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CLINICAL DIAGNOSIS
CASE EXAMINATION AND THE
ANALYSIS OF SYMPTOMS
BY '
ALFRED MARTINET, M.D.
PARIS. PRANCE
With thb Collaboration of
Drs. Desfosses, G. Laurens, LioN Meunier, Lutier,
Saint-C^ne, and Terson
AUTHORIZED ENGLISH TRANSLATION FROM THE THIRD,
REVISED AND ENLARGED EDITION
BT
LOUIS T. deM. SAJOUS, B.S., M.D.
PHILADELPHIA
WITH 895 TEXT ENGRAVINGS AND SEVERAL
FULL-PAGE COLOR PLATES
COMPLETE IN TWO ROYAL OCTAVO VOLUMES
VOLUME II
Analysis of Symptoms
JS^
PHILADELPHIA
F. A. DAVIS COMPANY. Pubushers
1922
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COPYRIGHT. 1922
BY
F. A. DAVIS COMPANY
CoprriKbt, Great Britain. AH Rights ReierTcd
PRESS OP
F. A. DAVIS COMPANY
PHILADELPHIA. U.S.A.
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CONTENTS.
PART III.
SYMPTOMS.
PAQB
Albuminuria 649
Alopecia 661
Anemia 675
Aphonia and Hoarseness 680
Arhythmia 693
The normal heart rhythm 694
Extra-systoles (premature beats) 700
Paroxysmal tachycardia 707
Respiratory (sinus) arhythmia 710
Auriculoventricular dissociation (heart-block) 714
Alternation of the pulse 726
Perpetual arhythmia (auricular fibrillation) 728
Ascites 737
Asthenia and Fatigue 751
Chills 757
Coma 759
Constipation 766
Convulsions 770
Cough 777
Delirium and Delusions 785
Diarrhea 790
Dyspepsia 796
Dyspnea 809
Edema 825
Epigastric Pain 833
Epistaxis 843
Exanthemata 847
Elementary and essential facts in dermatology 847
Main symptomatic features and course of syphilis 855
Main symptomatic features and course of the eruptive fevers 858
Expectoration 865
Eyes, Disorders of the 876
Examination of the eye and its adnexa 880
The principal ophthalmologic disorders 894
The principal eye conditions met with in general diseases 913
fiii)
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IV CONTENTS.
PAOB
Fainting 925
Fe\^r 929
Frequent Pulse ' 942
Genital Ulcerations 951
Glandular Enlargements 956
Glycosuria 969
Headache 976
Hematemesis 993
Hematuria 1003
Hemiplegia 1014
Hemoptysis 1029
Hiccough 1039
High Blood-pressure 1043
Hypochondrium, Left, Pain in 1058
Hypochondrium, Right, Pain in 1068
Iliac Fossa, Left, Pain in 1085
Iliac Fossa, Right, Pain in 1089
Insomnia 1101
Itching 1106
Jaundice 1119
Joint Pains. Arthralgia. Rheumatism 1128
Loss OF Weight 1137
Low Blood-pressure 1 145
Lower Extremities, Pain in 1153
Lumbar Pain. Backache 1170
Neck, Swellings in the 1182
Nervousness 1193
Obesity 1206
Oliguria 1218
Pain in the Side 1225
Plethora 1236
Polyuria 1240
Precordial Pain 1245
Sleep, Morbid 1271
Slow Pulse. Bradycardia 1285
Sore Throat 1290
Tinnitus Aurium 1294
Tongue, Diagnostic Features Relating to the 1297
Tremor 1308
Upper Extremities, Pain in 1313
Vertigo 1323
Vomiting 1332
Index of the Principal Clinical Signs 1343
Index to Volumes I and II 1353
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ILLUSTRATIONS.
WIQ. PAGB
498. Hairs in alopecia areata 602
499. Alopecia areata in a child 662
500. Microsporia 663
501. Hairs affected with microsporia 663
502. Tinea tonsurans due to the small-spored fungus. Microscopic aspect of a hair 664
503. Pieces of diseased hair 665
504. Diseased hair in tinea tonsurans of the large-spored variety in childhood 666
505. A hair in tinea favosa 666
506. Celsus's keiion 667
507. Congenital temporal alopecia 668
508. Alopecia due to x-ray exposure 669
509. Seborrhea decalvans of the vertex 670
510. Alopecia following erysipelas 671
511. Syphilitic alopecia 672
512. Tinea decalvans causing almost complete baldness 673
513. Brocq's pseudopelade variety of folliculitis decalvans 674
614. Paralysis of right recurrent laryngeal nerve. View during respiration 682
515. Paralysis of right recurrent laryngeal nerve. View during phonatlon j. 682
516. Paralysis of both recurrent nerves r 682
517. Indei>endeut paralysis of the laryngeal muscles, with the cords relaxed 683
518. Independent paralysis of the laryngeal muscles, with "button-hole" glottis .. 683
519. Partial paralysis of the posterior muscles of the larynx 683
520. Paralysis of the tensor muscles of the vocal cords 683
521. Diagram showing the course of the recurrent nerves 684
522. Horizontal section of the neck showing the position cf the recurrent nerves .. 685
523. Roseate vocal cords in acute catarrhal laryngitis 686
524. Button-hole glottis 686
525. Edema of the arytenoids 686
526. Broadened vocal cords In chronic laryngitis 686
527. Thickening of the Interarytenold tissues 686
528. The larynx In beginning tuberculosis 687
529. Tuberculous vegetations in the Interarytenold region 687
530. Thickening of a single cord in tuberculosis 687
531. Infiltration of the arytenoids in established tuberculosis 087
532. Infiltration of the epiglottis and ulcerations of the cords 687
533. Ulcerations of the vocal cords (glottic variety) 687
534. Gumma of the larynx 688
535. Ulcerated gumma of the larynx 688
536. Sessile nodule on the free margin of the vocal cord 688
537. Pedunculated polyp of the larynx 688
538. Papillomas of the larynx 688
539. Nodules on cords 688
(v)
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vi ILLUSTRATIONS.
FIO. PAOB
540. MaHfenaDt inflltratlon and Teseutlons immobilisiDg the vocal cord 689
541. Papillary Tegetatlons in cancer of the larynx 689
542. Extensive cancerous Inflltratlon of the larynx 689
543. Recurrent laryngeal paralysis, during respiration. During phonation 689
544. Paralysis of both recurrent nerves in goiter 690
545. The three causes of paralysis of the laryngeal muscles 691
546. Diagram of the bundle of His 695
547. 548. Jugular and radial pulse tracings 696
549. Normal electrocardiogram 697
550. Diagram showing the succession of motor events in the normal heart 697
551. The pneumogastric nerves 698
552. The nerves of the heart 699
553. Diagram of the nervous system as related to the circulation 700
554. Premature contractions during an attack of gout 701
555. Diagram of ventricular extra-systole or premature beat 702
556. Diagram of auricular extra-systole 703
557. Diagram of aurlculoventricular extra-systole 703
558. 559. Tracings of ventricular extra-systole 704, 705
560. Tracing of auricular and aurlculoventricular extra-systole 705
561. Tracing of aurlculoventricular extra-systole 706
562. Diagram representing a brief attack of fxaroxysmal tachycardia 70S
563. Tracing of paroxysmal tachycardia 709
564. Tracing of respiratory (sinus) arhythmia 711
565. 566, 567. Tracings of sinus arhythmia 711, 712
568. Diagram illustrating respiratory (sinus) arhythmia 713
569, 570. Tracings of Cheyne-Stokee rhythm 713, 714
571. Normal heart tracing 715
572. Tracing showing a tendency to aurlculoventricular dissociation 715
573. Diagram of partial heart-block 716
574. Diagram of complete aurlculoventricular dissociation 717
575. Tracing of extra-systole 718
576. Tracing of partial heart-block 719
577. Tracing of delayed conduction 719
578. Tracing of partial heart-block 720
579. Tracing of complete dissociation 720
580. Tracing of total bradycardia 720
581. Electrocardiogram of complete dissociation 721
582. Bradysphygmia counteracted by belladonna. Marked dilatation of aorta. Car-
diac-hypertrophy 722 -.
583. Cardiogram and sphygmogram from preceding case 723
584. Diagram of the alternating pulse 727
585. Diagram of auricular fibrillation 729
5S6. Electrocardiogram illustrating the 3 leads in a case of mitral stenosis with
auricular fibrillation 730
587, 588. Tracings of auricular fibrillation 731
589. Diagram of the normal heart rhythm 732
590. Diagram of extrasystoles 732
591. Diagram of paroxysmal tachycardia 733
592. Diagram of sinus (respiratory) arhythmia 733
593. Diagram of aurlculoventricular dissociation 733
694. Diagram of the alternating pulse 734
595. Diagram of auricular fibrillation 734
596. Abdominal areas of flatness in ascites and various other abdominal disorders.. 741
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ILLUSTRATIONS, vii
FIO. PAGE
597. The causes of ascites 743
598. The syndrome of Increased porta) pressure 744
599. Normal rhythm of urinary elimination, and opsiuria 746
600. Tributaries of the porUl vein 747
601. Diagram showing the nerve paths concerned in reflexes of the respiratory
tract 778
602. Diagram of fluoroscopic picture In localized cancer of the stomach 807
603. Diagram of fluoroscopic picture In cancer of the pylorus 807
604. Diagram of fluoroscopic picture In ulcer on the lesser curvature 807
605. Diagram of fluoroscopic picture In callous ulcer 807
60<S. Diagram showing the nerve paths concerned In reflexes of the respiratory
tract 809
607. Diagram of a terminal bronchus under normal conditions and during a par-
oxysm of asthma 811
608. Cheyne-Stokes breathing as observed during quiet and profound sleep 813
600. Chart from a case of auricular fibrillation and mitral stenosis 818
010. Cheyne-Stokes breathing 819
Gil. Dyspnea of myocardial fatigue and general exhaustion ^... 819
612. General topographic anatomy of the abdomen » ^ 833
613. Sagittal section of the abdomen 834
014. Surface projection of involved area in appendicitis, pancreatitis and chole-
cystlUs 835
615. The artery of eplstazls 843
616. Primary chancre of the vulva 852
617. Florid syphilitic roseola 852
618. Hypertrophic mucous patches of the vulva 852
619. Ulcerated syphilomas of the nose 852
020. Chicken-pox 864
621. Small-pox 864
022. Scarlet fever 864
023. German measles 864
624. Measles -v 864
62.5. Flortd measles eruption 864
026. Smear of sputum In "hemorrhagic bronchitis" 866
627. Vartous forms of the splrochaeta bronchlalis 866
628, 629. The sputum in chronic serous bronchitis 868
630. Mucoid sputum in acute bronchitis 869
631. Mucoid sputum in an asthmatic attack 869
0.32. Mucopurulent sputum in chronic pulmonary tuberculosis 869
633. Mucopurulent sputum in acute pulmonary tuberculosis 869
634. Purulent sputum In gray hepatisatlon 809
035. Purulent sputum In abscess of the lung 869
636. Fetid sputum in gangrene of the lung 872
637. Fetid sputum In fetid bronchitis 872
638. Rusty sputum in pulmonary Infarction 872
639. Rusty sputum in acute lobar pneumonia 872
640. Bloody sputum In gangrene of the lung 873
641. Bloody sputum in pulmonary tuberculosis 873
642. Bronchial false membrane 873
643. Alveolar cells containing pigment or dust particles in pneumonokoniosis 873
644. Lid elevator 870
645. Terson's eye speculum (blepharostat) 876
646. Ophthalmoscopic mirror 877
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viii ILLUSTRATIONS,
FIQ. PAGE
047. Ophthalmoscopic lens 877
G48. Disc with stenopeic opening 877
649. Electric pocket-lamp with speculum 878
G50. Armaignac's test chart* with a special chart for illiterates and the clock-dial
for astigmatism 879
651. Examining a child 882
652. Bent hairpin to be substituted for the lid elevator in an emergency 882
653. Inspection of the inner surface of the lower lid 883
654. Seizure and eversdon of the upper lid 883
655. Fixation of the everted lid 884
656. Eversion of the lid with the aid of a probe 884
657. Outward traction of the already everted upper lid 885
658. Rolling the lid about dressing forceps 885
659. Complete eversion of the upper cul-de-nac 885
660. Expressing the lacrymal sac 880
661. Lateral illumination with a lens 886
662. Lateral Illumination (examination with two lenses) , 887
663. Palpation of the eye to estimate the extent of fluctuation 888
664. Illumination of the eye with the mirror 889
665. Partial cataract, seen by transmitted light 889
666. Letters which a normal eye should be able to recognise at 5 meters 890
667. Examination of the field of vision with the perimeter 891
668. Normal visual fields 802
669. Pustular (phlyctenular) kerato-conjunctlvitis 897
670. Corneal ulcer 897
671. Corneal pannus and the upper lid in granular conjunctivitis 897
672. Hyphema 898
673. Hypopyon 898
674. Iritis with cellular exudation In the anterior chamber 898
675. Syphilitic iritis with granulomatous node 899
676. Profapse of the Iris 899
677. Synechiae in irlUs , 901
678. Complete umbillcoid occlusion of the pupil 902
679. Opacities in ttfe lens a 902
680. Muscles of the left eye 905
681. Course of the optic nerve-paths from the eye to the brain 910
682. Right homonymous hemianopia ^ 911
683. Bi-temporal heteronymous hemianopia 912
684. Central scotoma in an alcoholic subject 912
685. Temperature chart in the respiratory type of influenza 930
686. Temperature chart in frank pneumonia in an adult 931
687. Temperature chart In a case of acute miliary tuberculosis 933
688. Infectious pericarditis 933
689. Typhoid fever, with recovery 934
690. Malaria. Intermittent fever of quotidian type 935
691. Malaria. Intermittent fever, finally quartan 935
692. Intermittent fever of hepatic origin. Bllio-sepUc fever. Reversed type of in-
termittent hepatic fever. Fever in relapsing Jaundice 937
693. Diagram representing a brief attack of paroxysmal tachycardia 943
694. Diagram of experimentally induced tachycardia 944
695. Pulse chart in tachycardic neurosis 945
696. Paroxysmal tachycardia 94O
697. Tracings from an attack of paroxysmal tachycardia 947
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ILLUSTRATIONS. ix
FIO. PAGE
e&a. Chart from a case of post-infectious pericarditis with extensive effusion 948
(S99. Diagram of experimental tachycardia, after exercises 949
700. Axillary lymph-nodes 951
701. Hard chancre of the penis 962
702. Chancroidal pus, stained with methylene blue 952
703. Scrapings from hard chancre 952
704. 705. Unusual papulohypertrophlc chancroids of the balanopreputial region . . . 952
706. A burrow in scabies 954
707. Deep-seated vulTar herpes 954
708. 709. Vegetations on penis 964
710. Superficial lymph-nodes and the related anatomic regions 957
711. The blood in Hodgkins disease 963
712. The blood In tuberculous or other Infectious glandular enlargement 964
713. Lymphatic leukemia 905
714. Myeloid leukemia 965
715. Acute leukemia 966
716. Lymphosarcoma 966
717. Cut showing the relationship between -the frontal, ethmoid, and sphenoid
sinuses 976
718. Cut showing the relationship between the ethmoid sinuses and covering mem-
branes of the braJn 976
719. Head's cranial zones 977
720. Elective areas of fibrous thickening over of the skull, nucha, and neck 987
721. Posterior branches of the cervical nerves 988
722. Diagram of fluoroscopic picture in localized cancer of the stomach 995
723. Diagram of fluoroscopic picture In cancer of the pylorus 995
724. Diagram of fluoroscopic picture in ulcer on the lesser curvature 995
725. Diagram of fluoroscopic picture in callous ulcer 905
726. The arteries of the stomach 996
727. Blood-vessels of the gastric mucous membrane 997
728. SecUon of gastric ulcer .^ 998
729. The syndrome of high portal pressure 999
730. Section through the region of the bladder and membranous urethra 1004
731. Sources of the internal pudlc vein 1005
732. The three-glass test 1007
733. Diagram of the structure of the kidney 1009
734. Bllharzia ova 1010
735. Areas of paralysis In hemiplegia of cerebral origin 1015
736. The striate arteries and capsular hemprrhage 1016
737. Branches of the middle cerebral artery 1017
738. Diagram of the motor and sensory paths in the brain and spinal cord 1018
739. Areas of paralysis in peduncular hemorrhage 1019
740. Areas of paralysis in inferior pontine hemorrhage 1019
741. Anatomic relations In the medulla and pons 1020
742. Areas of paralysis In bulbar lesions 1021
743. Areas of paralysis In section of the cervical cord 1021
744. The medulla and pons 1022
745- Diagram of pulmonary infarction 1032
746. 747. Diagram of pulmonary Infarction 1033
748. Aneurysm of the pulmonary artery 1034
749. Diagram of a pulmonary lobule 1035
750. Diagram Illustrating the pathogenesis of hiccough 1040
751. The phrenic nerves 1041
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X ILLUSTRATIONS.
Fia. PAGE
752. Pulse tracing showing the successive variations of pressure In an artery .... 1043
753. Diagram Illustrating the systolic, diastolic, and pulse blood-pressures 1044
754. Blood-pressure determinations made a few days apart 1044
755. Diagram of vlscortty, pulse pressure, and urinary output In a normal subject 1048
750. Diagram of viscosity, pulse pressure, and urinary output in a plethoric .
subject 1050
757. Diagram of viscosity, pulse pressure, and urinary output in a subject with
sclerotic disease , 1054
758. Succeeslve stages In the development of cardlorenal sclerosis 1055
750. The splenic fossa 1058
700. Topographic features of the spleen 1059
701. Sagittal section through the left hypochondrium 1060
702. Deep-lying structures In the right and left hypochondria 1061
7«.'J. Arab children with malarial enlargement of the spleen 1063
764. Left-sided abscess between the liver and diaphragm 1064
705. Perisplenic abscess 1064
766. Post-gastric abscess 1064
767. Abscess between the liver and stomach 1064
768. Orthodiagrams from a case of gaseous gastric distention 1065
769. Anatomic relations of the liver with the chest and abdomen 1069
770. Alcoholic hypertrophic cirrhosis with ascites 1071
771. Alcoholic atrophic cirrhosis with ascites 1071
772. Bantl's disease IO71
773. Hepatoptosls IO71
774. Biliary cirrhosis with greatly enlarged spleen 1071
775. Bdliary drrhosU with enlarged liver and spleen 1071
776. Hydatid cyst of the liver IO71
777. Nodular cancer of the liver IO71
778. Cancer of head of pancreas IO71
779. Relations of the abdominal organs, viewed anteriorly 10T2
780. Kink at the first flexure of the duodenum 1073
781. Normal relaUons of the right kidney with the hepatic flexure and duodenum 1073
782. Anteroposterior section of the liver 1074
783. Vertlcotransverse diagrammatic section through the gall-bladder 1075
784. Right-sided abscess between the diaphragm and liver 1075
785. 786. Points of tenderness In the right hypochondrium 1076
787. Evacuation of a subdiaphragmatic abscess IO77
788. Indslon of a subdiaphragmatic abscess 1078
789. Cavities that may be occupied by pus in peritonitis 1079
790. Normal relations of the sigmoid flexure and rectum io85
791. Radiographic view of the large intestine 1086
792. General topographic features of the abdomen IO90
793. Topography of the abdomen IO91
794. Topographic features of abscesses of appendiceal origin 1092
795. Combined appendicitis and adnexitis IO93
796. Radiographic picture of the cecun^ and appendix 1095
797. Vessels and nerves of the anterior abdomJnal wall 1097
798. Scabies. Places of election for burrows HH
799. Burrow containing a female itch-mite and her ova 1112
800. Sarcoptes scablei, female, dorsal aspect III3
801. Sarcoptes scabiet. female, ventral aspect 1113
802. Pedlculus capitis, male m^
803. Ovum of pedlculus capitis attached to a hair III4
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ILLUSTRATIONS. xi
no. PAQB
804. Phthlrtus pubis 1114
806. Pemculotfis or pbtWrtaels. Areas of election 1115
806. Chart of a case with loss of weight and lowered hlood-pressure 1137
807. Gradual retrogression In a cardlorenal case with good compensation 1138
806. Chart from a case of cardlo-arterlo- renal sclerosis 1139
809. Bilateral tabetic knee-joints 1156
810. Lumbosacral and hypogastric plexuses In the male 1158
811. Lumbosacral and hypogastric plexuses In the female 1150
812. The greater sciatic nerve 1161
813. Vallelx's points on the posterior aspect of the lower extremity 1162
814. Roussy's algn in left-sided sciatica 1163
815. 816. Roussy's sign In right-aided scIaUca 1164. 1165
817. The lumbar plexus • 1166
818. Relations of the Intervertebral foramina with the lumbar spinal ganglia .... 1167
819. The nerve paths from the spinal cord to the periphery 1168
820. Lumbar musculature 1170
821. The spinal muscles H'l
822. Transverse section through the lumbar region 1172
823. Posterior relations of the kidneys 11'7«'^
824. 825. Osteospondylltis of the vertebr» 11^4
826. 827. Intraspinal venous plexuses ^^'^'^
828- Diploic veins in the body of a vertebra ^^'^
829. Anterior surface of the neck ^^^'^
830. Lymphatics of the head and neck ^^^^
831. Adenollpomatoais ^^^^
832. Deep structures of the neck ^^^'^
833. Exophthalmic goiter ^^^^
834- Diagram of the symptoms and pathogenesis of exophthalmic goiter 1190
835. Longillnear subject 1210
836. Mediollnear subject ^211
837. BreviUnear subject 1211
838 to 841. Anterior, posterior, and lateral topographic features of the chest — 1226
842. Anatomic relations of the heart 1227
843. Anatomic relations of the Intercostal nerves 1228
844 to 847. Head's sones 1229, 1230
848. Segmental cutaneous distributions of the nerves of the trunk 1231
849. Cutaneous branches of the intercostal nerves 1232
850. Horizontal cross-section of the chest of a new-bom infant 1246
851. Orthodiagram of a case of a^rophagia with dyspnea on exertion and precor-
dlalgla 1251
852. The nerves of the heart 1257
853. Diagram of the nervous system as related to the circulation 1258
854. Tracings showing premature contractions 1262
855. Blood-pressure chart of a normal Individual 1262
856. Normal subject as regards the circulation 1263
857. Heart weakness 1263
858. 859. Cardiac neurosis 1263
860. Aortic aneurysm with elevated pulsating tumor 1267
861. Aortic aneurysm with pulsating tumor 1268
862. Diagram of the normal heart-rhythm 1285
863. Diagram of delayed conduction 1285
864. Diagram of partial heart-block 1280
865. Diagram of complete aurtculoventricular dissociation 1286
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xii ILLUSTRATIONS.
PIO. PAQB
866. Tracing of delayed conduction 1288
867. Tracing of partial heart-block 1288
868. Tracing of complete dlssodaUon 1288
869. Tracing of total bradycardia 1288
870. Tracing of bradycardia due to a gumma of the bundle of His 1289
^71. Tracing of total bradycardia due to depressive psychoneurosis 1289
872. Mode of production of tinnitus aurlum 1295
873. Dorsal surface of the relaxed tongue 1298
874. Extensive gummatous ulceration of the tongue 1302
875. Tertiary syphilitic sclerosis of the tongue 1302
876. Actinomycosis 1305
877. Macroglossla 1306
878. Tuberculosis of the tongue- 1307
879. Diagram concerning the innervation of the upper extremity 1313
880. Peripheral sensory distribution in the upper extremity (posterior adpect) .. 1314
881. Peripheral sensory distribution in the upper extremity (lateral aspect) 1314
882. 883. Common types of distribution of the sensory disturbances in section of
the radial nerve 1315
884. Peripheral sensory distribution in the upper extremity (anterior aspect) — 1316
885, 886. Palmar and dorsal disturbances of sensation in severe injuries of the
median nerve 1317
887. Nerve-supply of the muscles of the upper extremity 1319
888. Distrtbution of pain and hyperalgesia after repeated attacks of angina
pectoris 1320
889. Pathogenesis of vertigo 1324
890. Diagram illustrating aural vertigo 1328
891. The causes of aural vertigo 1329
892. Pathogenesis of vomiting 1333
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^^ Felix qui potuit rerum
cognoscere causas.^^
PART III.
SYMPTOMS.
In the practice of medicine the PROBLEM OF DIAGNOSIS is
often put before the physician in the folloiving manner: A pa-
tient comes to consult him because of some concrete abnormal
condition; he is coughing, he is losing weight, he is sleepless, he
has spat up blood, his skin is yellow, he has **kidney" pains, his
skin itches, he has attacks of fever, he suffers from headache,
he feels tired, etc. This presenting symptom must be traced
bcKk to its underlying cause. This is done by means of a verbal
and physical examination which enables the practitioner to group
about the principal symptom — principal at least in the patient's
estimation — the remaining necessary data, signs, and symptoms;
— in short, by a mental correlation of these data.
In the succeeding presentation of the subject a plan closely following
the observations of ordinary practice has been adopted. In it
have been collected the most frequently encountered symptoms,
and in relation to each of these symptoms, after a brief review
of the related anatomical and physiological features, the author
has endeavored to explain how, with the assistance of the previa
oiis or concomitant accessory symptoms, and in the light of
these data, a concrete diagnosis may be arrived at.
Wherever it has seemed possible, each section has been summarised
in the form of a diagrammatic, mnemotechnic table.
(647)
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ALBUMINURIA.
Albumin, white of egg^^^vpelv^ to
urinate. Presence of albumin in
the urine.
Albuminuria is a sign which should never be allowed to
pass unnoticed. The test for albumin in the urine should be
carried out as regulariy and routinely as auscultation of the
chest or palpation of the abdomen. Two observations will give
an idea as to its frequency of occurrence. Out of 1000 subjects
of both sexes and of all ages, the great majority suffering from
chronic conditions, examined in the author's office, 204, i.e.,
about one-fifth of the cases, showed albtunin. In over half of
these persons albuminuria had not previously been known to
be present. Out of 1000 soldiers from twenty to forty-eight
years of age under observation in a hospital, the great majority
suffering from acute or subacute conditions, the author found
128 instances of transient or permanent albuminuria, constitut-
ing about one-eighth of the entire number.
Thus, albuminuria occurs with extraordinary frequency and
under the most varied clinical conditions. Its symptomatic
value, while sometimes practically nil, may be very great. In
finding our way through the etiologic and pathogenetic maze
of the various forms of albuminuria, the didactic presentation
of the subject by Castaigne in his work entitled "Livre du mede-
cin" (section on diseases of the kidneys) will be extensively
availed of.
Clinically, albuminuria occurs in the form of :
I. Acute albuminuria, always symptomatic of an acute or sub-
acute, infectious or toxic, nephritis which is comparatively easily
diagnosed.
II. Chronic albuminuria, which, on the contrary, as we shall
presently see, arises from a great variety of causes and the
etiologic diagnosis of which is often a matter of considerable
difficulty.
(649)
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650 SYMPTOMS,
ACUTE FORMS OF ALBUMINURIA.
Acute albuminuria is met with almost exclusively in the
following four groups of cases : (a) Superficial and transitory acute
nephritis; (i?) typical acute nephritis; (c) hyperacute nephritis;
{d) acute exacerbation in. the course of a chronic nephritis.
(a) Superficial and transitory acute nephritis is a clinical
type which is mild and very common and the presence of which
should he ascertained through systematic examination of the
urine in all infectious or toxic diseases (sore throat, grippe, pneu-
monia, acute gastric indigestion, enterocolitis, etc.).
The albuminuria is the constant sign of such a nephritis; in
degree it generally ranges between 0.1 and 0.5 gram of albumin
per liter of urine, but it may become more pronounced. It
persists throughout the fastigium of the infectious or toxic dis-
order, but as a rule passes off shortly before the beginning of
convalescence. It is clinically limited to a moderate and transi-
tory albuminuria, accompanied by very " slight, temporary dis-
turbance of the renal functions, erythrocytes, leucocytes, and
granular casts appearing for a time in the sediment. Complete
and permanent recovery from it is the rule, though the physi-
cian should be somewhat guarded* concerning the passage of
these cases of nephritis into a chronic involvement, which is,
however, exceptional.
(&) T3^ical acute nephritis is met with under the same con-
ditions as the preceding group, i.e., generally in connection with
and during the course of an acute infection, definite or obscure.
It is characterized by three cardinal groups of signs by which it
may easily be recc^ized, and the following summary of which
is adapted from Castaigne.
1. The urinary syndrome, which may be summarized as
follows: The urine is scanty, highly colored, comparable to
turbid bouillon, sometimes reddish, and even occasionally ex-
hibiting hematuria. The specific gravity is high, and the re-
action distinctly acid ; chernical examination generally reveals
a marked diminution of the urea and chlorides, together with
a large amount of albumin. Histologic examination of the
urinary sediment shows the presence of red blood cells, leuco-
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ALBUMINURIA. 651
cytes, and casts of all kinds, among which the granular type is
always present. The various clinical procedures recently recog-
nized (blood-pressure, methylene blue test, and determination
of the blood urea) point to a manifest impermeability of the
kidneys.
2. Edema is seldom wanting in the typical forms. It is
sometimes localized in distribution, as in the lower extremities,
the eyelids, and even the glottis, but more often it assumes the
type of a generalized anasarca with effusion in the serous cavi-
ties— pleura, pericardium, and peritoneum — and even in the vis-
cera, particularly the brain, liver, and kidneys.
3. S3niiptonis due tb impermeability of the kidneys are
almost regularly present, but are, as a rule, limited to relatively
mild manifestations such as headache, cramps, tinnitus, ocular
disturbances, dyspnea, vomiting, etc.; in some instances, how-
ever, all the signs of a major attack of uremia may be witnessed,
ttz,, eclamptic seizures, acute delirium, and coma.
4. Evidences of an infectious process may be superimposed
upon the foregoing symptoms, involving either the kidneys
alone or the organism as a whole.
The lumbar pain, sometimes very pronounced, and which
may be the initial symptom, is due to an infectious process
localized in the kidneys; again, palpation will reveal enlarge-
ment of both kidneys in these cases.
Infection of the entire organism is manifested in more or less
pronounced fever, an enlarged liver and spleen, and leucocytosis
— all showing that the infection has not been exclusively local-
ized in the kidneys.
This is the type of albuminuria met with in typhoid fever, pneu-
monia, acute sore throat, scarlet fever, influenza, etc.
(c) Hyperacute nephritis is usually a result of the condition
of intoxication following exhibition of agents highly destructive
to the kidneys, such as corrosive sublimate, phosphorus, cantharides,
etc. The patients are previously healthy persons who have ingested
one of these poisons in considerable amount and develop almost
complete anuria on the same (fey ; the few drops of urine collected
by catheterization are found to contain much albumin and many
casts.
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652 SYMPTOMS.
In the majority o£ cases, anuria remains complete in spite
of all attempts at treatment and the patient dies in coma five
to ten days after the beginning of symptoms, generally without
having shown edema or convulsive manifestations.
Thus, anuria, coma, and death may be said to summarize the
clinical picture, the entire illness being gone through without the
patient developing any edema or. signs of advanced uremia. The
ratio of blood urea may rise very high. In one such case the
author found 5.60 grams of urea per liter.
This applies not only to the hyperacute nephritis following acute
intoxication in a previously healthy person, but likewise in the much
more uncommon cases of hyperacute nephritis appearing during
the fastigium in acute diseases such as typhoid fever, scarlet fever,
pneumonia, etc.
Recovery is altogether exceptional. Passing- mention may
be made of the marked therapeutic utility of isotonic or hyper-
tonic glucose or lactose solution in these cases.
(d) Acute exacerbations in chronic nephritis. — "These might,
by the uninitiated, be mistaken for acute nephritis. The prog-
nosis in these cases is that of the form of chronic nephritis upon
which the acute congestive exacerbation has been superim-
posed." (Castaigne).
CHRONIC FORMS OF ALBUMINURIA.
"The etiologic circumstances under which chronic albumin-
uria may be encountered are complex and should be divided
into several main classes, which the physician may call to mind
when confronted with a case of chronic albuminuria, He, 1.
Chronic nephritis. 2. Chronic infections. 3. Chronic toxic and
autotoxic states. 4. Circulatory disturbances.'' (Castaigne).
I. Albuminuria of chronic nephritis. — Albuminuria having
been found to exist, it is necessary to know what variety of
chronic nephritis is present and to what extent the renal func-
tions are impaired. A systematic investigation should, there-
fore, be made of:
(a) The elimination of chlorides, by examining for edema
and, if need be, estimation of the chloride balance.
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ALBUMINURIA, 653
(b) The elimination of nitrogen, by examining for the cus-
tomary signs of nitrogen retention and, in particular, by deter-
mination of the blood urea and, if need be, by calculation of
Ambard's coefficient
(c) The elimination of water, by determination of the systolic
and diastolic blood pressure and comparison of the 24-hour out-
put of water with the pulse pressure, as well as, if need be, by
calculation of Martinet's coefficient:
24-hour output
pulse pressure
Systematic study of these three forms of elimination leads
rationally to the following classification of the chronic nephri-
tides :
1. Simple chronic albuminous nephritis, exhibiting, apart
from the chronic albuminuria, no indication of chloridemia, azo-
temia (nitrogenemia), or hydremia; no edema, no azotemic man-
ifestations, and no elevation of blood-pressure.
2. Chronic chloridemic nephritis of Widal, or hydropigen-
ous nephritis of Castaigne, characterized chiefly by a retention of
chlorides which is clinically manifested in edema, without appre-
ciable high blood-pressure or nitrogen retention.
3. Chronic azotemic nephritis — or uremigenous nephritis, as
formerly designated by Castaigne — characterized mainly by
a nitrogen retention which is manifested in a rise in the blood
urea and a large number of the classical symptoms of the uremic
syndrome, znz,, headache and even rigidity of the neck, neuralgic
pains, vertigo, dyspnea, general torpor, myasthenia, coma, con-
vulsions, delirium, anorexia, nausea, vomiting, diarrhea, etc.
4. Chronic hydremic nephritis (of Martinet), or hyperten^
sive nephritis (of Potain and Widal), characterized by a reten-
tion of water which is manifested in high Wood-pressure,
hydremia (anemia and lowered blood viscosity), and consequently,
by predominant cardiovascular manifestations, such as accentuation
of the second aortic sound, sometimes gallop rhythm, various
forms of hemorrhage due to rupture of vessels (epistaxis; retinal,
meningeal, and cerebral hemorrhages, etc.) followed eventually
by cardiac impairment and dilatation, tachycardia, arhythmia.
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654 SYMPTOMS,
loss of compensation, etc. The condition begins with cardio-
renal sclerosis and leads ultimately to heart failure and uremia.
In contrast with the simple albuminous and chloridemic va-
rieties of nephritis, the last two forms, the azotemic and the hy-
dremic, frequently coalesce, so that, the azotemic and hydremic
syndromes being in combination, the clinical picture comprises
both the cl^ssfe uremic symptom-complex already referred to and
the equally wdl-known cardioarterial symptom-complex at-
tending cardiorenal fibrosis. By combined use of the three pro-
cedures now available: 1. Determination of blood urea. 2. Of
the blood-pressures, systolic and diastolic. 3. Of the extent of
hydremia and anoxemia (as estimated through the blood viscos-
ity, by refractometry, by estimation of proteins in the blood
serum, etc.), it is at present possible for us to differentiate, in
these ultimate complex processes, that which specially apper-
tains to nitrogen retention from that which refers to retention
of water, to anoxemia, to impaired cardiopulmonary function-
ing, and to cardiorenal insufficiency.
II. Albuminuria of Chronic Infections. — Albuminuria is very
often met with in the presence of chronic infections, such as
tuberculosis, syphilis, malaria, etc., and it is of advantage from
the standpoint of therapeutic indications to establish the con-
currence of a chronic albuminuria with one of the chronic in-
fections referred to. As in the chronic nephritides, however,
the prognosis is largely based, it would seem, on the functional
variety of nephritis present — simple albuminous nephritis, or
hydremic, chloridemic, or azotemic nephritis.
III. Albuminuria of the Intoxications. — **In this connection,"
states Castaigne, **three sorts of toxic actions may be distin-
guished :
**The strong toxics (cantharides, corrosive sublimate, and
arsenic in large amount) which induce acute, and in particular
hyperacute, nephritis.
**The weak toxics acting rapidly and not taken repeatedly
(taken in a single dose) which induce a temporary albuminuria.
''The toxics taken in small but repeated amounts, and acting
slowly (lead) : these give rise to all the varieties mentioned in
respect of the albuminurias of chronfc nephritis; thus, it may
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ALBUMINURIA, 655
be said that, in the case of intoxications as in that of infections,
etiologic data do not suffice to illuminate the prognosis/*
IV. Albuminuria of Autointoxications. — This comprises in par-
ticular the albuminurias of pregnancy, of diabetes, and of gout.
(a) Albuminuria of pregnancy. — With Castaigne, we shall
recognize a number of different varieties, which differ widely
in significance and seriousness.
1. Albuminuria of pregnant zvonten who already had albumin-
uria before pregnancy.
2. True albuminuria of pregnancy, in which the autointoxi-
cations of the latter condition are responsible for the albuminuria.
The prognosis in these cases is based upon a study of the renal
functions.
3. Albuminuria attending the pyelonephritis of pregnancy,
with pyuria, and the seriousness of which is dependent upon the
intensity of the phenomena of retention and infection.
4. The transient and mild albuminuria of labor.
5. Postptierperal albuminuria, dependent, on the whole, upon
infection, and the prognosis of which is that of the acute infectious
nephritides.
(b) Gouty albuminuria. — Measures should be taken to find
out whether the condition is:
1. A simple albuminous chronic nephritis. 2. A hydremic ne-
phritis with hypertension, secondary to spasm of the vessels or
to cardiorenal sclerosis. 3. A calculous pyelonephritis.
(c) Diabetic albuminuria. — The significance of this form is
closely analogous to that of gouty albuminuria.
V. Chronic Albuminuria of Circulatory Origin, — This type
is found dependent upon two main series of causes, inc., cardiac
and neuromotor disturbances (Castaigne).
(a) Cardiac albuminuria. — This is the albuminuria which
appears at the time of attacks of acute heart dilatation or failure
and seems to be dependent upon the disturbance in the return
circulation, i.e., venous stasis. It generally disappears when the
process of cardiac weakening ceases. Where it persists, it should
be studied along the same lines as were advised in the case of
chronic nephritis.
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656
SYMPTOMS.
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658 SYMPTOMS.
(b) Neuromotor albuminuria. — ^This is the form which ap-
pears following vascular disturbances after nervous conditions
such as epileptic seizures, cerebral hemorrhage, trauma to the
skull, etc.
"Cases of this kind may be hard to interpret, and the physi-
cian should not be in a hurry to make a diagnosis of uremia
because the patients show albuminuria consentaneously with
the cerebral manifestations ; only the classic tests will permit of an
accurate prognosis of these combined disturbances.'* (Castaigne).
CRYPTOGENIC OR "FUNCTIONAL"
ALBUMINURIA.
Aside from the above mentioned groups of acute and chronic
albuminuria which may be more or less readily referred to a
known cause, there occurs also a relatively large number of
cases of albuminuria which have not yet been completely worked
out, and for which tradition has preserved the term, very prob-
ably inaccurate, of functional albuminuria; the term cryptogenic
albuminuria, which mentions our ignorance of its cause without
making any premature assertion as to its nature, seems to the
author more rational.
The most frequent of these cryptogenic albuminurias are
those known as the fatigue, digestive, cyclic, orthostatic, and
intermittent and minimal albuminurias.
The albuminuria of fatigue, which occurs intermittently and
is slight in amount, appears only after prolonged, fatiguing ex-
ercise, such as hiking, running, horseback riding, etc., and gen-
erally disappears with rest.
The digestive albuminurias are those which arise or become
accentuated during the process of digestion, whether the sub-
jects be dyspeptic, enteritic, or normal. The relationship of
cause to effect can be established only by repeated, fractional
analysis of samples of gastric juice withdrawn at various stages
of digestion, every precaution being taken, moreover, to eliminate
orthostatic albuminuria.
The cyclic albuminurias are those appearing in a cyclic man-
ner, at certain periods of the day, generally between 1 and 3
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ALBUMINURIA, 659
o'clock P.M. Described more particulariy by J. Teissier and
Pavy, they seem to be dependent upon some degree of insuffi-
ciency (or debility) of the liver and kidneys.
In orthostatic albuminuria, the standing posture is the sole
necessary and sufficient factor of the albuminuria, which passes
off when the subject reclines. It is especially frequent in child-
hood.
The intermittent and minimal type of albuminuria, well de-
scribed by its name, is a slight (0.1 to 0.2) and intermittent
albuminuria, which appears and disappears without any sort of
periodicity, independently of all fatigue, digestive process, or
body posture; this constitutes the most cryptogenic of all the
forms of albuminuria.
Long considered to be of a "functional" nature — sine materia
— as well as mild, this form of albuminuria has been the subject
of a long series of discussions, which have led to the conclusion
that, like all the other forms of albuminuria, this clinical group
may be symptomatic of a large variety of morbid states, from
the mildest and most evanescent functional disturbance to the
most definite chronic nephritis, and that the accurate functional
diagnosis necessary for the institution of an appropriate, rational
and effectual plan of treatment can be secured only by a syste-
matic study of the renal functions (hydruria, chloruria, and
azoturia) by the required methods: 1. Hydruric balance: Blood-
pressure, daily output of urine, and blood viscosity. 2. Chloride
balance: Chloride test and examination for edema. 3. Nitrogen
balance: Determination of the blood urea.
Mention may also be made of artificial or simulated albu-
minuria, of which some instances were observed during the war.
Albuminuria is simulated by mixing some white of egg with
the urine, either before or after urination, or even by intraureth-
ral or intravesical injection of a solution of egg albumin. Strict
isolation of the suspected individual, careful watching, and col-
lection of the specimens of urine for examination under direct
supervision will readily lead to detection of the artifice. (See
Examination of the Urine.)
In this connection a final word may be said regarding the
relationship of albuminuria to fitness for military service. The
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660 SYMPTOMS,
main conclusion from the foregoing facts is that, on the whole,
albuminuria is of relatively slight, and renal functioning of para-
mount, importance in relation to the prognosis, and hence also
in relation to military fitness. The essential point, therefore,
is to ascertain the condition of renal functioning in each case.
The author is entirely prepared to subscribe, with a few slight
modifications, to the conclusions stated by Gilbert (RSunion midico-
chirurgicale de la Ve armie, Oct. 28, 1916) : An albuminuric sub-
ject, to be kept in the armed service, must answer the following
requisites: 1. A fixed amount of albumin, uninfluenced by exposure
to cold, the standing posture, food conditions, and fatigue. 2.
Absence of casts. 3. Blood urea normal, and urinary urea paral-
lel to the nitrogenous food in the diet 4. Absence of edema,
with a normal chloride balance. 5. No pronounced elevation
of blood-pressure (below 180), and no gallop rhythm. A de-
cision can be reached in such cases, therefore, only after pro-
longed and careful study.
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ALOPECIA (COMPLETE
OR PARTIAL LOSS OF
THE HAIRY APPEND-
AGES).
Lat. alopecia;
from the Greek n dXa>7f€;(^ta,
derived from ^ d^nrj^y
the fox.
"Comme il advient au regnart que son poil
chiet une fois ran, aussi est appeli le choir des
cheveux allopice"^
Lanfranc, folio 38, verse XIV
in LiTTRi, article Renard,
Even the general practitioner is frequently consulted by pa-
tients on account of loss of hair. While not a few uncommon
varieties of alopecia are very difficult to diagnosticate, even —
and perhaps, especially — for the specialists, in 9 cases out of 10
the general practitioner may rapidly make such distinctions as
are necessary for the application of suitable treatment.
According as the patient is a nursling, a child, an adult, or
an elderly person, the diagnosis should be oriented, a priori, to the
most frequent forms of alopecia at the patient's age.
In the Nursling. — In this group the condition is practically
limited to:
1. Occipital alopecia, the result simply of wearing away of
the hair on the pillow; the occiput is the area affected, and the
area is ovoid in shape with its long axis directed transversely.
2. Congenital alopecia. — As a matter of fact, it is more par-
ticularly as the patient grows older that this form of alopecia
begins to attract attention.
In the Ohild. — Special thought should be given to the possi-
bility of alopecia areata, ringworm, and cicatricial alopecia in
this group of cases.
1. Alopecia areata. — ^The following lines are reproduced from
Sabouraud's description of this condition: "This is a primary
» "As it happens to the fox that his hair falls out once a year, even so
is loss of the hair termed allopicia."
(661)
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662
SYMPTOMS.
form of alopecia, which is not preceded by any functional mani-
festation . . . The hair is lost either diffusely over a limited
Fig. 498. — Hairs in alopecia areata, viewed with a magni-
fying lens (Sabouraud).
region, or as a patch which becomes completely bald from the
start . • . The bald surface is irregular in outline, of varying
Fig. 499. — Alopecia areata in a child (Sabouraud) .
shape, smooth, and devoid of any abnormal feature. It may
become definitely limited or arrested, or even undergo recession.
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ALOPECIA. 663
at any time; on the other hand, it may extend until the entire
scalp and the body surface as a whole has lost its hairy cover-
ing. Upon the scalp, extending areas of the disease are marked
by the presence of the typical club-shaped hair stumps, either
singly or in groups or streaks . . . Such a hair, which is
suggestive of the exclamation point in ordinary printing type,
Fig. 500.— Microsporia (Sabouraud), Fig. SOL— Hairs af-
fected with microsporia,
seen with a magnifying
lens (Sabouraud).
is one in process of atrophy ; it is like a portion of a needle with
its point embedded in the skin, etc."
Alopecia areata generally sets in in children between four
and seven years of age and, aside from the severe and recurring
forms, is spontaneously recovered from in from six months to
two years.
2. Ringworm. — (a) Tinea tonsurans due to the small-spored
fungus (microsporia) is the commonest form among the tineas,
i,e., diseases of the epidermis and hair caused by a cryptogamic
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664 SYMPTOMS.
microparasite. "It is characterized by dry, scaly, grayish patches
2 to 5 centimeters in diameter, nearly round and with rather
well circumscribed margins. The very first glance at the af-
fected area reveals that the hairs at the surface of these patches
are less numerous than normally. Of these hairs, a very few
have retained their normal features. The others, the ringworm
hairs, are short, broken off at a distance of 3 or 4 millimeters
above the skin surface, decolorized, and apparently covered with
Fig. 502. — Tinea tonsurans due to the small-spored fungus. Micro-
scopic aspect of a hair (Magnified 3(X)X). Some of the spores are seen
by transmitted light (R, Sabouraud).
a grayish shell. The hairs thus affected break off flush with
the skin when depilated. Ten or twelve grayish pieces of hair
may thus be pulled out at once between the fingers. The possi-
bility of thus depilating the surface with the fingers distinguishes
this form of tinea from all others." (Sabouraud).
Microscopic examination of the hair will confirm the diag-
nosis.
"When heated between 2 slides in a drop of caustic potash
solution and examined at a magnification of 100 to 300 diameters,
such a hair reveals a cortex of very small and refractile spores,
arranged in irregular apposition and forming a kind of shell
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ALOPECIA. 665
about the hair. . . . The hair appears like a little rod covered
^vith glue and then rolled in sand/'
This condition is less frequently met with in Paris than the
succeeding one, and is rare in children of less than three or
more than thirteen years of age.
(b) Tinea tonsurans due to the large-spored fungus (tricho-
phyton or school type). — This is, in general, less frequent than
the preceding condition. When left untreated, it is characterized
by numerous small areas of involvement, each of which might
easily be covered by the fihger-tip, and which are marked by a
^^
Ck y^
Fig. 503. — Pieces of diseased hair viewed with a magnifying lens, being
seen as they appear beneath the scale (Sabouraud).
small aggregation of adherent scales, presenting the appearance
of a dry scab. The diseased hair is gummed over and sur-
rounded by the scale. In order to see it, the latter must be re-
moved and its deep surface examined ; there are then seen pro-
jecting from it little white rootlets, short and curved over. Mic-
roscopic examination of these rootlets will remove all doubt.
Upon preparation by the technic above described, the parasite
is found to consist of spores much larger than those of the pre-
ceding variety and disposed in regular series or chains and in
groups of parallel, slightly wavy filaments.
This variety of ringworm of the scalp, which is at present the
commonest among the school children in Paris, generally occurs
in girls four to fifteen years of age, though occasionally persist-
ing to the age of sixteen or eighteen years.
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666 SYMPTOMS.
(c) Tinea favosa. — In contrast with ringworm of the scalp,
which is more particularly a disease of urban populations, favus
is a rural variety of tinea.
Fig. 504. — Diseased hair in tinea tonsurans of the large-spored
variety in childhood (Sabouraud).
"It invades the scalp only in individuals of school age, but
as it is never spontaneously recovered from, it may be encount-
Fig. 505. — A hair in tinea favosa (Sabouraud).
ered at any period of life. In its ordinary form (favus scutulum)
the disease is characterized by one or more irregular but sharply
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ALOPECIA, 667
circumscribed patches, covered with sulphur yellow crusts,
aiul of the color as well as the consistency of clay. The in-
dividual, separate crusts are rounded, annular, and of all differ-
ent sizes, the largest, which measure 1 to 2 centimeters in diam-
eter, showing a series of wave-like circular elevations.
"Of these cup-like formations, the smallest form simply a
ring about the hairs. The cups are pierced by the hairs and
• Fig. 506. — Celsus's kerion (Sabouraud) .
partly embedded in the skin. They may be detached without
great difficulty, in pieces ; in their stead is left a bleeding wound
which appears to extend rather deeply in the tissues.
"A hair affected with favus exhibits a mycelial parasitic
growth composed of a few irregular, wavy, and frequently dead
filaments; in the latter condition their course is shown by a
clearly distinct air bubble of similar shape. The living mycelial
filaments consist of segments of rather variable size and shape,
with some spore-bearing portions."
(d) In connection with the above disorders may be men-
tioned certain trichophyton invasions of animal source, e.g.,
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668 SYMPTOMS.
from the horse, dog, cat, or sheep, tending toward suppuration
and leaving behind a permanent cicatricial alopecia. Among
this group is the so-called kerion of Celsus.
(e) Under the general term cicatricial alopecias may be in-
cluded the patches of alopecia, generally circumscribed in more
or less well-defined islets, which follow impetigo, furuncle, or
trauma. The scar-like fibrous condition of the skin in the affected
area, in conjunction with the history, inevitably lead to the
proper diagnosis if the case is carefully investigated.
(/) Congenital temporal alopecia is of importance only by
reason of the mistakes in diagnosis (alopecia areata) to which
Fig. 507. — Congenital temporal alopecia (Sabouraud),
it may lead. The condition occurs on either one or both sides
of the head — in the latter case symmetritally — and is marked
by an oval bald area 2 centimeters long and lyi centimeters
broad situated on the temple and directed obliquely upward
and backward.
(g) The diffuse alopecias of childhood comprise particularly
the infectious and post-infectious alopecias (typhoid fever, oste-
omyelitis, eruptive fevers, etc.), but are generally much less pro-
nounced in children than in the adult.
(h) Lastly, mention may be made of the alopecia following
application of the x-rays. The hair falls out twenty to thirty
days after depilation with the rays, and begins to grow out
again two and a half months after the exposure — unless there
results an actual radiodermatitis causing, even when slight, a
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ALOPECIA. 669
permanent alopecia, A mistake in diagnosis in this connection
cannot possibly be made. The regular, romided shape of the
bald area, suggesting a tonsure, is in itself sufficient evidence
for a positive diagnosis. The ritual alopecia of the clergy alone
exhibits such a circular shape of the bald area and the same
relatively large size.
4t 4t 4t
In the Adult. — In this group there are more particularly en-
countered: Seborrhea decalvans, the ordinary baldness of male
Fig. 508. — Alopecia due to- x-ray exposure (Sabouraud) .
neuro-arthritic subjects; the scaly alopecia pityrodes of women,
and the various infectious and post-infectious alopecias, a sepa-
rate place being reserved for syphilitic alopecia and various con-
ditions suggesting alopecia areata but as yet of uncertain origin.
(a) Seborrhea decalvans (the ordinary baldness of men). —
"This presents as its objective sign and fundamental lesion a
cylindrical plug of fat contained in the sebaceous duct and which
is caused by pressing on the skin to emerge from the duct in
the form of a small vermicular mass or rudimentary comedo.
This plug of fat is the seat of a bacterial colony consisting ex-
clusively of the microbacillus of seborrhea.
"The alopecia attending seborrhea is much less diffuse than
that of pityriasis ; it is located at the vertex, over the very area
at which baldness is later to result ... As a rule, the earlier
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670 SYMPTOMS.
in life seborrhea of the scalp sets in the more rapid its course.
When it begins at the age of 18 it results in complete baldness
at 25 years, some 200 to 400 hairs falling out each day. When
it sets in at the age of 25, it results in partial baldness only at
55 to 60 years ; from 50 to 60 hairs are lost a day, the number
varying according to the season of the year."
Sometimes this local condition appears to be associated with
Fig. 509. — Seborrhea decalvans of the vertex. Common baldness in
process of development (Sabouraud),
or secondary to that rather indefinite, though frequently en-
countered diathesis: neuro-arthritism.
(b) Alopecia pityrodes. — In women this plays a role as im-
portant as seborrhea does in man. One half of all women show
some evidence of this disturbance, which should be thought
of a priori by the physician whenever a young woman consults
him on account of loss of hair. From the age of 10 years to 20
years the affected scalp is found to be scaly and covered with
dandruff. Later there results an elimination, not of scales and
dandruff, but of the hairs themselves, which fall out whole with
their bulb-like follicles and are replaced by other shorter and
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ALOPECIA, 671
weaker hairs until finally alopecia is established — never amount-
ing, however, to complete baldness. The hair becomes more
sparse, shorter, less abundant and luxuriant, with open spaces
interspersed, but never with anything actually suggestive of
the seborrheic baldness of males, with its large, regular, elliptical,
smooth and polished areas of involvement.
(r) Infectious and post-infectious alopecia is of great practi-
cal interest. Influenza, the eruptive fevers, mumps, erysipelas,
Fig. 510. — Alopecia following erysipelas (Sabouraud),
and in particular typhoid fever, cause a more or less pronounced
loss of hair. "Slight alopecia may follow these conditions as
soon as they have terminated, particularly those which, like ery-
sipelas, are attended with intense local inflammation, but all of
them have a definite period for the production of alopecia. The
latter follozvs its cause after an interval of eighty- five days. In
different cases there may be five days' discrepancy, one way or
the other, from this time interval." (Sabouraud). The hair con-
tinues to fall out for about six weeks ; this occurs in a diffuse,
irregular manner, without ever terminating in true alopecia.
Restoration of the hair is constant in these <:ases.
A separate place in the classification may be set apart for
the alopecia? of chronic tuberculous subjects, suggesting alopecia
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672 SYMPTOMS.
areata; this form is occipital in situation and circumferential in
arrangement.
{d) Syphilitic alopecia is separated from the preceding group,
of which it constitutes merely a single type, because of its great
clinical importance. It appears about six months after the onset
of the disease — in the course of the second six months' period,
never later. "This lesion is temporoparietal and irregularly
Fig. 511. — Syphilitic alopecia, rather more pronounced
than usual (Sabouraud) .
diffuse, so that when the patient's hair is cut short the hairy-
covering over these surfaces appears as though chopped up
with poorly directed scissor cuts. At each of these points a tuft
of some 12 to 15 hairs will have disappeared, leaving behind
an open space; even in women with long hair these open spaces can
still be recognized. Upon examination of the eyebrows these
are found to show parallel streaks; the cervical glands are en-
larged; upon looking into the mouth mucous patches are to be
found. Or, general examination of the patient may reveal the
indurated remnant of the chancre, the inguinal lymphatic en-
largements, sometimes a still visible roseola, etc." (Sabouraud.)
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ALOPECIA. 673
Mention should here be made of the alopecia of old syphilitic^
and of congenital syphilitics, which resembles alopecia areata.
In the congenital cases, it is accompanied by the classical stig-
mata— dental dystrophies, facial dystrophies, interstitial kera-
titis, etc. (see Syphilis), of the condition and will assume the
form of an indefinitely protracted, recurring alopecia areata.
(e) Brocq's pseudopelade variety of folliculitis decalvans, on
the whole rather rare, is met with almost! exclusively in males
20 to 45 years of age and leads ultimately to the formation of
Fig. 512. — ^Tinea decalvans causing almost complete baldness in a dwarf
presenting all the stigmata of inherited specific infection (Sabouraud).
patches of alopecia measuring 1 or 2 centimeters on either side,
polycyclic, serpiginous, and separated by spaces surrounded by
normal hair. It exposes irretrievably more or less extensive sur-
faces, later coming to an end spontaneously. Its onset, course,
and termination remain wholly obscure.
In the Elderly. — ^At this period of life the conditions most
frequently met with are:
The advanced forms ofl seborrheic baldness of the adult;
A form of alopecia due to sclerosis of the follicles and repre-
senting, properly speaking, senile alopecia.
The alopecia areata of the fifties.
Cicatricial alopecia of varying origin.
43
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674 SYMPTOMS.
Of the first of these forms, nothing in particular need be said.
Regarding the second, only slight qualifications are required.
The process of sclerosis or fibrosis leads to connective tissue re-
placement and disappearance of the hair follicle. The scalp, de-
prived of its follicles, assumes a smooth, scar-like appearance.
In the period of the menopause, or the process of involution
taking place in women in the forties, there occurs a rather uncom-
Fig. 513. — Brocq's pseudopelade variety of folliculitis
decalvans {Sabouraud),
mon parietal and frontal form of alopecia areata consisting of
more or less extensive irregular patches, which are spontaneously
recovered from after one or two years.
In this period of life, finally, the scalp may exhibit, in the form
of cicatricial patches of alopecia of varying shape and extent, the
end-results of all of the foregoing possible causes of destruction
of the scalp : Traumatism, furunculous eruptions, necrotic acne,
cold abscesses, bone suppurations, burns, gummas, syphilitic se-
•questra, etc.
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AMPmrT A r^> ^"» from di^d, privative; alfia^ blood J
As a general rule, abnormal pallor, if associated with a pale-
appearance of the mucous membranes of the lips, gums, and
conjunctivae, is due to anemia. It is a fact, however, that simple,
essential, or primary anemia is very uncommon, whereas morbid
pallor is of very frequent occurrence. The reason for this is
that in by far the greater proportion of cases, if not invariably,
the anemia is secondary to or symptomatic of some other dis-
turbance, and that actually the diagnostic problem set before
the practitioner confronted with a pale individual is that of in-
'^estigating the condition which underlies the anemia.
Despite the recommendations made in current text-books,
confusion of the customary pallor of anemia with the yellowish
discoloration of incipient jaundice or the evanescent pallor of
nenous angiospasm could occur only as a result of gross care^
lessness on the part of the clinician. What is more to the point,
in the author's view, is that both in hyposphyxic cases and in
many tuberculous patients, actual anemia may be masked by a
certain amount of lividity, cyanosis, or even jaundice, particu-
larly in hemolytic icterus. Hence, exatmination of the blood is,
as a rule, indicated in cases exhibiting pallor. This examination
should relate more especially to the cell count and the estimation
of hemoglobin (see Blood examination), Hayem's classification
is generally followed: A^ (tmntber of red cells); R (hemoglobin
value) ; C=-^ (cell value).
Normally, ^ N=5,000,000; /?=5,0(X),000; G=l.
ANEMIC STATES.
1st degree: N and R, and hence also G, are very slightly reduced.
2d degree: N = 5,000,000 to 3,000,000: R = 3,000,000 to 2,000,000; G =
0.80 to 0.30 (extreme figures).
3d degree: N = 3,000,000 to 1,000,000; R = 2,000,000 to 800,000; G =
0.84 to 1.00.
4th degree: N = 1,000,000 to 300,000; R = 800,000 to 300,000; G =
0.88 to 1.70.
(675)
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676 SYMPTOMS.
In the 4th degree is comprised the group of the so-called "per-
nicious anemias," the confines of which have not as yet been thor-
oughly d^emiined, and which certainly occur in more than one
form or variety. Determination of the differential leucocyte count
is always necessary in these cases. The total white cell coiuit is
seldom increased ; much more frequently the number of white cells
remains normal or is diminished, in which eveiTt leucopenia is
present. In a general way, a plastic anemia may be said to exist
where blood repair is manifested in the appearance of young or
immature cells; there may be present a leucocytosis, with granular
myelocytes; nucleated red cells may be found in variable numbers,
vis,, erythroblasts with mitotic nuclei or with nuclei in a state of
pyknosis, many reds exhibiting multiple and manifest deformations,
microcytes or megalocytes, etc.
In the much less common condition known as aplastic anemia,
there is an absence of defensive reaction in the bone marrow and
hence also in the blood. There is a leucopenia with preponderance
of the mononuclear cells. Nucleated reds and myelocytes are
absent.
Anemia having been observed to be present, the next step
is to ascertain its cause, since — it cannot be too often repeated —
primary, idiopathic anemia is exceedingly rare.
The classification of A. Jousset appears to the author par-
ticularly serviceable because it possesses all of the three cardinal
virtues of clinical classifications, being both practical, etiologic,
and pathogenetic. It combines at once the causal diagnosis and
the (capitally important) diagnosis that affords rational thera-
peutic indications.
I. Anemias by spoliation may follow any traumatic, surgical,
or spontaneous hemorrhage. Included in this group, in particular,
are all the secondary anemias attending the hemorrhagic affections;
Hemophilia, purpura, scurTTy, epistaxis, metrorrhagia, hemoptysis,
hematemesis, cmkylostomiasis, etc.
The causal diagnosis is often self-evident in these cases. Special
mention should, however, be made of the occult gastrointestinal
hemorrhages attending ulcer and cancer cases, which require for
their detection a systematic examination of the feces (see Exami-
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ANEMIA,
THE ANEMIAS.
677
I. — Spoliatory Type.
1. Traumatic or operative hemorrhage.
2. Spontaneous hemorrhage in disorders attended with bleeding
(hemophilia, purpura, metrorrhagia, etc.).
3. Gastro-intestinal hemorrhage, manifest or occult (ulcers or neo-
plasms of the digestive organs).
II. — Toxic-infectious Tjrpe.
A. Infectious.
Chronic:
1. Malaria.
2. Syphilis
3. Tuberculosis.
Acute :
1. Acute rheumatism.
2. Typhoid fever.
3. Suppurative disorders.
B. Toxic.
1. Carbon monoxide.
2. Lead.
3. Mercury (?)
III.— Autotoxic Type.
1. Bright's disease.
2. Hepatic disorders.
IV.— Insufficiency of the Hematopoietic Functions.
Disorders of the blood-forming organs.
V. — Crjrptogenic Type.
1. So-called "primary,"
2. Chlorosis.
essential, or idiopathic anemias.
nation of feces; Tests for blood). Hookworm ova are likewise
detected only by examination of the stools; the patient's environ-
ment will generally aflFord a serviceable indication, as in miners
[and in the endemic foci of the disease in the Southern U. S. —
Translator] .
II. Anemias due to Toxic Action on the Erythrocytes. — In-
fectious and Post-infectious Anemias.
In the first sub-group are placed the three major chronic
infections : Malaria, tuberculosis, and syphilis. These are three of
the most frequent causes of chronic anemia; if the practitioner will
constantly bear them in mind he will never err when seeking the
source of many chronic anemias apparently cryptogenic to a su|>er-
ficial observer. Should cancerous anemia logically be classed with
the preceding forms? At any rate it should and can be classed
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678 SYMPTOMS.
with them clinically, whether the anemia be due to manifest or
occult hemorrhage, to toxic action on the red cells, or to both of
these factors combined.
In the second sub-group are the three major acute infections:
Typhoid fever, acute rheumatism, and the various suppurative dis-
orders. In these cases the relationship of cause to effect is gen-
erally obvious.
Toxic Anemias Proper. — The three common forms of intox-
icaticTn are those due to carbon monoxide, lead, and mercury.
The first of these is by far the most common. It may be said
to be practically endemic in our cities throughout the cold
season, when houses are artificially heated. The imperfect
draught through most chimneys, the frequent use of heating
devices under conditions of slow or restricted combustion, and
the insufficient ventilation of living rooms are the effective fac-
tors in this form of poisoning. There results the well-known
carbon monoxide winter anemia with its customary clinical mani-
festations consisting of dizziness, headache, and tinnitus, all
refractory to any form of treatment.
Lead anemia comes next in frequency. The occupation of the
patient (painter, plumber, etc.), the examination for other signs
of lead poisoning (blue line on the gums, tremor, and high blood
pressure), and sometimes the history of former attacks of lead
colic, readily afford a positive diagnosis.
Mercurial anemia appears to the author much more uncommon,
at least in his own district, if indeed it exists at all.
III. Autotoxic Anemias. — In this group Bright's disease takes
first place and hepatic disorder comes second.
Brighfs disease induces anemia both by causing hydremia and
through an autotoxic factor. To it may be ascribed the pallor
of persons with arteriosclerosis (the aged) and of cases of acute
and chronic nephritis with or without edema. It constitutes,
with cancer, by far the most frequent cause of abnormal, lasting,
and progressive pallor coming on after the age of 45. In pale
subjects an examination should always be made for albumin,
edema, and high blood-pressure.
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ANEMIA, 679
Hepatic disorder (hepatism) is, as is well known, attended
with particular risk to the red blood cells; one need merely
recall the time-honored and of late thoroughly illuminated con-
ceptions as to hematic and hemolytic icterus, to realize the
frequency of occurrence of such cholemic anemias (see Jaundice),
lY. Anemias due to Insufficient Regeneration of Erjrthro-
cytes. — Perhaps it may be justifiable to place in this group the
anemias secondary to affections of the blood-forming organs:
Splenomegaly, multiple adenopathies, leukemias, and bone mar-
row disturbances; impairment of the nervous and digestive or-
gans with consequent poor nutrition ; and polyglandular insuffi-
ciencies.
V. Cryptogenic Anemias of obscure or as yet unknown ori-
gin. These are the anemias that do not fall into any of the
preceding groups. It is more rational to confess frankly our
lack of knowledge by the term "cryptogenic" than to disguise it
with the word "essential." Chlorosis, an anemia of development,
appearing at puberty and disappearing at its termination, may
perhaps be appropriately classed in this group until further light
is thrown upon it. In this form of anemia hemoglobin reduction
is more pronounced than red cell reduction, the latter often
being very slight.
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APHONIA AND Fa, privative; ^hjttJ, sound;']
HOARSENESS. [ deprived of voice. J
Aphonia seldom entails complete suppression of the act of
phonation, such suppression being observed almost exclusively
among the deaf and dumb and in hysterical mutism ; it is char-
acterized rather by dysphonia, hoarseness, and a muffled, raucous,
discordant quality of the voice.
For practical purposes aphonia may be divided into:
Acute aphonia, evanescent and generally of slight import.
Chronic aphonia, lasting and generally of serious import.
Acute Aphonia. — Acute laryngitis, — This may be roughly
divided into:
(a) Acute post- vocal laryngitis, practically a traumatic condi-
tion, occurring among speakers, actors, lawyers, "criers," vocal
professionals, etc. This represents practically a "sprain" of the
vocal cords.
(h) Acute catarrhal laryngitis of infections: Acute colds, erup-
tive fevers, measles, scarlet fever, grippe, etc.
(c) Acute congestive or irritative laryngitis, that of smokers
and alcoholic subjects.
Chronic Aphonia. — Three main groups of causes are opera-
tive :
1. Chronic laryngitis. 2. Organic diseases of the larynx. 3.
Paralytic disturbances due to pressure upon the nerves to the larynx,
1. Chronic laryngitis, the commonest causes of which are
chronic fatigue of the larynx, as in criers, vendors, orators, etc.,
and chronic descending infections of the nasopharynx, which
Laurens has aptly designated as the "morning drop of the
larynx."
2. Organic diseases of the larynx, chiefly represented by
tuberculosis, syphilis, and benign or malignant tumors. The cHni-
(680)
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APHONIA AND HOARSENESS. 681
cal and laryngoscopic features of these several affections will be
found in condensed form in the tables on pages 686 to 690. As
for their distinguishing features, the following resume is borrowed
from Georges Laurens (Oto-rhino-laryngologie du medecin prati-
cien, p. 380) :
'^Unquestionably, for the well-trained physician, the results ob-
tained by a4iscultation of the lungs, bacteriologic examination of
the sputum, specific treatment, and histologic examination of a
piece of tissue from the interior of the larynx may facilitate the
differentiation of these laryngeal disorders, vis., syphilis, cancer,
and tuberculosis ; the laryngoscopic picture, however, affords singu-
larly accurate supplementary information.
"The three affections are characterized by excrescences, a tumor,
or ulcerations.
**(a) Tumor or excrescences in the larynx,
"The syphilitic gumma is recognized by its location, being situ-
ated in the anterior portion of the larynx, including the epiglottis
and the true vocal cords; by its red, smooth, and circumscribed
aspect, and by its rapid course.
'* Tuberculous vegetations are multiple, irregular, and associated
with other lesions in the vicinity.
''Cancer results in the formation of a single, non-pedunculated
tumor involving the vocal cord or the epiglottis, without any lesion
of the adjoining mucous membrane, and immobilising the vocal
cord.
"(b) Laryngeal ulcerations,
"An ulcerated gumma exhibits a sanious base, punched out
red margins, and infiltration of the surrounding tissues.
''Tuberculous ulcerations exhibit dentate, irregular, and torn
margins, and are multiple.
"Ulcerated cancer exhibits granulations and fungous outgrowths,
and is sanious, bloody, painful, and unilateral."
3. Paralyses of the Larynx. — ^The following excellent didactic
article on paralytic conditions of the larynx is likewise borrowed
from Laurens's work.
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682
SYMPTOMS.
PARALYSES OF THE LARYNX.
By Dr. G. Laurens.
Let the reader recall the two functions of the larynx : Respiratory
and phonatory. During respiration the vocal cords move apart
and the glottis is partly opened; during phonation the cords are
Fig. 514. — Paralysis of right re-
current laryngeal nerve. During
respiration the left vocal cord is
seen to move while the right re-
mains motionless.
Fig. 515. — Paralysis of right re-
current laryngeal nerve. During
phonation the cords are seen in ap-
proximation, presenting a normal
laryngoscopic picture.
approximated and vibrate, and the glottis is closed down. All these
movements are carried out by the muscles of the larynx, some of
which are constrictors (closing the glottis) and others dilators
(partially opening it).
Fig. 516. — Paralysis of both recurrent nerves.
Within the tissue of the cords themselves are muscles (the
tensor muscles of the vocal cords), the functioning of which insures
phonation and relaxation, of which causes hoarseness.
All the muscles of the larynx but one are supplied by the recur-
rent nerves. Paralyses of central, myopathic, or recurrent origin
are encountered' (Fig. 523). The last-named variety is that occur-
ring most frequently.
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APHONIA AND HOARSENESS.
683
I. Paralyses of the Recurrent Nerves. — These may be either
uni' or bi- lateral,
(a) Unilateral paralysis, an aortic aneurysm, for example,
exerting pressure on the left recurrent laryngeal nerve. In this
instance, the corresponding vocal cord will remain motionless.
The outstanding symptom is hoarseness.
Fig. 517. — Independent paralysis of Fig. Sl8. — Independent paralysis of
the laryngeal muscles. the laryngeal muscles.
The tensor muscles of the cords (the thyroarytenoids) are paralyzed, the
cords relaxed, and the glottis presents a "button-hole" appearance.
(b) Bilateral paralysis, resulting from compression of the
recurrent by a tumor of the esophagus or of the thyroid gland.
This condition is rare. When it occurs, the cords cannot be
separated, but remain in absolute contact.
The symptoms are hoarseness and dyspnea.
Fig. 519. — Partial paralysis of the
posterior muscles of the larynx (ary-
tenoids). An isosceles triangle is
formed behind the glottis.
Fig. 520. — Paralysis of the tensor
muscles of the vocal cords (crico-
thyroids). The vocal cords exhibit
a wavy outline.
II. Independent Paralyses of Laryngeal Muscles. — These are
frequently of myopathic origin, following an attack of lar>'ngitis,
or hysterical. Their presence is manifested by hoarseness.
Figures 517 to 520 show the condition of the glottis in these
varieties of paralysis.
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684 SYMPTOMS.
Interpretation of a Case of Laryngeal Paralysis. — Given a
patient who has consulted the physician on account of hoarse-
ness or dyspnea, and in whom the laryngoscopic picture has
revealed laryngeal paralysis.
What data should he thereupon secure for diagnostic, prog-
nostic, and therapeutic purposes?
He should proceed by exclusion, proceeding from the simple
to the more complex.
'-- .2
.•3
4...
-o
Fig. 521. — Diagram showing the course of the recurrent nerves, which
supply the muscles of the larynx. /. Right recurrent nerve. ^. Left re-
current nerve. 3. Cancer of the esophagus. 4. Thyroid enlargement. 5.
Aortic aneurysm. 6. Tracheobronchial adenopathy. 7. Bifurcation.
First Possibility, — If the condition is a unilateral paralysis in-
volving the entire cord, with the larynx otherwise normal and
not in a state of hyperemia, the paralysis is one of the recurrent
nerve. Let the practitioner recall his anatomy and ascertain by
examination of the neck and chest which organ is causing the
pressure. He should auscult, use the x-rays, the esophagoscope,
etc., and will come to suspect some particular organ of causing
the trouble.
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APHONIA AND HOARSENESS. 685
Following are the possible causes of pressure on these nerves,
and hence, of paralytic conditions of the larynx:
1. Cancer of the esophagus. — The left recurrent nerve is situ-
ated behind the trachea, in the angle between the latter and
the esophagus. Consequently any growth in this organ will exert
pressure on the nerve and cause paralysis of the larynx.
2. Thyroid gland. — Enlargement of the thyroid gland, or of a
goiter, whether developing in the left or the right lobe of the organ,
exerts pressure on the recurrent nerve and paralyzes it. Such
a condition may also be the result of thyroidectomy, in the course
of which the nerve may be injured.
3. Aortic aneurysm. — The arch of the aorta is in close anatomic
--2
Fig. 522. — Horizontal section of the neck showing diagrammatically
the position of the recurrent nerves and the structures that may exert
pressure on them. /. Trachea. 2. Left recurrent nerve. J. Right recur-
rent nerve. 4. Esophagus. 5. Cancer of the esophagus. 6, Goiter. The
left recurrent nerve is thus seen to be particularly exposed to pressure
from two directions.
relationship wth the recurrent nerve. When dilated, it may
cause paralysis of the nerve.
4. Tracheobronchial adenopathy, developing at the bifurcation
of the trachea, frequently causes pressure on the laryngeal
nerves.
For clinical purposes, the greater frequency of left sided recur-
rent paralyses on account of their esophagoaortic origin should
be kept in mind.
Great significance attaches to this type of paralysis from the
standpoints of diagnosis, pathogenesis, and treatment. Hoarse-
ness will thus have led the physician to discover an aneurysm
of the aortic arch or of the right subclavian artery. The treat-
ment, however, is ineffectual.
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APHONIA AND HOARSENESS.
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APHONIA AND HOARSENESS. 691
Second Possibility. — If the examination of the nedc and chest
has given negative results, the points of origin of the recurrent
nerve in the brain must be at fault. Hence, the physician should
make an examination of the nervous system for tabes dorsalis,
disseminated sclerosis, etc. The neuropathologist will be able
to put his finger on the exact origin of the paralysis. — ^The prog-
nosis will depend upon the cause found.
Third Possibility. — If the hoarseness has appeared in the course
of an attack of influenza or acute laryngitis; if it is an expres-
Y
Fig. 545. — ^The three causes of paralysis of the laryngeal muscles.
1. Paralysis of the recurrent nerves is by far the most frequent ; any form
of pressure at any point on the course of the nerve is sufficient. The course
of the left recurrent nerve below, in front of, and above the aorta is shown
in Fig. 545.
2. Myopathic paralysis is rather frequently observed. It is produced as
follows: Following an ordinary catarrhal laryngitis the patient is seized
with hoarseness. This occurs from the fact that the inflammation of the
mucosa has extended to the underlying tissues and set up a species of myo- ;
sitis. The prognosis in this form of paralysis is favorable.
3- Paralysis of central origin, following disease of the brain and spinal
cord, is much rarer.
sion of isolated paralysis of one or both vocal cords, and if the
mucous membrane of the larynx is still inflamed, the paralysis
is unquestionably of myopathic origin. The prognosis is favorable.
Treatment. — This is unavailing in paralysis of central. origin
and very often, too, in pressure paralysis of the recurrent
nerve.
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692 SYMPTOMS.
It IS useful in the myopathic disturbances, i.e., in the paraly-
sis following acute laryngitis; also in hysteria, in intoxications,
and in syphilis.
The measures then to be recommended should comprise vocal
rest, inhalation treatment (if there are still evidences of catarrh
and laryngeal hyperemia), strychnine, electricity, bromides
with suggestion treatment (in hysteria), and if need be, external
vibratory massage. In cases of cord paralysis in which the cause
cannot be found the physician should not hesitate to prescribe
antisyphilitic treatment ; pleasant surprises for the patients can-
not but thus sometimes result
Recurrent paralyses are by far the commonest, constituting
perhaps 95 per cent, of all cases of laryngoplegia.
The remaining 5 per cent, are represented by:
Peripheral neuritis, as in diphtheria, alcoholism, syphilis, and
diabetes.
Spinal lesions, as in tabes dorsalis.
Bulbar lesions, as in syphilis, tumors, softening, pachymenin-
gitis, labio-glosso-laryngeal paralysis, disseminated sclerosis,
tabes dorsalis, etc.
Cerebral lesions at the foot of the third frontal convolution
and of the subjacent fibers.
Lastly, a word concerning hysteria and malingering.
Aphonia is one of the easiest symptoms to simulate, but is
also one of the easiest artificial symptoms to detect, thanks to
Zuber's sign. When the aphonic malingerer is ordered to
whistle, he insists he cannot do it; the true, non-malingering
aphonic subject is generally able to whistle without any trouble,
since the facial nerve is involved in this act, and is unaffected
by the disorders causing hoarseness.
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ARHYTHMIA
{Irregularities of
heart action,)
a, from a, privative^ I>v6(i6^^ measure.
Irregularities of heart action.
Cardiac arhythmias, manifested, in cursory clinical examina-
tion, by more or less distinct and pronounced irregularities of
the pulse, constitute a very common condition. Their semeio-
logic significance is always pronounced and sometimes exceedingly
great. The study of the arhythmias has undergone a complete
renaissance in recent years, and marked clinical benefit has re-
sulted. While certain of the arhythmias, as yet incompletely in-
vestigated, remain very difficult to interpret, the majority, on
the contrary, are now well understood from the standpoint of
pathologic physiology. Little mention need here be made of
the as yet insoluble problems relating to these disturbances,
attention being paid, as seems fitting in such a work, only to
the facts that may yield useful practical deductions, i.e., con-
clusions of actual therapeutic service.
Careful and judicious digital palpation of the pulse, combined
with correct auscultation and a critical study of the associated
clinical manifestations, proves sufficient in 90 per cent, of cases
for proper interpretation of the more commonly encountered
arhythmias. The graphic method (see the section on technic),
always to be recommended where it can readily be applied, is
sometimes indispensable. It is the procedure of choice for the
study of the arhythmias. In the subjoined brief presentation
of the subject, extensive and legitimate use will be made of the
results secured by this procedure.
In this section only a few typical examples of the cases of
arhythmia most often met with in practice will be given — cases
which every physician will certainly have occasion to observe,
which he may rather easily discover, and with which, therefore,
he should be familiar.
(693)
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694 SYMPTOMS.
In practice, the most frequently encountered forms of arhythmia
are:
1. Extrasystoles or premature contractions.
2. Paroxysmal tachycardia.
3. Respiratory (sinus) arhythmia.
4. Auriculoventricular dissociation or heart-block.
5. Alternating pulse.
6. Perpetual arhythmia or auricular fibrillation.
THE NORMAL HEART RHYTHM.
In order to interpret most of th^e arhythmias with some
■degree of accuracy, a short resume of the facts now established
regarding the contraction of the normal Heart may appropriately
be given.
The cardiac cycle consists, as is well known, of a series of
rhythmic movements, of contractions or systoles alternating
with periods of rest or diastoles. The several movements con-
stituting the cardiac cycle take place in regular succession in
the following order: Auricular systole, ventricular systole, gen-
eral diastole, auricular systole, ventricular systole, general dias-
tole, etc.
All recent anatomic, physiologic, and physiopathologic inves-
tigations have tended toward the conclusion that this rhythmic
succession of movements of the heart is caused by a stimulus
of as yet unknown. nature which, starting in the upper part of
the right auricle in the neighborhood of the sinus of the su-
perior vena cava, is transmitted from this point through the
auriculoventricular septum to the bundles of muscle fibers con-
stituting the myocardium. This apparatus for transmission of
the excitomuscular impulse, or neuromyocardial propagating
bundle, has been termed the bundle of His, after the anatomist who
first described it.
The bundle may diagrammatically be conceived of as follows
(Fig. 546) : It originates in the sinoauricular node, a little mass
of specialized tissue consisting of muscle cells interspersed with
a rich network of nerve terminals of the cardiac nerves, and
located in the upper part of the right auricle, near the opening
of the superior vena cava.
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ARHYTHMIA. 695
The rhythmic stimulus of unknown nature elaborated in this
center is transmitted along a thin neuromuscular tract, the auric-
uloventricular btmdle, to a secondary center, the auriculoventricular
node, whence it is further distributed to the myocardial bundles of
each ventricle by two main branches and their subdivisions.
For practical purposes it may be said that the systolic stimulus
originates at regular intervals of about one second in the sinoauricu-
lar node (the node of Keith and Flack) ; that it brings about con-
traction of the auricles at this moment ; that it is transmitted along
V,C., vena cava,
V,P., pulmonary vein.
P., pulmonary artery.
A., aorta.
A.D., right auricle.
A.G., left auricle.
V.D., right ventricle.
F.C, left ventricle.
/. Sinoauricular node.
2. Auriculoventricular bundle.
3. Auriculoventricular nucleus.
4^ 4'. Terminal neuromyocardial rami-
fications of the bundle.
Fig. 546. — Diagram of the bundle which transmits the neuro-myo-
cardial stimuli (bundle of His).
the auriculoventricular bundle to the auriculoventricular node (the
node of Tawara), such transmission normally taking about one-
fifth of a second ; that it then brings about ventricular systole through
transmission of the excito-contractile impulse to the myocardial
muscle fibers along the branches of the above mentioned auriculo-
ventricular bundle. Both auricles and ventricles then lapse into a
condition of rest and lose their irritability for a period of two- to
three-fifths of a second, after which the cycle of contraction above
described is again reproduced.
Objective representation of this cycle is well afforded either
in polygrams showing simultaneously arterial contractions such
as those of the radial, which accurately register the ventricular
systole with a delay of approximately one-tenth of a second
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696
SYMPTOMS.
(time of transmission of the pulse wave to the radial artery),
and the pulsations of the right jugular vein, which represent
for practical purposes the pulsations of the superior vena cava
and the right auricle; or, in a good cardiogram taken with the
patient in left lateral decubitus (Pachon).
» » 1 < ■ « » »'■■» '» w ■ < » I I ■ I !■ i|*|»| ■• i»««'«^w "••'••fi »• Ilia*
Ri^
^ er
s e
Fig. 547. — Case 157. Normal pulse. Rj, right jugular.
Rr, right radial.
A few samples of polygrams showing a normal rhythm and
typical from the standpoint just referred to are herewith pre-
sented.
On a polygram the beginning of the systolic expansion of
Rj.
9 e r
Rr.
Fig. 548. — Case 504. Normal pulse. Rj, right jugular.
Rr, right radial.
the radial artery is very easily located, being at start of the
ascending line; if, taking into account the time required for
transmission of the ventricular systolic contraction to the radial
artery (about Y^o second), one turns from the radial tracing to
the jugular tracing at a point preceding the above-mentioned
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ARHYTHMIA. 697
point by Y\o second, the point corresponding in time to the ven-
tricular systolic contraction is obtained. The jugular tracing
then becomes very easy to interpret (Figs. 547 and 548). Each
cardiac cycle is reflected in the jugular tracing by three eleva-
tions :
Fig. 549.— Normal electrocardiogram {Daniel Rvutier) .
1. A presystolic wave, a, corresponding to auricular systole, and
presystolic in respect of the ventricular contraction. This is gen-
erally represented by the letter a (auricular).
2. A systolic wave, c, immediately following the preceding, from
which it is separated, as a rule, only by a very slight depression ;
V,"
y. normal
Fig. 550. — Diagram showing the succession of motor events in the
normal heart. The auricle A contracts first and sends its impulse to the
ventricle F along the bundle F. The ventricle at once begins to contract.
The time of transmission, which is approximately the same as the dura-
tion of auricular systole, is about % second. R, radial tracing; /, jugu-
lar tracing. Marks at the top : Time in fifths of. a second.
it corresponds to ventricular systole. It is generally represented
by the letter c (carotid) because the earlier observers, Mackenzie
among others, ascribed it to the carotid pulsation, which, how-
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698 SYMPTOMS.
ever, does not seem always to be the case. At all events this
notation will here be preserved.
Fig. 551. — The pneumogastrics (Landois).
3. A post-systolic wave, v, distinctly separated from the wave
preceding it, c, and from that which follows it, a, in the next
cardiac cycle by 2 definite depressions, x and y. This wave is
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ARHYTHMIA. 699
generally represented, in accordance with Mackenzie's notation, by
the letter v (ventricular), Mackenzie ascribing it, or at least its
terminal portion, to relaxation of the right ventricle and opening
of the tricuspid orifice. The exact significance of this wave has
been the subject of prolonged discussion and is still being discussed ;
as a matter of fact it is one of the most fixed and constant and
often one of the most pronounced features of the venous pulse
Pneumog.
nerve.
pve.
)Qll.
Recurrent nerve.
Middle ai
cardiac z rve.
LIB.
Phrenic nei
plexus,
rdiac
Fig. 552.--The nerves of the heart (Hirschfeld).
tracing; it corresponds practically to the diastolic rebound of the
radial pulse, to the opening of the tricuspid valve and the closure
of the sigmoid valves. The notation 7', is thus highly appropriate
for it, provided there be attached to it the meaning valvular,
which is more comprehensive. Actually it marks the termination
of ventricular systole and the beginning of general diastole of the
heart.
The normal electrocardiogram lends itself to the same con-
siderations (Fig. 549).
The successive movements of the normal heart and the trans-
mission of the neuromyocardial impulse of contraction may be
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700
SYMPTOMS.
represented in a diagram which will greatly facilitate presenta-
tion of the subject of the arhythmias (Fig. 550).
The apparatus having to do with intracardiac conduction
may be and unquestionably is influenced and partly controlled
by the vagus and the sympathetic. Some of the cardiac arhyth-
mias are known to originate in the extracardiac nervous mechan-
ism, consisting chiefly of the bulb, the vagus, and the sympa-
thetic; it seems desirable, therefore, to reproduce and show in
a diagram the distribution of these nerves (Figs. 551 to 5S3).
These illustrations will doubtless facilitate comprehension of
certain forms of arhythmia.
Mf^uMat
Ihtebra/ yanfff/a
toikinknd
Heart
Fig. 553. — The nervous system as related to
the circulation. Connections of the vagus and
sympathetic nerves.
DISTURBANCES OF RHYTHM.
EXTRA-SYSTOLES (PREMATURE BEATS).
The normal cardiac rhythm is produced, we have seen, by
an impulse which, starting at regular intervals from the sinoau-
ricular node, or node of Keith and Flack, passes down along the
conducting system previously described, awakening in succes-
sion a contraction of the auricle and then of the ventricle. The
process goes on as if the entire cardiac rhythm were governed
by the primary contractions of the auricle, these in turn regu-
larly setting off secondary contractions of the ventricle.
An extra-systole or premature contraction is an extraordinary,
premature systole occurring independently of the above-men-
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ARHYTHMIA.
701
(a)
ib)
November 20, 1911
16
November 29, tqtt
' v^^xp-N^XI^^^^xT^^
VSs5.8
IS Nov, 29, 191 J, 5 minutes after the preceding
86
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15
December 8, 19^
jW-
vy-v-.^
V5.5.6 *
/w-./^.W->/\
IS
December 16, 191 r
»"»VA
nTK/^-vP-
VS«<k2
.r-sT-jvp^JX,
Fig. 554. — Premature contractions (extrasystoles) during an attack of
gout, (a) Bigeminal and (b) trigeminal pulse.
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702
SYMPTOMS,
^ tioned regular succession of contractions. Everything takes
place as if the initial stimulus arose at an abnormal point — inde-
pendently of the sinoauricular node — either in the auricle, in the
ventricle, or in the intermediate auriculoventricular node. Hence
there are 3 kinds of extra-systoles: Auricular, ventricular, and
auriculoventricular. These are sometimes rather hard to differ-
entiate.
An extra-systole* is generally felt by the patient as a precordial
thump accompanied by slight discomfort and an evanescent
tendency to fainting.
tiiiiiiiiiiiiiiliiiiiiiiiiiiiltl
Fig. 555. — ^Ventricular extra-systole or premature beat. The third
ventricular contraction takes place too soon. The third auricular con-
traction, taking place during the period of lost ventricular irritability
(refractory period), fails to induce a contraction of the ventricle. /,
jugular; R, radial; A, auscultation.
It is detected by the physician upon palpation of the pulse in
the form of an intermittence in the latter, a pause of unusual
length, suppression of one pulse wave, a "misstep of the heart."
Sometimes an ordinary beat is very closely followed by a very
small beat succeeded by a long pause ; at other times there is felt
but one ordinary pulsation, followed by a long pause.
Auscultation yields significant results (Figs. 555 and 556)*
If the extra-systole is strong enough (and sufficiently late in
respect of the preceding contraction) to open the sigmoid valves,
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ARHYTHMIA,
703
the double sound of the preceding systole is at once followed
by a double echo sound due to the extra-systole, and then by
I I I I I I I I t I I f I I I I I I I I I I I I I I I I I
f^\^^J^\/r^r^A->^\^>V
II 1 1 1 1 II I I 1 1
Fig. 556.— Auricular extra-systole. /, jugular; R, radial;
A, auscultation.
a prolonged pause. The rhythm has been reduplicated and now
includes four sounds. If the extra-systole is too weak (and
I I I I I I I I t I I I I I I I I f I I I I I I I I I I f
II II I III I I I i
Fig. 557. — Auriculoventricular extra-systole.
comes too soon after the preceding contraction) to open the
sigmoid valve, the double sound of the preceding systole is fol-
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704 SYMPTOMS.
low^d by a single souml due to the ventricular contraction in the
extra-systole (the rhythm now entailing 3 sounds), and then by
a long pause.
These extra-systoles may recur at quite irregular intervals, de-
void of any regular rhythm. If, on the other hand, they occur in
series at regular intervals they constitute allorhythmias. If each
regular systole is followed by an extra-systole, the pulse assumes
a bigeminal character; if the extra-systole recurs regularly after
2 regular systoles, the pulse is trigeminal; after 3 regular sys-
toles, quadrigeminal, etc. (Fig. 554).
Such are the simplest and most fundamental clinical observa-
tions that can be made without the help of any form of instru-
ment.
9
Fig. 558. — Case 205. Ventricular extra-systole. Pulse,
74; pressure, 2i%q.
The foregoing diagrams will have afforded a good demonstra-
tion of the nature of the phenomenon (Figs. 555, 556, and 557).
Differentiation of the several varieties of extra-systoles is
attended with greater difficulty, requiring the application of the
graphic method ; it may even prove difficult when this procedure
is availed of.
Ventricular extra-systoles are distinguished from auricular
extra-systoles by the 3 following features:
1. The total duration of the cycle consisting of an ordinary systole
and a ventricular extra^systole is equal to that of a cycle formed
of two ordinary systoles; this duration is appreciably less, however,
in the case of a cycle consisting of an ordinary systole and an auric-
ular extra^systole. This sign is the simplest, most constant, and
most readily observed of the signs differentiating these 2 varie-
ties of extra-systoles. It can be recognized even in a simple
radial tracing (Fig. 558).
2. On polygrams, if the extra-systole has forced open the sig-
moid valves, it is shown in the tracing by a premature contraction
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ARHYTHMIA, 705
followed by a more or less prolonged pause, which is always
definitely more prolonged than the normal diastolic pause (Figs. 558
and 559). If the extra-systole has not opened the sigmoid valves,
the radial tracing shows no evidence of any premature inter-
polated elevation; one merely notes the absence of one beat,
and a diastolic pause of manifestly abnormal duration. The
jugular tracing, when distinct, is rather characteristic of one or
Fig. 559.— Ventricular extra-systole {Daniel Routier).
the othes variety of extra-systole. In ventricular extra-systole
a rise synchronous with the extra-systolic elevation at the radial
artery is observed during the abnormal pause; in auriculoven-
tricular extra-systole, the extra-systolic jugular pulse wave often
occupies exactly the place which should have been occupied by
the auricular elevation, and since it brings together simultane-
ously the auricular and ventricular systoles, it is single and is
frequently definitely higher than the normal systoles that pre-
Fig. 560. — Auricular and auriculoventricular extra-systolci
(Daniel Routier).
cede and follow it; in auricular extra-systole, the interpolated
extra-systolic jugular tracing represents in miniature the events
occurring in an ordinary cardiac cycle with its three waves: a,
presystolic or auricular; c, systolic or ventricular, and v, post-sys-
tolic or valvular (Figs. 558, 559, 560,* 561).
It should not be overlooked that in some instances the trac-
ing's are rather hard to interpret; under these circumstances
electrocardiography may be of service.
46
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706 SYMPTOMS.
3. Again, whereas in ventricular extra-systoles the normal
rhythm of the heart, aside from the premature contraction itself,
is not disturbed, this is not true of the auricular extra-systoles,
in which, even apart from the extra-systole, the heart rhythm
may exhibit more or less irregularity.
The extra-systole or premature contraction is by far the most
common form of arhythmia encountered in cardiologic practice.
We have already seen the high degree of accuracy with which
the physiopathologic diagnosis may be established in these cases.
On the other hand, much discussion is still going on regarding
the prognosis ; the extra-systole, indeed, is a common reactive mani-
+-¥4-
Fig. 561. — Case 72, Auriculoventricular extra-systole.
festation on the part of the myocardium which m<iy be observed
under the most varied circumstances. Dyspepsia and aerophagia
frequently induce extra-systoles of reflex origin, practically devoid
of significance from the cardiac standpoint; yet these same ex-
tra-systoles may be expressions of more or less marked degen-
eration of the myocardium.
In short, the extra-systole per se is of no prognostic significance ;
all depends upon the circulatory symptoms and signs which
accompany it.
For practical purposes, there may be differentiated:
1. Fimctional, reflex extra-systoles (aerophagia, dyspepsia,
or nervousness) or toxic extra-systoles (gout) — intermittent,
temporary extra-systoles generally unaccompanied by any dis-
turbance of the circulation save occasionally a temporary eleva-
tion of blood-pressure (neurocardiac erethism), and devoid o£
any prognostic significance as regards the heart and circulation.
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ARHYTHMIA, 707
2. Lesional extra-systoles, as a rule practically permanent,
occurring in conjunction with some myocardial lesion and ac-
companied by the ordinary signs of myocardial and vascular
degeneration which will be repeatedly mentioned hereinafter —
changes of blood-pressure, stasic phenomena, dyspnea on ex-
ertion, signs of aortic degeneration, etc. In this event the extra-
systole is a sign of myocardial degeneration which, taken in
conjunction with the others, leads to the usual guarded prog-
nosis of myocarditis.
In brief, detection of extra-systoles should lead the practi-
tioner to make a complete, systematic examination of the cir-
culatory system. If the examination proves negative, the prog-
nosis will be definitely favorable, viz,, that of aerophagia, dys-
pepsia, or gout; if, on the contrary, it leads to detection of the
customar}*^ signs of myocarditis, the prognosis rendered should
be that of myocarditis. There is no doubt but that the extra-
systole may be, in the eyes of the patient, the first, significant
sign showing the presence of degenerative myocarditis — it is
from this viewpoint that its detection is of such interest to the
cardiologist.
PAROXYSMAL TACHYCARDIA.
Consideration of paroxysmal tachycardia is here taken up di-
rectly following that of extra-systoles because recent cardiologic
investigations have led to considering paroxysmal tachycardia as
consisting of extrc^sy stoles, generally of the auricular type, occur-
ring in uninterrupted succession for a period or paroxysm which
may last from a few sevonds to several weeks.
The subjoined diagram will satisfactorily illustrate the process
and may take the place of a definition (Fig. 562).
The diagnosis of paroxysmal tachycardia is relatively easy:
It may be put down as an axiom that any tachycardia exceeding
110 beats per minute, sudden in onset, unaccompanied by exoph-
thalmic goiter, not appearing in the presence of a febrile disorder,
and the rate of which is not appreciably modified by shifting from
the recumbent to the vertical posture, is paroxysmal tachycardia.
Difficulty of recognition arises only in individuals seen for the
first time, whose history is not known, and who, in conjunction
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708
SYMPTOMS,
with more or less pronounced tachycardia or tachyarhythmia,
exhibit evident manifestations of cardiac impairment,' such as
dilatation of the heart, edema of the lungs, congestion of the
liver and spleen, reduced urinary output, edema, etc. It may
be hard to find out whether the paroxysmal tachycardia was the
initial manifestation of the trouble or whether, on the other
hand, the tachyarhythmia observed is merely an evidence of
heart failure. The sudden onset, accurate graphic studies, and
the therapeutic test will settle the question of diagnosis under
such circumstances.
The onset is always abrupt — and is frequently perceived by
••••«iiiii^»rist
I I I I I I I I |. fi I 9 •
Fig. 562. — Diagram representing a brief attack of paroxysmal tachy-
cardia consisting of eight successive auricular extra-systoles (premature
contractions). A ventricular contraction takes place in conjunction with
each of these extra-systoles. Note the abrupt onset and termination of
the attack and the unusual prolongation of the final pause.
the patient as a kind of sudden thump in the precordium, a sen-
sation of unleashing of the heart, or a pronounced palpitation
coupled with general malaise; — at times, however, no subjective
sensation is awakened.
The duration may be extremely short — ^the attack consisting
merely of a series of premature beats varying from a few to
several dozens in number. The attack generally continues from
a few hours to a few days, more rarely a few weeks.
Sometimes the paroxysm is unaccompanied by any appre-
ciable subjective sensation. Usually, however, there are ob-
served digestive disturbances, such as flatulence, regurgitation, nau-
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^ ARHYTHMIA. 709
sea, and vomiting, and cardiac manifestations, some of the anginose
type, e.g., distressing dyspnea or a sensation as of constriction,
gripping, pressure by a tight band, or squeezing, others of the
type of inadequate heart action, e,g,, congestion of the liver and
lungs, cyanosis, venous engorgement, etc.
Usually the attack ends abruptly, as it began. Very exception-
ally sudden death has been witnessed; sometimes, though very in-
frequently, the heart-muscle is observed gradually to give out,
death taking place from asphyxia.
As in the case of extra-systoles, the prognosis' ol paroxysmal
tachycardia is much less dependent upon the tachycardia per se
than upon other attendant factors, particularly the pre-existing
state of the myocardium.
'Tkhjc)>snxjs26.ity," *h^
J
Fig. 563. — Paroxysmal tachycardia {Daniel Routier).
For practical purposes one may, as with extra-systoles, dis-
tinguish :
The functional paroxysmal tachycardia of the neurotic, the
abnormally impressionable, and the sphygmolabile, unassociated
with any appreciable pathological changes and exhibiting, in
the intervals between attacks, a perfect circulatory balance, with
absence of any permanent symptom. This form of paroxysmal
tachycardia is not, as a rule, of serious import.
The organic paroxysmal tachycardia associated with or even
dependent upon manifest lesions of the myocardium or endo-
cardium, consisting most frequently of cardioarteriorenal scler-
osis or of mitral stenosis. The prognosis in these cases is that
of the underlying disease, aggravated by a paroxysm which, by
its prolonged duration, may in itself constitute a cause of rapid
exhaustion of the heart-muscle.
Thus, under such circumstances the author witnessed death
in seven days from progressive cardiac failure in a patient 80
years old, suffering from well compensated cardiovascular-renal
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710 SYMPTOMS.
sclerosis, who was seized with paroxysmal tachycardia (heart-
rate 170 to 180) one evening. Dyspnea was rather pronounced,
the respiratory rate ranging from 22 to 48; the heart-sounds
were muffled and unequal; no cough, no fever, no expectoration,
no edema, and no congestion of the liver or lungs; there were
marked borborygmi and meteorism, and dyspnea and arhythmia
recurred upon the slightest attempt to take food; the least ex-
ertion brought on a feeling of constriction, pressure, and op-
pression, with anginose manifestations.
Although not a complete failure, treatment by mustard packs,
digalen, camphor in oil, sparteine, oxygen injections, etc., proved
insufficient. Progressive weakening of the heart action was
witnessed, with associated congestion of the bases of the lungs,
paroxysmal seizures of cardiac dyspnea, reduced urinary output,
and polypnea. Death supervened on the seventh day.
The author's other cases of the same disorder recovered after
paroxysms lasting from a few hours to a few weeks.
In short, the pathological lesions present along with the
syndrome, and the duration of the tachycardial attack, are the
main factors governing the prognosis. Generally the prognosis
as regards continuance of life is favorable, even in the presence
of advanced sclerotic lesions.
RESPIRATORY (SINUS) ARHYTHMIA.
Respiratory or sinus arhythmia is, next to extra-systolic
arhythmia, the form of heart irregularity most frequently en-
countered in practice. It is definitely known to be the mildest
of the several forms of arhythmia.
The description of the normal heart rhythm already given
will greatly facilitate comprehension of this form of arhythmia.
In accordance with the physiopathologic observations already
recalled, the normal rhythm of the heart is dependent upon a
stream of regular stimuli starting rhythmically in the sinoau-
ricular node (node of Keith and Flack) and transmitted thence
in succession to the auricular myocardium and the ventricular
myocardium by the conducting system previously referred to.
This sinoauricular node, however, is itself manifestly under
the control of the vagus or pneumogastric nerve, which exerts
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ARHYTHMIA.
711
an inhibitory effect upon it. Destruction of the pneumogastric,
more especially of the trunk on the right side, or its physiologic
suppression by the administration of atropine, which paralyzes
1HW1»>||I|'|IH||IIII III
I i ■ 1 1 I I 1 1 I
Respiration.
Right radial.
Fig. 564. — Case 236. Respiratory (sinus) arhythmia.
it, consequently accelerates the heart-rate; stimulation of it, on
the other hand, slows the heart.
As a rule, in man, this brake-like or inhibitory action of the
vagus is not noticeable. In certain individuals, however, par-
Respiration
Fig. 565. — Case 236. Sinus arhythmia.
ticularly in the majority of children, as well as in a few adults
(and always in dogs), this action is plainly present and is mani-
fested in a pronounced arhythmia, affecting both the frequency
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712
SYMPTOMS.
and the amplitude of the heart-beats, and distinctly subordinate
to the respiration. Even a cursory examination, with simulta-
neous palpation of the radial pulse and the respiratory rhythm
(inspiration and expiration), reveals a manifest relationship be-
■ 11 I'H^ I M
111! » mil nil II I I II I II I llnTI ijll
^
/.^..>gwi^H'^Jhl4-^»^^
.t{J^^,^
Fig. 566. — Case 236. Sinus arhythmia.
tween the arhythmia and the time of the respiratory movements,
the circulatory irregularity being observed to consist of an ac-
celeration of the pulse occurring with inspiration and a slowing
of the pulse with expiration.
]1^.f..lf,.\f?f.^'!\f'.\.''!t.\
Fig. 567. — Case 263. Sinus arh)rthmia. Cardiogram.
E, expiration ; /, inspiration.
The tracings herewith reproduced (Figs. 564 to 567) clearly
illustrate this close interdependence between the circulation and
respiration. As a matter of fact, the phenomenon is merely the
expression of a normal condition to an exaggerated degree, and
may almost always be recorded if, while a tracing is made, the
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ARHYTHMIA, 713
respiratory movements are purposely amplified to the point of
deep inspiration and forced expiration.
a c
AaXV-^'A^^W^
Fig. 568. — ^Diagrram illustrating respiratory (sinus) arhythmia. A and
V stand, respectively, for the auricular and ventricular contractions, taking
place in normal succession. The arhythmia here consists of an alter-
nate acceleration and slowing of the auriculoventricular cycles, due to
actual arhythmia of the initial stimulus originating at the sinus.
This form of arhythmio., representing at most the exagger-
ated expression of a normal process, perhaps points to an in-
VV V VVVV'VVnivS
Fig. 569. — Case 36 ter, Cheyne-Stokes rhythm. H., 61 years; Feb. 28,
1913; sitting position; pulse, 100 (?) ; pressures, ®*9i8o; viscosity, 6.4.
creased irritability of the sinoauricular node. At all events
it is certainly devoid of all prognostic significance, and yields
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714 SYMPTOMS.
but a single therapeutic indication, vis., that of allaying all
apprehension on the part of the patient and his family, and
therefore of ordering no treatment, which might simply lead
the patient to fear and believe that some abnormal condition
was really present in his case.
The above diagram will s^sist the reader in understanding
the probable mechanism of this form of arhythmia (Fig. 568).
As a matter of interest there is also reproduced herewith
a tracing from a case of respiratory arhythmia in which condi-
tions were manifestly far different from the group previously
referred to; the tracing was obtained in an azotemic patient
during an attack of cardiorespiratory dyspnea of the so-called
'*Cheyne-Stokes type" (Figs. 569 and 570).
Fig. 570. — Case 36 ter. Cheyne-Stokes rhythm (continued),
(To be read from right to left).
AURICULOVENTRICULAR DISSOCIATION.
The diagrams already presented in illustration of the normal
heart rhythm, extra-systoles, and paroxysmal tachycardia are of
further marked utility in defining and describing auriculoventricular
dissociation or heart-block.
The normal rhythm of the heart is dependent upon regular
transmission of a stimulus to contraction from the sinoauricular
node (of Keith and Flack) from the auricle to the ventricle along
the bundle of His (Fig. 571).
If this process of transmission is protracted or delayed owing
to some hindrance to conduction, as shown in Fig. 572, a tend-
ency to heart-block will occur which will be shown in tracings
by increased length of the a-c interval and by the appearance
of a short pause between the end of auricular systole and the
beginning of ventricular systole. This constitutes auriculoven-
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ARHYTHMIA, 715
tricular dissociation of the first degree, or better, a tendency to-
ward heart-block (Fig. 572).
If transmission is interrupted from time to time, if some
«^
A
r
^ normal
Fig. 571. — Normal tracing.
obstacle to conduction results in its being occasionally broken
oflF, some of the auricular systoles will fail to send their con-
tractile impulses to the ventricle.
M/M>*^A/''^Ay^
Fig. 572. — ^Tracing showing a tendency to auriculoventricular dissociation.
Delayed conduction. Prolongation of the o-r interval.
Suppression of some of the ventricular contractions will oc-
cur under these conditions. This constitutes auriculoventricu-
lar dissociation of the second degree or incomplete (partial)
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716
SYMPTOMS.
heart-block (Fig. 573). If the interruption, at first accidental
and irregular, increases and becomes regular and rhythmic, the
degree of dissociation may be expressed in some definite ratio.
Thus, if the ventricle responds once out of twice to the auricu-
lar stimulus, the heart-block is stated to be of the 2:1 variety;
if it responds only once out of three times, of the 3:1 variety,
and so on.
The ultimate degree of aiuiculoventricular dissociation, or
complete heart-block, is produced when all conduction between
I9IIIIIIIIIII Itlltlllllllfl
II II
I I I I
Fig. 573. — Partial heart-block. Incomplete auriculo-
ventricular dissociation.
the auricle and ventricle is arrested, as illustrated in Fig. 574;
the auricles and the ventricles contract independently; their
respective rhythms are completely dissociated and unrelated.
The auricular rate is about 72 to the minute, while the ventricu-
lar is 30. There is said to be present a bradycardia through
auriculo-ventricular dissociation.
The foregoing statements constitute the simplest descrip-
tion that can be given of auriculoventricular dissociation or
heart-block (Figs. 571 to 574).
The seat of this form of arhythmia is plainly the bundle of
His. This bundle has been found diseased in most of the cases
of auriculctventricular dissociation coming to autopsy; yet this
systematic investigation has given absolutely negative results
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ARHYTHMIA.
717
in a certain number of instances. One is therefore led to the
conclusion that, as in the case of extra-systoles or tachycardia,
there may occur, aside from the organic, permanent auriculo-
ventricular dissociation due to disease of the bundle of His
(gumma, fibrosis, post-infectious or post-rheumatic degenera-
tions), cases of functional, transitory auriculo-ventricular disso-
ciation (digitalis block, temporary block in rheumatism and in-
fectious diseases, stimulation of the vagus, etc.).
For practical purposes, syphilis, rheumatism, and connective
• I f I I I I t I I I t I f I I I I t I I I I I I I I 1 f 1
\ \ \ \ \ \ \
\ \ \ \
Fig. 574. — Complete auriculoventricular dissociation. The auricles and
ventricles contract inco-ordinately and independently.
tissue degenerations are dominant in the etiology of auriculo-
ventricular dissociation.
Finally, it may be added that, in regard to the semeiology of
bradycardia, it is necessary to distinguish instances of bradycardia
which might be termed fascicular, being due to disease or defective
functioning of the bundle of His and auriculoventricular disso-
ciation, and the nodal or total forms of bradycardia, the result
of deficiency in the process of stimulus production in the sino-
auricular node, and imaccompanied by auriculoventricular disso-
ciation.
Diagnosis. — ^The problem of diagnosis of auriculoventricular
dissociation, as it is placed before the unspecialized practitioner,
may seemingly be presented as follows:
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718 SYMPTOMS.
The diagnosis of incomplete auriculoventricular dissociation
is practically limited to a differentiation of this condition from
extra-systole. Radial palpation and simultaneous auscultation of
the heart permit of easily and almpst positively settling the
question. In auriculoventricular dissociation, the pause noted
at the radial artery is coupled with complete absence of heart-
sounds, since no ventricular contraction takes place (Fig. 573) ;
in extra-systole, on the other hand, the pause at the radial is
coupled with one or two heart-sounds due to the superadded
I I I I I I I I I I I I I I I I I I I I I I I I I I I I • I I I
R.
All I III I I I I I I
Fig. 575.— Extra-systole (premature contraction).
extra-systolic contraction of the ventricles (Fig. 575). In the
first instance there is present the ordinary rhythm merely slowed
down in two phases, or rather, consisting of the two sounds,
systolic and diastolic; in the second instance there is a three-
phase rhythm comprising the two normal systolic and diastolic
sounds followed by the systolic sound of the extra-systole, or
a four-phase rhythm (echo rhythm) if the extra-systole, having
forced open the sigmoid valves, is accompanied by a second,
diastolic sound (Figs. 575 and 576).
The diagnosis of complete auriculoventricular dissociation
which is ohjectizfely manifested in a very pronounced bradycardia
(30 to 40), iy made as follozvs:
1. Is there present bradycardia or bradysphygmia?
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ARHYTHMIA.
719
2. Is the dissociation functional in type (usually of extra-cardiac
origin and due to abnormal excitation and defective functioning
of the pneumogastric nerve) — or is it organic (of intracardiac origin
and due to a syphilitic or rheumatic fibrotic disease of the bundle
of His) ?
• I •• I I I I I I I
• I I I I I f I I I i
II II I I I I
Fig. 576. — Partial heart-block.
Auscultation will promptly answer the first question, as it
did in the case of extra-systoles. Combined palpation of the
radial artery and auscultation will show that for every radial
pulsation noted there are two contractions of the heart — one
a systole and the other an extra-systole.
Fig. 577. — Delayed conduction (^Daniel Routier),
In answering the second question the following clinical feat-
ures should be availed of:
1. Functional bradycardia (of extracardiac origin) is, as a
rule, transitory, terminating upon cessation of its original cause ;
organic bradycardia (of intracardiac origin), however, is perma-
nent
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720
SYMPTOMS.
2. Administration of 2 milligrams of atropine, by paralyzing
the cardiac terminals of the vagus, will generally cause func-
tional bradycardia to disappear for a time ; organic bradycardia,
on the other hand, is not perceptibly influenced by it.
Fig. 578.— Partial heart-block (Daniel Routier),
3. Change of posture {e.g., passing from recambency to the
erect posture and ince versa), exertion, deep or forced inspiration,
fever, and locomotion cause a distinct change in the rate in
4.5J3.D/5SOC complete
Fig. 579. — Complete dissociation {Daniel Routier) .
functional bradycardia; in organic bradycardia, on the other
hand, they exert no appreciable effect.
Many recent investigations have seemed to show that these
indications are not of absolutely positive significance.
Fig. 580.— Total bradycardia (Daniel Routier).
For the practitioner specializing in cardiology, the problem
of diagnosis is often markedly facilitated and illuminated by
the employment of graphic procedures, whereby auriculoven-
tricular dissociation may be recorded in the jugular, radial, and
cardiac tracings, as shown in the annexed diagrams for which
the author is indebted to his colleague, Daniel Routier (Figs.
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ARHYTHMIA. 721
577, 578, 579, 580).^ Electrocardiography will almost certainly
settle the question when availed of as a last resort in doubtful
cases (Fig. 581). The most characteristic indications in the
tracing are:
1. Abnormal prolongation of the a-c period.
2. A pause — ^which may be very brief — between the end of a
and the beginning 'of c in cases of incomplete dissociation.
3. Dissociation of the auricular rhythm a in the jugular trac-
ing from the ventricular rhythm (radial pulsations and apex-
beat) in cases of- complete dissociation.
It should be noted that in the complete form of dissociation
there is often perfect adaptation of the system to the new circula-
tory rigime, the slowing of the systolic contractions being com-
Fig. 581. — Complete dissociation. Electrocardiogram (Daniel Routier).
52. 11. 12. Aur. = 62; ventr. = 17. Lead I, ord. 1 cm. = 1 millivolt;
absc. 2H^ cm. = 1 meter.
pensated for by their increased power, objectively manifested
in the resulting full, large pulse — very striking upon palpation
and in the tracings — and in an increase of both the systolic and
diastolic blood pressures. The ventricle, well filled in the course
of a prolonged diastole, empties itself completely as the result
of a powerful contraction.
Proper diagnosis of auriculoventricular dissociation is a mat-
ter of great prognostic and therapeutic importance. When func-
tional, it is unattended with risk, as a rule, and terminates as
soon as its original cause is removed. When organic, it points
either to serious myocardial degeneration, of which it constitutes
in Itself an especially dangerous local manifestation, or to the
localization of some destructive or degenerative process, such as
1 For further details the reader is referred to Routier^s thesis entitled
"Etude critique sur les dissociations auriculo-ventriculaires/' Paris, J. B.
Bailliere, 1915.
46
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722
SYMPTOMS,
syphilis, rheumatism, or some infectious disorder, in the bundle
of His.
The study of auriculoventricular dissociation, and more particu-
larly of bradycardia, is intimately related to that of Stokes-Adams'
disease. The features presented in this condition are well
known. The patient suffering from it is subject to syncopal,
^-*^ ^
./r^
Marked basal
^syetolic murmur
Short
Fig. 582.— Oct 16, 1911. Case 263 his. H., 59 years. Bradysphyg-
mia counteracted by belladonna. Marked dilatation of aorta. Cardiac
h)rpertrophy. Elevation of the subclavians.
epileptiform, or syncopo-epileptiform attacks. The attack is
heralded by a kind of aura, characterized by general malaise,
tinnitus aurium pallor of the face, etc.; it is associated with a
paroxysmal slowing of the pulse, with pauses — actual periods of
asystole in the literal sense of the word — which may continue
for ten or more seconds. The disorder may be present to any
extent and with any degree of frequency, varying from the
transient mental confusion similar to that which an extra-sys-
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ARHYTHMIA.
723
tole causes in some subjects to the serious syncopal attack with
prolonged cardiac arrest which may result in death.
Before Charcot's time such a condition was ascribed mainly
to the myocardium, which had sometimes been found in a state
of degeneration ; in accord with Charcot's view, it was attributed
chiefly to the extracardiac nervous system (medulla or vagus
11. 16. 1911
4. 10. 1912
■ ■ M'l^ri^i'i^
2. 12. 1913, 8
Fig. 583. — Case 263 bis. Cardiogn^m and sphygmogram taken at differ-
ent stages in the course of the case referred to in Fig. 582.
nerve) ; after the discovery of heartrblock, however, it came to
be ascribed wholly to auriculoventricular dissociation, due, in
turn, to disease of the bundle of His. At the present time there
exists a tendency to revert toward a much more eclectic con-
ception of the condition, according to which the Stokes- Adams
syndrome — slow pulse with syncopal or epileptiform attacks —
may be caused by any functional disturbance or any organic
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724 SYMPTOMS,
change capable of inducing^ a pronounced slowing of the pulse-
rate:
1. Organic disease or functional disorder of the medulla or of
the pneumogastric,
2. Organic disease of the bundle of His and at times more
particularly of the node of Keith.
3. Or even extensive and severe disease of the myocardium with-
out any special localisation in the organ.
At all events, the author has encountered Stokes-Adams'
disease in two cases in which auriculoventricular dissociation
seemingly could with justification be excluded.
In the first of these cases (Figs. 582 and 583), the patient
was a man aged 59 years, suffering chronically from rheumatism
and with a past history of jaundice, exhibiting an extensive
aortic lesion and a marked systolic murmur at the base of the
heart, succeeded by a rolling sound which continued throughout
the short pause, and who for several years previously had
noticed a slow pulse (55) in the morning on awakening. For
the preceding seven or eight months this patient had been sub-
ject to periods of dizziness and confusion consentaneous with
a slowing of the pulse to 48; for the last six months he had
been subject to sudden, alarming, quasi-syn copal attacks with
sudden pallor and transient amnesia which had compelled him
to give up completely his ordinary occupation. Having been
obliged at the time to stay abed for seven weeks because of
complete inability to rise without syncope, he had found that
when recumbent he felt very well and was in complete posses-
sion of his mental faculties, whereas if he sat up he felt faint
and was completely amnesic. A strict diet and treatment with
a combination of adonis and theobromine had made him, if any-
thing, worse; a more generous diet had enabled him to leave
his bed, and a stay in Savoy brought about some general better-
ment. Bradycardia (?) and syncopal attacks continued, how-
ever, and it was under these circumstances that the patient came
to consult the author. The man showed an extensive and mani-
fest aortic lesion (pronounced systolic murmur continued as a
rolling sound during the short pause, and a clanging sound in
diastole). The pulse rate was remarkably low (33), but the
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ARHYTHMIA. 725
heart-beats were double as compared to the pulse (66). Aus-
cultation elicited the characteristic "echo rhythm" — ^Toc Toe,
toe toe. The radial tracing was typical, showing a bigeminal
pulse the result of extrasystoles, with the second pulsation im-
palpable, producing the condition termed bradysphygmia. The
systolic blood pressure was 165 mm., the diastolic, 85 mm., and
the blood viscosity, 4. No albumin.
In short, there were present aortitis and myocardial degenera-
tion, bradysphygmia due to bigeminal extrasystoles, and syncopal
attacks.
The author merely prescribed, along with a liberal diet, the
following pills:
Extract of belladonna 0.01 gram.
Extract of adonis 0.10 gram.
To make one pill. — Five pills a day.
Almost immediately the dizziness and malaise passed off,
and the pulse rate rose to 60 through disappearance of the extra-
systoles. The blood pressure rose slightly to 175 to 180 mm.,
systolic, and 85 or 80 mm., diastolic. The patient gradually re-
sumed his former occupations. His restored condition has now
been maintained for six years.
In a second case (No. I64bis), encountered' in a patient 54 years
of age, likewise having an aortic lesion and suffering from at-
tacks sometimes of a syncopal and at others of an epileptoid
type, with marked slowing of the pulse, tracings made in the
intervals between attacks showed no abnormality of heart
rhythm save a slight tendency to slowing of the rate (58), with
practically normal blood pressure (145 and 95 mm.) and a
slightly increased viscosity (4.5).
Prognosis. — The prognosis depends:
1. On the nature of the dissociation: If functional, it is gen-
erally not of serious import and terminates when its toxic, dia-
thetic, or infectious (rheumatism, pneumonia, or typhoid) cause
is removed.
2. On the grade of the heart-block: Manifestly the slight,
partial, and temporary grades of block are less serious than the
pronounced, complete, and permanent forms.
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726 SYMPTOMS.
3. On the other myocardial or endocardial lesions simultane-
ously present: The prognosis in complete, permanent auriculo-
ventricular dissociation is grave, in the first place because it is
an expression of a particularly serious localization of the myo-
carditis, and secondly and more especially, because it is usually
accompanied by deep-seated and extensive myocardial degenera-
tion.
4. On the syncopal and epileptiform attacks which may ac-
company the condition.
(a) In the milder form, there are noted brief fainting spells
with transitory unconsciousness, facial pallor, and a very short
period of pulselessness.
(b) In a more advanced form, the unconsciousness is supple-
mented by convulsive movements of the face and upper extrem-
ities. It should be noted that incontinence of urine and biting
of the tongue are, as a rule, absent. The condition of the cir-
culation at the time is characterized by absence of the ventricu-
lar contractions, resulting, in turn, in pulselessness, and by per-
sistence of the auricular contractions, manifested in rapid wave-
like movements along the veins of the neck.
(f) Death may be observed — ^though exceptionally — in the
course of an attack or a series of attacks of the type above de-
scribed.
ALTERNATION OF THE PULSE.
None of the forms of arhythmia previously referred to, vis.^
extra-systoles, paroxysmal tachycardia, sinus arhythmia, and
bradycardia, in itself supplies any definite prognostic indication.
The fact was sufficiently stressed that these disorders do not,
taken alone, constitute accurate prognostic factors, and that each
of these varieties of arhythmia is of markedly variable sig^ifi-
cartce according as it is of a functional or organic tiature, and
that, on the whole, the condition is of clinical value and sig-
nificance only as a factor taken in conjunction with the other
existing disturbances. This is by no means the case, however,
with the two forms of arhythmia still to be described, vis.,
the alternating pulse and perpetual arhythmia, to both of which
attaches a definite and serious clinical signification. The former.
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ARHYTHMIA, 727
being an expression of deep-seated myocardial degeneration, is
considered by Gallavardin as **a highly important sign — ^perhaps
tlie best sign — of inadequacy of the left ventricle," while the
latter points to auricular fibrillation.
The alternating pulse consists essentially in the alternate
occurrence, at practically normal, regular, and equal intervals,
of a large beat and a small beat. There is strictly speaking, no
arhythmia, but simply a regular alternation of two unequal
beats. At the most, the small beat may be slightly delayed due
to a slight retardation of cardio-peripheral conduction.
1 I I I I I i I I I I 1 I I I I I I I I I I I I I I I
Fig. 584. — Diagram of the alternating pulse. Strong and weak
contractions take place in alternation.
A bigeminal pulse the result of extrasystoles might possibly
be confused with the alternating pulse, being likewise attended
with an alternation of large and small pulse beats. In contrast
with the alternating pulse, however, the extrasystole or small
systole comes closer to the preceding than to the following beat ;
in the alternating pulse, the small beat is closer to the succeeding
than to the preceding beat. If careful palpation and ausculta-
tion fail to settle the question, an ordinary sphygmographic
tracing will promptly do so.
True alternation of the pulse is of the gravest prognostic
import, and Lewis does not hesitate to compare it with sub-
sultus tendinum, optic neuritis, and risus sardonicus as a sign
of the most unfavorable portent Frequently it is associated
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728 SYMPTOMS.
with cardiac dyspnea, anginal attacks, and Cheyne-Stokes breath-
ing. But even when present alone, its sombre prognostic im-
port is retained: It is a certain indication of deep-seated myo-
cardial degeneration and of advanced exhaustion of the heart-
muscle.
A few recent observations, those of Gallavardin among others,
have seemingly tended toward reduction of the gravity of the
prognosis in these cases. The author has personally o"bserved
three distinct cases of alternating pulse with respective survival
periods of six, seven and a half, and fifteen months.
PERPETUAL ARHYTHMIA (AURICULAR FIBRILLATION).
Perpetual arhythmia, the delirium cordis of olden times, was
for a long period a puzzle to cardiologists. To electrocardiog-
raphy we owe, if not an absolute, complete elucidation of the
condition, at least an explanation which accotmts for the great
majority of cases and affords the best view into its mode of
production.
Perpetual arhythmia consists, as the term implies, of a per-
manent arhythmia characterized by extreme irregularity and
baffling all description. The succeeding systolic contractions
are irregular both as to duration and intensity.
Prolonged discussions as to the exact pathogenesis have been
indulged in; — electrocardiography seems to have definitely
shown that this type of arhythmia is dependent upon a special
condition of auricular activity which is well expressed by the
term auricular fibrillation.
The following description of this condition is borrowed from
Thomas Lewis: "When we inspect the normally beating heart
of an animal, the systoles of both auricle and ventricle are readily
discerned. The movement of the auricle is a sharp flick, most
clearly perceptible in the length of the auricular appendix, for
in this line the shortening is greatest. When the auricle is
forced into fibrillation or delirium, the appearances are quite
distinctive ; the muscular walls are maintained in a position of
diastole; systole, either complete or partial, is never accomp-
lished; the structure as a whole rests immobile; but close ob-
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ARHYTHMIA.
729
servation of the muscle surface reveals its extreme and incessant
activity, rapid and minute twitchings and undulatory movements
are visibk over the whole. It is believed that the tissue mass
has suffered functional fragmentation and that a number of small
areas give independent birth to new impulses. . . . The effect
of the auricular confusion upon the ventricle is two-fold. The
normal, regular and co-ordinate contractions in the auricle are in
abeyance and consequently the ventricle is robbed of the regular
impulses which form its accustomed supply. These are replaced
by numerous and haphazard impulses, escaping to the ventricle
-^
Fig. 585. — The auricular muscle fibers fail to contract in co-ordinate
and rhythmic fashion. The auricular tissue is dissociated into a large
nimiber of small areas contracting independently. Some of the auricular
impulses reach the ventricle at wholly irregular intervals, awakening
there contractions which are both frequent and irregular. /, jugular; R,
radial.
from the turmoil which prevails in the upper chamber; the
change in the action of the ventricle, when the auricle fibrillates,
is consequently profound. Its rate of beating rises considerably
and the contractions follow each other in a completely irregular
fashion."
. The above diagram will give an approximate idea of the me-
chanism involved (Fig. 585).
Electrocardiography plainly demonstrates the fact that the me-
chanism above described is actually operative. The P wave char-
acteristic of auricular systole is suppressed and is replaced by a
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730 SYMPTOMS.
series of rapid, irregular oscillations of slight amplitude, ffff
(Fig. 586). ^
Sometimes the fibrillary twitchings of the auricle may even
be discerned rather clearly on a good polygraphic tracing (Figs.
587 and 588).
Electrocardiography alone yields an objective observation
and reliable record of auricular fibrillation.
For clinical and practical purposes the diagnosis may, how-
ever, be made either with or without the help of graphic pro-
cedures.
Fig. 586. — Electrocardiograms illustrating the 3 leads in a case of
mitral stenosis with auricular fibrillation. The R wave is very small
with Lead /, whereas 5 is pronounced; with Lead ///, R appears the
highest. There are evidences of hypertrophy of the right ventricle. The
ventricle is beating very irregularly. There is no P wave, but on the
other hand there are found a number of rapid oscillations, /, /, resulting
from the fibrillation of the auricles {Cambridge Association),
The following 3 practical rules may be given in this connec-
tion :
1. Any case of tacJty-arhythmia unth a heart-rate exceeding 130
is nearly always associated with auricular fibrillation and per-
petual arhythmia (the factor of irregularity comprised in the
arhythmia excludes instances of increased heart-rate due to fever
or emotion, as well as tachycardia of the nervous or paroxysmal
types, etc.).
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ARHYTHMIA. 731
2. Any persistent arhythmia coupled with signs of advanced
cardiac impairment is almost always dependent upon auricular
fibrillation. The probability becomes practically a certainty if
the arhythmia is associated with tachycardia.
3. Any case of arhythmia, even if unaccompanied by manifest
signs of existing cardiac impairment, any arhythmia which is in-
creased by acceleration of the pulse, such as might be induced
by moderate exercise, is likely to be a perpetual arhythmia. The
Fig. 587. — Auricular fibrillation {Daniel Routier).
other types of arhythmia, on the other hand, and in particular
extrasystolic arhythmia, are reduced or even disappear under
the influjMice of pulse acceleration.
The polygraphic method records an extreme and permanent
arhythmia in these cases. The radial tracing consists of unequal
and irregular systoles, constantly varying in duration and power ;
the jugular tracing generally assumes the so-called "ventricular
type," showing a series of oscillations synchronous with the
^^''-'^■'^'^X^'^j,/'^^
Fig. 588.— Case 248. H., 56 years; 169 cm.; 64.8 kilograms. Auricu-
lar fibrillation (perpetual arhythmia).
6. 23. 1913; pulse, 72 (?) ; pressures, i3%oo (?) ; viscosity =
4.3. H = 1200. Albumin absent.
ventricular contractions, but with absence of the a wave charac-
teristic of auricular systole. Sometimes, on the most successful
tracings, there is noted a series of minute and rapid presystolic
undulations, an aictual expression of auricular fibrillation (Figs.
587 and 588).
Electrocardiography records auricular fibrillation more or
less clearly (Fig. 586).
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732
SYMPTOMS.
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ARHYTHMIA, 735
Is tricuspid insufficiency always present in perpetual arhyth-
mia, and does recognition of the presence of perpetual arhythmia
necessarily mean recognition of the presence of tricuspid insuffi-
ciency? Some observers have thought themselves justified in
giving a positive answer to this question. The author, however,
has met with many cases of perpetual arhythmia in which there
were no apparent signs permitting of recognition of the presence
of tricuspid insufficiency. This latter condition has seemed to
him relatively frequent in these cases, but not constant.
Auricular fibrillation and perpetual arhythmia are always as-
sociated with and probably dependent upon a deep-seated degen^
eration of the myocardium and advanced cardiac insufficiency.
Their signs are therefore likely to be observed in association
with those of myocardial degeneration and heart weakness,
znc, dyspnea on exertion, cyanosis, venous stasis, passive con-
gestions, hepatic engorgement, edema, reduced output of urine,
etc. ; and it is very hard to say whether any one of these symp-
toms is dependent upon them or even whether they are exagger-
ated through the presence of fibrillation and arhythmia — which,
however, is very probably the case.
Attacks of paroxysmal fibrillation with manifest recrudes-
cence of both the arhythmia and the associated symptoms —
dyspnea, cyanosis, edema, etc. — may be witnessed. Other pa-
tients, however, seem hardly influenced by the condition. The
same is true, indeed, of paroxysmal tachycardia ; probably these
reactions, seemingly so diflFerent, are both actually dependent
upon the state of the myocardium ; if it is but slightly impaired,
the general circulation is comparatively little influenced by recru-
descence of the arhythmia; if, on the other hand, it is profoundly
degenerated, the usual signs of cardiac insufficiency will rapidly
appear.
Mitral stenosis, myocardial degeneration, and arterio-renal
sclerosis are the conditions nearly* always associated with per-
petual arhythmia.
The prognosis of perpetual arhythmia must therefore always
be guarded, since auricular fibrillation in itself constitutes a
positive sign of more or less advanced degeneration of the myo-
cardium and a probable sign of widespread degeneration.
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736 SYMPTOMS,
Nevertheless — and in this condition the therapeutic test is often
conclusive — certain instances of perpetual arhythmia are mark-
edly reduced by well-directed drug treatment, while others are
completely refractory. The prognosis is obviously profoundly
influenced by these factors. On the whole, the same conclusion
always follows, vis,, that the prognosis is governed much more
by a study of the contractility of the heart muscle than by a
study of its conductivity.
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ASCITES.
[dax^Sy a water-bag; an abdomen havingX
the shape of a water-bag. J
Ascites^ derived from the word d(T;^6$, a water-bag, on ac-
count of the resemblance of the abdomen distended with serous
fluid to such a vessel, consists of an intraperitoneal serous effu-
sion (hydroperitony, dropsy of the peritoneum, dropsy, etc.).
Becognition of Ascites.— Accumulation of fluid in the peri-
toneal cavity is generally a slow, gradual process ; in the excep-
tional cases of ascites spoken of as a frigore, due to sudden ob-
struction of the portal vein, effusion may take place rapidly.
Though sometimes obvious^ especially when it has attained
a certain size, when the abdominal parietes are relatively thin,
and when the fluid is freely movable, its recognition may in
other instances be attended with considerable difficulty when,
as is frequently the case, the parietes are thick and infiltrated,
when the effusion is of slight or moderate extent, when its
mobility is limited owing to adhesions, etc.
Clinically, its recognition is to be based on a systematic ex-
amination of the case:
Inspection.
(a) Shape of the Abdomen. — 1. Vertical position: Abnormal
prominence of the hypogastrium and the iliac fossa.
2. Recumbent position: The flanks broaden and flatten out,
like the abdomen of an amphibian; the fluid moves about, on
the whole, according to gravity, therefore passing to the de-
pendent side when the patient is in lateral decubitus.
3. Occasionally the umbilicus, turned out like a glove finger,
forms a small, soft, fluctuating, depressible, translucent tumor.
(6) Condition of the Skin. — The skin is frequently smooth,
white, even, polished, and shining; sometimes thickened, infil-
trated, and edematous; at times erythematous. Striae compar-
able to tttose of pregnancy may be noticed upon it.
47 {7i7)
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738 SYMPTOMS.
(f) Superficial Venous Circulation. — ^The accessory portal
veins, normally only slightly developed, enlarge, sometimes to
a considerable size, in the event of obstruction to the blood-
current through the portal vein. The circulation is in part re-
established through these vessels, whence there occurs dilata-
tion of the subcutaneous veins of the abdomen, with the pro-
duction of a prominent network of veins between the pubis and
the xiphoid appendix, especially on the right side, in the form
of a peri-umbilical venous plexus.
(d) Sometimes there is concomitant hydrocele, owing to per-
sistence of the vagino-peritoneal duct
Palpation. — ^The abdomen exhibits an even, tense, sometimes
elastic^ and firm enlargement
The fluid present masks the intestinal mass and forms an
obstacle to detailed examination of the abdominal viscera,
whence the necessity of puncture in cases where such examina-
tion is imperative.
Percussion. — Flatness manifestly varies in extent according
to the amoimt of effused fluid.
1. Its primary localization is over the iliac fossae and the hy-
pogastrium (fluid) ; the umbilical and epigastric regions are gen-
erally the seat of tympanitic resonance (intestines), the transi-
tion from flatness to tympany being, however, gradual.
2. A small effusion may be unrecognizable on percussion ;
but if the patient is turned on the side, the fluid will collect on
that side and flatness be detectable.
3. The flatness exhibits movable margins, which vary accord-
ing to the patient's position if the ascites is movable and free;
it is fixed, however, if the effusion is encysted or walled off (Fig.
596).
Combined Palpation and Percussion. — ^This procedure yields
one of the most important indications of ascites, viz., fluctuation.
With one hand applied flat over one side of the abdomen,
the physician taps lightly with the other on the opposite side,
either by light percussion or by flipping a finger; the former
hand notes a sensation as of a blow or wave. It is often useful
to have some one else apply the ulnar border of one hand along
the linea alba, in order to prevent transmission of* wave-like
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ASCITES. 739
movements of the abdominal parietes, which would constitute
a source of error.
At all events, fluctuation is almost pathognomonic of ascites,
as it occurs in the absence of ascites only in a few exceptional
cases of ovarian cyst with thin walls.
Vaginal Palpation. — ^With this procedure, a doughy, firm con-
dition in the culs-de-sac is occasionally found.
Sometimes vaginal palpation may prove of service in aflford-
ing an early diagnosis of ascites (descent and reduced weight
of the uterus, and extreme mobility of the cervix).
Functional Evidences.
(a) Chiefly manifestations due to distention and pressure.
1. Increased size of the abdomen: The patient can no longer
button up his trousers.
2. Digestive disturbances: Constipation due to pressure on the
intestines, resulting in paralysis (Chopart's law: Any muscle
underlying an inflamed serous membrane is paralyzed). Indi-
gestion and tympanites.
3. Urinary disturbances: Dysuria, diminished secretion of urine,
oliguria, and opsiuria, chiefly on account of the loss of fluid
resulting from the ascitic accumulation.
4. Cardiopulmonary dyspnea due to pressure on the diaphragm,
causing reduced lung expansion and displacement of the heart.
5. Edema of the lower extremities, due either to the same cause
as the ascites or to pressure exerted on the inferior venae cavae.
{b) Functional disturbances attending the primary disorder
(cirrhosis, peritonitis, etc.).
With What Oonditions Might Ascites be Oonfounded?— (a)
Abdominal Meteorism. — Here, resonance and tympany are in-
creased ; yet, in truth, ascites is frequently accompanied by mete-
orism; in fact, meteorism may conceal an ascites. The best
differential sign in these cases, in the author's estimation, is the
displacement of the dullness upon assumption of lateral decu-
bitus, the dullness appearing in the most dependent area, at a
point previously resonant.
(&) Edema of the Abdominal Wall. — ^The finger leaves a
depression in the parietal tissues; dullness is uniformly distrib-
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740 SYMPTOMS,
uttd, knd fluctuation is absent. Abdominal edema and ascites,
however, frequently coexist
(f) Retention of Urine. — The bulging and dullness are dis-
tinctly located in the hypogastrium, with their convex aspect
directed upward — the opposite of the condition in ascites. Urine
is passed by overflow; palpation of the hypogastrium is more
or less painful.
In the event of doubt, which is seldom excusable, catheteriza-
tion of the bladder will dispel both the doubt and the abdominal
enlargement.
(d) Pregnancy. — ^The enlargement is hard, in the median
line, rounded, pyriform, and hypogastric in situation. Palpation
reveals that the uterus is the cause of the bulging. The convex
aspect is directed upward — the opposite of the condition in as-
cites. On the whole, the mere thought of the possibility of
pregnancy is enough to eliminate this source of error. If doubt
should nevertheless exist, the other signs of pregnancy should
be examined for, vis., cessation of menstruation, secretion of
colostrum and other mammary changes, progressive enlarge-
ment, and after four and a half months, the diagnostic fetal
signs.
{e) Ovarian Cysts. — ^The following distinguishing features
may with advantage be recalled:
1. Shape of the abdomen. — Globular, and with umbilicus nor-
mal, in ovarian cyst.
Flattened out and with prominent umbilicus in ascites.
2. Flatness. — In ascites : Flatness in the lumbar regions ; umbili-
cal region resonant; flanks flat; the .flat area is, in a general
way, convex below ; the areas of flatness are movable and vary
with the position of the patient.
In ovarian cyst: Resonance in the lumbar, iliac, and epigas-
tric regions ; flatness rather median and hypogastric in location,
and sometimes umbilical, with convexity directed upward; flat-
ness is not changed by altered position of the patient.
3. Fluctuation. — Practically constant in ascites; exceptional in
ovarian cyst.
4. History of case. — Often negative in ovarian cyst.
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ASCITES.
741
Dorsal decubitus.
Lateral decubitus.
Fig. 596. — Abdominal areas of flatness in ascites and various
other abdominal disorders.
1. Frank ascites of hepatic origin. 2. Encysted ascites of the peritoneal
type. 3. Ovarian cyst. 4. Pregnancy; retention of urine.
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742 SYMPTOMS.
Always positive in ascites, comprising such features as he-
patic disorder (cirrhosis), cardiac affections, general impairment
of health (tuberculous peritonitis), some serious organic affec-
tion (cachexia), etc.
Notwithstanding all these distinguishing features, many mis-
takes are made; the possibility of coexisting ascites and cyst
further complicates matters.
Oaases of Ascites. — In the presence of ascites, attention
should be particularly directed to the liver, peritonetim, and heart.
The diagnosis is based largely on the history of the case,
the existing physical signs, the course of the ascites, and the
nature of the fluid withdrawn by puncture.
(a) Ascites of Hepatic Origin (General Type: Atrophic Cir-
rhosis; Typical Ascites). — ^The. onset is slow, gradual, more
rarely abrupt, rapid after exposure to cold; the fluid is free in
the abdomen, movable, and fluctuation is readily elicited.
The history includes a more or less well-defined precirrhotic
stage, characterized by manifestations of increased portal pres-
sure (hemorrhoids, collateral circulation), indigestion and gas-
tro-intestinal disturbances, catarrhal disorders, meteorism, diar-
rhea, hepatic congestion and incipient jaundice, reduced output
of urine, etc.
1. The course of the disease is progressive.
2. The liver is always found diseased, generally reduced in
size (Laennec's atrophic cirrhosis), sometimes enlarged (hyper-
trophic or alcoholic cirrhosis of Hanot and Gilbert) ; the spleen
shows enlargement; there are manifest evidences of portal hy-
pertension, together with distinct impairment of nutrition. As-
cites may be encountered in syphilis of the liver or in primary
or secondary nodular cancer.
3. The fluid obtained by puncture is serous and poor in fibrin,
cellular elements, and protein material.
4. Nevertheless, it is well to bear in mind that peritonitis
may and frequently does accompany many forms of cirrhosis,
and that cases of fibrous, alcoholic, tuberculous, and syphilitic
hepatitis are quite often associated with localized peritonitis
(perihepatitis) or generalized peritonitis of a similar. or hybrid
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ASCITES, 743
type (e.g., alcoholism with tuberculosis, alcoholism with syphilis,
syphilis with tuberculosis, or even alcoholism with tuberculosis
and syphilis).
(b) Ascites of Peritoneal Origin (General Type : Tuberculous
Peritonitis). — 1. The ascites is of moderate extent, often but
slightly fluctuating, and advancing by alternate exacerbations
and recessions.
The fluid is but slightly movable, and frequently encysted.
Cardiac obstrui Dyscrasias
hezia, Bright's
disease)
Hepatic obstruct
blebitis
Inflammation
of the peritoneuzE
Fig. 597. — ^The causes of ascites.
Cardiac. — Hepatic. — Peritoneal. — Pylephlebitic. — Dyscrasic.
Sometimes there are coexisting dull and hard infiltrations, best
palpated after puncture.
2. The concomitant signs should be looked for, vis., peritoneal
and pleural friction rubs, pleural effusion, ganglia, signs of pleu-
ropulmonary, genital, or articular tuberculous disease or typho-
bacillosis, fever, vomiting, etc.
3. The ascitic fluid is serofibrinous, containing a much larger
amount of fibrin, protein, or cells than that of mechanically
produced ascites. In short, it presents the typical features of
inflammatory exudates. Guinea-pig inoculation will give posi-
tive results in the presence of tuberculosis. Certain laboratory
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744 SYMPTOMS,
procedures are available for examining ascitic fluid for the tu-
bercle bacillus (Jousset's inoscopy).
4. It is well to note that tuberculosis of the peritoneum com-
prises by far the greatest number of the cases of peritonitic ascites,
but that one should also think of the possibility of cancer of the
Low blood-pressure
Pre
the
AS
Rais
P
hemorrhage
Hen
Fig. 596. — The syndrome of increased portal pressure.
peritoneum in an old, cachectic individual. The reactions involving
the lymph-glands; examination of the fluid, which generally
contains red blood cells; the history of the case, and the sub-
.sequent course of the disease, will soon confirm the latter diag-
nosis if the possibility of the condition is merely recollected.
Nor should it be forgotten that tuberculous peritonitis with
ascitic effusion may occur in any grade of severity, from the mild-
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ASCITES. 745
est forms, such as the long standing idiopathic ascites of young
girls, running a slow course, without fever or constitutional
disturbances, and nearly always ending in spontaneous recovery
(dropsy of the peritoneum), to the most serious varieties, such
as the ulcero-caseous forms which lead so quickly and inevitably
to the hectic state.
Finally, reference should be made to the frequent, not to
say constant, participation of the pleura in the process of peri-
toneal tuberculous involvement, almost always constituting
more properly a pleuro-peritoneal tuberculosis. At all events and
for practical purposes, in the presence of a suspicious peritoneal
disorder the physician should systematically examine the pleurae
and always perform an exploratory puncture of the pleura; this
procedure will supply a solution of the problem in the majority
of cases.
(c) Ascites of Cardiac Origin (General T3rpe: Heart Failure).
1. One of the most specific features of these cases is that here
the ascites clearly follows other manifestations of edema, as in
the lower extremities, scrotum, and lumbar regions — in contrast
with what occurs in cirrhotic and peritonitic ascites, — and that
it is frequently combined with hydrothorax.
2. The diagnosis is clear from observation of the attending
circumstances, the coexisting heart failure, and the physical
sig^s of cardiac disease. At the most, doubt might occur in the
very advanced cases in which — ^the primary hepatic cirrhosis
having led to secondary cardiac insufficiency, or, on the other
hand, primary heart disease having resulted in cirrhosis of car-
diac origin — a combined cardio-hepatic inadequacy, manifested
in both heart failure and hepatic cirrhosis, has been produced.
A careful inquiry into the past medical history as regards the
heart and liver, along with observation of the course of the
edema and the heart sounds, will nearly always settle the ques-
tion of priority, even though such an aim is of academic rather
than practical interest, since the therapeutic indications, like the
disturbances of function, are in close combination in these cases.
Other Oauses. — Apart from the above three cardinal sources
of ascites, mention should be made of :
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746
SYMPTOMS.
1. The Ascites of Nephritis. — This is, on the whole, rather
uncommon and is associated with the usual signs of Bright's
disease (see Albuminuria and Edema). The high urea content
in the ascitic fluid of azotemic cases should be borne in mind.
This diagnosis should not be accepted unless one has become
convinced from careful examination of the absence of hepatic
cirrhosis, peritoneal inflammation, or heart weakness.
The differential features include, more particularly: Albu-
minuria and, in the absence of all cardiac inadequacy, precession
of the edematous manifestations (lids, extremities, and scrotum).
2. The Ascites of Cachexia. — ^This is likewise an exceptional
^2 4 8 " U
Meal Meal
Fig. 599. — Normal rhythm of urinary elimination (above).
Opsiuria (below).
form, and one which, upon thorough investigation, can nearly
always be relegated to one of the three above-mentioned groups,
7n2., hepatic, peritoneal (tuberculous or neoplastic), or cardiac
ascites.
3. Chylous Ascites. — Also a rare form, at least in our own
countries, and doubtless of varied and complex causation.
The fluid withdrawn is whitish, opalescent, milky in appear-
ance, containing little protein but much fat, which is dissolved
by ether, thereby clearing up the fluid. Its composition is some-
what similar to that of pus (hyperleucocytosis).
In the presence of this form of ascites there have been de-
tected filariasis (Lancereaux), tuberculosis (Courtois-Sufiit),
chronic inflammation of the peritoneum (Letulle), and pressure
on the thoracic duct by enlarged mediastinal glands (Strauss).
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ASCITES. 747
•15
•16
S -H7
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« —20
7
« -21
9 -22
H
II -23
--2*
Fig. 600. — ^Tributaries of the portal vein (after Birard and Vignard).
X. Internal mammary vein. 2. Superior vena cava. S- Inferior vena cava.
4, Suprahepatic vein. 5. Liver. 6. Trunk of the portal vein. 7. Gastro-
duodenal veins. 8. Pancreas. 9. Duodenum. 10. Mesentery. ;/. Ileo-
colic vein. 12. Ileocecal angle. 13. Appendicular veins. 14. Appendix.
75. Spleen. 16. Stomach (opened). 77. Intrahepatic tributaries of portal
vein. j8. Celiac axis. 19. Tail of the pancreas. 20. Pancreatic veins.
^i. Inferior mesenteric vein. 22. Mesocolon. 23. Descending colon. 24.
Colosigmoid vein. 2). Sigmoid flexure.
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748
SYMPTOMS.
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ASCITES.
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750 SYMPTOMS,
4. The Ascites of Pylephlebitis. — An altogether exceptional
form characterized by its sudden onset, its exceedingly prompt
recurrence after puncture, the attendant pain, diarrhea, vomit-
ing, and hemorrhage in the digestive tract, the splenic enlarge-
ment, and the pronounced development of collateral circulation
in the abdominal wall.
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ASTHENIA AND [from a, privative; aOevogj strength^
FATIGUE. L Deprived of strength. J
The term fatigue relates to a sensation too commonly experi-
enced and well characterized to require definition. At most
need it be said that all grades of fatigue may be encountered,
from the mild, temporary, almost pleasant sensation of fatigue,
manifested in a desire to rest, to- deep, persistent, and lasting
exhaustion, almost completely depriving the individual of will
power and of the ability to act. Lastly, it is necessary to make
a distinction between "paralysis," or abolition of voluntary
movements of some portion of the body, and "fatigue," which
merely renders motion distressing or actually painful ; as a mat-
ter of fact, however, "paresis" is in some respects closely allied
to "fatigue."
Fatigue as a symptom is too common and ordinary a mani-
festation of most infectious, toxic, or depressive states to lend
interest even to an attempt at a complete semeiologic descrip-
tion in this connection. The scope of this chapter will there-
fore be restricted:
1. To recalling the commoner clinical states in which fatigue
occurs as a symptom.
2. To recalling under what circumstances fatigue, by virtue
of its unusual persistency, intensity, or variety, assumes definite
clinical significance and is sometimes practically pathognomonic.
The feeling of fatigue may be physiological, i,e,, normal, after
prolonged physical or mental exertion, after some form of shock
to the system, violent emotion, or prolonged test. In this in-
stance it is merely accidental and temporary. It yields readily
to rest, sleep, and removal of the cause.
Fatigue may assume an abnormal, pathologic type by virtue
of:
Its intensity (exhaustion, profound asthenia).
(751)
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752 SYMPTOMS,
Its duration (yielding neither to rest nor to removal of the
cause).
Its special modalities, being frequently periodic in type.
Its location, often in the lumbar regions.
It may be succinctly recalled that the more usual causes of
pathologic fatigue may be:
I. Nervous. — Nervous fatigue results naturally from over-
work, repeated emotion, and in particular from insomnia of what-
ever cause.
It is met with almost constantly, either as a subsidiary or
principal manifestation, in the majority of organic diseases of the
nervous system, and in particular in all paralytic states, to which
no further reference will be made.
Its diagnostic significance may be very great in all forms
of depressive psychoneuroses, zH:!,, neurasthenic and neurastheni-
form states, anxiety neurosis, cerebrocardiac neuropathy, psy-
chasthenia, general asthenia with gastrointestinal atony, ptosis,
and impaired nutrition, sympatheticotonia, etc. It is constant in
all these conditions and sometimes predominant and overmastering;
it is nearly always associated with insomnia. The cause will
always be found to be overstrain, physical or mental; sexual
excesses, or some emotional shock, the patient himself not gen-
erally connecting, however, the two groups of phenomena. Once
this cycle has been established, vis., excessive excitability ("emo-
tionalism,** suggestibility) and asthenia (insomnia), it tends, as
an actual vicious circle, to persist, the "emotionalism" and sug-
gestibility engendering or accentuating the asthenia and insom-
nia, and the asthenia and insomnia, in turn, engendering or ac-
centuating the "emotionalism" and suggestibility.
The diagnosis is generally easy, an inquiry into the patient's
mental state yielding conclusive results. It is to be borne in
mind, however, that a diagnosis of primary psychoneurosis
should never be made except after a process of exclusion, and
that the practitioner should always make certain that it is not
symptomatic of some somatic disorder such as tuberculosis,
arteriosclerosis, syphilis, azotemia, etc.
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ASTHENIA AND FATIGUE.
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754 SYMPTOMS.
n. The humoral caases of fatigue are legion. Any form
of intoxication, whether endogenous or exogenous and toxic or
toxinic, may cause asthenia. However defective the following
classification may be — and it must be confessed that many of
the groups overlap— it may be adopted, even if merely for mnemo-
technic purposes.
(a) Anemias. — In this group fatigue is continuous and is
associated with the customary indications of anemia, viz., pallor
of the mucous membranes, reduction of red cells, reduction of
hemoglobin, etc., together with anorexia, indigestion, etc. The
main object, however, should be, trace the cause of the anemia
(see Anemias).
(b) Hyposph3rxic States. — ^These involve a special circulatory
syndrome characterized essentially by low blood-pressure and
relatively high blood viscosity, these causing all the usual mani-
festations of impaired circulation, vis,, cyanosis, lowered super-
ficial temperature, dyspnea, and undue fatigability (see Low blood-
pressure).
(c) Conditions of Glandular Insufficiency. — Particular atten-
tion will here be paid to Addison's disease and myxedema.
1. Addison's disease (adrenal insufficiency). — Addison's disease
constitutes simply a very serious, but exceptional, form of adrenal
insufficiency, which recent observations, particularly those of Ser-
gent, have shown to be so common in, all infectious and post-infec-
tious states (typhoid fever, scarlet fever, dysentery, malaria, chol-
era, tuberculosis, etc.). During the course of these disorders the
3 cardinal signs should be systematically looked for: Asthenia,
low blood-pressure, and Sergenfs white line.
2. Myxedema. — ^The characteristic doughy infiltration of the
tissues (myxedema), the repeated intermissions in the progress
of the disease, and the permanent asthenia lead to the diagnosis.
(rf) Diathetic States (Metabolic Disorders).
1. Obesity. — This in itself is often dependent upon insufficiency
of several of the ductless glands, and particularly of the thyroid,
which allies it in some respects to myxedema. Asthenia should
lead to a suspicion of the latter condition (see Obesity).
2. Diabetes. — Ordinarily the diabetic is a supernormal, over-
active, indefatigable individual. Asthenia of unknown origin may.
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ASTHENIA AND FATIGUE, 755
however, at times lead to the detection of an incipient diabetes in
a previously healthy subject; acetonemia or azotemia will do the
same in a subject with glycosuria of long standing (see Glycosuria),
(e) Autotoxic States.
1. Uremia (and especially azotemia). — ^A persistent, overpow-
ering asthenia in conjunction with general torpor occurs almost
constantly in azotemia.
2. Arteriosclerosis (senile degeneration). — The same state-
ment 2q)plie& to arteriosclerosis.
III. The infectious causes of "fatigue" and asthenia mani-
festly induce them through poisoning of the nervous and mus-
cular tissues by toxins and through adrenal insufficiency.
Strictly speaking, they should therefore be included in the groups
already given. Let it be again repeated that in the classification
herein adopted *'dogmatic logic" is deliberately sacrificed in the
interests of "practical pragmatism."
The infectious forms of fatigue are often plainly evident ; this
applies to most of the asthenic conditions witnessed in conjunc-
tion with acute infections, e.g., typhoid and post-typhoid asthenia,
influenzal and post-influenzal asthenia, diphtheritic and post-
diphtheritic asthenia, etc. In any case careful inquiry should
be made to determine (1) whether this post-infectious asthenia
is not concealing incipient tuberculous disease, and (2) whether
It is accompanied by pronounced signs of adrenal insufficiency
(low blood-pressure, asthenia, Sergent's white line).
Particular attention should be paid to the chronic, sluggish,
cryptogenic forms of asthenia. In this connection especially
should the physician refuse to be satisfied with such "easy"
diagnoses as "anemia" or "neurasthenia," but should, on the
contrary, make a deliberate search for the three great chronic
infections (tuberculosis, syphilis, and malaria) and the three
main varieties of intoxication already referred to (uremia, gly-
cosuria, and hyposphyxia).
No detailed reference need be made to the well-known signs
of these disorders. Yet it may be recalled in conclusion that
any case of persistent, unaccountable asthenia should lead one
to the particular thought of the possibility of incipient tubercu-
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756
SYMPTOMS.
losis, evidences of which should be sought with great care,
vis., (1) Functional: weakness, lassitude, dyspnea on exertion,
anorexia, loss of weight, slight vesperal fever, night sweats, cough,
frequent heart rate, and hemoptysis. (2) Physical: reduced breath-
ing capacity, slight impairment of resonance at one apex, in-
creased vocal resonance, and persistent abnormalities of respira-
tion at one apex (rough, jerky breathing; rough, prolonged, and
blowing expiration; friction rubs, etc.).
Fluoroscopy, while of very great value, has in no wise de-
tracted from the significance of the above time-honored physical
signs.
Systematic clinical examination will automatically yield a
solution to these problems, provided it is, or attempts to be,
thorough and comprehensive.
Systematic Clinical Examination of Asthenic Subjects.
I. Determination of blood-
pressure, systolic and
diastolic
High blood-pressure.
Low blood-pressure.
Arteriosclerosis, nephritis, azotemia.
Hyposphyxia, tuberculosis, adrenal in-
sufficiency.
2. Blood examination.
Low red cell count.
Hyperviscosity.
Hyperazotemia.
Wassermann reaction.
Anemia.
Hyposphyxia, azotemia, tuberculosis,
adrenal insufficiency, acetonemia.
Azotemia.
Positive: Syphilis.
3. Temperature.
Hyperthermia.
Infectious states (tuberculosis, malaria,
etc.).
4. Auscultation.
Lungs.
Heart
Tuberculosis.
(Accentuation of second sound, gallop
rhythm: Nephritis, arteriosclerosis).
5. Urine examination.
Sugar, acetone.
Albumin.
Diabetes, acetonemia.
Albuminuria (azotemia).
6. Examination of reflexes
and nervous reactions.
1. Psychoneuroses.
2. Sergent's white line: Adrenal insuffi-
ciency.
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r%xjjT T c {French: Frissons, from frigere,]
A chill consists essentially of a sudden tremor of varying ex-
tent and varying duration, usually accompanied by a sensation
of cold and followed by a sensation of warmth.
At least three grades of chills may be recognized :
Cryesthesia or chilliness^: An unpleasant sensation of cold, with
very slight tremor.
Shivering,
An actual major chill, involving the entire body and attended
with chattering of the teeth, diffuse and violent trembling, and an
intense feeling of cold.
All true chills, except the nervous or emotional chills, are
followed by fever. As a general rule, a definite chill accom-
panied by an abrupt rise of temperature is symptomatic of the
onset of an infectious disease, by far the most frequent of such
disorders being pneumonia, grippe, malaria, tonsillitis, and sep-
ticemia.
The commonest causes of chills may be enumerated as fol-
lows :
Pyogenic and septicemic infections :
Pneumonia, tuberculosis, appendicitis.
Septic wounds.
Suppurative disorders of the liver and kidneys; biliary and
urinary infections.
Tonsillitis.
Vegetative endocarditis.
Phlebitis,
Empyema.
Erysipelas,
Malaria.
Renal and hepatic colic.
Nothing special need be said concerning:
(757)
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758
SYMPTOMS,
The chill from exposure or "a frigore,"
The emotional chill, or shivering "with fright" or "with horror/'
or simply the psychoneuropathic chill. Some nervous degen-
erates, apparently "constitutional shiverers," are always ready
to shiver on the slightest provocation.
Causes.
Fbykb.
BLOOD Ex-
Clinical
MEANS or
amination.
SIGNS.
lUCOYKBT.
Nervousness.
None.
Negative.
Neuropathic
stigmata.
Suggestion.
Discipline.
Septic states.
Remittent
Polymor-
Local or deep-
Dressings,
phonuclear
seated vis-
operation, and
leucocy-
ceral infec-
drainage.
tosis.
tion.
Infectious en-
docarditis.
Collargol in-
jections.
Phthisis.
Remittent.
Frequently
Stethoscopic
General and
leucocy-
and fluoro-
local treat-
tosis.
scopic pulmon-
ary evidences.
Tubercle bac-
illi in sputum.
ment. Hy-
gienic meas-
ures.
Spontaneous
recovery.
Pneumonia.
Continued.
Frequently
Stethoscopic
Hygienic treat-
•
leucocy-
evidences.
ment. Gen-
tosis.
Characteristic
sputum.
eral measures.
Spontaneous
recovery.
Hepatic colic.
Remittent
Not char-
Hepatic colie
Morphine.
or inter-
acteristic.
or gastralgia.
Operation.
Diet
mittent
Frequently
jaundice.
Pain in right
hypochon-
drium.
Malaria.
Intermit-
Leucopenia.
Splenic enlarge-
Quinine.
tent (at-
Malarial
ment
Arsenic.
tacks at
parasites.
definite in-
tervals).
Tsrphoid fever.
Continued.
Leucopenia.
Typhoid state.
General treat-
Agglutina-
Rose spots.
ment
tion test
Splenic enlarge-
Diet.
Blood cul-
ment, etc.
Cold baths.
ture.
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nnuiA \X(i(ia. Drowsiness J suspension]
i^UMA. 1^ ^y ^^^ mental fv/nctions. J
Coma consists of a state of profound somnolence with more
or less complete loss of consciousness, sensibility, and motility.
While it is the most striking feature of the syndrome resulting
from apoplexy, it may be and frequently is met with under other
circumstances.
It could hardly be confused with the deep sleep of convales-
cents or hysterical cases, or with syncope or asphyxia.
The deep sleep of convalescents is a quiet sleep, with the
pulse regular and respiration normal. It is seldom so profound
that the patient cannot be awakened by some sharp stimulus,
and the history of the case will generally exclude the idea of
coma.
The sleep of hysterical patients might more readily lead to
confusion. Only rarely, however, will the previous history and
the features of the onset of the attack fail to point the way to
a proper diagnosis, which will be thoroughly illuminated, fur-
thermore, by systematic investigation of the hysterogenous
zones.
Systematic diagnosis of hysterical pseudo-coma may be said
to be based on the following clinical findings:
1. If the onset was sudden, the patient falling, this fall oc-
curred without the patient receiving any severe blow or any
wound or traumatism; no biting of the tongue, and no relaxa-
tion of the sphincters. •
2. Frequently there are noted contracture, winking of the
lids, and various movements of the eyeballs, which are absent
in true coma.
3. The patient, while apparently insensitive to pain, noise,
and light, reacts to an exaggerated degree, on the other hand,
to pressure upon a hysterogenous zone, to a cold affusion, or
to appropriate suggestion in a loud voice. The author has wit-
(759)
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760 SYMPTOMS.
nessed many seizures of this type, sufficiently striking to alarm
an experienced hospital staff, suddenly cease upon suggestion
that the patient was to be "immediately placed in isolation in
the special quarters" or to be "subjected to cauterization with
the hot iron." Much oftener, indeed, it yielded to brief occlusion
of the nose and mouth.
4. Lastly, these hysterical pseudo-comatose states are fre-
quently associated with postures apparently unconsciously as-
sumed, but plainly semi-voluntary to the close observer; the
same applies to the pseudo-delirium encountered in these sub-
jects.
S3mcope is ordinarily of short duration. The sudden loss
of consciousness, pallor, weakness, and even almost complete
arrest of the heart-beats, the rapidly beneficial effect of the hori-
zontal posture, elevation of the legs, and stimulating injections,
will preclude any prolonged hesitation.
In asphyxia, the history of the case, the cyanosis, the livid ap-
pearance, and the reduced temperature of the lower extremities
will obviate any mistake.
The ordinary causes of coma may, for practical purposes,
be enumerated as follows:
Toxic causes: Exogenous: Alcohol, opium.
Endogenous: Uremia, acetonemia, acidosis
(diabetes).
Cerebral causes: Vascular: Apoplexy, hemorrhage, throm-
bosis, or epilepsy.
Inflammatory : Meningoencephalitis.
Neoplastic : Brain tumors.
Traumatic: Skull fractures.
Infectious causes: Malaria, rheumatism, typhoid fever, or in-
fectious jaunSice.
Circulatory causes: Stokes- Adams' disease.
Coma having been clinically encountered, the causal diag-
nosis, which is of prime importance both because of the prog-
nosis it affords and the indications it gives for treatment, is
based chiefly upon the history of the illness and, in particular, on
the results of clinical examination. The history and clinical findings
must be systematically collated.
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COMA. 761
The history is of prime imfrortance,
1. Has there been some traumatic injury, fall, or contusion
preceding the coma? If so, fracture of the skull.
2. Does the patient give a history of similar seizures before,
and is he subject to convulsive attacks? Epilepsy, eclampsia,
uremia.
3. Has the patient been intemperate? Had he been on an
alcoholic spree before the coma came on? Alcoholism.
4. Has the patient had syphilis? Has he previously had treat-
ment for this disease? Was he under treatment at the time?
Brain syphilis.
5. Did the patient have nycturia, vertigo, albuminuria, etc.?
Interstitial nephritis, arteriosclerosis, uremia, etc.
6. Was the patient in a rundown state; did he pass very
much water; had he had itching and digestive disturbances for
a few days, etc? Diabetes.
And so on . . .
In short, the practitioner should <:arefully take note of all
information supplied by the relatives as to the patient's previous
medical history ; such information will often yield highly service-
able clinical indications.
The direct clinical examination is of much greater importance
stUL
As in other conditions, it should be conducted systematically
and comprehensively. The following lines of inquiry are, how-
ever, particularly essential:
1. Is hemiplegia present? (See Hemiplegia), With decrease of
muscle tone on one side of the body ; sometimes conjugate devi-
ation of the head and eyes, an exaggerated patellar reflex on one
side, and the Babinski ^ sign or plantar reflex. Hemiplegia, if
present, will usually constitute a clinical expression of brain
hemorrhage or softening; it may be met with in uremia, and
in some forms of meningitis in childhood.
2. Is fever present? And if so, was it present before the
coma (typhoid fever, cerebral rheumatism, tuberculous menin-
gitis, cerebrospinal meningitis) ? Or was it present along with
the coma (pernicious malarial fever) ? Or did it come on after
the coma (certain forms of cerebral hemorrhage) ?
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762
SYMPTOMS.
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COMA.
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764 SYMPTOMS.
3. Is sugar or albumin present in the urine? The presence
of sug^r would suggest diabetic coma; in' this case the exami-
nation should be supplemented by tests for acetone and diacetic
acid and by a determination of urinary acidity (see Technical
Procedures), thus confirming the diagnosis. The presence of
albumin would suggest uremic coma, which is confirmed or ex-
cluded by determination of the blood urea. Where the latter
exceeds 1 gram (it exceeded 5 grams in one of the author's
cases),, the diagnosis of uremic coma is assured
4. Is there high blood-pressure? A systolic pressure exceed-
ing 220 millimeters (Pachon instrument); especially if asso-
ciated with manifest cardiac hypertrophy, gullop rhythm, and
albuminuria, certainly justifies a diagnosis of uremia with or
without -cerebral hemorrhage, arteriosclerosis, interstitial neph-
ritis, etc. The finding of the **blue line" on the gums of a worker
in lead will lead, on the whole, to the same inferences.
5. Is there some manifest evidence of syphilis? The finding
of osteoperiostitis, glandular swellings, a typical eruption, sus-
picious pigmented scars, etc., may bring to mind the possibility
of a specific cerebral arteritis.
6. A marked reduction in the pulse rate would suggest Stokes-
Adams* disease, brain tumor, or opium intoxication.
7. Examination of the blood (urea content and Wassermann
reaction) and, in difficult cases, examination of the cerebrospinal
fluid (cytologic study and Wassermann reaction), should, if pos-
sible, be systematically carried out. They will often enable the
practitioner to decide at once upon a diasrnosis of uremia (where
the blood urea exceeds 1 g^am),. of brain syphilis (positive
Wassermann), of cerebromeningeal hemorrhage (many red cells
in the cerebrospinal fluid), of tuberculous meningitis (lymphocy-
tosis), of cerebrospinal meningitis, etc.
The more usual causes of coma in private practice are, in
the order of their frequency:
Apoplectic coma (hemorrhage and softening of the brain).
Uremic coma.
Alcoholic coma.
Post-epileptic coma.
Diabetic coma.
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COMA. 765
Combinations of these forms may, of course, occur, the com-
binations, alcoholism with uremia, alcoholism with apoplexy,
alcoholism with ajcetonemia (diabetes), and uremia with apo-
plexy being the most frequent.
These forms undoubtedly make up over 95 per cent, of the
cases of coma seen in general practice.
The remaining 5 per cent, consist chiefly of:
Infectious and post-infectious coma (lobar pneumonia, ty-
phoid fever, infectious jaundice, malaria, and puerperal infec-
tion).
Post-traumatic coma (fracture of skull).
Inflammatory, meningo-encephalitic coma.
Toxic coma (opium, morphine).
Neoplastic coma (brain tumors).
Demential coma (paretic dementia).
According to Pierre Marie, brain compression plays an impor-
tant role in the productfon of post-hemorrhagic coma, and complete
coma is actually dependent upon brain hemorrhage (Presse med.,
June 6, 1914). It may be of service to reproduce here the follow-
ing practical conclusions, which Marie deems may be formulated
in this connection:
In a patient presenting the signs of cerebral hemorrhage who,
three hours after the attack, is in profound coma, the question
of performing a decompression operation may be considered
(an extensive extravasation of blood is in all likelihood present).
In any patient suffering from cerebral hemorrhage who, after
having at first presented only a partial coma, falls progressively
into a deep coma a few hours or days later, the performance
of a decompression operation should be seriously thought of
and the decompression carried out as soon as possible (in this
instance the condition present is rather a secondary edema).
At this operation a large decompression opening should be made
over the hemisphere on the sound side and not over that into which
the cerebral hemorrhage has occurred.
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CONSTIPATION fConstipatio, fnym constipare,!
[ to squeeze together. J
Constipation is characterized by infrequency of the intestinal
evacuations and an abnormally hard consistency of the feces. What
are the actual extremes of constipation ? No one, to the author's
knowledge, has as yet supplied a satisfactory definition in this
direction, and none will be rashly attempted here, nor will a
complete semeiologic account of constipation be presented. The
subject matter will, in fact, be limited to a succinct resume of
the more important clinical forms of the condition.
Constipation appears to depend, in general:
Either upon a decrease of the peristaltic contractions (hypo-
tonia) or, on the other hand, upon spasm.
Or upon a decrease of the intestinal secretions (hypocrinia).
Or upon an increase of absorption of the intestinal contents.
Little space will be devoted to accidental constipation^ the
cause of which is, as a rule, easily ascertained
The latter is not true, however, of habitual constipation, a
"menace to society" much more certainly than is purgation, de-
nounced, not without justification, by Moliere and Burlureaux.
Much care should be paid to the detection of the cause of this
type of constipation, and especially to finding out whether, in
the individual case, it is of atonic or spastic origin.
Accidental Oonstipation.
(a) Intestinal obstruction: Strangulated hernia; peritoneal
bands.
(fe) Acute abdominal disorders.
1. Appendicitis.
2. Peritonitis.
3. Hepatic or renal colic, etc.
(f) Lead poisoning (lead colic).
(d) Certain acute disorders of the nervous system: Menin-
gitis, etc.
(766)
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CONSTIPATION. 7^7
Habitaal Constipation.
1. This may be dependent upon some local abdominal cause
capable of inducing habitual constipation, either mechanical
(pressure or kink) or reflex.
2. It may be due to some more general cause.
1. Local Causes. — ^These comprise all abdominal disorders
capable of producing pressure on the intestine, kinking, or re-
flex spasm.
(a) Pressure. — Pregnancy, retroversion of the uterus, fibro-
myoma, or ovarian cyst in women; prostatic hypertrophy in
men, and a tumor of the kidney, spleen, or mesentery, or a
stricture, cicatricial band, or peritoneal adhesion in either sex,
may so obviously be the cause of obstinate constipation as to
require no further mention.
(b) Kinks. — The causal influence of enteroptosis, whether
due to loss of fatty support, pregnancy, obesity, perineal im-
pairment, peritoneal bands, or congenital malformations, has
always been in some degree realized. Systematic fluoroscopy
of the abdomen has, however, demonstrated for it a paramount
role in the production of habitual constipation. Relaxation of
tissues, lack of tonicity, and atony of the abdominal wall gener-
ally act in conjunction with the actual kink.
(c) Reflex Spasm. — This is the obvious mode of production
of constipation dependent upon painful affections of the bowel
or of neighboring organs — anal fissure, hemorrhoids, chronic
appendicitis, cystitis, salpingo-oophoritis, pyelonephritis, prosta-
titis, etc.
2. General Causes.
(a) The most frequent general causes are, perhaps, simply
habit and sedentary life. Education rapidly accustoms the civ-
ilized human subject to inhibit on various occasions the impulse
to defecate. Propriety, occupation, professional necessities, and
likewise the low and repulsive conception attaching to the act
of defecation, exert an inhibiting influence, consciously or un-
consciously, which leads to gradual suppression of the function,
constipation being thus established. To these may be added a
number of auxiliary factors such as the disgusting foulness of
some civil or military privies ; the false prudishness— doubtless
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768 SYMPTOMS.
to be deplored, but quite justified— of young girls; the sedentary
life imposed by various occupations; the wearing of corsets;
lack of physical exercise, gradually leading to more or less
marked atony of the muscles of the abdominal wall, and, ulti-
mately, in women, pregnancy and the impairment of the ab-
dominal wall frequently resulting, at least among civilized popu-
lations; all these factors account for the fact that constipation,
which is exceptional in animals and savages, and but moderately
frequent in men, is practically constant in women, particularly
those living in cities.
(b) The diet of city dwellers, nearly always defective, is
another factor, consisting as it does of white bread, meat, fowl,
fish, eggs, potatoes, rice, pastes, pastry, confections, cheese, alco-
holic beverages, and water — articles which leave too little resi-
due: "Where there is nothing left the bowel-, like the king, is
bereft of his prerogatives." The same is true, indeed, of a diet
insufficient in amount.
(c) Various metabolic and otiier chronic disorders may like-
wise induce constipation in one way or another:
1. Constipation is rather frequent in neuro-arthritic cases,
comprising those with gout, diabetes, etc.
2. It is regularly present in diseases leading to asthenia and
cachexia, such as chlorosis, anemia, senility, various cachectic
disorders, and infectious diseases. Prolonged recumbency is,
furthermore, not a negligible factor in these cases.
3. The atonic, asthenic type of gastrointestinal dyspepsia, so
frequent in women and nearly always associated with ptosis
and dilatation of the organs concerned, is another of the commonest
causes of constipation, acting through the three combined fac-
tors, reduced secretion, lack of tone, and kinks, with the forma-
tion of "dead areas" in the digestive tract.
In this connection the term gastrointestinal dyspepsia is to be
taken in its broadest sense, comprising motor, secretory, or
secretomotor insufficiency of the digestive tract — stomach, duo-
denum, and bowel — and of the related glandular organs — the
liver and pancreas. The marked importance attached, for ex^
ample, to duodenal dyspepsia as a result of modem investiga-
tions is well-known.
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CONSTIPATION. 769
4. Lastly, various nervous afiFections, functional (hysteria,
neurasthenia, overwork) or organic (tabes, myelitis, etc.), are
accompanied by habitual constipation.
The etiologic and pathogenetic diagnosis of constipation is
of paramount importance, since by elucidating the causes of the
disorder it often supplies direct indications for treatment, as, e.g,,
by psychotherapy, massage, mechanotherapy, electric proced-
ures, diet, etc. Whatever be the cause, however, one should
always endeavor to distinguish the atonic from the spastic type of
constipation. This distinction is sometimes self-evident, but in other
instances it is difficult or even impossible to make, the two forms
coexisting, both as regards time and space, i.e,, either following
upon one another or being actually present simultaneously at
separate points of the digestive tract. Fluoroscopy is of the
greatest assistance imder these circumstances.
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CONVULSIONS
(CONVULSIVE
SEIZURES).
Convulsio, /rom convellere, to shake;
sudden and involuntary contractions
of the muscles.
The term convulsions is applied to sudden, involuntary con-
tractions of the muscles. Tonic convulsions consist of contrac-
tions of relatively long duration, causing a condition of almost
continuous rigidity, combined with shaking movements result-
ing in only slight displacements of the parts. Clonic convul-
sions are made up, on the other hand, of more or less regular,
rapidly alternating contractions, resulting in more or less ex-
tensive involuntary movements.
Some types of convulsions, e,g,, those of chorea, athetosis, tics,
and tremors present such highly characteristic features that their
diagnostic recognition is an easy matter. These forms will not
be considered in this chapter, nor will reference * be made to
partial convulsions such as blepharospasm, spasmodic torticollis,
writer's cramp and occupational spasms in general. Actual, more or
less diffuse comnilsions need here alone be considered.
The only serious mistake in actual observation that can be
made is that entailed by malingering. Only exceptionally does
such an imposition escape detection by an experienced and well-
posted observer; the convulsions are always defective in the
sense of being pushed to excess — the subject attempting too
"dramatic" a representation — or in being unnatural — the subject
being a "novice." Yet the author has met with some "accom-
plished artists" in this connection whose duplicity was exposed only
with great difficulty.
The observation of an actual, not an artificial, convulsive
state having been made, the second and highly important step
is next to be taken, zns., that of finding out its cause.
In most instances the clinical history obtained from the patient
himself or his relatives will enable the physician to place the case
(770)
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CONVULSIONS. 771
in one of two groups: (a) The convulsions appear in an acute
manner, (b) They are chronic, i.e., habitual, occurring repeatedly
at intervals of varying length.
I.— ACUTE CONVULSIONS.
A. If the patient is a child, special thought should be given
— and, as a rule, the circumstances under which the convulsions
appeared will afford a pointer as to the diagnosis — to:
(a) Convulsions of Reflex Origin. — Usually unattended with
fever :
Dental.
Digestive, particularly due to colic and intestinal parasites.
Auricular, due to foreign bodies in the ear or to otitis media.
Acute otitis media is one of the most frequent causes of reflex
convulsions in children; further, as is generally realized, it is one
of the commonest and most often overlooked disorders. One
should never forget to palpate the mastoids and examine the ears
in a child with eclamptic manifestations.
(b) Convulsions of Febrile Origin. — Such convulsions are a
frequent accompaniment of the eruptive fevers and are generally
not of serious import.
(c) Convulsions of Meningoencephalic Origin. — These are
associated not only with fever, but also with evidences of meningo-
encephalic disorder such as Kemig's sign, headache, vomiting,
disturbances of respiration, etc. The marked diagnostic value of
lumbar puncture in these cases is familiar to all.
(d) Convulsions of Neuropathic Origin.
1. Infantile eclampsia, a very common disorder, is met with
in children as a symptom of various diseases, or as a neurosis
in which it constitutes in itself the entire disturbance.
2. In the latter form, or idiopathic eclampsia, there is always
present an underlying neuropathic condition, or spasmophilia,
consisting of abnormal irritability of the nervous system.
3. Spasmophilia is often due to an acid intoxication of the
blood following one of a variety of digestive disturbances which
gradually induce poisoning of the system.
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772 SYMPTOMS.
4^ The acidosis disturbs the metabolism of the lime salts,
which may be said to be essential for normal functioning of the
nerve cells.
5. In the pathogenesis of eclampsia are also involved changes
in certain of the endocrin glands, especially the parathyroids,
which lead to insufficiency of these glands.
6. This insufficiency results in eclampsia because the para-
thyroids are no longer carrying on their antitoxic role in the
system, while at the same time there is disturbed assimilation
of lime salts.
It is certainly a fact that, whatever may be the exciting cause
of infantile eclampsia, some individuals are particularly predisposed
to it, i.e., that there does occur a true spasmophilic tendency based
upon nervous disorder with exaggerated irritability of the nerv-
ous system and often accompanied by an abnormally acid con-
dition of the body fluids, or acidosis, probably favored by con-
genital insufficiency of the endocrin glands.
B. The patient is an adult.
(a) The convulsive syndrome results from some pre-existing
febrile disorder, such as typhoid fever (of the ataxo-adynamic
variety), cholera, or malaria (convulsive form of pernicious mal-
aria).
(b) There may or may not be fever, but such fever as exists
is manifestly accidental and the history of the case supplies the
diagnosis:
(a) The convulsions may follow some injury to the skull asso-
ciated with fracture, extravasation, meningeal hematoma, etc.
(b) They may follow:
1. A dog bite: Rabies (so-called "hydrophobic" seizures, visceral
spasms, etc.).
2. A contaminated wound: Tetanus (trismus; consciousness
completely preserved).
(c) They may follow an acute intoxication, premeditated or
accidental:
1. Strychnine, the type of convulsive poisoning.
2. Opium, cocaine, or theobromine, in which they constitute a
much more exceptional event.
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CONVULSIONS, 77i
(d) They may develop at labor in an albuminuric woman:
Puerperal eclampsia.
(c) The acute convukive seizures may occur m the course
of some chronic disorder unattended with fever. These are al-
vrays cases of chronic systemic intoxication.
(a) Uremia. — This is shown to exist by the albuminuria, high
blood-pressure, and enlarged heart, sometimes attended with
gallop rhythm; the edema, which, however, is frequently lack-
ing; the practically pathognomonic increase of the blood urea,
and the history (headache, vertigo, vomiting, and insomnia).
(b) Lead Poisoning. — This is suggested by the subject's occu-
pation (painter, etc.), the characteristic blue line on the gums,
sometimes by paralysis of the extensor muscles of the forearm,
by the high blood-pressure, and frequently by the history (head-
ache, insomnia, and lead colic).
(c) Diabetes. — Here, indeed, the acute manifestations are gen-
erally of the comatose variety; in any event, the urine exami-
nation, always indispensable, though perhaps more particularly
so in the comatose and convulsive cases than in others, including
tests for sugar, albumin, and acetone, and a determination of the
urinary acidity, will point to the proper diagnosis.
(d) Alcoholism. — This tends toward many different forms of
convulsions, and from various causes: Convulsive attacks in the
course of delirium tremens; convulsive uremic attacks super-
imposed on the alcoholism (cirrhosis of the liver or interstitial
nephritis), and hystero-epileptiform seizures in neurotic alco-
holics.
This is a matter of great practical importance to resident
physicians in hospitals, asylums, homes, dispensaries, and to
police surgeons.
1. Absence of albumin from the urine and a moderately tense
pulse will, in all likelihood, exclude uremia; subsequent determina-
tion of the blood urea will, if necessary, set the diagnosis straight.
2. An alcoholic spree is obviously capable of bringing on an
epileptic attack in a person predisposed to such seizures. Biting
of the tongue during the attack, with resulting drivelling of
blood-stained fluid, the incontinence of urine, the violence of
the convulsive movements, the initial cry, and the abruptness
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774 SYMPTOMS,
of the attack, frequently with bruising due to a sudden fall;
observation of inherited dystrophic stigmata, and the profound
coma which follows the convulsive attack, are as many presump-
tive indications of alcoholic convulsions.
3. A hysterical seizure may, be started by an alcoholic debauch.
The absence of profound coma after the attack ; the semi-volun-
tary, semi-conscious character of the movements, during which
the patient neither wounds himself nor receives any hard blows ;
sometimes the incoherence of speech, the resistance offered to
passive opening of the lids, the absence of aura, of the initial
cry, of tongue-biting, and of relaxation of the sphincters, to-
gether with the "artificial," "overdone," "exaggerated," "theatri-
cal" quality of the proceedings which strikes the experienced
onlooker — all these features are in favor of an hysterical origin
of the seizure.
4. Uremia, hysteria, and epilepsy having all been excluded,
simple alcoholic toxic convulsive attack constitutes the remaining
diagnostic alternative.
IL— CHRONIC CONVULSIONS.
Convulsions may occur in a chronic or at least a recurring
form. The preceding section (on acute convulsive seizures oc-
curring in the course of some chronic disorder unattended with
fever) should properly be included in the present group, from which
it was separated simply because, in practice, the clinical problem is
put before the physician under far different conditions. In the
cases considered in the preceding section the practitioner is wit-
nessing an acute convulsive attack concerning which he has little
or no definite information, whether the patient has been picked
up on the street or has been seized for the first time with an
attack which took his family unawares and unprepared. In the
group of cases now to be considered, on the other hand, similar
attacks have already occurred. A diagnosis has been rendered,
which may have been either correct, wrong, or misleading; in
any case, much useful information can be obtained, either from
the patient himself or his relatives, concerning his pre-existing
condition. In these cases the stumbling-block does not lie in
the paucity of information, but very often instead in an excess
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CONVULSIONS, 77i
of contradictory or even incorrect information which may or
may not be intentionally misleading.
The majority of cases of chronic or recurring convulsions are
due either to uremia, epilepsy, hysteria, diabetes, alcoholism, pro-
gressive general paralysis, or Stokes-Adams^ disease (paroxysmal
slow pulse).
Uremia of the convulsive type is a very common disorder,
which should always be thought of in the case of a middle-aged
or elderly patient or of a syphilitic. Presence of albumin in the
urine, repeated finding of a high blood-pressure, and the coex-
istence of usual signs of chronic uremia (headache, vomiting,
pruritus, insomnia or abnormal somnolence, etc.) will serve to
orient the diagnosis ; blood urea determination will confirm it.
Epilepsy should be suspected in the presence of inherited
stigmata of the disorder (malformations of the skull, teeth, etc.),
unfavorable family antecedents (epilepsy, alcoholism, dementia,
or syphilis), and a history of certain disturbances during child-
hood (arrested development in certain parts, convulsive attacks
in childhood, night terrors, or enuresis), and its existence is
confirmed by the features of the attack already specified.
Hysteria. — As is well known, the problem of hysteria has
been thoroughly gone over in recent years, and but little remains
of our former conceptions of the disease. A diagnosis of hysteri-
cal convulsions is justified only by careful study of the patient's
psychoneuropathic reactions, his suggestibility, and the obser-
vation of an inveterate mythomania, together with the special
features of the convulsions themselves, previously referred to.
Diabetes. — In this disorder the uranalysis, which should be a
routine procedure, will supply the diagnosis. Yet it should be
borne in mind that uncomplicated diabetes never causes convulsive
attacks, and that such attacks occurring in the presence of diabetes
constitute almost certain evidence of either hyperacidosis or uremia
as a complication of the disease. Routine estimation of the urinary
acidity and performance of the tests for acetone and diacetic acid
(see Uranalysis) will settle the question of acidosis and enable the
physician to expect and sometimes to prevent the threatening and
so often fatal coma. Examination for albumin and casts and
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776 SYMPTOMS.
determinations of the blood-pressure and blood urea will, on the
other hand, settle the question of uremia.
Chronic alcoholism is revealed by the usual evidences, rns,,
tremor of the extremities, exaggerated reflexes, gastrohepatic
and cardiorenal disturbances, and an abnormal "satiny" softness
of the skin, particularly over the abdomen. The latter sign,
mentioned by Cabot, is actually a very frequent indication of
alcoholism; it seems to be especially characteristic in persons
engaged in manual labor, whose epidermis is normally thick
and rough. Chronic alcoholism gives rise to convulsive attacks
only in the event of an acute alcoholic excess or in a hysterical,
epileptic, or uremic individual (see above).
Progressive general paralysis is detected by a careful inquiry
into the changes occurring in the patient's mentality and affec-
tive faculties, which the relatives will nearly always describe:
Changed handwriting, which is sometimes illegible; inability to
carry out correctly certain elementary mental tasks such as
adding or multiplying figures; peculiar optimism not justified
by attendant facts; inability to keep the attention fixed any
length of time on one subject; singular absent-mindedness, bi-
zarre and strange actions, and impairment of memory. Later,
unconsciousness, megalomania, and paralytic phenomena. A
specific history is nearly always present.
The period of general torpor or coma nearly always follow-
ing a severe convulsive attack is usually attended with a more
or less pronounced slowing of the pulse rate, which may descend
to 60, 56, or 54, without any special morbid significance. Where,
however, a convulsive and comatose attack is associated with
bradycardia falling below 40, a diagnosis of Stokes-Adams* dis-
ease may be almost certainly made. This appellation should,
in the author's estimation, be temporarily retained, as it desig-
nates precisely the clinical syndrome, paroxysmal bradycardia with
convulsive and syncopal attacks, without stating definitely its nature,
which appears to differ in the individual cases (see Arhythmia and
Slow pulse).
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CX)UGH.
Cough is so common a symptom in disorders of the respira-
tory tract that these two conditions are naturally conceived of
as bearing an almost necessary relationship the one to the other
and the equation, cough=respiratory disease, is almost inevi-
tably accredited.
Cough of respiratory origin, i.e., dependent upon some dis-
turbance in the respiratory tract, is, indeed, the commonest type,
representing about nine-tenths of all cases of cough that come
under the physician's care. Little space need here be devoted
to this form, as the practitioner's attention in these cases is al-
ways strongly drawn toward the respiratory tract and syste-
matic investigation is thereupon alone required to ascertain the
cause.
This does not apply, however, in cough of extra-respiratory
origin.
Occasionally a patient presents himself complaining of cough,
in whom most careful examination reveals nothing wrong in
the laryngotracheobronchial tree. Usually it is a fatiguing, par-
oxysmal sort of cough — a cough which is disheartening alike to
the patient and the physician, as the ordinary measures of treat-
ment for cough prove a complete failure.
For this form the term "reflex cough" has been coined —
certainly an improper designation since cough is always reflex,
being a defensive reaction of the system to a peripheral stimulus
starting nearly always in one of the sensory terminations of the
pneumogastric distributed to the mucous membrane from the
vocal cords to the terminal bronchial ramifications, but which
may originate very differently in different cases.
Such "reflex" coughs, or better, coughs of extra-respiratory
origin, can be mastered only by being familiar with their mode of
production, by tracing out their cause, and by instituting a
strictly causal line of treatment.
(777)
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778 SYMPTOMS.
Clinical Features. — ^There are a number of special features
which impart to cough of extra-respiratory origin a special clinical
aspect.
It is a dry cough, a "useless" cough — meaning by this that
it is purposeless, avails nothing, and that it cannot result, unless
bronchitis is simultaneously present, in the expulsion of actual
sputum; at the most it may sometimes be ifollowed by the ejec-
tion of a little mucus or saliva.
It isf often a paroxysmal type of cough, i,e,, one ordinarily con-
sisting of a long series of expiratory jerks, brief, occurring at
Efferent motor f^espk-atoiy center in meduKa Afferent sensory
Btfm
/^
Fig. 601. — Diagram showing the afferent and efferent nerve paths con-
cerned in the reflexes of the respiratory tract.
short intervals and .separated by relatively few inspiratory move-
ments. It is particularly distressing on account of the long dura-
tion of the paroxysms and their frequent recurrence.
Lastly, it is a type of cough which is produced, ordinarily,
under certain very special circumstances. In cases of pleurisy
(pleuritic cough being, indeed, comprised in this group as the
pleura or lung covering is physiologically an extra-respiratory
structure), the existing cause' is some change in the position of
the patient; in some dyspeptics it is brought on by food stasis
(gastric cough) ; worm cough of intestinal origin is a well-known
form in children ; laryngologists describe, further, a nasal cough
and a pharyngeal cough. In one of the author's patients, ap-
parently free of all neuropathic taint, endless paroxysms of
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COUGH, 779
cough were started by rather strong odors, such as those of
violets and of musk.
Mode of Production of Cough. — Physiologic, clinical, and ex-
perimental studies of cough lead to a rather definite conception of
its manner of production. This consists of a peripheral stimulus
transmitted to one or more nervous centers and then sent back
along centrifugal trunks to the muscles of expiration.
The nervous center of coughing is probably closely allied to the
respiratory center in the medulla at the nucleus of origin of the
pneumogastric, to the floor of the third ventricle and the corpora
quadrigemina, and to a few auxiliary centers.
The centripetal nerve paths are probably represented by the
pneumogastric; hence, the almost constant cough noted in affec-
tions of the mucous membranes of the respiratory tract supplied
by this nerve. The exciting impulse may, however, originate
instead in the pleural, pharyngeal, esophageal, gastric, or intes-
tinal branches of this nerve; hence the possibility of having a
cough symptomatic of disturbances of these various structures
(pleural, pharyngeal, esophageal, gastric, worm cough, etc.).
On the one hand, as with other reflexes, all sensory nerves,
including the cranial sensory nerves, may be conceived of as act-
ing like the pneumogastric on the expiratory center, stimulation
of these nerves thus being the starting-point of expiratory re-
flex effects. For practical purposes, the trigeminal nerve is, after
the pneumogastric, in most intimate relationship with the re-
spiratory center; this is the nerve which presides over sensory
impressions from the face and the nasal portion of the respira-
tory passages; in its sphere of action are generally to be sought
the exciting causes of cough where examination of the pneu-
mogastric has proven negative. An important role in the path-
ogenesis of the cough reflex may also attach to the glossopharyn-
geal. Participation of this nerve in respiratory phenomena had
been overlooked and unsuspected until it was demonstrated by
Laborde in his experiments on rhythmic tractions on the tongue.
These experiments showed that the part played by this nerve
as an exciting factor of cough, whatever the underlying cause
may be, must be duly taken into account, since its sensory fibers
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780 SYMPTOMS.
bear an immediate relationship to causes of local irritation that
may arise anywhere in the region of the pharyngolaryngeal vesti-
bule.
Sneezing is the most frequently occurring reflex that involves
the nasal mucous membrane. Clinically, however, sneezing often
precedes cough. The physiologic mechanism of the two reflexes
is practically the same; most physiologists believe in the exist-
ence of a nerve center common to both these acts, and nasal
cough is a condition recognized by all clinicians.
The centrifugal pathways are many, and need not be enumerated
here. Particular reference may, however, be made, as expiratory
nerve routes, to the pneumogastric (motor nerve to the smooth
muscle tissue in the bronchi) and to the intercostal nerves; and as
inspiratory centrifugal routes, to the phrenic nerve (motor nerve
to the diaphragm), the spinal accessory supplying the sterno-
cleidomastoid, and the cervical and brachial plexuses supplying
the trapezius, scaleni, and intercostals.
Lastly, the manifest inhibitory influence of the will or emotions
on cough leads us to the belief that the stimuli emanating from
the cerebral centers are conducted, along pathways as yet unknown,
to the reflex, automatic centers in the medulla oblongata. This
central cu:tion may, indeed, be provocative as in hysterical cough,
as well as inhibitory, as in the checking of the "useless" cough of
consumptives as a result of a peremptory command
Therapentic Indications. — The complexity of the mechanism
concerned in the act of coughing and the multiplicity of centripe-
tal routes along which the exciting stimulus may be conducted sug-
gest, a priori, the thought that there is not and cannot be any
"specific" treatment for the symptom, cough.
Again, cough which leads to expectoration and to evacuation
of the bronchi is a useful cough, which must be spared or, at most,
somewhat reduced. This applies to the majority of coughs of
respiratory origin. On the other hand, reflex cough is generally
a useless or even harmful manifestation, which must be ener-
getically combatted.
Rational treatment should aim: 1. To reduce the sensitiveness
of the mucous membrane from which the reflex starts. 2. To
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COUGH. 781
reduce the irritability of the nerve center concerned in the reflex.
3. To act if possible on the centrifugal pathways. 4. To inhibit
cough through the influence of the higher brain on the bulbar
center, eg., by suggestion.
The first indication, which consists in influencing the mucous or
serous membrane from which the reflex starts, is generally merged
with the causal treatment. This is the problem requiring the
greatest amount of clinical good sense; it can be solved only
after an accurate diagnosis has been attained. In a worm-in-
fested individual, a vermifuge remedy will clear up the whole
disturbance ; in a dyspeptic, proper dieting proves the best rem-
edial measure. Where the disordered mucous membrane is ac-
cessible to external applications, a local anesthetic will often give
excellent results; thus, in two particularly rebellious cases that
had proven refractory to most active internal drug treatment,
almost immediate results were obtained by placing temporarily
in the nasal cavities a wad of absorbent cotton moistened with
1 per cent, cocaine hydrochloride solution. In cough of gastric
origin, internal use of a preparation containing chloroform and
cocaine answers the same indication.
The indication which consists in reducing the reflex irritability
of the medullary center is generally fulfilled by opium and its
derivatives. Upon opium are based the many official prepara-
tions intended for use in controlling cough. It is often power-
less, if not indeed directly injurious, in the so-called "reflex
coughs," except pleural cough. The author has had under ob-
servation a patient suffering from paroxysmal cough of naso-
pharyngeal origin in whom a few centigrams of extract of opium
brought on paroxysms with such regularity as to exclude the
idea of a mere coincidence. The value of bromides in these
cases has already been amply stressed. The so^alled "Meglin's
pills" have also frequently proven successful in the author's
hands :
I^ Extract of hyoscyamus seeds ^
Extract of valerian r of each, 0.05 gram.
Zinc oxide J
To make one pill. Three pills to be taken daily, morning, noon
and evening.
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782 SYMPTOMS.
The third indication, viz., that of acting on the centrifugal nerve
paths, is on a more doubtful physiologic plane; yet experience
shows that often two fly blisters placed over the course of the
phrenic nerve, one in the cervical region, above the clavicle and
between the two heads of sternocleidomastoid, and the other
at the lower costal margin over the "phrenic point," act most
favorably on certain forms of paroxysmal cough, particularly
those — and they are frequent — associated with hyperesthesia
over the course of the phrenic nerve.
Finally, a central inhibitory effect is induced by suggestion dur-
ing waking hours, the physician asserting before the patient that
his cough is purposeless and convincing him of the possibility
and necessity of his arresting his cough by a mere effort of the
will. The following anecdote, related by Troisier, is quite typi-
cal in this connection: "During my visit at Falkenstein, I was
seated at the dinner table ; I had been given the place of honor,
next to the master; a consumptive physician was sitting not
far from us. He was coughing and coughing without cessation.
Dettweiler whispered to me: *You see that physician who is
coughing; well, I shall tell him after dinner that he must either
cease coughing or take his meals alone in his room, because his
cough is unnecessary.' That very evening, at supper, our unfor-
tunate colleague was in his usual place, but he did not cough
a single time throughout the entire meal."
On the whole, and by reason of its very commonness, cough
is a symptom which, taken alone, is of no great semeiologic sig-
nificance. It is clinically serviceable, as a rule, only by virtue
of the associated symptoms and signs, viz., expectoration, stetho-
scopic findings, fever, etc.
Yet a few varieties or modalities of cough are deserving of
brief mention. From the start, a distinction can and should be
made between:
1. The easily executed, expulsive, expectorating cough of re-
spiratory affections in the productive stage, and
2. The distressing, "useless," dry cough of beginning broncho-
pulmonary infections (before the productive stage) and of extra-
respiratory infections (typically pleuritis, pleurisy, or worm
cough). The following should also be mentioned:
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COUGH. 783
3. A form of cough which is both mufHed (low-pitched) and
well-transmitted, ''brassy," metallic, usually accompanied by
harsh breathing and occurring in the presence of tracheobron-
chial con:^)ression (as in aneurysm, deep-seated goiter, and medi-
astinal tumors).
4. The nervous cough, habit cough, or "tic cough" of psycho-
paths.
This occurs mainly under two sets of conditions:
(a) As a "defensive" or "disguising" cough, occurring con-
sciously or unconsciously when tbe patient is embarrassed and
desires a momentary interruption in his speech.
(fc) As a "suggested" cough, after the physician, in questioning
the patient, has asked him whether he coughs.
In this connection two equally unfortunate suggested inter-
pretations, personal or familial, are to be guarded against:
(a) A patient with incipient tuberculosis, desirous of giving
the impression that he is not ill, ascribes his cough to habit (a
pseudo-psychopath) .
{b) A psychopathic, obsessed patient, ascribing his cough to
tuberculosis, exaggerates the cough (a pseudo-consumptive).
5. The well-known "stridulous," barking, "croupy" cough of
croup (diphtheria) or of false croup (laryngismus stridulus).
6. The chronic, habitual, common cough of bronchopulmonary
disorders, viz., tuberculosis, emphysema, chronic bronchitis,
bronchiectasis, chronic pulmonary congestion, impaired heart-
action, etc.
7. The so-called "effort cough," generally dependent upon
some cardiac disorder and brought on, seemingly, by dilatation
of the heart, more particularly of the right auricle. As a matter
of fact, in old persons it is often hard to set apart that which,
in cough, is due to the heart and that which is due to the lungs,
i.e., to distinguish "heart cough" from "lung cough." Heart
weakness, indeed, favors stasis and infection of the lungs; on
the other hand, any bronchopulmonary disorder tends to accen-
tuate the cardiac inadequacy and the dilatation of the right
heart: The cough is then actually and literally of "cardiopul-
monary" origin.
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784 SYMPTOMS.
8. Postural cough with corresponding expectoration. The
patient coughs especially if he lies on one side, right or left,
and the cough is accompanied by copious expectoration. This
combination is rather pathognomonic of a bronchial cavity
(bronchiectasis or actual cavity) evacuation of which is favored
by some definite posture.
9. The "pharyngeal" cough of smokers and drinkers is ac-
companied by hawking and scraping and sometimes by nasal
discharge, and is more marked in the morning owing to accumu-
lation of secretions in the nasopharynx during the night.
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DEXrIRIUM AND [from de, out of lira, groove^ oiU\
DELUSIONS. L of the groove^ to wander. J
Obviously the aim here sought can merely be to recall the
fundamental clinical facts relating to delirium and delusions, Le.,
those facts with which any practitioner not specializing in psy-
chiatry should be familiar.
To supply a good definition of delirium is not easy. Grasset's
definition may here be accepted: "Such conditions may be
termed delirium as are characterized by disturbances of reason-
ing power and of judgment, with the reaching of conclusions
which the subject believes to be correct and exact/' Seglas,
quoted by the same author, refers to the fact that delirious con-
cepts may, in different cases, be either vague, indeterminate, or
precise and distinct; fixed or changing, polymorphous or uniform;
diflFuse, monotonous, or systematized (even to the point of "crys-
tallization'* or stereotypy) ; plausible, impossible, silly, fantastic,
absurd, incoherent, contradictory, contrasting, antagonistic, etc.,
and he studies them in succession in such varying forms as
deliriums (delusions) of self-accusation, persecution, self-defense,
grandeur, hypochondria, negation, enormity, mysticism, eroti-
cism, metabolism, body transformation, etc.
For clinical purposes, the large aggregate of different types of
delirium may be divided into the three following subgroups, vis,,
oniric delirium, partial or systematized delirium, and delirium of
interpretation.
1. Oniric or dream-like delirium is by far the commonest form
the non-specialized practitioner has occasion to witness. The
patient is then constantly in a condition resembling sleep — he is
dreaming. The typical delirium of this subgroup is delirium tre-
mens. Lasegiie's celebrated definition may be recalled in this
connection: "Delirium tremens is a dream which is being lived;"
this is the essence of the so-called oniric delirium. The following
50 (785)
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786 SYMPTOMS,
description of its essential features is from Reg^s : "Oniric delir-
ium is an actual somnambulistic state, a second state. Like any
other second state, it is brought into play through subconscious
or unconscious activity; it dominates the subject to the point of
making him live through and act his subconscious or unconscious
life . . . lastly, like a second state, it is always susceptible to
hypnotic influence. This form of delirium is, literally, a dream
delirium. Indeed, it originates and runs its course in sleep; it is
made up of extemporaneous associations of ideas, of hallucinatory
reproductions of former images and recollections, of scenes of
family or occupational life, of visions u^ally impleasant, and
of strange, impossible combinations which are eminently mobile
and changeable or, on the other hand, to some extent fixed, and
which impose themselves more or less completely upon the
patient's belief. In its mildest form, such delirium is exclusively
nocturnal and evanescent; it ceases upon awakening and reap-
pears only in the evening, either at twilight or not until later
when slight somnolence comes on. In a more pronounced form,
it again ceases upon awakening, but only incompletely, and
recurs during the daytime as soon as the patient shuts his eyes
and dozes. Lastly, in its most pronounced form, delirium fails
to disappear in the morning and continues as such throughout
the day, like a prolonged dream."
This is the typical delirium of intoxications and of acute or
subacute infections. It is th(*^ delirium of the toxic and infectious
psychoses in general, of gastrointestinal autointoxications, of alco-
holism, of drug intoxications {opium, salicylates, belladonna, etc.),
of pneumonia, of typhoid fever, of malaria, of ^uremia, of eclamp-
sia, etc.
This, it should be repeated, is the common, ordinary type of
delirium which the practitioner sees by far the most frequently.
Its extraordinary frequency in children is particularly well-
known; the "dream delirium" is one of the commonest features
of children's diseases ; it goes hand in hand with fever and accel-
erated pulse rate in these cases.
2. Systematized or partial forms of delirium (paranoia), gen-
erally chronic and quite distinct from the preceding types, are
made up of ''functional psychopathic states characterised by perma-
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DELIRIUM AND DELUSIONS, 7%7
nent, fixed, and systematically interconnected ideas, developing in
a certain direction and following a logical course" (Amaud).
Amaud presents the following classification of these forms:
1. Acute Systematized Delirium : Acute paranoia.
2. Chronic Systematized Delirium: Chronic paranoia.
(a) Depressed, — Delusion of persecution running a systema-
tized course.
Self-accusatory and melancholic delusion of persecution.
Primary systematized self-accusatory delusion.
Systematized hypochondriac delusion.
(b) Expansive. — Ambitious (megalomania).
Religious.
Erotic.
The clinical course, now established, of chronic systematized
delirium is as follows, according to Grasset:
A. Period of anxiety or subjective analysis (hypochondriac
insanity), characterized by strange, anesthetic disturbances; the
patient is very introspective, and discovers in these disturbances
some concealed motive, some allusion to his person or circum-
stances.
B. Period of delirious (delusive) explanation (delusion of per-
secution, religious delusion, erotic delusion, political delusion, de-
lusion of jealousy, etc.) ; the subject imagines an explanation for his
sufferings, for his anxiety, and for the surprising amount of atten-
tion which he believes is being paid to him. He discovers the
**formula for his delusion" ; it is his hallucination which he is inter-
preting; hence the term "period of delusive explanation."
C. Period of transformation of personality (delusion of ambi-
tion) ; from being persecuted, the subject becomes ambitious
or megalomaniac ; his entire personality is transformed ; he be-
comes a prince, a king, a prophet, or the Deity.
D. Magnan recognizes a fourth period of dementia, which is a
common mode of termination in this kind of psychosis as well
as in many others.
This is the typical delirium of chronic infections with second-
ary degenerative changes in the nerve centers.
Progressive general paralysis, though much less systematized
and coherent than the chronic systematized delirium above de-
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788 SYMPTOMS.
«
scribed, nevertheless presents some of its rather characteristic stages,
especially the third and fourth. Two clinical signs point to it
particularly, vis., a very special "euphoric mental puerility" with
amnesia and loss of the autocritical sense (Sicard and' Roger), and
the characteristic dysarthria with jerky, tremulous, drawling speech,
which is unmistakable.
3. Delirium of interpretation, a chronic systematized psy-
chosis, founded on delusional interpretations, separated in 1902
by Serieux and Capgras from the group of the systematized de-
lusions, is defined and described by these authors as follows :
"Delirium of interpretation is a chronic psychosis in which
the proliferation of manifold interpretations and progressive radi-
ation of a predominant concept result in the organization of a
complex delusive romance which may lead to variable reactions.
Delirium of interpretation is a constitutional psychosis, the origin
of which is to be sought, not in the action of some toxic agent,
but in a psychopathic predisposition, in developmental anomalies
of the cerebral centers which hold in dependency perversions of
judgment, gaps in the critical sense, and disturbances of affectivity;
they are essentially the result of a congenital malformation.
"Whereas some systematized psychoses are based upon pre-
dominant and practically permanent sense disturbances, delirium
of interpretation consists of a delusional system in which the
hallucinations always remain an incidental occurrence and are
even, as a rule, entirely wanting. Lucidity and mental activity
are retained throughout the disease; weakening of the intellect
appears only after a lapse of time, from the effects of senile
evolution; some subjects are seen retaining their mental alert-
ness thirty years after the beginning of the mental disturbances.
The disorder, while incurable, is thus not one attended with
progressive dementia.
"When in the presence of a subject suffering from delirium
of interpretation, one is first of all struck by his correct deport-
ment ; the observer is sometimes deceived by the brilliancy of
his conversation and the accurate logic of his reasoning pro-
cesses, and is rather disposed to consider him at most as a
thinker along fallacious lines, with a tendency to look upon
all events from a peculiar angle, and to systematize all exter-
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DELIRIUM AND DELUSIONS. 789
nal or internal phenomena upon the basis of a questionable
preconcept
'*The imperative need of referring all to his own person
and of interpreting everything in a certain direction, and of
emitting, on the whole, only affective judgments marred by
errors appears as the sole morbid condition in such a subject
"The mistaken interpretation, the delusion of personal sig-
nificance is, indeed, the fundamental manifestation of this psy-
chosis. The autonomy of a morbid entity cannot, however, be
based merely upon a single sign. Delusional interpretation plays
an important role in a number of other psychoses and even in
simple passional states. To warrant a diagnosis of delirium of
interpretation, a whole group of characteristics must be present,
zns., (1) multiplicity and organization of delusional interpretations;
(2) absence (or paucity) of hallucinations, and their casual occur-
rence; (3) retention of lucidity and mental activity; (4) progres-
sion through gradual expansion of the interpretations; (5) incura-
bility, without terminal dementia."
* * *
The reason that the author has — with Grasset — deemed it
proper to recall the main clinical features relating to the various
forms of delirium (or delusion) considered very broadly as "dis-
turbances of the reasoning power and of judgment" is that
definition and delimitation of the various forms of delirium is a
difficult* matter; that the types above recalled and described
condense into a small compass a number of psychiatric facts
indispensable for everyday practice, and that they will bring
to mind various fundamental and necessary acts of psychologic
discrimination.
As a matter of fact, in general practice the term "delirium" is
applied particularly to the common, ordinary form of the disturb-
ance, i.e., to confusion of ideas and the presence of mental images
associated with mistaken interpretations and often hallucinations —
in a word, to oniric delirium, for which careful clinical study
will always detect some cause, either:
1. Toxic (alcohol, opium, belladonna, salicylates).
2. Autotoxic (uremia).
3. Or infectious (typhoid fever, pneumonia, malaria, etc.).
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DIARRHEA. [Suappelv, to /low through.}
Diarrhea is characterized by the passage of liquid stools.
Only the most practical, fundamental, and essential facts re-
quired in the interpretation of this very common symptom can
here be presented.
In diarrhea, liquid stools are passed with variable frequency.
In general, diarrhea seems to depend upon:
Either an exaggeration of the persistaltic contractions (hy-
perperistalsis, intestinal hypersthenia).
Or an exaggeration of the intestinal secretions (hypercrinia).
Or diminished absorption of the intestinal contents.
Clinically, diarrhea may be met with under the following cir-
cumstances :
I. Lesions of the intestinal walls, whether there be irrita-
tion or pathologic changes in the mucous membrane, as is the
case in all instances of toxic, infectious enterocolitis,
A. Infectious or parasitic enterocolitis.
(a) In this group are included ordinary acute enterocolitis,
typhoid fever, and cliolera, of which mere mention is here sufficient.
It should be particularly borne in mind, however, that the greater
number of instances of common acute enterocolitis are as yet not
accounted for ; the characteristic clinical complex may be summar-
ized as comprising diarrhea, fever, leucocytosis, and albuminuria.
(fc) Chronic parasitic dysenteriform diarrhea with paroxysmal
recurrences requires more thorough consideration. As matters now
stand, these dysenteriform types of diarrhea may seemingly be
classified, for practical purposes, as follows:
Ordinary colon bacillus dysenteriform diarrhea, acute or chronic.
These cases yield to interruption of feeding, with restriction of the
patient to water by the mouth ; to castor oil, and to lactose.
Amebic dysenteriform diarrhea, acute or chronic. Ravaut and
Maute have plainly demonstrated the selective action of emetine
and of arsphenamine in these cases.
(790)
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DIARRHEA. 791
BacUlary dysenteriform diarrhea (acute or chronic dysentery),
amenable to irrigations with silver salts and to antidysenteric serum.
Dysenteriform diarrhea due to trichomonas (flagellates).
Tuberculous dysenteriform^ diarrhea, with presence of tubercle
bacilli.
These causal distinctions, now absolutely necessary as evidenced
by the specificity of the methods of curative treatment, can be
established only by bacteriologic examination of the stools (see
Examination of the Stools).
(c) By way of a reminder there may also be mentioned here
intestinal cancer which, however, causes obstruction much more
frequently than diarrhea, except where the lesion is situated low
down.
B. Toxic enterocolitis. — In this group are met the actually
toxic and drug forms of enterocolitis (enterocolitis due to mercury,
arsenic, digitalis, colchicum, etc.), and the alimentary forms (botul-
ism, etc.).
There is also the autotoxic or diathetic enterocolitis of uremia,
gout, and diabetes.
Some forms of hyperacute gastroenterocolitis result in a clin-
ical picture well described by Lesieur (choleroid state, reduced
output of urine, and uremia), which may be accounted for by
intense but diflfuse and superficial inflammatory lesions of the
digestive tract, particularly the small intestine (congestion with
hemorrhage, prominence of the follicles).
The bacteriologic basis of enteritis seems to be variable,
different combinations of bacteria being found; a constant fea-
ture, however, is weakness and insufficiency of the liver and
kidneys. This constitutional or acquired weakness sometimes
transforms the clinical picture of gastrointestinal infection into
that of auto-intoxication and azotemia. Hence the appropriate
designation "uremigenous gastroenteritis" proposed by Lesieur.
In all such cases the history or the coexisting diathesic mani-
festations will clear up the diagnosis.
II. Diarrhea of Nervous and Vasomotor Origin.— Enteric
neuroses are very frequent.
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792 SYMPTOMS.
Diarrhea upon emotion and the enter orrhea of exophthalmic
goiter constitute, as it were, an experimental verification of the
neuropathic diarrheal flux that may be met with, frequently in
alternation with constipation, in the course of the majority of
neuroses. Many instances of paroxysmal diarrhea ascribed to
dietary indiscretions are really due to this cause.
In most of these cases the cause of the diarrhea remains
wholly obscure. The physician finds neither infection (no fever
nor leucocytosis), nor ulceration (no blood in the stools), nor
food poisoning (no dietary indiscretion). The diarrheal flux
may supervene even while a most stringent diet is being ad-
hered to, but nearly always appears in conjunction with over-
work, insomnia, nervous shocks, or prolonged stress. It is hard
for the uninitiated to avoid the conclusion that an intestinal
neurosis exists and to suspect as cause a diminution of vaso-
motor tone due to abnormal excitation of the sympathetic, seem-
ingly evidenced by the low blood-pressure, high pulse rate, ex-
cessive emotional susceptibility, general asthenia, tendency to
fainting, and vasomotor disturbances (showing a curious simi-
larity to Graves's disease!) There appears to be some physio-
pathologic relationship between hyperperistalsis and low periph-
eral blood-pressure, occurring in conjunction with vasodilata-
tion in the splanchnic area.
It seems not unlikely that the so-called "mucous enteritis" is
not a true colitis, but rather a spastic enteroneurosis with alter-
nating diarrhea and constipation and excessive mucous secretion.
Diarrhea of circulatory origin is equally well-known, e.g.,
the diarrhea of atrophic cirrhosis, to which Portal referred when
he said: *'Wind precedes the rain," alluding to the sequence of
tympanites and diarrhea met with in cirrhosis. The same con-
dition may occur in cardiac, renal, cardiorenal, and cardiohepatic
disorders, although constipation is rather frequently observed
under these circumstances.
Mention should also be made of the diarrhea, at times pro-
fuse, which may follow reabsorption of edemas, hydrothorax,
and ascites, a feature affording a definite indication for purgation
in the presence of these disorders.
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DIARRHEA. 793
rn. Diarrhea of Digestive Origin. — The causes in this group
are complex and varied.
Any condition of gastrointestinal dyspepsia, especially if
associated with intolerance of fats ("hyposthenic dyspepsia/*
insufficiency of the liver and pancreas), is almost necessarily
accompanied by diarrhea with passage of an excess of fats in
the stools (hypersteatorrhea) .
Diarrhea of gastrointestinal digestive origin is thus, on the
whole, a manifestation of actual indigestion, subdivision of
which may be attempted as follows:
1. Botulism, food intoxication, ptomain poisoning, — The many
undoubted cases of collective intoxication, as by cream puffs,
game, etc., are manifestly produced in this way.
2. Overeating, — In these cases the digestive limit or capacity
is exceeded; this is the well-known indigestion of released
schoolboys and soldiers on leave.
3. Fat intolerance. — An expression of insufficiency of the liver
and pancreas.
4. Achylia gastrica.
5. Pronounced, abrupt discharge of bile occurring in overactivity
of the liver and resulting in sharp diarrhea in the morning after
eating.
According to Cabot, the relative frequency of the various
causes of diarrhea is as follows :
1. AciUe enteritis:
(a) Cryptogenic, five-sixths of all cases.
{b) Specific (typhoid, dysentery, cholera, toxic disturb-
ances), one-sixth of the cases.
2. Chronic enteritis:
(a) Cryptogenic, nine-tenths of all cases.
(&) Of known causation (digestive insufficiency), one-tenth
of the cases.
3. Cancer of the intestine,
4. Pernicious anemia,
5. Mucous colitis.
6. Intestinal neuroses and exophthalmic goiter.
7. Tuberculosis.
8. Fat intolerance.
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794 SYMPTOMS,
Certain signs and symptoms occurring in conjunction with
diarrhea sometimes permit of rather accurate localization of the
causal disturbance.
The presence of blood and pus in the stools (bloody, glairy
stools) is characteristic of ulceration. in the large bowel, of varying
origin (infection or neoplasm).
The presence of mucus and false membrane is often charac-
teristic of an intestinal neurosis.
The customary significance of fat-laden stools is well-known ;
steatorrhea points to insufficiency of the liver and pancreas.
Fluoroscopy after a bismuth meal and proctoscopy, moreover,
permit of a most valuable direct examination of the bowel (see Tech-
nical procedures, in Part II).
Frequently, indeed, direct, gross, macroscopic examination
of the feces affords highly serviceable information. This ele-
mentary clinical procedure is just cts essential as uranalysis, taking
the temperature, or examining the pulse. The '^offending body"
must always be sought, or at least the "evidence" or "witness"
of it.
The patient, then, should always be ordered to collect and keep
the feces for examination.
The following features of the stools should be noted:
Frequency : Four, 6, up to 100 a day — the latter in the pres-
ence of rectal tenesmus, as in dysentery.
Amount: From a few hundred grams to several liters, as in
cholera and choleroid forms of diarrhea, whence the enormous
loss of water from the tissues.
Consistency: Serous, albuminoid (glairy), mushy, pasty.
Color: Brown, as in normal stools.
Dark green: Excessive bile content in certain cases of jaun-
dice; in infantile diarrhea, or after administration of calomel.
Decolorized, gray, clayey: Obstructive jaundice.
Red or rust-colored: Dysentery.
Black, "coffee-ground": Melena, bismuth, or krameria (rhat-
any).
Colorless, serous, "rice water": Cholera and choleroid diar-
rhea.
Odor: This is always more or less unpleasant
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DIARRHEA. 795
Exceedingly malodorous : Putrid diarrhea in botulism, putre-
factive gastrointestinal indigestion, and in street cleaners, anato-
mists, and workers in sewage.
Distinctly acid: In gastrointestinal indigestion with fermen-
tation.
No odor in serous stools.
Kind: Ordinary fecaloid type
Bilious.
Serous.
Watery.
**Stony": Intestinal concretions and coproliths; gall-stones.
The macroscopic examination referred to will frequently re-
veal abnormal constituents of the stools:
Intestinal parasites: Tenia, ascaris, oxyuris.
Undigested food (li enteric diarrhea) : Acute indigestion, ex-
cessive peristalsis.
Fats {fatty stools) : Fats present in oily droplets, spherules,
or larger fatty masses (affections of the liver and pancreas)
Blood: Red: Hemorrhoids.
Black: Melena.
Intestinal shreds: Dysentery.
Blood-stained, glairy material: Neoplasm.
Pus: Infectious or neoplastic enterocolitis.
Mucus and membranous formations: Mucomembranous entero-
colitis, intestinal neuroses.
Intestinal sand: Mucous enterocolitis.
Rice-bodies: Flakes of epithelial cells: Cholera and choleroid
diarrhea.
The above brief review suffices to illustrate the very great
semeiologic value of a mere macroscopic examination of the
stools. Correlated with the medical history, other clinical mani-
festations (temperature, general condition, coexisting digestive
disturbances, urinary evidences, etc.), and examination of indi-
vidual organs (liver, stomach, intestinal canal, etc.), it will generally
lead promptly to a correct diagnosis.
In puzzling cases it should be supplemented by chemical, micro-
scopic, and bacteriologic examination of the stools (see Examina-
tion of the Feces), which is frequently indicated.
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DYSPEPSIA \^^' *''*' ni^ti, coction, digestion; disturb-']
' [ ance of digestion^ particularly gastric. J
The term dyspepsia is here employed in its semeiologic sense,
and is applied in a general way to any disturbance of gastric
digestion complained of by the patient or observed by the phy-
sician. The author would not have attempted to deal with this
extensive and complex subject — at least under the above com-
prehensive term — had he not found certain features of it already
partly considered in a section of Cabot's **DifIerential Diag-
nosis," upon which some of the material which follows is based,
and had not his colleague Leon Meunier consented to draw up
an authoritative plan of diagnosis for ulcer and cancer of the
stomach.
The author's aim will have been fulfilled if, upon reading
this section, the practitioner becomes convinced that dyspeptic
manifestations, indigestion, and vomiting are in most instances
of extragastric origin; that painstaking and complete investiga-
tion of all the organs is necessary, particularly in all cases of
chronic indigestion, and that in a patient complaining of such
disturbances, merely applying the term "dyspepsia'* and ordering
some indefinite antidyspeptic treatment amount to nothing, or
are even worse than nothing.
The very great majority of the causes of indigestion are unre-
lated to the stomach, or at least to any particular disease of the
stomach. On the other hand, there is not a single organ in the
human body which may not be a source of gastric symptoms.
Nausea, dyspeptic disturbances, the vomiting of pregnancy,
uremia, and brain tumor are familiar illustrations of this clinical
aphorism. As a matter of fact, the heart and the stomach may
with equal frequency and in an equal degree be disturbed by
remote and slight organic causes. The stomach is, moreover,
as frequently free of any pathologic changes in subjects com-
(796)
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DYSPEPSIA, 797
plaining of dyspepsia as is the heart in subjects complaining of
palpitations or in whom tachycardia is observed.
The truly "gastric" causes of indigestion or dyspepsia may
practically be reduced to two, vis,, cancer and tdcer. Nervous dys-
pepsia, the gastric neurosis, is of extraordinary frequency ; but only
exceptionally does it originate in the stomach. The same is
true of many other varieties, such as dyspepsia with hyperchlor-
hydria; dyspepsia dependent upon constipation or symptomatic
of appendicitis; gastroptosis, ordinarily the result of general
atony with multiple visceroptosis, alcoholic gastritis, etc. In
short, most varieties of dyspepsia are not, strictly speaking, of
gastric origin, and do not constitute gastric disorders.
What clinical possibilities, then, should come into our minds
when a patient complains of gastric symptoms, and of gastric
symptoms alone?
1. In the presence of a pregnant woman who has not yet reached
the menopause, one should always think first of all of a possible
pregnancy. As is well known, under these circumstances any
symptoms may be observed, from a simple condition of nausea
in the morning to the uncontrollable vomiting of pregnancy—
as is true, moreover, in many toxic states of the blood, such
as alcoholism, uremia, lead poisoning, etc. These digestive
symptoms occur with such frequency that they may properly
be included among the minor evidences of pregnancy. The
classic indications of this state should under these conditions
be sought, vis,, cessation of menstruation, increased size of the
uterus, secretion of colostrum, etc.
2. Uremia, manifest or latent, is also a very frequent condi-
tion, and one present far oftener than it is diagnosticated. Many
obstinate dyspeptic disturbances, either mild (nausea, anorexia,
aversion to food) or severe (vomiting, hematemesis), originate
in this way. Uremia should always be thought of in the pres-
ence of chronic dyspepsia coexisting with albuminuria, edema,
and a definite elevation of blood-pressure, and particularly if
blood examination discloses a high content of urea. Especially
should it be thought of, a priori, in any individual who after pass-
ing the fortieth year, and having had a "good digestion" up to
that time, loses his appetite, experiences nausea or even vomit-
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798 SYMPTOMS.
ing, becomes sallow and loses weight, and in whom examina-
tion of the stomach gives practically negative results. The above
mentioned evidences — albumin, high blood-pressure, edema, and
hyperazotemia — should be carefully searched for, and the appro-
priate antinephritic treatment will remove all doubt as to the
renal origin of the dyspeptic disturbances.
3. Tuberculosis, pulmonary or elsewhere situated, may like-
wise be a cause of many instances of indigestion in the absence
of any internal (cancer or ulcer) or external (food or drug
poisoning) gastric cause. As is well known, incipient tubercu-
losis often takes on the appearances of anemia and dyspepsia;
anorexia and loss of weight are common in this stage of the
disease. In these cases of '^cryptogenic" dyspepsia one should
proceed, therefore, to a careful investigation in this direction,
the temperature being taken morning and evening, careful aus-
cultation carried out in a quiet room, and an x-ray examination
practised.
As a matter of fact, the opposite mistake is also made, and
an attack of nervous dyspepsia with anemia and loss of weight
too often labelled pulmonary tuberculosis without any adequate
reason. The fact cannot too often be repeated : One should be
a "realist" in clinical work, and like St. Thomas, one must be
desirous to come into actual touch, i,e., to establish by contact
with our senses, the sufferings of our patients and the theories
evolved in our minds.
Furthermore, tuberculous patients — apart from the ordinary
causes of dyspepsia to be mentioned later (rapid eating, poor
teeth, excessive intake of fluid, etc.), and to which they are sub-
ject like other patients — are very often and very particularly the
victims of two serious sources of error regarding the stomach,
vie, drug intoxication (opium, morphine and its substitutes caus-
ing hypopepsia and apepsia; creosote and its derivatives, anti-
pyrin, pyramidon, etc., inducing ar "gastritis medicamentosa"),
and alimentary overwork the result of ill-considered overfeeding.
4. Numerous cases of indigestioit in women are the result
of inanition. In this connection the- author cannot do better than
to quote literally from Cabot, having nowhere found a better
or more judicious critical exposition of the abuse of dietetic
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DYSPEPSIA. 799
measures among dyspeptics. "This [inanition] comes about as
follows: Something, we need not now inquire what, produces
an upset of digestion. The patient attributes it to certain food,
probably what she took last, just before the attack occurred.
Accordingly, in future she omits this article of diet from her
bill of fare. The indigestion recurs, an article of diet is ag^n
blamed, and something else is cut out of the diet because she
thinks it hurts her. So in this way food after food is given up,
until the patient gets down to a regimen of slops or their equiva-
lent. We have now a typical vicious circle. The patient is ill-
nourished because she is dyspeptic, and she is dyspeptic because
she is ill-nourished. We can break this circle by forcing her to
eat despite grievous suffering. An ill-nourished stomach will
complain, yet it must be nourished nevertheless. If we can per-
suade the patient to undergo such suffering, we can honestly
hold out the hope that at the end of it she will break her chain,
will get back her nutrition, and lose her symptoms. The trouble
is that ordinarily the physician does not believe this himself.
He has not seen enough cases in which forcing the patient to eat
achieves this happy result; but anyone with extensive hospital
experience knows that what is called "dieting" — that is, cutting
out of one's diet most of the foods that ordinary people live on
— is usually a most pernicious process, and leads to a great
deal of long and unnecessary suffering. Most cases of this
type can be cured by nothing in the world but forced feeding.
"The greatest improvement that I have seen in the manage-
ment of stomach cases in the last twenty years has been the recog-
nition of causes outside the stomach and the successful attack
upon these*causes. Next to this, the greatest improvement has
been through giving up our habits of making strict, narrow diet
lists which result in more or less chronic starvation. Whatever
we do for a gastric patient, we must not starve him. We must
get in food enough to maintain the caloric needs of the body,
and the greatest error in the treatment of the past has been the
failure to recognize this necessity."
5. Cholelithiasis is a very common cause of paroxysmal pains,
very often ascribed to the stomach. After cancer and ulcer have
been correctly excluded, one may state that it is almost always
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800 SYMPTOMS.
a mistake to attribute really severe pain to the stomach. In
other words, the only disorders of the stomach causing severe
pain are cancer and ulcer. All the other varieties of dyspepsia
run their course with their usual assortment of symptoms and vary-
ing combinations of flatulence, heart-bum, discomfort, nausea, sen-
sations of constriction or oppression, and vomiting, but without
violent pain.
Gall-stones often induce attacks of pain situated in the epi-
gastrium and not in the gall-bladder region. Overlooking of
this fundamental fact leads to many mistakes. If the patient
has repeated attacks, some will sooner or later become localized
in or be referred to the right hypochondrium, but in the
earlier stages of the disease such localization is very frequently
lacking.
Allied to the gastralgia of cholelithiasis are the obstinate dyspep-
tic phenomena, with delayed pain and eructations, dependent upon
adhesions between the gdl-bladder and the neighboring viscera
(stomach, liver, transverse colon, etc.) the result of a former chole-
cystitis with pericholecystitis. These may assume the extremely
grave form of pyloroduodenal stenosis, with vomiting and absolute
intolerance of food.
6. Angina pectoris may be overlooked and treated as a form
of dyspepsia when the pain is felt in the epigastrium, is preceded
and accompanied by flatulence and eructations, as is frequently
the case, and comes on after meals. These three observations of a
digestive character, especially when made in combination, lead
to many mistaken diagnoses of various gastric aflfections. De-
termination of the blood-pressure, careful auscultation, and
painstaking inquiry relative to the patient's medical history and
the factors/ which brought on the attack will usually reveal in
definite fashion the existence of angina pectoris. One of the
most constant features of angina pectoris is its almost inevitable
occurrence under the influence of bodily fatigue and emotion,
and its subsidence under rest and quiet. Disturbances of gas-
tric origin do not have this feature. In the majority of cases
of angina pectoris the pain, even if it starts and culminates in
the epigastrium, radiates to the precordial region and sometimes
even into the left arm.
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DYSPEPSIA, 801
Yet, in truth, the diagnosis is frequently a nice matter, at least
when based merely on cursory clinical examination. This is due
to the facts that: 1. Many discomforts manifestly referable to the
stomach, particularly aerophagia and the gastric neuroses, are fre-
quently accompanied by anginose symptoms. 2. The anginose
S)mdrome (see Precordial pain) is of very variable origin and
gravity, but if it be recognized that true angina pectoris always
constitutes an outward manifestation of myocardial weakness or
an aortic or periaortic lesion or the — very frequent — combination
of these two conditions, the clinical examination should be directed
definitely along these lines. The objective evidences of myocardial
impairment and aortic lesions should be sought, and if such exami-
nation proves negative, the angina theory resolutely discarded.
7. Gastralgic crises of tabetic origin. — ^The possibility of
tabes as the cause of violent, paroxysmal, uncontrollable "crises"
of sudden onset and disappearance should always be thought of.
Indeed, if, in accordance with the precepts presented in the sec-
tion on systematic organization of clinical examinations, testing
of the patellar reflex and for the Argyll-Robertson pupil is never
omitted, many unrecognized cases of tabes will be detected and,
iir consequence, many gastralgias treated as ulcer of the stomach
referred to their true, tabetic origin; even more particularly
should these procedures be remembered in gastralgia occurring
in known cases of tabes. Gastric ulcer or cancer may, however,
be present in combination with tabes. The fact of having de-
tected tabes does not warrant the practitioner's dispensing with
an investigation for the signs of ulcer or cancer.
As an exceptional condition, brief mention may be made of
the possible presence of gastralgia of syphilitic origin resulting
cither from the so-called "hourglass" shape of the stomach,
probably due to a cicatricial band remaining after cure of a
specific lesion, and which fluoroscopy after a bismuth meal will
reveal de visu, or to specific ulcerations, which appear to be un-
common.
*8. Dyspepsia and gastralgia due to lead occur much oftener
than they are diagnosticated. Painters, printers, and workers
in rubber are particularly subject to them ; on the other hand, they
need hardly be thought of in persons who are not manual work-
si
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802 SYMPTOMS,
ers. Any una«ccountable dyspepsia or loss of appetite coming
on in an individual who handles lead should be presumed to be
of saturnine origin. If to the dyspepsia are added colic and
marked anemia, and if the gum margins exhibit the character-
istic bluish-gray lead line, a mistake in diagnosis is inexcusable.
In the premonitory stages, however, one cannot do more than
presume the existence of lead poisoning; in any case, application
of the classical precept *'sublata causa, tollitur effectus" is in
order; abstention from all contact with lead, proper diet, and
the exhibition of diuretics and laxatives will bring about rapid
improvement if lead poisoning exists. The patient, thus fore-
warned, should thereafter take whatever precautions or carry
out whatever procedures he may deem appropriate.
9. Cancer oi the large intestine deceives many clinicians, even
when very well posted, when it is manifested, as is often the
case, in irregular periods of nausea, pain, and even vomiting, in
the absence of any notable or appreciable intestinal symptoms.
A bismuth meal or enema followed by systematic fluoroscopic
examination will sometimes alone settle the diagnosis.
Simple fecal obstruction of atonic and aged patients may,
indeed, give rise to wholly similar manifestations. The author
will always retain a recollection of a patient seen in the late
Dr. Landrieux's service, in which he was an intern at the time.
This patient, about 60 years of age, cachectic, anemic, of a straw-
yellow color, presented upon palpation a tumor of the size of
the fist between the umbilicus and the right hypochondrium ;
digestive disturbances were very marked, consisting of anorexia,
aversion to meats, frequent vomiting, constipation, etc. Dieula-
foy, from whose service the patient had recently issued, had made
a diagnosis of cancer of the stomach, which seemed to the author
plainly warranted.
Months elapsed without any notable change in the situation,
when one day, a large dose of castor oil resulted in the evacuation
of several chamberfuls of stercoral masses, together with disap-
pearance of the abdominal tumor and rapid betterment in the diges-
tive disturbances.
The subject was seen again in subsequent years, and the im-
provement thus initiated was observed to have been maintained.
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DYSPEPSIA. 803
10. Organic affections of the nervous system, as well as
arteriosclerosis, are very often causes of indigestion; the head-
aches and vertigo which frequently accompany indigestion in
these cases should draw the practitioner's attention to the arter-
ies, kidneys, and brain. It should be recollected that sclerous,
specific, or neoplastic lesions of the brain may induce for weeks
or even months headaches of the so-called "bilious'' type ascribed
to indigestion or, if unilateral, decorated with the term "migraine."
These mistakes are obviated by careful anamnesis, determina-
tion of the blood-pressure, uranalysis, inspection of the ocular
fundi, and a search for the indications so often overlooked by
the patient or masked, vu:,, paresthesias of the extremities, slight
evanescent attacks of paresis, aphasia, mental confusion, con-
vulsive twitches, etc.
11. Alcoholic gastritis, a common disorder in some classes
of society, and not exclusively in the lower strata, is easily diag-
nosticated if merely kept in mind: (a) By observation of the
ordinary signs of chronic alcoholism, vi::., tremor of the extremities,
abnormal excitability, various evidences relating to the mucous
membranes, etc. (fe) By eliciting a history of habitual intemper-
ance, which should be carefully inquired into in any class of society
by minute questioning regarding the use of spirituous beverages,
(r) By the nature of the dyspeptic disturbances, taz,, anorexia,
aversion to food, and especially the vomiting of mucoid material
in the morning — a frequent and characteristic finding, (rf) At
times by the simultaneous presence of other visceral manifesta-
tions directly or indirectly related to alcoholism, vis., hepatic cir-
rhosis, arteriosclerosis, progressive mental deterioration, etc.
12. A most frequent clinical type, particularly in women, is
that aflforded in the following syndrome of gastrointestinal dys-
pepsia:
Poor or capricious appetite; a sensation of discomfort,
weight, or tension in the stomach during the digestive period,
continuing for a varying period of time; stasis of food in the
stomach, manifested clinically, apart from the unpleasant sen-
sations already mentioned, by regurgitation of food several
hours after meals and by succussion splash in the empty stomach
in the morning; gastrointestinal fermentation, distention after
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804 SYMPTOMS,
meals, and eructations. These patients state that they are
greatly relieved by belching, and lay much stress on this fact.
Generally there is manifest sluggishness of the bowel, with hab-
itual constipation, sometimes interrupted by attacks of diarrhea;
mucomembranous enterocolitis is frequently present, as are also
disturbances due to reaction on the liver (slight jaundice, painful
congestion of the liver, etc.) ; frequently the patient appeals to
the physician on account of disturbed heart action (palpitations,
tachycardia:, etc.), or for more or less definite nervous disturb-
ances, such as migraine, general malaise, vertigo, headache, gen-
eral weakness, and psychasthenia.
Upon examination there is found almost invariably a relaxa-
tion of the abdominal wall, with lessening of the normal ten-
sion of the abdomen; palpation gives a particular impression
of softness and atony; it excites no defensive reaction or reflex
tension. Needless to state, ptosis of the viscera is constant, con-
sisting of descensus of the kidney, liver, stomach, or even the
uterus.
Low blood-pressure is an almost constant finding; the hypo-
sphyxic syndrome is frequently present, and respiratory insuffi-
ciency is the rule.
From the purely clinical standpoint, this condition may seem-
ingly be designated as a h3rposthenic gastrointestinal dyspepsia
(hypomotor and hyposecretory), with stasis, fermentation, ptosis
of organs, and various reactions elsewhere, e.g., upon the liver,
heart, kidneys, and nervous system.
It should be repeated that few clinical types occur as fre-
quently in women as this one. This is sufficiently shown by
the large number of investigations that have been made on the
subjects of visceroptosis, dilatation of the stomach, movable kid-
ney, flatulent dyspepsia, etc., all of which are simply particular
modalities of the foregoing major type.
In truth, these are cases of inadequate circulation, respiration,
or neuromuscular action as plainly as they are cases of digestive in-
sufficiency. They are general hyposthenics, the functions of all
their organs being below normal (see Hyposphyxid).
13. Lastly, one should not forget the reflex dyspepsia of ap-
pendiceal origin, with or without nausea and vomiting.
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DYSPEPSIA. 805
Having concluded this lengthy, albeit incomplete, enumera-
tion of the possible causes of indigestion and gastralgia, there
remain to be mentioned the commonest and most important
causes of these conditions, in the author's estimation.
The first four are functional:
1. Bad teeth.
2. Rapid eating.
3. Aerophagia.
4. Psychoneuroses and mental depression; overwork.
The last two are organic:
1. Gastric ulcer.
2. Cancer of the stomach.
Bad teeth, so exceedingly frequent a condition, particularly
among the poorer classes, is a common, manifest, and unfortu-
nately too often overlooked cause of dyspepsia. Patients will
come to the physician already provided with strict dietetic regu-
lations and most expertly written prescriptions, in whom but
one point in the examination has been omitted, viz,, that of look-
ing at the patient's teeth — an initial and necessary step in any
examination of the digestive tract.
Rapid eating goes hand in hand with bad dentition; the
profound and patient; studies of Fletcher should be recollected
in this connection. Ke-education of mastication is sufficient
treatment for curing a very large number of dyspeptic cases.
The most elementary clinical investigation, indeed, will afford
conclusive evidence in support of the two following axioms :
A person zvho masticates his food correctly is almost never a
dyspeptic (apart from obvious dietary indiscretions).
A person who masticates his food insufficiently is always a
dyspeptic.
Practical conclusion: In all dyspeptics, whatever be the type
of dyspepsia, the prescription should begin with the time-honored
but often neglected warning: Eat slowly, masticate the food thor-
oughly, and moisten it well with saliva,
Aerophagia is very frequently combined with rapid eating,
and gives rise to similar dyspeptic symptoms consisting of a
feeling of weight and distention, meteorism, sometimes with
cardiac manifestations, dyspnea, palpitation, or even premature
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806 SYMPTOMS,
beats, all very easily accounted for by the anatomic relationship
between the fundus of the stomach and the diaphragm. Obser-
vation of the unconscious aerophagic reflex and percussion of
Traube's space insure a prompt diagnosis.
Psychoneuroses, mental depression, and overwork induce or-
dinary manifestations of dyspepsia, either chronic or oscillating
like patient's ''humor*' itself. That mental factors powerfully
influence gastric digestion and, conversely, that disturbances of
gastric digestion powerfully influence the patient's "morale"
or "humor" is a clinical fact which is well expressed in the
old-fashioned word "hypochondria" and the truth of which or-
dinary observation will easily prove.
The older authors, e,g., Chomel and Grisolle, considered dys-
pepsia a neurosis of the stomach. Subsequent organicist, path-
ologic, and chemical investigations for a long time eliminated
this conception which, however, has never been completely
abandoned. The most recent investigations point back' in its
direction ; unquestionably the nervous system in the widest meas-
ure regulates the secretion and motility of the stomach, and the
latter is one of the most sensitive organs in the body, upon
which react most frequently, through the solar plexus, all causes
of nervous disturbance, whether depressive or stimulating.
As a matter of fact the majority of dyspeptics are psychopaths.
Bourget estimated that the "dyspeptics through psychic dis-
turbances" made up three-fourths of the practice of physicians
specializing in the digestive tract. Mathieu and Roux write that
nervous dyspepsias are frequent. Dubois, of Bern, asserts that
"90 per cent, of dyspeptics are cases of psychoneurosis." The
latter estimate appears to the author too high, and is probably
accounted for by the fact that Dubois is a neurologist. The
author's experience leads him to conclude, with Bourget, that
psychopathic dyspepsias make up about three-fourths of all dys-
pepsias.
Disappointments and constant worry exert a marked influ-
ence. How many "hypochondriac" employes show restoration
of spirits and digestive capacity through mere promotion to a
position sought for a long period! How many ladies, terribly
dyspeptic, with a daughter to be married off, find their digestive
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DYSPEPSIA,
Ulcer and Cancer of the Stomach.
807
Catheterization of the Fasting Stomach.
(a) Food stasis Pyloric stenosis and, if true
stasis, cancer of the py-
lorus.
Wash water contains jReichmann
free HCl.
Wash water, with 1
per cent, acetic solu-
tion, contains chem-
ically demonstrable
blood.
(b) No food
stasis.
(probably py-
loric ulcer).
Ulcer of the body of the
stomach (simple or can-
cerous).
Examination of the Stomach after a Test MeaL
(a) Free HCl
in excess.
(b) Free HCl
reduced to-
ward 0.
Ether capsule dis-
solved in less than
one hour.
Ether capsule not dis-
solved.
Probable ulcer.
Probable cancer.
Examination of Feces after a Milk and Vegetarian Diet
Presence of
blood chem-
ically demon-
strable.
Blood disappears after
a few days rest.
Blood still present.
Blood is present in
feces but not in acid-
ulated wash water
^ from stomach.
Probable ulcer.
Probable cancer.
Duodenal ulcer or ulcer on
duodenal aspect of py-
lorus.
Fluoroscopic Examination (Principal types).
Small, con-
tracted stom-
ach with les-
sening of
peristaltic
contractions.
Filling-defect
in stomach
(apparent ab-
sence of a
portion of the
gastric shad-
ow).
Diffuse
cancer.
Localised
cancer.
"Amputation"
of the py-
loric region
and delayed
evacuation
of bismuth
meal.
Stomach
presenting
bilocular ap-
p ea ranee
(due to
spasm).
Cancer of
pylorus.
[Diverticular
a aspect (ap-
parent ad-
dition to gas-
tric shadow).
Ulcer on
lesser
curvature.
Callous
ulcer.
Blood Examination.
Increased antitryptic power of the serum Cancer.
Cytologic Examination.
Microscopic examination of the wash water after gastric
lavage.
Study of centrifugation sediment
Presence of neoplastic cells Cancer.
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808 SYMPTOMS.
power suddenly improved at the wedding feast! Unfortunately,
in these patients, except in the case of single persons, the physi-
cian's role is necessarily a rather restricted one.
Ulcer and Cancer of the Stomach. — ^The importance of such
diagnoses as those of ulcer or cancer of the stomach is obvious.
At the author's request, Dr. Leon Meunier consented to formu-
late a vade mecum of the laboratory procedures indispensable in
the diagnosis of ulcero-cancerous affections (see the preceding
page).
Aside from the classical symptoms of ulcer and cancer of
the stomach, viz., late pains, vomiting, hematemesis, cachexia,
etc., it is important to be able to make a diagnosis in the earliest
stage of these lesions, since often the only effectual treatment,
prompt operation, depends for its practicability upon such early
diagnosis.
In the annexed synopsis are presented the various methods
of examination which should be availed of when ulcer or cancer
of the stomach is clinically suspected, together with the results
obtainable therefrom.
It should be noted that any one of these procedures is rarely
sufficient to afford a positive diagnosis, but that their combined
results often lead to a strong probability.
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DYSPNEA. [8vg, ill; nvelv, to breatJie.]
Dyspnea is characterized by a difficulty in breathing; it is usvially
associated with increased frequency of respiration (polypnea)
and sometimes, as will be seen later, by changes in the ampli-
tude of the respirations. In brief, the essential feature of dysp-
nea is distress, or even at times pain, attending the respiratory
exertion.
EfTarentirwtor n^spirdtorf center inmedalla MTerent sensory
£)pirc
"^
Fig. 606. — Diagram showing the afferent and efferent nerve paths con-
cerned in the reflexes of the respiratory tract (cough, asthma, etc.).
Pathogenesis of dyspneic and asthmatic attacks.
All grades of dyspnea are met with, from the dyspnea on exer-
tion, appearing only u|x>n more or less marked or prolonged motor
activity, to orthopnea, in which extreme dyspnea compels the
patient to brace himself against furniture or a window in order
to breathe.
Some attacks of paroxysmal dyspnea are known as asthma.
It is not within our plan to discuss the physiology of regula-
tion of the respiratory rhythm and the pathologic physiology of
dyspnea. It should be noted, however, that the automatic reg-
ulation of the respiratory function is effected both by a chemical
and a nervous process.
(809)
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810 SYMPTOMS,
1. Chemical. — The concentration of carbon dioxide in the blood.
2. Nervous. — Through the pneumogastrics, which embody two
kinds of fibers: (a) The fibers inhibitory to inspiration and acceler-
ator to expiration which are excited by the expansion or dilatation
of the lungs, (b) The fibers inhibitory to expiration and acceler-
ator to inspiration, which are excited by deep expirations, as in
the majority of instances of dyspnea; these are inoperative dur-
ing ordinary breathing. Any morbid state which leads to an
excessive concentration of carbon dioxide in the blood or which
by any route directly excites the respiratory center in the me-
dulla, or indirectly through the pneumogastric nerves, is capable
of inducing dyspnea in the physiopathologic sense.
The number and variety of the causes of dyspnea are such
that the semeiologic value of this condition is rather limited.
In general, however, one may state that there is present:
1. Either a manifest or latent lesion of the respiratory system.
Or a manifest or latent lesion of the circulatory system.
Or some grave toxic-infectious state (uremia, acetonemia).
As with most other symptoms, one must likewise reckon with
the possibility of neurotic dyspnea (due to nervous inhibition).
2. The clinical significance of dyspnea varies in importance and
precision according to the degree to which the symptom is independ-
ent of other manifestations, i.e., is observed in the absence of
fever, changes in the lungs or heart, acceleration of the pulse rate,
and neurotic stigmata. One may almost make the assertion that
any dyspnea sine materia, in the accepted sense of this term, is
either a toxic dyspnea, usually uremic or acetonemic, or a neurotic
dyspnea.
3. Some forms of dyspnea possess per se a more or less char-
acteristic significance :
A. Thus, sometimes dyspnea affects more particularly the
act of inspiration, or, on the contrary, the act of expiration:
(a) Inspiratory dyspnea is characteristic of obstruction of the
upper respiratory passages ; thus, it is met with in edema of the
glottis, croup, diphtheria, laryngeal spasm, tumors of the larynx,
foreign bodies of the larynx, trachea, or bronchi, retropharyn-
geal abscess, Ludwig's angina, or pressure on the trachea (as by
intrathoracic goiter, aortic aneurysm, etc.). Particularly difficult
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DYSPNEA.
811
inspiration may be noisy and assume a stridulous quality which
is practically pathognomonic of pressure on the larynx or
trachea.
(fe) Expiratory dyspnea is frequently accompanied by whistling
sounds; as is well known, it is one of the most characteristic
features of emphysema and of asthma. It is met with exception-
ally in edema of the lungs.
(c) Mixed dyspnea affecting both inspiration and expiration is
by far the most frequent form and likewise the least character-
istic.
Fig. 607. — Diagram of a terminal bronchus under normal conditions
(A) and during a paroxysm of asthma (B) (Abrams). During the
asthmatic attack, the spasm of the circular fibers in the bronchial wall
(B) causes retention of air in the air-vesicles, difficulty of expiration,
and dilatation.
B. Kinetic and Static Dyspnea. — One should also carefully
distinguish :
(a) Kinetic dyspnea, or dyspnea on exertion, motion, and ex-
ercise, which is merely an exaggeration of a nonnal event and which
appears only upon exertion, such as walking, ascending stairs,
exercising, etc. The clinical signification of such dyspnea is
quite distinct and of great value. Any exercise, exertion, or
muscular contraction demands increased function on the part of
the cardiopulmonary system, which is normally manifested by
a temporary acceleration of the heart rate, a rise in blood pres-
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812 SYMPTOMS,
sure, an increase in the frequency and amplitude of the respira-
tory movements, and an increased elimination of carbon dioxide
from the lungs. The tachycardia and polypnea induced by ex-
ercise are thus absolutely normal phenomena and being such,
are not accompanied by cardialgia, palpitation, or dyspnea and
subside rapidly after cessation of the exercise. If the exercise
taken is too violent or too prolonged, or the reserve cardio-
pulmonary power of the individual in question is slight, there
will occur an excessive, prolonged dyspnea, palpitation, or tachy-
cardia.
Kinetic dyspnea on exertion is one of the first and most valuable
indications of insufficient cardiopulmonary function. The sub-
ject notices that he can no longer take a rather prolonged walk
or ascend the stairs — ^as he could previously do without the least
difficulty — without experiencing dyspnea. The dyspnea on exer-
tion, at first accidental (after a copious meal) or slight (occur-
ring only after relatively violent exercise), gradually becomes
habitual and pronounced, requiring for its production only a
very moderate amount of exercise.
If sought, it will be found present in all cases of chronic
cardiopulmonary insufficiency, including weakened heart action,
anoxemia, inadequately compensated heart aflfections, and
chronic bronchopulmonary disorders such as emphysema, chronic
bronchitis, and fibrosis of the lungs.
(fc) Static dyspnea continuing while the individual is at rest
either represents the final stage of the preceding type of dyspnea
or is the expression of a toxemia.
Brief mention may here be made of the influence of posture
and of rest at night.
Dyspnea, of whatever source, is almost invariably increased
by the horizontal position, and diminished or relieved by the
sitting posture. In extreme cases, indeed, the patients lean for-
ward, with their elbows on their knees, or sit at the edge of
the bed or are able to rest only when seated in an armchair.
Various factors are doubtless operative in this phenomenon, the
most important being the pressure on the mass of abdominal
viscera and on the diaphragm.
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DYSPNEA,
813
As for the influence of rest at night, it may be stated that,
with the exception of "dyspnea on exertion" which, as the term
implies, passes oflf after rest, the majority of instances of dysp-
nea, whether of cardiopulmonary or of toxic-infectious origin,
become worse at night. In a certain proportion of cases this
may be ascribed to an unfavorable influence of the horizontal
position customarily assumed at night; yet this recrudescence
of dyspnea is the rule even in subjects who remain in the sit-
ting position at night. Many plausible explanations have been
vouchsafed to account for this fact, e,g,, the disturbing influence
Uremic Coma. Chejme-Stokes Breathing.
15" • 15** I 1Q*» [ lO" ' 1j5" i 15"
/Ip/iea \4/kfjDiMim llRe^tations ^fRe^iSMfon^, ^finea
• ' 1 I
J L-
frequency
Fig. 608. — Cheyne-Stokes breathing observed during quiet and pro-
found sleep. Systematic observation for eighteen minutes showed ten
stereotyped respiratory "cycles" absolutely like that represented above in
duration, rhythm, amplitude, and auditory manifestations.
Case 613. Albuminuria, 6 grams to the liter ; blood urea, 2.10 grams ;
blood-pressure, 269ieo ; no edema. Other evidences of uremia : Headache,
vomiting, flow of viscid saliva, convulsive seizures, etc.
of the night and darkness on the patient's imaginative processes,
the period of maximal organic intoxication, a tendency to inhibi-
tion of the respiratory center during sleep, etc.
C. Che3me-Stokes Bireathing. — Special mention should be
made of a particular type of respiration known as the Cheyne-
Stokes rhythm, so called after the names of two observers
(Cheyne, 1816, and Stokes, 1854) who made a special study of
it. Tt consists of a series of respirations of progressively in-
creasing frequency, amplitude, and noise production (ascending
phase), followed by respirations occurring at increasing in-
tervals and becoming smaller and more quiet (descending phase),
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814 SYMPTOMS.
after which there appears a stage of complete apnea with cessa-
tion of all breathing (period of apnea), the cycle thereafter
beginning anew.
This sort of breathing is observed in its pure form only if
the subject, completely relaxed and unconscious, is in a deep
sleep. In the waking state it is always more or less interfered
with by mental reactions arising from anxiety, pain, etc.; in the
presence of coma, on the other hand, the rhythm is disturbed
by the complications attending this stage, vis., congestion of
the bases of. the lungs, partial obstruction of the pharynx and
larynx, paralytic phenomena, etc. Yet it is, as a rule, readily
detected if the least attention is paid to the respiratory rhythm.
The stages of apnea are particularly characteristic. "
When the condition is observed in its pure form during sleep
one is always impressed with the accurate control character-
izing the phenomenon, which recurs with mathematical regu-
larity, as in the case herewith illustrated.
Sometimes, though exceptionally, the foregoing rhythm of
respiration is present, but without any stage of apnea (Biot's
breathing). Such respiration possesses the same clinical signifi-
cance.
Cheyne-Stokes breathing is almost universally looked upon as
an indication of serious impairment of the bulbar centers, which
have a tendency to *'go to sleep" and the activity of which is ex-
cited only by such a carbon dioxide stimulation as attends be-
ginning asphyxia.
By far the most frequent cause of it is uremia, and the prog-
nosis is usually very unfavorable.
From the standpoint of semeiology alone, the various kinds
of dyspnea may be grouped as follows:
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DYSPNEA. 815
Dyspnea of Respiratory Origin.
Type case: Pneumonia.
Foreign bodies in the respiratory passages.
Pressure (pharyngeal, cervical, or medias-
tinal); acute and chronic pleuropulmon-
ary disorders.
Dyspnea of Circulatory Origin.
(a) Cardiac
Type case: Heart failure.
(b) Dyscrasic.
Type case: Uremia.
Cardiac insufficiency, hyposystoly, hypo-
sphyxia, inadequately compensated heart
affections (cardiac pseudo-asthma).
Anemia or anoxemia.
Uremia or acetonemia.
Intoxications (certain asphyxiating gases).
Febrile disorders.
Dyspnea of Nenrons Origin.
Type case: Hysteria.
Neuroses. Neurocardiac erethism.
Asthma, certain forms of.
Bulbar affections.
L— DYSPNEA OF RESPIRATORY ORIGIN.
This IS usually obvious, the relationship of cause to eflfect
being in most instances readily demonstrable.
Such is the case in foreign bodies in the respiratory passages ;
in pressure and obstruction of the pharynx, larynx, or trachea
(as in nasopharyngitis, adenoid vegetations, laryngeal diphtheria,
tumors of the larynx, and tumors or glandular enlargements in
the neck) ; in bronchitis — especially capillary bronchitis; in bron-
chopneumonia, congestion of the lungs, lobar pneumonia, pleu-
risy, pleuropneumonia, etc., further discussion of which would
seem superfluous.
These instances of dypsnea of pleurobronchopulmonary origin
are produced, on the whole, in the same way, vie, through suppres-
sion of a more or less extensive portion of the functionating lung
surface, owing either to compression, as in pleurisy or pneumo-
thorax; to encroachment upon the bronchi, as in bronchitis; to
encroachment upon the air vesicles, as in pneumonia and bron-
chopneumonia, or to inadequate motion of the ribs and dia-
phragm, as in emphysema, etc.
The paroxysmal attacks of dyspnea commonly known as
asthmatic seizures, which may, as will be seen, be of very vari-
able origin, hardly exhibit any special differential features ac-
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816 SYMPTOMS,
cording to their varying cause ; the two essential and characteristic
factors are: A pneumospasmodic disturbance (the paroxysmal
dyspnea) and a secretory disturbance (the catarrhal condition).
No lengthy description of these features need here be given.
Their essential characteristic is paroxysmal dyspnea, together
with bradypnea or slow breathing. It is in tracing the under-
lying cause of the asthmatic state that the therapeutist is called
upon to display the highest degree of clinical common sense and
carry out the most painstaking inquiry, for upon this investigation
curative treatment mainly depends. No form of clinical investi-
gation is more difficult, and while at times the physician may
succeed in detecting the exciting factor at once, more often a
prolonged and painstaking search is required, since "anything
may happen in asthma, and even, in the presence of certain
bizarre manifestations, to be skeptical would be a mistake"
(Brissaud).
In practice, the following 6 groups of causes, which are by
far the commonest (Moncorge), should be examined for: 1. Neu-
roarthritism. 2. Causes relating to the lungs. 3. Cardio-arterio-
renal causes. 4. Gastro-hepato-intestinal causes. 5. Toxic-infec-
tious causes. 6. Nasal hyperexcitability. As may be noted,
according to this almost the entire field of internal medicine will
have to be gone over.
Mention should be made again of the fact that chronic bron-
chopulmonary affections — particularly emphysema, asthma, and
chronic bronchitis — necessarily react upon the right heart, and
that at a more or less advanced stage of the disorder dyspnea
is as much of cardiac as it is of pulmonary origin.
It should be recalled, furthermore, that many lung manifesta-
tions are merely a symptomatic expression of some general morbid
condition, such as uremia or cardiac inadequacy; this is true, e.g.,
of passive congestion of the bases of the lungs, of acute and sub-
acute edema of the lungs, of many instances of chronic bronchitis,
and of many asthmatoid conditions. Cardiorenal insufficiency is
at the bottom of a very large number of acute and chronic respira-
tory manifestations.
For these various reasons, the semeiologic study of dyspnea
associated with some definite localized disorder in the respiratory
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DYSPNEA. 817
tract necessarily indicates a careful examination of the heart
and kidneys, both for diagnostic and for prognostic purposes.
IL— CARDIAC DYSPNEA.
As for so-called "cardiac dyspnea" one cannot do better than
quote the succinct, profound, and clinically excellent presenta-
tion of the subject by Ribierre:
"From the start, dyspnea on exertion (appearing upon climb-
ing stairs, steeply inclined streets, etc.) is accompanied by painful
sensations behind the sternum and in the epigastrium, and to these
painful sensations is attached from the outset an element of angor,
although they are evanescent and quickly disappear at rest.
"Next there is decubital dyspnea, coming on suddenly just be-
fore or during sleep and likewise accompanied by precordial angi-
nose pains, frequently radiating to the back, shoulders, and arms.
Sometimes the dyspneic element clearly predominates over the
painful element ; there exists then an asthmatoid dyspnea or, in
accordance with the rather questionable term sanctioned by us-
age, a cardiac pseudo-asthma.
"When one takes into consideration the special features attend-
ing these painful manifestations, angina pectoris at once comes to
mind. Is It wise, on account of slight symptomatic differences
relating to the duration and severity of a symptom, to perpetuate
former misconceptions and establish a definite distinction between
these anginose pains, constituting a supposed angina minor (which
ought not to be fatal!), from the true angina, which ends fatally?
Here again, the subsequent course of the case will bring out the
true state of affairs. Not infrequently, indeed, there are seen to
appear, in subjects who had previously exhibited only this rela-
tively mild syndrome, the major phenomena of insufficiency of
the left ventricle, vis., a most typical angina pectoris, and also
edema of the lungs, of which no detailed description is here re-
quired. Since the investigations of Merklen, it is no longer possible
to ignore the close relationship existing* between the painful dyspnea
of high pressure cases and angina pectoris and edema of the lungs,
nor the relationship of these syndromes with left ventricular insuffi-
ciency."
52
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818 SYMPTOMS.
The above word picture is particularly applicable to the cardiac
dyspnea of high pressure, aortic, cardiorenal, and nephritic cases.
In insufficiency of the right ventricle, dyspnea on exertion sets
in gradually, without concomitant precordial pains. Then the
dyspnea becomes continuous, making it impossible for the patient
to remain in dorsal decubitus and being progressively supplemented
Fig. 609. — Case 826. Heart failure, auricular fibrillation, and mitral
stenosis. H., 1888 ; 164 cm. ; 57 kilogr.
by the classical symptoms of impaired heart action, viz., painful
enlargement of the liver, jugular stasis, increasing cyanosis, re-
duced output of urine, edema, albuminuria, etc., heart failure fin-
ally occurring after a varying period. This clinical picture is more
particularly that of the dyspnea of mitral stenosis and of chronic
lung disorders, such as pulmonary fibrosis, adhesive pleuritis, bron-
chiectasis, emphysema, etc.
In the later stages of cardiac disorders, there is combined in-
sufficiency of the right and left sides of the heart, the result being
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DYSPNEA. 819
the .classical picture of complete cardiac insufficiency, involving
both the right and left auricles and ventricles.
Lastly, it should be mentioned that in simple fatigue of the
myocardium there may be observed in a very 'mild form a kind
of dyspnea suggesting Cheyne-Stokes breathing (Fig. 611).
Cardiac asthma. — Cardiac asthma consists, according to
Merklen's definition, of a paroxysmal dyspnea complicating dis-
turbances of pulmonary circulation and of the- cardiac function.
xvAVffll^^
a
Fig. 610. — Cheyne-Stokes breathing, a, apnea; b, ascending
phase; c, descending phase.
Cardiac asthma generally occurs in subjects presenting un-
mistakable evidences of insufficiency of the heart, such as diffi-
culty in walking, dyspnea on exertion, dyspnea in recumbency,
habitual breathlessness, and attacks of threatened pulmonary
edema manifested by slightly reddish albuminous expectora-
tion, gallop rhythm on auscultation, reduced blood-pressure, etc..
At times there are mild, incipient seizures occurring occasion-
ally, either at the moment of retiring, or during sleep, or even
.AfM ...jJi
d b a
Fig. 611. — Dyspnea of myocardial fatigue and general exhaustion.
a, apnea; b, ascending phase; descending phase absent.
several times in a single night These are the result of a weak-
ness of the myocardium which is favored by the reduction of
circulation that naturally occurs during sleep and which passes
off on awakening. Sometimes these attacks recur as soon as the
patient attempts to fall asleep again. Occasionally, after taking
cold, or a heavy meal, or some emotional impression, there is
a severe, dramatic attack with anginose manifestations.
Oppression is greater in cardiac asthma than in nervous as-
thma; this is because of an interference with pulmonary circu-
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820 SYMPTOMS,
lation, which, however, is not always readily detected. Fre-
quently, indeed, there is elicited on auscultation merely an ex-
aggeration of resonance, due to a species of acute emphysema
of the lung brought on by spasm of the muscles of respiration.
In other instances, there develops a more or less extensive pul-
monary edema, generally confined to the bases of the lungs.
Serous transudation may be sufficiently free to lead to the ex-
pectoration of albumin-laden sputum stained with blood — a proc-
ess which brings some relief to the patient. In such instances,
cardiac asthma and acute edema of the lungs coexist. Finally,
the tracheal rale may be noted in the absence of rales in the
lungs.
Cardiac asthma may be complicated with angina pectoris, and
this complication is met with particularly in subjects poisoned
by tobacco, suffering from sclerosis and atheroma of the coron-
aries, or subjected to a severe degree of overwork. The left
heart reacts to the distention in common with all reservoir-like
organs with muscle tissue in their walls, eg,, the bladder; hence
the pains felt by the patient. These pains cease when the heart
is dilated.
During an attack, auscultation of the heart is frequently im-
practicable. Sometimes one may note gallop rhythm, which is
an expression either of cardiac insufficiency in general or a mitral
insufficiency from dilatation, which disappears a^ soon as the
heart has become restored to its normal dimensions.
Cardiac asthma may eventually terminate in fatal syncope.
In such instances, the extremities become cold, there is incon-
tinence of urine and feces, the patient is covered with sweat,
his sight becomes dim, and death supervenes very quickly. In
many instances the fatal termination occurs only after the lapse of
one or two hours. Some patients pass into a comatose state.
As a rule, however, the case does not die if the necessary meas-
ures are taken in due time, and the physician always has reason
to hope for termination of the attack, even under what appear
to be most unfavorable circumstances.
Cardiac asthma is the result of sudden insufficiency of the
left ventricle; it is due to an abrupt turn for the worse in a
latent heart disorder.
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DYSPNEA. 821
The attacks of asthma are, as Merklen puts it, prepared for
by pathologic changes or functional disturbances of the myo-
cardium, the chief causes of which are tobacco abuse, alcoholism,
overwork, and impaired coronary circulation. They are directly
brought on by any factors tending to produce or increase the
dilatation of the heart. The most important of these causes are
those which induce peripheral vaso-constriction — exposure to
cold, emotional impressions, indiscretions of diet, excessively
long tramps or prolonged work, sexual excesses, intercurrent
diseases, influenza, and pneumonia.
Thus, the subject of cardiac dyspnea would be a fairly lucid
one were it not rendered obscure by the cardiac neuroses, i.e.,
those individuals who, apart from any acute or dironic organic
lesion of the heart or its separate layers (endocarditis, pericar-
ditis, myocarditis), and even in the absence of any true — e.g.,
congenital or constitutional — myocardial weakness, or of any
known disease of the nervous system, suffer from some symp-
tom-complex preeminently involving the heart. As a matter of
fact, it is these cardiac neuroses which are accompanied by the
most numerous and distressing cardiac or pseudo-cardiac symp-
toms, the most important of which are dyspnea, choking sensa-
tions, or angor with radiation of pain to the arm and neck (nerv-
ous angina, etc.).
Differentiation of cardiac neurosis and organic disease is not
always an easy matter. Auscultation may be difficult and
misleading; various types of arhythmia — extrasystoles, nodal
rhythm, etc. — may be observed in either condition ; the same is true
of the customary hypertrophy of the left ventricle and even
in greater degree of the subjective manifestations, such as dysp-
nea on exertion, sensations of constriction, or even an anginose
syndrome, palpitations, phrenocardia, etc. Nevertheless there
are some differential points.
(a) The first and most important is, perhaps, the neuropathic
substrate over which cardiac neurosis always runs its course. The
cardiac symptom-complex above referred to is but a portion of
the neuropathic picture, always more or less distinct and gener-
ally supported by heredity and the extracardiac neuropathic
manifestations, particularly digestive and mental.
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822 SYMPTOMS.
(6) The second is the frequency and severity of the symptoms
occurring at night, viz., insomnia, anxiety, dyspnea, and even angor
and cardiac pseudo-asthma, incomparably more frequent, im-
pressive and seemingly more "dramatic," as a rule, than in cases
of organic heart disease. These nocturnal psychosomatic dis-
turbances are very definite in neuro-cardiac cases.
(c) N euro-cardiovascular instability and mobility constitute the
external evidences of excessive nervousness, the pulse frequency
and blood-pressure being affected to a surprising extent by the
slightest disturbing causes. The same is often true of the aus-
cultatory signs, which are far from being as relatively fixed and
constant as those present in organic disease.
{d) Absence of the customary etiologic factors of organic heart
disease is, as a rule, noted, vis., rheimiatic, typhoid, s)rphilitic,
diphtheritic, or other infections, plethora and auto-intoxication,
gout, uricemia, etc.
(e) Lastly, the circulatory functional test (see the Circulatory
system) clearly demonstrates the heightened vasomotor reactions
and the usually considerable margin of safety in the reserve
power of the myocardium.
III.— DYSCRASIC DYSPNEA.
One of the most salient features of this type of dyspnea is
that of being for a long period sine materia, and the fact that
neither the time-honored and already somewhat obsolescent
routine examination of the circulation, nor an examination of the
respiratory system, reveal any disorder or organic disease which
might plausibly account for it.
Whereas, however, the objective cardiopulmonary evidences
and the classic symptoms already mentioned are ordinarily lacking,
and while such dyspnea, considered from this already antiquated
standpoint alone, are sine materia, such is far from being the case
if they are studied and listed with the assistance of the modem
methods of examination.
Actually, most cases of this type of dyspnea may, clinically,
be placed in one of the three following groups :
1. Anoxemia. — ^At bottom, in these cases, there is a func-
tional cardiopulmonary insufficiency unattended by any recog-
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DYSPNEA, 823
nized disease, but in which modem means of investigation gen-
erally elicit: (1) Insufficiency of respiration (the spirometer
showing a breathing capacity below 2 litres in an average sub-
ject). (2) Low blood-pressure, with the systolic at 120 milli-
meters or less and the pulse pressure at 15 to 35 millimeters. (3)
Increased blood viscosity, 4.5 and upwards, or at least a relatively
high viscosity, 4.2 and upwards. Fluoroscopy and orthoradiography
demonstrate this lowered functional and nutritive state of the heart
and lungs even more rapidly, showing microcardia (the small *'drop"
heart), insufficient breathing particularly manifested in a rela-
tive reduction of the excursions of the diaphragm, reduced clear-
ing of the lung margins during inspiration, and the presence
in these parts, especially at the bases of the lungs, of zones
which hardly exhibit any clearing at all during inspiration.
These are cases of hyposphyxia (see Low blood-pressure),
2. Uremia. — Whether manifest or latent, uremia is perhaps,
after hyposphyxia, the commonest cause of dyscrasic dyspnea.
Apart from the customary but often misleading evidences of
uremia, vis,, headache, nausea, itching, cramps, numb fingers,
sleeplessness, albuminuria, etc., there are now available certain
practically pathognomonic signs, one of which in particular, viz.,
hyperazotemia, or an excessive amount of urea in the blood —
0.60 or more — should be examined for by determination of the
blood urea in all suspected cases. High blood-pressure, exceed-
ing 200 millimeters, the presence of traces of albumin, and the pas-
sage of an excess of urine of low specific gravity at night, in a dysp-
neic subject, are in themselves almost pathognomonic of azot-
emia, especially if the dyspnea assumes at times the so-called
Cheyne-Stokes character. In uremic poisoning the azotemia is
much more active in causing dyspnea than the chloridemia,
which appears to act rather in a mechanical manner (through
hydremic plethora and edema of the lungs).
3. Acetonemia. — As is well known, some cases of dyspnea,
in which indeed the prognosis is highly unfavorable, are asso-
ciated with the presence of acetone in the urine and with urinary
hyperacidity (see Uranalysis), This is the case in the dyspnea,
sometimes fatal, witnessed in the final stages of some cases of dia-
betes. The precise mode of production of this kind of dyspnea is
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824 SYMPTOMS,
still being widely discussed. One need here merely recall that such
dyspnea is always accompanied by acidosis, which is expressed,
among other manifestations, in urinary hyperacidity, and by cu:e-
tonemia (test for acetone), and that it is met with chiefly in the
terminal stage of diabetes (diabetic coma).
From the above the reader will have gained an idea of the
importance of chemical studies of the urine and blood in the
presence of dyspnea unattended with definite cardiopulmonary
pathology.
As possible causes of dyscrasic dyspnea may be mentioned :
1. Some forms of intoxication: Asphyxiating gases.
2. Certain febrile conditions,
IV.— DYSPNEA OF NEUROPATHIC ORIGIN.
This type of dyspnea is mainly represented by hysterical
polypnea, which can, as a rule, be readily differentiated by means
of the following features:
1. There is very marked polypnea, the rate of respiration reach-
ing or exceeding that noted in the final stages of cardiopulmonary
diseases.
2. It occurs in the absence of any marked or even appreciable
lesion of the heart or lungs; cough is practically absent and
expectoration nil.
3. Such polypnea may be greatly reduced or even completely
removed by distraction of the patient's attention, as by an in-
teresting conversation ; it may cease while the patient is answer-
ing questions ; in any event, it is never continuous, but is paroxys-
mal, coming on in distinct attacks.
4. This syndrome is present in conjunction with the psycho-
pathic state characteristic in these subjects, evidenced by sug-
gestibility, distortion of the truth, mythomania, etc.
5. There is absence of the other signs of true dyspnea: No
cyanosis, little or no acceleration of the heart rate, no reduction
of urinary output, no edema, no azotemia, etc.
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KDEMA. lol^fM, from oiSelv^ to swell]
Edema consists of a serous infiltration of the subcutaneous
cellular tissues or of visceral tissues, as in edema of the meninges
— involving- the pia mater, — of the lungs, etc. The ordinary
edema of the subcutaneous cellular tissues will here alone be
considered. Its characteristic feature is the lasting* depression
in the edematous region made by any form of pressure (depres-
sion from pressure with the finger, grooves from folds of the
clothing or pillow, depression with central groove upon pinch-
ing, depression en masse by lying on an edematous region, etc.).
While sometimes obvious where the swelling has caused a
marked change in the shape of an affected part, careful exami-
nation is frequently necessary for the detection of edema: In
the lower extremity it appears more particularly in anterior
pretibial tissues, in the region of the malleoli, and on the pos-
terointernal aspect of the thigh. In some subjects the lower
lids constitute a seat of election, exhibiting a characteristic
prominence. In patients confined to bed one should not forget
to examine the sacral region and the posterointernal aspect of
the thighs. In persons who still leave their beds and walk
about, it often appears only after they have been standing for
a more or less prolonged period, so that, while absent in the
morning, it reaches its maximal degree in the evening before
retiring. At the very beginning it may sometimes be elicited
only by noting an unusual sensitiveness of the cellular tissue to
palpation, constituting a species of pre-edematous hyperesthesia.
In established edema, the skin is, as a rule, tense, shining, and
pale (white edema of kidney cases) ; in heart cases, with impaired
heart action and hyposphyxia, the skin may assume a livid, purplish
tint (blue edema of heart cases) ; in inflammatory edema, as in
suppurative lesions and lymphangitis, the color ranges from pink
to red (red edema of infection) ; in hard, chronic edema the color
(825)
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826 SYMPTOMS,
may become darker, a bronze shade appear, and pigmentation of
the skin occur {bronzed edema of -chronic cc^es).
The usual consistency of edematous tissues is soft ; the finger
sinks into them as though into butter ; if the illness is prolonged,
and the edema becomes chronic, the cellular tissue undergoes
sclerosis and the condition becomes a hard edema. This is the
case, in particular, in the chronic edema of cases of varicose veins,
of lymphangitis, of myxedema, and of elephantiasis.
The cause of edema is often plainly apparent, the case being
either one of heart disease, with cyanosis, dyspnea, oliguria, an
overburdened disordered heart, and arhythmia; or one of chronic
nephritis, with pallid skin, gallop rhythm, and more or less
pronounced albuminuria; or one of malignant disease of the
stomach, greatly emaciated, cachectic, and with the lower ex-
tremities enormously swollen; or one of puerperal phlebitis,
with fever, leucorrhea, etc.
Sometimes, and even frequently, more than a single cursory
examination is required. While an experienced clinician will
almost always be able to get right to the point by virtue of
practical knowledge previously acquired, a less experienced
practitioner would do well to carry out the following funda-
mental steps in the process of diagnostic analysis:
Edema may be due to either a local or a general cause.
The local causes of edema should be examined for:
(a) Skin and cellular tissues. — Infections and toxic infections
of these tissues, — Furuncle, carbuncle, lymphangitis, abscesses, and
erysipelas are always accompanied by local edema. Are not
the three cardinal signs of infection, known since the early his-
torical ages, swelling, redness, and pain? Mere recollection of
the fact is sufficient. Allied to these conditions are certain dis-
orders, rare in the Western countries, involving the lymphatic
tissues (pressure or obliteration, of bacterial or parasitic, e,g.,
filarial, origin) and causing edema of the type of elephantiasis.
Certain poisonous bites, mosquito or snake bites, etc. — ^pro-
duce a similar effect.
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EDEMA, 827
Axrute eczema may be attended with edema.
For the sake of completeness the post-traumatic form of
edema, particularly following fractures, may be referred to.
(b) Veins. — Phlebitis, whether primary or secondary, and
whether infectious (as is the rule) or dyscrasic (as is much
less common) or neoplastic (as is much rarer still), is nearly
always attended with edema confined to the affected limb. It
is seldom wanting, even during the pre-obliterative stage.
Pain more or less limited to the course of a vein, sometimes
the feeling of the vein as a characteristic cord, the observation of
more or less extensive edema, the knowledge of some previous
infectious disorder (puerperal infection, typhoid fever, rheumatic
fever, etc.) or of a gouty tendency or a tuberculous or neoplastic
affection causing cachexia (phlegmasia alba dolens) are the very
features required for a diagnosis of phlebitis.
General cau8e8.-^The above causes being, as will have been
noticed, easy to exclude, the various possible general causes
remain to be considered.
In the presence of a definite, manifest edema, one should think
mainly of the three commonest causes, viz., cardiac, renal, and hemic
(dyscrasic), and secondarily, the former having been excluded, of
the three exceptional causes, viz., hepatic, nervous, and dystrophic.
I. Cardiac edema. — ^This is a characteristic feature of cardiac
insufficiency or hyposystoly. The diagnosis is obvious in the stage
of asystoly or complete decompensation: Marked edema, constant
dyspnea, tachy-arhythmia, oliguria, edema of the bases of the lungs,
passivq congestion of the liver, cardiac dilatation, and frequently,
the observation of a definite heart lesion.
At the outset of heart disease one should look carefully for
the minor evidences of impaired heart action, viz., dyspnea on
exertion, nycturia, orthostatic oliguria, vesperal edema of the lower
extremities, and persistent pulse acceleration after exertion (see
Functional tests of the circulation).
In these cases water retention and chloride retention are
often closely parallel.
II. Renal edema. — ^This is perhaps the most frequently en-
countered of all the varieties of edema; often it is present in
association with the preceding variety.
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828 SYMPTOMS,
Here again, the diagnosis is sometimes obvious, as in acute
nephritis where it develops suddenly, accompanied by fever, pro-
nounced albuminuria, and even hematuria, and in long-standing,
established chronic nephritis.
In early cases a special examination for it is frequently neces-
sary, edema being looked for in the lids, the cheeks (as shown
by map-like formations on the face, found in the morning and
due to pressure by folds of the pillow), and the malleoli. Its
appearance is generally preceded by a stage of pre-edema, or better,
of internal, invisible edema, demonstrated by periodic weighing
of the patient and by determination of the chlorides, which will
indicate in a parallel and synchronous manner any increase of weight
and retention of chlorides.
In all instances the physician should carry out a systematic,
complete investigation of the renal functions (see Examination of
the urinary system), including examination for albumin and casts,
and determination of the amount and rhythm of urinary excretion,
the systolic and diastolic blood-pressure, elimination through the
kidneys, chlorides in the urine, and blood urea. Such an investi-
gation is particularly necessary in the course and during the after-
math of infectious diseases, especially scarlet fever.
Renal edema is, as is well-known, related mainly to retention
of the chlorides.
III. Hemic or dyscrasic edema. — This form, the mode of
production of which is as yet quite uncertain, is the one met with
in anemias of the pernicious type and particularly in the final stage
of cachectic disorders (tuberculosis and malignant growths).
Whether it be true or fiction, it is related that Trousseau, who
had been suffering* for a long time from digestive disturbances
resulting in loss of strength and pain, declared to Dieulafoy,
his pupil, that he was afflicted with a growth of the stomach
and forecast an early, unfavorable termination because of the
presence of edema of the lower limbs which could not be ac-
counted for by the condition of the heart or kidneys. His diag-
nosis and prognosis unfortunately proved to have been well
founded. In old subjects one should always look with suspicion
upon such insidious edemas that cannot be shown to be either
of cardiac or renal origin.
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EDEMA, 829
Much less commonly, one of the following types of edema
may be encountered:
1. Edema of hepatic origin, nearly always of mechanical caus-
ation, vis., pressure upon the inferior vena cava in advanced cir-
rhosis of the liver. Gilbert has, furthermore, described a preascitic
edema met with early in the course of hepatic cirrhosis.
The supposedly established theory of an hepatic form of edema
was seriously discredited by a few clinicians. In 1893 Hanot wrote :
"Changes in the liver cells account for the cases of localized
edema either about the malleoli or in the face in the absence
of albuminuria. There exists an hepatic form of edema just as
there is a renal edema and the former may be an early sign of
disease." Le Damany, in a later contribution on the subject {"Les
hepatites hydro pigenes," 1914), concluded that there may be a
defective elaboration of protein material in the liver, by virtue
of which, such material being retained in the tissues, it may
secondarily induce retention of water and chlorides. Certain
puzzling clinical combinations, e.g., pronounced edema with but
little ascites, preascitic edema, and extreme ascites without
edema, occur, indeed, which argue against the purely mechanical
causation of edema of hepatic origin.
2. Edema of nervous origin. — Edema may be witnessed in
the presence of peripheral neuritis, of spinal affections such as
tabes and syringomyelia, of hemiplegia, of epilepsy, of paralysis
agitans, and of exophthalmic goiter. Generally, however, if
one carefully eliminates the edemas of cardiorenal origin which
may occur in the presence of these disorders, one finds that, as
a rule, the condition present is merely a dystrophic pseudo-
edema in which the characteristic sign of pitting on pressure
cannot be elicited.
3. Dystrophic edema. — This is the so-called "trophedema" of
Henry Meige: "The term trophedema, without further qualification,
may be applied generally to the dystrophic edemas of as yet un-
known cause, but seemingly of nervous origin.
"Chronic trophedema is characterized by a white, firm, pain-
less edema affecting one or more segments of one or several
limbs and persisting throughout life without notable prejudice
to the health of the individual. Sometimes the condition occurs
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830 SYMPTOMS,
singly. In other instances it is an inherited and family disorder.
It may also be congenital.
"One may describe as acute trophedema the so-called neuro-
pathic, circumscribed, angioneurotic, neurovascular, and inter-
mittent edemas, etc. — transitory edematous involvements some-
times accompanied by thermic manifestations, by disturbances
of sensation, by pain, by changed color of the skin, and fre-
quently also by trophic skin disturbances, eruptions, or ulcera-
tions. This group of conditions make up what is known as
Quincke's disease." (Henry Meige).
Special Localized Edema. — Lastly, certain local forms of
edema require mention, znc, edema of the lower extremities, edema
of the upper extremities, and edema of the face and lids.
(a) PulHn^ss of the face and lids.
1. Puffiness of the face and slight edema of the eyelids are
normal conditions upon awakening in some individuals. This is
due to an unusual relaxed, flaccid state of the tissues in these
persons. Such a quasi-normal edema is seen most frequently
in women and obese subjects.
2. Puffiness of the face is a well-known feature upon awakening
after alcoholic sprees.
3. It is likewise of frequent occurrence in pregnancy, and seems
to be one of the component features of the facies of pregnancy. As
in the preceding forms, however, it is well none the less to test
the urine for albumin.
4. It is met with in eczema, erysipelas, and sunburn,
5. BlepharO'Conjunctivitis is also attended with puffiness of the
eyelids.
6. Edema of the surrounding tissues in dental abscess is char-
acteristic.
7. Furuncles in the nostrils frequently induce a marked edema
of the infrapalpebral or even the palpebral portions of the face.
8. Tumors of the neck and mediastinum — aortic aneurysm,
posterior forms of pericarditis, Hodgkin's disease, Ludwig's angina,
and much more exceptionally, thrombosis of the superior vena cava,
cause edema of the face and neck, sometimes very widespread,
extending at times to the upper portion of the thorax and to
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EDEMA, 831
the root of the upper extremities. Of all these causes, aortic
aneurysm and pericarditis are the commonest
9. The doughy facies of myxedema should likewise be borne
in mind.
10. Certain druff intoxications (iodine, bromine, antipyrin) in-
duce congestion of the mucous membranes with facial edema.
11. Finally, mention may be made of angioneurotic edema or
Quincke's disease, characterized by the sudden appearance of
edema of the extremities, accompanied by edema of the mucous
membranes. Often this condition is restricted to the lids (idio-
pathic edema of the lids).
(b) Edema of the upper extremities. — ^This is met with:
1. In septic disorders involving the upper extremities and the
axilla.
2. In phlebitis, much less commonly, however, than iu the lower
limbs.
3. In gout, likewise much less commonly than in the lower limbs.
4. In cervical and mediastinal pressure:
(a) Lymphatic enlargements, cervical and mediastinal,
(fr) Malignant growths of the breast and mediastinum,
(c) Aortic aneurysm,
(rf) Hodgkin's disease (mediastinal lymphoblastema).
5. In malignant metastases in the mediastinum or axilla.
It should be noted that :
1. Renal edema is rare in the upper extremities, and is seen
only in a late stage, in the period of anasarca.
2. The same is true of edema of cardiac origin, which is only
exceptionally observed in recumbent subjects who have been lying
on one of their arms, causing venous obstruction and hindrance to
the return circulation. It should be carefully remembered that
cardiac edema is a dependent or ^'gravity" edema.
(c) Ekiema of the lower extremities. — In contrast with the
assertions made above concerning the upper extremities, the fol-
lowing kinds of edema nearly always appear first in the lower
limbs :
1. Edema of cardiac origin.
2. Edema of renal origin.
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832 SYMPTOMS.
As in the case of the upper extremities, edema is here met
with in the presence of:
1. Septic affections of the lower extremities, and particularly
of the feet.
2. Phlebitis, relatively common in this region, particularly as
puerperal phlebitis, phlegmasia alba dolens, post-operative phle-
bitis, etc.
Much commoner still is varicose edema, due to phlebosclerosis,
almost always absent on arising from recumbency, but reaching
its height before retiring, after having been in the vertical posture
all day.
3. Gout, the seat of election of which, as is well known, is in the
great toe.
4. Abdomino-pelvic pressure:
{a) Utero-ovarian tumors and cysts (cysts, fibromas, malignant
or inflammatory swellings).
(fr) Rectovesical malignant growths.
(c) Primary or secondary enlargements of pelvic and abdominal
lymphatics.
(rf) Various abdominal tumors and cysts (hydatid cysts, various
new growths).
5. Malignant metastases.
6. Lastly, the lower limbs are the seat of election of the so-
called ''cachectic" edemas, of varying and complex causation.
The pathogenesis of edema and its significance in pathologic
physiology have been the subject of very many investigations in
the course of the last ten or fifteen years. To present an outline
of this subject, however important it is and tempting the occasion,
does not come within the scope of this work. The reader desirous
of obtaining an idea of some of the later studies on the causation
of edema is referred to current medical periodicals.
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EMOASTRIC PAIN. [*^' X; CI&aT^]
The pit of the stomach or epigastrium, a region bounded
above by the xiphoid appendix and the lower costal margins,
lb.
Diaphragm.
m.
5.
Xiphoid
append.
Lesser
curvature.
Liver.
Pleura.
Gall-bladder.
Pylorus.
Liver. !oloii.
colon.
Ascend, colcm. *'
Cecum.
Sigmoid flex.
Fig. 612. — General topographic anatomy of the abdomen (Poirier).
and below by a line passing midway between the umbilicus and
the xiphoid, overlies, from before backward, the anterior aspect
of the liver, the anterior surface, upper border, and posterior
surface of the stomach, the pancreas, the celiac axis, and the
53 (833)
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834
SYMPTOMS.
solar plexus; still farther posteriorly is the lesser peritoneal
cavity, and lastly, the aorta, which can often be seen or felt
pulsating in the epigastrium in thin individuals with atonic
musculatures.
Pain is frequently referred to the epigastrium, either as a
Diaphragi
Live
Oastrohepadc li
Stomac
Traniver
mesocolo
Tranrverae colo
Spigelian lobe.
Pancreas.
Spinal column.
Duodenum.
Great omentui
Mesentery.
Small intestine
its mesentei
Bladd4
Symphysis pub
Rectum.
Seminal vesicle.
Prostate.
Tunica vaginal
TesUe
Fig. 613. — Sagittal section of the abdomen.
dull, heavy sensation, especially after meals as in many dyspep-
tics— or as an acute and almost lancinating or even a piercing
pain, coming on a few hours after or independently of the meals,
as in gastric ulcer, the gastralgic form of calculous attacks, or
the gastric crises of tabes — or brought on exclusively by pres-
sure or percussion, as in many instances of congestion of the
liver or gastric neuroses (hyperesthesia of the solar plexus).
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EPIGASTRIC PAIN. 835
Epigastric pain is generally an expression of some gastro-
hepatic disorder, such as gastrohepatic congestion, hyperchlor-
hydria and its attendant manifestations, gastric neurosis, ulcer
or cancer of the stomach, or cholelithiasis of the gastralgic
type.
Much more exceptionally it is an expression of disease of
some adjoining organ, e,g,, pancreatitis, pericarditis, or abdom-
inal aneurysm, or of disease of some remote structure, e.g.,
appendicitis.
Among the possible causes mention should also be made of
tabes dorsalis, with its frequently dramatic attacks of pain in
Fig. 614. — A, Surface projection of involved area in appendicitis; P,
of involved area in pancreatitis ; V, of involved area in cholecystitis.
the epigastrium (gastric crises), the pathogenesis of which is
still rather obscure, and to which the term abdominal angina
has been applied.
Hepatic Syndromes. — The pain of active or passive congestion
of the liver is generally latent, being elicited only by palpation or
percussion. It. is most constant in the epigastrium in these cases.
From the semeiologic standpoint, it is equivalent to congestive ten-
derness of the liver. Whenever it is met with, further investigation
to ascertain its origin is indicated.
1. Disorders of the biliary passages— cholelithiasis (hepatic colic,
sensitiveness of the gall-bladder, jaundice, and the evidences of
hype rchlorhyd ria ) .
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836 SYMPTOMS.
2. Disorders of the liver— <iyspeptic congestion due to excessive
intake of alcoholic beverages and meats, precirrhotic hyperemia,
abscesses, infectious jaundice, syphilis, or malaria.
3. Disorders of the heart in particular, passive congestion of
the liver with tenderness being one of the most patent and con-
stant signs of cardiac insufficiency (reduced function or actual
heart failure).
Gastric Syndromes. — Pain thus caused exhibits very different
features in two practically opposite conditions affecting the stomach,
zfis., the syndrome of hyperchlorhydria, and gastric neurosis with
ptosis and gastrointestinal atony. Indeed, the combinations of
gastric symptoms are so protean that almost anything may occur,
even an apparent coexistence of the two syndromes referred to.
Little space need be devoted to the well-known "hyperchlorhy-
dric syndrome" — pain oh gastric evacuation, "hunger pain" — the
main feature of which is a combination of tardy stomach pains,
sometimes quite severe and of the "burning," boring type, coming
on periodically several hours after meals, and generally allayed by
alkalies or bland foods, and a more or less pronounced hyperchlor-
hydria or even sometimes a gastroduodenal ulcer.
The pain in these cases had formerly been ascribed to irritation
of the sensory nerves of the stomach, when exposed by an ulcer,
by the unduly acid gastric contents. As with any other careful
clinical observation, the observed fact remains unimpeachable, and
its interpretation alone has been subject to revision. The finding
of the symptoms of "hyperchlorhydria" in persons with normal
gastric acidity, physiological experimentation, and x-ray observa-
tions tend to show that gastric hypertonicity, pylorospasm, and
exaggerated peristaltic movements play an important, if not pre-
dominant, role in the causation of this pain. That the oncoming
of the pain is delayed is because it appears particularly during the
period of evacuation of the stomach, consentaneously with especially
forcible contractions of the pylorus. There is thus likewise ex-
plained the observation of the syndrome referred to in many chronic
disorders of the intestine and biliary passages causing excessive
peristalsis in these structures. Examination of the very large ag-
gregate of clinical and experimental data available leads, at any rate,
to the conclusion that hypertonicity of the stomach and intestines
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EPIGASTRIC PAIN. 837
and gastric hyperacidity, generally in combination, are the fnain
factors of the syndrome of hyperchlorhydria.
These "theoretic" considerations have here been referred to at
some length because they afford important therapeutic indications:
Excessive peristalsis indicates administration of belladonna, and
hyperacidity, of alkalies — ^both often remarkably efficient measures.
These considerations are completely applicable to the diagnosis
and treatment of gastric ulcer. The s)rmptoms of hyperchlor-
hydria, x-ray examination, and systematic testing of the stools for
blood after the institution of a special diet are the main factors
leading to a diagnosis, an obvious, outward demonstration of which
may, however, in some cases be supplied in the form of actual hema-
temesis. In addition to the remedial measures already mentioned
a protective "dressing" of bismuth in the stomach should be applied
in these cases.
As for gastric neurosis with gastroptosis (dilatation of the
stomach), gastrointestinal atony, frequently hyperacidity, in short,
hyposthemc dyspepsia, the pain manifestations attending it are far
different. These are dull pains coming on immediately after inges-
tion of food, with marked hyperesthesia of the solar plexus (per-
manent induced epigastralgia), sensations of weight or puffing,
various local discomforts, vasomotor disturbances, etc. — ^all super-
imposed upon an asthenic and neuro- and psychopathic make-up
which is frequently characteristic. It should be borne in mind,
however, that occasionally, accidentally the pains may, in a few
of these cases, assume the type met with in the "syndrome of hy-
perchlorhydria ;" one of the surprises sometimes encountered in
fluoroscopy is the observation of such a ptotic and habitually atonic
stomach contracting with very great vigor, at the time of evacuation.
Observations of this sort are, in this connection at least, in favor
of the hyperperistaltic theory of the causation of pain in these
cases, the pain thus representing an actual "colic of the stomach.*'
The pain in cancer of the stomach is of very variable descrip-
tion, being sometimes almost nil, and only slightly elicited by palpa-
tion; at other times, a dull pain, with sensations of weight in the
epigastrium and distention in the same r^on; more rarely it pre-
sents the delayed and "boringf' attributes of the ulcer upon which
the cancer has been superimposed (degenerated ulcer). Thus, in
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838 SYMPTOMS,
these cases study of the pain may be misleading. The diagnosis
should be based especially on the finding of blood in the feces (on
a meat-free diet), the frequently pathognomonic results of fluoro-
scopic examination, the age of the patient, the degree of impair-
ment of ntttrition, and later on, the direct detection of a gastric
tumor (see Dyspepsia),
Cholelithiasis is frequently attended, as already pointed out,
with the syndrome of hyperchlorhydria, and differentiation from
duodenal ulcer and hypersthenic dyspepsia is frequently a dif-
ficult task. A positive diagnosis in some instances may be
reached only by careful examination for gall-bladder signs, such
as gall-bladder pain and tenderness, radiation of the pain to the
right shoulder, slight or* distinct jaundice, definite attacks of
hepatic colic, and a history of former infections (typhoid fever,
etc.).
All of the preceding conditions giving rise to epigastralgia
are very common. The following are much less common, or in-
deed, strictly speaking, are exceptional :
The epigastralgia of pericarditis presents absolutely no dis-
tinctive feature ; it is a dull, or even latent, pain, readily awakened
by pressure. When one has had the opportunity to see and
follow up cases of "already diagnosticated" pericarditis, the pain
will regularly be thought of ; in the opposite event, it will always
be overlooked. Dyspnea, cardiac acceleration, and sometimes
precordial pain will attract the observer's attention. Systematic
examination of the case, including fluoroscopy, will afford a
positive diagnosis.
The epigastric pain of pancreatic origin is met with under
two quite different clinical conditions:
1. In the chronic form. — This is often the pancreaftco-
biliary syndrome of Dieulafoy (former gallstone disease, obstruc-
tive jaundice, loss of weight, pain, and sometimes a pancreatic mass
in the right intercostoumbilical region). Yet, as Dieulafoy so cor-
rectly said, "even supposing that the maximum of pain is observed
at the pancreatic point, that is, a point 4 or 5 centimeters to the
right of, above, and laterally from the umbilicus (pancreaticochole-
dochian region), it is not always easy to find out whether the pain
is to be attributed to pancreatitis or to stones in the bile-duct"
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EPIGASTRIC PAIN, 839
Doubt may persist even after operation. Twenty-five years ago
the author had under observation, with the late Dr. Guinard, a case
of chronic obstructive jaundice with marked loss of weight in a
patient manifestly suffering from gall-stones; the operation showed
a large stone blocking the bile-duct, which was removed, and also
a scirrhous growth of the head of the pancreas. De visu, the diag-
nosis of cancer of the head of the pancreas was decided upon and
the prognosis corresponding to this condition issued. The patient
not only recovered, but **bloomed out" again, and lived fifteen years
longer. The condition present was an interstitial pancreatitis second-
ary to calculus in the bile-duct — s, condition of which little or
nothing was known at the time, and which Dieulafo/s work was
instnxmental in bringing to general notice.
2. Hyperacute epigastric pain, 7vith pancreatic operitoneal
hemorrhage. — ^Dieulafoy's account of the "pancreatic tragedy'
should be read over in this connection. "Terrific and generally fatal
symptoms suddenly develop at a time when little apprehension ex-
isted and in persons not exhibiting jaundice at the time. The
patient is seized with violent pain in the umbilical region, in the
epigastrium, and in the hypochondriac regions. The highly distress-
ing and excruciating pain is accompanied by vomiting, prostration,
and a tendency to syncope; there is general abdominal hyperes-
thesia, constipation is absolute, and there is not the least passage
of gas. In the presence of such a condition one thinks of an acute
peritonitis, an attack of poisoning of some sort, or perforation of
the stomach, duodenum, or gall-bladder ; one thinks of appendicitis,
or of intestinal obstniction, but none of these conditions exist, and
I have applied to the attack the term 'pancreatic tragedy' in order
to establish a clear distinction between it and all other conditions
that may resemble it. At the operation or the autopsy, indeed,
there is found, not a peritonitis, not a perforation of some organ,
not an appendicitis, not an intestinal obstruction, but the major
pathologic witnesses of the tragedy, vis,, the white foci (candle-
grease spots) of fat necrosis, with which are frequently associated
pancreaticoperitoneal hemorrhages — lesions consecutive to an at-
tack of c^ute pancreatitis, nearly always superimposed, in turn,
upon a chronic pancreatitis." The diagnosis, rarely correctly made,
is based, on the whole, upon the history of pancreaticobiliary trouble,
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840
SYMPTOMS.
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842 SYMPTOMS,
the **tragic" syndrome above described, and particularly upon
actual inspection of the lesions found upon laparotomy, which is
indicated whatever condition may be thought present.
Aneurysm of the abdominal aorta may be suspected — at least
at first — only in the presence of the following combination of
clinical indications: Pain in the epigastrium and diffuse, deep-
seated pulsations in the same region. Careful fluoroscopic ex-
amination with the patient in an oblique position can alone afford
a positive diagnosis.
Appendicitis, whether acute or chronic, may be attended with
epigastric pain and even nausea and vomiting — epiphenomena of a
syndrome of peritonitis or "peritonism" or hyperperistalsis, the fre-
quency of which has already been referred to. Only very excep-
tionally, however, will careful clinical examination not reveal the
right iliac fossa as the probable source of the disturbance. For
the required further discussion of these cases the reader is referred
to the section on Vomiting.
Concerning gastralgia in tabes the same may be said as of
epigastralgia in pericarditis, vis., whoever has seen and followed
one such case will always have the condition in mind^ while
whoever has not will never think of it. The onset is generally
sudden, with extremely severe pain in all respects suggesting
that of gastric ulcer or of hepatic colic ; with unusual obstinacy,
so that even morphine brings only partial relief ; with vomiting,
often uncontrollable ; the duration of pain a few hours to a few
days, and the cessation of pain sudden like the onset These
features will put the well-posted observer on the right track.
Furthermore, systematic examination of the patient (which
should never be omitted) will often discover a number of char-
acteristic evidences, vis., a history of syphilitic symptoms, loss
of knee-jerks, Argyll-Robertson pupil, impaired equilibration,
ataxia, etc. The attacks are often exactly similar as to onset,
course, and duration, and the patient, having in mind an earlier
diagnosis of his case, may even supply the diagnosis himself.
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EPISTAXIS. 1^ Naaalhemorrhage. J
Epistaxis may be defined as a hemorrhage in the nasal cavities.
This symptom, when present, is obvious, and cannot be
mistaken for any other unless, in posterior epi^t^is — which,
Fig. 615. — ^The artery of epistaxis. Terminal distribution of the
sphenopalatine artery. Upon raising the tip of the nose with the fore-
finger and inserting a speculum, the observer will notice in many per-
sons, at the lower anterior portion of the septum, a small group of
diverging arterial branches. If ulceration occurs at this point — usually
on account of insertion of the finger — copious hemorrhage from one
of these vessels will occur. This is the source of the majority of •
cases of epistaxis {Laurens),
however, is uncommon — the blood, unwittingly swallowed, is
later discharged by vomiting (suggesting hematemesis) or
passes out with the stools (suggesting melena). The mere
recollection of the possibility of these altogether exceptional
mistakes is sufficient completely to guard against their occur-
rence; in the event of doubt, rhinoscopic examination, advan-
tageous in any case, and often essential, will settle the question.
There are many possible causes of epistaxis,
(843)
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844 SYMPTOMS.
Locally, epistaxis may be of traumatic (blow on the nose) or
operative origin (the latter following, for example, removal of one
of the turbinates, etc.) ; further reference to these obvious causes
would be superfluous. In 90 per cent, of cases, according to G.
Laurens, epistaxis is due to a localized, varicose erosion of the
anterior inferior portion of the nasal septum. This is a clinical
feature to be carefully remembered, since all local treatment (caut-
ery, packing, pressure, etc.) is necessarily based on it.
General causes of epistaxis may be divided into 2 groups,
vis,, the mechanical or circulatory and the dyscrasic or hemic.
Like all other attempts at a simple, easily remembered classi-
fication, this division is in some respects questionable, most
causes of epistaxis acting in a *'mixed" manner, i,e,, both mechan-
ically (through low blood-pressure and reduced resistance of
the vascular walls) and dyscrasically (through hydremia, low-
ered viscosity, disturbances of coagulation of the blood, etc.), as in
chronic nephritis or arteriosclerosis. The division above made is
merely of didactic value — which is the essential point herein.
The mechanical causes comprise all factors resulting in con-
gestion of the nasal mucosa, which is an exceedingly vascular
and erectile tissue.
(a) Passive, venous congestion of the nasal mucosa, due to
increased venous blood pressure in the superior vena cava. Un-
der this heading belong mitral and tricuspid lesions with loss
of compensation, heart failure in general, and pressure upon the
veins of the neck or mediastinum; these are, on the whole,
relatively uncommon causes of epistaxis, which are readily de-
tected by virtue of the accompanying cyanosis, turgescence of
the veins, dyspnea, frequent and irregular heart action, and even
a cursory examination of the chest.
(&) Active, arterial h)rpcrcmia of the nasal mucosa, due to
high blood-pressure, is by far the most frequent cause of epistaxis.
All disorders attended with high blood-pressure, including
plethora, gout, and in a greater degree, arteriosclerosis, aortic insuffi-
ciency, and Bright's disease are, par excellence, conditions favoring
epistaxis of the recurrent type and sometimes of alarming extent.
In the same group are, the epistaxis of vicarious menstruation, those
of hemorrhoids and of the menopause, and in some degree, that
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EPISTAXIS, 845
of puberty, Epistaxis is the most frequent type of hemorrhage wit-
nessed in these conditions of high pressure with hemorrhagic tend-
encies, apparently because, most fortunately, the vessels of the nasal
mucous membrane constitute a vascular locus minoris resistentiae
or actual safety-valve affording, in the presence of dangerously high
blood-pressure, a "providential bleeding"' and a warning often of
marked service when its significance is duly appreciated by the
physician and patient It may, however, in a given person occur
in alternation with most varied types of hemorrhage, as in an arterio-
sclerotic patient with high blood-pressure, under the author's ob-
servation for over ten years, who developed every spring either
epistaxis, hemoptysis, or hemorrhoidal bleeding and was finally
rendered hemiplegic by cerebral hemorrhage. In all these cases sys-
tematic blood-pressure estimations will supply the diagnosis as well
as the prognosis, and bring out the various indications as to treat-
ment Systematic uranalysis, determination of the blood viscosity,
and also, of course, general clinical examination, are essential in
all instances.
The dyscrasic causes or blood changes, such as lowered coag-
ulability, hydremia, etc., very frequently co-operate with the pre-
ceding causes in the production of the severe forms of epistaxis.
As is well-known, certain blood disorders, including anemias
and leukemias, frequently tend toward hemorrhage production.
Cell counts, hemoglobin estimations, and the differential leucocytic
count are the main diagnostic factors in these cases.
Other disorders, vis,, the purpuras and hemophilic conditions
are as yet only rather imperfectly defined from the hematologic
standpoint. Marked delay in coagulation is always noted. These
states are frequently related to more or less obvious deficiencies of
the hepatic, renal, and polyglandular functions. Indeed, clinically,
the concept of inherited deficiency and the frequent, identical repe-
tition of the hemorrhagic manifestations will compel the practi-
tioner to make a provisional diagnosis of this nature — since these
are clinical cases of a complex and probably dissimilar nature.
Ever since remote ages there have been noted cases of epistaxis
symptomatic of z^arious liver conditions. As a matter of fact this
form of epistaxis is of very variable origin:
1. Dyscrasic infectious epistaxis in infectious "grave" icterus.
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846
SYMPTOMS,
2. Dyscrasic non-infectious epistaxis of hepatic secretory insuffi-
ciency.
3. Dyscrasic and mechanical epistaxis in cirrhosis, particularly
of the atrophic variety.
4. Mechanical epistaxis in congestion of the liver — either passive
congestion, as in increased venous pressure in the liver and cirrhosis
of cardiac origin, or active hyperemia, as in the increased arterial
blood-pressure of plethoric or gouty enlargement of the liver, etc.
Infections. — Lastly, many infections are either especially and
primarily producers of hemorrhage, or may occur in a hemorrhagic
form. This applies particularly to:
1. Typhoid fever, — Epistaxis is, as is well-known, frequently
a preliminary symptom in typhoid. In the hemorrhagic form, epis-
taxis may go hand in hand with hemorrhage from the bowel.
2. Eruptive fevers, particularly measles, chicken-pox, varioloid,
and scarlet fever.
3. "Rheumatism" and "infectious pseudo-rheumatism" in some
of their "purpuric" forms.
EPISTAXIS.
1. Traumatism . .
2. Operation —
3. Inflammation
(a) Passive venous
congestion.
(b) Active hyptt-
emia (far more
common).
(c) Dyscrasias.
Local Causes.
(Obvious).
(Obvious).
(Erosion of the anterior inferior portion of the
septum; rhinoscopic examination).
General Causes.
1. Heart disease with loss of compensation, im-
paired heart action (cyanosis, auscultatory
evidences, and often low blood-pressure).
2. Pressure in the region of the superior vena
cava, as by a tumor of the neck or medias-
tinum (cyanosis, sometimes edema, collateral
circulation, and signs of tumor).
1. All disorders attended with hipjh blood-
pressure: Plethora, gout, arteriosclerosis,
B right's disease.
2. Certain physiologic states: Menopause and
puberty.
3. Vicarious menstruation or hemorrhoidal
flux.
1. Anemias, leukemias, purpura, and hemo-
philic states.
2. Liver disturbances: Infectious jaundice, cir-
rhosis, or hepatic congestion.
3. Infections promoting hemorrhage: Typhoid
fever, the eruptive fevers, infectious rheuma-
tism, etc.
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EXANTHEMATA.
if 6>, out of; ivdog^ flower; i^dvOefia^
from i^dvdetVy to bloom. A skin
eruption.
Skin eruptions are of such frequent occurrence that it has
seemed absolutely necessary to devote a semeiologic section to
a brief presentation of the various types of eruption. These
various types, however, by virtue of their actual frequency and
number, do not lend themselves well to condensation into a
short, yet comprehensive article. After prolonged hesitation the
author decided to employ the following plan :
1. To give a didactic account of certain elementary facts in
dermatology, based on the writings of an authority on the sub-
j ect — Sabouraud.
2. To recall, in a short synopsis, the main clinical features
of the great chronic infectious skin disorder of temperate
climates, vis., syphilis.
3. To recall, in condensed, tabular form, the more essential facts
concerning the eruptive fevers.
4. To request the reader to refer to special works on derma-
tology for further details.
L ELEMENTARY AND ESSENTIAL FACTS IN
DERMATOLOGY.
(After Sabouraud)*.
There are some eruptive diseases that involve the entire surface
of the body or the greater portion of it. Such are the exanthematic
{eruptive) fevers.
On the other hand, there are skin disorders which, without ever
extending to involve the entire cutaneous surface, have no definite
seat of election and may be noted in any portion of the body. Such
are the epitheliomas.
* See Sabouraud's Dermatologie topographique, p. 581.
(847)
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848
SYMPTOMS.
EXANTHEMATA.
Primary Charactkb-
Dermatolooic
o ■• K V I n L.na T
ISTIC FEATDRB.
Appellation.
DCiHBIVwvU X.
1. Some skin disorders
Simple squam-
Ichthyosis (congenital).
are characterized
ous skin af-
Desquamation in febrile states
solely by dry scales
fections.
and eruptive fevers (scarlet
and exfoliation of the
fever).
Pityriasis in various forms:
homy layer, without
redness or oozing of
fluid.
— simplex.
— (tinea) versicolor (mycotic).
— rosea of Gibert.
— rubra pilaris.
Dry eczema.
Psoriasis.
2. Flat elevations, with
Urticarial af-
Nettle rash.
itching, exactly re-
fections.
Dermographism (vasomotor
sembling nettle rash.
neurosis).
Toxic urticarias.
Food poisoning.
Drug poisoning.
Idiopathic urticarias of un-
known cause.
3. Parasitic lesions, les-
Parasitic skin
See Pruritus.
ions due to scratching,
affections.
Scabies. Pediculosis. Fleas.
attended with itching
Bedbugs. Mosquitoes.
and easily confused
with prurigo.
4. Papules, widi itching,
Papular and
Papular syphilides.
smaH dry, elevated,
lichenoid skin
Lichen planus.
flat, discrete, circu-
affections.
Papulonecrotic tuberculides.
lar, tablet-like lesions
Prurigo (with
Prurigo in various forms:
or lesions grouped in
itching, pap-
symptomatic;
thick, cross-lined
ules and Uch-
senile;
patches.
enification).
diathetic, and
regional or circumscribed.
5. Vesicles, small, clear
Vesicular and
Eczema (initial eczematous ves-
collections of fluid
exudative skin
icle, patch of eczema, with
slightly raising the
affections.
itching, oozing, crust forma-
superficial epidermis;
like "small pearls"
tion, desiccation, and licheni-
fication).
embedded in the epi-
Miliaria sudoralis.
dermal layer. When
Chicken-pox.
broken, the vesicles
Vesicular urticaria.
discharge fluid.
Diffuse impetigo.
Pemphigus foliaceus.
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EXANTHEMATA.
EXANTHEMATA (conHnued).
849
Pbimabt character-
Dermatologic
Semeioloot.
istic FBATUBE.
Appellation.
6. Pustules, or puru-
Pustular and
Staphylococcic pustules.
lent vesicles. Rup-
ulcerative
Furuncle. Carbuncle.
tured pustules be-
skin affec-
Acne pustules.
come more or less
tions.
Phlyctenosis strcptogenes.
superficial ulcera-
Ecthyma.
tions.
Small-pox. Varioloid. Chic-
ken-pox.
Bullous and
Urticaria bullosa.
icles, "balloon-like"
pemphigoid
Erythema multiforme bullosa.
and constituting the
eruptions.
Bullous drug eruptions.
so-called pemphigoid
Acute infectious pemphigus.
Various forms of pemphigus
eruptions.
(vegetating, foliaceous,
traumatic, or hysterical).
Painful, multiform dermatitis
(Duhring, Brocq).
8. Purpura, consisting
Purpura and
Hemophilia.
of blood macules.
purpuric
Rheumatic purpura (peliosis
ecchymotic spots, or
eruptions.
rheumatica).
extravasations into
Werlhoff's disease.
the skin which pres-
Acute febrile purpura.
sure with the finger
Cachectic purpura.
cannot dissipate.
Toxic purpura.
Purpuric eruptions in eruptive
fevers (exanthemata with pur-
pura).
9. Erjrthematous mac-
Measles and
Measles.
ules, hyperemic spots.
rubeoliform
Rubella.
temporarily dissipated
eruptions.
Febrile roseolae (typhoid
by pressure with the
fever, small-pox, puerperal
finger.
fever, etc.).
Syphilitic roseolae.
Drug roseolae.
Roseola due to serum disease.
10. Diffuse erythema,
Scaxiet fever
Scarlet fever.
, scarlet red, more or
and scarla-
Scarlatinoid rash in small-pox.
less extensively dis-
tinoid erup-
Recurrent exfoliative scarla-
tributed.
tions.
tinoid erythema.
Toxic scarlatinoid erythemas.
Mercurial rash.
11. Erythrodermias con-
Enrsipelas and
Febrile erysipelas.
sisting mainly of ery-
erythroder-
Exfoliative erythrodermias.
thematous lesions
1. Generalized, afebrile, and
with edematous infil-
primary.
tration of the dermal
2. Secondary (traumatic.
layer.
mercurial, and arsenical
eruptions).
54
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850
SYMPTOMS,
EXANTHEMATA (continued).
PRIMARY CHARACTBR.
I8TIC PBATURB.
DERMATOLOOIC
Appellation.
Sbmeioloqt.
12. Dyschromia, melan-
odermia, vitiligo,
scleroderma, and
morphea.
Dyschromia.
Sderodermm.
Symptomatic dyschromias, as
in albinism, pigmented nevi,
lentigo, ephelides*, xero-
derma pigmentosum, and
neurofibromatosis.
Nervous dyschromias, as in
Addison's disease, tubercu-
lous melanodermia, pig-
mented syphilis, leprous dis-
colorations, and vitiligo.
Hematic dyschromias, as in
lymphadenosis, leukemias,
mycosis fungoides, malarial
cachexia, and bronzed dia-
betes.
Toxic dyschromias, as in pois-
oning by arsenic, antipyrin,
silver, or lead.
Dyschromias of local causa-
tion, as by heat, counter-
irritation, or pediculosis.
Scleroderma.
13. Tumors of the skin;
cutaneous neo-
plasms.
Skin tumors.
Retention cysts and the like
benign tumors: Milium, se-
baceous cysts, wens, hygro-
mas, etc.
Small, transmissible benign
tumors: Molluscum contag-
iosum, warts, and papillomas.
Parasitic tumors : Blastomy-
cosis, bothriomycosis, and
keloids.
Circumscribed congenital skin
deformities or nevi: Pig-
mented nevi, vascular nevi,
and verrucose or fibroma-
tous lymphangiomas.
Dermatomyomas.
Dermoid cysts.
Fibroraas. ^
Lipomas.
Xanthomas.
Sarcomas.
Mycosis fungoides, cutaneous
lymphadenosis; papillary or
pearl-like epitheliomas, rod-
ent ulcer, etc.
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EXANTHEMATA. 851
Again, there are some which have elective locaHzations, yet
spread over the entire body surface and therefore require a gen-
eral description. Such is scabies.
These disorders are in themselves very many, and necessitate
a classification for the practitioner. Such a classification should
be planned on lines sufficiently simple so that the physician will be
able, without any previous dermatologic study, to ascertain easily
the dermatologic type to which any disorder under observation
belongs.
Condensed in the tables presented on the succeeding pages
will be found:
The main symptomatic features and course of syphilis.
The main symptomatic features and course of the eruptive
fevers.
4c 4t ♦
The following statistical matter, collected by Halperin at
Camp Lee, Petersburg, Va., gives a good idea of the ^proxi-
mate and respective frequency of the various skin disorders in
young recruits upon their arrival in camp. Among 8000 sub-
jects examined during the week following their incorporation
Halperin found:
Skin Conditions in 8000 Recruits.
Syphilis (open lesions) 125 Brought forward 443
Tinea versicolor 109 Sebaceous cysts 3
Pustular acne 75 Ringworm 3
Psoriasis 40 Erythrasma 2
Scabies 20 Herpes zoster 2
Seborrheic eczema 18 Varicose ulcers 2
Chronic eczema 16 Purpura 2
Folliculitis 11 Pediculosis pubis 3
Alopecia areata 8 Pediculosis Corporis 1
Ichthyosis 8 Parapsoriasis 1
Urticaria 5 Lupus vulgaris 1
Erythema multiforme 4 Acne rosacea 1 .
Lipoma 4 Keloid acne 1
443 "465
Again, the war resulted in a renaissance of artificial or simu-
lated eruptions. Such eruptions may be of an eczematoid aspect,
or pustular, or pemphigoid, or may suggest mucous patches,
sloughs, etc.
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Explanation of the Annexed Plate.
Tjrpical Manifestations of Ssrphilb in its Several Stages.
1. A primary chancre of the vulva, fully developed. The appearance is
quite characteristic. If it be further recollected that the chancre is indurated
and accompanied by multiple, painless, inguinal glandular enlargement, with
the central node particularly enlarged, an accurate mental conception of the
ordinary syphilitic chancre and its accompaniments will be had. (Photo by
Dr. Ravaut).
2. A florid roseola of the "peach-bloom" variety, distinguished from the
non-specific "roseolai^* eruptions only by the history of a chancre and the
subsequent secondary manifestations on the skin and mucous membranes,
together with the Wassermann reaction, which is always positive in this
stage. (Photo by Dr. Ravaut).
3. Hypertrophied mucous patches of the vulva, which, when so typical
as those presented, could hardly be confounded with any other condition
involving the genitals. One should get accustomed to looking for smaller
and more discrete patches than these. (Photo by Dr. Brocq).
4. Ulcerated syphilomas of the nose, which increasingly accurate diagnosis
and energetic treatment are rendering daily more uncommon. Note the regu-
lar, "cyclic" appearance of the ulcers, with their indurated margins and
necrotic bases; these lesions are attended with surprisingly little pain. The
most striking advantage of arsphenamine and mixed (iodide and mercury)
treatments is that they will heal and "dissipate" such ulcers as these within
a few days. (Photo by Dr. Brocq).
The author's thanks are due to Drs. P. Teissier, Brocq, and Ravaut, who
kindly consented to select from among their valuable collections some excel-
lent autochrome reproductions of skin conditions, thus enabling him to place
before his readers a few of the types of cutaneous disturbance most com-
monly met with.
(852)
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Ill
IV
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EXANTHEMATA. 853
The diagnosis in these cases of malingering is always diffi-
cult, the patient obstinately refusing to confess his own re-
sponsibility in the matter. As in other forms of malingering, the
suspicious appearance of the patient, the unusual sort of erup-
tion, the lack of harmony between different symptoms and signs,,
the durajtion of the disease and its unaccountable recurrence, in
short, the incoordinate or, on the other hand, repeatedly co-
ordinate course of the disorder will eventually lead to a pre-
sumption and probable diagnosis of the condition.
On succeeding pages will be found a few chromo-typographic
typical illustrations of the chief infectious eruptive disorders.
These will assist in making one familiar with the characteristic
eruptions of rubella, measles, chicken-pox, small-pox, and scarlet
fever, and ipso facto with the typical features of vesicular (chicken-
pox), morbilliform (rubella and measles), scarlatinoid (scarlet
fever), and pustular (small-pox) skin disorders.
GENERAL REMARKS CONCERNING THE DIAG-
NOSIS OF SYPHILIS.
Syphilis, tuberculosis, and alcoholism are unquestionably
three of the greatest scourges with which the human race is
compelled to contend. No more imperative task devolves upon
the practitioner than that of detecting them in whatever form
they may appear.
As for syphilis in particular, such endeavor is all the more
necessary in that: 1. The earlier the diagnosis is made, the
greater the chances of radically effective treatment. 2. We are
possessed of antisyphilitic remedies which are extremely power-
ful if administered early and with due energy and wisdom.
The succeeding tables, together with the annexed illustra-
tions, will give a general idea of the clinical manifestations of
syphilis and, properly comprehended and availed of, will greatly
facilitate its diagnosis. Let it be particularly borne in mind that
the skin and mucous membrane eruptions of syphilis are merely
the outward manifestations of a deep-seated septicemia; that
the entire system is impregnated with the syphilitic virus, and
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854 SYMPTOMS.
that especially the cardiovascular and nervous systems are
always, or nearly always, more or less attacked by the infection.
Hence, let it not be thought that a syphilitic has been cured
simply because he has been freed of all manifestations of the
disease aflfecting the skin and mucous membranes; and let it
not be asserted that an individual never had syphilis before
because he has retained no obvious stigmata of the disease.
The diagnosis of syphilis, to-day as in the past, remains, as
was happily stated by Foumier, one of a series of morbid states
based on a definite diagnostic triad, ids., the history, the existing
signs of syphilis (in the skin, mucous membranes, and internal
organs), and a practically specific serum test (the Wassermann
reaction). This statement must be adhered to with precision,
judicious consideration, and common sense, if the practitioner
is to avoid making one of two almost equally fearsome mistakes,
vis., either of overlooking syphilitic infection which is still a
source of danger, or of burdening an individual free of syphilis
with an obsessive and depressing idea that he is syphilitic. Few
problems in diagnosis bring so actively into play the moral
responsibility of the practitioner.
The three classic laws relating to congenital syphilis may
here be recalled:
Law of Colics (1837) : A child born syphilitic of a syphilitic
father generally does not infect the mother if she shows no signs
of the disease, and she may nurse it without risk. To this we
may add, with Carle (of Lyons) : But she should be placed un-
der treatment at once, as she harbors specific infection.
Law of Profeta (1865) : The healthy child of a syphilitic
mother cannot contract syphilis during lactation nor through any
form of contact. To this we may add, with Carle: But the
child should be kept under observation, and even given treatment
if indicated, as he is often syphilitic himself. Most cases of late
inherited syphilis are merely exhibiting delayed symptoms of an
unrecognized congenital syphilitic infection.
Law of conceptional syphilis (Diday; Fournier) : A syphi-
litic fetus in utero may infect its mother through the placental
vessels, with resulting appearance of secondary symptoms in the
pregnant mother without any primary stage.
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EXANTHEMATA.
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SYMPTOMS.
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Explanation op the Adjoining Plate.
The commoner types of infectious exanthemata.
1. Chicken-pox (varicella), the type of the vesicular exanthemata.
2. Small-pox (variola), the type of the pustular exanthemata, illus-
trating clearly the essential eruptive lesion (the pustule).
3. Scarlet fever (scarlatina), the type of the scarlatinoid exanthemata,
affording a good illustration of the maximal degree of eruption at the natural
skin folds.
4. Rubella (Grerman measles), a rare, seasonal, epidemic, contagious
disorder characterized ''by a general glandular enlargement, itching, and
a rash" (Sabouraud).
5. Measles (rubeola), the type of the "morbilliform" rashes.
6. Florid measles, almost purpuric in appearance, constituting, from
the eruptive standpoint alone, a manifest transitional form between the
morbilliform rash (hyperemic) and the purpuric eruption (hemorrhagic).
The author is indebted to Prof. Pierre Teissier for the six original
pictures comprised in this plate.
(864)
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[6^, out ofy pectus, chest; expulsmi]
of ahnormal secretions from the J
respiratory tract
Expectoration is, together with cough, the commonest mani-
festation of affections of the respiratory tract. While sometimes
devoid of any great diagnostic importance, under certain other cir-
cumstances it assumes an exceedingly characteristic significance,
as in hemoptysis, putrid sputum, sputum containing false membrane,
etc. It may even be practically pathognomonic, as in the case of
"rusty sputum."
Macroscopic examination of the sputum is very often sufficient,
when taken in conjunction with the other clinical evidences, to
indicate the correct diagnosis.
Microscopic, cytologic examination yields useful information,
but is seldom indispensable.
Microscopic, bacteriologic examination, including particularly a
search for the tubercle bacillus, is, on the other hand, ordinarily a
very necessary adjunct to the clinical examination of the patient.
Presence of the tubercle bacillus in the sputum is an indication of
an already advanced tuberculous infection of the lung, and all the
physician's endeavors and procedures (stethoscopic, fluoroscopic,
hematic, etc.) should aim toward the making of a much earlier
diagnosis. None the less, the sputum should be examined for
tubercle bacilli almost routinely, even in many instances of ordinary
acute bronchitis, and in all cases of chronic bronchitis.
The tables hereinafter presented will show in a condensed form
the various possible types of expectoration, their macroscopic and
microscopic features, and their semeiologic value.
Mention should be made of a very simple chemical method of
examining the sputum (the albumin test), the exact semeiologic
significance of which has not as yet been definitely ascertained
(see page 196).
55 (865)
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866 SYMPTOMS.
Lastly, reference must be made to a peculiar affection known
as Castellani's hemorrhagic bronchospirochetosis, apparently car-
ried into France by Asiatic laborers and soldiers, and studied anew
Spiroch<£ta hrofi"
chialis.
Red corpuscle.
Mononuclear cell.
Polymorphonu-
clear leucocyte.
Pharyngeal cell.
Lung cell.
Heart cell.
Various micro-
organisms.
Fig. 626. — Smear of sputum in "hemorrhagic bronchitis."
Immers. object. Mb Stiassnie, ocul. 1. Fresh specimen (yiolle),
during the war by Violle, Dalimier and others (Presse medicale,
July 5, 1917; July 18, 1918, and Mar. 10, 1919). The condition
Fig. 627. — ^Various forms of the Spirochata bronchialis,
Immers. object %5 Stiassnie, ocul. L Stained by the Fontana-
Tribondeau method {Violle) .
generally consists of a relatively mild bronchitis but one which is
accompanied by bloody sputum containing innumerable spirochetal
organisms. The period of incubation is short (one to two days) ;
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EXPECTORATION. 875
soon the patient begins to complain of slight pain in the tracheo-
bronchial region, is seized with harsh, annoying cough — almost
exclusively at night, and expectorates a certain amount of mucus
and blood. The sputum presents a characteristic appearance, being
homogeneous, rose-colored, and comparable to currant jelly; it is
copious and soon becomes mucopurulent and greenish. After a
few days' intermission a fresh exacerbation occurs with elimination
of the same kind of sputum. The latter contains enormous numbers
of the Spiroch(£ta bronchialis, which are characteristically variable
in their morphologic features. This germ is met with only in the
discharge from the lungs.
Where the possibility of this disorder has not been kept in mind
and bacteriologic examination of the sputum has been omitted, a
mistaken diagnosis of tuberculosis is almost sure to be made.
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EYES, DISORDERS OF THE.
EXAMINATION AND SYMPTOMATOLOGY OF
THE EYES.
By a. Terson, M.D.
In his daily practice the non-specialized physician will neces-
sarily be compelled, sooner or later, to see, first and alone, diseased
eyes and cases of poor vision.
The occasions of this sort vary.i
Fig. 644. — Lid elevator.
Sometimes it is an emergency, medical or surgical, because of
traumatism, relating to the eye or the rest of the body (with secon-
dary visual disturbance), or because of a rapidly progressive spon-
taneous disorder (suppurative conjunctivitis, corneal ulcer, glau-
Fig. 645.— Terson's eye speculum (blepharostat).
coma, detachment of the retina, etc.), which compels him to make
a provisional diagnosis and institute provisional treatment — without
postponing too long a special, thorough consultation, at which
the necessary accurate conclusions may be reached.
Occasionally some eye complication will develop in the
course of another disease which is already under treatment.
1 For further details the reader is referred to Terson's "Ophtalmologie
du medecin praiicicn," 2d Ed., Masson et Cie., 1921.
(876)
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EYES, DISORDERS OF THE. 877
Finally, the physician will often be called upon to state ''what he
thinks" of some eye condition or other before the services of an
ophthalmologist are sought
It will therefore not be without utility here to devote a few
pages to describing for the practitioner a line of conduct to be fol-
lowed by him when confronted with a manifest lesion of the eye
Fig. 646. — Ophthalmoscopic mirror.
and its adnexa, or with some visual disturbance unattended with
any apparent lesion. Furthermore, examination of the eyes is
sometimes of assistance in the rendering of a diagnosis and a
prognosis as to zision, and even as to life, in the presence of a
general disease.
In any event, after the first visit, or even after a mere conver-
Fig. 647.— Ophthalmoscopic lens. Fig. 648. — Disc with stenopeic
opening.
sation, the physician must be able to judge in due time whether he
should seek the help of a specialist. Putting himself in the patient's
place, he will have to make up his mind whether he can conscien-
tiously continue to treat thd patient alone in a satisfactory manner,
"A good physician," said La Bruyere, "is one who has specific
remedies, or who, if he has none, allows others who have them to
treat his patient." It seems doubtful if any better fundamental
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878 SYMPTOMS.
rule of professional behavior could be found, even in text-books on
medicine.
The practitioner will, of course, undertake only a brief, ex-
oscopic examination, covering mainly that which is visible to
the unaided eye. Examination of the eye-grounds, endoscopy of
the countless "hidden" disorders of the inner membranes of the
eye, and a host of other procedures of mensuration and func-
tional determination are not within his province and can be
learned only by prolonged training in the living human subject.
Among the elementary instruments in the following list are,
however, to be found included an ophthalmoscope and its lens,
Fig. 649.— Electric pocket-lamp with speculum*
the mirror being used solely to obtain pupillary reflection,
without any attempt to examine the posterior segment of the
eyeball.
Minimum Instrumental Requirements. — ^Two lid elevators
(Fig. 644) ; one blepharostat (Fig. 645) ; a simple ophthalmo-
scope, with lens (Figs. 646 and 647) ; a decimal test chart (Fig.
650) for the purpose of quickly distinguishing normal from de-
fective vision; three concave lenses of — 1, — 2, and — 3 diopters,
respectively; three convex lenses, of +1, +2, and +3 diopters,
and a disc with central stenopeic opening (Fig. 648) (for which
a visiting card with a hole put through it may be substituted).
An electric pocket lamp is always serviceable. When com-
bined (Fig. 649) with an ear speculum (A. Terson), it supplies
a sharp beam of light for pupillary examination. It may also be
used in diaphanoscopy.
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EYES, DISORDERS OF THE.
879
Obviously, it would be advantageous for the practitioner to
measure the field of vision and record it on. special sheets, and like-
wise, to probe the lacrymal passages, etc. Much experience with
these procedures is required, however, if they are to yield conclu-
sive results and be carried out without serious mishaps (injections
and catheterization).
E B
PAT
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Fig. 650. — Armaignac's test chart, with a special chart for illiterates and
the clock-dial chart for the detection of astigmatism.
One should have on hand ampoules of 2 per cent, and 1 per
cent, solutions of cocaine hydrochloride ; of 1 : 1000 adrenalin solu-
tion ; of 1 per cent, pilocarpine nitrate solution, and of 0.5 per cent,
atropine sulphate solution. Such ampoules, which do not deteriorate
and are convenient for carrying about, are frequently just as use-
ful for diagnostic purposes as for the prompt institution of
treatment.
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880 SYMPTOMS.
I. EXAMINATION OF THE EYE AND ITS
ADNEXA.
Even if it is only superficial, an ophthalmologic examination
should be carried out patiently and systematically if any conclusion
is to be reached from it. Examinationr from a point some distance
from the eye is insufficient. Countless foreign bodies in the con-
junctiva and even on the cornea, pupils occluded because of iritis,
and cases of chronic glaucoma, granulations, dacryocystitis (even
purulent) have been overlooked, sometimes for months, because the
examiner failed to get close enough to the eye, used neither a lens
nor a lamp, and neglected to ez^ert the eyelids and to make a direct'
examination of the eye or the lacrymal sac. And yet innumerable
eye washes, useless or actually prejudicial, have been prescribed
during these wasted periods.
The observer must see the tissues properly with the necessary
lens and illumination ; he must also adopt means for examining by
direct contact the eyeball, the lids, the lacrymal sac, and the region
of the orbit, and must check up the functions of both eyes, whether
the patient is seen at his home or in the office. Mere impressions
and suppositions are not sufficient; the physician must be actually
certain of anything that conditions permit him to be certain of.
In the patient's home, he should have with him the few articles
already mentioned for the clinical examination (including a folding
pocket test chart, mounted on muslin). Two alternative conditions
may present themselves : Either the patient is unable to get out of
bed or he is able to sit on a chair.
If the patient is in bed, the observer should try to have him sit
up, and should himself sit on the edge of the bed or on a chair drawn
close to it. If the patient cannot be moved at all, lateral illumination
of the eyes can always be obtained by having some one hold a lamp
for the purpose. If the patient is sitting in a chair, opposite the
physician's, he should be examined first in daylight and then with
artificial illumination. The daylight should never stream directly
into the patient's eyes, but should reach them from the side.
In the physician's office, which can be turned into a dark room
at the appropriate time by means of shades, the test chart should
be hung at a distance of 5 meters from the chair on which the pa-
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EYES, DISORDERS OF THE, 881
tient sits, with his back turned toward the light. The source of
artificial light may be a common lamp, a gas burner (not an incan-
descent mantle), or a frosted electric bulb. Candle light is gen-
erally quite inadequate.
ELEMENTARY OFFICE EXAMINATION OF THE EYE.
PreUminary Verbal Examination. — After having rapidly
made note of the general deportment, position of the head
(photophobia), and facies of the patient, the physician inquires
of him or of his associates (if an infant or child) what caused
them to seek medical advice — e.g., impairment of vision, ocular
or periocular pain, annoying secretions, a structural defect, etc.
Care should be taken to bri^g out how long the morbid con-
dition of one or of both eyes has been present ; what the patient
is still capable of in the way of near and distant vision ; whether
the eyes water and the lids are stuck together in the morning on
awakening; whether the pain is constant, intermittent, and spon-
taneous or induced by certain activities or labors ; whether the
morbid condition began suddenly, rapidly or ran a slow course ;
whether both eyes began to be affected at the same time,, and
lastly, whether the disorder is ascribed to some definite cause,
local or general and old or recent.
The above verbal examination, brief but concise, should be fol-
lowed by the local examination, which is concluded, in turn, by a
supplementary verbal inquiry dealing, in addition to any points that
may have been overlooked or suggested by the local examination
itself, with the present and past medical history and the family
history, the latter extending two generations back. The last step
consists, where indicated, of a complete examination of the patient,
including a review of his general health, his habits as regards
hygiene, and his mode of life and' occupation.
Local Examination. — The physician first washes his hands
thoroughly with soap — in full view of the patient — and then be-
gins with the direct examination, which comprises, as in the
case of any other structure, two objective procedures, exoscopy
and endoscopy, and thereafter a third, no less indispensable pro-
se
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882 SYMPTOMS.
cedure, vis,, examination of the functions of the eye and its
adnexa.
The external examination (exoscopy) should be made, first in
daylight, then by artificial light. For the specialist, the latter
method is frequently sufficient.
Fig. 651. — Examining a child.
The older children and adults should be seated in front of the
physician; small children and unruly patients in general should be
placed with the head low and the extremities held by other per-
sons (Fig. 651).
Fig. 652. — Bent hairpin which may be substituted for the lid
elevator in an emergency.
In examining the cornea and pupil — points of major importance
in the external examination — no direct contact with the eyelids is
required in docile patients and where the eyes give little or no pain.
In the case of painful and watery eyes, the lids should be carefully
dried with absorbent cotton, the observer's index fingers covered
with a thin layer of cotton, and these fingers, slightly bent, then ap-
plied at the ciliary margin. If the fingers are placed farther in,
the lids come together and prevent inspection of the cornea.
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In cases where the fingers do not suffice, lid elevators (Fig. 644)
or the adjustable blepharostat (Fig. 645) should be used. A hair
pin bent over at the curved end (Fig. 652) may, with due care, be
availed of where no other instrument is at hand.
In rare instances, instillation of a 1 per cent, solution of cocaine
hydrochloride (stronger solutions are useless except under certain
special conditions) five minutes before the examination is required.
The specialist also uses adrenalin under certain definite circum-
stances. The examination of the eye, one region after the other, is
then promptly proceeded with.
Eyelids. — The size and shape of the palpebral fissures of the
two sides should be compared, the patient opening and closing the
Fig. 653. — Inspection of the inner Fig. 654. — Seizure and eversion of
surface of the lower lid. the upper lid (1st step).
eyes. Altered direction of the lashes should be looked for with a
hand lens.
The lids are palpated for nodular masses, which may or may
not be tender.
The lids should be everted in any disorder causing pain. The
lower lid is merely pulled well down, the patient being meanwhile
asked to look strongly upward (Fig. 653).
Turning the upper lid requires more dexterity. It must be
turned without causing pain and ivithout exerting pressure on the
eye.
It is absolutely essential that the patient should look down.
He should be instructed to look at his knees. The lashes are next
seized between the thumb and forefinger of the left hand (Fig. 654) ;
the tip of the forefinger of the right hand then tilts back the tarsus
and holds the lid in the everted position (Fig. 655).
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SYMPTOMS,
If the physician's fingers are( not small enough for the purpose,
the forefinger may be replaced by a probe, a grooved director, a
bodkin, or some other thin, smooth object (Fig. 656). If eyelashes
are few or wanting, the margin of the lid itself is pinched up.
It is very necessary that the patient should continue to look
STEADILY downward during all these manq>ulations.
When performed gently and methodically, such an instantaneous
turning back of the lids causes no pain in a docile patient who does
not insist upon looking upward, which hinders the procedure.
It is quite useless to attempt to turn the lid with one hand, be-
tween two fingers; the procedure already described is preferable
and less unpleasant to the patient.
Fig. 655. — Fixation of the everted lid
(2d step).
Fig. 656. — Eversion of the lid with
the aid of a probe.
In some cases it may be necessary to investigate, in addition, the
upper cul-de-sac, which forms a deep pocket beneath the lid that
has already been turned back.
Among several procedures available for the purpose, the fol-
lowing are the most effective :
The first consists, after having turned the lid back, in introduc-
ing the elevator into the cutaneous recess of the lid, which is thus
drawn forward, allowing the observer to glance into the cul-de-sac
(Fig. 657). The second, or thorough, procedure, which exposes
the entire cul-de-sac, consists, after instillation of cocaine followed
by subcutaneous injection of the local anesthetic and a ten minutes'
wait, in having the patient lie down and seizing the lid horizontally
with forceps and rolling it about the latter (Fig. 658). With this
procedure, no foreign body, tumor, granulations, etc., may be over-
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EYES, DISORDERS OF THE.
885
looked, as may, on the other hand, be the case if one merely turns
the lid or passes a smooth curet blindly into the cul-de-sac, as text-
books invariably recommend.
Fig. 657. — Outward traction of the already everted upper lid with an
elevator inserted into the fold of skin for the purpose of inspecting the
upper conjunctival cul-de-sac.
Lacrymal Duct. — The physician should ascertain whether the
lower lacrymal punctum is not everted and therefore useless; he
should make firm pressure on the lacrymal sac to see if any secre-
Fig. 658.— Rolling the lid about dress- Fig. 659. — Complete eversion of the
ing forceps (1st step). upper cul-de-sac (2d step).
tion will exude from it (Fig. 660). The procedure of making sure
of the permeability by injection into the lacrymal passages and
catheterization with an olive-tipped probe belongs to the field of the
eye specialist. One may, in any case, instil a colored solution such
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886
SYMPTOMS,
as argyrol or coUargol and have the patient blow his nose fifteen
minutes later to see if the solution has passed into the nasal cavity,
but this gives no information as to the degree and number of the
stenoses that may exist.
Fig. 660. — Expressing the lacrymal sac.
Examination of the Eyeball. — (a) Cornea. — The cornea
should always be examined in a darkened room] with lateral illumi-
.".1 z r rl~I-I"-W.'vC<"-."-.T».-v>»
D
Fig. 661. — Lateral illumination with a lens.
nation, concentrated on the eye with a lens (Fig. 661) ; if need be,
an additional hand lens may be used (Fig. 662).
(6) Conjunctiva and Sclera. — Color, vessels, deformations,
etc.
(c) Iris and Pupil. — The surface of the iris should be care-
fully examined for fissures, spots, prominence or retraction, abnor-
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EYES, DISORDERS OF THE, 887
mal shape, etc., and likewise, the contents of the anterior chamber
(aqueous humor, blood, pus, cellular exudate, etc.), the outline of
the pupil, the si::e of the pupil, and its motor responses, all in the
darkened room.
A comparison of the two eyes should always be made.
If the least irregularity of the pupil is noted, two drops of 2
per cent, cocaine should be instilled; at the end of half an hour this
will accentuate the peculiarities of shape (from synechiae, etc.).
Complete examination of the motor functions of the pupil —
response to light and convergence, or to convergence alone {Argyll-
Robertson pupil) — ^has already been mentioned in this work (see
Fig. 662. — Lateral illumination (examination with two lenses).
p. 481), and likewise the manner of eliciting the pupillary reflexes.
The significance of these tests will be referred to later.
One cannot insist too strongly upon the necessity on the part of
the practitioner of informing himself de visu as to the actual condi-
tion of the cornea and pupil (adhesion or its absence, and normal
or abnormal reflexes) if he wishes to avoid overlooking certain par-
ticularly serious disorders (corneal opacity and ulcer, occlusion of
the pupil, etc.) which prompt recognition and treatment would have
checked before damage hard to undo had resulted.
Palpation. — Note should always be made of the comparative
tension of the two eyes. The practitioner should confine himself to
digital palpation. He should never press one finger against the eye.
Both forefingers must be used (Fig. 663), and employed in exactly
the same way as for eliciting fluctuation in an abscess, and after
having requested the patient to look down. One may then note the
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SYMPTOMS.
firmness or hardness of increased tension, which is sometimes stone-
like {glaucoma), or the lowered tension and flaccid condition in cer-
tain other disorders.
Pressure may be exerted, if need be, to elicit the oculocardiac
reflex (see p. 482). In some forms of keratitis, the sensibility of
the eye to contact should be tested with horsehair, a fine probe, or
a wire previously passed through an open flame.
Endoscopy. — ^The specialist examines the fundus of the eye
with his perforated mirror and lens. This form of examination.
Fig. 663. — Palpation of the eye for the purpose of estimating
the extent of fluctuation.
which requires prolonged training and an ability to distinguish the
numerous varieties of intraocular disease, is not available to the
practitioner who has not gone through the course of studies required
for the purpose.
Nonetheless, the practitioner incapable ot examining the fundus
of the eye may, by illuminating the pupillary region, obtain some
information concerning the degree of transparency of the crystal-
line lens and vitreous body. The pupil should preferably be first
dilated by instilling 2 per cent, cocaine solution, and after waiting
half an hour, light is thrown on the eye with the mirror (Fig. 664),
the patient meanwhile rotating the eye in various directions. There
will thus appear, when present, conditions of partial opacity of the
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EYES, DISORDERS OF THE.
889
lens (Fig. 665), cellular deposits, synechice of the iris, and floating
bodies in the vitreous humor. All these abnormalities appear black,
contrasting with the red of the illuminated fundus. At the least
movement of the eye, the corpuscles in the vitreous body, will be
observed in motion and thereby distinguished from fixed opacities.
Fig. 664. — Illumination of the eye with the mirror.
The pupillary field may exhibit several colors (partial cataract,
dislocation of the lens, swellings, or detachment of the retina).
When a patient states that his vision became impaired suddenly,
and the pupil appears alternately dark grayish and reddish under
simple illumination with the mirror, without a lens, and with the
eye in motion, one should think of the possibility of detachment of
Fig. 665. — Partial cataract, seen by transmitted light.
the retina, and find out whether^ the patient sees a hand better in
one portion of the visual field than elsewhere.
Diaphanoscopy. — The specialist may likewise be led to practice
diaphanoscopy, with a lamp (Fig. 649) held over the cocainized
eye; such an examination is sometimes conclusive (growths, foreign
bodies in the lens, etc.).
Movements of the Eyes. — ^With his head held steadily in one
position, the patient should be required to move each eye in all
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890 SYMPTOMS.
directions, the eye not under test being meanwhile covered; one
finds out thus whether there is free ocular motion or motor in-
capacity. The physician notes whether diplopia is present, and if
so, whether it disappears (binocular diplopia) or persists (monoc-
ular diplopia) when one eye is covered.
Orbitoscopy. — The condition of the walls and accessible con-
tents of the orbit should be summarily ascertained by palpation. If
exophthalmus exists, diaphanoscopy, examination of the sinuses,
and fluoroscopy — the latter also very useful in the detection of in-
traocular foreign bodies — should be availed of.
Examination of the Ocular Functions.— In many instances
this may come before any other procedure, even endoscopy.
(a) Visual Acuity. — ^Testing visual acuity requires the use
of a special test chart (Fig. 650), placed at a distance of 5 meters
T c N D z p
Fig. 666. — A normal eye should be able to recognize these letters at a
distance of 5 meters (16% feet).
from the patient, in a good light. If no such chart is available,
the practitioner may nevertheless eliminate instances of normal
visual acuity if the above line (Fig. 666) can be read off with
each eye at a distance of 5 meters, in a good light, the other eye
being meanwhile covered.
By means of the test chart, the visual capacity (acuity) of each
eye is ascertained in turn ; it is also necessary, however, if vision is
insufficient, to find out whether this condition is due to a defect of
refraction (myopia, hyperopia, or astigmatism) alone or in com-
bination with some disease of the eye.
Looking through a perforated disc (the stenopeic opening in
Fig. 648) or through a pinhole in a card is in itself sufficient to im-
prove vision in persons with defective refraction. The remaining
procedures (testing with lenses, optometry, skiascopy, etc.) are the
particular concern of the eye specialist. The visual power of an
illiterate subject or of one with word blindness can be tested by
having him hold in his hand a card cut in the shape of a fork and
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EYES, DISORDERS OF THE. 891
turn it in the directions in which he sees the prongs of the letter E
pointing on the special test card (Fig. 650).
In some patients vision is so poor that it can be estimated only
by the distance at which fingers can be distinguished or a candle
seen, etc.
(b) Field of Vision. — Defects in the field of vision show exactly
the situation and extent of existing intraocular lesions; testing the
visual field yields valuable information regarding various conditions
Fig. 667. — Examination of the field of vision with the perimeter.
of the brain, especially through detection of the presence of hemi-
anopia. The results obtained localise the lesions in the eye without
or before their observation by ophthalmoscopy.
Study of the visual field likewise localizes them in the cranial
cavity and in the brain.
The field of vision is tested with the light coming from behind.
The campimeter or better the perimeter (Fig. 667) are the usual
instruments employed for the purpose. One of the patient's eyes
is closed or blindfolded and the examiner moves a white or colored
pointer over various points in the field, at first working in from the
regions inaccessible to the eye. The patient says "I see it" as soon
as the test object passes into his visual field. His head must be held
still throughout the test and the eye must fix the central mark
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892 SYMPTOMS.
directly in front of him. The examiner records on the chart, with
a line, the limits obtained in the test and then compares them with
the normal field (Fig. 668).
An approximate idea of the visual field may be secured without
the special apparatus. The patient keeps his head motionless, covers
one eye with his hand, and looks steadily at the forehead of the ob-
server, who moves about in front of the eye thus fixed a finger or a
piece of white paper held in, forceps. He is thus enabled to ascer-
tain whether there exist any extensive scotomata (defects) — lateral,
superior, or inferior, — or any concentric contraction (retinitis pig-
mentosa, neuritis, or neurosis) of the field of vision.
Fig. 668. — Ndrmal visual fields.
The white area represents the field of vision for white. The con-
tinuous line indicates the limit of the field of vision for blue. The line
indicates the limit of the field of vision for red. The line
indicates the limit of the field of vision for green.
The peripheral defects having first been investigated, there re-
main to be detected central and paracentral defects, positive scoto-
mata (black spots) or negative scotomata (gaps). The central
scotoma is the most peculiar type, and is met with in the presence
of ambly<^ia (due to alcohol or tobacco) and disease of the macula
lutea.
To make a rough test for central scotoma the patient may be
asked to distinguish the color of discs of red or green paper of the
size of a ten cent piece or less.
Accurate examination of the field of vision is nearly always
referred to the eye specialist
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EYES, DISORDERS OF THE. 893
After any examination of the eye and its adnexa, the question of
possible simulation, a frequent occurrence in industrial accidents,
hystero-pithiatism, etc., should, if it arises, be put up to the specialist
for solution.
Following is the outline of a complete examination of the eye
and its adnexa. From among the procedures enumerated the prac-
titioner will select those which he is able satisfactorily to carry out.
Plan of Examination for an Eye Disorder.
General appearances: Brief verbal inquiry.
Examination (always compare the two eyes).
1. Eyelids, on both their external and internal surfaces. The con-
junctival culs-de-sac.
2. Lacrymal passages.
3. Conjunctiva and sclera.
4. Cornea (lateral illumination).
5. Surface of iris and anterior chamber.
6. Pupils: Reflexes and size.
7. Crystalline lens, with or without artificial dilatation of the pupil
(cocaine).
8. Test of visual acuity (distant vision) and for refractive defects
(myopia-hypometropia, hyperopia, and astigmatism).
9. Test of the accommodation and of near vision.
10. Test of the field of vision.
11. Test of ocular motility.
12. Test of binocular vision.
13. Test of color vision.
14. Test of intraocular tension and sensitiveness (palpation). The
oculocardiac reflex.
15. Endoscopy of the eye (ophdialmoscopy), relating to the lens,
vitreous body, choroid and retinal layers, and the optic nerve.
16. Illumination by transmitted light (diaphanoscopy). Fluoroscopy
and radiography.
17. Examination of the orbit (orbitoscopy) and of the periorbital
sinuses.
18. Special examinations (prospective railway employees, soldiers, or
emigrants; industrial accidents, etc.): Detection of malin-
gering.
19. Examination of the face and cranium (nose, ears, teeth, lymph-
nodes, etc.) and of the neck (thyroid gland, etc.). A more or
less exhaustive examination, as in a patient with some inter-
nal disorder (organs in general, heart, liver, urine, blood, com-
prehensive examination by the latest methods, various tests,
blood-pressure, bacterioscopy, biopsy, etc.). History. In-
herited disorders. Supplementary verbal examination.
20. Name, age, occupation, address, diagnosis, treatment, date, case
number, prescription, and certificate if required.
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894 SYMPTOMS.
In short, after thorough examination of the eyes a complete
examination of the patient is generally necessary in order to con-
firm the results of the eye examination: After the ophthalmopathy
comes the ophthalmopath himself. It is unnecessary here to empha-
size how much of added accuracy may be contributed by examina-
tion of the cranium, nose, heart and vessels, kidneys, urine, blood
and its reactions, etc. — of all the bodily functions and the physical
and mental circumstances of life — ^to the diagnosis, the prognosis,
the intelligent and causal direction of local and general treatment,
and hygiene after recovery.
The local examination, however well conducted, becomes of con-
clusive significance only when supplemented by a complete general
examination, and a satisfactory general examination, in turn, must
include an inquiry into all organs and functions, apart from cer-
tain exceptional cases.
II. THE PRINCIPAL OPHTHALMOLOGIC
DISORDERS.
Eye disorders may be divided, for the purposes of the un-
specialized practitioner, into two main groups. In the first group,
there exists an obvious morbid condition, visible to the naked eye,
in the ocular and periocular region. In the second, the patient com-
plains of pain or disturbed vision, but the eye shows no externally
manifest lesion, or no lesion discernible without some special, com-
plicated technical procedure.
The following facts will lead to definite recognition or to pre-
sumption of certain morbid conditions, while awaiting more en-
lightened inquiry.
A. Disorders Attended with Externally Obvious Lesions. —
Discharges. — (a) Lacrymation. — Using a lamp and hand lens, the
physician should make a very careful examination of the cornea
(erosion, foreign body, slight keratitis, etc.), the iris, tlie con-
junctiva (cul-de-sac and deep aspect of the lids, which should
always be everted), the ciliary margin (intumed lashes), and the
lacrymal apparatus — in conformity with the directions outlined
under Examination of the eye — in order to ascertain whether the
lacrymation results from some lesion of the eye or from a disorder
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EVES, DISORDERS OF THE. 895
of the lacrymal apparatus. In the newborn, congenital dacryo-
cystitis, nearly always unilateral, is readily mistaken for conjunc-
tivitis if one n^lects to compress and empty the lacrymal sac.
(b) Catarrhal, pseudomembranous, and purulent excretions. —
These result from the presence of catarrhal, pseudomembranous, or
purulent conjunctivitis. Bacterioscopy is indicated.
Conditions Affecting the Lids. — Aside from congenital defects
(coloboma, etc.), there may occur: (a) Edema: 1. Passive and
chronic, in heart disorders, nephritis, etc., or disorders in the vicinity
(tumors of the orbit, etc). 2. Acute: Urticaria and transient
edema.
(b) Infectious edema: Local disorders (furuncles and styes,
malignant pustule, erysipelas, subcutaneous abscess, herpes zoster,
etc.) or neighborhood disorders [lacrymal sac, orbit, sinuses, or eye
(conjunctivitis, keratitis, iritis, etc.)].
(c) Emphysema: Comes on abruptly, nearly always upon
blowing the nose violently (involvenfent of the lacrymal passages,
nose, and sinuses).
(d) Ulcerations and tumors, identical with those affecting the
skin in other regions.
(e) Skin disorders of all kinds, similar to those of the hairy sur-
faces (blepharitis ciliaris marginalis) or of various regions of the
body.
(f) Abnormal position of tissues. — Eversion (ectropion), cica-
tricial or non-cicatricial. Inversion (entropion), with or without
ingrowing lashes (trichiasis). Adhesion to the eyeball (symbleph-
aron). Tics, spasms, and contractures; one should carefully ascer-
tain whether the condition is one of purely nervous disease or
whether the eye is itself affected (photophobia and blepharospasm
in keratoconjunctivitis, folliculo-adenoid conjunctivitis, etc.).
Lagophthalmos (the eye unable to close in facial paralysis). Ble-
pharoptosis, which may be either complete through paralysis of the
levator muscle (3d pair), with or without paralysis of the extrinsic
muscles; or incomplete, through paralysis of the cervical sympa-
thetic (Claude Bernard's syndrome, with myosis, enophthalmus, and
slight ptosis). Ptosis of conjunctival origin {granular conjunc-
tivitis, etc.). Ptosis merely of cutaneous nature, through dermato-
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896 SYMPTOMS.
lysis of the lids. One should always examine the pupils, ocular
motility, and the condition of the conjunctiva in ptosis.
Abnormal Conditions and Appearances of the EyebalL — 1.
Congenital anomalies (anophthalmia, cyclops, microphthalmia, albin-
ism, etc.).
2. Megalophthalmia (glaucomatous buphthalmia, extreme my-
opia, or intraocular tumor).
3. Hypotonic atrophy of the globe.
4. Disturbances of motility with various types of abnormal posi-
tions, with or without oculomotor paralysis, and with or without
characteristic diplopia (see the table on Diplopia, p. 908).
5. Retraction of the eyeball (enophthalmus). — Due to cachexia
and general disorders. Unilateral in Claude Bernard's syndrome
and certain cases of trauma to the face and orbit. Sometimes alter-
nates with exophthalmus.
6. Prominence of the eye (exophthalmus). — May result from
direct traumatism (foreign body, hematoma, fracture, etc.) or in-
direct traumatism (pulsating exophthalmus, sometimes spontane-
ous) ; from inflammation, as in rheumatic tenonitis (a species of
post ocular synovitis) ; orbital abscess ; osteoperiostitis in syphilis,
tuberculosis, mycoses, or sinusitis ; orbitocranial phlebitis or thrombo-
phlebitis (exophthalmus often bilateral) ; from tumor, benign (con-
genital or hydatid cysts, etc.) or malignant; or from exophthalmic
goiter (the incomplete, unilateral cases should be watched for).
Examination of a case of exophthalmus necessitates painstaking
investigation of both eyes and of all their functions, of the adjoin-
ing cavities (nose and sinuses, ear, cranium, and mouth), radiog-
raphy, and a general examination of the patient.
Diseases of the Conjunctiva. — Varipus tumors (benign, as in
papilloma, pinguicula, etc., or malignant, as epithelioma and sar-
coma, the latter frequently melanotic). Special dystrophies such as
pterygium (fan-like fold of the conjunctiva between the caruncle
and cornea). Lithiasis, manifested in small yellowish concretions.
Conjunctivitis. — Secreting: Pseudomembranous, catarrhal, or
purulent. Vegetating: Granulations, follicles, etc. Eruptive: Pus-
tules, vesicles, and various skin disorders (erythema multiforme,
pemphigus, psoriasis, etc.).
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EYES, DISORDERS OF THE,
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One should avoid confusing conjunctivitis with keratitis, scle-
ritis, iritis, or glaucoma, these being much more serious diseases
which require prompt treatment of a different kind.
These last disorders are eliminated only by exclusion. Close ex-
amination can alone reveal, indeed, whether the cornea, pupil, intra-
Fig. 669.— Pustular (phlyctenular)
kerato-con j uncti vitis.
Fig. 670.— Corneal
ulcer.
ocular tension, and vision are normal. Only after '.having made
certain of the integrity of the other portions of the eye should the
observer look for thel distinguishing features of the several forms
of conjunctivitis. At the same time he should find out whether the
Fig. 671. — Corneal pannus and the upper lid in granular conjunctivitis.
conjunctivitis is not complicated with keratitis (Fig. 669) or some
other affection of the eye.
The physician should never allow himself to be led into error by
faint resemblances to certain disorders.
The most important thing in. the diagnosis of conjunctivitis is
to make sure of the precise condition of the other portions of the
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898 SYMPTOMS.
eye and its adnexa, and actually to see that they are in a normal
condition.
Diseases of the Sclera. — General inflammation (diffuse scleritis)
or superficial (episcleritis) or deep (parench)rmatous scleritis) focal
inflammation.
There is less of a bright red color (violet) than in conjunc-
tivitis, and the conjunctiva is smooth, with vegetations or secretions.
Congenital brown spots (not to be confused with supra-and intra-
ocular tumors).
Cornea. — (a) Opacity and keratitis: Without ulceration
(superficial, parenchymatous, or deep-seated) or with ulceration
(Fig. 670). There should be a detailed examination with the lamp
and hand lens. The observer should ascertain if there is not some
Fig. 672.— Hyphema Fig. 673.— Hypopyon Fig. 674.— Iritis with
(blood in the anterior (pus in the anterior cellular exudation in
chamber). chamber). the anterior chamber.
lesion in the vicinity — dacryocystitis, blepharitis, or conjunctivitis —
or a foreign body; if the eye is not hard (glaucoma), and whether
the opacity is of long standing (cicatricial leucoma) or recent Sen-
sation of the cornea should be tested with a piece of wire, being
sometimes abolished (neuroparalytic keratitis).
(b) Vascularization, a frequent condition during repair of
ulcers, congenital syphilitic interstitial keratitis, etc. Vasculariza-
tion (Fig. 671) of the upper portion of the cornea (pannus) often
points to granular conjunctivitis (in such a case the upper lid, seat
of the disease, should always be everted).
(c) Ectasia, transparent (keratoglobus, keratoconus) or opaque
(staphyloma).
(d) Tumors about or in the cornea, sometimes melanotic. Con-
fusion with an extravasated intraocular tumor is to be avoided.
Anterior Chamber. — Contents normal or abnormal: Hyphema
(Fig. 672), hypopyon (Fig. 673), cell deposits (Fig. 674), foreign
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EYES, DISORDERS OF THE.
899
bodies, dislocated lens, etc. The depth of the anterior chamber
may be reduced or increased; sometimes it is entirely emptied (the
iris being then glued to the cornea).
Glaucoma (characterized by intraocular hypertension). — 1.
Acute: Intense congestion of the eye, paroxsymal pains, pupil
dilated, eye very hard on well-conducted palpation (see Examinor-
tion of the eye), but only slightly sensitive to pressure; vision
markedly impaired.
It should not be confounded with acute iritis. Signs of the lat-
ter: Eye red, pupil contracted and irregular, intraocular tension
normal or subnormal, palpation very painful, vision interfered with.
2. Chronic : But little redness, intraocular tension more or less
excessive, field of vision contracted (on the nasal side), pupil free
Fig. 675. — Syphilitic iritis with granulo-
matous node.
Fig. 676. — Prolapse of the iris.
of adhesions. Iridescent vision about lights, such as that of a
candle.
Instillation of atropine is to be avoided where a precise diag-
nosis has not been made, for atropine markedly aggravates glau-
coma— 2L mistake too often made.
Ophthalmomalacia. — ^Transient or permanent hypotonia (with
atrophy of the eye).
Iris. — Anomalies. Inflammatory conditions (iritis) and nodular
formations (granulomata in syphilis, tuberculosis, leprosy, the
mycoses, etc.).
The DIAGNOSIS of acute iritis is based: 1. On the special type
of redness of the eyeball, such redness being especially pericorneal,
like a radiating areola, with distorted outline of the narrowed pupil,
some parts of the iris becoming adherent to the lens (synechia) ;
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900 SYMPTOMS,
the pupil appears ragged and fringed (Fig. 675). 2. On the sub-
jective disturbances: Spontaneous pain, increased on palpation,
interference with vision, and photophobia. The upper lid is some-
times swollen. Detailed examination of the cornea excludes the
existence, or demonstrates the coexistence, of keratitis, which causes
redness of the same order as that of iritis.
Some cases of chronic iritis are not attended with redness nor
pain, being featured by the disturbance of vision combined with
observation of pupillary cohesions.
Iritis is distinguished from acute glaucoma, first of all, by pal-
pating the eyeball, which is hard in glaucoma; next, by noting that
glaucoma exhibits a dilated, mydriatic pupil instead of .the myotic
pupil of iritis. Some cases of chronic iritis may be complicated
with increased intraocular tension {secondary glaucoma), but ex-
amination of the pupil shows the iritic synechias
Iritis should not be mistaken for conjunctizntis, in which the
redness is diffuse, not merely pericorneal, and the pupil free, with
vision but slightly or not at all interfered with. The secretions,
eruptions, and swelling (chemosis) complete the diagnosis of con-
junctivitis in the absence of any iritic corneal complication.
Tumors: Cyst, sarcoma, etc.
Prolapse of the iris (in ulcerous or traumatic perforation),
forming a small, black, projecting mass.
Displacements: Prominence or retraction in certain disorders
'of the lens and vitreous body. Tremulousness (iridonesis) in dis-
location of the lens, etc.
Abnormal Conditions of the Pupils. — A comparison of the two
pupils as to shape, size, and spontaneous or induced mobility should
always be made.
One should note the outline of the pupil, which is sometimes
notched (congenital coloboma), wavy or angular te^V/toM/ adhesion
(glaucoma, tabes, etc.), or irregular and adherent to the lens or cor-
nea {synechicE), It is of capital importance to detect these adhe-
sions (iritis) of the "fringed** pupil. In doubtful cases, dilatation
with cocaine (2 per cent.) will reveal the smallest synechiae (Fig.
677) after waiting twenty minutes, thus obviating the unpleasant
features (visual disturbance persisting for about ten days and inter-
fering with reading) of atropine, which may be reserved for the
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EYES, DISORDERS OF THE. 901
treatment of iritis after it has been duly diagnosed. The adhesions
of iritis should not be confounded with the threads of a congenitally
persisting pupillary membrane ; the latter do not start from the mar-
gin of the pupil, but from the anterior surface of the iris.
Mydriasis and Myosis. — Where uni- or bi-lateral myosis is pres-
ent, one must exclude : The use of a myotic, some disease of the
nervous system (tabes, etc.), paralysis of the cervical sympathetic
[disease in the cervical region (enlarged glands) or in the medias-
tinum should be looked for] with slight ptosis, and intoxication by
opium, morphine, etc.
Where there is mydriasis, one must exclude: The use of a
mydriatic (sometimes surreptitious), oculomotor paralysis, paral-
ysis of the iris and ciliary muscle (diphtheria, syphilis, etc.), cere-
brospinal diseases, lesions of the orbit, and certain intoxications
Fig. 677. — Synechiae in iritis.
(belladonna, spoiled meat, etc.). The physician should think of
incipient general paralysis where the pupils are markedly unequal
and insensitive to light.
An indispensable proceeding is to ascertain the mobility or
IMMOBILITY of the pupil to light and accommodation, and then to
test the consensual reflex.
The Argyll-Robertson pupil {lack of response to light coupled
with response to fixation and convergence) is a sign of nervous
syphilis (tabes, general paralysis, etc.), hut very many syphilitics do
not show it.
Finally, there are cases in which :
1. When light is thrown into one eye, its pupil fails to contract,
but the opposite pupil responds, through the consensual reflex; the
condition then present is a paralytic mydriasis with peripheral in-
volvement of the ciliary and pupillary nerves due, e.g., to syphilis.
If light is thrown in the opposite eye, the pupil responds, but the
pupil of the first eye remains motionless.
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902 SYMPTOMS.
2. Light is thrown in a single eye and both pupils remain
motionless. If now light is thrown in the other eye alone, both
pupils respond. This condition is the result of a complete blindness
of the first eye due to local (peripheral) disease of the retina and
optic nerve.
In so-called "hysteric" blindness and in blindness of cortical
origin the reflexes are retained, as a general rule.
Pupillary Area. — ^The pupillary opening overlies the anterior
surface of the lens. The observer should ascertain whether there
is not some exudate, with partial or total occlusion of the pupil
(Fig. 678) and pigment deposits (former iritis).
Fig. 678.--Complete, urn- Fig. 679.— Opacities in the lens (partial
hilicoid occlusion of the cataract), contrasting as black spots in the
Qupil. pupil illuminated with the ophthalmoscopic
mirror.
The condition of the lens should be investigated — ^whether it is
clear or opaque (cataract, partial or total, acquired or congenital,
and of many possible varieties).
The observation of a grayish hue of the pupil, very commonly
present in old persons, yet unaccompanied by opacity, should not
lead to the conclusion that cataract exists. The pupil does not seem
to be of a clear black when looked at by daylight; yet the lens is
found to be clear on closer examination.
Aside from the cases in which there is advanced, intense, and
unquestionable opacity, as seen on lateral illumination with a lamp
and by use of the hand lens, the physician should not commit him-
self until after he has illuminated the interior of the eye with the
ophthalmoscopic mirror, which, after dilatation of the pupil with 2
per cent, cocaine (and waiting 20 minutes), will reveal, contrasting
in black against the red background of the eye, the slightest lens
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EYES, DISORDERS OF THE. 903
opacities (Fig. 679) of incipient cataract — ^not yet sufficiently
marked to prevent reading and writing.
Without being trained in examining the retina and optic nerve,
the practitioner may employ for this purpose the mirror and any
available source of light, the patient being meanwhile shaded by a
screen (Fig. 664).
The patient should be requested to move his eye about while
the light is being directed at him with the mirror; very often the
pupillary area will appear filled with moving objects, floating
particles, detached retina bobbing about a dislocated and mov-
able lens, crystals, etc.
Som« eyes that prove unilluminable, the pupil continuing to
exhibit an ebony black appearance, are the seat of tumor, hemor-
rhage, black cataract, etc.
Limiinous Pupil. — Where, in a child, the pupil presents a
glowing, illuminated (cat's eye) appearance, there is frequently
present a glioma of the retina, a tumor which destroys the eye
and is generally fated in spite of enucleation.
B. Disorders Unattended with External Lesions, thoagh some-
times Attended with Internal Lesions, Visible only by Endoscopy.
— Pain. — Pain in or near the eye, without any visible pathologic
condition, must be differentiated from headache and migraine —
though these are often present in addition.
After having carefully investigated (by palpation, etc.) whether
the pain is not the result of some inflammatory condition which is
not yet superficially manifest (beginning stye, keratitis, iritis^ over-
looked foreign body beneath the lid or in the cornea) or of increased
intraocular tension {glaucoma), the physician should proceed to
eliminate simple migraine and especially ophthalmic migraine with
scintillating scotoma and images of luminous bands, sometimes with
transient hemianopia.
He should next think of facial neuralgia (making pressure over
the points of emergence of the trifacial branches about the orbit)
and tic douloureux ; a prospective eruption {herpes zoster) should
be kept in mind. Neurasthenic and hypochondriac patients some-
times experience for years paroxysms of ocular neuralgia (delayed
recurrent keratalgia) in eyes that have previously been subjected
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904 SYMPTOMS,
to some form of traumatism, often of trifling degree (erosion from
contact with the finger nail or with a house plant, etc.). Very care-
ful examination is necessary in such cases.
Pain after Close Work. — Refractive disorders {astigmatism,
hyperopia, presbyopia, and sometimes marked myopia) should be
excluded. Headache of this type, which is very common, demands
the wearing of glasses, in conjunction with general treatment of
coexisting disturbances (neurosis, anemia, intoxication, etc.).
Latent strabismus and insufficiency of and excessive strain in con-
vergence, as well as slight forms of diplopia, may likewise be the
cause of the pain.
Miscellaneous Visual Disturbances. — ^Impaired Vision on One
or Both Sides. — The patient complains of blurred vision with
one or both eyes ; or he may be unable to see anything, not even
light ; yet the eyes seem normal.
Where the patient is still able to see a few objects he should be
placed 5 meters away from the test card (Fig. 650), with the latter
well illuminated and the patient's back to the light, and his ability
to distinguish some of the letters ascertained.
The observer may hold the perforated disc (stenopeic open-
ing) in front of each eye in turn, the other eye being meanwhile
covered; or a card with a pinhole may be substituted. If vision
is improved thereby, some error of refraction (myopia, hyper-
opia, or astigmatism) is present, with or without disease of the
fundus, and the patient will derive more or less benefit from the
use of concave, convex, or cylindric lenses, which the practi-
tioner may try to select if they are available, but accurate pre-
scription of which requires the intervention of the eye specialist.
Where, on the other hand, the stenopeic opening reduces
vision, some disease of the fundus exists, or an amblyopia due to
a post-ocular cerebral or neuropathic disorder.
Here again an examination by the specialist is necessary to
settle the question and determine which, among the numerous
possible disorders, has been the cause of the blindness or visual
impairment in one or both eyes.
Nyctalopia. — Improvement of vision as the light of day dimin-
ishes, occurring in subjects who are dazzled in broad daylight (alco-
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EYES, DISORDERS OF THE, 905
holic amblyopia, some cases of cataract, certain diseases of the fun-
dus, etc.).
Hesperanopia. — This term, proposed by the writer, and more
accurate than the old term hemeralopia (which is etymologic-
ally nonsensical), refers to a sudden reduction of vision as the
light of day declines. The subject then becomes nearly blind. There
are cases of transitory hesperanopijsi (in overworked or poisoned in-
dividuals and disorders of the liver and kidneys) and cases of per-
manent hesperanopia, already present in childhood (retinitis pig-
mentosa chronica). It is essential to have the eye-grounds ex-
amined in such cases, particularly where the subject is a child who
seems helpless and has difficulty in getting about towards evening
(crepuscular amblyopia).
Phosphenes. — This symptom is an evidence of retinal irrita-
tion, which is sometimes of serious degree in myopic subjects; it
may be a forerunner of detachment of the retina. It is also
present in a variety of affections of the retina and choroid. There
are even blind subjects who continue to be inconvenienced by
luminous visions. The condition should not be confounded with
the paroxysm of ophthalmic migraine with scintillating scotoma.
Muscae volitantes. — These are most commonly present in
myopia, in overworked individuals, and in neurasthenia. They
may sometimes be present for years, or even indefinitely, irre-
spective of normal vision. Examination of the fundus will show
whether the lens, vitreous body, and internal membranes remain
in a normal condition and will permit of making a more accurate
prognosis.
Disturbances of Color Vision. — These may be temporary, as in
alcoholic and tobacco amblyopia, affections of the retina and choroid,
diabetes, etc., or congenital, as in Daltonism (color blindness; to
be excluded by special tests).
Colored Vision. — Erythropsia (red vision) in neuroses, after
cataract extraction, etc. Various phenomena of colored audition.
Iridescent Vision. — When a patient sees the colors of the rain-
bow when looking at an open flame (candle), the intraocular ten-
sion should always be tested, this symptom being often an accom-
paniment of glaucoma.
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906 SYMPTOMS.
Photophobia. — Where, in the presence of photophobia, the cor-
nea and iris are both found normal, a disorder of the retina or of
the lens (cataract) is to be feared. Some neurasthenics, however,
are subject to paroxysms of photophobia although vision and the
eye are and remain normal.
Vertigo. — One should first of all determine whether the patient
is not suffering from double vision; the writer's advice has fre-
quently been sought on account of vertigo attributed to the stomach,
previously treated by diet and antidyspeptic remedies, where the
actual cause was paralysb of a nerve or muscle of the eye.
JVhen a patient complains of vertigo, the physician should close
one of the patient's eyes, which will cause the vertigo to disappear
at once if some form of ocular paralysis is responsible.
Vertigo also occurs in connection with deep-seated disorders of
the eye, with unsuitable glasses, with overstrong lenses, and with
general disorders.
Diplopia and Polyopia. — One should at once ascertain, by
having the patient close one eye, whether he is not seeing double
with a single eye; in some neuroses, indeed, and especially in in-
cipient cataract, there occurs a monocular diplopia or polyopia, the
patient seeing, e.g., seven or eight gas jets where there is but one,
with one of his eyes.
Where the subject has to use both eyes to see double, paralysis
or contracture of some muscle exists, or there may be a mechanical
deviation of the eye on account of orbital disease (tumor or
abscess).
A person suffering with diplopia generally shows a faulty posi-
tion of the eye, due to loss of power of one muscle and attraction
of the eye by the normally antagonistic muscle. Ordinary strabis-
mus, or squint, does not cause diplopia, and in spite of the faulty
position, each eye, when examined independently, is capable of
rotating in all directions; paralysis is not present under these cir-
cumstances. Faulty position and diplopia are the result of the
physiologic peculiarities of the nerves and muscles of the eye (Fig.
680). In paresis with but slight muscular weakness, however, or
where a single muscle, such as the inferior oblique or inferior rec-
tus, is weak, the faulty position is almost imperceptible, and the
localizing diagnosis is based on the diplopia alone.
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EYES, DISORDERS OF THE. 907
It is well to place a red glass before an eye in order to find out
with which eye the fed image is seen (crossed diplopia— or hotnony-
mous when on the same side), and to hold a lighted candle 2 meters
in front of the patient.
Objective and Subjective Signs of Paralyses. — Complete
paralysis of the oculomotor nerve (3d pair) which supplies both
the superior, inferior, and internal recti, the inferior oblique, and
the constrictor of the pupil and levator palpebral superioris,
results in :
Ptosis, mydriasis, paralysis of accommodation {reading being
impossible except with a strong convex lens), divergent strabismus,
and horizontal crossed diplopia, i.e., a condition in which the
false image is projected to the side opposite that of the paralyzed
eye.
] Sup. rectus
Sup. oblique
Int. recttiil^. ^' ■■^iw Ext. rectni
Inf. oblique
Inf. rectus
Fig. 680.— Muscles of the Ufi eye, with their respective distances
from the cornea and functions.
Internal rectus, adductor ; external rectus, abductor ; inferior rec-
tus, depressor, inward rotator, and adductor; superior rectus, elevator,
inward rotator, and adductor; superior oblique, with its pulley, depres-
sor, inward rotator, and abductor; inferior obuque, elevator, outward
rotator, and abductcM*.
Paraljrsis of the abducens (6th pair), which supplies the ex-
ternal rectus or abductor muscle, results in convergent strabismus,
with the false image on the same side (horizontal homonymous
diplopia).
Paralysis of the patfaeticus (4th pair), which supplies the
superior obUque or inward rotator, depressor, and abductor
muscle, results in vertical homonymous diplopia, with deviation
upward and toward the unaffected side.
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908
SYMPTOMS,
Lastly, there occur instances of independent paralysis of a
nerve-branch supplying but one of the muscles innervated by the
oculomotor, either in one eye or in both, and in which determina-
tion of the exact type of involvement is a complex matter. There
being no distinct defect of position, the diagn'osis is gradually elab-
orated through analysis of the existing diplopia. By moving the
candle about before the eyes, at first horizontally and then vertically,
the head meanwhile being kept motionless, a progressive widening
of the distance between the images is noted (in the direction of the
paralyzed muscle).
Puech and Fromaget clearly summarize the significance of dip-
lopia in the table reproduced below. Examination shows, indeed :
1. In //i^ direction in which the function. o/ the affected muscle
is normally exerted:
False image, increase of the diplopia and progressive increase
of the distance between the images, limitation of movement, an
altered direction, of the face and the inclination of the head,
2. In the direction opposite to the physiologic function of
the affected muscle:
Faulty position of the eye and diminution of the diplopia.
Later, after having precisely determined whether the diplopia is
of the HOMONYMOUS or CROSSED variety, the following:
A. — Homonjrmous Diplopia. |
Paralyzed
Muscle.
Affected Eye.
1. In the horizontal direc-
External
The distance between the
tion :
rectus.
images steadily increases
on the paralyzed side.
f above:
Inferior
The upper image corre-
2. In the vertical 1
oblique.
sponds to the affected
direction:
eye.
I below:
Superior
The lower image corre-
oblique.
sponds to the affected eye.
B.
—Crossed Dip
miopia.
1. In the horizontal direc-
Internal
The distance between the
tion:
rectus.
images increases in the
direction of the motor
action of the paralyzed
muscle, and, hence toward
the normal eye.
2. In the vertical f ^^^^^•
direction: ( below:
Inferior
rectus.
The upper image is that of
the affected eye.
Superior
The lower image is that of
rectus.
the affected eye.
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EYES, DISORDERS OF THE. 909
The general practitioner scarcely needs to undertake such in-
vestigations: He may Hmit himself to the immediate diagnosis of
the more easily recognizable forms of paralysis with obvious devia-
tion and muscular weakness — those involving the oculomotor and
abducens — and to blind-folding one eye to abolish diplopia and ver-
tigo ; in any kind of paralysis he should then, without further ado,
proceed with an investigation of the cause and with causal
treatment.
A consultation with the specialfst later will determine the fur-
ther details of the condition, and will also, if the occasion exists,
differentiate paralysis from contracture, which is much less
common.
Ophthalmoplegia. — Diffuse forms of paralysis, congenital or
acquired, inherited and familial, oi the neri'es and muscles of the
eye. "
Where all the centers (progressive nuclear ophthalmoplegia)
of the motor nerves to the eye fail\in succession, the patient,
with his drooped lids, with difficulty raised by wrinkling the
forehead, and his eyeballs fixed in their orbits, is said to present
the ophthalmoplegic Hutchinson's facies.
Ophthalmoplegic migraine (with sudden and recurrent failure
of all the muscles) is frequently a benign condition, from which
recovery occurs withifi a fe%v days-; in some instances, however, it
is attended with dangerous intracranial disturbances, infectious or
neoplastic.
Paralysis of Associated Movements. — Cases occur in which,
in both eyes, whereas other movements of the eyes can still be made,
there exists a paralysis of the associated movements, vertical
(paralysis of ele7'ation or of depression of the eyeball) or lateral,
owing to disease of the association fibers connecting the centers and
convolutions. An ophthalmo-neurologic consultation should be held,
as in any other form of paralysis, to determine the cause and seat
of the lesion. A complete examination of the patient should be
made, with determination of any co-existing syndromes, such as
that of Millard-Gubler (pontine lesion with paralysis of the ab-
ducens and. facial on the same side and hemiplegia on the opposite
side) and that of Weber (peduncular lesion with oculomotor paral-
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910 SYMPTOMS.
ysis and opposite paralyses of the face and extremities) — syndromes
to be referred to again later in this work.
Abnormalities of the Visual Field. — (a) Peripheral con-
traction.— ^This may be concentric or excentric and monocular or
binocular.
In glaucoma, the patient presents, if the disease is of long
standing, an excentric and internal contraction of the visual field.
Fig. 681. — Course of the optic nerve-paths (with their direct and
crossed fasciculi) from the eye to the brain; c, c', cuneus; a, b, decussa-
tion of the optic tracts (chiasm).
He is unable to see an object placed in front of his eye, and sees it
only when it is moved toward the temporal region.
An extreme degree of concentric contraction (some fieMs
are only of the size of a dime) may be observed in retinitis
pigmentosa, in optic atrophy — e.g., in tabes — and in various in-
stances of amblyopia unattended with ophthalmoscopic lesions
(hystero-pithiatism, etc.).
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EYES, DISORDERS OF THE, 911
(ft) Bilateral contraction with obscuration of one-half
OF THE VISUAL FIELD: Hemianopia.^ — In hemianopia there is
complete normalcy of the eye-grounds and inspection of Fig. 681
will show what the homonymous or homolateral (on the same side)
and the heteronymous varieties of hemianopia consist of.
Central vision is retained and the patient is able to read.
Where hemianopia is suspected on account of the position of
the patient, who turns his head in such a manner as to direct toward
external objects that portion of the eye which is still functionally
available, and ot\ account of the absence of lateral vision of per-
sons, o£ dishes on the table (the patient sees his glass, but nothing
Fig. 682. — Right homonymous hemianopia the result of disease of the
left optic tract at d (Fig. 681) or of its cerebral origin, c.
which adjoins it), or of the word following that which he is read-
ing, it is easy to localize the intracranial situation of the lesion
responsible. This can be done by copying the accompanying dia-
gram and by interrupting the optic fibers, either between the brain
and the optic chiasm, at d, for example, showing that there is
homolateral homonjrmous hemianopia, right- or left- sided (Fig.
682), or in the region of the chiasm, at the crossed or non-crossed
fasciculi, heteronymous or heterolateral, binasal or bitemporal
hemianopia (Fig. 683). There also occur complicated cases, with
patch-like defects, atypical forms, double hemianopia, etc.
1 This condition has often been termed hemio^io or hemianopsia; the
writer prefers to substitute for these the term hemianopia, which expresses
the gap in the field of vision and conforms in its termination to the cus-
tomary, general nomenclature, as in diplopia, hy per mtir a pia, nyctalopia.
etc
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912 SYMPTOMS.
For practical purposes, homonymous hemianopia (Fig. 682) is
nearly always the result of a cortical lesion in the occipital region
and cuneus (softening, syphilitic arteritis, hemorrhage, etc.). It is
generally accompanied by apoplectic strokes, hemiplegia, aphasia, or
Fig. 683. — Bi-temporal heteronymous hemianopia (in acromegaly) , due
to pressure on the optic chiasm (crossed fasciculi).
psychic blindness. Consultation with the ophthalmologist and the
neurologist is quite indispensable.
Cro.y.y^rf hemianopia of the bitemporal type (Fig. 683) is fre-
quently the result of acromegaly, the enlarged pituitary body
Fig. 684. — Central scotoma in an alcoholic subject.
exerting pressure on the optic chiasm (a, b) ; whence a characteris-
tic form of visual field (see Eye conditions met with in general
diseases),
(c) ScoTOMATA. — The patient complains of spots or gaps in the
CENTRAL or PARACENTRAL PORTIONS of the visual field, and not at
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EYES, DISORDERS OF THE, 913
its periphery. Central scotomata (Fig. 684) indicate defective func-
tioning of the macular region of the retina and are the most annoy-
ing to the patient. In some cases they are due to disorders of the
fundus, in others to special disturbances, among others alcoholic
and tobacco amblyopia. They impart the sensation of a spot or
hole, a gap (the patient failing to see certain words in a printed
line), or of poor color perception. They should not be confused
with hemianopic defects.
In all visual disturbances, with or without obvious pathologic
change, one should keep in mind the possibility of simulation,
which the specialist may be called upon to settle, in conjmon with
artificially induced disorders of the eye.
III. THE PRINCIPAL EYE CONDITIONS MET WITH
IN GENERAL DISEASES.
The majority of diseases, whether acute or chronic, may be at-
tended at some time in their course, sometimes even before their
manifest onset, and sometimes during or even after convalescence,
by some organic or functional disturbance of the eye.
It may happen, indeed, that an ocular disturbance appears a long
period ahead, as the initial manifestation of a disorder that is to be-
come obvious and generalized only a long time after. Iritis may be
the initial localization of a gouty or rheumatic state which will sub-
sequently involve other regions ; retinal hemorrhages sometimes pre-
cede albuminuria, etc. The eye condition is thus the harbinger of a
latent general disease. In these cases a complete examination of the
eye patient and inquiry into his family history, together with a
thoroughgoing plan of treatment, calculated to improve all bodily
functions and all conditions that might be considered subnormal,
constitute "the best thing to do" while awaiting the conclusive evi-
dence to be afforded by the subsequent course of events.
Again, while several general diseases are attended by well-
known and customary eye complications, these do not always occur;
or there may occur others, of very varied type and much more un-
expected. To cite one example: Diabetic cataract is familiar to
all, but many diabetics do not show it or suffer exclusively from
58
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914 SYMPTOMS,
iritis, amblyopia, and less ordinary eye affections; yet these are
characteristic to an ophthalmologist.
Finally, assuming a loftier view, one may recall how the assimi-
lation and sometimes the identification, in general and compara-
tive MEDICINE, of the ocular disturbances — regional states com-
parable to those observed in other portions of the body and in other
organs — is a matter of compelling interest and affords a solution
for many ophthalmologic or general problems which could not be
solved by men restricted to their own special field, medical or sur-
gical. As far as the writer is concerned, he has always believed
and taught, through the last twenty-five years, that an eye condi-
tion is, as a rule, in all respects, even as regards treatment, an oculo-
general syndrome. There is no doubt but that the other specialties
would derive benefit from a similar, daily confrontation of observa-
tions, as well as from a like joint conclusion as regards the etiology
and treatment.
Diseases of the Kidneys. — Many cases of Bright's disease re-
main free of ocular disturbances throughout One should be wary
as regards coincident disorders (hyperopia, myopia, etc.), non-
pathognomonic complications such as iritis, cataract, paralyses of
eye muscles, etc., and those due to a concomitant disease, and
should have a complete examination of the eyes made in these cases.
Edema of the lids, bilateral and of varying degree (less common
than is generally believed), retinitis with hemorrhages and white
spots, accompanied by edema of the optic nerve, are more character-
istic. The patient has difficulty in reading or cannot read at all, but
can still get about. ^ Blindness is rare, unless some complication
occurs such as detachment of the retina, glaucoma, etc. The eye
disease is recovered from, however, only if the nephritis is likewise
cured.
Retinitis sometimes precedes the appearance of albuminuria
{prealbuminuric retinitis) in patients with arteriosclerosis and high
blood-pressure.
It occurs frequently in combined glycosuria and albuminuria.
Retinitis with white spots is rather the result of the azotemic
condition ; edematous neuro-retinitis, of chloridemia, and the retinal
hemorrhages, of high blood-pressure. These several types, while
sometimes present independently, are rather usually combined.
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EYES, DISORDERS OF THE. 915
Thus, the patient almost never becomes blind, but in the many-
cases of incurable nephritis the appearance of retinitis is an un-
favorable omen. Statistical records show that "ocular" nephritics,
with few exceptions, die sooner, generally not surznving longer than
two years.
Some patients with albuminuria and high blood-pressure suffer
attacks of transitory amaurosis, unaccompanied by disease of the
eye-grounds and followed by return of vision.
Diabetes. — Aside from retinal hemorrhage and mixed forms
of retinitis (diabetes with albuminuria), diabetic patients may
suffer from cataract of different varieties (soft, white, and bi-
lateral in young subjects) and more or less operable under local
and general precautions; acute or chronic iritis; hemorrhagic
glaucoma; amblyopia with central scotoma (of the toxic type,
similar to that in alcoholic amblyopia) ; optic atrophy ; paralysis
of the motor nerves of the eye ; rapidly progressive myopia, etc.
The urine should always be examined in eye disease, especially
when deep-seated.
Gout. — Iritis, sometimes hemorrhagic; scleritis or sclero-
tenonitis.
Arthritis Deformans. — Iritis, iridochoroiditis, scleritis, or
anterior sclerochoroiditis.
Diseases of the Heart and Vessels. — (a) Heart Disorders. —
In the last stage, edema of the lids, the optic nerve, and the orbit ;
sometimes retinal hemorrhages, glaucoma, and hemorrhagic glau-
coma. Embolism and thrombosis of the retina in chronic endocar-
ditis, causing sudden blindness on one side, which is often per-
manent
Pulsation of the retinal vessels is frequently present in aortic
insufficiency and at times in mitral insufficiency.
Spontaneous subconjunctival ecchymoses, sometimes preceding
cerebral hemorrhage, occur in arteriosclerosis and high blood-
pressure.
Inequality of the pupils is observed in aortic aneurysm (pressure
on the sympathetic).
(b) Major hemorrhages. — Certain profuse hemorrhages, as
in hematemesis, intestinal hemorrhage, metrorrhagia, epistaxis,
wounds, etc., lead either at once or later, severed days after the loss
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916 SYMPTOMS.
of blood, to bilateral disturbances of vision which may go on to
blindness, partial or complete, curable or incurable (complete or
partial optic atrophy).
(c) Blood disturbances. — A thorough examination of the blood
by the latest methods is of exceedingly great importance in the
majority of diseases of the eyes and their adnexa, both as regards
diagnosis, prognosis, and treatment. One should not be too positive
in concluding that syphilis is absent where thej Bordet-Wassermann
reaction is negative; in the writer's experience, intensive antisyph-
ilitic treatment has often brought about a recovery undeii these cir-
cumstances in a wide variety of eye disorders. An investigation for
syphilis should always be made, even in the presence of manifest
tuberculous disease, which is often combined with syphilis.
A study of the blood should be made in chlorotic anemia, leu-
kemia, Hodgkin's disease, hemophilia, etc., where localized ocular
involvement exists.
Various Infectious Diseases. — Eruptive fevers. — Measles. —
Conjunctival hyperemia, chiefly in type (like pterygium) ; styes, ab-
scess of fhe lid, pustular keratoconjunctivitis, blepharitisi or dacryo-
cystitis.
Small-pox and Chicken-pox. — Pustular formations in or about
the eye ; seriou§ corneal ulcers and abscesses; iritis, iridochoroiditis,
or optic neuritis ; orbital abscess ; chronic ulcerative blepharitis with
misplaced lashes. Persons in whom a vaccinal eruption is at its
height should.be cautioned not to touch their eyes with their fingers
(vaccine blepharitis and keratitis).
Scarlet fever. — Conjunctivitis, sometimes with false mem-
branes; dacryocystitis; albuminuric retinitis.
Note. — In all eruptive fevers with eye or lid involvement the
physician should ascertain daily, with the lamp and hand lens,
the exact condition of the cornea and pupillary margin.
Diphtheria. — Paralysis of accommodation with mydriasis; the
patient is unable to read, unless a strong convex lens of +3 or +4
diopters is used, or a 1 per cent, solution of pilocarpine nitrate is
instilled and he waits half an hour for its effect. Paralysis of eye
muscles; pseudomembranous conjunctivitis.
The pupils and vision should always be examined in the presence
of any kind of sore throat.
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EYES, DISORDERS OF THE. 917
Grip. — ^Herpes of the cornea, transient or lasting; iritis, etc.
Grip initiates, relights, or aggravates the majority of eye disorders.
Mumps. — Inflammation of the lacrymal glands (dacryoadenitis) ;
conjunctivitis, iritis, or optic neuritis.
Typhoid fever. — Optic neuritis, paralysis of ocular muscles, etc.
Malaria. — Obstinate herpes comeae, iritis, retinitis, floating par-
ticles in the vitreous humor, optic neuritis.
Acute and recurrent rheumatism. — Iritis, scleritis, or sclero-
tenonitis; causal role in other eye affections more doubtful.
Erysipelas. — Abscess of the lid; dacryocystitis, conjunctivitis,
corneal ulcer, iritis, optic neuritis ; phlebitic orbital infections. Some-
times a (**curative") erysipelas causes improvement in a rebellious
eye affection (granular conjunctivitis, leprosy, etc.).
Anthrax. — Malignant pustule and edema of the lids.
Leprosy. — Leprous nodules of the lids, conjunctiva, or cornea;
iritis ; paralysis of the orbicularis muscle.
Tuberculosis. — Almost any of the syndromes — whether inflam-
matory or in nodular foci — affecting the eye and its adnexa may be
of tuberculous origin. One should exclude or detect syphilis, ac-
quired or congenital, and the other affections frequently present in
combination.
Syphilis. — Chancre of the lids or conjunctiva. Pustules, papules
or patches. Gummas and syphilomas of the lids, conjunctiva, lacry-
mal sac, lacrymal gland, orbit, cornea, sclera, or interior of the eye
(perforating gumma of the iris and ciliary body). Intraocular in-
flammatory states, acute or chronic (iritis, choroiditis, retinitis, optic
neuritis, etc.). Optic atrophy, with or without tabes. Paralysis of
oculomotor muscles. Frequent anachronisms in the various mani-
festations (early tertiary or delayed secondary manifestations).
Syphilis in its acquired or congenital forms should always be
looked for in the presence of ocular disorders. Any of the afore-
mentioned eye conditions may be met with in congenital syphilis,
with a special predilection, however, for interstitial keratitis, chorio-
retinitis, congenital cataract, buphthalmus (infantile glaucoma),
strabismus, and nystagmus. Tuberculosis is frequently present in
association. The therapeutic test by means of antisyphilitii treat-
ment— which should not be neglected in spite of the results of the
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918 SYMPTOMS.
blood or other tests, whether positive or negative— of tentimes yields
unexpected benefit..
Mycoses. — A definite differentiation of these disorders from
syphilis, tuberculosis, and the other infections of the eye and its
adnexa should be made.
Diseases of the Respiratory Tract — (a) Nose. — Dacryo-
cystitis, lacrymal stenosis in the presence of rhinitis and ozena, with
or without serious corneal ulcers. Adenoid growths are often pres-
ent in combination with follicular conjunctivitis (likewise an
adenoid condition) and with pustuloscrofulous (or phlyctenular or
impetiginous) conjunctivitis. Exophthalmus may be produced by
extension of nasal tumors.
(fc) Sinuses. — Many ocular and periocular conditions develop
in sinusitis (optic neuritis, iritis, detachment of the retina, orbital
abscess and orbitocranial phlebitis, paralysis of ocular muscles, etc.).
Examination of the nose and sinuses is imperative in most
affections of the eyes and especially in affections of the lacrymal
passages and orbit, just as examination of the eyes is necessary in
disorders of the nasopharynx and sinuses.
(c) Larynx, trachea, bronchi, and lungs. — Pupillary dis-
turbances (mydriasis or myosis) may occur in cases of tumor or
enlarged glands through paralysis or irritation of the sympathetic
(slight ptosis, enophthalmus, and myosis in Claude Bernard's syn-
drome). Mydriasis on the side of a diseased lung (pleurisy, pleu-
ral pneumonia, tuberculosis, etc.) is rather common. Consumption
generally runs its course, however, without any special eye dis-
turbances.
Herpes comeae, iritis, and optic neuritis occur in influenza and
pneumonia.
An extensive subconjunctival ecchymosis sometimes occurs in
whooping-cough, but is unattended with risk, no hemorrhage in the
fundus of the eye taking place.
Diseases of the Ears. — Iritis, choroiditis, optic neuritis, orbito-
cranial phlebitis, paralyses of ocular muscles — especially the abdu-
cens distribution — are met with in otitis and mastoiditis ; nystagmus,
spontaneous or induced, may be encountered.
Diseases of the Digestive Tract. — (a) Teeth and Mouth. —
Infections, such as orbital abscess and phlebitis, iridochoroiditis.
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EYES, DISORDERS OF THE. g\g
optic neuritis and keratitis. Mixed or reflex complications (neur-
algia, amaurosis, blepharospasm, glaucoma, paralyses of ocular
muscles, etc.). Coexisting disorders may be exemplified in the
oculodental stigmata of congenital syphilis, rickets, etc. Mikulicz's
syndrome, involving the lacrymal and salivary glands.
(ft) Esophagus. — Tumors, resulting in Claude Bemam's syn-
drome.
(c) Stomach and Intestine. — Enterogenous autointoxication
and intestinal infection take part in very many eye disorders.
Blindness, transient or permanent (optic atrophy), may follow
hematemesis or intestinal hemorrhage. Intraocular metastases of
visceral cancers. Ocular parasites of intestinal origin.
(d) Liver. — Choroiditis, chorioretinitis, retinal cirrhosis (retin-
itis pigmentosa with hesperanopia) , or retinal hemorrhages. Xan-
thoma of the lids, conjunctival icterus, or lithiasis conjunctivae.
Metastases in the liver are frequent in melanosarcoma of the
eye.
Diseases of the Skin. — ^Any skin disorder may occur primarily
or secondarily on the eyelids; many occur likewise on the conjunc-
tiva and even on the cornea. Similarly, diseases of the hair may
occur in the eyebrows and eye-lashes.
Blepharitis ciliaris or marginalis corresponds to the various
types of skin disorder, viz., eczema, seborrhea, folliculitis, sycosis,
etc., the exact nature of which should be inquired into in each in-
dividual case.
Among the most noteworthy general pathologic conditions,
special mention should be made of erythema multiforme, with its
huge conjunctival papules directly on the eyeball; of acute cutaneous
edema, sometimes alternating with acute glaucoma — further prov-
ing that acute glaucoma is a condition of acute edema occurring in
the eye and associated with increased intraocular pressure (A. Ter-
son), and of pemphigus, which gradually results in complete fusion
of the eyelids with the immobilized ocular globe (symblepharon).
Diseases of the Ductless Glands. — (a) Thyroid gland, — ^Ex-
ophthalmic goiter, complete or fruste (incomplete or truncated; uni-
lateral, dissociated, etc.), with exophthalmus, Graefe's sign (de-
layed motion of the upper lid when the patient looks down), tachy-
cardia and tremor. Sometimes there are inequality of the pupils,
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920 SYMPTOMS.
paralyses of ocular muscles, etc. Reduction of pulse-rate on testing
the oculocardiac refle?^.
The condition of the cornea should be watched in marked exoph-
thalntus (the cornea being examined with a lamp and hand lens) in
order to detect any incipient ulceration and to be able to apply the
emergency treatment (tarsorrhaphy, etc.).
(&) Adrenal glands, — Asthenia of the eyes, etc.
(c) Pituitary body. — Exophthalmus, nystagmus, and paralyses
of ocular muscles in conjunction with the acromegalic facies. Pro-
gressive optic atrophy.
The fields of vision should always be tested — bitemporal hemi-
anopia with loss of the two outer halves of the visual fields on
account of pressure* on the two crossed fasciculi of the optic nerve
at the optic chiasm (see Fig. 683).
(rf) Testicles and ovaries. — Effects on the eyes may be of the
asthenic, hypersthenic, or toxic types, — ^to be determined with a
varying degree of probability in the individual case.
Diseases of the Reproductive System. — (a) Male. — Gonor-
rheal ophthalmia, direct or metastatic, with scleritis, iritis, optic
neuritis, or dacryoadenitis.
(fc) Female. — Iridochoroiditis and deep-seated infections of
metritic origin, following the menopause, etc. Menstrual asthen-
opia. Optic atrophy following profuse metrorrhagia.
Retinal hemorrhages and neuroretinitis during pregnancy, the
nephritis of pregnancy (sometimes necessitating induction of labor),
or lactation. Pulsating exophthalmus. Metastatic intraocular sup-
puration (puerperal sepsis).
Purulent conjunctivitis of the newborn. Serious accidents to
the eyes (exophthalmus or orbital fracture) due to use of the for-
ceps or various other obstetrical procedures.
Diseases of the Nervousi System. — Hysteropithiatism. — Am-
blyopia and amaurosis, with sudden blindness, total or partial. The
eye-grounds are normal and the pupillary reflexes are preserved. —
Concentric contraction of the visual field with inversion of the color
fields. In some instances, anesthesia of the conjunctiva, blepharo-
spasm, facial hemispasm, strabismus, or spasm of accommodation
(special, transient myopia).
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EVES, DISORDERS OF THE. 921
Examination of the eyes is imperative, to obviate confusion (or-
ganic disturbance or simulation). ,
Neurasthenia. — Ocular asthenia (asthenopia) while at work;
muscae volitantes, ophthalmic migraine, or periocular neuralgia;
transitory contraction of the visual field due to fatigue.
Epilepsy. — Frequency of refractive defects and eye disorders,
stigmata of inherited syphilis, alcohol and tobacco amblyopia, etc.
iNsANiTY.-r-Attacks of ocular hyperemia. Auto-mutilation of
the eye, in several instances extending to the rapid tearing out of
both eyes, the preliminary incision about them being made with the
sharp finger nails.
Idiocy. — Stigmata of inherited syphilis; congenital anomalies.
Meningitis. — Mydriasis or myosis. Optic neuritis. Irido-
chorioretinitis. Tubercles of the choroid. Paralyses of ocular
muscles. Total or partial optic atrophy. Nystagmus. Strabismus.
Intracranial thrombophlebitis. — Exophthalmus, generally
bilateral. Paralyses of ocular muscles. Optic neuritis.
Encephalitis of various types. — ^Lethargic encephalitis, among
others, exhibits paralyses of the ocular muscles in successive groups
or "waves;" paralysis of associated movements (convergence);
ptosis; nystagmus.
Hydrocephalus. — Optic neuritis and atrophy; paralyses of
ocular muscles; nystagmus and strabismus. Coexisting signs of
congenital syphilis or tuberculosis.
Brain softening, cerebral hemorrhage, etc. — Amblyopia;
word blindness; hemianopia, usually homonymous, permitting of
localization of the disease in the hemisphere opposite to that of the
field defects (see Fig. 682).
Tumors. — Edema and venous congestion of the optic nerve
owing to increased intracranial pressure. Paralyses of ocular
muscles. Hemianopia. These signs, while frequently present, may
be lacking or present with conditions other than tumor. They con-
firm the diagnosis of endocranial tumor, but seldom suffice in them-
selves to localise it.
Involvement of the cerebellum, peduncles, or pons. — Syn-
dromes of Millard-Gubler or of Weber (p. 909), in conjunction with
other localizing neurologic syndromes ; optic neuritis.
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922 SYMPTOMS.
Myelitis. — Optic neuritis (optic neuromyelitis), sometimes pre-
ceding the myelitis.
Tabes dorsalis. — ^Argyll-Robertson pupil; pupillary inequality;
frequently myosis. Irregularity of the pupillary outline (oblique-
ovaloid pupil of A. Terson). Sclerous atrophy of the optic nerve,
as yet incurable and becoming bilateral in spite of the latest forms
of treatment. Highly intensive treatment further accelerates the
reduction of vision, notwithstanding the fact that these patients are
known to be syphilitic. Paralyses of ocular muscles, transient or
persistent.
General paralysis. — Inequality and irregularity of the pupils
with mydriasis and paralysis of the iris. Toward the final stage,
optic neuritis and atrophy, and motor paralyses.
Friedreich's ataxia. — Nystagmus; sometimes optic atrophy.
Little's disease. — Strabismus; nystagmus; stigmata of in-
herited syphilis.
Disseminated sclerosis. — Nystagmus; paralyses of ocular mus-
cles ; rarely, sclerosis of the optic nerve.
Intoxications. — Alcohol and tobacco. — Amblyopia, bilateral
from the start, with central scotoma.
Far vision is impaired, but the subject, while dasded by bright
light and nearly blind in broad daylight, has much better vision in
the evening (crepuscular improvement).
Near vision is greatly interfered with ; the patient is unable to
read, and distinguishes certain colors poorly (green and red), espe-
cially over a small area, on account of the central scotoma. While
he recognizes the color of a sheet of red paper, he is unable to state
the color of disc of red paper o£ the size of a dime. When the
disease is sufficiently advanced, he mistakes a dime for a silver
dollar.
This condition, if taken at the start and treated by a strict diet
and suitable remedies, may be completely recovered from if the sub-
ject does not resume his harmful habits.
The practitioner should always have an examination of the eyes
made in order to exclude certain very serious mistakes (diabetic
amblyopia, macular chorioretinitis, retrobulbar neuritis, optic
atrophy, etc.) and diagnose coexisting disorders.
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EYES, DISORDERS OF THE. 923
Many other forms of poisoning (lead, male fern, pelletierine,
iodoform, etc.) may give rise to toxic neuritis and a variety of
ocular and oculomotor disorders of a lasting or transient nature.
Ingestion of large amounts of quinine at a single dofse sometimes
induces temporary blindness, which terminates either in recovery
or in partial and lasting sclerosis of the optic nerves.
Atoxyl has been the cause of many cases of optic atrophy and
incurable blindness.
Naphthalene, when ingested, yields an experimental form of
cataract (in animals).
Botulism may bring about optic neuritis and paralyses of the
ocular muscles, including those of accommodation.
Ophthalmic Signs and Reagents Indicating Death. — Exami-
nation of the eye is of assistance in distinguishing actual from ap-
parent death and in obviating premature burial, whether under ordi-
nary or unusual circumstances (wars, epidemics, or catastrophes).
Loss of the winking reflex, loss of corneal sensibility, dilatation
of the pupil following myosis (frequent in the agonal state), a dull
appearance of the eyes, and complete opening or closure of the lids
(a very variable condition in different subjects and according to the
manner of death) constitute merely presumptive evidence. The
pupils of a corpse will often react for several hours, especially to
myotics (eserine and pilocarpine) and electric stimulation. Palpa-
tion of the eyes may be practised; they become particularly flaccid
at the end of several hours.
In S. Icard's procedure (subcutaneous staining injection of fluo-
rescin, which fails to diffuse in a dead body ) , the eye may assume a
greenish tint in a living subject; but this phenomenon is very in-
constant.
Lecha Marzo has made an investigation such as had already
been made in other regions of the body, of the existence of a post-
mortem acid reaction of the tears, which are neutral or alkaline in
the living subject, by placing a piece of litmus paper beneath the
eyelid. Unfortunately the time of appearance of the acidity, as
well as its intensity, are highly variable after actual death. Dis-
tinct acidity, it is claimed, is never present, however, in a living
subject in a condition of apparent death.
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924 SYMPTOMS.
Instillations of irritants and mechanical stimuli (scraping or
chemical or actual cauterization of the conjunctiva or of the up-
turned lids, etc.) may be tried, and will induce redness and hyper-
emia in an inert living subject. Instillation of ether (d'Halluin)
may, however, not be without risk to the cornea. The writer pre-
fers the introduction of a wheat-grain-sized amount of powdered
ethyl-morphine hydrochloride (dionin), a substance used in daily
practice without harmful results, and which induces redness and
swelling, often of considerable extent, of the conjunctiva in the eye
of a living subject.
One need not limit himself to the ocular tests of death, but they
should be utilized among the routine measures for the determina-
tion of death.
The foregoing summary considerations on the subject of com-
bined ophthalmology and general medicine may have served at least
to suggest to the practitioner the marked importance of an objective
and functional examination, whether positive or negative, of the
eyes and their adnexa in the diagnosis and prognosis of almost any
disorder affecting the human body — not to mention the cases in
which such an examination, as yet so frequently neglected or inade-
quately performed, actually permits of apprehending, arresting, or
curing a disease of the eye itself.
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FAINTING [From aiv, with, and x&JVtBiv, to cvi.^
[ Faintneas, fainting spell. J
(SYNCOPE).
True S3mcopc consists of a sudden, temporary cessation of
the heart's action. It is exceedingly uncommon. On the other
hand, faintness, semifainting, or lipothymia (from ^htislv, to
relinquish, dvfzdg, spirit) is met with rather often, and is char-
acterized by a more or less complete loss of consciousness ap-
parently dependent upon a reduction of varying degree in the
blood flow (ischemia) through the brain. The nervous and
circulatory systems are so intimately interdependent that psy-
chic and circulatory manifestations are in close association, and
the most reliable sign of syncope and of lipothymia, which sign,
moreover, allows of their immediate differentiation from coma,
asphyxia, etc., is the combined observation of a more or less
complete loss of consciousness with weakened and sometimes
slowed heart action, the latter sometimes passing into actual
cessation of the heart beats for a varying period of time. Syn-
copal states, then, are characterized:
1. By a more or less profound state of fainting and uncon-
sciousness, with more or less complete muscular relaxation.
2. By a marked weakening of the pulse (small, feeble pulse)
and of the heart beats.
3. By certain associated vasomotor and secretory disturb-
ances, ins,, pallor of the face and lips, cold sweat, cold ex- '
tremities, etc., which impart in some degree to syncope the ^
appearances of death.
It should be noted that frequently, just before the termina-
tion of syncope, a short general convulsive seizure is observed,
independently of any epileptic tendency.
Thorough realization of the three above mentioned characteris-
tic features will suffice to eliminate, usually at the first glance,
artificial fainting spells, "theatrical faints," and "suggestive syn-
(925)
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926 SYMPTOMS.
copal states" so prevalent in certain quarters, and seemingly
in all historical periods, judging from the high percentage of
**swoons" referred to in the romantic literature of all ages and
all climes. '*Clarisse Manson," wrote Lenotre (the celebrated
witness of the Fualdes episode), "succeeded in holding in
anxious suspense the attention of the entire world for two whole
years merely by swooning, a proceeding which she carried out
to perfection and repeated indefinitely without becoming fa-
tigued."
Syncope and syncopal states are met with chiefly under the
following conditions:
1. Ordinary fainting, probably due to acute anemia of the brain
(by vaso-constriction or nervous cardiovascular inhibition) acting
upon predisposed individuals when in a confined or poorly venti-
lated room, in the presence of a crowd, or unexpectedly witnessing
some accident or a hemorrhage. The sight of blood-shed regularly
causes faintness in some persons who may properly be said to be
hemophobic, and in these individuals personally experienced pain
or hemorrhage has, of course, an even more certain eflFect in this
direction. The wearing of a. corset or other tight garment, and
either the period of digestion or that of fast, plainly predispose to
fainting in some persons. In short, at the bottom of the condition
there are always found: 1. Some emotional impression (anxiety,
apprehension, pain, fear, terror, etc.). 2. An emotional neuro-
cardiovascular predisposition, finding its ultimate expression in an
exaggeration of the nervous vasomotor and inhibitory reflexes.
Allied to ordinary fainting are the faintness and lipothymic
attacks of patients with low blood-pressure, of convalescents, of
septic cases, and of cases of visceroptosis, accounted for in each
case by a manifest state of neurovascular weakening.
2. Certain minor forms of epilepsy are commonly considered
related to ordinary fainting, but in these cases the vasomotor
manifestations characteristic of syncopal states, zns,, small pulse,
coolness of the extremities, etc., are, as a rule, absent. Yet
it must be admitted that some of these conditions are very simi-
lar to syncope. They should always be thought of in the pres-
ence of recurring pseudolipothymic attacks or repeated faints
ot obscure causation.
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FAINTING. 927
3. Certain cerebrocardiac forms of arteriosclerosis, especially
if accompanied, as is the rule, by aortitis, may lead to particu-
larly dangerous syncopal states. The fatal syncope of the major
forms of angina pectoris belongs in this group. It is mainly
the possibility of such an occurrence that furthers an unfavor-
able prognosis in the latter disorder. Yet it should be mentioned
and repeated that even in the major forms of angina pectoris,
even in the presence of definite and extensive aortk lesions,
such as dilatation or actual aneurysm, and even wijth a rather
marked elevation of blood-pressure, fatal syncope is exceptional
and, in any case, perhaps, is generally long delayed. The author
has had, and still has, under observation such subjects for peri-
ods of ten or twtlve y^ars or over.
For practical pmrposes the following general rule may be
adopted :
Syncope is ordinarily a mild condition in young individuals;
on the other hand, it is always a serious, at times a dangerous, and
sometimes even a fatal, occurrence in old persons,
4. The fainting of paroxysmal bradycardia (Stokes- Adams'
disease) is easily diagnosticated if one merely takes care to count
the pulse (see Arhythmia: Auriculoventricular Dissociation). A
subsequent thorough general examination and, if need be, a good
polygraphic tracing will eliminate all doubt.
5. Chloroformic syncope is, as is well known, a dangerous
manifestation. Following are the warning signs of this condition,
as recalled by Desfosses:
(a) Respiration: Arrest of respiration occurring together with
pallor of the face.
(&) Facial appearance: "If the face is seen suddenly to become
blanched or dusky, and the pupil to dilate, this means that the
respiration, or perhaps the pulse, has just stopped; the result is
'white syncope.' The patient is in extreme danger."
(c) Condition of the pulse: "If the pulse stops, there is present
cardiac, syncope, a very serious or 'white syncope' ; but as a rule
the arrest of respiration will already have served to warn the care-
ful anesthetist."
(d) Examination of the eye: "If the pupil, after having been
contracted, suddenly dilates, the corneal reflex should be tested at
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928 SYMPTOMS.
once; if present, vomiting and return to consciousness are to be
apprehended; if not present, a severe syncopal attack is to be
feared."
6. All weakening, exhausting, debilitating illnesses lead to a mani-
fest predisposition to faintness, which may pass into actual syncope.
The mere change from the horizontal to the vertical position is
sufficient, in many convalescents, to bring on a lipothymic attack.
Sphygmomanometric study of these cases reveals in this connec-
tion a considerable d^free of tachycardia with markedly low blood
pressure. As is well known, in such cases a post-infectious
adrenal insufficiency, with low pressure, asthenia, and Sergent's
white line, is nearly always found. This seems to be the case, in
particular, in attacks of pernicious malarial fever (of the syncopal
type).
7. Cases of syncope in the presence of extensive pleural effu-
sion, with large areas of flatness, have been reported. "Do not
wait till the patient faints to tap," wrote Trousseau. Doubtless
it is through having followed this rule that the author has never
witnessed syncope in these cases, neither spontaneously nor
during the process of tapping.
8. Any extensive hemorrhage, e.g., the intestinal hemorrhage
of typhoid fever, the intraperitoneal hemorrhage of extra-uterine
pregnancy, postpartum hemorrhage, internal hemorrhage follow-
ing wounds of the chest or abdomen, or an uncontrolled ex-
ternal hemorrhage, bring on a syncopal condition which may
pass into fatal syncope.
Syncopal states are, as a rule, easily distinguished, as was
previously pointed out, from "s3mcopomorphic" hysterical seiz-
ures by their shorter duration (hysterical coma persists for min-
utes or hours; syncope only for seconds), the existence of an
actual provocative cause, and especially, the observation of
actual cardiac and vasomotor disturbances, such as slowing, or
suppression of the pulse, pallor, cold sweat, cooling of the tis-
sues, etc.
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FEVER. [Febris, from ^eSofiai, to tremble.]
In practice, the words "fever," "pyrexia," and "hyperthermia"
are often used indiscriminately, without marked disadvantage.
A patient is spoken of as having "fever" when his temperature
is continuously above the normal.
The rectum and the floor of the mouth are the points of election
for taking the so-called ''central" or "internal" temperature. In
adults the normal internal temperature ranges between 37° and
37.6° C. (98.6° and 99.68° F.), the physiologic oscillations of tem-
perature during the 24 hours, and the difference between the mini-
mal or morning and the maximal or evening temperature being
sometimes as great as 0.5 to 0.6° C.
The axilla and the inguinal fold are the points of election for
taking the so-called ''peripheral" or "superficial" temperature. In
adults the normal superficial temperature ranges between 36.4® and
37° C (97.52° and 98.6° F.), with diurnal oscillations of 0.5 to
0.6° C. There is thus a mean interval of 0:5° C. between the in-
ternal and superficial temperatures. The sources of error, how-
ever, vis., sweating, cooling of the surface, and faulty mode of
application of the thermometer, are much more pronounced over
the surface.
Preference should, therefore, be given wherever possible to the
internal temperature. Ordinarily the internal, rectal, and oral tem-
peratures are the same ; but sometimes they are markedly different ;
it should be borne in mind that a local inflammation or hyperemia,
as in proctitis, hemorrhoids, high portal pressure, etc,, may result
in a localized h)rperthermia unaccompanied by true fever {i.e,,
there is no actual pyrexia). The author has seen patients considered
febrile and kept in bed for weeks or even months because of a
rectal temperature persisting in the neighborhood of 38° C.
(100.4° F.), but having no true fever, as was later proved by regu-
lar and careful notation of an absolutely normal buccal temperature
59 (929)
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930 SYMPTOMS.
(37° to 37.4° C— 98.6° to 99.32° R), a pulse rate of 60 to 72,
and the absence of all symptoms, in spite of persistence of the
rectal temperature in the vicinity of 38° C. All these were cases
of proctitis, hemorrhoids, portal hypertension, or congestion of the
liver. Sometimes . repeated introduction of the thermometer, two
or more times a day, or the local use of irritant antiseptics seem
to be the exciting cause of the local irritation.
In a general way, as is well known, fever is an indication of the
Fig. 685. — Respiratory type of influenza.
presence of infection. Clinically, the equation, fever = infection,
is justified in 19 cases out of 20. There remains, however, a small
percentage of non-infectious fevers, to be briefly discussed later.
To review all the causes of fever would thus entail a tiresome enum-
eration of all the infections, with the further addition of a few non-
infectious forms of pyrexia.
As a matter of fact, the solution of the clinical problem of fever
is sometimes immediately manifest; erysipelas, herpes, the eruptive
fevers, etc., become plainly apparent sooner or later.
In other instances the cause remains for a long time, if not
permanently, obscure, and for a solution of the problem application
of the most recent technical procedures is required.
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FEVER. 931
From the exclusive standpoint of practical diagnosis, a useful
clinical division of fever is that into:
Fevers of short duration, lasting altogether not over two
weeks.
Fevers of long duration, persisting over two weeks without
descending to normal.
Intermittent fevers, or recurring fevers, made up of variable
periods of pyrexia separated by intervals of apyrexia.
Little need be said concerning the fevers of short duration,
since in these cases either the diagnosis becomes more or less
Fig. 686.^Frank pneumonia in an adult
plain sooner or lat^, or, if the cause remains obscure (as is
often the case) , more or less prompt recovery occurs in any case,
thus settling the main practical question of import to the patient
as well as to the physician.
In this group of fevers are encountered:
The eruptive fevers or exanthemata: Measles, scarlet fever,
rubella, etc., and diphtheria. .
Common or specific infections of the respiratory tract: Catarrhal
conditions, acute bronchitis, sore throat, pharyngitis, pneumonia,
bronchopneumonia, etc. ; also influenza, etc.
The ordinary gastro-intestinal infections: Febrile gastric up-
sets, acute gastro-enteritis, appendicitis, etc.
Acute infections of the various other systems and structures:
Acute arthritis, lymphangitis, pelvic infections, sinusitis, erysipelas,
poliomyelitis, etc.
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932 SYMPTOMS.
In truth, most of these fevers of short duration are actually
of unknown etiology and origin, or at least are "non-specific," and
many of the terms applied to them, such as cold, grippe, influenza,
febrile pains in the limbs, ephemeral fever, rheumatoid fever, etc.,
are none other than makeshift "clinical labels" applied to "cryp-
togenic fevers," generally mild and of brief duration.
Further, some of these conditions, persisting for unduly long
periods, may pass into the group of the fevers of long duration,
to be next considered, and conversely, a few of the clinical states
ordinarily attended with fever of long duration may be cut short
in some unusual way and fall into the present group. The possible
occurrence of such exceptional cases should be kept in mind. For
practical purposes the general division given above nonetheless re-
mains of marked clinical service.
The fevers of long duration are attended with a more urgent
need of proper diagnosis because in them prompt recovery,
which would quickly solve the clinical problem in spite of the
physician's doubt, fails to occur.
In 90 per cent, of cases the underlying condition is either
tuberculosis, typhoid fever, septicemia, or deep-seated suppura-
tion.
The remaining 10 per cent, of cases refer to a wide variety
of conditions, including rheumatic feVer, influenza, meningitis,
chronic appendicitis, leukemia, syphilis, cancer, etc.
Cabot's statistics, referring to 784 febrile cases recorded at
the Massachusetts General Hospital, are as follows:
Typhoid fever 586
Sepsis 70
Tuberculosis 54
710 (90 per cent).
Meningitis 27
Influenza 10
Acute rheumatism 9
Leukemia 5
Cancer 2
Syphilis 2
Trichiniasis 2
Cirrhosis 2
Gonorrhea 2
Scattering 11
74 (10 per cent).
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FEVER, 933
These statistical results manifestly do not in the least represent
those of private practice; the disproportionately great number of
typhoid cases is accounted for by the special concentration of these
Fig. 687. — Temperature chart in a case of acute miliary tuberculosis with
onset suggesting typhoid fever (Letulle and Debri),
cases in the Massachusetts General Hospital. In private practice
tuberculosis, deep-seated sepsis, and the indefinite infections labelled
Fig. 688. — Infectious pericarditis.
influenza and rheumatism greatly exceed typhoid fever. Yet, on
the whole, in private practice as in the statistics above presented,
it may be said that 98 per cent, of the cases of prolonged fever
fall, in the order of frequency, under the five following headings:
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934 SYMPTOMS.
Tuberculosis, sepsis of visceral origin, influenza, rheumatism, and
typhoid fever.
In tuberculosis, certain localizations of the infection are practi-
cally obvious, e.g., tuberculosis of the bones and joints, lymphatics,
peritoneum, meninges, reproductive organs, and pleura. It is par-
ticularly the pulmonary and the renal forms that may remain latent
for a rather long period. The diagnostic means at the physician's
disposal in modern special procedures are known to all: Ausculta-
tion, fluoroscopy, inoscopy, inoculation, etc.
Among the septic conditions one should think:
Fig. 689.-— Typhoid fever, with recovery (IVidal and Sicard).
1. Of infectious vegetative endocarditis, malignant and septic,
very insidious, but revealed to a certainty by careful auscultation,
by the characteristic temperature curve (the large oscillations of
septicemia), and sometimes by complications (embolism).
2. Of puerperal and post-puerperal infections, generally obvious.
3. Of visceral infections, viz., in the order of frequency:
Appendicular and peri-appendicular infections.
Cystic (gall-bladder), pericystic, and hepatic infections.
Urinary infections, renal and perirenal.
Genital infections, pelvic, prostatic, etc.
Gastrointestinal infections.
4. Of pleural infections.
5. Of lymphatic infections, lymphangitis, erysipelas, or abscesses.
Deep-seated visceral abscesses, particularly those of the kidney
and liver, are at times the hardest to detect because local symptoms
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FEVER, 935
are often absent. All the resources of modem clinical investigation
are to be availed of in such cases. It is in respect of these cases
that the author has committed and seen committed the greatest
Fig. 690. — Malaria. Intermittent fever of quotidian type (Laveran).
mistakes in diagnosis. The possibility of these conditions should
always be thought of in prolonged "cryptogenic" fever.
In influenza with protracted fever, the chief problem, on the
Fig, 691. — Malaria. Intermittent fever of quotidian t)rpc, then
tertian, and finally quartan {Laveran),
whole, is to ascertain whether a threatening tuberculous infection
is not concealed behind the screen of the acute infection, and if
some deep-seated complication (liver, kidney, etc.) has not stepped
in and changed the usual course of the disease. The diagnostic
problem merges with that above referred to.
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936 SYMPTOMS.
In acute articular rheumatism and the post-infectious rheumatic
states, the joint involvement and the history generally render the
diagnosis obvious.
The diagnosis of typhoid fever, the paratyphoid fevers, and
typhobacillosis is founded on the frequently typical temperature
curve, the sometimes very definite clinical picture, and especially
on the modem methods of blood examination — serum diagnosis,
blood cultures, and inoscopy.
Many cases of prolonged, obstinate febricula in childhood and
even in adults, with temperatures of 36"* to 37** C. (96.8'' to
98.6^ F.) in the morning and 37.5^ to 38.2^ (99.5'' to 100.76° F.)
in the evening — accompanied at the latter period* by slight malaise —
wrongly ascribed to tuberculosis, are undoubtedly of pharyngeal
origin,
♦ ♦ ♦
The above mentioned febrile affections make up, as already
pointed out, 98 per cent, of all cases of prolonged fever. The
remaining 2 per cent, comprise a great variety of disorders, such
as secondary syphilis (always to be kept in mind), meningitis (soon
revealed by headache, Kernig's sign, etc.) and meningococcal con-
ditions (often associated with herpes), the leukemias, rapidly grow-
ing malignant tumors (particularly cancer of the liver), Hodgkin's
disease, Malta fever, etc.
Mention should also be made of certain exceptional and gener-
ally obvious conditions, such as wounds and diseases of the brain
(cerebral hemorrhage, acute delirium, tumors, and skull fracture),
belladonna poisoning, and toxic gas poisoning.
The majority of these clinical conditions are, as may be noticed,
non-infectious.
Along with tliis group may be cited the highly characteristic
pyrexia of exophthalmic goiter, always of moderate degree, vis,,
38"* C. (99.5** F.) or below, accompanied by a frequent pulse, gen-
erally reaching its maximum in the morning — as does likewise the
pulse rate — and its minimum in the evening. With this form of
pyrexia may, with Leopold-Levi, be contrasted the customary
hypothermia of cases of thyroid insufficiency, both these condi-
tions being associated, moreover, with the usual concomitant dis-
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FEVER. 937
turbances of disordered thyroid function, vis., circulatory disturb-
ances (vasomotor or congestive), secretory disorders (hyper-
idrosis), and sensory symptoms (itching, burning sensations, etc.).
December Januaiy
Intennltteiit feff«r ct hepttio orlsln (euppttrattve aagloctioUUs).
Hay AsrU
Blllo-feptlo fei?«r. Berersed type of intermittent hepatic ferer.
Aaguit
Fever in relapilng Jaundice (Weil-Matlileu's disease).
Fig. 692.— Intermittent types of fever of hepatic origin (Lereboullet) ,
This type of hyperthermia may occur in nervous, neuroarthritic
patients, during rapid growth, in persistent juvenility, in the vari-
ous Basedow disorders, in thyro-testicular cases, at all periods of
the reproductive life in the female, and in some high pressure
cases.
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938
SYMPTOMS.
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Local evidences.
Irregular, erratic fever.
Local evidences. Aus-
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s.
Continuous fever. Rose
spots. Enlarged spleen.
Typhoid state, etc.
Headache, backache, in-
fluenzal tongue, respir-
atory catarrh.
Signs of arthritis, some-
times with secondary
involvements of endo-
cardium and pleurae.
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Infective
focus.
Heart.
Lungs.
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Overwork.
Poor nutrition.
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carriers.
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Cold and damp-
ness.
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culosis.
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arthritis
(rheuma-
tism).
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FEVER.
939
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940 SYMPTOMS.
This fever of neuropathic origin may be compared with the
so-called purely "nervous," "hysterical," or "psychic" fevers, our
knowledge of which is as yet very deficient. How shall one ac-
count for the "admission fever" noticed when a patient enters a
hospital, apparently a very real pyrexia, and the "Sunday fever,"
observed when visitors are admitted? In truth, many different
factors may be operative under these circumstances.
Intermittent Fevers. — In practice this group of fevers is repre-
sented in our climes by malaria, detected from the history (fonner
residence in a malarial district), the intermittent type of the fever,
the enlarged spleen, and examination of the blood for the causal
parasite.
Relapsing fever is very exceptional in temperate climates.
It should not be overlooked, however, that this intermittent or
recurrent form of fever may be caused by non-specific, non-exotic
infections, foremost among which are:
Hepatic intermittent fever (bilio-septic fever), especially fre-
quent in angiocholitis and quite precisely reproducing the appear-
ances of malarial intermittent fever, sometimes even to the extent
of showing a maximum of temperature in the morning, constitut-
ing a "reversed" type of fever (Gilbert and Lereboullet). The
fever may be remittent or even at times continuous in type (see
page 937).
Urinary intermittent fever (uroseptic fever), especially com-
mon in pyelonephritis, involves precisely the same considera-
tions.
Yet, while these infections may present the appearances of an
attack of sudden onset, running a more or less rapid course, well
maintained and with typical recurrences, they never exhibit
the characteristic feature of regular intermittence shown in the
true malarial paroxysms.
♦ ♦ ♦
In conclusion, it may be well to recall, with Edmond Lesne,
the following point of practical importance, viz,, that "the in-
ternal TEMPERATURE OF THE BODY MAY BE CAUSED TO RISE BY ONE
OF A NUMBER OF DIFFERENT FACTORS," which may be enumerated
thus: •
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FEVER. 941
(1) Elevation of the external temperature; (2) tetanic muscu-
lar contractums; (3) lesions of the nerve centers; (4) infections.
When present in combination, these several factors bring
about the so-called ** hyperthermic fevers," e-g., in meningitis at-
tended with convulsions.
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FREQUENT PULSE.
Tachycardia, or frequent pulse, is marked by a more or less
pronounced and persistent acceleration of the heart beats. Nor-
mally, in sitting or recumbent subjects, the pulse frequency
ranges from 60 to 80 in different individuals, at different times
of the day, in accordance with the intervals before or after a
meal, etc. For practical purposes, tachycardia or frequent pulse
can hardly be said to exist unless the rate exceeds 90; it may
attain and even exceed 200.
Accelerated heart action is a ccwiimonly and easily observed
condition. Its clinical meaning is sometimes obvious and of slight
import ; under other circumstances, however, its significance is so
great as to make of it a separate morbid entity, viz., paroxysmal
tachycardia, a condition which has excited wide interest among
modem clinicians. Rather frequently the proper interpretation of
a frequent pulse proves a matter of considerable difficulty.
For practical purposes, the frequent pulse may be said to occur
in three separate modalities which lend themselves to rapid differen-
tiation: 1. More or less permanent tachycardia. 2. Attacks of
paroxysmal tachycardia. 3. Temporary, accidental attacks of tachy-
cardia.
I. More or Less Permanent Tachycardia. — This is met with
under two groups of circumstances, sometimes clearly defined
and separate, at others in combination.
(a) In the presence of a recognized heart lesion, such as myo-
carditis, pericarditis, and valvular disorders, especially aortic.
{h) In the absence of any recognised heart lesion:
(1) Graves's disease (exophthalmic goiter).
(2) Tachy cardie neuroses.
(a) The frequent pulse occurring as a symptom of organic
heart lesions should generally be attributed to a more or less
pronounced weakness of the myocardium. The reduction in the
(942)
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FREQUENT PULSE.
943
tachycardia following rest, good hygiene, and digitalis when
properly administered constitutes evidence of the truth of this
supposition. The results of the static and dynamic tests of the
circulation may be said to afford also an experimental demon-
stration. This type of frequent pulse is met with in associa-
tion with myocarditis (particularly post-infectious), pericarditis,
and endocarditis, especially aortic. The diagnosis should be
based on: 1. The presence of the characteristic clinical signs
of these conditions. 2. The results of the special test of the
circulation already referred to. 3. The effects of treatment, as
by rest, diet, and digitalis. What remains in the way of a
I I I I I 4 I I
• I«|4I|I||1||
• I I I I I I
Fig. 693.— Diagram representing a brief attack of paroxysmal tachy-
cardia consisting of 8 auricular extra-systoles. With each auricular im-
pulse there corresponds a ventricular contraction. Note the abrupt onset
and termination of the attack and the abnormal prolongation of the
terminal pause.
tachycardia under these circumstances constitutes an index
either of irreducible myocardial weakness or of a concomitant
tachycardic neurosis.
Tt should be borne in mind, moreover, that in some individ-
uals the most varied forms of tachycardia may be observed
occurring in succession, viz., tachy-arhythmia, paroxysmal tachy-
cardia, persistent tachycardia of the Graves's disease type, pre-
mature contractions, etc. These cases are exceptional, but many
instances of them have nevertheless been recorded.
{b) "Yet," as Gallavardin correctly writes, "it must be con-
fessed that bordering on these sinus tachycardias of known origin
there occurs a vast group of tachycardias of poorly determined
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944 SYMPTOMS,
origin, generally appearing in young or adult subjects, and concern-
ing which comparatively little is known. Some of these cases are
unquestionably to be ascribed to a fruste Graves's disease, for, in
spite of the absence of any ocular sign of this disorder, careful
examination often elicits a small nodular goiter or merely a neck
slightly broadened at its base, with slight diffuse enlargement of
the thyroid lobe (usually the right). In other instances, however,
nothing is found upon examination of the thyroid. These cases
are well known, and no physician exists who has not seen some
of them; it would seem well to group them provisionally under
the generic term tachycardic neuroses. The accelerated heart
Fig. 694.— Heart weakness. (H., 1893; 165 cm.; 60 kilogr.)
Experimentally induced tachycardia.
action, an aggregate of symptoms of disturbed function, some-
times highly distressing (palpitations, breathlessness on exertion,
and various painful reactions), and lastly, the absence of any notice-
able cardiac lesion constitute the basic symptomatic triad which
may serve as a foundation for all the cases of this kind."
The frequent pulse of Graves's disease origin is obvious from
the recognized symptomatic accompaniments of this condition,
vis,, tachycardia, exophthalmos, hyperthyroidism, and second-
arily, tremor and vasomotor disturbances.
The tachycardias of cryptogenic origin (tachycardic neu-
roses) already mentioned are, aside from the absence of exoph-
thalmus and of hyperthyroidism, identical with the tachycardia
of Graves's disease.^
iSee Martinet: "War and the Cardiac Neuroses" (Presse mid,, Nov.
5, 1915).
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FREQUENT PULSE, 945
Both forms are enhanced by exercise, are only rarely accom-
panied by dyspnea or premature contractions, and are but
slightly or not at all influenced by compression of the eyeballs
or treatment with digitalis ; a moderate elevation blood-pressure
is nearly constant in these cases. A very common, if not con-
stant, phenomenon should also be referred to, viz., inversion of
the temperature and pulse rate, the pulse frequency diminishing
while the body temperature ascends. Gallavardin has made a
special study of this phenomenon, and the author of this work
has frequently had occasion to see it. Tachycardia of this type
Fig. 695. — ^Tachycardic neurosis (Case V, 458, H.,
1896, 178cm.;65kilogr.).
Note the rise in heart-rate each morning.
is at its maximum in the morning and its minimum in the
evening.
The author freely agrees with the conclusions expressed by
Gallavardin :
"In the two instances (fruste Graves's disease and tachycardic
neuroses), the clinical syndrome is really the same. There is the
same variability in the heart acceleration, the same morning type
of tachycardia, the same change in the temperature and pulse rate
cycle, and the same clinical features, with continuous or temporary
tachycardia. The condition may always be summarized as an in-
tense excitation of the sympathetic, with not only a cardio-acceler-
ator, but also a vasoconstrictor and blood-pressure-raising and even
00
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946 SYMPTOMS.
a thermic action. One must actually make bold to state that these
two varieties of patients differ only as regards the neck enlarge-
ment,
"Hence two modes of interpretation are allowable. Is one deal-
ing with two thyroid disorders, the one with a manifest goiter, the
other with some concealed change in the thyroid (small adenomas,
defects in the internal secretion), or merely with two pathogeneti-
cally distinct syndromes of sympathetic excitation, the one of thy-
roid origin and the other of unknown causation? While the first of
these two theories seems the most likely and many authors have
already spoken of cases of fruste Basedow's disease, without goiter,
and with tachycardia alone present, it will be wise, before reaching
a conclusion, to await positive proof.'*
Tachyc parojys 26.2 13, *-
Fig. 696. — Paroxysmal tachycardia {Routier).
In this group of casts belongs the continuous post-emotional
form of frequent pulse.
II. Attacks of paroxysmal tachycardia, coming on, as the term
implies, in paroxysmal outbursts, starting and ending abruptly.
The very nature of the attacks of tachycardia, their marked clinical
autonomy, and their rather clearly elucidated pathogenesis, as de-
veloped in late years, which makes of them actual extra-systolic
seizures brought on by the coming into play of an abnormal center
of cardiac motor excitation — ^all these facts contribute to their for-
mation into a special group of tachycardias which are really abnor-
mal, arhythmic, and, as a rule, readily distinguished.
The diagnosis of this disorder is rather easy. It may be put
down as a definite rule that any tachycardia exceeding 110, of
abrupt onset, unaccompanied by exophthalmic goiter, not coming
on in association with some febrile disorder, and the rate of zvhich
is not greatly altered by passage from the recumbent to the up-
right posture, is a paroxysmal tachycardia. The only difficulty
arises in subjects seen for the first time, whose history is not
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FREQUENT PULSE.
947
known, and who, in conjunction with tachycardia of varying de-
gree, present obvious signs of heart failure, such as dilatation of
the heart, edema of the lungs, congestion of the liver and enlarged
spleen, reduced urinary output, and edema. In such cases it may
Right jugular.
1
Right radial.
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Fig. 697.— Case 1219, Mar. 18, 1915 (F., 1867; 158 cm.; 48 kilogr.).
Attack of paroxysmal tachycardia of a few minutes' duration (/, be-
ginning; ^, middle; j, end of attack) in an improved case of exophthal-
mic goiter at the menc^ause. Note the abrupt onset, abrupt termination,
and clearly extrasystolic terminal period.
be difficult to ascertain whether the paroxysmal tachycardia was
the initial morbid manifestation or, on the other hand, the tachy-
arhythmia witnessed is not a secondary result of the impaired heart
action. The sudden onset, accurate graphic records, and the thera-
peutic test with digitalis will settle the question.
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948 SYMPTOMS.
III. Temporary, accidental attacks of tachycardia are those
in which there is simply acceleration of a heart beating in normal
rhythm. The most common and manifest causes of such attacks
may be briefly recalled as follows:
(a) Fever. — Pulse acceleration and hyperthermia are the two
characteristic, clinical, and essential features of fever. As is well
known, in some kinds of fever, as in meningitis, peritonitis, etc.,
there may be noted a discrepancy between the degree of hyper-
thermia and the increased pulse rate, and such a discrepancy is
in itself a clinical indication of by no means negligible value.
Fig. 698.— Case V, 750 (H., 1897; 168 cm.). Post-infectious
pericarditis with extensive effusion.
It should also be remembered, as will be mentioned again later,
that hyperthermia may exert a sedative, slowing action on certain
forms of continuous tachycardia (Graves's disease, tachycardic at-
tacks). In one case of pericarditis with extensive effusion (in
which puncture was carried out) which the author had occasion
to observe closely for a long period, two successive attacks of acute
suppurative otitis media caused, in addition to marked fever (39°-
40° C), an equally pronounced slowing of the pulse, which was
reduced in the two attacks from 124 to 104 during the period of
fever, rising again to 120 or above in the interval and after the
second attack. Herein lies a rather odd application of the well-
known aphorism: similia similibus curantur.
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FREQUENT PULSE, 949
(&) Exertion. — That the pulse rate rises during exertion, and
ascends to a degree varying with the extent of the exertion and
its duration, is a matter of common observation. Upon the basis
of this fact the author has devised a test of induced tachycardia
brought on by a standard amount of exertion, which affords some
measure of information concerning the reserve power of any given
heart. In a general way it may be asserted that after a medium
amount of exertion the acceleration of the pulse as compared to
the rate while at rest is less, and the return to the status quo ante
after cessation of exertion more rapid, according to the amount
of reserve power possessed by the heart.
^ ^ SltUng
mmtrnn^ Recumbent
I I I StandiDg
L L L Dipping exercises
1*2*3* Time in minutes
it,,
^PSfi ^1 Blood-pressures
Ma"
!••••• Pulse frequency
Fig. 699.— Normal individual (H., 1884; 149 cm.; 46.5 kilogr.).
Experimental tachycardia, after exercises.
(c) Posture. — Acceleration of the pulse due to passage from the
recumbent to the upright posture, or orthostatic tachycardia, is
likewise a well-known event. Prevel seems to have found out an
essential factor in this, form of tachycardia, ascribing it largely to
visceroptosis, making of it an abdominocardiac reflex, and demon-
strating that it can be reduced or eliminated by the wearing of
an abdominal support.
{d) Emotion. — The well-known ''doctor's pulse," an emo-
tional tachycardia which the physician regularly observes, es-
pecially at his earlier visits, should not lead him into error; it
generally subsides after he has been talking with the patient
for a few minutes. Pulse acceleration is one of the most con-
stant somatic signs of the emotional syndrome. There actually
exists an emotional tachycardic constitution — a true tachycardic
neurosis.
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950
SYMPTOMS.
(e) Pain. — Many forms of visceralgia bring on an evanescent
reflex tachycardia, the source of which may be as likely fotmd in
the uterus as in the pleura.
(/) Certain kinds of intoxication, among the foremost of which
should be placed coffeeism and teaism, caffeinism (caffeine) and
theobrominism (theobromine). At first the heart acceleration is
transitory and present only during the period of intoxication ; later,
however, there may be seen to develop an actual tachycardic neu-
rosis. Hence the rule, which is, on the whole, frequently justified,
of forbidding the use of tea and coffee in persons with "excited"
hearts.
Lastly, it may be noted that while the heart-rate is in normal
subjects entirely independent of cerebral volition, 15 authentic cases
have been recorded in medical literature of individuals who could
at will markedly increase the frequency of their heart beats.
TACHYCARDIA.
I. ParoxjrsmaL
II. Temporary. AccidentaL Easily referred to the follow-
ing causes:
1. Fever: Febrile pulse acceleration.
2. Exertion: Pulse acceleration on exertion.
{Experimental pulse ac-
celeration (cardiac
functional test).
4. Emotion: Emotional pulse acceleration.
5. Pain: Algic pulse acceleration.
6. Intoxications: Toxic pulse acceleration (tea, coffee, caffeine, kola,
theobromine).
III. Continuous.
A. In the presence of a recognized heart lesion: Frequently a re-
active effect of heart weakness or failure.
B. In the absence of any recognized heart lesion.
B^. Graves's disease:
(a) Cardinal symptoms: Accelerated pulse, exophthalmos, hyper-
thyroidia (goiter).
(&) Accessory symptoms: Tremor, vasomotor disturbances, exces-
sive nervousness.
B*. Tachycardic neuroses. Features same as those of Graves's
disease, with the exception of the goiter and sometimes the
exophthalmos. "These two kinds of disorder differ only in
the appearance of the neck." (Gallavardin).
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GENITAL ULCERATIONS.
Recognition of the cause of ulcers on the genitals is, on ac-
count of the frequent presence of syphilis, of great clinical im-
portance. A condensed tabular presentation of the main facts
in this connection seems, therefore, appropriate.
Fig. 700. — Axillary lymph-nodes, with the afferent and efferent
lymphatic vessels {Sappey).
1, 1. The two most dependeDt nodes of the inguinal chain, alike remarkable
because of their size. £. Inferior lateral inguinal node. S, S. Mesial inguinal
nodes, receiving lymphatic vessels from the scrotum, perineum, anal region, and
upper and inner portion of the skin of the thigh. 4. Superior mesial inguinal
node, receiving vessels from the urethral canal, the surface of the glans, and the
skin of the penis. 5, 5. Superior medial and lateral inguinal nodes. 3 or 4 in num-
ber, receiving lymphatic vessels, from the abdomen below the umbilicus. 6, 6.
Lymphatic vessels of the anterior and inner portion of the thigh. 7. 7. Vessels
from the outer aspect of the thigh. 8, 8. Vessels from the buttocks. 9, 9. Ves-
sels of the lumbar region. 10, 10, 10. Vessels of the anterior abdominal wall be-
low the umbilicus. 11, 11. Lymphatic vessels of the scrotum. If. Lymphatic ves-
sels of the prepuce. IS, IS. Lymphatic vessels of the skin of the penis. H.
Lymphatic trunk coursing about the corona of the glans. 15. Mesial trunk con-
nected with the preceding. 16. Umbilicus.
(951)
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952
SYMPTOMS.
Fig. 701.— ^Hard chancre of the penis (Sabouraud),
Fig. 702. — Chancroidal pus, stained
with methylene blue.
Fig. 703. — Scrapings from hard
chancre. (Giemsa stain).
Figs. 704 and 70S. — Unusual papulohjrpertrophic chancroids of the
balanopreputial region (Marcel F errand).
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GENITAL ULCERATIONS.
GENITAL ULCERATIONS.
953
Macroscopic
Appbabanci.
Incubation
PERIOD.
Glandulab
Bnlabgbmbnts.
ASSOCIATED
CLINICAL
EVIDENCES.
CODBSE.
Vabious Tests,
micboscopic
Examination.
Hard Chancre.
1. Flat ulcer,
non-suppura-
tive, generally
single.
2. Resting on
a plate of car-
tilaginous in-
duration (see
Fig. 701).
Fourteen to
twenty-eight
days after
coitus.
Later on, rose-
olar eruption,
mucous
patches,
patchy alo-
pecia, etc.
In contrast to chan-
croidal glandular
enlargement, the
non - inflammatory
nature of the
glandular enlarge-
ments attending
chancre is to be
noted.
1. Ricord's Plei-
ades.
Secondary syphilitic
multiple glandular
enlargement.
Multiple, elastic,
movable, and pain-
less glands.
2. Indicating (pri-
marily enlarged)
gland, or satellite
of the chancre,
somewhat larger.
Apart from the initial specific lesion, ssrphilis may be manifested
on the glans penis in several other ways:
1. Papules: Secondary papular syphilides, varying in number.
(Recognized from the history, absence of lymphatic reaction, and
the effects of specific treatment).
2. Gummas: Rather rare; gummatous nodules undergoing absorp-
tion under treatment or terminating in vicious and deforming scars.
3. Chancriform gummas: Similar to the initial lesion (false rein-
fection, false S3rphilis redux, etc.); no roseolar eruption and no
glandular enlargement
Later on, the sec-
ondary stage.
Positive Wasscr-
mann test.
Negative reinocu-
lation in the same
subject upon in-
sertion by punc-
ture of material
from the initial
lesion.
Ultra-microscopic
examination.
Giemsa stain.
Schaudinn's pale
spirochete (see
Fig. 703).
Chancroid.
\. Vesiculo-ul-
cerations.
2. Then suppu-
rating ulcers.
3. Then mul-
tiple punched-
out ulcers,
suppurating
freely, with-
out induration
(see Figs. 704
and 70S).
Appear four to
eight days
after coitus.
1. Single bubo,
soft, painful, ter
minating in suppu
ration and ulcera
tion.
2. Ganglionic soft
chancre, ulcerated
and suppurating.
In some in-
stances : pha-
gedenic tend-
ency.
Ordinarily,
rather quick
recovery with-
out sequelae.
Positive reinocula-
tion in the same
subject upon in-
sertion by punc-
ture of pus from
the original
lesion.
Bacillus of Ducrey
(see Fig. 702).
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954 SYMPTOMS.
ed
ita.
)enlng
to the
irrow.
Fig. 706. — A burrow in scabies Fig. 707. — Deep-seated vulvar he)i>es
(Darier). (Darter),
Figs. 708 and 709. — Vegetations on penis (Musee de Saint-Louis),
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GENITAL ULCERATIONS.
955
GENITAL ULCERATIONS {continued).
Macroscopic I
ASSOCIATED Clinical
Appearanci.
Glandular
Evidences.
Incubation period.
ENLARQBMBNTS.
Course.
Various Tests.
. , ...
Herpes.
1. Vesico-pustules
Glandular reaction
Sometimes recurrence
grouped together, then,
very slight or
in situ with discour-
2. Superficial, circinate,
wanting.
aging obstinacy.
polycyclic ulcerations.
One or two days after
irritation or without
appreciable cause.
Scabies.
1. Round, red, flat, al-
Glandular reaction
1. Itching in nocturnal
most papular spots.
very slight or
paroxysms.
2. Sometimes distinct
wanting.
2. Lesions due to scratch-
burrows.
ing.
3. Similar lesions on the
3. Lesions at the points
of election : Groins,
prepuces, in the groins
and axillae, etc.
armpits, forearms, etc.
Characteristic feature of
4. Characteristic bur-
the acquisition of an
rows.
itching affection by
Itch parasites in the
contact
burrows. (See Para-
sitology and Itching.)
Cauliflower or coxcomb genital vegetations.
1. More or less promi-
Glandular reaction
Persistent, rebellious.
nent papules ulti-
very slight or
and recurrent owing
mately forming, by
proliferation :
wanting.
to a manifest predis-
position to epithelial
2. Excrescences, tumor-
proliferation.
like masses, or vege-
tations, attended with
a varying degree of
suppuration.
Perhaps of gonorrheal
origin.
Genital diabetides. |
Nothing characteristic:
Glandular reaction
Refractory to all meas-
Oozing erosions and
very slight or
ures other than anti-
eczematoid balanitis.
wanting.
diabetic treatment.
Glycosuria.
Balanitis. |
More or less copious
To be examined for:
and rebellious suppu-
Diabetes (see above).
ration, most pro-
Mercurial poisoning.
nounced over the glans
Potassium iodide pois-
and prepuce.
oning.
Erosive circinate bal-
anitis.
Vegetations, herpes,
chancre, etc.
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GLANDULAR
ENLARGEMENTS.
Adenitis or adenopathy [dbyiP gland] consists generally of a
morbid enlargement of one or more lymphatic ganglia.
It is rather hard to define exactly at what degree of enlarge-
ment ^'adenopathy" begins.
Indeed,' in stout individuals none of the lymph glands, even
those superficially situated, are normally palpable; in very thin
persons, on the contrary, they are easily palpable at certain
points, vis,, in the inguinal and axillary regions; in no indi-
viduals are they normally distinguishable in regions other than
those just mentioned.
The diagnosis of glandular enlargements is hardly open to
error. Lipomas are of an altogether different, soft and lobulated
consistency; sebaceous cysts (wens) are embedded in the skin
proper, and their localization is usually quite different from that
of glandular enlargements ; actinomycotic skin infiltrations are intra-
dermal in situation.
Morbid enlargements of these lymphatic ganglia generally corre-
spond to certain definite areas or anatomic regions.
Considering for a moment only the readUy and actually access-
ible glandular regions, it may be considered a general rule that
swollen glandular masses correspond to the several anatomic divi-
sions of the body as follows:
Inguinal glands. — These drain the reproductive organs, the
lower extremity, and very exceptionally react to pelvic or ab-
dominal affections.
Axillary glands. — These are related to the thoracic wall, in-
cluding the breast, and the upper extremity, and very exception-
ally react to thoracic tumors.
Post-cervical glands. — These drain the mouth, throat, face,
and cranium.
Submaxillary glands. — Related to the lower jaw.
(956)
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GLANDULAR ENLARGEMENTS. 957
Supraclavicular glands. — These exceptionally exhibit metas-
tasis from cancer of the stomach.
It should be remembered, however, that the majority of lym-
phatic enlargements completely escape our examinations by
reason of their depp situation in the body.
Thus, abdominopelvic tumors and infections almost inevitably
give rise to inaccessible deep mesenteric and prevertebral glandular
Si:
Su] cla
xlll
Bi) Bpil
chl<
Fig. 710. — Superficial lymph-nodes and the related anatomic regions.
swellings in the abdomen, and only in exceptional instances to
enlargement of the inguinal glands. Tumors and infections in the
chest almost inevitably give rise to inaccessible tracheobronchial
glandular enlargements, and only exceptionally to enlargement of
the cervical and axillary lymphatics.
Such a condition is, on the whole, the rule ; thus, cancer of the
stomach, tuberculous peritonitis, infections of the biliary tract, gas-
tric and duodenal ulcers, in fact, the great majority of abdominal
disorders that are hard to diagnose are unaccompanied by any ap-
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958 SYMPTOMS,
preciable enlargement of superficial lymphatic glands. Only ex-
ceptionally and in the terminal stage, and only in certain forms,
are enlarged supraclavicular glands found in cancer of the stomach.
The tonsils, as is well known, like the follicles of the intestine,
may and should be looked upon as actual submucous, pharyngeal
and intestinal, lymphatic ganglia. The frequency with which they
become diseased and the common occurrence of sore throat and of
intestinal folliculitis, specific or non-specific, is also a matter of
common observation. Do these infections take place usually through
the blood stream or through the alimentary tract? Do they con-
stitute oftener a portal of entry or a focus of secondary involve-
ment? An answer to this question is of marked theoretical as
well as practical (therapeutic) importance; from our present ex-
clusive standpoint of semeiology, however, it is of' much less sig-
nificance.
Finally, mention may be made of the lymphadenomas^ or neo-
plastic enlargements of lymphatic foci normally not palpable.
In this work space will not permit of more than a review of
certain common clinical observations susceptible to everyday appli-
cation in the causal diagnosis of glandular enlargements.
In whatever region a glandular enlargement be situated, it
may present itself to the examiner in one of the four following
forms :
(a) Simple glandular hypertrophy or painless adenopathy
of intermediate extent and generally involving several lymph nodes.
This includes the syphilitic adenomas, lymphatic hypertrophies with
or without accompanying leukemia, cold tuberculous glandular
swellings, and lymphatic enlargements which one is compelled to
qualify as cryptogenic, since in last analysis their exact nature is
beyond our ken, e,g., the lymphatic enlargements of convales-
cence, of the **lymphatic temperament" ('iymphatism'*), etc.
The syphilitic gland enlargements deserv^e especial mention
both on account of their frequent occurrence and their diagnostic
signification, sometimes practically pathognomonic.
Glandular swelling is a constant appurtenance of the syphilitic
chancre. It involves either a single, large, hard, sluggish node,
which never suppurates ; or a group of nodes in the center of which
is one larger than the rest.
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GLANDULAR ENLARGEMENTS. 959
In the secondary stage, the lymph-glands become enlarged in all
parts of the body, including not only the glands corresponding to
the lesions on the skin and mucous membranes in the secondary
stage, but also those of other regions; the epitrochlear and post-
cervical glands are of prime diagnostic import in this connection.
(b) Inflammatory glandular hypertrophy or painful adeno-
pathy, involving one or more glands, with or >vithout suppura-
tion. This is the ordinary type of septic adenitis following local
infection: Cervical and submaxillary lymphatic enlargements,
etc., in sore throat and infective disorders of the mouth or
pharynx; enlarged inguinal and femoral glands in wounds and
infections of the lower extremities and infective disorders of the
genital organs (gonorrhea, balanoposthitis, and chancroid) ; en-
largement of the axillary glands in infections of the upper ex-
tremities, and secondary lymphadenitis in boils or carbuncles in
any portion of the body. These 'disturbances may result in the
production of glandular abscesses or, as is more common, un-
dergo absorption.
General infections of the type of "grippe" may cause tem-
porary painful enlargement of "glands" that have been latent
for a number of years.
(r) Caseous glandular enlargement, or gland softening. This
is generally the result of tuberculous lymphadenitis, the usual pre-
cursor of the so-called "cold abscesses," which, if improperly treated,
become adherent to and break through the skin, leaving the per-
manent, highly characteristic scars still rather frequently noticed
in the cervical region.
Adhesion of lymph-glands to the skin is met with particularly
in the septic and tuberculous varieties of lymphadenitis.
(d) Hard, nodular, scirrhous glandular enlargements. — ^These
are usually the result of neoplastic metastqsis from cancer, either
manifest or latent; on the whole, they are generally secondary
malignant glandular enlargements. Some varieties are of great
clinical import, e.g., the secondary enlargement of the axillary
lymphatics in cancer of the breast and the rather exceptional
supraclavicular enlargements in malignant growths of the
stomach.
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960 SYMPTOMS.
Cervical lympjiadenitifly a very common disorder, and one
readily observed in the exposed neck region, deserves especial
mention. Of all gland swellings these are the most accessible,
and they should be examined for as a routine.
Submaxillary and post-maxillary lymphadenitis is almost
constant in children, being dependent upon one of the ordinary
infections of the mouth or pharynx (sore throat, dental infection,
etc.), which few individuals escape.
Lateral cervical adenitis is also extremely common. The naso-
pharynx is the usual portal of entry to the infecting germ in these
cases, and the tubercle bacillus is the commonest of the infecting
germs. The submaxillary and stemomastoid series of glands gen-
erally become involved at practically the same time. All different
varieties may be observed, from the multiple slight enlargement
of several nodes (micropolyadenitis) to the caseous lymphadenitis
terminating in cold abscess. Scrofula and tuberculous infection
appear to be the commonest causes of these glandular affections.
Occipital adenitis, manifest about the margins of the hairy
scalp, on either side of the occiput, is encountered chiefly in the
presence of scalp infections (as in phthiriasis or impetigo) ; ac-
cordingly, it is seen more especially in children in the form of
tender gland swellings which never undergo suppuration.
Syphilitic glandular enlargements occur in the cervical region
in two equally characteristic forms :
(a) SxERNOMASTOro ADENOPATHY IN CHANCRE OF THE TONSIL. —
This occurs as an initial indication of primary general syphilitic
glandular enlargement, represented by a single large node (ganglion
indicateur) , beneath and at the middle of the stemomastoid mus-
cle, of the size of a walnut or hazelnut, and rendering the muscle
tissue prominent above the surrounding surface, and a conjoint
group or "pleiad" of smaller nodes underlying the whole neck
region on the same side, hard, painless, and rolling beneath the
finger. Careful inspection of the patient's throat will reveal a
chancre of the tonsil on the same side, or, if it has already been
absorbed, the patient will recall having had a tonsillitis on one
side lasting a few weeks.
Chancre of the tip of the tongue or of the lips gives rise to
enlargement of a suprahyoid node, "single, movable, and rolling
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GLANDULAR ENLARGEMENTS. 961
beneath the finger like a little rubber ball, the feel of which it
exactly reproduces.*' (Sabouraud.)
(&) Secondary syphilitic adenopathy is chiefly post-cervical,
the nodes extending along the neck like a string of beads, mov-
able, elastic, and practically insensitive. These should always
be systematically examined for, and if they are found, the other
signs, stigmata, and the history of the disease should likewise
be sought.
Neoplastic glandular enlargements are secondary to cancer
of the tongue or lips.
Cancer of the base or lateral portions of the tongue reacts on
the submaxillary and postmaxillary glands, and later on the
stemomastoid group.
Cancer of the lips or of the tip of the tongue gives rise at
first to suprahyoid glandular enlargement Later, it extends to
all the other lymph nodes in the region.
Thefee glandular enlargements are hard, nodular, and scir-
rhous, tending to become adherent and to infiltrate the surround-
ing tissues.
The lymphadenosis of Hodgkin's disease generally appears
first in the cervical region and is predominant in this location
for a long time in the form of multiple, sometimes very large
masses (varying in size from an almond to an orange), hard,
insensitive, freely movable, not adherent to the skin, and never
undergoing suppuration. Examination of the blood shows a
moderate leucocytosis with lymphocytosis (see below).
♦ ♦ ♦
Special reference should be made to the apparently primary
tumor growths of the lymphatic and adenoid tissues. These com-
prise the large group of the lymphomas, lymphadenomas, and
lymphosarcomas, with or without leukemia.
The glandular enlargements are generally made up of hyper-
trophied nodes exhibiting structurally one of several different
types :
1. The first and commonest type is characterized by hyper-
plasia of lymphoid tissue similar to the normal tissue of the
61
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962 SYMPTOMS,
lymph-nodes, i.e., by proliferation of the lymphocytic cells
(lymphocytomatosis) .
2. A second, less common type is that which reproduces mye-
loid tissue, or the tissue of which bone marrow is composed, and
is characterized by the presence of myelocytes and nucleated
red cells (myelomatosis).
3. More rarely, the growths are made up of large mononu-
clear cells with basophilic non-granular protoplasm and clear
nuclei (macrolymphocytes or primitive cells), like those seen
in acute leukemia.
4. The last group brings together a number of very different
kinds of tumors, all characterized by a special malignancy of
growth (malignant or atypical lymphadenosis). It includes:
(a) Lymphosarcoma, consisting of sarcoma cells.
(fe) Granulomas, the hybrid structure of which is character-
ized by a combination of lymphoid and myeloid hyperplasia with
neoplastic and inflammatory proclivities.
The condition of the blood reflects, as a rule, that of the
blood-forming organs; hence the need of blood examination in
the diagnosis of lymphatic adenopathies.
The ease with which this mode of examination may be carried
out renders it accessible to the practitioner,-
A mere leucocyte count will show whether the case is one of
leukemia.
Qualitative examination is, however, equally indispensable
for revealing a lymphocytemia or a myelemia, which, even in
the absence of leukemia, then becomes the main clinical feature.
A few stained, dry blood preparations will readily permit of
ascertaining the leucocytic formula.
Yet the typical blood reaction may be lacking (though un-
commonly), especially at first; in this event, removal of a bit
of the glandular tissue for histologic study may be of great
assistance.
Clinically, with the aid of the blood examination, one will be
able to distinguish :
(a) Hodgkin's disease (lymphadenoma, aleukemic lymph-
adenosis. Trousseau's adenosis).
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GLANDULAR ENLARGEMENTS. 963
In this condition the glandular enlargement develops slowly,
at the angle of the jaw, in the submaxillary region, or along the
carotid chain of glands, often symmetrically ; other glands then
appear and fuse with the primary group, thus forming a mass
which is sometimes of considerable size (up to that of a man-
darin orange). This development takes place in the course of
several months or even years. The enlarged nodes are freely
movable beneath the skin, and never undergo ulceration or sup-
puration.
Similar ganglionic masses occur in the axillae and groins.
Fig. 711. — Blood in Hodgkin's disease. /. Lymphocjrte.
^. Red cell. j. Polymorphonuclear leucocyte.
Hypertrophy of the spleen, liver, tonsils, testicles, etc., may
likewise be observed.
Blood Examination. — Cell Count. — The red cells show a
slight decrease, numbering 4 to 5 millions.
The white cells do not show a leucocytosis, numbering 3000
to 5000.'
Or, there may be a moderate increase of the white cells — ^to
about 25,000 — constituting a subleukemia.
Differential Count. — Generally there is a lymphocythemia :
True lymphocytes: 60 to 90 per cent.
Polymorphonuclear leucocytes: less than IQ per cent.
Rarely, myelemia (presence of myelocytes or granular mono-
nuclears and of nucleated red cells).
Rarely, an ordinary pol)rmorphonuclear increase.
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964 SYMPTOMS.
Rarely, again, the differential count may be normal.
The DIFFERENTIAL DIAGNOSIS of Hodgkin's disease involves espe-
cially the elimination of:
1. Infectious glandular enlargements.
In these there are either no blood changes or there is pol)rmor-
phonuclear leucocytosis.
2. Tuberculous lymphadenitis.
In these cases either the blood formula remains practically nor-
mal or there may be a polymorphonuclear leucocytosis.
(b) Lymphatic leukemia, the ordinary form of which is the
splenogang^lionic form, is characterized by gland enlargements,
_./-..3
Fig. 712. — Blood in tuberculous or other infectious glandular en-
largement. /. Large mononuclear. ^. Polymorphonuclear leucocyte. 3.
Lymphocyte.
either slowly or rapidly progressive, in the neck, the submaxil-
lary and nuchal regions, the axillae, and later in the inguinal
regions.
Enlargement of the spleen is neither constant nor pronounced
in these cases.
Blood Examination. — Cell Count. — The red cells show a
decrease, frequently slight.
The white cells show a leucocytosis, often less marked than
in myeloid leukemja — 100,000 to 250,000, occasionally up to
900,000.
Differential Count. — True lymphocytes: 90 to 99 per cent.
Polymorphonuclear leucocytes: barely 10 per cent.
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GLANDULAR ENLARGEMENTS.
%5
Eosinophiles : none.
(r) Myeloid leukemia, uncommonly.
Enlargement of the lymph-glands is uncommon in myeloid
(spleno-myelogenous) leukemia, which is characterized mainly
by enlarged spleen and liver, etc.
Fig. 713. — L)rmphatic leukemia. /. Large lymphocyte. 2. Small
lymphocyte. 3. Polymorphonuclear leucocyte.
Blood Examination. — Cell Count. — The red cells show a
marked reduction, to about 3 millions.
Fig. 714. — Myeloid leukemia, /. Neutrophilic myelocyte. 2. Eosino-
philic myelocyte. 3. Small lymphocyte. 4. Large lymphocyte. 5.
Nucleated red cell. 6. Polymorphonuclear neutrophilic leucocyte.
The white cells are increased to about 300,000, up to 1 million.
Differential Count. — The myelocytes or granular mononu-
clears predominate.
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966
SYMPTOMS,
Nucleated red cells are present in varying numbers.
(d) Acute leukemia. — The various groups of lymph-nodes,
particularly the cervical and submaxillary, are involved, but
Fig. 715. — Acute leukemia. /. Macrolymphocyte. ^. True lymphocyte.
3. Polymorphonuclear leucocyte.
hardly reach the size of an almond. Enlargement of the spleen
is slight.
There is tonsillar hypertrophy, suggesting an acute tonsillitis..
^/— Ji
Fig. 716. — Lymphosarcoma. /. Eosinophile. ^. Polymorpho-
nuclear neutrophile.
Hemorrhages, pronounced anemia, and fever.
Blood Examination. — Cell Count. — The red cells show a
marked decrease.
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GLANDULAR ENLARGEMENTS, 967
The white cells are increased to 50,000 or 100,000; sometimes
200,000, or even 900,000.
Differential Count. — Polymorphonuclears: below 10 per cent.
Eosinophiles : none.
Macrolymphocytes or primitive cells: 80 to 90 per cent.
(Non-granular mononuclear cells with voluminous proto-
plasm, basophilic, and with clear nuclei.)
{e) Lymphosarcoma. — In this condition the lymphatic tumor,
generally located in the neck, shows rapid progression, attains
a considerable size within a few months, and produces a rounded
prominence covered with a pronounced network of veins, some-
times ulcerated, and capable of leading to copious hemorrhage.
Blood Examination. — The blood shows little change. There
is a moderate degree of leucocytosis with excess of polymorpho-
nuclears, with or without eosinophilia.
(/) Lymphatic granulomatosis. — Enlarged glands form masses
of varying size, running a rather rapid, malignant course.
Blood Examination. — Generally there is a leucocytosis of
30,000 to 50,000.
Differential Count. — Polymorphonuclear leucocytes increased.
Eosinophilic polymorphonuclears increased.
Myelocytes sometimes present.
Before concluding this section a word or two must be said
concerning the moot question of the lymphatic temperament or
diathesis, now needlessly obscured by discussions as to termin-
ology and pathogenesis (inter-relationship — as yet uncertain — of
scrofula, the lymphatic diathesis, tuberculosis, and "arthritism").
Clinically there is no doubt of the existence of a lymphatic
diathesis. Children in general, and certain children in particular,
exhibit a marked tendency to excessive reactions on the part of
the lymphatic channels and nodes, and in some of them, this tend-
ency is expressed in a variety of clinical manifestations, chiefly
involving the skin and mucous membranes, which, in the aggre-
gate, justify us in speaking of a lymphatic temperament — ^an actual
diathesis, constitution, or special morbid predisposition — some-
times called lymphatism.
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968
SYMPTOMS.
With exclusive reference to the actual clinical evidences, these
manifestations may be grouped as shown in the subjoined table:
Clinical Manifestations of the Ljrmphatic Constitution.
pbimabt.
SECONDARY, WITH A TBND-
BNCT TO RBCUBBSNCB.
Skip
Scaly eruptions. Intertrigo.
Prurigo.
Eczema. Impetigo.
Multiple abscesses.
Mucous mem-
branes
Desquamative processes
and various evanescent
catarrhal states.
Sore throat.
Pharyngitis.
(Gastro-enteritis).
Coryza (hay fever).
Laryngitis (false croup).
Bronchitis (asthma).
Conjunctivitis.
Blepharitis.
Balanitis.
Vulvo-vaginitis.
Lsrmphatic
structures ...
Hypertrophied palatal and pharyngeal tonsils. En-
larged cervical, inguinal, axillary, or other glands.
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pj Yco^TTRTA Fy'^^^^^ sweet substance; ovpelv, to wri-1
• [ nate. Pi'esence of sugar in the urine. J
Since uranalysis should be carried out as a routine in the process
of examining a patient, glycosuria is a condition which ought
not to be overlooked. Even accidental or alimentary glycosuria is
almost certain to be detected if the test for sugar is repeated at
each examination, as it should be.
In the event of doubt, glycosuria may be clinically considered
to exist whenever there is distinct reduction of Fehlingf s solu-
tion (see Technical procedures).
The following figures will give an idea of the frequency with
which glycosuria clinically occurs:
Out of 2000 subjects of both sexes suffering from various
chronic disorders examined in the author's office, 106, or approxi-
mately 5 per cent., showed glycosuria; in two-thirds of these pa-
tients the condition had previously been overlooked.
Out of 1000 military subjects, suffering for the most part from
acute disorders, examined in a hospital, 6, or approximately 0.5
per cent, showed glycosuria; the condition had previously been
overlooked in 4, i,e,, two-thirds of the cases.
Diabetes mellitus is a clinical symptom-complex characterized
by permanent, or at least lasting, glycosuria, usually associated with
polyuria, polydipsia, polyphagia, and autophagia, none of these
symptoms being, however, necessarily present in all stages of the
disease, while the essential, characteristic manifestation is habitual
glycosuria with hyperglycemia.
Diabetes is put down as a clinical symptom-complex and not
a disease, because the diabetes or permanent glycosuria is not
always due to the same cause nor attended with constant patho-
logic evidences — ^as is also true, indeed, of the accidental, tempo-
rary forms of glycosuria,
(969)
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970 SYMPTOMS.
Clinical observation and experimental work have shown that
a temporary or a permanent (diabetic) glycosuria may be produced
either :
1. By hyperglycophagia (so-called "alimentary glycosuria"),
including muscular hypoglycolysis (due to insufficient exercise).
2. By disease of one of various organs.
(a) The liver. — Hepati<: diabetes, occurring in two forms (Gil-
bert and Camot) : Excessive hepatic actiznty (hypertrophy, conges-
tive states, etc.), and insufficient hepatic activity (cirrhosis, oblitera-
tion of the portal vein, etc.).
(b) The pancreas (pancreatic insufficiency). — Pancreatic dia-
betes, a well-known condition clinically, and one also experimentally
reproduced (von Mehring and Minkowski).
(c) The kidneys (renal insufficiency). — Renal diabetes, experi-
mentally demonstrated through the production of phloridzin gly-
cosuria.
(d) The adrenals (hyperepinephria). — Adrenal diabetes, ex-
perimentally demonstrated through epinephrin glycosuria.
(e) The thyroid (hyperthyroidia). — Thyroid diabetes (hyper-
thyroidia, Graves's disease).
3. By lesions of the nervous system. — The manner in which
this form of glycosuria is produced was demonstrated experi-
mentally by Claude Bernard in 1849, sugar appearing in the urine
upon production of a lesion of the medulla.
(a) Organic disease, especially bulbospinal: Brain tumors, gen-
eral paralysis, disseminated sclerosis, tabes dorsalis, etc.
(b) Neuroses and psychoses: Chorea, Graves's disease, etc.
(c) Traumatic lesions.
4. By disturbed general nutrition.
(a) Neuroarthritic glycosuria, dependent upon a chronic dis-
turbance of general nutrition, usually inherited and variously asso-
ciated or combined with the various so-called "arthritic" disorders,
vis,, gout, obesity, lithiasis, etc.
(b) Toxic states, acute or chronic. Those clinically most famil-
iar, though generally evanescent, are caused by chloroform or
chloral hydrate; the most important, however, because frequently
overlooked, are the^nore or less lasting forms of glycosuria brought
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GLYCOSURIA, 971
on by the insidious intoxications by illufninating gas and carbon
monoxide.
The foregoing simple etiologic classification gives a sufficient
understanding of the various well-known theories as to the causa-
tion of glycosuria, vis., the hepatic theory, the pancreatic theory,
the nervous theory, and tlie glycolytic theory. These theories hold
good in certain individual cases and explain certain clinical forms
of glycosuria, but are not sufficiently comprehensive. They apply
in some forms of the condition, but not in all.
As matters now stand, if one takes into account all known
clinical and experimental data, it becomes necessary either to limit
one's efforts to special studies of each of the innumerable varieties
of glycosuria or, adc^ting broader conceptions of the pathogenesis,
to put it down as a fact that the diabetic symptom-complex is the
obvious organic expression of a lesion or disturbance of function
at some point of the glycotrophic nutritive system.
This glycotrophic nutritive system, which is highly complex,
is governed and coordinated by the organic cerebrospinal nervous
system, which insures functional cooperation in this system, thus
rendering it possible to have a glycosuria of nervous origin through
glycotrophic incoordination.
The glycotrophic system consists essentially of a group of gland-
ular organs, vis,, the liver, pancreas, and in fact the entire digestive
tract, the adrenals, the thyroid, etc., charged with the task of elab-
orating sugars, presiding over their conservation (glycogenesis)
and destruction (glycolysis), and whose overactivity or insuffi-
ciency, inducing disturbance of sugar nutrition, brings on a diabetes
of glandular origin.
Yet this glycolytic property, while more especially possessed by
certain individual organs, ap^pears to be a functional attribute of
cell nuclei in general, so that any general disturbance of cell nutri-
tion— usually combined, indeed, with the glandular disturbances
above mentioned — may bring on a form of glycosuria that may
properly be described as a dystrophic diabetes of arthritic or toxic
origin.
Brief reference may here be made to the ingenious theory in-
volving the role of the endocrine glands (thyroid, adrenals, and,
in part, the pancreas). This theory presupposes that the glycolytic
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972 SYMPTOMS,
reaction in the cell nuclei can occur only in the presence of catalyz-
ing reagents or complements set free in the system by the endocrine
glands; in the absence of these indispensable complementary fer-
ments, the glycolytic reaction is held not to occur, glycosuria there-
fore resulting. In truth, this theory, while opposed by the actual
known instances of diabetes induced by hyperepinephria and hyper-
thyroidia, is based upon the definite observations well described by
Minkowski and leading to the conclusion that glycosuria may be
brought on by suppression of the internal secretion of the pancreas,
which in the normal animal proceeds to exert its action upon the
other glycotrophic organs through the medium of the circulation.
At all events, the brief causal and pathogenetic review just pre-
sented will have imparted some conceptions as to the occurrence of
the syndrome of diabetes, accounted for by one of a variety of
causes, and the causal treatment of which — ^the only rational means
of therapy — should be adapted to each clinical form.
However limited our knowledge may as yet be in this con-
nection, it is thus nevertheless indispensable to make a systematic
study of each case and try to trace back the initial cause of the
nutritional disorder.
"Before undertaking to treat a diabetic subject, one should study
the case with care not only as regards the existing symptoms but
also as regards the patient's habits and character. The results
obtained depend, indeed, upon a host of circumstances apart from
the nature of the diabetic disorder per se: The patient's occupa-
tion and tastes and the general type of his associates frequently
offer hindrance to successful results from the physician's advice."^
(Le Gendre).
This careful preliminary investigation will sometimes enable the
physician very readily to dispel incipient diabetes. "My advice was
sought a few years ago," wrote Lepine, "by a manufacturer about
fifty years of age, free of inherited morbid taints. He was leading
a normal life and was not subject to worry; his diabetic condition
had set in about two years before.
"After prolonged questioning I finally learned that during the
preceding three years he had made a change in his daily routine
1 Diabete in "Traiti de midecine" vol. i, Masson et Cie.
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GLYCOSURIA. 973
which he wrongly deemed of little consequence; he had taken up
his abode directly at the factory, whereas previously he had walked
to and from the factory twice daily, thus covering a distance of
8 kilometers. Upon finding out this fact, I recommended that he
take a walk for two hours each day. I also adjusted his diet.
The glycosuria disappeared."
Such easy cases as this are exceptional ; yet they are sometimes
met with in practice. The above example shows how intelligent
and painstaking an inquiry is required before prescribing treatment.
A clinical classification of cases of diabetes, however imperfect
it may be with our present restricted knowledge, is of marked
service in defining the general lines of antidiabetic treatment in
the various cases.
For want of a better one, the following least defective, oldest,
and most practical classification will here be adopted:
Stout Diabetics, without Impairment of Nutrition. — These
are usually cases of "neuro-arthritic" diabetes, or hepatic dia-
betes through overactivity of the liver; this is the diabetes of
plethoric or of florid gouty persons with enlarged and congested
liver, a sluggish intestine, and taking but little exercise. Such
diabetics generally appear very well nourished, stout, red com-
plexioned, and show marked endurance; they eat and drink
heartily and are in a general sense high livers.
In these patients the body weight is definitely above the average,
and the same is true of tlie daily output of urea, which exceeds
0.40 gram per kilogram of weight ; the glycosuria is of intermediate
degree, ranging from 0 to 60 grams. If the urine is systematically
collected at fairly regular intervals after and between meals, the
sugar elimination will be found to be intermittent, or, if it is con-
stant, a marked recrudescence after meals will be noted.
This is the commonest type of case, and these are also the most
favorable cases from the standpoint of treatment, proper and well
planned general hygiene and diet being suflicient for successful
results. Marked benefit accrues from restriction of the total intake
of food, special reduction of carbohydrates, and systematic exercise.
Thin Diabetics, with Impaired Nutrition. — ^This is the dia-
betes of young subjects and of those with serious disease of the
pancreas or certain lesions of the liver.
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974 SYMPTOMS,
The disease in these cases is attended with rapid loss of weight,
progressive asthenia, and a tendency to cachexia. The general ap-
pearance is one of physical debility, and resistance to fatigue is
slight.
The body weight is distinctly below the average; polyuria and
glycosuria are very marked, the former amounting to 3 liters a day
and the latter to over 100 grams. The amount of sugar excreted
may exceed the intake of carbohydrates. Examination of the urine
collected at regular intervals shows that glycosuria is constantly
present and that the influence of the meals on it, though present,
is much less marked than in the preceding group of cases.
These are the worst cases from the standpoint of treatment.
Often it is impossible to arrest denutrition and prevent cachexia.
The prognosis is most unfavorable.
Nervous Diabetes. — This group includes, indeed, several very
diflFerent forms of the disorder; but, if one excludes the cases
manifestly dependent upon some obvious lesion of the nervous
system and in which the glycosuria is to be considered only as
a bulbar manifestation of the organic disorder present, there re-
mains a rather clear-cut clinical type, vis,, the diabetes of city
dwellers, business men and others overburdened with mental
work or continually subjected to emotional impressions and oc-
cupational stress and worry. The predominating clinical feature
in these cases is nervousness and irritability. The urinary evi-
dences are likewise very changeable ; the polyuria and glycosuria
vary markedly from one week to another or from one day to the
next, without apparent relationship to the diet, and an obvious,
direct connection can be made out between the degree of over-
work and worry and the glycosuria and general condition of
the patient. Oxaluria and phosphaturia are frequently present
in these cases.
Obviously, in these subjects, general hygiene, mental rest if
possible, country life, a regular mode of living, and nervine
medication are the chief therapeutic indications.
The above varieties having been enumerated, there remain cer-
tain indefinite cases, of varying etiology and symptomatology, such as
post-infectious diabetes, toxic diabetes, traumatic diabetes, etc..
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GLYCOSURIA. 975
complex in their pathogenesis and not precisely compatible with
the groupings already referred to. In these cases clinical inves-
tigation should be especially painstaking and intelligent, since a
rational and sometimes effectual causal treatment may be
worked out upon discovery of the exciting cause of the condition.
The author is well aware that the above mentioned groupings
are arbitrary and are not adequately supported by clinical or patho-
logic data ; yet they are, for the present at least, worthy of adoption
from the practical standpoint, i.e., for prognostic and therapeutic
purposes.
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HEADACHE
(CEPHALALGIA).
[xe^Hxki^^ head; d>lyo$, ^in,l
headache. J
Headache is one of the commonest of clinical symptoms. A
definition of the term cephalalgia is scarcely necessary ; in a gen-
eral way, it refers to pain, generally diffuse in character, experi-
enced in any portion of the cranial region.
Fig. 717. — Cut showing the close ana-
tomic relationship existing between the
frontal, ethmoid, and sphenoid sinuses
and the covering membranes of the brain.
The ethmoid sinuses are diagrammatic-
ally represented.
Fig. 718.--Cut showing the
close anatomic relationship exist-
ing between the ethmoid sinuses
and the covering membranes of
the brain.
This region includes :
1. The cranial contents: Cerebrum, cerebellum, the brain mem-
branes, and the intracranial vessels and nerves.
2. The cranicU cavity with its annexes: Frontal, maxillary, and
ethmoid sinuses, and the auricular and orbital cavities.
3. The pericranial tissues: Pericranial muscles, insertions, and
fasciae (frontal, occipital, and temporal), and in particular the
occipital (nuchal muscles) and temporal muscular masses; also
the skin and cellular tissue of the frontal and temporal regions and
of the scalp.
(976)
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HEADACHE (CEPHALALGIA), 977
All these tissues, with the exception of the brain itself, are
provided with sensory nerves; furthermore, while the brain itself
is actually insensitive, the brain arteries are provided with sym-
pathetic plexuses, and the dura mater and pia mater and their
extensions are abundantly innervated ; thus, many deep-seated brain
disorders, e.g., tumors, may give rise to inveterate headache, pos-
sibly through meningeal or vascular irritation.
This structural complexity accounts, at least in part, for the
exceeding frequency of cephalalgic reactions, of which even the
subjoined enumeration will give only an incomplete idea:
Fig. 719. — Head's cranial zones. NF, nasofrontal : 6th upper thoracic
segment : Disorders of the pulmonary apexes and of the base of the heari.
T, temporal : 7th thoracic segment : Disorders of the bases of the lungs,
the left ventricle, and the upper gastric region. AP, anterior parietal :
8th thoracic segment. PP, posterior parietal : 9th thoracic segment. O,
occipital : 10th thoracic segment.
1. The scalp itself may be the source of the morbid impulses,
as from parasites, wigs, hats, or dyes.
2. The muscle mass and fasciae of the nuchal region may be
the seat of fibrous deposition, of inflammation, or of painful infil-
trations the importance of which will later appear.
3. The cranial sinuses, frontal, ethmoid, and auricular (middle
ears), by virtue of their contiguity to the nasopharyngeal mucous
membrane, are particularly exposed to the catarrhal states and in-
fections which so often affect the latter surface.
4. The intracranial membranes (meningeal and vascular) are
likewise frequently subject to congestive or inflammatory painful
conditions.
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978 SYMPTOMS,
5. The trigeminal region, rendered hypersensitive, it seems, by
the refinements of civihzation, is subjected to the abnormal irrita-
tion of affections of the eyes, nose, and teeth. It might further
be stated, apparently with sufficient justification, that the chief cen-
ter of cephalic sensation, "the headache center," if one may use
such an expression, is principally made up of the "trigeminal cen-
ters."
6. Many clinical observations compel recognition of the occur-
rence of reflex headaches brought on through morbid excitation
of extracranial regions, sometimes very remote, probably owing
to more or less intimate connections between the pneumogastric
centers and the fifth pair. Thus, Head has described certain cephalic
zones which he considers particularly "exposed" and painful in
the presence of disorders of the thoracic or abdominal viscera.
Diseases of these viscera are well-known to cause hyperesthesia
and reflex pain in certain definite zones of the thoracic and ab-
dominal walls. If this pain exceeds, however, a certain degree of
intensity, a similar hyperesthesia and pain tend to set in in a corre-
sponding cranial zone. The general law of pain distribution, as
conceived by Head, is as follows : The higher up the affected por-
tion of the trunk, the more anterior the affected zone of the encepha-
lon. Thus, according to Head, the relationships existing between
the trunk and head may be given as follows:
Six upper thoracic segments, naso-frontal area.
7th thoracic segment, temporal area (held to be one of the most frequent
types).
8th thoracic segment, vertical (anteroparietal) area.
9th thoracic segment, parietal area.
10th thoracic segment, occipital area.
The hyperesthetic zone of the seventh thoracic segment, which
corresponds to a visceral disorder at the base of the lungs, the
upper portion of the stomach or the left heart, including more par-
ticularly the mitral region, is, indeed, often attended with tem-
poral headache.
Reflex headaches of more remote source, e.g., from the uterus
or ovaries, have also been reported.
7. Lastly, the close connections existing between the cortical and
subcortical centers of head sensation and the special sense centers
(visual, auditory, gustatory, and olfactory in particular), as well
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HEADACHE (CEPHALALGIA), 979
as the general and special hyperesthesia of hypercivilized subjects,
account for the headaches of special sense origin induced in algic-
hyperesthetic persons by marked or prolonged special sense excita-
tion, e,g., too much light (as illustrated in the headache and neu-
ralgia met with on the Cote d' Azur, or Southern Coast of France),
sharp, discordant sounds, strong or nauseous odors, unpleasant
tastes, etc.
If one considers, furthermore, that all of the foregoing head-
ache-producing stimuli may be direct or indirect, circulatory, in-
flammatory, toxic, etc., a conception will be had of the very great
frequency of the syniptom headache, the multiplicity of its causes,
and the practical impossibility of supplying a complete, practical,
and logical classification.
For want of a better classification and in full knowledge of the
attendant shortcomings and of the frequently artificial nature of
distinctions thus made between different groups of headaches, the
following classification, which is the least inconvenient, will be
adopted herein:
Headaches of toxic and toxinic (infectious toxins) origin.
Headaches of neuralgic and neuropathic origin.
Headaches due to pressure (inflammatory, meningoencephalitic,
or neoplastic).
Headaches of reflex origin.
Headaches of muscular origin.
Headaches of toxic origin are very common and often diffi-
cult to diagnosticate, being highly variable as to type, severity,
localization, and duration.
In this group may be mentioned the prodromal headache of
infectious diseases. In general these are poorly localized and of
intermediate severity; they usually diminish in the morning and
show exacerbation in the afternoon and evening; they are often
associated with a gradual rise in the temperature; after the pro-
dromal period they generally subside or diminish. This prodromal
type of headache is particularly marked in typhoid fever, malaria,
and influenza. The first of these disorders may be suspected upon
careful examination of the temperature curve and search for the
other prodromal signs (epistaxis, dizziness, diarrhea, appearance
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980 SYMPTOMS,
of the tongue, enlarged spleen, etc.), and its existence may be later
confirmed by the Widal test and blood culture. Malaria is recog-
nized from the periodicity of its febrile paroxysms and their cfiar-
acteristic successive stages; examination of the blood for malarial
parasites may definitely settle the question. Influenza is generally-
recognized from the existence of an epidemic at the time, the sudden
onset, the respiratory catarrh, and the rapid course of the
disease.
Headache of uremic orig^ seems to be most pronounced in
the presence of azotemia. Often a comparative remission in the
mornings will be noted. Frequently attending the digestive form,
it is accompanied by nausea, vertigo, mental confusion, and some-
times vomiting; it frequently presents the appearance of migraine;
high blood-pressure is almost constantly present; determination
of the blood urea will definitely settle the matter. In the high
pressure forms without marked azotemia, which seem to occur
rather frequently in interstitial cases with excessive output of urine
of low specific gravity, without albuminuria, but with markedly
high blood-pressure, the toxemia is often less pronounced, and
the headache is perhaps less dependent upon this factor than upon
the lack of elasticity of the arteries with increase of the blood-pres-
sure in the cranial cavity. Such conditions induce headache which
varies with every change in the circulation and frequently assumes
a pulsating character. Renon has called attention to a special form
of morning headache occurring in high pressure cases and accom-
panied by polyuria, excessive output of urine at night, acute albu-
minuria, and hypertrophy of the left ventricle.
The headache of stercoremia or constipation is generally of
the toxic type, and the frequent association of the cause with the
eflfect is usually known to the patient himself.
A much more severe variety is the bilious headache which,
in some individuals, recurs at irregular intervals and ranges from
a simple persistent feeling of frontal weight to a lancinating,
throbbing, boring pain. It is commonly associated with nausea and
vomiting; the vomitus first brought up consists of more or less
digested food, and that appearing later, of mucus and bile. This
type of headache is due partly to the presence of toxic sub-
stances in the blood, but mainly to the brain congestion resulting
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HEADACHE (CEPHALALGIA), 981
from repeated vomiting. Very common and annoying concomi-
tant symptoms are palpitations and vertigo.
A form of headache recurring regularly in the morning, gener-
ally of slight intensity, and passing off after breakfast and a walk
in the open air, is that due to insufficient ventilation of the bedroom.
In such cases the gas pipes and chimneys should be examined
with great care since, aside from the fatal risks which an intoxica-
tion of this sort may entail (as exemplified in the death of Zola
and of Tarbe des Sablons), a mild but continuous intoxication may
in the course of time induce a very obstinate type of headache
together with marked alterations of the blood. Apparently also
belonging in this category is the inveterate winter headache of city
dwellers, coextensive with the cold season of the year and artificial
heating of the houses, and absent throughout the warmer period
and during life in the country.
Toxic headache du£ to tobacco or alcohol is, as a rule, easily
recognized.
Lastly, mention may be made of the headache, sometimes very
characteristic, of cases of lozv blood-pressure or hyposphyxia (see
Low blood-pressure) — an occipital variety of headache which is en-
hanced by recumbency, obstinate, resistant to all the usual treat-
ments for headache, not influenced by seasonal or digestive factors,
and always associated with low pressure and a relatively high blood
viscosity.
The term headache of nervous origin is manifestly only a
makeshift used to designate headaches the cause of which ap-
pears to reside in a functional disturbance of the nervous system
per se, although as a matter of fact careful clinical analysis
nearly always leads to the detection of some proximate cause,
reflex, congestive, anemic, or toxic.
The most characteristic form is migraine, a unilateral type of
headache recurring at regular or irregular intervals in plainly
neurotic patients whose family history reveals the frequency of
migraine among their forebears and collateral relatives, espe-
cially women. Migraine is a very severe type of headache of the
boring, throbbing type, generally accompanied by very distinct
ocular symptoms. Sometimes the pain begins in one eye and
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982 SYMPTOMS.
extends over the whole of the same side of the head; at other
times, the converse condition occurs. The patient often experi-
ences an impression as of luminous particles in the affected eye ;
the skin vessels are engorged, and there iscommonly nausea and
vomiting.
These attacks may last several days and are regarded by
neurologists as representing "nervous discharges" for the pro-
duction of which an inherited predisposition as well as an ex-
citing cause are required. In very many cases there are present re-
fractive errors and disturbances of ocular motility which demand
careful examination, since much may be done in this direction to
reduce the frequency of the attacks. While migraine may, like
epilepsy, be looked upon as the result of an inherited nervous
instability, it is none the less worthy of note that, in a given
subject, the attack is often brought on by tbe same cause. The
treatment is very difficult, and it is a source of great consolation
for the patient to know that his attacks will become much less
frequent during the second half of his life.
Recognition must be given to the occurrence of a headache
of the migraine type of pituitary origin, detection of which is
facilitated by observation of the ordinary signs of disturbed pituitary
function, vis., increasing coarseness of the features, thick lips,
prognathism, thick eyebrows, mustache in women, hairiness of
the body and extremities, tendency to acromegaly, hig^ blood-
pressure, etc.
Administration of preparations of the whole pituitary gland
generally causes this type of headache and the other attendant
symptoms to disappear. '
Facial neuralgia is often attended with pain which may sug-
gest cephalalgia. The pain may be severe, lancinating, of sud-
den onset, and be accompanied by tender points along the course
of the affected nerve. In bad cases, pronounced local edema may
be superadded. One should always bear in mind the fact that
the neuralgias and, in a general way, all the headaches of nerv-
ous origin may be purely toxic or anemic.
Neurasthenia and hysteria are often attended with headache,
the distinguishing feature of which is a feeling of pressure or
numbness at the vertex, or of compression or constriction over
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HEADACHE (CEPHALALGIA). 983
the lateral regions ("en casque")* One may here recall, more-
over, the variety of neurasthenia so well described by Krishaber
under the name cerebrocardiac neuropathy, owing to the predomi-
nance of cerebral (headache, insomnia, and depression) and car-
diac (palpitations, tachycardia, angor, etc.) manifestations.
Usually there are found in combination with the headache
neuropathic symptoms such as exhaustion on slight effort, alter-
nating periods of exaltation and depression and, in a general
way, nervous irritability. One should not forget, as already
pointed out, that these headaches of so-called "nervous" origin and
their proximate causes themselves are often the expression of
some form of reflex irritation of a weakened nervous system, and
that both headache and neurasthenia may actually be the result
of a latent hyperesthesia of the eyes, nasal mucosae, or stomach.
Pressure headaches may be the result of
Inflammation: Meningo-encephalitis, syphilis.
Tumor.
Endocranial abscess.
Glaucoma.
The differential diagnosis in these forms is often a matter of
great difficulty and sometimes requires the assistance of a neuro-
logist. As a. rule, they are characterized by their constancy,
increasing severity, and nocturnal exacerbations; they are ac-
companied by fever in the acute diseases, such as meningitis;
exceptionally, however, even in the case of brain abscess, they
may be attended with subnormal body temperature. Examina-
tion of the cerebrospinal fluid and testing for Kemig's sign are
indicated in all instances. Marked assistance may be had, both
as regards causal diagnosis and localization of the disease focus,
from examination of the fundus of the eye or observation of a
localized paralysis.
A very severe form of headache, often mistaken for neur-
algia, is that due to acute glaucoma. The possibility of this
diagnostic error is enhanced from the fact that there is fre-
quently edema with points of hyperesthesia around the orbit and
the patient thinks he sees luminous particles. Such a mistake
is attended with serious consequences, for glaucoma, even when
Digitized by VjOOQIC
984 SYMPTOMS.
properly treated, may lead to deep-seated visual disturbances,
and an overlooked and consequently untreated glaucoma may
induce complete blindness in a few hours. In glaucoma the eye
is red and lachrymal secretion profuse, but the cardinal factors
in the diagnosis are painful tension of the eyeball, a turbid and
insensitive condition of the cornea, and wide dilatation of the
pupil, which reacts poorly to light and to myotics.
Special reference should be made to syphilitic headache,
which is of great diagnostic importance. In this connection the
two commonest types of this kind of headache should be re-
called: 1. Secondary syphilitic headache, deep-seated, with a
feeling of weight, continuous, with vesperal exacerbations, ap-
parently dependent, on the whole, upon an actual process of
secondary syphilitic congestive meningo-encephalitis with cere-
brospinal hypertension, as shown by lumbar puncture. 2. Ter-
tiary SYPHILITIC HEADACHE, circumscribcd, boring, persistent, with
nocturnal exacerbations, and dependent upon a gumma. The
Wassermann reaction and the efficacy of antisyphilitic treatment
bring convincing proof to the diagnosis.
The headache of brain tumor is often localized, increased by
percussion, and sufficiently severe to cause the patient to cry
out; it appears in paroxysmal attacks and is generally accom-
panied by vomiting, dizziness, and pupillary disturbances.
^Headache of reflex origin. — This form, as already implied,
is steadily increasing in frequency, apparently because of the
gradual heightening of civilization which, by increasing sensory
acuity and developing specialized functions, is bringing about
the formation of a series of normal or morbid reflexes which are
absent among savages. Prolonged, patient study of his case will
enable the physician to find out whether a headache is reflexly
dependent upon some ocular, digestive, genital, or other source
of irritation.
This type of headache is among the most frequent symptoms
of ocular disorders, and such a cause may be suspected where
the pain is particularly localized in the superciliary, frontal, or
temporal region, and where, being absent on rising in the morn-
ing, it thereafter gradually increases with increasing use of the
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HEADACHE (CEPHALALGIA). 985
eyes and becomes very marked upon constant use of the eyes for
some task requiring minute ocular adjustment. The severity of
such headache bears no relationship to the extent of the ocular
disorder; slight refractive defects often cause much more severe
headaches than marked defects. Patients frequently have ob-
vious refractive errors without experiencing any symptom of
eye-strain, owing to an instinctive compensatory reaction. Thus,
many persons with hypermetropia are able to see objects dis-
tinctly, without apparent ocular fatigue, by continuous contrac-
tion of the ciliary muscles. If, however, they overwork or lose
the hypertrophy of their ciliary muscles either by reason of
abuse or through disease, vision becomes difficult and close work
impossible.
< Myopic persons, whose distant vision is improved when the
ciliary muscles are completely relaxed and consequently almost
atrophied, similarly suffer from frequent headaches whenever
they undertake any continuous work requiring some accommo-
dative effort. The same result is often brought about by over-
correction of myopia, when the latter is estimated solely with
the objective procedures employed by opticians.
Very distressing headaches are also induced by even a slight
degree of astigmatism.
Under normal conditions the ocular muscles maintain the
eyeball in such a position that the rays of light from a distant
object fall directly upon the macula lutea without requiring any
exertion on the part of the individual. Frequently one group of
muscles is too strong or too weak, so that a parallel position of
the two eyeballs is obtained only by dint of overcontraction of the
weaker muscles. Generally the muscle is able to carry out its
task and the tendency to deviation can be detected only by
special tests; the constant exertion entailed by binocular vision
may, however, lead to a number of distressing nervous symp-
toms, particularly headache. Sometimes the weaker muscles
become momentarily insufficient and temporary strabismus is
then noticed; in other instances, the strabismus is permanent.
Where there is continuous, permanent strabismus, the patient
gets in the habit of disregarding completely the image from one
of his eyes, and great patience is then required to convince him
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986
SYMPTOMS,
that he "sees double"; he is not making any effort to combine
the two images and hence does not suffer from asthenopia and
generally has no headache.
Headache of nasal origin is less common than that due to
eye-strain. It is generally localized in the frontal region and
associated with some obvious nasal disorder. It is the result of
irritation of the terminals of the fifth pair in the nasal mucous
membrane. For example, swelling of the mucous covering of
the turbinates in acute rhinitis is accompanied by a dull headache,
particularly if the nasal cavities are too small to permit of this
mucous swelling without morbid pressure ; this sort of headache
is very often relieved by the use of vasoconstrictor astringents,
such as cocaine or adrenalin. Headache recurring regularly at
certain seasons or when the wind blows from a certain direction
is often of reflex nasal origin. In subacute rhinitis the headache
is more marked in the morning owing to the accumulation of
mucous secretions in the nasal cavities during the night. An
ulceration of the nasal mucosa exposing the nerve terminals may
be the cause of a reflex headache. This is also, as is well known, an
important symptom in sinus inflammations.
Head, as already mentioned, made a special study of the
zones of cutaneous hyperesthesia and the corresponding cranial
headache zones as they occur in disorders of the thoracic and
abdominal viscera governed by the vagus nerve. The following
table epitomizes his conclusions :
Head's Zones.
Zones of cutaneous
CORBESPONDINO
DEEP Viscera Associated
HYPEBE8TUE8IA.
CRANIAL Zones.
With These Zones.
3d and 4th cervical.
Naso-frontal.
Apex of lung, liver, stom-
ach, aortic orifice.
2d, 3d, and 4th
Pretemporal.
Lung, heart, aortic arch.
dorsal.
5th and 6th dorsal.
Fronto-temporal.
Intermediate portion and
base of lung, left ven-
tricle, upper gastric
region.
8th and 9th dorsal.
Antero-parietal and
Stomach, liver, upper por-
parietal.
tion of small intestine.
10th dorsal.
Occipital.
Liver, intestine, ovaries,
testicles.
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HEADACHE (CEPHALALGIA), 987
Utero-ovarian disorders are a frequent cause of reflex head-
ache, whether the condition present be ulceration or dis-
placement. This type of headache is often localized in the occip-
ital region and becomes accentuated during the menstrual
periods. Indeed, headache is so frequently present at these
periods that it seems almost a normal accompaniment of the
menstrual process.
Fig. 720. — Elective areas of fibrous thickening over of the
skull, nucha, and neck.
Lastly, many persons are subject from time to time to slight
headaches, perhaps partly reflex, as a result of exposure to cold
or of an emotional impression or dietary indiscretion.
The foregoing list, in spite of its already tiresome length, is
far from exhausting the possible causes of headache. There is
one group, not yet referred to, which has been the subject of numer-
ous investigations in late years, 7t;?., that of the headaches of
muscular origin, seemingly dependent upon connective tissue in-
filtration of the muscles of the neck, particularly of the nuchal
region, and of the head, nearly always accompanied by excessive
muscular tone with a tendency to rigidity and frequently an arthritis
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988 SYMPTOMS.
sicca of the vertebral articulations. Palpation of the back of the
neck and particularly of the skull over the fascial insertions en-
ables one directly to observe the presence of such fibrous thicken-
ings. The headache in these cases may assume one of three types
(Hartenberg) :
Trapezius,
Splenius,
Small occipital nerve.
Great occipital nerve.
Sd cervical nerve.
4th cervical nerve.
Fig. 721. — Posterior branches of the cervical nerves {Soulii).
1. Frank migraine with unilateral pain, arterial throbbing,
scotomas, and vomiting.
2. Neuralgia, definitely localized and associated with the
presence of tender points.
3. Indefinite headache with a feeling of weight or a crushing
or dragging sensation.
Hartenberg, who has made a special study of this variety of
headache, ascribes these infiltrations to a cervical myocellulitis. **I
feel justified in incriminating," he states, "as the chief exciting cause
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HEADACHE (CEPHALALGIA). 989
of these infiltrations, an insufficiency of arterial, venous, and lym-
phatic circulation, due, in turn, to insufficient muscular activity.
Indeed, local exposure to cold and reduction of temperature,
which reduce both tissue metabolism and circulation, distinctly
favor the production of these lesions. Again, I have observed
them particularly in subjects leading a sedentary life^ and those
who take physical exercise are free of them.
"Cellulitis thus appears to us as a species of tissue rust due
to insufficient physical activity. It constitutes a stigma of pre-
mature senility in overcivilized. subjects who have replaced
muscular labor by brain work."^
The series of causes above enumerated shows how difficult
the differential diagnosis sometimes is. In truth, often it is
obvious and does not require any very prolonged examination,
e.g., in the headache of infectious diseases, of acute meningitis,
of migraine, etc. In other instances, again, a painstaking clinical
study is required. On the whole, there are a certain number of
points which should never be forgotten during such studies, and
which, correctly illuminated, will yield a positive diagnosis in
95 per cent of cases of obstinate chronic headache :
History of the Illness.
1. Are there paroxysms, sometimes at regular intervals
(monthly), or with ocular disturbances, nausea, etc. (migraine)?
2. Is the headache periodic, and accompanied by attacks of
fever (malaria) ?
3. Are there clear-cut past evidences of specific infection
(syphilis) ?
4. Have there ever been manifestations of a psychoneurosis
(neurasthenia) ?
Etc.
Daring the clinical examination, one should always examine:
1. The eyes, including the retina (albuminuric retinitis, vas-
cular disturbances, evidences of intracranial disease).
The pupils (reaction to light, Argyll-Robertson pupil, showing
a specific meningo-encephalitis).
The intraocular tension (glaucoma).
iHartenberg: Presse mid., Feb. 14, 1912, p. 134.
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990
SYMPTOMS,
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HEADACHE (CEPHALALGIA).
991
Rigid-
ity of
the
neck.
Kernig's
sign.
Areas of
indura-
tion.
Rigid-
ity.
1
1
+
1
■f
+ So
i+
+
High
pres-
sure.
Cephal-
algic
changes.
0 High
pres-
sure.
■ 1
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^1
Wasser-
mann
1
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Occa-
sionally
albu-
min.
Occa-
sionally
albu-
min.
Occa-
sionally
albu-
min.
o
o
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+ SO
o
+ SO
+ s°
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nocturnal
recrudes-
cences.
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Glasses worn.
Myopia, presby-
opia.
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nary.
Digestive.
Utero-ovarian.
Sedentary life.
Insufficient exer-
cise and fresh
air.
s
I
CO
^1
Nasal
disturbances
(sinusitis).
1
Visceral
disorders
(reflex
headaches).
Indurative
muscular
headache.
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992 SYMPTOMS,
2. The ears, middle and internal (otitis, brain abscess).
3. The nose and its annexes (maxillary and frontal sinuses).
4. The temperature (toxic-infectious headache).
5. The blood-pressure (headache of high-pressure cases, of
uremia, of hyposphyxia).
6. The urine (albuminuric, indicanuric, or acetonemic headache).
7. The blood (determination of the blood urea for uremia, Was-
sermann reaction for syphiUs).
8. If need be, the cerebrospinal fluid (high pressure and the
white cell formula, e.g,, lymphocytosis in tuberculous meningitis
and polynucleosis in ordinary meningitis, etc.).
9. The muscle insertions on the cranium and nuchal region
(headache of muscular origin).
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HEMATEMESIS. [-^^l^^l/^'iST""]
Hematemesis consists of the vomiting of blood. The pres-
ence of blood in vomited material is frequently obvious; if it is
doubtful, blood should be tested for by the usual procedures em-
ployed for the purpose [See Blood examination: Microscopic ex-
amination (red cells, hematin crystals) ; spectroscopic examination
(hemoglobin spectrum); chemical examination (Meyer's test)].
The diagnostic problem is put before the practitioner in the
following terms :
A. Is hematemesis taking place?
I. And first of all, is it blood that has been brought up?
(a) If the vomited material is bright red blood, there is no dif-
ficulty in recognizing it, and all that is necessary is to exclude the
possibility of hysterical simulation.
(&) If it is coffee ground vomit, it may be confused (in rare
instances) with the black vomitus of a patient who has taken in
succession a preparation of ergotin and gallic acid and one of ferric
chloride (ink formed in the stomach) ; also with biliary black vomit.
1. Microscopic examination shows more or less distorted red
corpuscles and crystals of hematoidin or hematin.
2. Spectroscopic examination permits of easy diflFerentiation.
3. Frequently the coexistence of intestinal hemorrhage obviates
the need of these procedures.
4. Sometimes there are only traces of blood.
In the latter event, the most serviceable procedure for clinical
purposes consists in mixing in a test-tube some tincture of guaiac,
ozonized oil of turpentine, and gastric juice. If blood is present,
even in small amount, a characteristic blue color will appear (see
Blood examination: Weber's test).
II. It is blood. Where is the seat of the hemorrhage?
(a) It is from the pharynx, the nose, or the mouth; inspection
of these cavities will settle the matter.
«3 (993)
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994 SYMPTOMS.
{b) It is from the esophagus:
Former indications of disease of this canal (dysphagia, post-
sternal pain, fluoroscopy after ingestion of bismuth) alone permit of
establishing such a diagnosis.
The above causes having been excluded the following question,
which is that of greatest clinical importance, arises :
(c) Did the blood issue from the stomach or the respiratory
tract? Isi there hematemesis or hemoptysisf
1. Particular import attaches to this question in view of the fact
that entrance of a few drops of blood into the larynx in the course
of hematemesis* is sufficient to induce cough, and conversely, that
in hemoptysis blood may be swallowed and then expelled in the act
of vomiting. Accordingly, although the blood in hemoptysis is gen-
erally red, foamy, and mixed with air-laden mucous discharges,
this sign is absolutely unreliable,
2. Consequently, the diagnosis is based on the concomitant
signs. In hemoptysis the physician will note the customary evi-
dences of disorders attended with this condition (tuberculosis, hy-
peremia, or apoplexy of the lung, or valvular heart disease) ; in
hematemesis, gastric manifestations predominate (dyspepsia, epi-
gastric pain, dilatation of the stomach, etc.).
3. The practitioner may be greatly puzzled in the event of simul-
taneous presence of gastric and pulmonary disease {gastric ulcer and
pulmonary tuberculosis),
4., In theory, the differential signs of hematemesis and hemo-
ptysis may be summarized thus :
Hemoptysis.
Hematemesis.
History of lung disturbance.
The blood is expectorated.
It is red, foamy, and frothy.
It may be mixed with sputum.
The onset of hemoptysis is often
heralded by a pricking sensation
in the larynx.
It may be accompanied by nausea
and pain in the chest.
It is rarely followed by discharge
of blood from the bowel.
History of a gastric, hepatic, or
splenic disorder.
The blood is vomited up.
It is black, compact, and free of
air admixture.
It may be mixed with bile or food
debris.
The onset of hematemesis is
often heralded by a feeling of
dizziness or faintness.
It may be accompanied by nausea
and pain in the epigastrium.
It may be followed by discharge
of blood from the bowel.
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HEMATEMESIS,
Ulcer and Cancer of the Stomach.
995
Catheterization of the Fasting Stomach.
(a) Food stasis Pyloric stenosis and, if true
stasis, cancer of the py-
lorus.
'Wash water contains Reichmann (probably py-
(b) No food
stasis.
free HCL
Wash water, with 1
per cent, acetic solu-
tion, contains chem-
ically demonstrable
blood.
loric ulcer).
Ulcer of the body of the
stomach (simple or can-
cerous).
Examination of the Stomach after a Test MeaL
(a) Free HCl
in excess.
(b) Free HCl
reduced to-
ward 0.
Ether capsule dis-
solved in less than
one hour.
Ether capsule not dis-
solved.
Probable ulcer.
Probable cancer.
Examinajdon of Feces after a Milk and Vegetarian Diet
Presence of
blood chem-
ically demon-
strable.
Blood disappears after
a few days' rest.
Blood still present
Blood is present in
fe.ces but not in acid-
ulated wash water
. from stomach.
Probable ulcer.
Probable cancer.
Duodenal ulcer or ulcer on
duodenal aspect of py-
lorus.
Small, con-
tracted stom-
ach with les-
sening of
peristaltic
contractions.
Fluoroscopic Examination (Principal types)
'Amputation" Stomach
Filling-defect
in stomach
(apparent ab-
sence of a
portion of the
gastric shad-
ow).
of the py-
loric region
and delayed
evacuation
of bismuth
meal.
presentmg a
bilocular ap-
p ea ranc e
(due to
spasm).
Diverticular
aspect (ap-
parent ad-
dition to gas-
tric shadow).
Callous
ulcer.
Ulcer on
Diffuse Localized Cancer of lesser
cancer. cancer. pylorus. curvature.
Blood Examination.
Increased antitryptic power of the serum Cancer.
Cytologic Examination.
Microscopic examination of the wash water after gastric
lavage.
Study of centrifugation sediment
Presence of neoplastic cells Cancer.
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996 SYMPTOMS,
B. Hematemesis has occurred. What is its cause?
I. The hematemesis occurs under certain special circum-
stances, independently of any local disorder which might facili-
tate discovery of the causes of the bleeding*.
(a) It occurs in the course of an infectious disease: Hemor-
rhage-producing disorders such as scurvy, purpura, hemorrhagic
smallpox, infectious endocarditis, typhus fever, plague, perni-
cious malarial fevers, grave icterus, and yellow fever.
en
gastric branch
istroepl-
artery
Gai
Hepatic
Gastrohepatic
Pyloric
Right gi
epiploic
Fig. 726. — The arteries of the stomach.
{b) It may follow phosphorus or arsenic intoxication.
Ic) It may be substituted for hemorrhoidal or menstrual
bleeding.
(d) In predisposed subjects, especially hysterical persons, it
may come on following some pronounced emotional impression,
slight traumatism to the epigastrium, or exposure to cold. The diag-
nosis in these cases is based on:
1. Persistence of the disorder in spite of all treatment.
2. Relatively slight impairment of the general condition in spite
of copious hematemesis.
3. The presence of permanent stigmata of hysteria, such as
anesthesia, and contraction of the visual fields.
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HEMATEMESIS. 997
The fact should be borne in mind, however, that gastric ulcer
is not uncommon in neuropathic subjects.
(e) Again, attention should be called to the possibility of
hematemesis where persons are exposed to a sudden reduction of
atmospheric pressure, as exemplified in the "Zenith" balloon disaster.
(/) Lastly, mention may be made of the hematemesis of uremia
and of unrecognized strangulated hernia in old persons (Robin).
II. In cases of exactly opposite type, the hematemesis is recog-
nized as being of local origin, and the seat of the hemorrhage is
localized in the stomach, its annexa, and other organs.
Capillary network
about oriflcea of glands
Periglandular
capillary network
Vertical yein
Small artery
Submucous vein
Fig. 727. — Blood-vessels of the gastric mucous membrane (Brinton).
(a) Stomach: 1. M^y he mentioned sls occasional causes: In-
ternal or external traumatic injuries, miliary aneurysms, thrombo-
sis, embolism, amyloid infiltration, and venous stasis of cardiac
origin.
2. As common causes: Cancer and ulcer (see p. 995).
3. Some difficulty attends the differentiation of hematemesis due
to ulcerations of the stomach in the presence of chronic gastritis,
particularly of uremic origin. All the symptoms combine to mis-
lead the clinician ; under these circumstances Robin's predept should
be called to mind: "You should make a diagnosis of cancer only
when you cannot do otherwise."
(b) Auxiliary digestive organs.
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998 SYMPTOMS,
1. Diseases of the liver.
In cirrhosis of the liver, especially atrophic cirrhosis, hemateme-
sis sets in rather early, in the pre-ascitic period, and is then associated
with the usual clinical signs of the pre-cirrhotic stage; sometimes
it is very copious, and in some instances it has been known to cause
death. It seems to be dependent both upon varicose vessels of the
esophagus and upon altered nutrition. Undoubtedly it occurs very
often. Like the succeeding forms, it is largely secondary to the
syndrome of high portal pressure (see Fig. 729).
Hypertrophic cirrhosis and cancer of the liver; mention should
Fig. 728. — Section of gastric ulcer (Dieulafoy). U, ulcer farmed at
the expense of the mucosa M and the muscularis mucosae mm ; a, a sub-
mucous arteriole destroyed at the point /», where a large number of red
cells are collected; the fatal hemorrhage has taken place at this point;
. t\th, a thrombosed vein; sm, submucous layer; mtr and ml, muscular
layer; s, serous coat; /, ^, 3, miliary abscesses in the depths of the mucous
layer.
also be made of grave icterus, which is attended with hematemesis
for various reasons, some local and others general.
2. Pressure on the portal vein by tumors of the hilum or of
neighboring structures (pancreas, etc.).
3. Embolism of the mesenteric, hepatic, or splenic ar-
teries, e.g., in the course of infectious endocarditis.
(c) Disorders of neighboring organs.
1. Duodenum: See Dyspepsia.
Ulcer of the duodenum may be attended with hemorrhage, in
which the blood travels back toward the stomach. The diagnosis
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HEMATEMESIS. 999
is based on the frequency of intestinal hemorrhage, the different
seat of pain, and the result of clinical examination according to
Meunier's procedure (see p. 75).
Varicose conditions of the duodenum occur under the same cir-
cumstances as varicose conditions of the esophagus or stomach (syn-
Low blood-presBure
hemorrhage
Fig. 729. — The syndrome of high portal pressure (portal hypertension).
drome of portal hypertension). Ulcers may also follow extensive
bums of the body surface.
2. Esophagus:
Varicose vessels of the esophagus are met with particularly in
cirrhosis of the liver or cancer. The customary evidences of eso-
phageal tumor are present under these circumstances, vis,, dys-
phagia, pain, regurgitation of food, results of examination with the
sound, etc.
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1000
SYMPTOMS.
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HEMATEMESIS.
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1002 SYMPTOMS,
3. Circulatory system.
Heart failure ; aneurysm of the aorta or celiac axis. The diag-
nosis is based on the usual symptoms of these disorders. Hemor-
rhage from ruptured aortic aneurysm is generally of the fulminating
type.
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HEMATURIA. [,„"i!SXfc.]
Hematuria is jone of the commonest and most important mani-
festations of disease of the urinary tract. For clinical purposes the
term hematuria will be held to refer to cases in which blood in the
urine is visible to the naked eye.^
The physician should, in the first place, make certain that
hematuria actually exists by himself directly examining, if possible,
the suspected specimen of urine obtained from the patient.
He should exclude, then, either by direct inspection of the
urine or by microscopic or spectroscopic examination, pseudo-hema-
turia due to ingestion of drugs (see below) and hemoglobinuria,
and should, furthermore, guard against making a serious error
where blood from the female genital tract is mixed with the urine,
as in menstruation or metrorrhagia.
The actual existence of hematuria having been positively estab-
lished, he should next endeavor to ascertain the source of the
hemorrhage and its cause, without waiting for further symptoms to
appear.
Hematuria often occurs abruptly, during apparent good health,
in a subject previously free of any symptoms referable to the
urinary tract. Under these circumstances it constitutes an alarm
signal, practically a useful manifestation of a disorder as yet latent
or circumscribed, early recognition and treatment of which may
result in complete cure — which is all the more advantageous in that
the more distressing phases of the disease will thus have been
forestalled.
1 It should be borne in mind, however, that there may occur a micro-
scopic hematuria, which sometimes plays an important part in the diag-
nosis of renal calculus, according as microscopic examination of the cen-
trifugated urine, before or after walking, shows the presence of red blood
cells in greater numbers in the urine collected after exertion or fatigue.
(1003)
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1004 SVMPTOMS.
Too often, however, it happens that the physician, reassured by
the absence of other clinical signs, rests content with the mere ob-
servation of the presence of hematuria; only much later, when the
hematuria recurs, when it alarms the patient, and when other symp-
toms appear such as a local swelling, fever, and pain, does he think
of carrying out a complete examination of the patient.
die
Bulb of urethra
Fig. 730.
This mode of procedure is all the more to be deplored in that,
thanks to systematic clinical study and especially to the modem
means of examination, one is able very early, and even in the ab-
sence of any other symptom, to detect the cause of the bleeding.
In the presence of hematuria two questions arise: Where
does the blood come from? and What is the cause of the hemor-
rhage?
It will be well to consider the special features presented by
the hemorrhage according as it comes from one or another por-
tion of the urinary tract, as well as the attributes afforded to
it by its various possible causes.
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HEMATURIA. 1005
I. The blood comes from the urethra or the prostate. — The
blood appears at the start of micturition. It is an initial hemor-
rhage, the blood in the urethral canal, washed down by the urine,
appearing with the first drops of urine that pass out.
Fig. 731. — Sources of the internal pudic vein, H, and the vesical vein,
V (Farabeuf). The pin passing through the lower and outer surface
of the bladder represents the dividing line between the two venous cur-
rents, pelviovesical, F, and perineopudic, H.
This initial type of hematuria is of small amount, and follows
either a traumatized state of the urethral canal (acute urethritis,
injury during coitus, rupture of the urethra, or false passage dur-
ing catheterization) or a lesion of the prostatic urethra (varicose
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1006 SYMPTOMS.
vessels of the prostatic region, cancer of the prostate). The diag-
nosis is based particularly on the history.
Where initial hemorrhage is more pronounced, blood appears
at the meatus independently of micturition. The condition is
then an actual urcthrorrhagia, the amount of which bears a re-
lationship to the seriousness of its cause. Such urethrorrhagia
is met with chiefly as a result of rupture of the urethra, either
from external traumatism (fall or blow on the perineum) or
internal traumatism (serious false passage).
Sometimes blood coming from the posterior urethra or pros-
tate independently of micturition passes back into the bladder,
and if the bleeding is of considerable degree, the entire amount
of urine may be discolored by it; upon inserting a catheter and
washing out the bladder, however, the urine in the latter will
rapidly become clear.
II. The blood comes from the bladder. — Vesical hematuria
may be terminal or total. Terminal hematuria, characterized by
the appearance of blood, generally in moderate amount, at the
end of micturition, at the moment when the bladder is complet-
ing its evacuation by means of a few forcible contractions, is in-
dicative of a lesion of the neck of the organ, as in gonorrheal
cystitis.
Disorders involving the body of the bladder produce more
abundant hemorrhage; the blood may in these cases be com-
pletely mixed with the urine, which issues red from the beginning
to the end of micturition and may be deeply colored.
The vesical origin of total hematuria may be established as
follows :
When the blood is derived from the bladder, the depth of dis-
coloration of the urine increases as the close of micturition is
approached. If the patient is caused to urinate into three glasses,
the first two glasses show less discoloration than the third ; lastly —
an important indication — a bleeding bladder is hard to wash out.
Thus, given a patient with hematuria. A catheter is inserted
and, upon slow injection of fluid into the bladder several times,
the wash water tends to come back clear at the beginning of
its expulsion, but as the bladder is further emptied, the later
wash water shows increasing discoloration, which is the more
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HEMATURIA. 1007
marked according as the bladder is allowed to empty itself more
completely. If, furthermore, one waits until the bladder is thor-
oughly empty, the bleeding at once recurs, sometimes in the
form of an outflow of almost pure blood.
Vesical hematuria is met with:
(o) In trauma of the bladder; here the circumstances under
which the hematuria arose point definitely to the source of the
bleeding.
(h) In cystitis — ^tuberculous, calculous, or neoplastic cystitis,
or simple hemorrhagic cystitis.
R.K. L.K.
-Iff
111
-111
Three glasseB equally henuituric.
Total hematuria = Renal.
Last glass colored or more deeply
colored.
Terminal hematuria = Vesical.
First glass colored.
IniUal hematuria = Urethral.
Fig. 732.
(r) In the absence of all signs of cystitis, in certain tumor
formations — papilloma, angioma, and beginning cancer.
(rf) In some forms of congestive prostatic enlargement in
which hemorrhage occurs into the bladder.
As a general rule, the practitioner should not be satisfied with
a diagnosis of hematuria of vesical origin based on the observa-
tion of other bladder signs such as pain, tenesmus, pyuria, etc.;
bladder manifestations may occur in the presence of hematuria
of renal origin, and to depend upon such evidences may lead to
serious mistakes.
The only absolute rule, which must be remembered as a defi-
nite axiom, is that any total hematuria believed to be of vesical
origin points to the necessity of cystoscopic examination of the
bladder.
III. The blood comes from the kidney or ureter. — Hematuria
of renal origin is a form of total hematuria in which the urine
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1008 SYMPTOMS.
shows a uniform discoloration from the beginning to the end of
the act of micturition. In contrast to that which occurs in vesi-
cal total hematuria, the wash water finally becomes quite clear
or, if there is continuous oozing in the kidney, the results of irri-
gation will always be sufficiently marked to permit of immediate
cystoscopy.
There are three great causes of renal hematuria which should at
once come to the practitioner's mind, viz., tuberculosis, stone, and
cancer.
In each of these three disorders, bleeding may appear abruptly,
without any previous or coexisting symptom. It is essential that
the physician be familiar with this fact, since it is in these cases
that early hematuria constitutes an actual benefit, enabling him
to act early in the disease and under the best possible conditions.
Usually certain other signs assisting in the diagnosis are pres-
ent in conjunction with the hematuria.
In incipicjit tuberculosis of the kidney, there are present certain
mild vesical symptoms, such as frequent urination, a light pul-
verulent deposit at the bottom of the chamber, and slight pain
in the bladder, and sometimes enlargement and sensitiveness of
the kidney are also present (see Examination of the Kidney: Renal
points of tenderness, p. 335).
In more advanced tuberculosis of the kidney, there are present
polyuria, pyuria, a more or less remote history of cystitis, and
enlargement of the kidney.
In renal calculus, hematuria often appears abruptly, without any
previous attack of pain. Some kidney stones induce absolutely
no pain. In other instances, however, pain is a prominent feat-
ure (dull pain in the kidney region, renal colic, and expulsion of
stones). Finally, renal hematuria of calculous origin is often
(but not always) brought on by fatigue, walking, horseback
riding, etc.
In cancer of the kidney, hematuria may appear very early and
be the only symptom. At a later stage, however, it occurs in con-
junction with pain, enlargement of the kidney, and cachexia.
Apart from these three main causes of renal hematuria, there is
one other which is of relatively frequent occurrence, zns., hema-
turic nephritis, with or without pain. This form of nephritis is
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HEMATURIA. 1009
sometimes associated with only trifling general manifestations,
and the diagnosis is made chiefly by ureteral catheterization;
upon examination of the separated urines, the hemorrhage is found
to be often bilateral (either concomitantly or alternately on the
right and left), the kidneys exhibit impaired functional power,
and casts are observed. The pain in this forni of nephritis often
disappears after renal decapsulation.
Fig. 733. — Diagram of the structure of the kidney. Shaded gray, a
renal pyramid, with its apex dipping into a calyx, and its base sending
several processes (the pyramids of Ferrein) into the cortical substance
(white). In relief, the arterial vessels (interlobar artery, arterial arcade,
and interlobular and glomerular arteries). In black, a few uriniferous
tubules, the course of which is from glomeruli to the apex of the renal
pyramid (Laederich),
IV. The hematuria is of hemic origin. — The appearance of
the urine in this event is naturally the same as in hematuria of
renal origin, but the cause of the condition has less to do with
changes in the kidneys, which are nearly always present, than
with a blood dyscrasia of infectious or toxic origin, such as :
1. Hemorrhage- provoking disorders of the type of purpura, hem-
ophilia, scurvy, and the leukemias. Recently there have been re-
64
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1010 SYMPTOMS,
ported instances of actual '^vesical purpura," either in conjunc-
tion with purpura of the skin or even occurring independently.
2. Hemorrhagic forms of various infectious diseases, such as
typhoid fever, malaria, small-pox, typhus fever, yellozv fever, septi-
cemia, and icterohemorrhagic spirochetosis.
3. Certain forms of poisoning associated ivith hemorrhage, such
as cantharis poisoning (blistering) and phosphorus poisoning
(an exceptional condition aside from speciaHzed industrial occu-
pations).
Separate recognition must also be given to hematuria of para-
sitic origin of the type of bUharziasis, a condition met with ex-
clusively in tropical countries or in individuals coming from such
Fig. 734. — Bilharzia ova.
countries. The finding of the parasitic oya in the urine will alone
suffice for diagnostic purposes.
Finally there remain the crjrptogenic hematurias of unknown
origin, including vicarious hematuria, occurring in place of the
menstrual flow; the diathetic hematurias, renal "epistaxis," etc.
In any case of total hematuria, the physician must strenuously
endeavor to find out the source and the cause of the bleeding.
Cystoscopy will of itself generally permit of establishing the
origin of a vesical hematuria.
Catheterization of the ureters, by enabling the practitioner to
collect separately the urine from the two kidneys, will give an idea
of the actual functional capacity of each kidney, permit of cyto-
logic and bacteriologic studies of the individual urines, and lead
accurately to discovery of the cause of the bleeding.
Radiography is likewise of considerable service.
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HEMATURIA.
1011
FALSE HEMATURIA.
Mention should also be made of the false or pseudo-hematurias,
in which the urine is colored red by one of a number of different
drugs.
Red discoloration of the urine by various drugs
{pseudo-bloody urine). ^
Antipyrin:
Pyramidon:
Sulphonmetfaanum :
Phenol and its Salts:
Cryogenin:
Cascara:
Senna:
Rhubarb:
Blood-red color.
Cherry-red or salmon color.
Brownish red color.
Reddish brown color.
Reddish dark yellow with a species of iridescence.
Reddish yellow or brown (red if urine is alkaline).
Reddish yellow or brown (red if urine is alkaline).
Reddish yellow or brown (red if urine is alkaline).
* *
For clinical purposes, the commonest causes of hematuria ap-
pear to be those given in the following table :
After Jacquot, Union pharmaceutique, 1916.
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1012
SYMPTOMS.
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HEMIPLEGIA.
iffiuyvg^ half; nXrc/uv^ to strike; more
or less complete loss of motion in
one side of the body.
The term hemiplegia refers to a paralytic condition restricted to
one lateral half of the body, right or left. Hemiplegia may be com-
plete or incomplete according to the degree of paralysis. As a rule
its presence is very readily observed.
For practical purposes the diagnosis of hemiplegia necessarily
entails an answer to each of the two following questions:
1. Where is the lesion located?
2. What is its nature?
I. Location of the lesion. — The site of disease, usually located
at some point along the pyramidal tract, may be either cerebral
(cortical or capsular), mesocephalic (peduncular or pontine), bul-
bar, or spinal. Clinically, hemiplegia of cerebral origin is far
more frequent than all other varieties combined. These various
types of hemiplegia are rather easily distinguished by virtue of
the following features :
A. Paralysis of cerebral origin is of the hemiplegic type, in-
volving more or less completely the face and the upper and lower
extremities. It usually sets in with an apoplectic attack; is some-
times associated with conjugate deviation of the head and eye-
balls, and spares the muscles having synergistic bilateral motor
functions.
The sensory functions are seldom affected ; the tendon-reflexes
are, as a rule, exaggerated ; there is inversion of the plantar reflex
( see Reflexes: Babinskis sign). Muscular atrophy is never present
at the outset and seldom later. On the contrary, secondary con-
tracture frequently occurs at the end of two or three months.
Cortical hemiplegia, usually induced by cerebral softening as a
result of embolism or thrombosis, is distinguished from capsular
hemiplegia, the result of cerebral hemorrhage, by the following
features :
(1014)
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HEMIPLEGIA. 1015
Hemiplegia of cortical vrigin {cerebral softening):
Hemiplegia complete or incomplete.
Aphasia frequently present.
Tendency to recession of paralysis in the days following the
stroke.
Hemiplegia of Cerebral Origin.
Paraljmis of the lower branch of the facial and of the extremities
on the side opposite the lesion.
Gsion.
Paralyi iralysls
Fig. 735.
Hemiplegia of capsular origin (cerebral hemorrhage) :
Hemiplegia complete and permanent.
No aphasia.
Tendency to extension in the days following the stroke.
Initial reduction of body temperature.
Early contractures.
Conjugate deviation of the head and eyeballs.
More frequent involvement of the right side.
(These diflferential features, however, are not absolutely reliable).
B. Paralysis of mesocephalic origin, relatively uncommon, oc-
curs in the form of an alternate (crossed) hemiplegia, the extremi-
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1016 SYMPTOMS.
ties being paralyzed on one side and the face or eyeball on the
other.
1. Alternate hemiplegia of peduncular (upper pontine) origin
results in the so-called syndrome of Weber, with paralysis of the
face and limbs on the side opposite to that of the brain lesion,
and oculomotor paralysis on the same side. As shown in the
annexed illustration :
Anatomic Features.
Fig. 736. — Striate arteries — capsular hemorrhage. /. Internal carotid.
2, Anterior cerebral artery, j. Middle cerebral artery coursing through
the Sylvian fissure. 4. Internal striate arteries. 5. External striate
arteries. 6. The artery of cerebral hemorrhage, with a miliary aneurysm
in its course. 7. Cerebral hemorrhage. 8. Caudate nucleus. 9. Optic thal-
amus. 10, Internal capsule. //. Claustrum. 12. External capsule. 13.
Lobule of the insula. 14, Lenticular nucleus or extraventricular nucleus
of the corpus striatum.
(a) The lesion of the pyramidal tract and geniculate fibers
before their decussation results in paralysis of the face and ex-
tremities on the side opposite to that of the lesion.
(fc) The lesion of the oculomotor or 3d cranial nerve at its
origin causes, on the same side as the brain lesion, paralysis of
the superior rectus, inferior rectus, internal rectus, inferior ob-
lique, pupillo-constrictor, and levator palpebrae muscles, such
paralyses, in turn, resulting clinically in blepharoptosis, mydriasis,
divergent strabismus, paralysis of accommodation, and crossed
horizontal diplopia.
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HEMIPLEGIA. 1017
2. Alternate hemiplegia of pontine {lower pontine) origin re-
sults in the so-called syndrome of Millard-Gubler, .with paralysis of
the limbs on the side opposite to that of the brain lesion and
paralysis of the face and internal oculomotor on the same side.
As shown in the annexed illustration :
(a) The lesion of the pyramidal tract before its decussation
results in paralysis of the extremities on the side opposite to that
of the lesion.
(fc) The lesion of the facial or 7th cranial nerve at its origin
results in paralysis of the face on the same side as the brain lesion.
Fig. 727. — Branches of the middle cerebral artery. Cerebral softening.
J. Middle cerebral artery. 2, External orbital artery. 3. Inferior frontal
artery. 4. Ascending frontal artery, 5. Ascending parietal artery. 6,
Inferior parietal artery. 7. Artery to angular gyrus. 8. Temporal arteries,
p. Near the origin of the Sylvian artery are to be seen the perforating
(anterolateral) arteries.
It should be noted that in embolism (as by a piece of valve, vegetation,
or clot), the occluding foreign body rarely enters the innominate artery,
which opens obliquely into the arch of the aorta, but nearly always passes
into the left carotid, which forms an almost direct prolongation of the aortic
arch. Thus, hemiplegia due to embolism is almost always a right-sided
hemiplegia, due to a lesion of the left cerebral hemisphere.
(c) The lesion of the external oculomotor (abducens) or 6th
cranial nerve at its origin results in paralysis of the external
rectus muscle on the side of the brain lesion, i.e., clinically in con-
vergent strabismus with homonymous diplopia (displaced image
on the same side).
The aphasia bundle passes down from Broca's convolution to
the anterior portion of the internal capsule and from there to the
bulbopontine centers of articulate speech production.
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1018 SYMPTOMS.
The geniculate bundle passes down from the foot of the ascend-
ing frontal convolution, passes through the internal capsule at
the genu, decussates at the pons (see below), and terminates in
the centers of the facial and hypoglossal nerves.
■ Geniculate flbera
(facial).
■ Tmo'i?).' ''•"' ^ Eil Apha-la bundle.
B Sensory tract. ^ Gray matter.
Fig. 738. — Diagram of the motor and sensory paths in the
brain and spinal cord.
The pyramidal tract passes down from the central convolutions,
passes through the internal capsule in its posterior and middle
portion, behind the geniculate ganglion, and decussktes with the
pyramidal tract of the opposite side at the bulbar pyramids, after
giving off a direct bundle which remains in the corresponding
half of the cord.
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HEMIPLEGIA. 1019
Peduncular hemarrhage.
Weber's syndrome or superior alternate hemifrfegia.
>
A
sLfion^*
^^
Fig. 739. — /'. Paralysis of the extremities on the side opposite the brain
lesion. 2. Oculomotor paralysis on the same side as the lesion, (a)
Ptosis. (6) Outward deviation of the eye owing to persistence of func-
tion of the fourth and sixth cranial nerves.
Inferior pontine hemorrhage.
Syndrome of Millard-Gtibler. Inferior alternate hemiplegia.
2
Fig. 740. — /. Paralysis of the extremities on the side opposite the brain
lesion. 2. Paralysis of the face on the same side as the lesion, j. Paral-
ysis of the sixth cranial nerve on the side of the lesion, causing conver-
gent strabismus through deviation of the eye inward and downward.
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Anatomic Relations.
Cerebral peduncles
Left genicula nlculate fibers
Left pyramidal rramldal tract
Right oculo-
motor Den ft oculomotor nerve
Right
geniculate fibers- ns
ft geniculate fibers
Right oculo- . « . ^
motor nerve- Left sixth cranial
nerve
Right facial nen ''t facial nerve
ive
Hypoglossal nen
Right pyramidal tra< ramidal tract
Fig. 741.
1. High lesion involving peduncle and pons.
Superior alternate hemiplegia.
1. Involvement of the pyramidal tract above its decussation : Paralysis of
the extremities on the side opposite the lesion.
2. Involvement of the facial above its decussation : Facial paralysis on the
side opposite the lesion.
3L Involvement of the oculomotor on the side of the lesion : Oculomotor
paralysis on the side of the lesion (superior rectus, inferior rectus, internal
rectus, inferior oblique, constrictor of the pupil, and levator palpebrse super-
ioris), whence:
Blepharoptosis, mydriasis, paralysis of accommodation, divergent stra-
bismus, and crossed horizontal diplopia.
2. Inferior pontine lesion.
Inferior alternate hemiplegia.
1. Involvement of the pyramidal tract above its decussation : Paralysis of
the extremities on the side opposite the lesion.
2. Involvement of the facial below its decussation : Facial paralysis on the
side of the lesion.
3. Involvement of the abducens at its point of origin: Paralysis of the
external rectus on the side of the lesion, whence :
Convergent squint with homonymous diplopia (false image on same
side).
3. Bulbar lesion (very rare).
1. Involvement in the vicinity of the olive, affecting the hypoglossal and the
pyramidal tract above its decussation.
2. Involvement of the pyramidal tract above its decussation : Paralysis of
the extremities on the side opposite the lesion.
3. Involvement of the hypoglossal at its point of origin : Paralysis of the
tongue on the side of the lesion.
(1020)
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HEMIPLEGIA,
Bulbar lesion.
Lesion
1021
Fig. 742.—/. Paralysis of the extremities on one side. 2. Paralysis
of the tongue on the opposite side.
Section of the cervical cord (extremely rare).
Spinal hemiplegia.
Brown-S6quard'8 ssmdrome.
S
8 /
Fig. 743. — I. Paralysis of the extremities on the side of the lesion. 2,
Hemianesthesia on the side opposite the lesion, s. Face unaffected.
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1022 SYMPTOMS,
The sensory tract originating from the posterior columns of the
spinal cord ascends to the bulb, where it decussates at the pos-
terior portion of the cerebral pedvmcles, passes through the in-
ternal capsule in its posterior part, and terminates in the occipital
convolutions.
C. Hemiplegia of bulbar origin is exceedingly uncommon.
I. Olfactory
II. OpUc
III. Oculoi
IV. Pathetic ne
V. Trifacial ne
te of
VI. Abducens ne ^
VIII. Auditory ne
VII. Facial nerve
IX. Glossopharyngeal
X. Pneumogasti
XII. Hypoglosi
XI. Spinal accessory n(
I. Cervical n<
Fig. 744. — The medulla and pons.
The commonest example of superior bulbar paralysis is that at-
tending polioencephalomyelitis, the cardinal syndrome of which is
external ophthalmoplegia, i,e,, paralysis of all the muscles of the
eye except the pupillary muscles.
The commonest example of inferior bulbar paralysis is that of
labioglossolaryngeal paralysis, attended with paralysis and atrophy
of the lips, tongue, muscles of mastication, soft palate, and laryn-
geal muscles, resulting in progressive disturbances of deglutition,
respiration, and circulation.
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HEMIPLEGIA.
1023
' (a) The lesion of the pyramidal tract before its decussation
(see p. 1020) results in paralysis of the extremities of the opposite
side.
(fc) The lesion of the hypoglossal nerve at its origin causes
paralysis of the tongue on the same side as the lesion.
D; Hemiplegia of spinal origin, a condition wholly exceptional
in the absence of traumatic injury of the cervical cord, results in
the so-called syndrome of Brown-Sequard, in which there is paralysis
of the limbs on the side opposite to that of the lesion, anesthesia
likewise of the opposite side, and the face and eyes uninvolved,
E. Finally, one should not overlook the possibility of a purely
functional hemiplegia, independent of any nervous lesion.
Hysterical hemiplegia is diflferentiated from the organic hemi-
plegias already described by the following features :
Differential Diagnosis.
Obganic Hsmiplboia.
Hysterical Hemiplboia.
The tendon and skin reflexes are
affected:
There is exaggeration of the
patellar reflex, abolition or dimi-
nution of the skin reflexes, and
inversion of the plantar reflex
(toe phenomenon or Babinski
sign).
The tendon and skin reflexes are
unchanged. The toe phenom-
enon (Babinski sign) is absent.
The disturbances of sensation de-
crease as one ascends from the
distal to the proximal portions
of the extremities.
The anesthesia or hypoesthesia
present is of the hemianesthetic
type.
There is usually no facial paral-
ysis, although there is some-
times glossolabial spasm on the
opposite side.
The patient is suffering from
heart disease, arteriosclerosis,
syphilis, uremia, or other con-
dition.
The patient is generally young,
most often of the female sex,
and exhibits stigmata of hys-
teria and neuropathic evidences.
The syndrome appears abruptly,
frequently after some emotional
impression.
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1024 SYMPTOMS.
II. What is the cause of the hemiplegia?
Certain general features of nervous disease may, in the first
place, be referred to.
The brain is more frequently affected by disorders of vas-
cular origin (thrombosis or hemorrhage) than by inflammatory
disorders (meningo-iencephalitis) .
The spinal cord is more frequently involved in inflammatory
degenerative processes, acute (myelitis) or chronic (systema-
tized sclerotic processes), than in vascular lesions.
The peripheral nerves are oftenest affected by intoxications
(alcoholism, lead poisoning, etc.), infections (diphtheria, typhoid
fever, etc.), and traumatic injuries.
It is impracticable and would be tiresome to review all the
possible causes of hemiplegia.
Let it be borne in mind that practically ps per cent, of all hemi-
plegias are dependent upon arteriosclerosis, Bright's disease, syph-
ilis, alcoholism, or rheumatism (endocarditis), and that these several
causes can be almost always discovered by the following plan of
examination :
1. History: Age, vertigo, mental impairment (arterio-
sclerosis).
Polyuria, nycturia, albuminuria, etc. (Bright's disease).
Specific history (syphilis).
Intemperate habits (alcoholism).
Acute rheumatism or other acute infection.
2. Auscultation: Aortic evidences (arteriosclerosis, specific
aortitis).
Aortic evidences with gallop rhythm (Bright's disease).
Mitral or mitro-aortic evidences (rheumatism).
3. Examination of the urine: Albuminuria and casts
(Bright's disease, arteriosclerosis).
4. Blood-pressure determination: Pressure particularly high
in arteriosclerosis and Bright's disease.
5. Special features of the hemiplegia per se,
(a) A right-sided hemiplegia without apparent cause, after a
short period of dizziness, with or without an apoplectic stroke, and
without temperature changes, generally points to softening of the
brain due to thrombosis in an arteriosclerotic subject.
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HEMIPLEGIA,
1025
(8) A right- or left- sided hemiplegia, appearing after an apo-
plectic stroke in a middle-aged or old subject is generally dependent
upon cerebral hemorrhage, the commonest causes of which are
Bright' s disease ^nd arteriosclerosis.
The predisposing influence" of plethora in males and of the
menopause in women may here be noted.
(c) An incomplete right-sided hemiplegia, appearing abruptly,
without a stroke, in a young or adult subject suffering from mitral
or mitro-aortic endocarditis is induced by cerebral embolism occur-
ring as a complication of endocarditis,
(rf) A right-sided, progressive hemiplegia, appearing without
an apoplectic stroke in a young or adult subject who is syphilitic is
generally due to syphilitic arteritis.
{e) A hemiplegia appearing more or less abruptly in a young
or adult subject addicted to alcoholism, and soon accompanied by
contractures or even convulsive attacks of the Jacksonian type
should direct the observer toward the thought of a hemorrhagic
pachymeningitis in an alcoholic individual,
(/) The following brief tabular statement of the diagnostic
featuresi of facial paralysis should be kept constantly in mind :
Facial Paralysis.
Medical
causes
(fl) Peripheral
I (b) Central
Both branches are involved; in-
fluenzal neuritis, and the ordi-
nary so-called "rheumatic"
facial paralysis.
C Lower branch alone involved;
\ cerebral hemorrhage or soften-
L ing, or tumor of the cortex.
Traumatic
causes . ..
(a) Intratemporal
{b) Extratemporal
{Fractured skull, foreign body in
the mastoid, or mastoid opera-
tion.
Wound of the face by a missile
or by an operation in the paro-
tid region.
(After Pauchet).
6. Blood examination (blood obtained by cupping or vein
puncture).
65
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1026
SYMPTOMS.
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HEMIPLEGIA.
1027
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1028 SYMPTOMS.
(a) The W.assermann reaction, if positive, will confirm the
diagnosis of syphilis if it has already been rendered, or will draw
the observer's attention in that direction in doubtful cases.
(fc) Determination of the blood urea: Blood urea exceeding
0.80 gram indicates the presence of uremia.
Much might be written concerning the relationship of uremia to
hemiplegia. Formerly it was practically an established custom to
consider the terms relatively antagonistic. At the present time one
cannot help noting that these two conditions bear most intimate
clinical interrelationships, and that hemorrhages (including cerebral
hemorrhage), high blood-pressure, azotemia, and albuminuria are
practically common accompaniments of arteriosclerosis and nephr-
itis. Concomitance of the two conditions is, indeed, the clinical
rule. Most of the author's cases of sclerosis with hemiplegia have
been azotemic, and many of his uremic subjects have shown a
terminal hemipl^ia. Such are the actual facts in this connection.
7. Examination of the cerebrospinal fluid. — ^This is of espe-
cial service for the detection of :
1. Hemorrhagic states : Cerebral and meningeal hemorrhage
(red blood cells in the cerebrospinal fluid).
2. Inflammatory states: Meningitis (leucocytosis; presence
of pathogenic bacteria).
The annexed clinical table summarizes the iacts already re-
called.
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«i7iurrki>T»vcTC faW* hlood; nrvCLg, spitting. Spitting']
inii.MUi'l Yblb. 1^ of blood. (See Expectoration.) J
Hemoptysis, defined as the expectoration of blood set free in
the air passages, is very often an obvious occurrence ; yet rather
frequently the fact that the blood expectorated has come from
the broncho-pulmonary tract requires to be investigated, verified,
and proven. Hemoptysis and hematemesis are often confused,
and even more frequently, more or less deeply blood-stained dis-
charges of nasal, lingual, gingival, or laryngeal origin are put
down as constituting hemoptysis.
Epistaxis. — Production of bloody expectoration by epistaxis,
especially of the posterior variety, is a very commonly observed
occurrence. Where expectoration of blood attends an anterior
"external" epistaxis, the source of the blood is obvious; where,
however, it is not accompanied by "nosebleed," examination of
the pharynx and even the nasopharynx is indicated. Naso-
pharyngeal hemorrhage is generally of dyscrasic origin (hemo-
philia or high blood-pressure) or the result of ulceration, rupture
of a varicose vessel, or ani adenoid inflamrtiation which careful
examination cannot fail to detect.
The only real, though slight, diagnostic difficulty arises from
the fact that blood shed in the nose or pharynx may actually be
swallowed or coagulate in the nasopharynx itself and be dis-
charged only by a spell of coughing. Under these conditions
the blood is more or less mixed with mucus from the stomach
or nasopharynx and may, upon hasty examination, be deemed to
have issued from the lung or stomach. The opposite mistake,
which consists in carelessly ascribing to the nasopharynx a
hemorrhage actually occurring in the stomach or lung, is much
more serious.
Let it be repeated once again that a careful general examina-
tion— including that of the nasopharynx — will inevitably and
(1029)
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1030 SYMPTOMS.
promptly lead to a correct determination of the source of expec-
torated blood.
The lingual origin of blood expelled from the mouth may be
noted in the event of a bite of the tongue, traumatic or "epi-
leptic," or of a tuberculous or neoplastic ulceration. Mention of
this cause of blood spitting, which could confuse only a very
careless or inexperienced practitioner, is required merely for
the sake of completeness and because it is customary to do so.
Bleeding from the gums is extremely common, even inde-
dendently of scurvy and hemophilia, which are themselves ex-
ceptional disorders. The ubiquitous pyorrhea alveolaris, various
diathetic disturbances, and even abuse of the tooth brush may
induce swelling and "inflammation" of the g^ms and render
them both sensitive and prone to bleed. Under these circum-
stances the least contact with the gums results in oozing which
stains all sputum with blood and gives rise to "pseudo-hemo-
ptysis." A most casual examination of the gums will discover the
actual source of the bleeding to be in these structures.
Hemorrhage in the larynx may result either from traumatism
or from ulceration. The former is readily excluded. Ulcerations
are always either syphilitic, tuberculous, or cancerous ; they are
always attended with hoarseness and local pain ; they are always
preceded by a period during which the attention was drawn to
and fixed upon the larynx. Examination of the larynx with the
mirror will always demonstrate the laryngeal source of the
bleeding.
The only real difficulty in diagnosis is that sometimes met
with in the differentiation of hemoptysifl from hematemesis, which
may constitute a most puzzling problem (see Hemat erne sis).
As a rule, there is little trouble in this connection :
The preliminary symptoms are different, being
Digestive in hematemesis and respiratory in hemoptysis.
The manner in which the blood is expelled is likewise different.
In hemoptysis there are attempts at coughing and the blood
is liquid, red, and foamy.
In hematemesis there is retching and the blood is clotted,
dark colored, without admixture of air, but mixed with food
material; sometimes intestinal hemorrhage coexists.
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HEMOPTYSIS. 1031
All these signs, however, are unreliable.
In hemoptysis there may be dark colored blood (pulmonary
hemorrhage) and in hematemesis red blood (gastric ulcer).
In hemoptysis the preliminary cough may be wanting, while
on the other hand there may be concomitant vomiting and con-
sequently admixture of blood with food material.
In hematemesis the blood may or may not be mixed with bile
or food material.
After careful deliberation and thorough examination the con-
clusion may eventually be reached that hemoptysis has occurred.
♦ ♦ ♦
The diagnosis of "true hemoptysis" having been correctly made
— ^and definitely established, i.e., on the whole, the presence of
blood in the sputum either being obvious or having been demon-
strated by suitable hematologic procedures; the supposition of
hematemesis having been excluded, sometimes a difficult matter,
as the author has seen mistakes in this ccmnection made (and later
proven) by experienced observers; and the oropharynx, gums,
tongue, and nasopharynx being readily eliminated as sources of
bleeding by a mere citrsory examination, provided it is actually
carried out, — ^the cause of the hemoptysis is generally^ very easily
found if the following fundamental propositions are kept in mind :
1. Eleven-twelfths of all instances of true hemoptysis are of
cardiopulmonary origin and are due to one of two following
causes :
(a) Pulmonary tuberculosis in any one of its stages, from the
pretuberculous congestive stage to the stage of cavity pro-
duction.
(b) Infarction of the lung, generally secondary either to a
mitral disorder, particularly mitral stenosis; to some cardio-arterial
disorder which has advanced to the stage of decompensation with
stasis, or to phlebitis in any of its stages, from the pre-obstructive
stage to the stage of disintegration of the intravascular clot.
Pulmonary tuberculosis is a far more frequent cause than in-
farct of the lung. As for the latter, its cause is nearly always
obvious upon any sort of careful examination (mitral stenosis,
heart failure, puerperal, infectious, or post-operative phlebitis, etc.) ;
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1032 SYMPTOMS,
frequently, moreover, infarction is marked by a sudden pain in the
side with cough, dyspnea, and even orthopnea, an area of fine
rales, etc.
Thus, any case of hemoptysis unattended with cardiovascular
disease (heart disease or phlebitis) may be considered to be in
all likelihood tuberculous. Furthermore, the hemoptysis of ad-
vanced tuberculosis, in the stages of softening or cavity forma-
tion, cannot fail to be recognized, as its source is quite obvious.
Doubt may arise only in connection with the premonitory
Fig. 745. — Diagram of pulmonary infarction. The embolus, having
become detached at some point in the inferior vena cava {v, c. i.) or its
tributaries, or in the superior vena cava {v. c. s.) or its tributaries, passes
through the right auricle {o. rf.), is discharged into the pulmonary artery
(a. />.), and lodges in one of the lobes of the lung, giving rise to an infarct
which finds its clinical expression in : 1. A sudden sharp pain in the side.
2. Blood-spitting (hemoptysis). 3. The physical signs shown in Figs. 746
and 747.
hemoptysis at the very beginning of tuberculosis, accompanied
by little in the way of general or auscultatory evidences, or even
occurring at a time when the disease is as yt^t entirely latent.
Any true hemoptysis of obscure, cryptogenic origin should be
considered of tuberculous nature imtil proof to the contrary is
obtained, and the patient kept under careful observation as re-
gards body weight, temperature, general health, and examina-
tion of the lungs ; this is a clinical axiom from which the practi-
tioner should never depart, lest he take upon himself a most
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HEMOPTYSIS,
1033
serious responsibility and meet with egregious disappoint-
ment
The only real difficulty in these cases lies in the possibility of
simultaneous mitral stenosis and pulmonary tuberculosis; only
rarely, however, will careful observation of the patient's general
condition and temperature and systematic, repeated ausculta-
tion of the lungs fail sooner or later to afford a distinction be-
tween the manifestations appertaining to one or the other of
these disorders.
Certain instances of hemoptysis, due exclusively to mitral
stenosis and associated with marked and persistent hyperemia of
Phjrsical signs.
■^ Weakened or muffled breathing.
Ck^ Surrounding area of crepitant rales.
Figs. 746 and 747. — Pulmonary infarction.
a pulmonary apex, may, however, hold the diagnosis in suspense
for a time.
2. One twelfth of all instances of true hemoptysis may be
referable to exceptional or obvious or, on the other hand, with
difficulty detected causes.
Among the obzious causes, traumatism is the most important;
thus, a chest wound or contusion, a fractured rib, or gas poisoning
are obvious conditions.
The majority of acute and, particularly, chronic affections of
the lungs may ultimately be associated with hemoptysis. Ac-
cordingly, hemoptysis may be met with in pneumonia, chronic
bronchitis with dilated bronchi, abscess of the lung, broncho-
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1034 SYMPTOMS.
pulmonary gangrene, and syphilitic or cancerous involvement.
Frequently the clinical evidences present in conjunction with the
hemoptysis are such, especially in bronchiectasis and pulmonary
abscess or gangrene, as to make the diagnosis perfectly plain ;
syphilis and cancer, however, require a painstaking examination
for their detection, and especially, the actual thought of their
possible presence on the part of the physician.
Fig. 748. — Aneurysm of the pulmonary artery {Letulle and Natlan-
Larrier. Microphotogr. by E. Normand. X5). n, ruptured wall of the
affected artery; c, tuberculous cavity bounded by a layer of caseous
material; x, a diverticulum of the aforesaid cavity; />, pulmonary vein,
occluded and included in the caseous layer about the cavity.
Hemorrhagic disorders, including the infectious purpuras, in-
fectious jaundice, hemophilia, leukemic conditions, etc., as well
as some severe forms of typhoid fever and malaria, may likewise
lead to hemoptysis, but in these disorders the hemorrhage takes
place in the presence of a clinical picture so definite as to leave
little chance of any actual difficulty in diagnosis. One of the
author's patients with arteriosclerosis and high blood-pressure
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HEMOPTYSIS, 1035
developed every spring, in April and May, for over ten years, a
varied assortment of hemorrhages, usually in the form of epi-
staxis, sometimes as hemoptysis and less frequently as hemor-
rhoidal hemorrhages of almost alarming extent ; the tenth year,
he developed a severe cerebral hemorrhage resulting in perma-
nent hemiplegia.
In addition to these hemorrhagic disorders mention should be
made of the congestive hemoptysic attacks of gouty patients; the
author has seen several instances of this condition. The history of
gout, the congestive nature of the pulmonary attack — ^which gen-
Fig. 749. — Diagram of a pulmonary lobule {Miller). B, terminal bron-
chus; y, vestibule; At, atrium; S, air-sac (infundibulum) ; C, air-cell
(alveolus) ; Ar, artery; V (at the right), vein.
erally involves the bases of the lungs and sometimes assumes the
appearances of acute edema — and the ovemourished aspect of the
patient directly suggest the diagnosis in such cases. Uremia may
give rise to a similar condition, the source of which is ascertained
by blood-pressure estimation and determination of the blood urea.
Aortic aneurysm may likewise lead to hemoptysis, under two
very different groups of circumstances. There may occur either
slight, intermittent hemoptysis, due to the presence of a slight
fissure at an area of adhesion of the aneurysm to the trachea and
sometimes compatible with life for a more or less prolonged
period, or else rupture of the aneurysm into a bronchus or the
trachea with fatal hemorrhage. From the diagnostic standpoint,
either the presence of aneurysm will already have long been
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1036 SYMPTOMS.
known at the time of the hemoptysis, the significance of which
will therefore be obvious, or the aneurysm will have up to that
time remained latent, either because of insufficient clinical ex-
amination or on account of a remarkable degree of tolerance of
the disease by the patient, who has not as yet consulted a physi-
cian. In no case of this type, to the author's knowledge, has
careful clinical examination failed to elicit some sign or other
of a mediastinal mass (bronchial murmur, collateral circulation
over the upper part of the thorax, pressure manifestations, pupil-
lary inequality, elevation or broadening of the arch of the aorta,
inequality of the right and left pulse, etc.).
Few symptoms, the reader will note, are of such definite
semeiologic significance as hemoptysis. Almost constantly it
constitutes an external expression of some pulmonary or cardiac
disorder, hemorrhagic diathesis, or manifest or latent congestive
state.
Does Vicarious Menstruation in the Form of Hemoptysis Act-
ually Occur? — Before concluding this section, mention may be
made of a very exceptional form of hemoptysis which has been the
subject of prolonged discussion and the diagnostic and prognostic
significance of which may be altogether different, vis., vicarious
menstruation through the lungs.
The reader's indulgence is requested by the author for de-
voting a disproportionate amount of space to this subject, but
the condition is a very peculiar and as yet variously regarded
one, and the following brief contribution to its study seems war-
ranted on condition that the reader makes good note of the fact
that this constitutes only a very exceptional form of hemoptysis.
According to many observers, particularly phthisiologists,
vicarious menstruation through the lungs is almost invariably
evidence of a manifest or threatening tuberculosis of the lungs.
The condition is, as a matter of fact, met with either singly
or repeatedly in not a few cases of pulmonary tuberculosis in
women. But the writer has also seen it in cases in which all
idea of an organic disease could be clinically excluded and in
which very prolonged later observation failed to show the exist-
ence of any morbid manifestation.
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HEMOPTYSIS, 1037
One case, among others, may be here referred to because the
period of observation was sufficiently prolonged to carry con-
viction. The patient was a young lady about twenty years of
age, free of any history of general disease, apparently in robust
health, having one child eighteen months old and another three
months old which she was nursing, and who, in November, 1901,
saw her menstruation stop suddenly on the second day and a
copious hemoptysis set in which continued for two days and
then ceased as it had come on, without apparent cause. The
patient, with whom the author had been acquainted for three
years, had had no discomforts during that time; her pregnancies
had been normal and unattended with any noteworthy difficul-
ties. The attack of hemoptysis referred to, aside from some
justifiable but temporary anxiety, was not associated with any
marked disturbance ; there was no rise of temperature nor of the
pulse rate, nor any dyspnea. Very careful auscultation gave
negative results.
Lactation was not discontinued and no special treatment was
instituted. Although kept under careful observation for a long
period, the patient showed no further untoward symptom. The
author has been seeing her at somewhat irregular intervals for
almost eighteen years, on account of illnesses of her husband or
children, and has not seen her health in the least impaired at
any time. No recurrence of the hemoptysis ever took place.
It would seem difficult to supply any more positive clinical evi-
dence than this.
An almost similar clinical picture was seen by the author in
a lady of thirty-five years; the ophthalmic test was negative.
From the ISth to 17th of May, 1908, he had occasion to observe
6 spontaneous hemorrhages, including 2 of copious epistaxis in
arteriosclerotic subjects, 1 of cerebral hemorrhage, 1 of hemop-
tysis in a consumptive, the case of vicarious hemorrhage already
referred to, and a case of vicarious epistaxis. In this more than
a mere coincidence was unquestionably involved; the subject
will be taken up again in a later publication.
Were the physician still to harbor any doubts as to the actual
occurrence of idiopathic hemoptysis vicariously substituted for
the menstrual flow, Ventura's case would certainly remove them
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1038 SYMPTOMS. .
(Gas. degli osped,. No. 129, 1907). This author gave the history
of a family in which substitution of periodic hemoptysis for
menstruation took place in three successive generations. The first
generation comprised three sisters; in one of them menstruation
was replaced by hemoptysis at monthly intervals. One of the un-
aflfected sisters had five female children, two of whom presented
the same clinical phenomenon as their aunt. Again, one of the
latter had four female children, two of whom showed the same
inversion of function. In none of these subjects was either
tuberculosis, syphilis, hemophilia, or cardiac disease discovered.
Finally, as an interesting clinical case, reference may be
made, although unrelated to hemoptysis, to a quite typical and
remarkable instance of menstrual substitution recorded by the
author at the Maison municipale de sante while in Danlos's
service.
The patient was a woman about forty years of age, short and
stout, who had had ten years before a child which she had nursed
for a long time (up to about two years) and who had had no men-
strual periods since that time but, on the other hand, had kept
on secreting milk continually, with periodic recrudescences, as
the author had occasion personally to observe. This woman
died of a brain tumor. At the autopsy a normal uterus but
atrophied uterine adnexa were found.
Thus, due recognition should be given to the actual occur-
rence of idiopathic hemoptysis, vicariously substituted for the
menstrual periods, in the absence of any organic disease in the
lungs or heart and of any hemorrhagic disorder of the blood.
The prognostic importance of this fact is self-evident.
4c 4c 4c
Bronchial Spirochetosis. — Castellani in 1905 described a special form of
bronchial infection observed in Ceylon and caused by spirochetes. In 1908,
American observers reported it from the Philippines, and others, in various
tropical lands. Experience during the great war led to the detection of a
considerable number of cases along the shores of the Adriatic and in Serbia,
Switzerland, Egypt, and France. The disorder is commonly mistaken for
tuberculosis, whether acute or chronic in form. The patients generally com-
plain of an obstinate! cough which gets worse at night and in the morning
and is associated with blood-stained expectoration. In the common, chronic
form of the disease, the patient is usually free of fever and the general
health may be slightly impaired. The diagnosis of the disease is based ex-
clusively on examination of the sputum for the organism termed by Castel-
lani Sptrochcpta hronchialis. It stains easily with the basic anilin stains, but
is negative to Gram's method (see p. 527).
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HICCOUGH.
Hiccough or hiccup consists of a clonic contraction of the
diaphragm. Its essential feature is a sudden inspiratory con-
traction of the diaphragm occurring in conjunction with a rapid
closure of the glottis; there result an abdominal spasm, inspira-
tion and sudden expulsion of air, consequent vibration of the
completely or partly closed glottis, and a hiccup sound which
may at times assume the characteristics of a bark.
A diagrammatic representation of the usually reflex patho-
genesis of hiccough is presented below.
The medullary center concerned adjoins that of the pneumo-
gastric and consequently the vomiting and respiratory (cough)
centers.
It appears to undergo direct stimulation, possibly through
the circulation, in the course of "grave infections'* and "agonic
states," the resulting condition constituting a terminal form of
hiccough.
The centripetal (afferent) routes of stimulation consist chiefly
of the pneumogastric nerve and secondarily ofJ the sympathetic and
certain cortico-bulbar fibers.
Through the pneumogastric (an appropriately named nerve) :
The center may be brought into activity by stimuli starting :
(a) From the abdomen (subdiaphragmatic region) :
1. From the stomach: This is the starting-point of hiccough in
4 out of 5 cases, e.g., very commonly in infants after nursing, in
dyspepsia (especially of the neurotic type), in dilatation of the
stomach, aerophagia, tachycardia, the ingestion of unduly hot or
cold food, and much less frequently in ulcer and cancer of the
stomach. In these cases the hiccough may be either continuous or
intermittent, appearing and disappearing for no evident reason or
when the subject takes food or a little fluid.
2. From the intestine : Helminthiasis.
3. From the peritoneum: Peritonitis, especially when situated
below the liver.
(1039)
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1040 SYMPTOMS.
4. From the female reproductive organs: Genitourinary and
uterine disorders.
(b) From the thorax (supradiaphragmatic region).
1. In diaphragmatic pleurisy: Actually a rare cause, the stimu-
lus being ordinarily inhibited by pain. The same is true in pneu-
monia.
2. In car dio pericardial disturbances : Hiccough is observed espe-
cially in pericarditis, particularly at the beginning, when the phe-
Medullanr center. ^^SSdS °'
1^6&r th© "v**"™ '*'•*"■ ««»Ti*oi»" anil thfl "i>oaf\li>atm>tr
center." This c
—possibly throu
tioDS and In age
Diaphragm
The stomach
ordinary blccouf
cold, etc.. or t
Fig. 750. — Diagram illustrating the pathogenesis of hiccough.
nomena of irritation are still predominant. Exceptionally the
author has seen it in lesions of the aortic arch, aortitis, and aneurysm.
The same is true of heart disorders, such as acute or chronic endo-
carditis, myocarditis, etc.
The SYMPATHETIC ROUTE may in all likelihood be one of the
afferent routes of stimulation of the phrenic nerve, chiefly in the
presence of heart disturbances.
Finally, the corticobulbar routes of stimulation are those involved
in psychoneurotic states (tic-hiccough), in hysteria (barking hic-
cough), and in meningitis.
The centrifugal (efferent) routes of transmission are chiefly
represented by the phrenic nerve which is the motor nerve to the
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HICCOUGH. 1041
diaphragm and the gross anatomic relationships of which should
always be kept in mind. Issuing from the cervical plexus, it
passes down, crosses the anterior aspect of the scalenus anticus
muscle, runs down along the internal border of this muscle,
enters the thorax, and passes, on the right side, between the sub-
clavian artery and vein, on the lateral aspect of the pneumo-
ScalenuB an
Phrenic d
Subclavian ai
Superior Tena cai
Phrenic nerve.
Fig. 751.— The phrenic nerves {Hirschfeld),
gastric, and along the superior vena cava, and on the left side, be-
hind the innominate artery, crossing the arch of the aorta. It
then courses on either side between the pleura and the pericar-
dium and ends in ramifications over the upper surface of the
diaphragm.
It receives the stimuli issuing from the pneumogastric :
1. Through the intermediation of the medullary center of
this nerve and through the anterior gray horns.
2. Through the cervical plexus (whence the phrenic nerve
originates from three roots), being connected with the pneu-
G6
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1042 SYMPTOMS.
mogastric through the gangliform plexus by means of one or
two nerve filaments.
It is enabled to receive the stimuli from the sympathetic by
reason of the many anastomotic connections between the cer-
vical plexus and the sympathetic.
The actual cortico-bulbar pathways are not as yet satisfac-
torily known.
Recoftnition of the cause of hiccough is based chiefly upon the
associated symptoms or physical signs, which may indicate gastric
disturbance, peritoneal or meningeal involvement, psychoneu-
rosis, etc.
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HIGH BLCX)D-PRESSURE.
Inspection of a sphygmographic tracing of the pulse, such as
that presented herewith (Fig. 752), in which variations of blood-
pressure within the artery under examination are elicited and
recorded, is sufficient to show that this pressure is a variable
quantity and that it exhibits both a high point corresponding to
cardiac systole (the maximal or systolic pressure) and a low
point corresponding to diastole (the minimal or diastolic pres-
sure). There is thus not one single blood-pressure, but several
TVT^^TU
. Systolic
Diastolic
Fig. 752. — Pulse tracing showing the successive variations of pressure
within the lumen of an artery.
blood-pressures. The maximal pressure corresponds to but a
very brief portion of the cardiac cycle, the point of culmination
of the systole. The minimal pressure, on the other hand, consti-
tutes the permanent, basic pressure below which the pressure
never descends; it will be seen at once that this latter pressure
is at least as important to know, and perhaps even more impor-
tant, than the maximal pressure. The difference between the
maximal or systolic and the minimal or diastolic pressures, the
differential or pulse pressure, bears a manifest relationship to
the force of the pulse and consequently to the cardiac contrac-
tion. The diagram herewith presented will demonstrate at once
the main features and mutual relationships of these several
grades of pressure (Fig. 753).
All of these three grades must be taken into account if an
approximate idea of the general circulatory condition in a given
subject is to be obtained.
(1043)
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1044
SYMPTOMS.
The maximal or systolic pressure has long been, and still is, the
kind of blood-pressure investigated by the majority of cardiologists.
Yet it is certainly insufficient to afford an exact idea of the cir-
culatory balance in a given case. Convincing evidence of this is
relatively easily given. Following are two sphygmomanometric
tracings (Fig. 754) taken from the same patient, the one directly
It
160
I
Pulse pressure
Diastolic pressure
ryy/V/V/VI
(90)
I.
Fig. 753. — Diagram illustrating the systolic, diastolic, and pulse
(differential) blood-pressures.
during an attack of heart failure, and the other during convales-
cence with a normal condition of circulatory equilibrium. The
systolic and differential pressures are the same, vis,, 200 milli-
meters Hg, in the two cases, but the minimal and differential
pressures show, on the contrary, pronounced changes. This
single example, taken from among many others, is sufficient to
200
200
^VTV
Fig. 754. — Blood-pressure determinations made in a single individual,
a few days apart, the patient having heart failure in A, but restored
compensation in B,
show that henceforth it will be necessary to be able to determine
both the systolic and the diastolic pressures ; this is one reason,
and perhaps the most important one, which led the author to
adopt the Pachon oscillometer in his blood-pressure studies.
The normal systolic pressure ranges from 140 to 160 milli-
meters Hg (Pachon) in different individuals; exceptionally, the
writer has found it 130 or 170.
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HIGH BLOOD-PRESSURE, 1045
This observation is in itself of considerable practical impor-
tance, showing that the concept of high blood-pressure is act-
ually a relative or individual quantity. A person whose normal
systolic blood-pressure was 130 would already be suffering from
a marked increase in blood-pressure at 190 millimeters Hg; on
the other hand, 190 would, constitute but a moderate degree of
hypertension in a patient whose normal pressure was 170.
High systolic blood-pressure starts then, in the writer's
opinion, at 180 millimeters Hg.
For practical purposes three grades of high blood-pressure
may be recognized:
Slight hypertension, from 180 to 200, generally observed in
plethoric or full-blooded subjects and in the obese, gouty, or dia-
betic; generally a result of overeating.
Intermediate hypertension, from 210 to 250, likewise observed
in many of the plethoric subjects already enumerated, but also in
certain number of cases of arterial and renal sclerosis.
Marked hypertension, from 260 to 350, almost exclusively met
with in arteriosclerosis and interstitial nephritis.
This rough, simple nomenclature shows that the equation, high
blood-pressure = arteriosclerosis, is to a large extent in error, and
that, aside from organic (vasculorenal) hypertension, there occurs
also a functional (neurohemic) hypertension. This distinction is of
decided importance, for the treatment to be instituted is quite dif-
ferent in the two instances.
It should be borne in mind, moreover, that: (1) The sys-
tolic arterial pressure, like all other systemic coefficients (pulse
rate, temperature, urinary output, etc.), exhibits normal varia-
tions of 20 to 30 millimeters Hg in the course of the day, rising
from morning to evening, after meals, after exercise, etc. (2)
In some sphygmolabile, angiospastic subjects sudden, tem-
porary, and pronounced changes of pressure amounting to 40 or
50 millimeters, or even more, may be witnessed.
Whence 2 practical deductions: (1) In any g^ven subject
the blood-pressure should be taken, as much as possible, at the
same hour of the day, midway between meals, in order to obtain
comparable readings. (2) True, continuous high blood-pressure
should be considered present only after several pressure deter-
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1046 SYMPTOMS.
minations, made at intervals of several days, have actually
shown it to exist.
The minimal or diastolic pressure, or constant pressure,
varies within limits much more restricted than does the systolic
pressure.
In the normal subject, it commonly ranges between 80 and 100
millimeters Hg; 80 corresponding to the normally low systolic
pressures of 130 to 140 millimeters (Pachon instrument), and 100
to the normally high systolic pressures of 150 to 170 millimeters.
It is thus seen to be relatively stable as compared to the systolic
pressure.
Increased diastolic pressure is met with under the following four
circumstances :
1. In cases of markedly high systolic pressure with good com-
pensation (260 millimeters or higher), in which the sustained
diastolic pressure may reach 120 millimeters or even exception-
ally 130 millimeters.
2. In cases of heart failure, heart failure being associated much
oftener with an increase of diastolic pressure than with a reduction
of systolic pressure ; these two pressure indications may, indeed,
coexist; in fact, they are usually present together.
3. In cases of uremia,
4. In cases of plethora with venous congestion, especially in in-
dividuals exhibiting; the syndrome of increased portal pressure.
In short, high diastolic pressure is generally associated — if,
indeed, it is not actually its true sphygmomanometric expres-
sion— with high venous pressure, loss of cardiovascular balance,
heart weakness, or heat failure.
The highest diastolic reading the author has recorded was
190 millimeters, in a case of uremia with heart failure.
Thus, the diastolic pressure is seen to be of at least as great
diagnostic and prognostic significance as the systolic pressure.
Were it necessary to summarize the relative portent of high
systolic and high diastolic pressure in one brief, epigrammatic,
almost crude phrase, the matter might be expressed as follows:
High systolic pressure is the balistic high-pressure having to do
with rupture, hemorrhage, and apoplexy.
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HIGH BLOOD-PRESSURE. 1047
High diastolic pressure is the static high-pressure having to do
with loss of cardiovascular balance, venous congestion, and heart
failure.
The differential or pulse pressure, consisting of the difference
between the systolic and the diastolic pressures, commonly
varies in the same direction and almost to the same extent as
the systolic pressure in persons in a state of satisfactory cardio-
vascular balance ; thus, •/ absolutely necessary, the curve of varia-
tions in the systolic pressure, practically parallel to that of the
variations in the differential pressure, may be sufficient in fol-
lowing up the circulatory function in a subject with good cir-
culatory balance.
In a subject on the road to heart failure, on the other hand,
the differential or pulse pressure decreases much more quickly
or rises much more slowly than the systolic pressure. Discrep-
ancy is shown between the courses followed by these two kinds of
pressure. To estimate the progression of heart failure, the pulse
pressure seems to the writer to be essential.
Thus, one is led to consider the pulse pressure as a reflection
or sphygmomanometric expression of cardiac power. Indeed,
constitutionally weak individuals with congenitally small hearts
show a low pulse pressure (20 to 40 millimeters Hg) ; well com-
pensated cases of arteriosclerosis with **ox hearts" show an
enormously high pulse pressure (100 to 250 millimeters) ; cases
of heart failure with low pulse pressure generally show a grad-
ual gain in the pulse pressure as the heart recovers its func-
tional power and the output of urine undergoes a corresponding
increase, etc.
A rather absurd objection is sometimes made to this rela-
tionship of the pulse pressure to cardiac power, which at least
has the advantage of bringing out in striking fashion the impor-
tance of the diastolic pressure; and, strangely enough, this objec-
tion has been raised by the very persons who have overlooked
the latter variety of pressure. Thus, it has been said that it is
absurd to believe that any relationship exists between the pulse
pressure and cardiac power. Take two individuals, for example :
The first shows 160 millimeters as systolic, 90 as diastolic, and
70 as pulse pressure, and is in a satisfactory state of circulatory
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1048
SYMPTOMS.
balance; the second shows 260 millimeters as systolic, 190 as
diastolic, and again 70 as pulse pressure, but is already in a state
of complete decompensation, although the pulse pressure is the
same in the two cases. Quite so. The above remark is of exactly
the same order as would be one to the effect that, strangely
enough, a mover carried a trunk from the ground floor to the
second story without any trouble but gave out in going from
Blood of normal viscosity
Pulse pressure (p) normal
6
Normal daily output of
urine, H = 1500 c.c.
Hydruric coefficient:
H 1500
— = = 250<i.c.
P 6
Kidneys
Urine normal = 1500 c.c.
Fig. 755.— Normal subject (pulse pressure in centimeters of mercury).
the sixth to the seventh; yet he was carrying the same trunk
and the number of steps to be climbed was the same in both
instances. Precisely so ; but the man had been exhausted owing
to the five stories already climbed. The same applies to the
heart ; in order to climb the 70 steps from 190 to 260, the heart
had already to climb the 190 steps represented by the diastolic
pressure and was exhausted; on the other hand, the heart was
quite fresh in climbing the 70 steps from 90 to 160, having as
yet ascended only 90. Nothing, it would seem, could show more
definitely than this the importance of the diastolic pressure.
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HIGH BLOOD-PRESSURE. 1049
As a matter of fact — in general clinical work — cases of high
arterial pressure may be roughly divided into the four following
groups.
1. Plethoric cases.
2. Nervous (angiospastic) cases.
3. Renal (infected and poisoned) cases.
The natural ultimate ending in these three groups is repre-
sented in the last group.
4. Arteriosclerotic cases.
The first three categories correspond to perfectly distinct
clinical conditions, of different pathogenesis, and consequently
yield definite therapeutic indications. This classification, there-
fore, serves some practical purpose. Yet, in truth, these several
conditions may perfectly well occur in combination: A ple-
thoric subject (e.g., weighing 100 kilograms) may, in addition,
be angiospastic (abnormally emotional) and harbor infection
(syphilis). Under these circumstances he is very likely to travel
a precipitate journey along the road leading to arteriorenal
sclerosis (arteriosclerosis), this constituting the natural penulti-
mate stage in chronic high arterial pressure. A diagram illus-
trating the course followed by these instances of cardiorenal
sclerosis is presented herewith. It will be noticed, however, that
this next to last, almost incurable stage, that of arteriosclerosis,
is preceded by a long period of functional hypertension (ple-
thoric, angiospastic, and renal), in respect of which we are pos-
sessed, on the contrary, of very efficient remedial means. The
differential diagnosis of the several varieties of high arterial
tension is thus by no means merely an academic procedure.
I.— PLETHORA.
The term plethora actually applies to a very clear-cut and
frequent clinical state. It is not employed in current text-books
on internal medicine because the time-honored list of diseases
includes scarcely more than the disorders accompanied by
known organic lesions, definite humoral disturbances, or dis-
tinct symptom-groups.
The plethoric subject, indeed, is by no means an ill person in
the accepted sense of the word. Apart from slight, occasional
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1050 SYMPTOMS.
disturbances such as skin eruptions, hemorrhoids, etc., he is in
a flourishing state of health and apparently normal; in fact he
displays an excess of functional activity betokening unusually
intense vitality. He consumes large amounts of food and his
digestive functions are admirably performed — as, indeed, is like-
wise the case in diabetic, gouty, or obese cases. He takes in
large quantities of fluid and is polyuric, as are diabetic and gouty
^ T^iooH ftf ^i^h viscosity
6
ressure (/>) high
10
Increased daily out(>ut of
urine, H = 2300 c.c.
Hydruric coefficient:
H 2300
— = = 230c.c.
P 10
^8
\
Urine increased : 2300 c.c.
Fig. 756. — Plethoric subject (pulse pressure in centimeters of mercury).
patients. His complexion is ruddy and his appearance that of
robust health. Without his being, properly speaking, an obese
individual, his weight is nevertheless distinctly above normal,
e.g., 96 kilograms (212 pounds) as against a height of 187 centim-
eters (6 feet lyi inches); 74 kilograms (163 pounds) as against
a height of 166 centimeters (5 feet 5 inches), etc. He has
marked endurance, is very active, and the aggregate of work he
performs may be much above the normal — as in many gouty
and diabetic cases.
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HIGH BLOOD'PRESSURE, 1051
In short, without being at all ill, one might almost say that
the plethoric subject is a supernormal individual, a *'superman"
from the physiological standpoint. The heart, unusually power-
ful, hypertrophied, contracts with unusual vigor, this being re-
flected in a heightened pulse pressure. The blood, richer and
less watery, exhibits a higher degree of viscosity. The kidneys,
adapted to an unusually abundant circulation and nutritive
process, eliminate abnormally large amounts of water, salt, urea,
uric acid, etc. The digestive glands, richly supplied with blood,
are overactive in their secretion, with resulting polyphagia, poly-
dipsia, polyuria, plethora, etc.
The plethoric is thus an individual who is not, properly
speaking, abnormal, but supernormal, featured by his appear-
ance of flourishing health, his body weight which exceeds the
normal, and his high blood-pressure and viscosity.
He is, however, a candidate for obesity, diabetes, or gout, of
which he already presents many^ anatomical and functional
manifestations. He is a candidate for sclerotic vasculorenal dis-
orders. To the author's mind, it is precisely a great feature of
superiority of the sphygmo-visco-hydrurimetric methods that
they are sufficiently searching to disclose the morbid tendencies
long before any established and recognized pathological change
exists, hence enabling the physician to rectify them with much
greater certainty.
II.— NERVOUS ANGIOSPASTIC CASES.
Everything tends to show that this condition frequently con-
stitutes the intermediate stage between simple plethora and car-
diorenal sclerosis — that it represents in part what Huchard so
appropriately termed the stage of presclerosis.
In the course of the development of sclerosis, starting from
the simple plethoric subject, the present stage, that of prescle-
rosis, might be said to come 5 years after the onset, and that of
established, irremediable sclerosis 10 to 15 years after the onset.
At times, indeed, one is enabled to contrast the two clinical
types in an almost perfect manner. Thus, the case is recalled of
a man of 31 years, obese and suffering from lithiasis, 171 centim-
eters (5 feet 7 inches) tall and weighing 123 kilograms (271
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1052 SYMPTOMS.
pounds), florid and well compensated, with a pulse rate of 98,
systolic pressure 250, diastolic pressure 120, and viscosity 4.8;
and the case of his mother, 51 years of age, of the degenerated
obese type, 160 centimeters (5 feet 3 inches) tall and weighing
87 kilograms (192 pounds), an established case of sclerosis, with
nycturia, albuminuria, a pulse rate of 120, systolic pressure of
280, diastolic pressure 160, and viscosity 4.1.
One of the characteristic features of this condition, whether as
regards the pulse rate, the systolio and pulse pressures, the blood
viscosity, or the output of urine, is an altogether abnormal instabil-
ity or variability which is met with neither in the preceding stage —
practically normal from the circulatory standpoint — nor in the
subsequent stage in which permanent pathological changes have
occurred.
In the first stage balance is maintained by virtue of a gen-
eral, harmonious, and regular functional hypertrophy; in the
third stage, the system has adapted itself, either well or badly,
to permanent lesions constituting a permanent infirmity ; it con-
tinues on its course, limping along in a continuous, even man-
ner, as it were.
In the stage of the disease here especially under discussion,
however, the organism, not yet permanently altered, is not re-
signed to its fate and will not admit itself conquered. It strug-
gles against the approaching collapse by processes of compen-
satory hypertrophy ; but at times the functional adaptation be-
comes insufficient, there is functional disorganization, disordered
reactions, angiospasms, and various forms of insufficiency mani-
fested in the form of paroxysmal attacks of hydremia, angina,
myocardial weakness, etc. Ordinarily, under the mere influence
of a diet instinctively imposed upon himself by the patient,
everything returns to normal. But the transitory attacks of
hydremia with diminished *urinary output, high blood-pressure,
and increased blood viscosity, expressed in a sudden, marked
rise of the sphygmoviscosimetric index and betokening a forcible
reaction on the part of the heart against an abrupt vasculorenal
block due to angiospasm, are quite significant and characteristic.
They constitute the last cry of warning at the entrance to the
blind defile of sclerotic infiltration.
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HIGH BLOOD-PRESSURE, 1053
The outstanding feature of this stage is nervous erethism,
emotivity, and exaggerated tendency to angiospasm which, in pre-
disposed subjects, plays an important role in the pathogenesis of
arteriosclerosis, as Lancereaux, Bouveret, Potain, and Huchard
clearly saw and taught. Some cases may even reach ultimate scle-
rosis solely by the angiospastic route. The majority reach it, how-
ever, by the plethoric route; degeneration is promoted by angio-
spasm and infections.
III.— RENAL CASES. NEPHRITIS.
The marked influence of nephritis (excepting certain rare forms
of excessive renal permeability) in causing high blood-pressure
is an obvious clinical fact, whatever explanation of it be
adopted. Whether the nephritis be acute or chronic, of infec-
tious or toxic origin, it is nearly always associated with high
blood-pressure, which is slight or wanting in simple albuminous
nephritis, moderate in chloridemic forms, constant and some-
times very marked in the azotemic and hydremic forms. The
last-mentioned form, indeed, as is well known, was long termed
hypertensive nephritis, high blood-pressure constituting one
of the cardinal features of this type of the disease (see
Albuminuria).
Whether the nephritis be the result of a metabolic disorder
such as gout, or of some form of poisoning such as lead poisoning,
or of an infectious disease such as scarlet fever or typhoid fever,
high blood-pressure is one of its most constant symptomatic
manifestations, and frequently, indeed, it exhibits distinct
features in accordance with the clinical courses of these several
disorders.
A rational classification of these cases is afforded by system-
atic study of the renal functions (output of water, chlorides,
urea, albumin, etc.), in conjunction with blood-pressure deter-
minations.
IV.— ARTERIOSCLEROSIS.
Plethora, angiospasm, and infection, whether they do or do not
cause preliminary renal changes, and whether they are or are not
present in combination, in the long run induce degeneration of the
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1054
SYMPTOMS.
arteries and arteriorenal sclerosis or arteriosclerosis. In the pres-
ence of this common disorder, continuous elevation of blood-pres-
sure being the rule, the equation high blood-pressure = arterio-
sclerosis was long accredited, though this is manifestly an error,
as already noted.
The practitioner should make a methodical search for:
* Blood of normal or low viscosity
3.8
\ Pulse pressure (/>) very high
18
Daily output of urine
rather highly H = 1800 c.c.
Hydruric coefficient:
H 1800
— = =100 ex.
p 18
Kidneys
Urine output rather high : 1800 c.c.
Fig. 757. — Subject with sclerotic disease.
Evidences of peripheral fibrosis : Tortuous temporal vessels, in-
duration of the radial, brachial, and temporal arteries, intermittent
claudication, etc.
Evidences of chronic aortitis and cardiac hypertrophy: Accen-
tuation of the second aortic sound, gallop rhythm, and enlargement
of the area of heart dulness.
Ezndences of interstitial nephritis: Increased output of urine of
low specific gravity, low urea output in the urine, high blood-pres-
sure, slight albuminuria, reduction of the hydruric coefficient, and
hydremia (lowered blood viscosity).
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HIGH BLOOD-PRESSURE, 1055
One should bear in mind the frequent occurrence of hemor-
rhagic complications such as epistaxis, hemoptysis, and hema-
temesis.
^^■^•^^
Heart
Fig. 758. — Successive stages in the development of
cardiorenal sclerosis.
/. Normal.
2, Eusystoly. — Simple plethora. — Good cardiorenal compensation.
J. Hypersphyxia. — Hydremia. — Renal insufficiency.
4. Heart weakness. — Hydremia and anoxemia. — Cardiorenal insufficiency.
Mx, Systolic blood -pressure.
Mn. Diastolic blood-pressure.
V. Blood Viscosity.
H. Daily output of urine.
— . Hydruric coefficient.
The main diagnostic features of these disorders will be
found in the accompanying table.
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1056
SYMPTOMS.
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HYPOCHONDRIUM, \vn6, below; x^^^pog, cartilage;^
LEFT, PAIN IN. L below the ribs. J
For clinical purposes the left hypochondrium consists, as its
etymological derivation shows and without any need of further
definition, of that region of the abdomen which is situated be-
neath the lower and anterior margin of the thoracic cage on the
left side. Painful affections of the fundus of the stomach, the
5"
P
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R
Ipc
cd
e
ac
Fig. 759. — The splenic fossa.
FS, Splenic fossa. E. Stomach retracted to the right. R, Upper end
of right kidney, with the adrenal gland within. P. Section of tail of pan-
creas, or. Splenic flexure drawn down. cd. First part, e. Omentum of
descending colon. Ipc. Phrenocolic ligament, g. Sulcus formed between
the kidney and costal wall. D. Diaphragm, p. Thoraco-abdominal wall.
S. Sternum (Picon, after Constantinesco, in Poirier and Charpy),
spleen, the left kidney, and the splenic flexure of the colon are
the chief disorders which find clinical expression in this region.
Clinical Description. — Nine-tenths of all instances of pain in
the left hypochondriac region, coincidently with pains in the lower
(infracardiac) thoracic region on the left side, are of gastric origin
and are symptomatic of gaseous distention of the fundus of the
stomach, i.e., of flatulence, meteorism, and aerophagia. Percussion
leads to the discovery of a pronounced extension of Traube's space,
(1058)
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HYPOCHONDRIUM, LEFT, PAIN IN. 1059
frequently coupled with a tympanitic note. The patient, in addition
to experiencing pain in the hypochondrium and left side of the chest,
generally complains of heart disturbances, such as palpitations,
dyspnea, and even "missed beats" or extrasystoles, especially when
lying on the left side; he states that he is frequently relieved by
eructations ; not rarely, while he is talking, he may be caught in the
very act of swallowing air ; conscious or unconscious sialorrhea is an
almost constant accompaniment. These patients actually consult
8th rib
Spleen
Adren
PlBsure of lung
Lower border
Qaatric of lung
SplenI
Colon
Pleural cul-de-
sac
Fig. 760. — Topographic features of the spleen. Projection of the spleen
on the costal wall (Picou, in Poirier and Charpy).
the physician on account of heart disturbances such as palpitations,
precordial pains,, "missed beats," angor, dyspnea, etc., much oftener
than they do on account of the hypochondriac discomfort, thus
justifying the old clinical aphorism: "When a patient complains of
his heart, there are* 9 chances out of 10 of his being a neurotic dys-
peptic." Many instances of pseudoangina pectoris arise solely from
this cause. Gaseous distention of the stomach, having once been
detected, its cause remains to be discovered, whether it be a gastric
neurosis, gastric hyperacthnty, chronic intestinal disease, or even
cholelithiasis or appendicitis, without forgetting the most frequent
cause of all, vis,, aerophagia.
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1060 SYMPTOMS.
Frequency. — In the order of frequency, surgical affections of
the left kidney — nephrolithiasis, pyo- and hydro- nephrosis, peri-
nephric abscess, tuberculosis of the kidney, or neoplasm— come
next to the gastric disturbances. Certain details concerning the
pain of renal involvement are presented in the section on the
Ti
Fig. 761. — Sagittal section through the left hypochondrium, passing in
the middle of the space between the parasternal and nipple lines, in a
subject with marked dilatation of the stomach (Luschka),
right hypochondrium (q.v.). Pain on pressure is usually most
marked in the lumbaf region; it radiates along the left ureter,
over the iliac fossa, and even to the testicle. Bimanual palpation
may sometimes reveal the presence of a) tumor of the kidney;
finally, examination of the urine in some instances leads directly
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HVPOCHONDRIUM, LEFT, PAIN IN. 1061
to the diagnosis. Detection of perinephric abscess frequently
demands considerable clinical sagacity, and the author cannot
escape the recollection of a disastrous case of perinephric abscess
coming on insidiously in a pregnant woman and gradually mani-
fested in persistent pain in the left hypochondrium and lower
intercostal spaces, with fever and tenderness in the left lumbar
Spleen
Right adr« Left adrenal
Tail of
pancreas
Duodenum*'
TrauBTerse
colon**
Deacendlng
Descending
colon
Right \
E artery
artery
Fig. 762. — Deep-lying structures in the right and left hypochondria.
region, then in an alarming symptom-group of peritonitis, with-
out renal evidences being apparent at the time, and which, al-
though suspected to be of renal or perirenal origin by the first
three physicians called, was wholly overlooked by two eminent
consultants, who diagnosticated* a|>pendicitis and subsequently
failed to be enlightened, after a fruitless appendectomy, by a
pyemic state of daily increasing gravity and even a copious dis-
charge of pus from the urinary tract. This was one of the most
trying episodes of the author's entire medical career, and one
which he is unable to recall without a feeling of bitterness.
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1062 SYMPTOMS,
Pride, conceit, and absurd pretentions to a species of infallibility
may lead physicians to really criminal acts.
Although relatively common, the disorders most specifically
attaching to the left hypochondrium are the affections of the
spleen. All splenic enlargements, whether due to leukemia,
anemia, malaria, syphilis, or polycythemia, and whether or not
associated with hepatic cirrhosis or heart weakness, are accom-
panied by a varying degree of painful tension in the left hypo-
chondrium. Enlargement of the spleen having been noted, there
remains to be made, by means of the customary methods of
examination (history, blood examination, liver examination,
uranalysis, Wassermann reaction, etc.), a diagnosis of leukemia,
malaria, syphilis, cirrhosis, heart failure, etc.
Subdiaphragmatic abscess on the left side appears to warrant
a somewhat extensive consideration in view of the fact that little
attention is generally paid to it and because, although uncom-
mon, it is much less rare than one might suppose, the author
having personally observed a dozen cases, aside from others that
may have been overlooked.*
There are two anatomic varieties of subdiaphragmatic abscess
which may give rise to signs and, in particular, to pain in the left
hypochondrium. These are :
1. More often, abscesses of the perisplenic fossa (or gastro-
splenic fossa of Dieulafoy), bounded above by the diaphragm
and the left extremity of the left lobe of the liver, within by the
fundus of the stomach and the pancreas, posteriorly by the dia-
phragm and kidney, anteriorly by the diaphragm and the omen-
tum, externally by the diaphragm and ribs, and below by the
splenic flexure and the left mesocolic fold.
Abscesses collecting in this locality are secondary either to
abscesses of the spleen (infarct, malaria) or to a perforation of the
stomach situated -near the cardia or on the posterior wall of the
fundus.
In these cases the pain is located deeply in the left hypochon-
drium, the mass formed shows little tendency to encroach on
the epigastrium, pronounced enlargement of splenic dulness is
1 See also Martinet : "Des varietes anatomiques d'abces sous-phr6niques,"
Paris, 1898.
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HVPOCHONDRIUM, LEFT, PAIN IN. 1063
noted and left-sided pleurisy is almost constantly present; fre-
quently, beneath the false ribs of the left side, there is an actual
cake-like condition about the spleen.
2. Less commonly, there occur abscesses of the left inter-
hepato-diaphragmatic fossa, bounded on the right by the sus-
pensory ligament, posteriorly by the triangular ligament, below by
the upper surface of the left lobe of the liver and part of the
anterior aspect of the stomach, above and to the left by the dia-
phragm, anteriorly by adventitious adhesions between the dia-
phragm and the anterior root of the left lobe and by a varying
portion of the anterior abdominal wall.
Fig. 763.-.-Arab children of Algeria with malarial enlargement of the
spleen. The cross + shows the position of the umbilicus (Brumpt).
The cause of this type of abscess is invariably a perforation
of the anterior wall of the stomach.
In this variety the initial pain is predominantly situated on
the left and sometimes radiates toward the left shoulder; con-
vexity is especially pronounced on the left; Traube's space is
always modified ; frequently there are signs of left-sided pleurisy,
displacement of the heart-apex upward and inward, formation
of a mass below the ribs on the left side, and immobilization of
the left side of the chest.
The splenic flexure of the colon, forming, as is well known,
an extremely acute angle, is one of the "critical" points of the
intestine, and is one of the commonest sites of intestinal tumors.
Indeed, a neoplasm of the splenic flexure frequently causes no
local pain; careful deep palpation of the left hypochondrium
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1064 SYMPTOMS.
may, however, yield significant information which, when corre-
lated with a more or less pronounced symptom-group of obstruc-
tion, may lead to the diagnosis of tumor, to be subsequently con-
Fig. 764. — Left-sided abscess be- Fig. 765. — Perisplenic abscess. Ab-
tween the liver and diaphragm. Per- scess of the spleen : Infarction, raal-
f orated stomach, due to gastric ulcer, aria, gastric perforation.
Fig. 766. — Post-gastric abscess. Fig. 767. — Abscess between the liver
and stomach.
firmed by testing of the stools for blood and fluoroscopy follow-
ing a bismuth meal.
There is one symptom-group, however, which has not yet
been adequately described: Chronic pain in the left hypochon-
drium with periodic exacerbations, apparently the result of
gaseous accumulation at the splenic flexure and of defective
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HVPOCHONDRIUM, LEFT, PAIN IN.
1065
transit through the large intestine owing to excessive angula-
tion of the splenic colon — a condition admirably demonstrated
by fluoroscopic examination.
The possible occurrence of pain in the left hypochondrium in
cases of pneumonia involving the left lobe or of pleurisy lends itself
to the same observations as are made in the section on the right
h)rpochondrium (q^v.).
♦ ♦ ♦
As a suggestive instance of the disturbances — sometimes ap-
parently very serious — that may be brought on by the accumula-
tion of air and gases in the fundus of the stomach, with the re-
sulting pressure on the left side of the diaphragm and displace-
ment and distortion of the heart and aorta, the follgwing data per-
taining to a case of this type may be here presented :
Case 3596.
Fig. 768.
Man, 1862,
171 <
— ; 76 kilograms.
Pressures :
Pulse press., 100.
27 cm.
230
125-
Marked anginoid syndrome, espe-
cially pronounced on walking and
after meals. During attacks, the
patient is "rooted to the spot" and
unable to move. The stomach shows
a very large air bubble and there is
meteorism with marked pressure dis-
placement of the heart and distor-
tion of the aorta.
Case 3596.
Same patient three weeks later,
after treatment. Weight, 74.8 kilo-
grams.
IGO
Pressures : j^ . Pulse press., 60.
All anginoid manifestations have
disappeared. Locomotion and mod-
erate outdoor sports resumed. Met-
eorism has disappeared and the gas-
tric air bubble is markedly reduced.
The heart and aorta are restored to
their normal shape and position.
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1066
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HYPOCHONDRIUM, RIGHT, PAIN IN.
The right hypochondrium normally corresponds to the lower
border and anterior surface of the liver in its entire extent. As a
matter of fact, four-fifths of all pain disturbances in this region
originate in the liver or gall-bladder; yet by no means all pains in
the hypochondrium originate in these structures.
A brief review of the regional anatomy will suggest the various
possibilities in the interpretation of pain in this area.
The right hypochondrium is in its entirety in relationship with
the anterior surface and lower border of the liver, including, in its
middle portion, the fundus of the gall-bladder. Disorders of the
liver and other biliary structures constitute the chief pain-producing
agencies in the right hypochondriac region. Acute, paroxysmal
pains of the type of colic are especially characteristic of cholelithir-
asis, simple or with complications. It should not be overlooked,
however, that frequently this disorder is — like chronic appendicitis
— spontaneously manifested only in what appear to be ordinary
dyspeptic disturbances or in a pyloric symptom-group with tend-
ency to stasis and dilatation in the presence of adhesions uniting
the gall-bladder and duodenum. Jaundice occurs in about one:
fourth of all cases of cholelithiasis. Only in exceptional instances
(1 out of 20) will palpation! not induce a characteristic pain at the
fundus of the gall-bladder for a more or less prolonged period of
time during the intervals between the acute attacks.
Pain of hepatic origin is generally of a duller type, and is some-
times only brought out by palpation or percussion. Pain has to
be actually examined for in these cases. Sometimes it is latent;
active or passive congestion of the liver is by far the commonest of
the disorders of this organ inducing sensitiveness; it accompanies,
precedes, or heralds the oncoming of the majority of instances of
(1068)
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HYPOCHONDRIUM, RIGHT, PAIN IN. 1069
hepatic cirrhosis. As is well known, it is one of the most constant
symptoms of heart weakness or heart failure.
Lastly, one should always bear in mind the possibility of syph-
ilis of the liver, a fairly common but generally rather painless con-
dition (enlarged syphilitic liver, pseudocancerous form, syphilitic
a — .
^/.-..
Fig. 769. — Anatomic relations of the liver with the walls of the chest
and abdomen (Laederich), a. Projected outline of the upper border of
the liver, b. Lower border of the lung. c. Pleural cul-de-sac. d. Gall-
bladder.
lobulated liver, lobed liver, or syphilitic cirrhosis) ; of hepatic abscess
(history of malaria, fever, jaundice, pain, etc.), and of cancer, for-
tunately much more uncommon ("galloping" enlargement of the
liver with marked emaciation and rapid cachexia). In all these
cases, it is not the character of the pain but the associated signs and
symptoms and the clinical course which constitute the basis of the
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1070 SYMPTOMS,
diagnostic conclusion — as will be seen in the tabular summary at the
end of this section.
Immediately behind the liver are situated the angle formed by
the ascending and the transverse colon (hepatic flexure) and the
first flexure of the duodenum, to which, furthermore, the gall-blad-
der so frequently becomes adherent in the event of pericholecystitis.
A corollary of this is that pain in the right hypochondrium may
be symptomatic of a precolic or retrocolic high appendicitis, and
the incipient jaundice frequently present in these cases may still
further augment the difficulty of diagnosis. Indeed, the author has
seen the two following mistakes committed, viz,, a cholecystitis with
prolapse mistaken for an appendicitis and a high appendicitis
mistaken for cholecystitis. , Appendicitis may, as a matter of fact,
be the starting-point of subhepatic abscess. Ordinarily, and apart
from the particularly acute emergencies in which incipient or estab-
lished peritonitis prevents all precise localization, palpation will en-
able the practitioner to elicit an especial localization of the disturb-
ance in the right iliac fossa.
As for duodenal ulcer (see Dyspepsia) the particular type of
the pain, coming on spontaneously and periodically with a uniform
relationship to meals, the symptom-group of hyperchlorhydric in-
digestion which usually accompanies it, and the lower position of
the tenderness elicited by palpation between the right hypochon-
drium and the umbilicus will frequently permit of an easy diagnosis,
sometimes definitely confirmed by the advent of hematemesis. The
chief condition to be differentiated from duodenal ulcer is chole-
lithiasis.
Behind the lower surface of the liver, the hepatic flexure and
the duodenum is the right kidney, many disorders of which may be
manifested in pain in the right hypochondrium. Especial mention
should be made of nephrolithiasis and of kidney suppurations (pyo-
nephrosis) or perirenal abscess. Aside from the paroxysmal attacks
of renal colic, in the presence of which brief hesitation may occur
in the diflFerentiation from hepatic colic by reason of the practical
impossibility of making an, examination on account of the severe
pain, cholelithiasis is readily differentiated by the fact that the pain
or tenderness is most marked in the lumbar region, by the radiation
of the pain along the ureters and to the testicles, by the urinary
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FMg. 770.— Alcoholic hyper- Pig. 771.— Alcoholic atrophic Fig. 772.— Bantl's disease:
trophic cirrhosis with as- cirrhosis with ascites. Greatly enlarged spleen,
cites. atrophic cirrhosis, and as-
cites.
Pig. 773.— Hepatoptosis. Fig. 774.— Biliary clr- Pig. 775.— Biliary cir-
Movable lobe. rhosis with greatly enlarged rhosis with enlarged liver
spleen. and spleen.
Pig. 776.— Hydatid cyst of Fig. 777.— Nodular cancer Fig. 778.— Cancer of head
the liver (left lobe). of the liver. of pancreas. Dilated gall-
bladder.
(1071)
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1072 SYMPTOMS.
manifestations, and sometimes by the detection of gravel in the
urine. Similar considerations apply in thd case of pyonephrosis or
perirenal abscess, although in the latter instance, if the abscess
points — as is seldom the case — below the liver, the diagnosis may be
very difficult; differentiation is, however, of capital importance,
since the institution of proper operative treatment, viz,, lumbar in-
Fig. 7^9. — Relations of the abdominal organs, viewed anteriorly.
cision or subhepatic celiotomy, depends upon the decision reached.
To be particularly borne in mind, in order that they may be excluded,
if possible, by careful clinical study, are pericholecystitis, subhepatic
abscess of appendicular origin, and subdiaphragmatic abscess.
All the above mentioned disorders, capable of causing pain in
the right hypochondrium as an important or predominant clinical
manifestation are of abdominal origin, being hepaticobiliary, colo-
duodenal, or renal. Two thoracic disorders, right-sided pleurisy and
right-sided pneumonia, may also give rise to pain in this locality.
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HYPOCHONDRIUM, RIGHT, PAIN IN. 1073
Fig. 780. — Kink at the first flexure of the duodenum due to a nephro-
ptosis of the third degree. Pronounced dilatation of the first part of the
duodenum. , Hydronephrosis has been produced owing to multiple kinks
of the ureter. The patient had been admitted to Prof. Terrier's service
with symptoms suggesting intestinal obstruction. She died in a few days
without having been operated, and at the autopsy the only lesions found
were those here illustrated : / p.d., first portion of the duodenum, greatly
dilated above its flexure, r. Note the adhesions ad, c,d.
Fig. 781. — Diagram showing the normal relations of the right kidney
with the hepatic flexure and duodenum. The lower pole of the kidney
is generally situated behind the hepatic flexure. Exceptionally, this
flexure lies below the kidney (Alglave).
68
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1074 SYMPTOMS.
In pneumonia, such a location of the pain is the rule in involvement
of the lower lobe, and at times of the middle lobe of the right lung,
particularly in children. In these cases, indeed, pain in the right
hypochondrium is actually of threefold origin :
Cutaneous, or pain attending a superficial hyperesthesia (Head's
hyperesthetic projection zone).
Hepatic, or a deep seated pain due to the active congestion of the
liver attending infection.
Diaphragmatic, or pain due to an inflammatory pleural reaction.
Lung
Pleural cul-de-sac
P*®"'**^ Coronary ligament
ht kldpey
Trans'
Fig. 782. — Anteroposterior section of the liver (Charpy). The
section passes through the right hypochondrium.
Excepting in children, the diagnosis is very seldom held in sus-
pense for a long time in pneumonia. The same is true of pleurisy,
except in diaphragmatic pleurisy, in which the diagnosis is often
difficult.
Lastly, mention should be made of a variety of subdiaphragmatic
abscess located in the right hypochondrium, in the right interhepato-
diaphragmatic fossa, and bounded above by the diaphragm, to
the left by the falciform ligament and gastrohepatic omentum,
and below by the right half of the transverse colon and a double
transverse fold of peritoneum extending from the lower portion of
the ascending colon to the abdominal wall slightly below the tip
of the eleventh rib. This is one of the commonest varieties of
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HYPOCHONDRIUM, RIGHT, PAIN IN, 1075
subdiaphragmatic abscess. In the course of a study of the
several varieties of subdiaphragmatic abscess, made by the
Fig. 783. — Verticotransverse diagrammatic section passing through the
gall-bladder. The fundus of the latter exhibits a perforation. Below,
adhesions are shutting off the peritoneal cavity. An outpouring of bile
has occurred and the resulting abscess developed between the diaphragm
and the liver, which is pushed downward. (Right-sided inter-hepato-
diaphragmatic abscess).
Fig. 784. — Right-sided abscess between the diaphragm and liver.
author a number* of years ago, this variety was found to have
existed in 60 out of 146 cases. Such abscesses are sometimes
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rdera of the liTer
gall-bladder
( Pleurtsy
( Pneumonia
al diaordera
PneumonI
PleurlB ,„
j Hyperemia
Subdiaphra«m( IverK Syphilia
abscera I Cancer
all-bladder. Stone
:omach f rjice-
Stone) uodenuml*^
Abscess >l
Pyonephrosis)
ppendiclUa
Figs. 785 and 786. — Points of tenderness in the right hypochondrium, with
their respective causes and modes of radiation.
(1076)
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HYPOCHONDRIUM, RIGHT, PAIN IN. 1077
secondary to a disturbance of the liver, such as cholelithiasis or
abscess or suppurative hydatid cystic disease of the right lobe,
or may follow perforation of a duodenal ulcer.
The diagnosis is based on the initial pain, most marked in
the right hypochondrium and frequently radiating toward the
Fig;. 787. — Evacuation of a subdiaphragmatic abscess (i) of appendic-
eal origin through the chest wall below the pleura. /. Colon. 2. Liver,
displaced downward and inward 4. Right lung (Kelly).
right shoulder; on the epigastric prominence, extending mainly
toward the right side ; on the enlarged area of hepatic dulness,
or, on the other hand, in tlie case of gaseous abscesses, on the
percussion note over the liver and the lowered position of this
organ, the complete or incomplete immobilization of the right
half of the thorax, and the frequent association with a right-
sided pleurisy or even a phrenic neuralgia on that side. The
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1078 SYMPTOMS.
causal diagnosis should be based mainly on the history of the
case.
Finally, three rarer conditions may be referred to:
(a) An exceptional localization of herpes zoster, revealed by
Fig. 788. — Incision of a subdiaphragmatic abscess of appendiceal origin
in the 9th right costal interspace (Berard).
direct inspection of the painful area — a procedure indicated in all
regions of the body.
(fc) A special localization of the "girdle pain" of tabetic origin,
mere recollection of the possibility of which is sufficient, but which
should always be thought of in the presence of pain in the right
or left hypochondrium or the epigastrium, and which systematic
examination of the reflexes and station — always a necessary pro-
cedu/re — is sufficient to establish.
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HYPOCHONDRIUM, RIGHT, PAIN IN. 1079
(c) Hydatid cyst of the liver is usually painless, even where it
reaches a considerable size. In exceptional instances it may, how-
ever, give rise to attacks of pain suggesting gall-stones. The cause
of these attacks is by no means clear ; possibly a reflex contraction
Fig. 789. — Cavities that may be occupied by pus in peritonitis : /. In-
framesenteric space. 2. Pelvic cavity. 3. Supramesenteric space. 4-
Right paracolic space. 5. Interhepatocolic space. 6. Right and 8, left
subdiaphragmatic spaces, the latter separated from the preceding by the
falciform ligament (7). 9. Left paracolic space.
of the biliary passages occurs, constituting a species of painful
biliospasm (ChauflFard) ; or, more probably, there is obstruction of
the common bile duct by vesicles or membranes set free from an
hydatid cystic disease of the liver that has opened into the bile
passages (Dene).
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1080 SYMPTOMS.
Diagnosis of hydatid cyst simulating gall-stones (hydatid
hepatic colic) is a matter of great difficulty and sometimes quite
impossible where the clinical signs of cyst are wanting.
Courvoisier, in 1890, in his monograph on "The Pathology and
Surgery of the Biliary Passages," enunciated the following law:
'7n obstruction of the common bile duct by a stone, dilatation of the
gall-bladder is exceptional; under these circumstances the gall-blad-
der is t^ually contracted. In obstruction of the duct due to any
other cause, dilatation of the gall-bladder is the rule." This law
was confirmed but slightly modified by Terrier, who wrote: '7n
cases of occlusion of the common bile duct of internal causation,
the gall-bladder is ordinarily shrunken, whereas dilatation of the
gall-bladder is the rule when occlusion of the biliary passages is of
external causation."
Krahenbiihl, of Bale, in turn, corrects the law in the following
manner: "In cases of gall-bladder enlargement of long standing,
the occlusion of the common bile duct is ordinarily of neoplastic
nature; where gall-bladder enlargement is wanting or but temporary,
occlusion of the duct is usually due to stone."
Statistical records confirm the frequency of stones in cancer
OF THE GALL-BLADDER. Out of 41 cases of cancer of the gall-blad-
der the presence of stones was found mentioned in 36 instances, or
89 per cent. ; in 4 other cases, stones were not referred to, and in a
fifth case, the patient is said to have previously passed calculi with
his stools.
The relatively frequent coexistence of lithiasis and cancer of the
gall-bladder naturally suggests, as J. Dumont states, the thought of
a possible etiologic relationship between the two diseases. Is chole-
lithiasis the cause of cancer or merely a consequence of it ? A fact
justifying the belief that cholelithiasis precedes the cancer and con-
stitutes one of its predisposing causes (irritation theory) is that in
the overwhelming majority of cases (37 out of 41), the patients had
been suflFering for a long time, in some instances for decades, from
hepatic colic. (It may be added, to complement the above data re-
lating to cancer of the gall-bladder, that jaundice was present in 63
per cent, of the cases and that cancer occurred oftenest between the
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HYFOCHONDRIUM, RIGHT, PAIN IN. IQgl
ages of sixty and sixty-five and 5 times oftener in women than in
men). The pathogenetic role of cholelithiasis in cancer of the gall-
bladder is supported by the fact that the latter seems to be getting
more uncommon since operations for cholelithiasis have been per-
formed oftener and earlier in the disease. Thus, between 1890 and
1900, 140 operations for gall-stones revealed 17 instances of cancer
of the gall-bladder (12 per cent.); from 1901 to 1910, ;197 opera-
tions brought to light 16 cancers (8 per cent.), and from 1911 to
1919, 151 cases yielded only 9 cancers (6 per cent).
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1082
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ILIAC FOSSA, LEFT, [Ilia, the flanks; appertaining'}
PAIN IN. L to the flanks. J
Practically the same considerations apply to pains in the left
iliac fossa as to those in the right iliac fossa (to be discussed in
Am
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Fig. 790. — Normal position and relations of the sigmoid flexure and
rectum in the adult. The pelvis has been freely opened anteriorly by a
frontal section passing through the centers of the acetabular fossae
(Poirier) .
the succeeding section), the only important differences being
those attendant upon the presence of the appendix and cecum on
the right side in lieu of the iliac colon on the left.
(1085)
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1086 SYMPTOMS,
The annexed anatomical illustration of the region and the
diagnostic tabulation will give data serviceable in the clinical
study of this region.
Abdominal palpation, palpation from the rectum (and the
vagina in women), fluoroscopic examination after a bismuth
meal, and gross and microscopic examination of the stools are
s
Fig. 791. — Radiographic view of the large intestine (Tuffier, Aubourg).
the mam clinical procedures employed in investigating the left
iliac fossa,
Muco-membranotis enterocolitis (or mucous colitis), a very
common disorder, gives rise to pain localized in the left iliac fossa;
it is oftenest situated in the cecum and transverse colon. Again,
palpation of the left iliac fossa frequently reveals the descending
colon and sigmoid in a contracted condition, with reduced size, im-
parting the sensation of an elastic "sausage'* rolling beneath the
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ILIAC FOSSA, LEFT, PAIN IN. 1087
finger. This condition, when correlated with alternating diarrhea
and constipation and the discharge of mucus and false membrane,
generally affords an easy diagnosis. Pain is not constant in these
cases.
It should be borne in mind that tumors of the descending colon
and sigmoid may be particularly silent from the symptomatic stand-
point and be associated with very little local or general disturbance ;
even the degenerative process itself, similar to a small ring of metal,
is often hard to detect. In general, in any subject over fifty years
of age exhibiting irregularity of bowel action which had previously
been regular, or losing weight, the stools should be examined for
blood and x-ray studies carried out.
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1088
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ILIAC FOSSA, RIGHT, PAIN IN.
The semeiology of the right iliac fossa revolves chiefly about
the diagnosis of acute and chronic appendicitis.
Yet, appendicitis is not the only pain-producing disorder met
with in this region.
It would seem of interest in this connection to reproduce the
highly suggestive statistics recorded by Cabot in "Dijferential
Diagnosis/^
Relative frequency of the disorders causing pain in the right
iliac fossa (Cabot, 1747 cases).
Appendicitis 1169 cases 66% per cent
Pus-tube (and pelvic adhesions) 427 " 24 " "
Dysmenorrhea 81 " 4% " "
Extra-uterine pregnancy 23 " 1% ** "
Ovarian cyst with twisted pedicle 21 " 1% " "
Psychoneurosis and the fear of appendicitis . 17 " 1% ** "
Colica mucosa 5 " % " "
Ureteral stone , 4 " % - "
1747 cases.
To the above might well be added a few exceptional cases
of inguinal hernia with pain radiating to the iliac region and the
more frequent cases of obstruction in the ileocecal region due to
neoplasm, tuberculous disease, morbid or post-operative adhe-
sions, abnormal position of the cecum (ptosis, congenital dilata-
tion, etc.) ; in these cases, however, the pain is generally slight
and rarely localized in the iliac fossa.
Examination of this region of the abdomen is of such out-
standing importance as to warrant a description here of the sys-
tematic procedure to be followed.
The patient being relaxed and recumbent, and the abdomen
exposed :
The abdomen should first be examined as a whole, attention
being paid to any visible prominence of one abdominal region,
«» (1089)
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1090 SYMPTOMS,
due to meteorism, pus accumulation, or a tumor, and noting
whether the two sides of the abdomen show different motion in
respiration, as might occur through inhibition of one side of the
diaphragm because of an underlying process of peritonitis. One
Anterior aspect
Diaphragm
4th rih
Diaphragm
Left lung
Xiphoid LlTer
append.
Stomach
curyature
Liver
Spleen
Pleura
Spleen
Gall-bladder
Pylorui Stomach
H^^ TransT. colon
Descend, colon
TJmbllieus
Small intestine
Sigmoid
flssurs
Cecum
Sigmoid
Hezure
Fig. 792. — General topographic features of the abdomen
(T. Jonnesco, in Poirier and Charpy).
should also note whether respiration or coughing awaken any-
localized pain, and if so, at what point.
Skin sensation should be tested on the two sides by drawing the
finger over the skin, pinching, and the application of heat and
cold. Any existing anesthesia, dysesthesia, or hyperesthesia
should be noted. Where such sensory disturbances are found to
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ILIAC FOSSA, RIGHT, PAIN IN.
1091
be unilateral — hemianesthesia or hemidysesthesia — an examina-
tion should be made for the customary stigmata of the neuroses
(hysteria). If the disturbances show a metameric distribution
corresponding to one .of the zones of Head, the condition may be
regarded as a cutaneous expression of some deep-seated visceral
inflammatory process.
Fig. 793. — ^Topography of the abdomen, pp. The pancreatic point.
App. The appendiceal point.
Palpation is the chief factor in the examination of this region,
and too much care and attention cannot be given to its execution.
Both superficial and deep palpation should be practised. In the
acute, febrile, peritoneal stages the palpation should be particu-
larly light and cautious. It should be carried out with the tips
of the fingers, in a gradual manner. Sudden, forcible palpation
always excites a defensive reaction of the abdominal wall, even
in the normal subject and in the absence of all pain; the ab-
dominal muscles contract, form a barrier, and resist depression
by the palpating hand — a condition particularly to be avoided.
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1092 SYMPTOMS.
The patient being well extended in recumbency and eased in
mind, with his legs, if possible, slightly flexed, palpation is be-
gun and the various regions of the abdomen (right and left iliac
8
Fig. 794. — Topographic features of abscesses of appendiceal origin in
the order of their frequency : /. The commonest type of abscess, in the
right iliac fossa. 2. Pelvic abscess, s. Retrocecal and prerenal abscesses.
4. Abscess in the left iliac fossa. 5. Mesoceliac and infraumbilical ab-
scesses. 6. Right subphrenic abscess. 7. Portal and intrahepatic suppura-
tion. 8. Right-sided suppurative pleurisy, p. Left-sided prerenal abscess.
70. Infrasplenic abscess //. Left-sided suppurative pleurisy (Kelly),
fossae and hypochondriac regions, hypogastrium, and umbilical
region) lightly and gradually depressed, beginning with the
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ILIAC FOSSA, RIGHT, PAIN IN. 1093
regions manifestly free of pain at the time. If the subject is well
relaxed, the several abdominal regions can be depressed more
or less deeply without meeting with too much resistance, often
with the result that, by slow, "coaxing," gradual pressure the
deep-lying organs may be palpated. In the presence of some
inflammatory visceral disturbance, and particularly in appen-
dicitis, the palpating finger encounters over the site of pain a
firm resistance or insuperable reflex muscular contraction, con-
stituting the so-called **board-like rigidity." This sign, which
Fig. 795. — Combined appendicitis and adnexitis. The appendix (A) is
adherent to the ampulla (P) of the Fallopian tube, which is closed and
distended with pus. The inflammatory cyst (K) is partly covered over by
the omentum (E) (Berard).
is never absent, is the earliest and perhaps the most reliable indi-
cation of appendicitis.
Its exact features must, however, be carefully noted; in some
nervous, pusillanimous subjects there may occur a general abdom-
inal rigidity preventing palpation of any of the regions of the
abdomen, and under these circumstances the rigidity is devoid of all
diagnostic value. The same is true of the muscular contraction in-
duced by unduly rough palpajtion. But whenei'er a correctly con-
ducted palpation, after noting the absence of undue resistance in
other regions of the abdomen, meets with rigid contracture in some
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1094 SYMPTOMS.
definite area, the result is to be considered pathognomonic evidence
of a subjacent inflammatory insceral disorder.
By the same proceeding of palpation with one finger one should
endeavor to ascertain the point of maximum pain. The diagnostic
significance of the so-called McBurney's point is well known.
Palpation sometimes leads, moreover, to the detection of a
mass of varying size, sensitiveness, and evenness of outline,
such as an accumulation of feces, an abscess, or a tumor,
thorough examination of which will reveal its actual nature.
**On the second, third, or fourth day of acute appendicitis,
palpation over the right iliac fossa reveals a doughy condition
or broad area of induration which spreads out laterally, is ap-
parently connected with the abdominal wall, and forms a species
of thick, hard shield. This condition, if it possesses and retains
the characteristics just referred to, is an outward expression of
the Vailing off' process which has set in and gradually ex-
tended about the diseased area; such being the case, its pres-
ence is actually of favorable import.
"About the fifth or sixth day the temperature recedes and
drops more or less rapidly to normal, and the pulse rate de-
creases in parallel fashion; the hard *shield,' which has by this
time frequently extended over a broad surface, now ceases to
enlarge and becomes still harder in its central portion, while
softening and yielding at its periphery, and appears less and less
tender on palpation." (Lejars, Chirurgie d'urgence, p. 496).
Finally, it is of advantag^e, though not absolutely indispens-
able, to practise ''decompressive" palpation, which consists,
after more or less deep pressure at some region of the abdomen,
in suddenly removing the compressing finger, so that abrupt
release of pressure results. Sometimes it is noted that, whereas
pressure has been relatively painless, decompression causes
much pain. This seems, to all appearances, to be a reliable in-
dication of inflammation of the peritoneum beneath the palpated
area.
Percussion may prove of great service in the detection of an
abnormal, flat area in certain cases in which satisfactory palpa-
tion is practically impossible. It may, furthermore, be availed
of as a gentle method of palpation.
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ILIAC FOSSA, RIGHT, PAIN IN, 1095
The foregoing examination of the right iliac fossa should be
supplemented with the three following procedures :
(a) Manual and bimanual palpation of the right lumbar
region for the detection of any existing pus tracks in retrocecal
disease, to exclude the possibility of renal disorder, etc.
(fc) Vaginal palpation in women for the detection of diseased
2-
1-
Fig. 796. — Radiographic picture of the cecum and appendix twelve
hours after ingestion of bismuth magma. The cecum (/) and the ascend-
ing colon (2) appear dilated and segmented by the constricting bands
due to pericolitis. The appendix (3) is seen occupying a latero-intemal
position (Berard).
adnexa and pelvic infiltration of appendiceal origin, and rectal
palpation in males for prostatitis, ureteral involvement, and ex-
tensions of appendiceal suppurative foci into the pelvis.
(c) Gentle examination of the psoas muscles by flexion, exten-
sion, abduction, and adduction of the lower limbs against a slight
d^ree of resistance. Where the psoas is involved, e.g., if there is
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1096 SYMPTOMS.
appendiceal inflammation adjoining this muscle, such an examina-
tion of the latter is a painful procedure.
In conclusion it may be added that it is always well to examine
the right iliac fossa under anesthesia just before the operation.
"Before operating, one should never neglect to conduct a final
examination upon the well anesthetized patient in a state of com-
plete muscular relaxation. Frequently the yielding of the abdom-
inal wall, which is no longer rigid, will lead to the detection of a
more or less distinct prominence in the right iliac fossa, or upon
oblique inspection, a marked lack of symmetry of the two lateral
halves of the abdomen may become apparent.
"Examination by palpation will afford more exact information ;
generally the examiner will find one of the following conditions:
Either a definitely fluctuating pocket, tense, circumscribed, and
sharply defined at its mesial border ; a thick sausage-like mass, com-
pact, indistinctly or partially fluctuating, or with nodular surface
and poorly defined borders below and toward the median line, or a
small, hard mass, rounded or nodular, non-adherent and readily
mistaken for the appendix itself.
"Sometimes the tumor noticed in the waking state will seem
to have almost completely disappeared. It may be added that if,
when the patient has been anesthetized, iliac palpation continues to
give the impression of a diffuse doughy condition, while the ab-
domen fails to recede and remains prominent and tense, the pre-
vious apprehensions, of generalized peritonitis are to a singular de-
gree confirmed." (Lejars.)
The following summary reflections, of general application in the
diagnosis of abdominal disorders, are borrowed from Cabot
C Differential Diagnosis"),
Though it seems judicious and is in accord with current prac-
tice to differentiate the exciting causes of the various localized
and diffuse abdominal pains, as a matter of fact such distinctions
do not always hold good. Disorders such as appendicitis, theo-
retically attended with pain in the right iliac fossa, may very
readily cause pain localized even above the waist line. Again,
lead poisoning, which ordinarily gives rise to distinctly diffuse
pains in the last-named region, may instead readily cause a much
more circumscribed pain.
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ILIAC FOSSA, RIGHT, PAIN IN. 1097
Thus, the reader looking up in a certain chapter a variety of
pain commonly described as being localized in a certain region
may wonder at its absence from that point and at finding it else-
where. Again, some causes of pain may be found referred to in
Fig. 797. — Vessels and nerves of the anterior abdominal wall projected
upon the ceco-appendicular region. MB. McBurney's point. M. Morris's
point. L. Lanz's point. The dotted line pointing to MB shows the line
of the McBurney incision. The dotted line ML shows the Jalaguier in-
cision (Berard),
two different chapters (ovarian cyst with twisted pedicle, ectopic
pregnancy, etc.) because they are equally common on the right
and. the left sides of the body.
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1098
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ILIAC FOSSA, RIGHT. PAIN IN.
1099
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1100 SYMPTOMS.
In a general way, when the practitioner is seeking to find out the
probable cause of a pain in the abdomen, he should be guided by
the folloTving rules:
1. First of all he should suspect the gastrointestinal tract, and
if the most commonplace disorders, such as constipation and colitis,
can be excluded, he should think especially of appendicitis, peptic
ulcer, neoplasm of the stomach or large bowel, and the ultimate
consequences of these conditions, such as peritonitis and intestinal
obstruction.
2. Next he should suspect (in women) the generative tract —
salpingitis, ovarian cyst, uterine fibroids, and ectopic pregnancy.
3. The gall-bladder and bile-ducts should be particularly in-
vestigated in persons over middle age.
4. The urinary tract, especially in old men and young girls,
comes next in the list of causes of abdominal pain.
Clinical examination, the history, palpation, blood examination,
uranalysis, fluoroscopy, and cystoscopy are the most serviceable aids
in reaching a diagnosis.
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INSOMNIA.
I In, negative; somnum, 8leep;'l
I deprivation of sleep. J
Insomnia or agrypnia consists in a more or less complete and
lasting inability to sleep. It occurs in all grades, from simple
hyposomnia, characterized by shorter, lighter, more restless, and
less refreshing sleep than usual, to the obstinate and inveterate
complete insomnia, sometimes attended with a very unfavorable
prognosis.
The causes of sleeplessness are many. For practical purposes
they may be divided into the three following groups :
Insomnia due to pain.
Insomnia due to excessive nervous excitability.
Insomnia due to circulatory or respiratory disturbances.
Insomnia due to pain may be the result of any kind of pain, of
whatever situation and nature, including the most varied forms of
neuralgia, arthralgia, and visceralgia. To attempt to enumerate all
these causes would be tiresome to the reader and plainly superfluous.
At the most it will be well to call attention to the fact that some
"pain insomnias," when carefully traced, lead to the discovery of
certain "algias" which recur at night and are of special clinical
significance, such as the osteocopic pains of syphilis, sometimes the
neuralgias of tabes, and more frequently the myalgias and arthral-
gias of gouty subjects.
Again, it should be noted that itching or pruritus (see Itching)
of whatever cause (parasitic or toxic) may be the source of highly
obstinate insomnia. When correctly traced, this symptom leads to
the detection of numerous "incomplete" cases of diabetes, uremia,
and cholemia.
Lastly, it may be pointed out that the insomnias due to
special sense hyperesthesia and the psychosplanchnic neurosis
merge insensibly with the next succeeding group, affording a
good illustration of the fact that clinical conditions, with their
infinitely numerous variations, always tend to pass beyond the
(1101)
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1102 SYMPTOMS,
group limitations within which the physician, for his conveni-
ence, endeavors to confine them.
Insomnia due to abnormal excitability of the nervous system.
— Such nervous overexcitability may be the result:
1. Of some organic change in the nervous system (type condi-
tion: meningitis).
2. Of an overexcitation of functional origin (type condition:
psychoneuroses ) .
3. Of an intoxication or infection (type conditions: caffeinism
and t3rphoid fever).
In the first group are included the insomnias of meningitis, brain
tumor, general paralysis, and cerebral syphilis. In all these cases
the symptomatic combination of headache and insomnia exists.
The second group, that of the psychoneuroses, is much more fre-
quent. In it are comprised the so-called "nervous** insomnias de-
pendent upon overwork, excessive ideation, worry, mental excite-
ment (irritable weakness, emotivity, emotional impressions), mania,
psychoneuroses, hysteria, neurasthenia, obsession, phobia, and anx-
ious states. "In acute attacks of psychosis," states Regis, "insom-
nia is one of the first symptoms to appear; it is manifested particu-
larly in restlessness, dreaming, and nightmares. On the other hand,
restoration of the ability to sleep towards the close of a period of
mania or melancholia is of excellent prognostic import." In chronic
mental diseases insomnia is uncommon, except among insane subjects
harboring hallucinations or cenesthetic illusions. Insomnia as a
symptom should receive careful treatment in all psychoneurotic
states: A patient able to sleep is already half-cured under these
circumstances.
The third group, the insomnia of toxic and infectious states, is
more complex.
In this group some forms of sleeplessness seem to be instances
of true toxic insomnia due to direct stimulation of the cerebral cells ;
among these are the insomnias due to abuse of tea, coffee, alcohol,
tobacco, morphine, cocaine, etc.
As for the infectious and post-infectious insomnias, their mode
of production is unquestionably much less simple. Some appear to
be algic insomnias dependent upon some predominant painful dis-
turbance (headache, joint pain, or pain in the side), as in meningitis,
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INSOMNIA. 1103
acute rheumatism and pneumonia. Others seem to be true toxic-
infectious insomnias, of dyscrasic origin, due to the action of the
toxins of infection on the nerve centers, as in the early insomnia of
typhoid fever, of grippe, and of erysipelas. Lastly, an additional
g^oup, especially related to convalescence, appears to be dependent
upon neurovascular weakness, e.g., the insomnias of anemic and (w-
thenic cases (starvation, convalescence, sequelae to infections, etc.).
Insomnia due to circulatory or respiratory disturbances. —
Insomnia dependent upon some cardiopulmonary affection, — This is
the insomnia of heart failure, of lost compensation, of cardiopulmon-
ary disorders causing cough and dyspnea, of asthma, of chronic
bronchitis, etc. The causes are many and outstanding, z/is,, cough,
dyspnea, and toxic influences.
Thus, insomnia is a very common symptom and consequently one
of very restricted diagnostic value, except possibly in the psycho-
neuroses. This does not apply, however to its causal diagnosis,
for it is from such a study of its cause that the basis for rational
and effectual treatment can be found. A patient with heart weak-
ness is made to sleep by restoring circulatory balance; a coffee
fiend by withdrawing the drug, and a syphilitic subject by specific
treatment.
Even with reference to much less definite groups of cases,
however, rational use of special hypnotic remedies depends upon
a partial knowledge of the pathologic physiology of insomnia,
and as an illustration of this fact it seems of interest to consider
summarily the respective indications of chloral hydrate and of
morphine in this class of cases.
INDICATIONS AND CONTRAINDICATIONS TO CHLORAL
HYDRATE AND MORPHINE FOR HYPNOTIC PURPOSES.
Chloral hydrate and morphine are probably — ^and with reason —
the two most commonly employed hypnotics. They should not,
however, be thought of as being interchangeable. While they
may sometimes be administered with advantag'e in combination,
they actually meet wholly different indications and should be pre-
scribed only for definite reasons.
Chloral hydrate and morphine appear to be directly acting hyp-
notics, i.e., drugs inducing sleep by a selective, direct action upon
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1104 SYMPTOMS,
the nerve cell. This constitutes, however, about the only property
they have in common. Indeed,
L Opium and its derivative, morphine, exert, in moderate dosage,
— as Sydenham had plainly noted — ^a tonic action on the heart; under
their influence the heart beats develop increased amplitude and
power, the blood-pressure rises, and circulation through the viscera
becomes more active.
Chloral, on the other hand, is a cardiovascular depressant; un-
der its influence the heart beats become weaker and less frequent,
the blood-pressure is reduced, and visceral circulation is less
Active.
2. In the first stage, at least, opium and morphine produce evi-
dences of cerebral stimulation (a property availed of by morphin-
ists), in all likelihood through hyperemia of the brain and meninges
and direct nervous action. The sleep induced is frequently associ-
ated with dreaming; sometimes it presents features suggesting the
so-called "coma vigil.*'
Chloral sleep, on the other hand, is not preceded by any stage
of stimulation; it is in all respects comparable to normal sleep as
to general features and duration.
. 3. Finally, morphine is an analgesic agent of the first order,
being the type of the pain-relieving drugs.
Chloral, on the other hand, is neither analgesic nor anesthetic;
pain prevents chloral sleep from coming on, while loud noises
awaken the sleeping patient.
Such are the more salient diflFerences between chloral hydrate
and morphine. Their respective indications and contraindica-
tions are logically based on these differences in action.
Morphine, a cardiac and vascular stimulant, at least temporarily
a sPimulant of the brain functions, and an analgesic agent of the
first order, is especially indicated in insomnia dependent upon or as-
sociated with neurovascular zveakness or some painful disorder.
Such being the case, it is serviceable in pain insomnia, generally
due to neuralgia or visceral pain, as well as tabes dorsalis, cancer,
etc. In these cases, however, in order to obviate or postpone as
much as possible the risk of morphine habit, it is well not to
resort to it until after the entire list of pure analgesics, such as
acetphenetidin, antipyrin, exalgin, salipyrin, etc., has been exhausted.
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INSOMNIA. 1105
In the insomnia of anemic or asthenic subjects (inanition, con-
valescence, typhoid fever, pneumonia, etc.) or of persons with weak
heart action or low blood-pressure, morphine, with or without the
addition of heart tonics, remains the hypnotic remedy of choice.
In these cases, on the other hand, chloral hydrate proves ineffec-
tual or even usually does harm.
In the so-called nervous insomnia, however, dependent upon
overwork, excessive ideation, worry, mental excitement, mania,
alcoholism, meningeal congestion, and high blood-pressure, mor-
phine not only proves ineffectual, but is frequently even dangerous.
Chloral hydrate is the hypnotic of choice, in these cases.
Lastly, there occur a large number of hybrid clinical species,
and various "mixed" insomnias, which warrant combined use of
the two drugs to some extent.
Such, for example, is the insomnia of overworked anemic sub-
jects, the painful insomnia present in high blood-pressure (neu-
ralgia in a case of arteriosclerosis), etc. Under these circum-
stances the combination of chloral with morphine, while it doubt-
less fails to afford an ideal pharmacodynamic procedure, consti-
tutes a logical solution of the problem of sleep induction.
Were it necessary to summarize in one concise sentence the
above considerations, it might be stated that:
Opium and morphine are indicated in insomnia associated with
neurovascular weakness or pain; chloral hydrate, in insomnia re-
lated to neurovascular overactivity, without pain.
70
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ITCHING.
The least inaccurate definition of itching or pruritus would
appear to be that of Jaccoud, vk., pruritus is the sum of the sub-
jective sensations which awaken the desire and need of scratching.
The frequent association of pruritus with vasomotor disturb-
ances, as in dermographia, has led to the view that its cause may
be an organic or functional disturbance of the sympathetic nerves.
Many diflferent classifications of pruritus, based on its patho-
genesis and clinical features, have been formulated. The best,
for practical purposes, appears to be the following :
Toxic (and metabolic) pruritus.
Derma tosic pruritus (due to skin lesions).
Parasitic pruritus.
Keurotic pruritus.
Toxic pruritus or itching includes all those forms of pruritus
in which the cause seems to be actually some change in the tissue
fluids or blood, whether this change be metabolic (autotoxic) in
nature, or a true intoxication of food or drug origin (exotoxic).
Autotoxic metabolic pruritus is extremely common. It is
met with in diabetes {diabetic pruritus), in gout, in uremia, in ster-
coremia (constipation), in cholemia (itching in jaundice), in arter-
iosclerosis {senile pruritus), in dyspepsia, and in dysmenorrhea. Its
outstanding feature is plainly the conception of an altered humoral
state consequent upon the insufficiency of the liver and kidneys
which is characteristic of most of the above mentioned disorders.
Pruritus of alimentary origin is no less common, and the
large number of the persons predisposed to it is well known. The
more particularly prurigenous articles of food are crustaceans and
Other shell fish, preserved and salted meats, gam-e, stale fish,
spices, an excessive meat diet, fermented cheeses, and strawberries. *
A partial insufficiency of the liver and kidneys seems to be at
the bottom of these various types of food intolerance. Possibly
(1106)
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ITCHING. 1107
the factor of anaphylaxis is also concerned, as in the succeeding
group of cases.
Pruritus of pharmaceutic origin, due to coffee, tea, alcohol,
belladonna, cocaine, antipyrine, mercury, bromides, chloral hydrate,
opium and its derivatives, and the balsamic remedies. Abuse of
these drugs in some persons, and their use in ordinary dosage in
many, may be the source of itching with or without actual skin
disease.
Pruritus of hydatid origin should also receive recognition in
this group.
Dermatosic pruritos comprises all the skin aflfections which
give rise to itching. The commonest are: Prurigo, urticaria,
lichen, eczema, mycosis fungoides, chicken-pox, seborrhea, hy-
peridrosis, Duhring's dermatitis herpetiformis, the ringworms,
etc. One cannot resist the temptation to reproduce in extenso
Rrocq's lecture on the topic of pruriginous skin disorders :
"I am reviewing for you briefly how one may understand and
classify the pruriginous dermatoses which fall into the group
I term that of the simple skin reactions with pre-emptive pruritus
(Jacquet).
"1. When a patient is seized with pruritus and scratches him-
self, the integument, even though exposed to the trauma of
scratching and rubbing, may retain its normal appearance, show-
ing no structural change appreciable to the naked eye, i.e., no
eruption. One may thus say that it is not reacting in a visible man-
ner. This constitutes simple pruritus or pruritus sine materia.
This is the so-called idiopathic pruritus, a rather frequent condition
in private practice, especially among neurotics; senile pruritus be-
longs in this group.
"2. Under the influence of scratching and rubbing, the skin
may more or less rapidly exhibit a changed appearance ; it may
assume a slightly brownish tint; the creases in it become en-
hanced and more readily visible, deeper, and cross one another
in diamond-shaped fi.gures of varying regularity ; the appearance
at first becomes velvety, then rugose, owing to accentuation of
the dermal papillae and of the epidermis ; histologically, indeed,
there is produced a very marked hyperacanthosis. The process
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1108 SYMPTOMS,
may stop at this point, as is nearly always the case when the
pruritus is of general distribution; when it is circumscribed,
however, the skin lesions undergo further development, suggest-
ing at first species of papules arising through papillary and epi-
dermal hypertrophy, and later infiltrated, thickened, cross-hatched
plaques, more or less scaly and excoriated. These are the changes
characteristic of simple lichenification, 2l process which, like pruri-
tus itself, may be either diffuse or circumscribed; and as I
showed twenty-two years ago while attempting a complete dif-
ferentiation of these morbid types, these are lesions of a purely
traumatic origin, which may be either primary, i.e., show initial de-
velopment on a healthy skin, or secondary, i.e., become superimposed
upon any other pre-existing pruriginous skin disorder. When pri-
mary, the condition constitutes the lichen simplex of the older au-
thors, or, in our own nomenclature, diffuse pruritus or circum-
scribed pruritus with lichenification,
"3. Under the influence of scratching and rubbing the skin may
react by the production of an ordinary urticaria; it may react with
the so-called urticaria papulosa, characterized by small, papular
lesions, and the resulting sequence of changes tends toward the ap-
pearance of prurigo (see below) ; again, it may react with urticaria
bullosa, and the resulting sequence of changes tends toward the
appearance of dermatitis multiformis (see below).
"4. Under the influence of scratching and rubbing, especially
when the pruritus is localized on the inner aspects of the fingers,
the patient may note almost immediately the formation of certain
elevations of the epidermis filled with citrine, clear, serous fluid
and free of surrounding redness, the result being that the skin
appears as though peppered with boiled sago grains, closely
Siggr^gSited and sometimes so confluent as to form rather exten-
sive areas of raised epidermis, almost always discrete, or merely
in apposition. This is the clinical picture for which the term dys-
idrosis should properly be reserved; frequently, however, it is
present in combination with the following type of disturbance,
whence unfortunate mistakes are apt to result.
"5. Under the influence of scratching and rubbing, there de-
velop on the skin, sometimes without redness, but nearly al-
ways with a more or less striking erythema, fine vesicles of un-
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ITCHING, 1109
equal size, of the average size of a pinhead, and which dot the
epidermis in highly irregular fashion. The best plan for observ-
ing them plainly is to first dry the skin either with a piece of
fine cloth or with cotton impregnated with sulphuric ether, then
apply over the affected surface a piece of cigarette paper, over
which is placed a piece of glass to exert pressure. Serous fluid
from the vesicles is then seen through the glass to ooze out and
be absorbed by the paper, thus showing very clearly the shape
and arrangement of the little vesicles. If the latter have not yet
ruptured, one need merely make a few very light strokes with a
curette and then apply the cigarette paper and pressure glass.
To this objective morbid condition, definitely characterized by
the peculiar fundamental skin lesion just referred to, I apply the
term eczema vulgaris, true vesicular eczema, or amorphous eczema,
"6. Under the influence of scratching and rubbing there de-
velop minute lesions of a rather bright red color, slightly ele-
vated above the surrounding skin surface, exhibiting at their
center a slight lifting up of the epidermal layer by citrine serous
fluid, i.e., a small vesicle. These lesions may be scattered here
and there in complete disorder, especially on the extremities, but
exhibit a marked tendency to become agminated and confluent,
thus giving rise to red patches, dotted with minute vesicles simi-
lar to those of the preceding type and oozing more or less freely.
This is the disorder to which the term papulovesi<:ular eczema is
peculiarly applicable. It is made up of a number of transitional
stages which insensibly merge the true, common or amorphous
vesicular eczema with the true prurigoes to be next described.
"7. Under the influence of scratching and rubbing, the skin
reacts with bright red, acuminate, more or less urticarial papules,
exhibiting at their apices a slight tendency to elevation of the
epidermal layer by a little citrine serous fluid. As the attendant
itching is very marked, these urticarial papulovesicles (Tomma-
soH's seropapules) are nearly always found ruptured by the pa-
tient's finger nails; where, however, the lesion is permitted to run
Its course without traumatic interference, there arises spontane-
ously at its summit a minute brownish-yellow crust formed
through desiccation of the little apical vesicle. Such is the char-
acteristic fundamental lesion of prurigo. As I already stated in
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1110 SYMPTOMS.
discussing the diflferential diagnosis of one of our cases, if these
eruptive units remain separate and discrete, the morbid type
known as prurigo simplex exists ; if they show a tendency to come
together in clusters and form eczematized and lichenified
plaques, the condition is that known as Hehra's prurigo; if they are
very large, the condition present is prurigo ferox Vidali,
"8. Following scratching and rubbing there may be produced
in certain patients only a more or less marked lichenification of
various extent, together with acute out-croppings of eczema ves-
icles. E. Eesnier long ago classified this disorder among the
'diathetic prurigoes.' According to the nomenclature personally
adopted, it cannot be spoken of as a form of prurigo, since it
fails to exhibit the fundamental urticarial papulovesical charac-
teristic of this group. For it I shall therefore retain the term
pruritus with lichenification and ecsematous transformation.
"9. Under the influence of scratching and rubbing, the skin may
finally react in a much more complex manner. In some places there
form patches of erythema, elsewhere urticarial lesions, elsewhere,
either on healthy skin or over pre-existing patches of erythema,
vesicles or blebs of varying size, and sometimes even pustules.
These various eruptive types may be simultaneously present in the
same individual, constituting the multiform eruption par excellence;
they may instead occur in succession, one eruptive outburst being,
e.g., urticarial, another erythematous, another erythematovesicular,
another bullous, another actually multiform, etc. Furthermore, the
various eruptive lesions may be scattered in disorderly fashion;
they may be grouped together, and suggest either herpes, vulgaris or
the circinate lesions of ringworm, in which event the term derma-
titis herpetiformis (Duhring) is particularly applicable. The clin-
ical group as a whole should be termed that of dermatitis muHi
formis.
"Such, briefly summarized, is the vast series of the pruriginous
skin disorders with pre-eruptive pruritus (Jacquet) belonging to
the group of the primary skin reactions.
"It should be added, however, that under the influence of itch-
ing and the attendant scratching, other eruptions, which cannot, for
the present at least, be classed simply among the skin disorders with
pre-eruptive itching, may likewise develop with extreme ease and
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ITCHING. 1111
rapidity. In the front rank among these should be mentioned those
peculiar disturbances, intermediate between eczema and psoriasis,
which have been the subject of such extensive discussion of late
and to which we have applied the term psoriasiform parakeratoses;
now, among these psoriasiform parakeratoses there is one particu-
lar form which is frequently seen to develop under the circum-
Fig. 798.— Scabies. Places of election for burrows. None
are ever noted on the face or scalp.
stances alluded to: This variety is chiefly characterized, objectively,
by the presence of patches of varying extent of a more or less
bright red color, sometimes pale, sometimes rather dark, scaly, and
over which are formed vesicles similar to those of true vesicular
eczema. This condition is therefore actually deserving of the
appellation eczema; it is what most authors term seborrheic psori-
asiform eczema, but what I have referred to as eczematized psori-
asiform parakeratosis, wishing thereby to imply that in many in-
stances this clinical condition is in no wise related to seborrhea/'
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1112 SYMPTOMS.
Along with these various forms of dermatosic pruritus should
be mentioned the itching due to varicose conditions of the lower
extremities. These are always accompanied by trophic disturb-
ances.
The same applies to the localized forms of pruritus, such as
vulvar or perianal pruritus due to some local uterine, vaginal
(leucorrheal), urethral, anal or perianal (fistula or hemorrhoids)
discharge.
Parasitic pruritos is clinically represented chiefly by scabies
and the several varieties of pediculosis. These conditions should
always be kept in mind, though little should be said about them,
Fig. 799. — Burrow containing a female itch-mite and her ova.
even after the diagnosis is certain. The diagnosis of scabies — ^an
important one to render — should be basied chiefly on the transmis^
sion of an itching disorder (the patient "having slept with some one
who was frequently scratching himself"), on the special localisation
of the itching at the points of election shown in the annexed illus-
tration, and if necessary, by microscopic identification of the paror-
sites themselves. For the latter purpose one of the little burrows in
the skin should be opened up with a needle and the minute white
object at the bottom of it removed, likewise with the needle; the
female parasite is thus secured and may be examined with a hand
lens or microscope.
The following description of one of these burrows is reproduced
from Sabouraud:^
"The Burrow. — I am for the first time thus alluding to the
familiar burrow of scabies. This is because in any fairly extensive
1 Presse medicale, June 21, 1917.
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ITCHING, 1113
dispensary practice, the dermatologist will have twenty times made
a diagnosis of scabies on the basis of the localizations, of the dis-
order before having searched for a single burrow. The burrow is
• looked for in recent or doubtful, cases in which no light is thrown
on the condition by the history. What, then, is the scabies burrow ?
A homely comparison will give an idea of it at once, for every one
is familiar, from repeated observation, with the burrow of a mole
projecting above the surface of the ground in a field. The burrows
of the itch-mite are constructed similarly. They are most readily
Fig. 800. — Sarcoptes scabiei, female, Fig. 801. — Sarcoptes scabiei, female,
dorsal aspect (R. Blanchard). ventral aspect {R. Blanchard).
observed in uncleanly individuals working in dirty liquids, since
these liquids, entering the burrows by capillarity, stain them black.
To see them well when one is not familiar with them, the palm
of the hand in the children of the very poor should be selected.
The burrows may be accurately compared to the outline of the
spirochete of syphilis stained with silver nitrate, now a familiar
object owing to its frequent reproduction by photography as well
as by delineation. It appears as a wavy black line. Where the
burrow is not blackened with dirt, howerer, it is so hard to see
that the observer, in order to remove all doubt, should stain it
by placing a drop of ink or tincture of iodine over it, wiping it
off a moment later — a simple, but often useful procedure.
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1114 SYMPTOMS,
"The unblackened burrow is even harder to describe than to
descry. X-et the reader imagine that he has pushed a needle
through thick, horny epidermis, e.g., at the finger tip, without
Fig. S02.—Pediculus capitis, male. Fig. 803.— Ovum of Pediculus cap-
Enlarged 25 X (Brumpt), itis attached to a hair. Enlarged.
(Brumpt),
drawing any blood. When the needle is withdrawn, the track
made by it will be visible, the raised epidermis having been ren-
Fig. SOi.—Phthirius pubis. Enlarged 25 X. St. Stigma. Tr. Air-duct.
dered dull and whitish; the channel thus made is, however, a
straight one, while that of the itch-mite is always wavy. Other-
wise, the white, dull condition of the epidermis induced is exactly
the same. Such a channel is quite hard to see, and this is what
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ITCHING. 1115
makes the diagnosis of the disease so difficult, except under hos-
pital conditions. More commonly the lesions of scabies are ele-
vations, papules, or vesicles often opened by scratching, and the
long axis of which exhibits the same direction as the skin fold
at that point."
The diagnosis of pediculosis (phthiriasis) is similarly based on
the situation of the skin lesions (see illustration) and direct exami-
nation of the parasite. It should not be overlooked that these para-
Fig. 805. — Pediculosis or phthiriasis. Areas of election.
sites are not only unpleasant, but also dangerous, being known car-
riers of many instances of relapsing fever and of typhus fever.
The well-known maculce carulece above the pubis, characteristic of
pediculosis pubis, should be kept in mind.
Neurotic pruritus is met with chiefly under the three following
circumstances :
(a) In psychoses, neuroses, exophthalmic goiter, and as a sequel
to overwork, sorrow, and severe emotional impressions.
(&) In lesions of the peripheral nerves (causalgia).
(c) As a reflex manifestation of some deep-seated visceral irri-
tation, as exemplified in the itching of intestinal helminthiasis.
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1116 SYMPTOMS.
To recapitulate: Itching may, for practical purposes, be divided
into the following five gfroups of causes, which account for at
least 95 per cent of all cases:
1. Parasites: Scabies and pediculosis; in these cases the
diagnosis is based on:
(a) Localization of the itching: Head and neck in ordinary
pediculosis; dorsal surfaces of the hands and forearms, anterior
aspect of the axillae, inguinal regions, and penis in scabies; pubic
region in pediculosis pubis.
(fr) The skin lesions due to scratching.
(c) Direct observation of the parasite concerned with a good
hand lens or microscope.
2. Itching skin affections: Observation of the type of skin
disorder present enables the experienced dermatologist to ren-
der an immediate diagnosis.
3. Hepatic and renal insufficiency: Cholemia and azotemia,
(a) Blood-pressure estimation, uranalysis, the presence of other
evidences of azotemia (vertigo, cramps, epistaxis, and nycturia),
and in particular, determination of the blood urea will lead unmis-
takably to the diagnosis of azotemia,
(fc) The itching attending jaundice is a familiar symptom. One
should be able, however, to detect even an early cholemia, of
which itching is itself a valuable indication.
4. Metabolic disorders, in the front rank of which should be
placed diabetes. Pruritus in certain regions, e.g., the inveterate
pruritus vulvce of women, is particularly significant. One should
never omit examining the urine in a case of pruritus, for four dis-
tinct reasons — sugar, albumin, bile, and acidity. Glycosuria, nephr-
itis, cholemia, and acidosis are extremely common causes of itching.
5. Neuropathic states in which pruritus is an actual cutaneous
dysesthesia, accompanied by the usual characteristic evidences
of neurosis. The diagnosis of neuropathic pruritus should, how-
ever, be made only by exclusion, after having systematically
eliminated the causes already mentioned, %nz., parasites, skin
disorders, cholemia, azotemia, glycosuria, and dietetic or phar-
maceutic intoxication.
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ITCHING.
ITCHING.
1117
Cad SIS.
Special Pbatcbbs
AND Location
or ITCHING.
Urini
Examination.
Obnbral Condition.
Associated Clinical
Signs.
Parasitic.
Pediculosis.
Scabies
(burrows).
Scratch marks.
Special parasite.
Head and back of
neck.
Dorsal aspect of
hands and forearms.
Anterior aspect of
axillx.
Prepuce ; inguinal
regions.
Pubes.
Nocturnal paroxysms.
0
0
Denna-
toaic
Typical skin affec-
tions, such as pru-
rigo, urticaria, lichen,
eczema, seborrhea,
ringworm, chicken-
pox, mycosis, etc.
Sometimes al-
bumin if the
skin disorder
is generalized.
0
Cholemic
Generalized itching
sine materia, some-
times predominantly
on the lower ex-
tremities.
Scratch lesions late
in appearing.
Sometimes bile
pigments.
Nearly always
urobilin, and
frequently ali-
mentary gly-
cosuria.
Established or in-
cipient jaundice.
Bradycardia.
Familial cholemia.
Azotemic
Generalized itching
sine materia.
Sometimes nocturnal
paroxysms.
Scratch lesions late
in appearing.
Frequently
albumin.
Evidences of Bright's
disease and arterio-
sclerosis.
High blood-pressure.
Headache, vertigo,
epistaxis, nycturia,
etc.
Diabetic
Itching often localized
at the vulva, or skin
folds on flexor sur-
faces; extremely
marked and obsti-
nate.
Glycosuria.
The usual signs of
diabetes :
Polyuria, polydipsia,
poyphagia, etc.
Toxic
Generalized itching
sine materia, or urti-
carial, or dermatitis
medicamentosa (Ex. :
Exfoliative derma-
titis of mercurial
origin).
0
Or transitory
albuminuria.
Or transitory
urobilinuria.
Dietetic or pharma-
ceutic intoxication,
more or less obvious.
Yields more or less
quickly to removal
of the cause.
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1118
SYMPTOMS.
ITCHING (conHnued).
Special Features
Ubinb
GENERAL CONDITION.
Causes.
AND LOCATION
BXAM I NATION.
Associated Clinical
OF Itch I NO.
SIGNS.
Neuro-
General or local
0
(a) Psychopathic
pathic
itching sine materia.
disorder, neurosis,
exophthalmic
goiter, emotions,
overwork, etc.
(b) Peripheral neu-
ritis (causalgia).
(c) Remote visceral
irritation (helmin-
thiasis).
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JAUNDICE (ICTERUS).
The term icterus is applied in all cases in which — whether the
urine and stools are or are not aflfected — the conjunctivae and
skin exhibit a yellow or yellowish hue. In this work the word
icterus, in conformity with its etymologic derivation (from
lyTfpog, jaundice), will be taken as synonymous with jaundice
and as being free of any implication that the discoloration is of
biliar>% hepatic, or other origin.
Icterus or jaundice may be caused :
1. By retention and reabsorption of the bile and of the normal
biliary pigments : Hepatic jaundice.
2. Through a special change in the blood (hemolysis) : Hematic
(hemolytic) jaundice.
3. Through a special kind of intoxication (picric acid) : Picric
jaundice.
I.— HEPATIC JAUNDICE.
Hepatic jaundice, dependent upon retention and reabsorption of
bile and biliary pigments, is that which displays in its greatest inten-
sity the well-known symptom-group of jaundice with its cardinal
symptoms, viz,, jaundice of the skin and conjunctivae and urinary
jaundice (from canary yellow to mahogany color, with more or less
pronoimced decolorization of the stools), and its associated symp-
toms due to bile intoxication, viz., slow pulse, itching, loss of weight,
depression, oozing of wounds, etc.
It should be at once pointed out that this classical symptom-
group, which, as we shall see, is of markedly variable origin, ex-
hibits a diminishing degree of intensity of the jaundiced color
of the skin, conjunctivae, and urine in the following three classes
of cases :
Maximum intensity: Cholelithiasis, cancer of the pancreas,
and chronic obstruction of the bile duct.
(1119) '
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1120 SYMPTOMS.
Intermediate intensity: Catarrhal jaundice, benign infectious
jaundice, and picric jaundice^
Minimum intensity: Infectious, cirrhotic, syphilitic, and
hemolytic forms of jaundice.
Hepatic jaundice may be the result either of an obstruction or
impediment to the flow of bile or of disease of the hepatic lobules or
dyshepatia.
Intrinsic (Intracanaliculobiliary) Causes of Obstruction. —
Cholelithiasis, affecting the gall-bladder, but more particularly
the biliary canal or bile-duct, is by far the most important among
the possible causes of jaundice; tenderness of the gall-bladder,
acute attacks suggestive of hepatic colic, and the history will
generally point directly to the diagnosis.
Catarrhal jaundice comes next, with its usual accompaniment
of febrile gastric disturbance and running its course in one or
two weeks; as a rule the diagnosis of these cases occasions no
difficulty.
Exceptionally there have been reported instances of foreign
bodies that had passed out through the walls of the intestine (fruit
stones, grape seeds, and parasitic ascarides or hydatid disease) ; in
such cases the diagnosis can be made only as an unexpected finding
during an operation or at the autopsy. In the case of a cicatricial
stenosis following duodenal ulcer, the diagnosis would be made on
the basis of the history and the symptoms of duodenal disease.
Extrinsic (Extracanalicular) Causes of Obstruction. — 1. Out-
side of the liver: Usually, cancer of the head of the pancreas,
which is by far the commonest cause of jaundice of extrahepatic
origin. Exceptionally : Secondary tuberculous or malignant gland-
ular involvement at the hilum of the liver, peritoneal bands, ad-
hesions of the biliary channels, lower hepatic surface and colon on
the right side, tumors of the kidney, and aneurysm of the abdominal
aorta.
2. Within the liver: Cancer of the biliary ducts and liver,
hepatic abscess, and cysts of the liver.
Disease of the lobules of the liver, or dyshepatia, may result
from some intoxication or infection acting injuriously upon the liver
cells. It is generally manifest in the lengthy chain of infectious
jaundiced states, a mere enumeration of which will here suffice :
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JAUNDICE, 1121
Catarrhal jaundice, simple or prolonged, always benign, and
occurring sporadically and indigenously.
Benign infectious jaundice, or pseudocatarrhal infectious icterus.
Pleiochromic jaundice.
Recurring infectious jaundice.
Grave icterus, usually secondary to some pre-existing liver dis.-
turbance, such as cirrhosis, etc., or to an infectious disease, such as
typhoid fever, staphylococcic infection, malaria, etc.; exceptionally
as a primary disorder, as in phosphorus poisoning, yellow fever,
icterohemorrhagic spirochetosis, etc.
This type of jaundice is essentially characterized clinically by
a certain symptomatic triad, viz., (1) jaundice; (2) typhoid state,
and (3) various sorts of hemorrhage. According to the kind of
case the condition may be attended with hypothermia, as in
colon bacillus infection and phosphorus poisoning, or with fever,
as in yellow fever and staphylococcic or streptococcic infection.
Larrey, in his Memoires, already wrote of an "icteroid typhus"
which assailed the troops of the Army of Egypt in 1800. Dur-
ing the War of the Rebellion, over 70,000 American soldiers be-
came afflicted with jaundice. More recently, in Macedonia, the
belligerent armies developed many cases of grave malarial
bilious fever (intermittent bilious fever, hemorrhagic bilious
fever, hemoglobinuric bilious fever, etc.).
Special mention may here be appropriately made of an appar-
ently primary variety of infectious jaundice which has only of late
come to notice. It is manifested in a recurring febrile infectious
jaundice, ordinarily accompanied by myalgia and hemorrhage, and
brought on by a spirochete discovered and studied in 1913-1915 by
two Japanese authors, Inada and Ido, whence the term ictero-
hemorrhagic spirochetosis now generally applied to the disease.
This form' of infectious jaundice, often a grave disorder, is
probably identical with Larrey's icteroid typhus, with the epi-
demic remittent bilious fever of Laveran, and with the idiopathic
grave icterus of Kelsch.
It is manifested in a symptom-group characterized by sudden
onset, high fever (39-40** C), a pronounced typhoid state, a pro-
gressive jaundice of variable intensity, pains in the extremities,
myalgia (especially in the thighs and calves), and joint pains,
71
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1122 SYMPTOMS.
albuminuria, and a progressive azotemia which may attain to a
very high degree. In one of our fatal cases, the azotemia ulti-
mately rose to 6.80. The provisional diagnosis of spirochetosis
can be definitely established only by microscopic examination
for the causative germ.
As a matter of fact, icterohemorrhagic spirochetosis may ex-
hibit any grade of severity, from the form suggesting catarrhal
jaundice to that representing grave icterus. On the whole one
may, however, make out three stages in the course of the disease :
(1) A preicteric stage, with predominance of constitutional symp-
toms ranging from simple diffuse pains to continuous fever sug-
gesting typhoid; (2) an icteric stage, with more or less in-
tense and persistent jaundice and almost constant albuminuria;
(3) a stage of slow restoration, with gradual return to normal,
or, on the contrary, aggravation of the disease vrith progressive
azotemia and a fatal termination.
A positive diagnosis manifestly requires examination for the
spirochete. Its presence is best demonstrated by guinea-pig in-
oculations. Into one guinea-pig 5 cubic centimeters of blood are
injected and into another, 5 cubic centimeters of urine. Where
the result is positive, the animal dies in about a week, exhibiting
a yellow color of the scler3e, ears, and mucous membranes, and
bile pigment, albumin, and spirochetes in large numbers in the
urine and in sections of internal organs.
In hepatic, mechanical jaundice of the retention type, the bile
pigments retained in the blood and passing out in the urine are nor-
mal bile pigments (see Technical procedures) , and the icterus may
be said to be orthopigmentary.
In infectious, dyshepatic jaundice, the result of cell disturbance
and pathologic change, the bile pigments retained in the blood and
passing out in the urine are normal as well as abnonnal bile pig-
ments (see Technical procedures), and the icterus may be said to
be metapigmentary,
XL— HEMATIC JAUNDICE.
The hematic forms of jaundice, mainly dependent, apparently,
upon some disturbance of the blood, or at least accompanied and
characterized by such a disturbance, were already clearly discerned
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JAUNDICE. 1123
in the eighteenth century. Bianchi's concise reference to the matter
(1710), quoted by Boix, leaves no room for doubt in this connec-
tion: **Sunt duo primaria icteri genera: prima classis icterus e
tntio hepatis, alterius speciei uteri a causa solutiva sanguinis." The
profound studies of Giibler on hemapheic icterus are well-known to
all. The subject has, however, in late years been completely recast,
thanks particularly to the labors of the French clinicians Chauffard,
Gilbert, Widal, and their followers on the hemolytic forms
of icterus..
Clinical characteristics of hemol3rtic icterus :
1. Jaundice generally of slight or intermediate intensity.
2. Coloration of the stools.
3. Hemapheic character of the urine (see Urine) : Absence of
true bile pigments, presence of urobilin (acholemic, orthopigmentary
jaundice).
4. Absence of the ordinary signs of bile intoxication, in:^., ab-
sence of slow pulse, itching, xanthelasma, and loss of weight.
Characteristics referable to the blood:
1. Anemia.
2. Lowered resistance of the red cells (hemolytic reaction).
3. Granular red cells and autoagglutination of these cells.
Clinical varieties (the least obscure ones) of hemolytic
icterus :
1. Congenital, familial hemolytic jaundice (Gilbert's familial
cholemia; Chauffard's congenital icterus of the adult). As a mat-
ter of fact, all cases of congenital icterus in the adult should be
presumed to be of non-hepatic origin.
2. Acquired hemolytic jaundice: Simple jaundice of the
newborn, simple post-infectious hemolytic jaundice, hemolytic
jaundice of the type of pernicious anemia, and the jaundice of
idiopathic paroxysmal hemoglobinuria. ^
III.— PICRIC JAUNDICE.
Picric jaundice results, as the term implies, from picric intox-
ication, by the ingestion of picric acid. It is characterized :
1. By a yellow, icteric hue of the skin, conjunctivae and urine.
2. By coloration of the stools.
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1124 SYMPTOMS.
3. By the usual absence of bile pigments from the urine and
blood serum, picric acid being, however, present in these fluids (see
Uranalysis).
4. By the usual absence of the classic signs of bile intoxication,
vi::., by the absence of slow pulse, itching, and loss of weight.
The procedure described by Castaigne and Desmoulins, which
permits the detection of picric acid in the serum of patients with
jaundice, is particularly serviceable by reason of its simplicity,
reliability, and speed: Fifteen to 20 cubic centimeters of blood
are collected by wet cupping or vein puncture and placed in a
test-tube. An equal volume of a 25 per cent, aqueous solution
of trichloracetic acid is added. The tube is then closed with the
thumb and thoroughly shaken, the mixture poured on an ordinary
pleated filter, and the filtrate collected in a well cleaned test-tube.
In the absence of picric acid the filtrate is clear and colorless.
The presence of picric acid is shown by a yellow picric tint
of varying intensity upon inspection against a white background.
IV.— SYPHILITIC JAUNDICE AND JAUNDICE DUE
TO ARSPHENAMIN.
The relative frequency of jaundice occurring during arsphenamin
treatment has led to the publication of many contributions on the
subject which are rather contradictory, some considering the jaun-
dice as a syphilitic jaundice or hepato- recurrence awakened by the
treatment and amenable to more intensive medication, while others
look upon it as a toxic arsenical jaundice.
In truth, it would seem most extraordinary if the drugs of the
arsphenamin series were the only arsenical compounds which might
not, in high dosage, act prejudicially on the liver, and certainly
nothing is less definitely proven at the present time than that arsen-
ical treatment is indicated and effectual in these cases. For the
present it seems prudent to consider the jaundice which occurs un-
der these conditions as of toxic, arsenical nature, and to interrupt the
treatment or replace it by mercurial medication.
As for chronic jaundice, it should be recalled that Hanot's syn-
drome and the hemolytic types of jaundice particularly call for a
search for acquired syphilis in the former case and for syphilis or
inherited syphilis in the latter.
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JAUNDICE. 1125
V.~R£LATIV£ FREQUENCY OF THE SEVERAL
FORMS OF JAUNDICE
Clinically, the order of frequency of the several vareties of
jaundice above mentioned appears to be as follows:
Infectious jaundice, ranging from catarrhal to grave.
Cholelithiasis, simple or with complications.
Hemolytic icterus.
Tumors of the liver.
Cirrhosis and syphilis of the liver.
Cancer of the pancreas and biliary tract, etc. (extrahepatic
tumors).
Abscess and hydatid cyst.
Picric jaundice.
Consideration of the differential diagnosis of jaundice in the
subjoined table will be limited to the varieties just given.
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1126
SYMPTOMS.
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JAUNDICE.
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JOINT PAINS.
ARTHRALGIA.
RHEUMATISM.
(>6VfMrv(yfi6g^ from (>ev[ia, flux.
Rheumatism.
Pains in the joints (arthralgia) occur so often, in such a va-
riety of situations, and in so many forms that an analytic and
synthetic presentation of the subject would seem to be almost
an impracticable task, particularly since it brings up the ques-
tion, as yet obscure in many respects, of "rheumatism." Hence
the author's belief, departing from the plan followed in other
chapters of this work, that it is best here not to analyze the
"innumerable and protean joint disturbances," but to arrange
them in logfical grouping's from the standpoint of pathologic phy-
siology and to recall the general clinical rules which permit of
the makmg of a concrete diagnosis in these cases.
To give an idea of the frequency with which the term "rheu-
matism" is improperly applied to the most varying clinical con-
ditions, one need merely recall the figures published by Deaderick,
analyzingi 100 cases labelled "rheumatism" and detecting 53
mistaken diagnoses which were grouped thus:
Eighteen cases of syphilis with positive Wassermann reaction,
8 cases of neuritis, 4 cases of tuberculosis, 4 of flat foot, 2 of
neurasthenia, 2 of arteriosclerosis, 2 of tabes dorsalis, 1 of chronic
nephritis, 1 of chronic gastritis, 1 of progressive muscular
atrophy, 1 of malaria, 1 of pernicious anemia, and 1 of myelitis.
Joint Pains. — Rheumatism. — Whereas practically definite
pathologic and clinical concepts are expressed in the terms dia-
betes, gout, and obesity, this is far from being the case with the
term rheumatism. Usage has given to this word a vague, inac-
curate, extremely defective meaning because it is far too com-
prehensive ; this term we shall accept, however, without attempt-
ing useless explanations of it, the essentially practical aim of the
work making it necessary to exclude all hair-splitting and fruit-
less terminologic discussions.
(1128)
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JOINT PAINS. ARTHRALGIA. RHEUMATISM. 1129
Medical men are constantly speaking, then, of acute articular
rheumatism, of gonorrheal rheumatism, of tuberculous rheumatism,
of gouty rheumatism, of deforming rheumatism, of trophoneurotic
rheumatism, of muscular rheumatism, etc. There is no doubt that it
would be much better to use in most instances strictly concrete and
determinate pathologic terms such as arthritis, osteoarthritis, neu-
ralgia, myalgia, etc., following them with special qualifying words
such as gouty, gonococcic, tuberculous, saturnine, traumatic, etc.,
and to make of the qualifying term rheumatic itself a specific desig-
nation applying to certain relatively well defined clinical entities
such as acute, frank, rheumatic multiple arthritis, or progressive,
deforming, rheumatic multiple arthritis. Yet, we repeat, nosologic
usage has already settled the matter otherwise and has given to the
term rheumatism the very vague signification of a disorder charac-
terised especially by pains in the joints; we shall accept it thus,
faulty as it is — and all the more willingly since in practical work the
often difficult question of diagnosis between most varied sorts of
joint disturbance, infectious and metabolic, is continually arising
and it seems useful and eminently practical to attempt a compre-
hensive classification and general review of the clinical features of
the joint disorders most commonly encountered.
To find and keep to the proper path in the maze of joint dis-
turbances, it is necessary to refer back to the etiology whenever
the pathogenic cause of the condition can be determined. This
is, of course, not always, nor even often, the case; hence the
need of accepting, in lieu of a better one, the following* hybrid
classification, based partly on the etiology and partly on the
clinical features.
I. Acute joint disorders.
A. Acute articular rheumatism.
B. Infectious pseudorheumatism, or better, infectious arthritis
{ordinary joint infections, or specific, toxic-infectious disorders) :
gonorrheal, miscellaneous (post-influenzal,
tuberculous, post-pneumonic, puerperal,
syphilitic, post-anginal, post-typhoid,
scarlatinal, etc.).
polymicrobic,
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1130 SYMPTOMS.
C Acute gouty arthritis.
II. Chronic arthritides.
A. Chronic gouty arthritides,
B. Generalised chronic rheumatism,
(a) With erratic manifestations (articular, muscular, neural-
gic, etc.).
(&) With local manifestations (Heberden's nodes, campto-
dactylia, drumstick fingers, rhizomclic spondylosis, etc.).
(c) Progressive deforming rhetunatic polyarthritis (nodular
rheumatism).
C. Arthritis deformans, mono- or oHgo- articular.
III. Trophoneurotic. — Neurotrophic.
(a) Joint disorders following neuritus (z(ma), myelitis (tabes),
encephalopathy (hemiplegia), etc.
(&) Amyotrophic arthropathies due to spinal lesion, the latter
either primary or secondary to the reaction; of the joint inflammation
upon the neuraxis.
(c) Generalized dystrophy.
IV. Traumatic.
(Sprains, fractures near joints, wounds, and foreign bodies.)
The latter group is of interest in this connection only when
the traumatism results in local infectious or nutritional disturb-
ance.
The above simple classification is of real practical service ; it
is sufficiently clinical in type and seems deserving of recommen-
dation provided its somewhat restricted scientific basis is always
kept in mind. In other words, clinical use of this tabular scheme
necessitates familiarity with the three following clinical laws:
I. There is not necessarily any relationship between the cause
of a joint disturbance and its clinical modality. — ^Thus, gonor-
rheal joint disease may occur in any of the following forms :
Acute febrile arthritis (gonorrheal rheumatism).
Suppurative arthritis.
Plastic, fibrous, ankylosing polyarthritis.
Again, tuberculous joint disease may occur as:
Acute febrile arthritis (tuberculous rheumatism).
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JOINT PAINS. ARTHRALGIA. RHEUMATISM. 1131
Subacute serous arthritis (hydrarthrosis).
Suppurative osteoarthritis (white swelling).
Fibrous, ankylosing osteoarthritis.
Even the term tuberculous arthritism has been used by some.
Consequently :
II. A given clinical type of joint disturbance may result from
different pathogenic causes. — Thus, progressive deforming poly-
arthritis may be the end-result of acute rheumatism, of gonococcic
infection, of tubercle bacillus infection, and, even more frequently, of
as yet imperfectly defined causes, among which are mentioned pre-
eminently exposure to cold and dampness and, as a subsidiary fac-
tor, thyroid insufficiency.
Again, acute exudative febrile arthritis may be brought on, ordi-
narily by acute rheumatism, rather frequently by gonococcic infec-
tion, exceptionally by tubercle infection, etc.
III. There is no definite line of demarcation between the three
t3rpes of joint disturbance (toxic-infectious, dyscrasic, and neuro-
trophic).— Or at least, if a few perfectly definite clinical species
do exist, such as acute rheumatism, the gouty arthropathies, and
rhe tabetic arthropathies, most of the above mentioned clinical
species, of obscure and diverse etiology, do not constitute definite
clinical identities, but mere syndromes which may be brought on
by different pathogenic causes [toxic-infectious, humoral (ex-
ogenous and endogenous), or neurotrophic].
Further, it is readily conceived that some toxic-infectious dis-
order, reacting upon the functions of the endocrin glands, for
example, or upon the neurotrophic cells, might actually bring about
the humoral or trophoneurotic degenerative changes which
are recognized or suspected as being at the bottom of the major-
ity of the so-called diathetic chronic joint disorders — ^the various
forms of chronic rheumatism.
As in the case of diabetes or obesity, one is led, then, to the con-
ception of chronic rheumatism as a trophoneurotic clinical syndrome
affecting particularly the joints, of toxic-infectious or dyscrasic
origin, these tzvo pathogenic factors being present either separately,
in combination, or as a subordinate cause.
On the whole, the joint tissues react, whatever pathogenic
agent they may be subjected to, in but a few ways, vu:., pain,
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1132 SYMPTOMS.
congestion, inflammation, serous exudation, suppuration, and
fibrosis.
Any joint disorder, of whatever cause (traumatic, infectious,
dyscrasic, or nervous) may pass through three distinct stages:
Acute stage, chronic stage, and stage of deformity.
Some forms stop in the acute stage, as is generally the case
in rheimiatic fever; others in the chronic stage, as is frequently
the case in tuberculous arthritis ; a few begin in an. acute stage
and terminate in the deforming stage, as is frequently the case in
gonorrheal joint disease; certain disturbances, moreover, cause
deformity from the start, as in nodular rheumatism. All these
varieties are commonly met with.
The disease may attack from the start or in succession the
synovial membrane, the periarticular aponeuroses, the muscles
and tendons in the vicinity of the joint, the periarticular bony
surfaces, the nerves, and the marrow ; all the tissues, in fact, in-
cluding the. skin, cellular tissues, and vessels, may undergo tro-
phoneurotic degeneration — a matter of common observation in
chronic forms of rheumatism.
It seems not inappropriate here to present an excerpt from
the communication of P. Le Gendre to the Academic de medecine
on May 9, 1911, regarding the pathogenesis and prophylaxis of
the so-called "rheumatic" affections:
To explain the origin of the rheumatic disorders and their re-
crudescences, it is necessary to bring in two parallel series of
factors, zns., (1^ the intoxications and toxic-infectious states, and
(2) faulty hygiene of the locomotor apparatus.
The latter might be said to be the initial and primary factor,
producing a favorable soil for the activities of the former; it
would thus underlie the entire clinical history of rheumatism in
all its forms, both those set apart under the term pseudorheuma-
tism, and the gradually decreasing number which are still con-
sidered instances of true rheumatism.
In the case of the latter, Bouchard, through his studies of their
concurrence with other morbid conditions, brought out their rela-
tionship ivith the diseases due to slowing of the nutritive process,
such as obesity, diabetes, gout, migraine, calculous disorders, asthma,
etc., and with the so-called arthritic diseases. This implies that they
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JOINT PAINS, ARTHRALGIA. RHEUMATISM. 1133
are likewise dependent upon arthritism — the bradytrophic diathesis
of Landouzy, or dystrophic diathesis, if one uses the term proposed
by Fernet This relationship seems also to be shown by clinical
observation of the post histories of the patients themselves and their
family histories.
Might one not conceive of this relationship, however, as being the
result of the influence of faulty hygiene of the locomotor apparatus
upon general nutrition?
It is impossible that an apparatus of such importance in the
living system should not play a very prominent role in the ac-
tivity of interstitial metabolism. In it, along with the digestive
tract and the nervous system, are to be found the three great
sources of nutritive disturbances — acting through different
mechanisms but frequently in combination.
A diet which is defective through excess or improper selection
of foods, imperfect elaboration of the latter owing to impaired
digestive functions, autointoxication by poisons of gastrointestinal
origin resulting from prolonged stasis of the digestive residue in
one or another portion of the alimentary tract (dilatation of the
stomach, dyspepsia with ileocecal stasis, and coprostasis either of
liquid or solid matters in the colon), and defective functioning of
the liver — ^these, doubtless, are the causes of arthritism.
An excessive, disturbed functioning of the nervous system, in-
hibiting tissue metabolism or secretion by the endocrin glands which
supply the ferments indispensable for such metabolism, should also
be taken into account in the production of certain arthritic diseases,
and it has been necessary to appeal to it in the pathogenesis of
obesity, of diabetes, and of gout, according as the metabolic proc-
esses concerned were those of fat, sugar, or uric acid production, or
fat, sugar, or uric acid de3truction.
As a counterpart to these factors, we shall accept the view that
there occurs also a group of disorders characterized by slowed
nutrition which is dependent upon a primary disturbance of the
locomotor apparatus and that it is this disturbance which is at the
bottom of the so-called true rheumatic disorders — predisposing the
various constituent parts of this apparatusi to become unduly sensi-
tive to cosmic factors as well as to endogenous toxic influences, and
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1134 SYMPTOMS,
to react against them by such manifestations as pain, hyperemia,
exudation, or proliferation.
Perhaps this dystrophic state of the serous, fibro-connective,
osteo-cartilaginous, and muscular systems also predisposes them
to being more easily injured by exogenous bacterial or toxic
attacks and to reacting against the latter by various local changes
which may progress to the point of actual suppuration.
Among the characteristic effects of the bradytrophic diathesis
is an excessive sensitiveness of the vasomotor system; as Cazalis
and Senac have stated, it is a congestive diathesis, which favors
hyperemia, edema, and oversecretion ; it also exhibits an exces-
sive tendency to painful manifestations or algias. Thus, it carries
with it a tendency to react excessively to cosmic factors in the
production of congestion, edema, and exudation in the serous
membranes of the joints and the synovial coverings, and to trans-
late into pain all functional disturbances of the various constitu-
ent parts of the locomotor apparatus.
To recapitulate, the motor apparatus contributes in two re-
spects to the general functioning of the system.
Through its serous membranes, connective and fibrous tissues,
and marrow tissue, it constitutes a part of the connective tissue,
lymphatic, and leucocytic defensive system; it serves as a locus for
the unloading and destruction of bacterial agents and the soluble,
organic or mineral poisons of bacteria.
By the functioning of its masses of muscle tissue, it takes part
in the processes of nutrition; it uses up glycogen and forms lactic
acid and many other products of disintegration.
From the first of these standpoints, it is destined to be the seat
of infectious rheumatic disorders, or pseudorheumatism.
From the second standpoint, it may contribute to the production
of the bradytrophic diathesis, and when it itself takes the conse-
quences of the latter, becomes the seat of what is still termed true
rheumatism, with the associated extraordinary sensitiveness to cos-
mic influences.
Always at the bottom of the condition, however, is faulty
hygiene of the motor apparatus.
This pathogenetic conception is perhaps not actually a new
theory ; it is, at least, a more comprehensive interpretation of
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JOINT PAINS. ARTHRALGIA, RHEUMATISM. 1135
known facts and current views, capable of serving as a link be-
tween the older theories which are only apparently in disaccord —
it is thus a common meeting-ground for purposes of conciliation.
It offers the particular advantage of serving as a basis for
therapeutic, and especially prophylactic, indications.
In the prophylaxis of the arthritic dystrophy and of the nu-
tritive diseases — apart from the regulations concerning dietetic
hygiene, so much emphasized, and justifiably so, in modem con-
tributions, and apart from the hygiene of the nervous system,
which has been rather more neglected — highly important indica-
tions appear to the author to be as follows :
1. One should regulate the hygiene of the motor apparatus with
the greatest care, beginning in early childhood, in all children, but
more especially those the offspring of rheumatic individuals. There
should be sufficient, but never excessive — ^particularly regular — daily
exercise of all the motor structures.
2. One should place these structures in a state of defence against
cosmic agencies, particularly exposure to cold, by a systematic, pro-
gressive training toward tolerance of cold, by stimulation of the
skin functions. Instead of defending one's self passively against
cosmic influences, it is better to activate the play of the vasomotor
reflexes and skin excretions by dry rubbing or rubbing with alcohol,
cold affusions, and hydrotherapy of the "hardening" type.
Again, when the rheumatic tendency, i.e., the state of lowered
resistance of the motor apparatus to cosmic agencies and endogen-
ous onslaughts, has actually shown itself, one should look for and
overcome, insofar as is possible, any sources of infection and in-
toxication which the body may be harboring. These are detected by
a careful clinical study of the functional activities of the digestive
tract and the annexed glandular organs, the nasopharyngeal cavities,
the genital organs, and the endocrin glands, and by analysis of the
blood and urine. Though there are rheumatic subjects with excessive
uric, lactic, or oxalic acidity, there appear also to be some with
lowered acidity.
Sources of intoxication should be removed by the use of the
best procedures now known ; the emunctories should be assisted, and
insofar as is practicable, the faulty chemical state of the body
fluids should be corrected.
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1136 SYMPTOMS.
All this can be done without neglecting the use of remedies
that may allay the rheumatic symptoms or influence the patho-
logic results of the disorder — ^measures. selected from the phar-
maceutic realm and especially from physical therapy.
It is well to emphasize again the marked importance of look-
ing for some chronic or subacute focus of infection in the pres-
ence of cryptogenic joint affections. The nasopharynx and teeth
(caries or infectious processes) should, in particular, be investi-
gated. In the course of a study of 1000 cases of acute joint
disturbance more or less closely suggesting acute rheumatism,
Lambert {Jour, Amer, Med, Assoc, Apr. 10, 1920) found 253 in-
stances of inflammation of the nasopharynx and 683 of dental
infection. Such infections are of frequent occurrence in chronic
joint disorders. Indeed, the author has personally seen some
cases of subacute or chronic joint involvement clear up after ap-
propriate treatment of the teeth and nasopharynx had been given.
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LOSS OF WEIGHT.
The body weight is a factor of considerable clinical import-
ance. The scales are to be thought of as an essential piece of
medical equipment, as necessary as the clinical thermometer.
Along with the blood-pressure instrument, they constitute the
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Fig. 806.— Case 2500. F., 1860, 154 cm. Loss of weight.
thermometer of chronic cases, which will detect many instances
of as yet latent functional failure, and permit of accurately trac-
ing the course of many morbid states.
Experience has shown that for each individual there is a nor-
mal weight characteristic of health, which, in the event of perfect
functional equilibrium, ranges only between rather restricted
limits. The author's normal weight, as recorded for nearly thirty
years, has always ranged between 74 and 75 kilograms. Below
73, there appear unquestionable evidences of physical and mental
weakness (such a test was made ten times in the course of re-
72 (1137)
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1138 SYMPTOMS.
peated reduction cures) ; above 76, manifestations of plethora
develop.
Theoretic expressions of this physiologic body weight have
been vouchsafed, the simplest of which consists in the assump-
tion that the normal weight is equal in kilograms to the number
Fig. 807. — Case 252, 49 years, 160 cm. Gradual retrogression In a
cardiorenal case with good compensation.
of centimeters of height above one meter. Thus, for a person
measuring 170 centimeters it would be 70 kilograms, and for one
measuring 154 centimeters, 54 kilograms, etc.^
Observation shows that this rule is correct only for medio-
1 One hundred centimeters = 39.37 inches ; one kilogram = 2.2046 pounds
Avoirdupois.
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LOSS OF WEIGHT.
1139
linear individuals, of intermediate morphologic type, i.e., persons
the ratio of whose height to the biaxillary diameter is in the
neighborhood of 5.8 (5.6 to 6), as in the subject referred to below :
(Case 3049). Mediolinear, IJ^ (5.85), whose normal weight
is 68 kilograms.
In a brevilinear or stocky individual, with a broad biaxillary
diameter and in whom the ratio referred to is below 5.6, the
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Fig. 808. — Case 467. Cardio-arterio-renal sclerosis.
normal weight generally exceeds by a few kilograms the figure
obtained by the preceding calculation, as in the following subject:
(Case 399). Brevilinear, ^J^^- (5.44), whose normal weight
31 cm.
is 74 kilograms.
In a longilinear individual, on the other hand, the preceding
ratio being above 6, observation of subjects in a state of perfect
nutritive equilibrium yields lower figures, as in the following
case:
(Case 3207). Longilinear, Ms^ (6.20), whose normal weight
is 73 kilograms.
These three concrete, not theoretic, examples point clearly to the
necessity of taking into account at least the vertical and transverse
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1140 SYMPTOMS,
measurements in calculating theoretically the normal weight of an
individual.
The theoretic normal weight of a subject who is:
Mediolinear, is expressed approximately in kilograms by the
number of centimeters by which his height exceeds one meter,
Mediolinear: Height, 170 centimeters = weight, 70 kilograms.
Brevilinear : May exceed the above figure, the correction some-
times reaching one-tenth of the whole.
Brevilinear: Height, 170 centimeters = weight, 70 to 77
{70 + f^) kilograms.
Longilinear: Should be lower than the figure in mediolinear
subjects, the correction sometimes reaching one-tenth of the whole.
Longilinear: Height, 170 centimeters = weight, 70 to 63
(70 — p kilograms.
Even with due corrections, however, such theoretic, approxi-
mate results hold good only in subjects who are nearly normal;
continued concrete observation without preconceived notions
leads to the conclusion that in individuals with inherited con-
stitutional defects the foregoing rules do not hold good. There
are some constitutionally lean persons whose normal weight in
a state of physiologic equilibrium may be much below the theo-
retic figures previously mentioned ; again, there are constitution-
ally stout (obese) persons whose normal weight may be decidedly
above these figures. One of the author's patients (Case 2510),
an adult (bom in 1885), an unusually longilinear subject with
inherited dystrophy (g^™-. Index : 7.05 !) was observed to vary
from 52.8 to 61 kilograms. He could never be brought to weigh
more than 61 kilograms. This is, of course, a subject suffering
from constitutional hyposphyxia, asthenia, varicose vessels, etc.,
with a diabetic family history.
In this connection one might discuss the ethnic, familial, and
pathologic factors resulting in the development of special types
of constitution ; such a discussion, however, would lead us too
far afield.
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LOSS OF WEIGHT. 1141
Loss of weight may thus constitute a favorable process, and
one which the therapeutist will seek to obtain in many instances
where the patient's weight is above normal and this condition
is accompanied by pronounced disturbances such as plethora and
evidences of cardiovascular inadequacy. (See Plethora.)
At this point mention may be made of the remarkable rela-
tionship generally existing between the body weight and the
blood-pressure. In a high pressure case (plethoric or cardiorenal)
undergoing improvement, the weight and blood-pressure go hand
in hand (Figs. 806 and 807). In a low pressure case (anemia,
asthenia, and certain forms of hyposphyxia), the weight and
blood-pressure rise simultaneously. This is a point both of prog-
nostic significance and of actual practical import.
In the course of certain cases of arteriosclerosis the corres-
pondence of the weight and pressure is most striking, and where
this correspondence is observed to cease, the weight falling while
the blood-pressure is rising, certain aggravation of the sclerotic
process is indicated and the prognosis rendered less favorable.
This condition was noted in the case represented in Fig. 808,
which was under observation for a prolonged period.
In short, loss of weight generally goes hand in hand with dinti-
nution of blood-pressure, and gain in weight with elevation of blood-
pressure {at least in well compensated subjects). Lack of accord in
the progression of these two factors is of marked prognostic
significance.
Loss of weight is a very common clinical event, the cause of
which should be inquired into with great care. Its import is
sometimes obvious, as, for example, in the case of an individual
whose work has increased while the amount of food taken has dimin-
ished. The same is likewise frequently true where the loss of
weight is accompanied by manifest signs of some disease, such
as tuberculosis, typhoid fever, acute infections, gastric disorders,
enteritis, etc. But much oftener still, a careful inquiry to ascer-
tain the cause is required.
The author has made note of the various clinical cases which
came to him complaining chiefly of loss of weight which had
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1142 SYMPTOMS.
excited their apprehension. These cases may be classified in the
following groups, given in the order of frequency :
1 . Gastrointestinal disorders, and more particularly the frequent
and common forms of atonic (hyposthenic) gastrointestinal dyspep-
sia and acute or chronic enteritis. The main diagnostic features
connected with this group of cases will be found in the section on
Dyspepsia,
2. Infections, especially those of tuberculous and influenzal
nature, and secondarily all acute or chronic infections (choleroid
states and typhoid fever at one extreme and syphilis at the
other). The sequence of events in these cases is too obvious to
require further comment than the following, to wit: Where
the occasion presents, one should examine systematically for
the characteristic evidences of the infections (auscultatory signs,
sputum examination, leucocyte count, temperature curve, etc.),
and carefully avoid making the least premattwe statement involv-
ing the serious risk of a mistaken diagnosis.
3. Depressive psychoneuroses, together with exophthalmic
goiter and Addison's disease. During the course of the year 1918,
a large number of persons sought the author's advice on account of
loss of weight, in some instances very marked, e,g., 8 to 12 kilo-
grams (20 to 30 pounds) or more. In a few cases food restrictions,
particularly that referring to bread, seemed to be the main cause.
In the greatest number of instances, the loss of weight was accom-
panied by numerous evidences of general depression (insomnia,
weakness, exaggerated emotivity, pessimism, despairing thoughts,
"cafard," etc.). Examination of the body itself yielded practically
negative results, revealing, however, a reduction of blood-pressure
which was often very pronounced. The anxiety and worries under-
gone in that trying year were unquestionably the exciting cause of
this morbid condition, which the author is disposed to term depres-
sive psychoneurosis with impaired nutrition and low blood-pressure.
All these patients recovered under the threefold influence of tonic
medication, optimistic psychotherapy, and the final triumphant vic-
tory of the Allied cause.
Exophthalmic goiter is sometimes the source of a most striking
loss of weight, amounting practically to cachexia. The same is true
of Addison's disease.
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LOSS OF WEIGHT, 1143
4. Comparable with the foregoing types of cases are certain in-
, stances of loss of weight accompanied by temporary glycosuria in
overworked individuals, especially intellectual workers. The
author has seen a number of these cases among his colleagues in the
course of the last few years.
Such a loss of weight may, however, as is well known, be an
initial indication of diabetes, particularly the grave cases of pan-
creatic diabetes, but also sometimes in the so-called neuroarthritic,
hepatic, and nervous forms of diabetes.
Practical conclusion : Never omit uranalysis in a case of loss
of weight.
5. Tumors, in whatever situation, though more especially
tumors of the digestive tract, constitute the most dangerous
factor of loss of weight. Tumor should always be thought of in
an elderly person who begins to lose weight and whose general
condition exhibits continuous and inexorable deterioration. At
the least suspicion of trouble, a systematic examination must be
carried out, including inquiry for occult bleeding from the ali-
mentary canal through examination of the stools, careful exam-
ination of this canal by fluoroscopy after ingestion of a bismuth
meal, etc., and will very often settle the question. Pyloric steno-
sis, cancer of the large bowel and rectum, and cancer of the liver
are by far the commonest medical tumors ; the possibility of their
presence should always be borne in mind, and in particular, one
should never forget to palpate the rectum in all suspected
cases.
6. Arteriosclerosis is also a common cause of impaired nutri-
tion. The age of the patient, the high blood-pressure generally
existing, and the coexisting signs, generally multiple (tortuous
temporal vessels, signs elicited upon auscultation over the aorta,
nycturia, etc.), without taking into account the state of hydremia
frequently present and manifesting itself in lowered viscosity of
the blood, will insure the correct diagnosis.
7. Again, mention may be made, as regards more exceptional
C3^es, of certain intoxications, vis., alcohol in large amounts,
through the resulting gastrointestinal dyspepsia and hepatic cir-
rhosis, and morphine in chronic poisoning, both of which condi-
tions generally cause loss of weight.
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1144 SYMPTOMS.
8. Lastly, mention may be made, as a species of clinical curi-
osity, of a condition which, while rather common in an attenu-
ated form in women, is very uncommon in its well-marked form,
vis,, progressive lipodystrophy (Barraquer-Simons's disease),
characterized by a gradual and almost complete disappearance
of adipose tissue and subcutaneous cellular tissue from the upper
portions of the body, combined with adiposity of the parts from
the umbilicus down. In its attenuated form it sometimes leads
to a singular conformation which might be described thus :
Venus de Milo above the umbilicus and the Hottentot Venus
below it. In its pronounced form the face, chest, and abdomen
present a skeletal aspect, while the more dependent parts become
so overburdened with fat as to suggest elephantiasis. Whether
this condition is of endocrin or nervous origin has not as yet been
ascertained.
In brief, in cases of marked and persistent loss of weight, a
comprehensive examination is, as always, indicated ; the essential
procedures of examination, however, the various combinations
of which with the factor, loss of weight, will permit of definitely
grouping" 95 per cent, of the cases are the following :
(a) Blood-pressure determinations.
(b) The temperature curve.
(c) Uranaly sis (amount, specific gravity, sugar, and albumin).
(d) Careful examination of the digestive tract.
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LOW BLCX)D-PRESSURE.
Inclusion in this work of a short section on low blood-pres-
sure as a counterpart to that on' high blood-pressure already pre-
sented is warranted: 1. Because this condition is very fre-
quently met with. 2. Because it is often one of marked clinical
significance. 3. Because among chronic cases, at least, deter-
mination of the blood-pressure now appears to the author just
as essential as that of the temperature or pulse in acute cases.
In this section consideration of the subject of low blood-pressure
will be limited to a short discussion of the symptomatic import of
low systolic, diastolic, and pulse pressures, the reader being referred
for the definition of the terms systolic, diastolic, and pulse pressure
to the section on High blood-pressure.
Low systolic pressure may be put down as commencing at
120 to 130 millimeters of mercury, as determined with the Pachon
blood-pressure instrument. [The readings with this instrument
are somewhat higher than those afforded by the ordinary mer-
cury sphygmomanometer. — Translator.] The lowest readings
the author has met with in adults were 70 and 80 millimeters.
A continuous low systolic pressure is found almost exclusively
in anemias, in the tuberculous, in neurasthenics, in adrenal insuffi-
ciency (Addison's disease, post-infectious adrenalitis, etc.), and in
a rather important group of cases not specifically grouped until
lately, vis,, cases of low blood-pressure through debility of the car-
dio-arterial functions, congenital or familial, perpetuated or made
worse by a mode of life excluding all physical exercise — ^a condition
the author has described under the term hyposphyxia.
Low blood-pressure is one of the almost constant attributes of
the disorders causing cachexia, viz., tuberculosis, cancer, and de-
fective nutrition ; a progressive and inveterate low blood-pressure is
generally a forerunner of death.
(1145)
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1146 SYMPTOMS,
A temporary reduction of systolic pressure may be observed in
the course of infectious diseases and during convalescence from
them, as well as after hemorrhage or operative shock. The prog-
nostic importance of low pressure in the last-named class of cases is
well known ; in thoraco-abdominal wounds, progressive reduction of
blood-pressure points to a continuing hemorrhage.
Traumatic shock is a general somatic state met with after
wounds and characterized by a pronounced and persistent deficiency
of blood-pressure, with frequent pulse, pallor, sweating, shallow and
frequent respiration, and extreme weakness with a tendency to
syncope.
Low diastolic pressure, 80 millimeters or below (oscillometric
or auscultatory methods), is met with only in conjunction with the
low systolic pressure of anemic and cachectic cases and in aortic re-
gurgitation. The lowest reading obtained by the author in an adult
was 50 millimeters, in a case of pernicious anemia. Low diastolic
pressure is of diagnostic import only in aortic regurgitation, but in
this condition its significance is very clear-cut and may be expressed
as a definite rule : The combination of low diastolic pressure (80 mm,
or below) with high systolic pressure (170 mm, or above) is
pathognomonic of aortic regurgitation.
As for the significance of the pulse or differential pressure,
following are certain justifiable statements on this subject: The
pulse pressure is in a measure a sphygmomanometric reflection or
expression of cardiac power. Persons with constitutional debility
and congenitally small hearts exhibit a low pulse pressure (20 to
40 mm.), while well compensated arteriosclerotic cases with hyper-
trophied "ox hearts" show a very high pulse pressure (100 to 250
mm.). In cases of cardiac insufficiency with low pulse pressure the
pulse pressure rises in proportion as the heart regains its functional
power and diuresis takes place, etc.
In some cases of ''shock," the pulse pressure may be completely
obliterated. In these cases a fatal termination has, so far, always
occurred. The prognosis of "shock" is the less favorable in propor-
tion as the pulse pressure sinks lower and the oscillometric index
falls more rapidly.
Three points relating to low blood-pressure seem to require
further discussion from the practical standpoint, 7A2,:
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LOW BLOOD-PRESSURE, 1147
1. Low blood-pressure in tuberculosis.
2. Low blood-pressure in adrenal insufficiency.
3. Low blood-pressure in hyposphyxia.
1. Low pressure is so constantly present in tuberculous cases
that: (1) It may be considered an evidence of tuberculosis to
the same degree as cough, loss of weight, fever, anorexia, lassi-
tude, etc.; taken alone, it is of very little symptomatic value, but
in conjunction with the preceding manifestations it assumes
marked significance. (2) The finding of a normal or increased
pressure warrants the conclusion that either tuberculosis is ab-
sent or some complication, generally renal, is present; all the
tuberculous subjects in whom the author found high blood-pres-
sure were also suffering from nephritis.
Nevertheless — and this statement applies whenever one is deal-
ing with low pressure — one must always take into account the hyper-
tensive reaction of nervous origin which inevitably occurs at the
first blood-pressure examination. Whence the following ad-
monitions :
(1) At the first examination, one should make two successive
pressure determinations at a few minutes' interval. [The dis-
crepancy, often pronounced, between the first and second read-
ings (the latter always being lower) affords a good index of the
emotivity of the patient concerned.] (2) Further blood-pressure
determinations should be made at later examinations. The emo-
tional and accidental, temporary, hypertensive factor is thus
eliminated, and the morbid, essential, and permanent factor alone
kept in view.
2. Low blood-pressure is one of the three permanent evidences of
adrenal insufficiency (h3rpoadrenia). One may state that the
symptom-group low pressure, asthenia, and Sergent's white line is
pathognomonic of adrenal insufficiency, the extremely frequent
clinical occurrence of which has been discovered through recent
investigations. In its highest expression this condition is mani-
fested by the well-known classic syndrome of Addison's disease,
long since ascribed to degenerative changes in the adrenal glands
and accompanied by characteristic pigment changes in the skin and
mucous membranes. The conclusion from the recent investiga-
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1148 SYMPTOMS.
tions referred to seems to be that most instances of infectious,
post-infectious, or cachectic low blood-pressur^ are wholly or
partly the result of adrenal insufficiency, whether there exists an
actual adrenalitis or merely a temporary insufficiency (Loeper).
This interpretation, however, is still a moot point.
3. Hyposphyxia is a circulatory symptom-group a short dis-
cussion of which seems warranted in view of the fact that it has
been known and described only in relatively recent years.
Blood-pressure and blood viscosity, — The author has shown in
the course of the last few years that in subjects whose cardiovas-
cular system is well balanced and at no point impaired there exists
a rather close relationship between the differential or pulse pres-
sure, an expression of the power of the heart beat, and the viscosity
of the blood, an expression of the resistance opposed by the blood
to the circulation. With a low viscosity, as in anemics, there cor-
responds a low pressure; with a moderate viscosity, as in normal
subjects, a moderate pressure, and with a high viscosity, as in ple-
thoric, full-blooded persons, a high pressure. In short, in the per-
son who is normal from the cardiovascular, or better the circula-
tory standpoint, the pressure goes hand in hand with the viscosity.
The converse, however, is not always true, for reasons set forth
at length in an earlier work of the author's^ devoted to a study of
this question.
Furthermore, this relationship, which the author was enabled
to demonstrate only after extensive observations, will seem ob-
vious to any one who will call to mind the fact that the energy
required to cause a fluid to circulate in a given canal system is
proportionate to the resistance offered by the fluid, vis,, to its
viscosity.
Such is the natural relationship of the pulse pressure and
blood viscosity.
Clinical observation leads to the detection of two radically
opposed abnormal sphygmoviscosimetric types of cases in which
there is disharmony between^ the pulse pressure and the blood
viscosity.
1 Alfred Martinet : "Pressions arterielles et viscosite sanguine," Paris,
Masson, 1912.
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LOW BLOOD-PRESSURE. II49
The first type exhibits a pulse pressure which is high in com-
parison to the normal or low blood viscosity; these are hyper-
systolic, hypersphyxic cases, the permanent hypersphyxia being
represented by arteriorenal sclerosis.
The second type, which is the subject of the following brief
study, shows, on the other hand, a viscosity which is high as
compared with a normal or low pulse pressure : These are hy-
posphyxic cases.
The h5rposph)rxic syndrome. — Hyposphyxia consists of the
combination of an absolutely or relatively low pulse pressure with
a high blood viscosity. These two factors, simultaneously present,
constitute the highest expression of the condition of sluggish cir-
culation so frequently noted in young girls, sedentary indiznduals,
pretuberculous subjects, etc., and characterized especially by weak
pulse, a liznd skin surface, habitual coldness and cyanosis of the
extremities, a tendency to venous plethora, varicose veins, enlarge-
ment of the liver, unusual sensitiveness to cold, etc.
Hyposphyxia is almost constantly associated with pluriglandu-
lar insufficiency, of which it is a dominant feature and upon which
it depends. In hyposphyxics there are noted, indeed, gastrointes-
tinal dyspepsia due 'to inadequacy of the several digestive glands,
various disturbances long since attributed to insufficiency of the
endocrin glands (thyroid, ovaries, adrenals, pituitary, etc.), vis.,
headache, migraine, dysmenorrhea, asthenia, asthma, disturbed
nutrition of the hair, etc.
The hyposphyxic syndrome is specifically mentioned in many
descriptions of the syndromes due to insufficiency of glandular
functions.
Stress is to be laid on the fact that hyposphyxia is only a symp-
tom-group and not a definite disease entity, and that one may dis-
tinguish organic and functional forms of hyposphyxia, as well as
constitutional inherited, and accidental {e.g., post-infectious) forms.
Precisely the same is true of the syndrome of pluriglandular in-
sufficiency.
This ascendancy of the circulatory factor over the neuro-mus-
culo-trophic factor had already been clearly expressed by Bris-
saud in relation to feeble children (Bauer) and to mitral dwarf-
ism. "As soon as a certain degree of narrowness of the arteries
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1150 SYMPTOMS,
exists," he wrote, "the poorly nourished tissues and organs may
actually undergo development, but remain small and weak. The
stunted individual that results does attain complete development,
but without proper growth." (Henry Meige.)
From the standpoint of pathogenesis, this syndrome consti-
tutes, in last analysis, the outward manifestation of a circulatory
disturbance characterized by high venous pressure with stasis de-
pendent either upon some obstruction in the left heart (mitral dis-
orders) or in the right heart (tricuspid disorders), or, as is more
usually the case, upon a congenital underdevelopment of the heart
(constitutional cardiac debility), or an obstruction in the lung
(chronic tuberculous lung disorders), liver (cirrhosis or passive
congestion), or veins (varicose veins, phlebitis, and cutaneous
cyanosis).
Absolute or relative weakness of the cardiac contraction, peri-
pheral circulatory weakness through vascular myasthenia, and
respiratory weakness are met with in all these conditions.
The above state of circulatory dynamism, with a low pulse
pressure and high viscosity, points directly either to a congenital
weakness or underdevelopment of the cardioarterial system (con-
stitutional cardiac debility) or to an obstacle to the circulation
behind the left heart (mitral valve, lungs, right heart, or liver).
Venous plethora is the inevitable result and constitutes a mode
of adaptation or defensive reaction to an unusual condition of
the circulation.
The presence of this syndrome in a chronic form, constituting
an habitual circulatory state, chronic hyposphyxia, has been clin-
ically obsen^ed by the writer:
1. In subjects with certain lesions, chiefly obvious cardio-
pulmonary conditions and corresponding with clearly defined
nosologic entities, to which the term secondary organic hypo-
sphyxia is applicable.
. 2. In subjects apparently free of any organic heart or lung
disorder so far described, the appellation protopathic functional
hyposphyxia (neurocirculatory asthenia) may be used.
3. Occurrence of the syndrome as an acute or subacute, acci-
dental and temporary condition, acute ten:4)orary hyposphyxia,
has also been noted.
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LOW BLOOD-PRESSURE. HSl
Organic hyposphyxia has been observed by the writer :
1. In acute or chronic tuberculous cases, with the exception of
those with added renal complications.
2. In mitral disease, with or without compensation. Congenital
or acquired mitral stenosis affords the most striking examples of
this group. Doubtless the same applies to tricuspid stenosis.
3. In the majority of cases of chronic lung disturbance with
emphysema and bronchitis,
4. In kyphotic patients,
5. In some cases of uremia, or more correctly, azotemia.
Functional hyposphyxia has been very frequently witnessed.
This type is almost the rule in young girls and a large number
of women leading sedentary lives by choice or occupation (dress-
makers, pianists, clerks, etc.), with low breathing capacities and
weak musculatures. The author has also come across it in a
number of youths, scholars or students not interested in sports.
Often it is an inherited condition, dependent upon an actual,
congenital and familial cardiovascular hypoplasia. In one such
family, the grandfather, suffering from varicose veins, had al-
ways exhibited cyanosis and had cold, moist extremities; the
mother, also varicose, was likewise hyposystolic and showed a
high blood viscosity; the uncle had varicose veins and cyanosis
of the face, lips, and extremities; an aunt, cyanotic and with
varicose ulcers, was looked upon as having heart disease; another
aunt was in a similar state; as for the patient himself, he was a
cyanotic, sedentary individual with poor musculature, cold, moist
extremities, and a congested liver; his pulse pressure was 30
millimeters and his viscosity 5.5.
This type of disturbed nutrition, accompanied by many other
states of maldevelopment (dental, palatal, abdominal, etc.), fre-
quently forms part of the symptom-group of congenital syphilis.
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1152
SYMPTOMS.
LOW BLOOD-PRESSURE.
Anemias.
Hemorrhages.
Neurasthenia.
Cachectic states.
Tuberculosis.
Adrenal insuffi-
ciency.
Hjrposphyxia.
Organic
Functional
Low cell count; pallor of mucous membranes;
functional cardioarterial murmurs.
Traumatic or post-operative.
(Progressive reduction of blood-pressure after
trauma or an operation is always an indication
of persistent hemorrhage).
Neuropathic syndrome: Headache, insomnia,
constipation, asthenia, anxiety.
Cancer; senility; phthisic conditions.
Cough, fever, loss of weight, auscultatory signs.
' either lead to exclusion of
the diagnosis of tuber-
culosis,
or lead to the detection of
a renal complication.
High blood-pres-
sure should
Padiognomonic ssrmptom-group: Low blood-
pressure, asthenia, and Sergent's white line. .
' from Addison's disease or acute ad-
renalitis with rapid death,
All grades { to the temporary and mild forms
of post-infectious adrenal insuffi-
ciency.
Slow circulation (low pressure, high viscosity),
very often associated with pluriglandular in-
sufficiency (hypocrinia).
(Pulse small and frequent, lividity, sensitiveness
to cold, coldness and cyanosis of the extremi-
ties, venous plethora, etc.).
1. Tuberculous cases.
2. Mitral cases.
3. Chronic pneumopaths.
4. Kyphotics.
5. Azotemics.
6. Congenital cardiovascular dystrophy (includ-
ing congenital syphilis).
Sedentary life, cardiomuscular debility, etc.
Neurocirculatory asthenia.
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LOWER EXTREMITIES, PAIN IN.
The causal diagnosis of pain in the lower limbs is often ob-
vious, as in rheumatic arthritis, post-infectious phlebitis, acute
gouty attacks, etc. ; yet sometimes it presents insuperable diffi-
culties. Few portions of the body are more accessible and read-
ily examined; yet few are more complex, and none is the seat of
pains that may be due to such a large variety of causes.
Any of the tissues of the extremity, bones, joints, muscles,
veins, arteries, or nerves, may be the starting-point of painful
affections; the spinal cord, vertebral column, various trophoneu-
rotic disturbances, and various abdominopelvic disorders may
^ likewise cause more or less obstinate pain in the lower extremi-
ties. Proper diagnosis sometimes demands an extremely pains-
taking clinical investigation and penetrating analysis.
Any of the tissues, as we have seen, may be the starting-point
of painful affections. A succinct reference to each kind of tissue
may prove serviceable:
I. The Bones. — Traumatic conditions, such as fractures, con-
tusions, and sprains, generally self-evident, may be dismissed from
the start, leaving for our consideration osteoperiostitis; osteomye-
litis; osteosarcoma; an extremely common skeletal deformity, flat
foot, which should always be kept in mind precisely because of its
common occurrence, and the disorders of the bony spinal column,
foremost among which is Potfs disease.
(a) Osteoperiostitis. — This condition is characterized by the
presence of a more or less localized painful area along the shaft
of one of the bones of the lower limb, usually the femur or tibia,
together with a variable degree of swelling. Osteoperiostitis
may be :
Syphilitic, as suggested by the history, recurrence of the pain at
night (osteocopic pains), a positive Wassermann, and the efficacy
of mixed treatment.
78 (1153)
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1154. SYMPTOMS.
Tuberculous, though this form of osteoperiostitis is actually
much less common than tuberculous osteoarthritis.
Post-infectious, e.g,, post-typhoid; staphylococcic in the pres-
ence of recurring furunculosis or after sore throat.
(6) Osteomyelitis. — This is characterized by more severe and
more diffuse pains and larger oscillations of temperature; it is
generally post-infectious, e.g., typhoid (post-typhoid) or staphy-
lococcic (following sore throat or furunculosis).
(r) Osteosarcoma. — This is fortunately much less common, in
fact exceptional, and is characterized by a rapidly progressive and
generally painful enlargement involving the shaft of the femur. ,
A mere mention of the condition would suffice were it not neces-
sary to point out that it may sometimes be confounded with a
syphilitic gumma of the bone. Indeed, in a case of sciatica resist-
ant to all forms of treatment, in which the progressive develop-
ment of a swelling of the femur had led to a diagnosis of osteosar-
coma and a decision to amputate the limb, and the denials of the
intelligent patient, answering questions in good faith, the absence
of evidence of venereal diseasfe, and the existence of nearly adoles-
cent children free of any appreciable stigmata had seemed to war-
rant exclusion of the diagnosis of syphilis, the swelling was ob-
served to melt away like butter before the sun's direct rays as a
result of mercurial inunctions.
(d) Painful valgus flat foot should be thought of in any ado-
lescent complaining of pains in the legs and muscular contrac-
tures when he is fatigued, and the diagnosis may be made by the
print method, which consists in having the patient place his feet
over sheets of paper covered with lampblack. The footprints
thus obtained show, in such cases, that the inner border of the
foot is completely sagged down and that the foot is resting on
the ground over the entire extent of the sole and not on its three
normal pillars — posterior (os calcis), anterior (toes), and ex-
ternal (outer border of the foot).
(e) In this essential examination of the bony framework the
spinal column, particularly in its dorsolumbar region, should not
be neglected. This step in the examination is made necessary
chiefly by the possibility of Pott's disease:
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LOWER EXTREMITIES, PAIN IN. 1155
Whether the case be that of a child with unsteadiness of gait,
weakness of the legs, more or less definite pains in the lower
extremities, and impairment of general health ;
Whether it be that of a subject whose parents have them-
selves detected a lateral deviation of the spinal column giving
rise to pain ;
Or whether, especially in an adult complaining of pain, an
abscess pointing in the inguinal region brings definitely to light
a Pott's disease which careful examination of the spinal column
by inspection, percussion, motion, and fluoroscopy might have
disclosed many months before.
(/) Lastly, one should bear in mind the rare possibility of an
incipient osteomalacia, which would later be confirmed by charac-
teristic deformities, with exaggeration of the normal curves of the
bones, disordered locomotion, and pain on walking, becoming
fatigued, or local pressure.
II. The Joints. — It will not be necessary here to review all the
possible causes of joint pains, a special section having already been
included on thisi subject (see Joint pains). Systematic examina-
tion by inspection, palpation, mobilization, and if necessary fluoros-
copy, will in the first place locate the pain in one of the joints of
the extremity. The special features of the joint disturbance, the
history, onset, course, and simultaneous presence of other abnormal
conditions will, as a rule, lead quickly to classification of the dis-
order in one of the following groups : Acute articular rheumatism,
gonorrheal rheumatism, post-infectious rheumatism (scarlatinal,
typhoid, etc.), or rheumatism due to some metabolic disorder
(gout, arthritis deformans, etc.). Too much stress cannot be laid,
here as elsewhere, upon the advisability of examining the seat of
pain carefully and by direct inspection, of palpating and passively
moving it, in short, of locating with care the pain and the seat of
pathologic change, of precisely determining its nature, if possible,
and of not resting content with the vague term "rheumatism,"
which is just as devoid of true diagnostic meaning as "headache"
or "pain in the side."
Some joint involvements exhibit a rather pronounced selective
tendency.
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1156 SYMPTOMS,
Gout very frequently occurs in the joints of the great toe (meta-
tarsophalangeal joints).
Acute rheumatism of the lower extremities is located in the
knees in four cases out of five. The same is true of gonorrheal
arthritis.
Fig. 809.— Bilateral tabetic knee-Joints. (Glorieux and Van
Gehuchten, Revue neurologique, 1895).
Tuberculosis involves almost indifferently any of the joints;
yet its predilection for the knee (white swelling) and the hip
(coxalgia) is well known.
Malum cox(V senilis, the pathogenesis of which is as yet ob-
scure, involves, as the term implies, the hip in elderly subjects.
Nor should one forget the characteristic tabetic or Charcot
joints, with the attendant marked deformity, extreme laxity of the
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LOWER EXTREMITIES, PAIN IN. II57
involved joints and painlessness. If the condition is only kept in
mind, the diagnosis can be made by observation of the other indi-
cations of tabes — specific history, reflex disturbances (Argyll-
Robertson pupil), loss of the patellar reflex, etc.; astasia, abasia,
ataxia, lightning pains, sphincter disturbances, etc.
III. The Muscles. — Disorders of the muscles, tendons, and
serous membranes, occurring, respectively, in the form of myo-
sitis, tenositis, and bursitis, constitute possible localizations of
rather indefinite painful processes the origin of which may be
that described by Le Gendre, vie, "a defective functioning of the
locomotor apparatus either through lack of activity (sedentary
mode of life) or through excessive activity (overstrain)," which
renders it sensitive particularly to cosmic [meteorologic] influ-
ences that are normally not felt.
Mention may here be made of the myalgias, often accom-
panied by arthralgias without objective manifestations, which,
attended with an apparent typhoid state with sudden onset and
albuminuria, frequently features the first or preicteric stage of
primary infectious jaundice (hemorrhagic spirochetosis). Such
pains may dominate the clinical picture sufficiently to mislead an
inexperienced practitioner. Thus, the author saw a fatal case of
primary infectious jaundice which was admitted tp a hospital on
the third day of the illness with a diagnosis of ** rheumatism."
The patient, indeed, complained almost exclusively of pain and
cramps in the thighs and a feeling in the knees as of constriction
in a vice, without any redness or swelling but with a temperature
of 40° C, a pulse rate of 136, albuminuria, a small liver, and
incipient jaundice. This case succumbed in ten days with the
complete clinical picture of grave primary infectious jaundice —
small liver, progressive jaundice, albuminuria, hemorrhages, and
increasing hypothermia. The pains in the muscles subsided as the
jaundice grew more marked. A few spirochetes were found in the
blood and the urine.
To complete the enumeration, mention may be made of the
painful muscular spasms of nervous diseases, of tetanus, etc.
IV. The Veins. — Inflammations of the veins play a far more
important role in pain in the lower extremities than they do in the
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1158 SYMPTOMS.
case of pain of the upper limbs. Here phlebitis is much more
common, being either of chronic nature, as in chronic degenerative
phlebitis (varicose veins) or ck:ute or subacute infectious phlebitis.
^* Superior
mesent.
plexus
gf Inferior
mesent.
plexus
Hy
moid
(xure
sclati
idder
Fig. 810. — Lumbosacral and hypogastric plexuses in the male
(sources of the sciatic nerve) {Hirschfeld).
the latter especially post-infectious, post-operative or puerperal in
origin. The diagnosis of the condition is, as a rule, easy. The
mere finding of dilated veins, which in the chronic forms are par-
ticularly prominent with the patient in the standing posture, the
observation upon palpation of phlebosclerosis and frequently of
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LOWER EXTREMITIES, PAIN IN. 1159
induration around the vein, and the presence of trophic changes of
the skin lead to the proper diagnosis in chronic forms. In acute
and subacute phlebitis, the history (as of infection, a surgical pro-
cedure, or parturition), the fever, edema, special sensitiveness
1st saci
gangli
Hypogaatric
plexus
Great
sciatic
nenre
Visceral
nenres
Uterine
plexus
Fig. 811.— Lumbosacral and hypogastric plexuses in the female
(sources of the sciatic nerve) (Hirschfeld).
along the course of the vein, and sometimes the finding of a hard,
cord-like vein insure recognition of the existing disorder.
V. The Arteries. — Pain attending disease of the arteries in
the lower extremities is not of very frequent occurrence, but
when present is very obstinate. It is the result of arteritis of the
femoral or of the tibial or peroneal vessels. Arteriosclerosis,
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1160 SYMPTOMS.
gout, specific disease, and infections, especially typhoid fever, are
by far the most frequent causes — in fact, the only oties met with
in the author's experience.
As serviceable diagnostic indications of such a condition the
following features may be mentioned :
A distinct difference of blood-pressure in the two limbs ; grad-
ual diminution of the beats below the involved portion of the
artery; intermittent claudication (in the chronic forms) ; lowered
local temperature of the affected limb ; coldness and pallor ; some-
times, where the vascular distribution from a certain trunk is
actually obliterated and no collateral circulation forms, hypo-
thermia, vasomotor disturbances, and cyanosis occur and are fol-
lowed by the appearance of areas of necrosis of varying extent,
which may later result in mutilation of the part.
VI. The Nerves. — The sciatic nerve is the one by far the most
frequently involved in the lower extremities. One should remember
that the course of the sciatic nerve comprises a spinal portion, origi-
nating in the anterior branches of the last two lumbar and first four
sacral nerves; a pelvic portion, in which the sacral plexus, formed
by the convergence and subsequent fusion of the foregoing nerve-
roots, enters into direct or indirect anatomical relationship with
nearly all the pelvic organs; a gluteal portion, beginning at the
great sacro-sciatic notch, from which the single, combined trunk
of the sciatic issues at the gluteal fold, being ensconced in this
region in a musculo-osseous recess bounded within by the
ischium and externally by the greater trochanter; a deep, intra-
muscular femoral portion, in which the nerve is lodged in a ver-
tical muscular trough bounded externally by the long head of the
triceps and internally by the semitendinosus and semimembran-
osus, and finally, a terminal portion, in which it divides, four
fingerbreadths above the plane of the tibiofemoral joint, into its
two terminal branches, the external popliteal nerve, which, after
having passed around the external condyle of the femur and the
inner surface of the head of the fibula, continues through the
thickness of the peroneus longus and along the external and dor-
sal aspects of the foot, and the internal popliteal nerve, which
crosses the popliteal space obliquely, passes above the soleus
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LOWER EXTREMITIES, PAIN IN.
1161
(posterior tibial nerve) and extends to the plantar surface of the
foot, nearly the whole of which is innervated by it.
Brief reference to these anatomic facts was necessary because:
Sup. gluteal nerye
Nerve to pyriformla
Inf. gluteal nerye |
Post, cutaneous ner
Post, cutaneous neri^
of the thigh
Inf. gluteal nerye
Sciatic nerye
Nerve to semitendinosui
Nerve to semimem- J
branosus ]
Nenre to semitendinosui
Nerve to short head of
biceps
^erve to long head of
biceps
, popliteal nerve
Int. popliteal ner
Nerve to int. gastrc
nenoiius
;>opliteal nerve
to plantarls
to ext. gastroc-
us
Ext saphenous e
Fig. 812.— The greater sciatic nerve (Sappey). The small sciatic nerve
consists of the two small trunks designated above as the inferior gluteal
nerve and the posterior cutaneous nerve of the thigh.
1. The sciatic nerve must be investigated in every portion of
its course, from the lumbosacral vertebrae to the os calcis and the
sole of the foot. There are certain points which, on account of
their regional anatomic relationships, lend themselves especially
well to examination and the eliciting of tenderness. Valleix made
a special study of these elective points, whence the designation
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1162
SYMPTOMS.
"Valleix^s points" which has remained attached to them. These
points are shown in the annexed diagram.
Mention should be made of Lasegue's well-known, simple and
rapid maneuver, which consists in flexing the
thigh on the pelvis with the leg extended.
During this procedure the sciatic nerve, after
running a practically straight course with the
limb in complete extension, is forced into a
sharp curve in its gluteal course by the flexion
of the limb, and is thereby stretched like a
violin string when the bridge is raised into
position. The resulting tension at once excites
a characteristic pain along the nerve in the
presence of sciatica.
Lasegue's test is merely the simplest and
most commonly used of the various pro-
cedures of stretching the sciatic, which brings
on pain where there is disorder of the nerve.
It is plain that any form of motion, whether
active or passive, which causes stretching will
excite the same sort of pain or a character-
istic posture of the limb having for its pur-
pose to obviate the stretching of the nerve.
When the patient is standing and is asked to
pick up an object from the floor, keeping the
legs extended on the thighs, he will in-
stinctively and necessarily flex the involved
limb or move it backward in order to avoid
tension on the nerve.
When the patient is recumbent and is re-
quested to sit up, keeping his legs straight, he
will similarly, and for the same reason, flex
the affected limb (Sicard's ^'raised knee
V 11 • ' ^^9^")* thus exhibiting what appears as a
points on the poste- unilateral Kemig sign (G. Roussy).
rior aspect of the 2. The origin of the nerve pain may be at
lower extremity, and j^^^ ^^ ^^^ ^^^^^ ^^ ^j^^ ^^^^
their relationship to _ ^
the bony skeleton. The whole course of the nerve should be
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LOWER EXTREMITIES, PAIN IN. 1163
examined just as carefully to discover the cause as from the
symptomatic standpoint
Along the spinal portion of the sciatic bony changes should
especially be looked for, vis., Pott's disease, exostoses, spondylitis,
gumma, or cancer of the vertebrae ; and likewise meningeal disturb-
ances, such as acute or chronic meningomyelitis or the common con-
dition termed meningeal hyperemia. An undemonstrable, but
seemingly probable and frequent cause, judging from the percent-
age of cases in which the author found it and the therapeutic efficacy
Fig. 814. — ^Left-sided sciatica. Forward bending of the body is possible
only if the knee of the affected side is flexed (G. Roussy).
of hamamelis in large doses, is intraspinal venous hyperemia or the
"intraspinal varicose state," causing pressure upon and strangula-
tion of the nerve-roots upon their emergence from the bone (see
Lumbar pain).
Along the pelvic portion of the sciatic, disorders of the rectum,
prostate, bladder, Fallopian tubes and ovaries, and uterus may
be and frequently are the source of sciatic neuralgia or neuritis
through one of the four following factors: 1. Pressure, as by
primary new growths or secondary glandular enlargements. 2.
Hyperemia, as in inflammatory pelvic congestion or acute con-
gestion of hemorrhoids. 3. Reflex irritation from a remote struc-
ture, as in urethritis or orchitis. 4. Direct involvement in malig-
nancy or inflammation, as in tumor of the rectum or uterus.
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1164 SYMPTOMS.
From the above considerations the importance of a systematic
examination of the pelvic structures in the presence of sciatica
will readily be seen.
Along the femoral portion of the nerve, in the buttock, the con-
ditions oftenest met with as exciting causes of sciatica are trauma-
tism (falls, sudden impacts or blows) and coxofemoral arthritis and
periarthritis. In the femoral region a special search should be made
for factors resulting in compression, chiefly by bone, such as osteo-
periostitis, gumma, and osteosarcoma; in the popliteal space, the
Fig. 815. — Right-sided sciatica. In some instances, when the body
is being bent forward, the patient spontaneously tilts the affected lower
limb backward (G. Roussy),
commonest exciting causes are crypts, aneurysm, and fungous joint
inflammation.
Where, however, all these local causes of neuralgia and neu-
ritis can be excluded, an inquiry should be made for general
causes, some of which are still rather obscure :
Neuralgia a f rigor e (following exposure to cold).
Rheumatic (?) neuralgia.
Diathetic neuralgia ; diabetes should be remembered as a fre-
quent cause of obstinate sciatica.
Post-infectious neuralgia.
Toxic neuralgia; in this connection special attention should be
paid to alcoholism, with the attendant diffuse pains, lack of febrile
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LOWER EXTREMITIES, PAIN IN. 1165
temperature, absence of local inflammation and of signs of tabes
dorsalis, and sometimes the steppage gait in an inveterate alcoholic.
If still nothing can be found, the condition may be labelled
a simple, primary, or idiopathic sciatica, the physician thus
escaping the necessity of committing himself concerning the
actual nature of the disturbance.
It is plain that, apart from symptomatic, palliative treatment
of the neuralgia, which, indeed, is frequently all that is required,
an accurate causal diagnosis can alone supply a reliable basis for
curative treatment.
Fig. 816.— Right-sided sciatica. The patient, when in the sitting position,
is unable to extend the aflFected limb completely (G. Roussy).
One should always carefully examine for muscular atrophy
and electric reactions, which afford a distinction between neu-
ralgic sciatica, ordinarily a mild condition, and neuritic sciatica,
which is always serious and sometimes incurable.
The lumbar plexus, formed by anastomoses of the anterior
divisions of the last four lumbar nerves, and its branches — the
ilio-hypogastric, ilio-inguinal, external cutaneous, genito-crural,
obturator, and especially, the anterior crural — is, apparently, much
less frequently affected than the sdatic. Yet lumboabdofninal neur-
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1166 SYMPTOMS.
algia with its painful points (lumbar, iliac, abdominal and scrotal),
frequently encountered in pyelonephritic disorders ; external cutane-
ous neuralgia with its superior interiliac painful point, and especially
anterior crural neuralgiCy with its painful points dispersed along
the anterointernal aspect of the thigh, leg, and foot (tender points in
Qi
12th doraal
2d lumbar
3d lumbar
4th lumbar
Bxte:
Genlto-crural
Lumbosacral trunk
^ Sacral plexus
Fig. 817. — The lumbar plexus.
the inguinal region, the crural region, over the internal condyle, the
internal malleolus and the inner margin of the foot) are not very
uncommon, particularly that last mentioned.
Lumboabdominal neuralgia, as we have just seen, 15 an almost
constant clinical appurtenance of many pyelonephritic infections,
especially renal colic.
In anterior crural neuralgia a special examination should be
made for Pott's disease, psoas inflammation, appendicitis, typh-
litis, inguinal and femoral hernia, and in a general way for affec-
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LOWER EXTREMITIES, PAIN IN, 1167
tions in the pelvis, especially those involving the Fallopian tubes
or the ovaries.
Lastly, mention should be made of the lightning pains of tabes
dorsalis, exhibiting definite features in their paroxysmal occurrence,
lancinating, fulgurant, and boring character, but the diagnosis of
which should, in short, be based mainly on the major symptom-
group of tabes, vis,, specific history; reflex disturbances, such as
Transve
ntervertehral
oramina
Articulai
Fig. 818. — Relations of the intervertebral foramina of the lower lumbar
region with the lumbar spinal ganglia.
loss of the patellar reflex and the Argyll-Robertson pupil ; disturb-
ances of station and equilibrium (astasia), disturbances of motion
(ataxia), sphincter disturbances, etc.
In a striking synthetic study concerning cases of neurodocitis
and vertebral funiculitis, Sicard (Presse med., Jan. 7, 1918), gave a
good general account and excellent anatomic classification of the
changes occurring in the spinal nerves from their point of issue in
the spinal cord to their rearrangement in separate fascicular groups.
A good diagram condensing the essential facts in this connection
seems adequate at this point. Neurodocitis is a general term desig-
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1168 SYMPTOMS,
nating the changes resulting from compression of certain nerve-
trunks in the natural osseous,, fibro-osseous, or fascial canals. The
word funiculitis is here taken to signify a neurodocitis of the tis-
sues surrounding the intervertebral foramina.
Ordinary sciatic neuralgia is either a neurodocitis resulting
trom compression of the nerve at the great sacrosciatic notch, in
sma/f htanehes
Fig. 819. — ^The several sections of the nerve paths from the spinal
cord to the periphery. Ordinary sciatica is a funiculitis at the inter-
vertebral foramen.
the ischiotrochanteric space, or on the outer aspect of the fibula,
or a funiculitis of the intervertebral foramen of rheumatic, gouty,
or arthritic origin.
True lumbago is a bilateral rheumatic funiculitis involving the
2d, 3d, and 4th lumbar nerves.
Syphilis usually causes radiculitis and myelitis, while tuber-
culosis and cancer oftenest lead to funiculitis.
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LOl^BR EXTREMITIES, PAIN IN. 1169
However long and tedious the preceding enumeration may
have been, it constitutes only an incomplete list of the local dis-
orders; yet it includes the majority, at least, of the painful con-
ditions met with in the lower extremities. (In addition there are
to be thought of such discomforts as may arise from tight leggings,
corns, perforating ulcers, ill-fitting footwear, abscesses, lymph-
angitis, suppurative processes and the corresponding glandular
enlargements, etc. — all self-evident local disorders.)
As a parting piece of counsel, it may be stated that whatever
variety of pain in the lower extremity is complained of, one
should never fail to examine :
(a) The spinal column.
(b) The hip joint
(c) The region of the appendix,
(rf) The kidney region.
(e) The urine.
74
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LUMBAR PAIN.
BACKACHE.
Few symptoms are so frequently misinterpretea as lumbar
pain, backache, or, as popularly termed, **kidney pains." The
bar muBcles
HUB dorsl
mediuB
maxlmus
Fig. 820. — Lumbar musculature. The spinal muscles on the side
opposite to that of flexion are in contraction. The transverse folds of
skin over the spinal muscles on the relaxed side are readily seen (P.
Desfosses),
author has f)ersonally seen — ^an instance almost unbelievable, yet
absolutely authentic — a case of ordinary lumbago labelled Bright's
disease (needless to state, examination showed neither albumin,
casts, high pressure, nor any increase in blood urea), and con-
(1170)
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LUMBAR PAIN. BACKACHE. 1171
versely, an obvious case of Pott's disease of the lower dorsal
region with abscess formation, labelled lumbago.
Such mistakes may be accounted for in many ways.
First and foremost is the unfortunate habit of not examining
the painful region directly and by inspection. Only exception-
ally, indeed, is the lumbar region actually subjected to a sys-
tematic examination in a patient complaining of "kidney pains."
laliB colli
lUocoBtalis cerrl Icalla descendens
Longisslmus dors!
Sacrolumbal is
niocofltalis dorsl
Spdnalis dorai
lumbalis
niocofltalis lumb<
inaliB
Fig. 821. — ^The spinal muscles.
As a matter of fact, there are few regions of the body that de-
mand a more thorough and systematic local examination, since
very few regions exhibit painful manifestations originating in
such diverse and variously situated disturbances. While one
of the anatomic peculiarities of the region is the pres-
ence of the thick sacrolumbar masses of muscular tissue, which
act, to all" intents and purposes, as the muscles governing the
erect posture and are so frequently rendered painful by the most
varied pathologic states, the following regional anatomic divi-
sions should be kept in mind :
1. Muscular region : The sacrolumbar mass of muscle tissue.
* 2. The bony spine and the sacroiliac joints.
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1172 SYMPTOMS.
3. The spinal cord and nervous system.
4. Paravertebral organs : The aorta and lymphatic structures.
5. The abdominal viscera, including especially the kidneys,
spleen, liver, colon, and uterus.
When a patient comes complaining of "kidney pains" or back-
ache, the lumbar region should be exposed and a systematic ex-
amination of the structures above enumerated proceeded with.
1. The skin. — This is sometimes the seat of herpes zoster
(zona) covering a varying extent of surface.
dominis
Peritoneum
Small IntesUne '"» extemus
Iquus Internus
Abdominal i ransversalis
Inferior vena
> Psoas
Right kidney
Lumbar vertebra "(covered with
peritoneum
Spinal coi anterioriy)
scending colon
IratuB lumborum
Longisslmus dor
Spinal «'""" «°
-lumbalis
Fig. 822. — Transverse section through the lumbar region.
2. The sacrolumbar muscular system. — Palpation and inspec-
tion with the patient in various positions, especially the erect
posture, together with movements of anteflexion, extension, tor-
sion, and lateral bending will often lead to the discovery that the
seat of pain is actually in the muscle tissue, the condition being
a true lumbar muscular pain for which, seemingly, the term lum-
bago should be set apart, but which may yet be encountered
under very variable clinical circumstances, to wit :
(a) Acute lumbago, following a forceful straightening of the
flexed body, as in lifting a heavy v/eight, such as a trunk.
(&) Subacute lumbago, following a prolonged march, with
fatigue and exhaustion. This represents a "forcing^* of the
muscle, which becomes painful because of overwork, — a tondi-
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LUMBAR PAIN. BACKACHE, 1173
tion that might without impropriety be placed in the group of
**rheumatic disturbances the result of defective functioning of
the locomotor apparatus," masterfully described by Le Gendre.^
Undoubtedly there occurs, moreover, an acute or subacute lum-
bago of rheumatic origin which is very favorably influenced by
sodium salicylate.
Fig. 823. — Posterior relations of the kidneys. On the left side is seen
the main mass of spinal muscle (shaded), and projecting beyond it below,
the quadratus lumborum. On the right side the main spinal muscle
mass has been removed, exposing the quadratus lumborum and the lum-
bocostal ligament.
(f ) Subacute or chronic lumbago of psychoneurotic cases, ap-
parently the local clinical expression of an actual constitutional neu-
romuscular asthenia, and which may occur either as: 1. A localized
pain constituting an actual topoalgia. 2. A regional dysesthesia, with
morbid sensations of pressure, of sharp, fleeting pains, of heat, or of
cold, frequently with abnormal sensitiveness of the region to pal-
iLeGendre: Acad, de med., May 9, 1911.
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1174
SYMPTOMS,
pation, the whole constituting a vague neuromuscular syndrome. 3.
Deep pain, weakness, and exhaustion with lumbar muscle pains fol-
lowing strong emotional impressions; an actual paroxysmal emo-
tional lumbago superimposed upon a chronic psychoneurotic lum-
bago attending habitual asthenia.
The absence of definite local lesions, the history, the neurotic
stigmata, the habitual psychasthenia, the chronic course of the
morbid manifestations, and their recrudescence after emotional
Figs. 824 and 825. — Osteospondylitis of the vertebrse.
impressions are the most reliable diagnostic features of these
cases.
3. The spinal column, and more particularly the lumbar verte-
brae, with which we are here especially concerned, may be the seat
of many pathologic conditions causing lumbar pain.
(a) First and foremost should be placed the chronic inflamma-
tory states- or spondylitis of the vertebrae, their periosteum, and the
intervertebral joints, leading to the exostoses, adhesions, and anky-
loses frequently encountered in sedentary individuals after the
fourth decade of life. Some rough sketches illustrating these con-
ditions are presented herewith. Such instances of spondylitis are
met with among all the usual cases of arthritis deformans, and post-
infectious rheumatism, e,g,, after pneumonia, tonsillitis, typhoid
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LUMBAR PAIN, BACKACHE,
1175
fever, etc. The condition is, in short, a vertebral osteoarthritis, or
a deforming or post-infectious lumbarthritis. Nor is post-traumatic
spondylitis a rare affection.
The limitation of motion, the stiffness in the lumbar region, the
pain induced in the lumbar spine by flexion or torsion of the body,
the cracking sensations experienced by the patients themselves, the
chronic or subacute course of the disorder, the history, and espe-
cially the x-ray examination, will lead to the diagnosis.^ The dis-
order particularly to be excluded in these cases is Pott's disease.
(b) Pott's disease, the recognized evidences of which need
here scarcely be recalled: Localized pain, most marked in one
vertebra ; radiation of pain to the lower extremities ; cessation of
pain upon rest in recumbency and immobilization of the affected
region ; and ultimately, angular deformity at the point of involve-
ment and paretic disturbances of the sphincters and lower extremi-
ties, with exaggerated reflexes, abscess formation, etc.
Pott's disease should always be thought of in the presence of
chrdnic lumbar pain,
(r) Diac and sacroiliac osteoarthritis, the location of which
is determined by careful palpation.
1 Beclere, quoted by Leri (Presse nUd,, Feb. 28, 1918), had already pub-
lished in 1906 the following differential table relating to chronic rheumatism
of the vertebrae and rhizomelic spondylosis :
1. Chronic vertebral rheumatism.
First feature: Distortion of the
bodies of the vertebra consisting of
a broadening of the upper and lower
surfaces and exaggeration of the
circular concavity.
Second feature: The interver-
tebral discs are distinctly more
transparent than the bodies.
Third feature: Little or no sug-
gestion of a vertical opaque band
corresponding to the ligaments is
present
2. Rhizomelic spondylosis.
First feature: No distortion of
the bodies of the vertebra, which
are almost cylindrical in shape.
Second feature: The discs are
not more transparent than the
bodies.
Third feature: Both the bodies
and discs are covered by a broad
band with parallel borders; the
outermost portions of the verte-
bral bodies project beyond this
band; the processes of the verte-
bra exhibit a remarkable and un-
usual degree of transparency.
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1176 SYMPTOMS.
4. Inflammatory conditions of the spinal cord and vertebral
column cause well-known forms of backache. They are met with
chiefly in the following disorders.
(a) In acute meningomyelitis (acute meningitis; cerebro-
spinal meningitis), the diagnosis of which is based on the simul-
taneous presence of constitutional signs of infection, such as
fever and leucocytosis, in conjunction with the meningeal symp-
tom-group (headache, backache, Kemig's sign, etc.), and is con-
firmed by examination of the cerebrospinal fluid, showing an ex-
cess of lymphocytes or polynuclears, the presence of meningo-
cocci, etc.
(6) The onset of many infectious diseases, particularly influ-
enza, smallpox, and pneumonia, is, as is well known, frequently
marked by extremely severe backache. Examination of a num-
ber of specimens of cerebrospinal fluid obtained under these con-
ditions led to the surmise that the beginning of these disorders
is often accompanied by a sharp but temporary meningeal con-
gestion, which later passes off along with the backache which
is its clinical manifestation.
(c) Mention may here be made of an expression used in military
medicine, ins,, backache with fever {courbaiure febrile) — on the
whole a rather happy expression since it combines both the symp-
toms, backache and fever, which feature the clinical state to which
it refers. Unquestionably this term comprises a number of diflFerent
conditions and careful investigation would lead frequently to the
discovery of cases of "incomplete" paraityphoid or even typhoid
cases. On the other hand, it is certainly true that if the clinical
entities now recognized are eliminated from it there remains a large
percentage of undetermined, cryptogenic infections, usually tran-
sient and mild, but for which an accurate designation would be
hard to find.
(rf) The same sort of a sharp, temporary meningeal reaction
with backache and fever has been noted by the author in certain
cases of secondary syphilis running an acute, febrile course.
{e) The author has been led to consider as symptomatic of
venous congestion of the spinal and perispinal plexuses certain in-
stances of chronic lumbago in subjects suflFering from hemorrhoids,
with high venous pressure and low arterial pressure, the lumbar pain
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LUMBAR PAIN, BACKACHE. 1177
showing daily, almost periodic exacerbations; these cases were, as
a matter of fact, greatly relieved by counterirritation with fly blisters
and wet cupping over the lumbar region and medication directed
toward overcoming the venous congestion, vis., adrenalin, strych-
nine, and hamamelis. This condition must play an important role
in the lumbago of psychoneurotic subjects.
Lateral ant.
plexus
ant
irse
lexus iBverae
. plexus
us of the
jrvert
unen
iteral ant.
lexuB
Figs. 826 and 827. — Intraspinal venous plexuses.
(/) Lastly, it should not be forgotten that the spontaneous or
artificially induced pain in some cases of sciaticalgia may ascend
above the great sacrosciatic notch to the vicinity of the sacroiliac
joint or of the transverse processes of the lumbar vertebrae and the
lumbosacral masses of muscle tissue.
Examination for Lasegue's sign is of the greatest service in
these cases.
In the frequent instances of sciatica combined with kypho-
scoliosis or scoliosis, hyperesthesia and hyperkinesia of the lum-
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1178 SYMPTOMS,
bosacral muscular mass are constantly present. It is noteworthy,
however, that this hyperesthesia and hyperkinesia are in some
instances homologous {i.e., present on the same side as the sciatic
pain), while in others they are on the opposite side; no reliable
explanation of this fact can at present be vouchsafed.
This peculiarity is of importance in the exposure of maling-
erers. Where, in conjunction with the symptoms of sciatica,
there is noted spontaneous or induced hyperesthesia of the lum-
bar region on the opposite side, one may aimost certainly, unless
Fig. 828. — Diploic veins in the body of a vertebra.
the subject is thoroughly familiar with the clinical features of
sciatica, exclude the possibility of malingering.
5. The popular exp-ression "pain in the kidneys" correctly
suggests the anatomic relationships of the kidneys to the lumbar
regions. It is an actual fact that many renal disorders are accom-
panied by lumbar pain, the following succinct description of
which is borrowed from Cathelin :
"The first indication of reno-ureteral affections which plays
a predominant role in the patient's own estimation is pain, which
may be either spontaneous or artificially brought on by motion
or by pressure in the costovertebral angle, particularly at the
apex of this angle. It is seldom present anteriorly, yet radiates
either in the direction of the ureter obliquely downward and in-
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LUMBAR PAIN, BACKACHE, 1179
ward or along the iliohypogastric and ilioinguinal nerves, extend-
ing around the body.
**In other instances, it radiates even to the neck of the bladder
or the spermatic cord, as in stone, a fact accounted for by the
existence of the genital fibers of the ilioinguinal nerve.
"The pain may be located sympathetically (Guyon's reno-renal
reflex) in the opposite kidney, thus bringing in a disturbing factor
in the interpretation of the case. A patient with a stone in the right
kidney often experiences pain in the left kidney. The same sort of
thing is observed in renal congestion.
**The pain may be either slight, dull, and deep-seated or occur
in paroxysms introducing the symptom-group of renal colic (hydro-
nephrosis) or of nephritic colic (descent of a stone) ; while gen-
erally wanting in nephritis, in cancer, and in some common forms
of renal tuberculosis, it is present especially in certain cases of
movable kidney, in hydronephrosis, and in lithiasis, in which it is
increased by walking, riding in vehicles, violent exercise, and
motion in general,"
Physical examination of the kidneys, which should be com-
bined with the study of the functional signs, consists chiefly of pal-
pation and the finding of either a movable, a distended, a subcostal,
or a cancerous kidney, the organ, in the latter instance, being often
hard, irregular, and mobile.
Such a clinical investigation for tumor in the hypochondriac
regions is sometimes hard to interpret, on account of the pres-
ence of the liver on the right side and the spleen on the left.
By this procedure, however, one is enabled to ascertain the
exact position of the enlarged kidney, whether, thoracic or sub-
costal, its mobility, its smooth or lobulated surface, its consist-
ency (hard or soft; fluctuation in hydronephrosis), and its irreg-
ular shape (in certain instances of malignancy).
Among the further sources of information that may be availed
of by palpation are the three ureteral points of tenderness, viz., the
superior or paraumbilical point, corresponding to the renal pelvis;
the intermediate or iliac point, corresponding to the crossing of the
external iliac vessels, and the inferior or z*esical point, corresponding
to the interstitial, intravesical portion of the ureter, palpable
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1180 SYMPTOMS.
through the vagina in women and through the rectum in the male
subject.
6. Abdominal ptosis, various uterine disorders, and pregnancy
are the cause^ — frequently obvious— of many instances of lumbago.
The mere thought of them is often sufficient to make plain their
causal relationship to the lumbar discomfort. The author has seen
very many cases of obstinate lumbago yield to the wearing of a
suitable abdominal belt.
7. Exceptional forms. — Mention may be made of certain truly
exceptional causes of lumbar pain, viz., cholelithiasis, aortic aneu-
rysm, and vertebral and paravertebral tumors. The presence of
a painful point in the right lower lumbar region with contraction
of the muscles of the posterior wall in attacks of acute appendi-
citis has been pointed out by a number of authors.
Brief clinical examination will often discover very easily the
actual cause of lumbar pain. The following few questions are
sometimes conclusive in this connection :
1. How long has the patient been suffering from backache?
(a) The patient may have had it for a few days, the onset hav-
ing been sudden, after exertion or a forced march : True or rheu-
matic muscular lumbago,
(b) He may suffer from it in chronic fashion, with exacerba-
tions, and exhibit an asthenic appearance: Depressive psychoneii-
roses, spondylitis, Pott's disease, spinal and perispinal venous con-
gestion, chronic abdominal affections, or chronic nephritis.
2. The backache is closely accompanied by an infectious dis-
order: Meningomyelitis, onset of infectious diseases (such as in-
fluenza, small-pox, pneumonia, etc.), backache with fever, etc.
3. The lumbar pain is increased by the standing posture and
by flexor and extensor movements of the body : The seat of pain
may be in the spinal column (Pott's disease, vertebral osteoar-
thritis, etc.) or the lumbosacral muscle mass (traumatism, strained
back, rheumatism).
4. Is there pain on pressure or percussion, and if so, where?
In a vertebra : Vertebral osteoarthritis. Pott's disease.
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LUMBAR PAIN, BACKACHE. 1181
In the costovertebral angle : A renal disorder.
In a sacroiliac joint: Sacroiliac osteoarthritis.
Involving the last lumbar nerves and along the sciatic nerve:
Sciatic aigia.
5. Does the urine contain albumin, blood, or pus? A renal
disorder.
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NECK, SWELLINGS IN THE,
The limits of that which constitutes the neck are rather hard
to define. Anteriorly, it is bounded below by the angle formed
by the clavicles and sternum, above by the lower jaw and an
imaginary line extending from the angle of the jaw to the mast-
oid process. Posteriorly, it is bounded above by the mastoid
processes and, the external occipital protuberance, while below
its limits are indefinite ; it forms a continuous surface, in the ab-
sence of any prominent landmarks, with the dorsal region. This
constitutes the nuchal region, which is one of subsidiary import-
ance from the medical aspect. The anterior and lateral surfaces
of the neck, on the other hand, are frequently the seat of swell-
ings concerning which the practitioner's opinion is often in de-
mand, and although by far the greater number of these belong
rather to the domain of surgery, it seems essential to refer to
them briefly. The subject being, however, somewhat out of the
exact limits of the field covered by this work, the data presented
will be given merely in a brief, suggestive form, with just suffi-
cient detail properly to recall the various possibilities to the
reader's mind.
For convenience of description, it is advisable to divide the
anterolateral region of the neck into two median parts, the supra-
and infra-hyoid, and two lateral parts, the sternomastoid and the
supraclavicular, as represented in Fig. 829.
The patient comes to seek the practitioner's advice:
Either on account of a local or diffuse swelling in the neck, of an
acute and painful inflammatory type.
Or on account of a chronic enlargement of non-inflanimatory
nature. A swelling in the neck may even be discovered by the
physician in the course of a systematic examination without the
patient having previously been aware of its presence.
(1182)
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NECK, SWELLINGS IN THE. 1183
The acute inflammatory swellings in the neck comprise ade-
nitis, thyroiditis, and cellulitis of the neck.
Submaxillary adenitis, a frequent condition in children, is
generally of dental origin.
Adenitis below the angle of the jaw either originates from the
pharynx or occurs in conjunction with disturbances localized in the
unsdom tooth.
In suprahyoid adenitis a primary inflammatory condition
should be examined for in the lower lip and suprahyoid superficial
Diga8trl(
Mylotayoi<
Inten , . ^,
Externa ^«^**^ <^"^^
Oi »«®
Sternoi ige
Stemc
Cleidoma
Trapeziu
«v^»««-, (cut)
Fig. 829. — Anterior surface of the neck, showing the regional sub- '
divisions and underlying structures.
tissues. Allied to this is the serious condition known as suprahyoid
cellulitis, following Ludwig's angina, the primary source of which is
an inflammation of the floor of the mouth in the form of a sub-
lingual abscess.
In the infrahyoid region, an inflammatory swelling is neces-
sarily associated with laryngeal manifestations such as aphonia'
dyspnea, and suflFocative attacks. It follows an abscess of the
thyrohyoid and thyroepiglottic spaces, detected by palpation
from the pharynx: On following down the base of the tongue,
an edematous, tender, and sometimes fluctuating swelling is
found in front of and on the lateral surfaces of the epiglottis.
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1184 SYMPTOMS.
Stemomastoid adenitis is almost inevitably accompanied by
symptomatic torticollis, Tha source of infection is to be looked for
in the regions of the mastoid (mastoiditis) and of the pharynx
(phlegmonous angina).
DiflFuse cellulitis of the neck sometimes follows the form of
adenitis referred to ; much oftener, however, it develops directly,
in a predisposed subject, as a result of some infection of the
mouth or pharynx.
All of the above conditions are mainly surgicaL
Thyroiditis is chiefly a medical disorder. It appears in the
form of a uni- or bi- lateral swelling in the infrahyoid region repre-
senting the thyroid gland, the shape of which is reproduced
thereby; the enlargement is sensitive rather than painful, of
elastic consistency, and covered with healthy skin of normal hue
but crossed by dilated veins. The condition is accompanied by
dyspnea, cough, a rough quality of the voice, and sometimes by
frothy, blood-stained expectoration. The pain is worse on swal-
lowing. The disorder develops either spontaneously, with a sud-
den onset marked by a chill and fever, or in consequence of an
infectious disease. Resolution is the rule, and suppuration
exceptional.
Chronic Enlargements in the Neck. — ^These are by far the
more important from the medical standpoint.
A regional classification is necessary for practical clinical pur-
poses : A swelling may exist either on one of the lateral aspects
of the neck or in the median region.
Enlargements on the Lateral Aspects of the Neck.
1. Glandular enlargements. — Here again, involvement of
glands supplies the greatest number of enlargements.
• The usual causes of such enlargements are tuberculosis, syph-
ilis, lymphatic hypertrophy, and neoplasm; the main diagnostic
features of these conditions have already been given under Glandular
enlargements (q.v.).
Softened tuberculous l5miph-nodes are identified by their
fluctuation and non-reducibility. Where there is periadenitis,
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NECK, SWELLINGS IN THE. 1185
Fig. 830. — Lymphatics of the head and neck (Sappey).
/, /. Lymphatic vessels leading to the parotid nodes. -?, 2. Inferior
frontal lymphatics, j, S. Superior frontal lymphatics. 4, 4. Parietal
lymphatic vessels ; these pass vertically downward, anastomosing with the
neighboring vessels, and end in the mastoid nodes. 5, 5. Origin of these
vessels. 6, 6. Anterior suboccipital vessels, converging to form a single
trunk which, after a prolonged course, terminates in one of the lowest
cervical nodes. 7. Trunk resulting from coalescence of these vessels. 8.
Node in which this trunk terminates. 9, 9. Posterior suboccipital vessels,
terminating in two nodes located at the anterior border of the trapezius
muscle. 70, 10. The above two nodes. //. Large horizontal trunk start-
ing from the uppermost of these nodes and passing beneath the splenius
muscle to end in the submastoid nodes. 12. Vessels originating in the
superior mastoid nodes and passing through the sternomastoid to end in
the nodes located beneath this muscle, /j?. Parotid nodes. 14. ^4- Cer-
vical nodes and their afferent vessels. /% 13. Lymphatic vessels originat-
ing in the integument of the nose. r6, 16. Lymphatic vessels of the lips.
77. Subn)axillary nodes. 7^. Lymphatic vessels from the middle portion
of the lower lip. 19. Suprahyoid node in which the above vessels ter-
minate. ^. Large lymphatic vein.
75
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1186
SYMPTOMS.
with adhesion to the reddeiled and tense overlying skin, the diag-
nosis is extremely easy.
The differential diagnosis between tuberculous lymphadenitis
and lymphadenoma sometimes occasions difficulty: 'These two
forms of enlargement at first present common features. They may
be of the same size and shape, in either case consisting of several
lymph-glands; they are movable in respect of the skin and
Fig. 831. — Adenolipomatosis {Launois and Bensaude),
deeper tissues, though in some instances fixed by contraction of
the sternomastoid muscle; they have the same seat of predilec-
tion (angle of the jaw, submaxillary region, and carotid chain) ;
they may be symmetrically placed, and also appear at the same
age, though scrofulous adenitis is more frequent in early life.
Yet each of the conditions has its own particular features. Thus,
lymphadenoma is relatively uncommon, while tuberculous ade-
nitis is by far the commonest form of enlargement met with in
the neck. Lymphadenoma is of an even consistency and imparts
to the fingers a sensation similar to that of renal parenchyma.
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NECK, SWELLINGS IN THE. 1187
Tuberculous adenitis, on the other hand, may be of uneven con-
sistency and present some hard spots and other areas of soft-
ening. Tuberculous adenitis imdergoes suppiuration, while lym-
phadenoma never does. Consequently, whenever fluctuation, or
even periadenitis, is detected, or a sinus or the scar of a former
In
>tid
vical ganglion
t>Ud
tery
LStoid muscle
Hypoi
Middl
trie nerve
Con
Inferio
in artery
Fig. 832. — Deep structures of the neck (vessels).
abscess observed, a definite diagnosis of tuberculous adenitis
may be made. Finally, although lymphadenoma affords only
negutive signs, since at one period the same evidences are found
as in lymphatic tuberculosis, it should be borne in mind that
lymphadenoma may be diagnosed where an enlargement of con-
siderable size IS present; where lymph-nodes similarly affected
are found in the axillae and the inguinal and other lymphatic
regions; where an enlargement of the same nature is found in
another organ, either the testicle or the skin (mycosis fung-
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1188 SYMPTOMS.
oides) ; where enlargement of the spleen, tonsils, or thyroid gland
is simultaneously found, and finally, where the blood count
shows an increase of the leucocytes.
"If the swelling has developed rapidly and attained a consid-
erable size within a few months; if it forms a rounded prominence,
covered by a marked venous network, and especially if its surface
has become ulcerated and gives rise to free hemorrhages from time
Fig. 833. — Exophthalmic goiter.
to time, one should think of sarcoma, which may originate in any
of the structures constituting the neck and even the submaxillary
gland, but which, as a rule, starts in the lymph-nodes, or results
merely from transformation of a lymphadenoma, in which event it
is termed lymphosarcoma" (Rochard and Demoulin, "Manuel de
diagn ostic ch iru rgical" ) .
2. Mention should be made of the ossifluent abscesses (ab-
scesses from congestion with breaking down of bone tissue), the
existence of which is shown by the fluctuating character of the
swelling with slight reducibility (liquid tumor), the fact that
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NECK, SWELLINGS IN THE. Ugg
motion of the head generally causes pain, and examination of the
spine, which reveals either a bony deformity or the presence of
a well localized point of tenderness.
3. Lipoma, including the supraclavicular pseudolipoma of the
emphysematous and adenolipoma, probably comes next after gland-
ular swellings in frequency. A mere mention of lipoma is here
sufficient. An illustration of typical adenolipomatosis is presented
herewith (Fig. 831).
4. Finally, there are the vascular enlargements, or more
specifically, aneurysm, which is, however, an uncommon disorder,
even though the supraclaviculocarotid region is a point of election
for it. Aneurysms present four pathognomonic signs : They are of
fluid consistency, reducible, and pulsating, whether their beats, which
synchronize with those of the pulse, be visible or merely palpable;
lastly, they are the seat of a systolic blowing bruit which is audible
on auscultation. These are the well-known signs of arterial aneur-
ysms. Arteriovenous aneurysms are always consequent upon
traumatism, e.g., a bullet or stab wound; the bruit is continuous
with reduplication, and palpation yields the so-called "thrill," a
species of fremitus with periodic accentuation.
It is the. custom to explain how to differentiate aneurysm
from vascular goiter. A single sign is ordinarily sufficient for
the purpose: A p:oiter, even when vascular, ascends with the
larynx during deglutition while an aneurysm remains motionless.
Recognition of the site of an aneurysm is of marked import-
ance as regards operative intervention.
Carotid aneurysm is located in the sternomastoid region. The
bruit is transmitted in the cervical region. Only the temporal
pulse is interfered with.
Subclavian aneurysm is located in the infraclavicular region,
at a point lateral to the sternomastoid. The enlargement is elon-
gated in the transverse direction. The bruit is transmitted to-
ward the axilla. The radial pulse is interfered with.
Aneurysm of the innominate artery and aortic arch is located
in the suprasternal region, between the sternomastoid muscles.
Both the radial and temporal pulses are interfered with. The
bruit is transmitted toward both the neck and the axilla.
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1190 SYMPTOMS,
5. Sebaceous cysts, uncommon in this region, contained
within the skin, painless, and of firm consistency, could hardly be
mistaken for anything except a small encapsulated lipoma, and the
untoward result of such a mistake would be slight.
Exophthalmic Goiter
Nervous Factor Thyroid Factors
Sympathetic l^eurosis Dysthyroidia
C&€broytfikmf9V8tem
tAaAnos}
Vasomotor
nervtm io
skin 9t*d i
Sfmatgknds
(Swan and
a.
^5)
StomBch
Uver (intfrmiH^nt
htestina (di^rrheB)
^fCtr}eys(pofyuna)
Fig. 834. — Graves's disease. Exophthalmic goiter.
Symptoms and pathogenesis.
Enlargements in the Median Region of the Neck.
The suprahyoid region being rapidly dealt with by simple
enumeration of adcnolipoma and suprahyoid glandular swellings
(syphilis, lymphatic hypertrophy, or neoplasm), there remains to be
considered :
The infrahyoid region, in which, the exceptional eventualities
of cysts, tuberculous lymphadenitis, and cancer of the larynx (dis-
turbances of voice production and deglutition, blood-stained and
mucopurulent salivation, and laryngoscopic examination) having
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NECK, SWELLINGS IN THE. Il91
been likewise — and readily — eliminated, the remaining con-
dition is :
Enlargement of the thyroid gland, situated definitely below
the larynx, generally bilateral, and moving upward upon swal-
lowing owing to the fact that the gland is attached to the laryn-
gotracheal canal.
Congestion of the thyroid with temporary swelling of the
neck may, as is well known, be witnessed in pregnancy, after pro-
longed exertion, and in the course of infectious diseases (small-pox,
typhoid fever, eruptive fevers, etc.). It is essentially a transient
condition, as is true likewise of thyroiditis, but it may at times be
associated with the symptomatic picture of mild and fugacious
Graves's disease.
True, lasting enlargements of the thyroid (cysts and solid
enlargements) are, from the medical aspect, dominated by the ques-
tion of Grofves's disease and dysthyroidia. The problem which
arises, and which is the most important to the physician, is as
follows :
Is the condition a simple goiter (solid or cystic) without appre-
ciable disturbance of the function of the gland — without dys-
thyroidia?
Or is it a goiter with overfunctioning of the thyroid or hyper-
thyroidia (exophthalmic goiter) or with reduced function or
hypothyroidia (myxedema) ?
Briefly, in every goiter case, of whatever degree and variety,
one should look carefully for the signs of hyperthyroidia given
in the subjoined table, which covers concisely the main clinical
features and probable pathogenesis of the disturbances of thyroid
function.
Mention may here appropriately be made of the profound dis-
turbances of metabolism which generally accompany exophthal-
mic goiter and of which the metabolism of glucose serves as a
rather satisfactory index. In this connection one may also refer
to the possibility of the simultaneous presence of exophthalmic
goiter and diabetes, as emphasized by Marcel Labbe, and the
frequency of intermittent glycosuria and of alimentary glyco-
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1192 SYMPTOMS,
suria. Hyperglycemia is the rule in Graves's disease. American
writers (Goetsch and Lueders) have, moreover, called attention
to the fact that intramuscular injection of 0.5 cubic centimeters
of 1 : 1000 adrenalin solution in hyperthyroid subjects causes not
only a marked pulse acceleration and rise of blood-pressure but
also, as a rule, in the succeeding two hours, a varying degree of
glycosuria.
Chief Clinical Signs of Exophthalmic Goiter.
1. Enlargement of the thjrroid gland (goiter).
2. Exophdialmos and the associated ocular signs: Staring expres-
sion (Stellwag); failure of upper lid to move with the eyeball in
looking downward (von Graefe); deficient convergence
(Mobius).
3. Permanent tachycardia, respiratory arhythmia, palpitations, vaso-
motor manifestations (transient erythema, dermographia),
sphygmolability, and febricula.
4. Static tremor, exaggerated reflexes, nervousness, subjective sen-
sation of heat, and various spasmodic disturbances (asthmatoid
attacks, gastrospasm, spastic constipation, etc.).
5. Profuse sweats, unusual salivary secretion, and tendency to diar-
rhea on slight provocation.
6. Polyuria, frequent urination, and intermittent glycosuria.
7. Sexual perturbations.
Chief Clinical Signs of Hypothsrroidia.
1. Atrophy and sclerosis of the thsrroid, possibly, though rarely, in
conjunction with apparent hypertrophy, or, more frequently,
with a doughy condition of the tissues of the neck.
2. Doughy condition of the tissues, thickening of the integument,
with a swollen, waxy, myxedematous appearance (false edema,
firm and resilient).
3. Phjrsical torpor, sluggishness, inertia, sloA^ness of the move-
ments, and sensitiveness to cold.
4. Mental torpor, apathy, tendency to backwardness, and slowness
of mental reactions.
5. Diminution of the sweat and sebaceous secretions; skin dry and
scaly. Impaired nutrition of the skin and hairy covering.
6. Reduced urinary output (oliguria).
7. Sexual anorexia.
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NERVOUSNESS.
A definition of the term '^nervousness" is badly needed for
the very reason that it is so commonly used. What is the meaning
of the term "being nervous?" One may be nervous in a variety
of different ways, and the mere attempt to have patients who
describe themselves as being "nervous" give a definite account
of their symptoms (often an impossible task) is enough to show
that this term, as commonly used, is possessed of either vague or
variable meanings which make it unsuitable for legitimate clinical
use.
Unquestionably the proper thing to do is to decompose "nen^ous-
ness^' into its several primary factors and to make a systematic
search, in a patient considered "nervous," for the typical stigmata
and symptoms, both motor, sensory and special sense, mental, vis-
ceral and vasomotor.
I. Motor nervousness is manifested especially in restlessness
and exaggeration of motor responses. In one group of cases the
patient is shifty, restless, unable to keep still, and actually has "the
fidgets." Such motor excitement is, as is well known, practically
a normal condition in children. In the adult it is often associated
with mental excitement, insomnia, anxious states, etc. It is one of
the attributes of the emotive or nervous constitution.
In a second group of cases, the patient exhibits uncontrollable
contractions of var)ring frequency in some portion of the body:
Twitchings, contractures, tics, or tremor (see Tremor),
This form of motor nervousness is met with in chorea and the
choreiform states, in tics, and in many neurotic disturbances. A
particular search should be made for:
Somatic causes, foremost among which are :
1. Intoxications, principally alcoholism, less frequently cocaino-
mania, opium habit, lead poisoning, etc.
2; Hyperthyroidia: Graves's disease, exophthalmic goiter, in-
complete (fruste) Graves's disease, and, in a general way, over-
(1193)
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1194 SYMPTOMS.
activity of the internal secretions — thyroid and ovarian or testicular,
and hypercrinia.
Mental causes: Strong emotional impressions, overwork, and
passional states inducing psychoneurotic disturbances. Such
motor nervousness is often the external expression of a deep
mental injury. The patient has some poignant burden in his
heart; he rebels, and the pain experienced induces lasting nerv-
ousness. A historic example of this is that of the wandering, ill-
used Empress of Austria, Elizabeth.
II. General sensory and special sense nervousness is mani-
fested in an hyperesthesia, either general or selective, toward exter-
nal stimuli, — whether tactile, gustatory, auditory, olfactory, visual,
or cutaneous impressions be felt to an excessive or actually pain-
ful degree, or even awaken distressful motor or visceral reflexes.
The disturbance is especially evident as regards the auditory
function. The subject is startled by the least sound, jumps when
a door is opened, and complains of hyperacusis. Frequently such
a patient is, moreover, unable to stand bright illumination or
direct sunlight (as exemplified in the obstinate facial neuralgia
sometimes experienced on the Southern Coast of France). At
times olfactory hyperesthesia is manifest in that the subject is
able to perceive odors which persons considered normal cannot
smell, yet which analytic procedures show to be actually present.
Not rarely one observes in these cases a cutaneous hyperesthesia,
demonstrated by pricking with a pin or by mere grazing of the
skin surface, as well as a heightening of the tendon and skin
reflexes.
This "general sensory and special sense nervousness" is fre-
quently accompanied by neuralgia of varying kinds. There is thus
present an actual diathesis — an actual algic, hyperesthesic con-
stituHon,
Special mention should be made of the "general sensory and
special sense nervousness** manifest in a "meteorologic (cosmic)
hyperesthesia." These patients are actual meteorologic esthe-
siometers or, as they frequently describe themselves, "regular
barometers." They are oversensitive to variations of tempera-
ture, of barometric pressure, and of humidity, to electro-magnetic
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NEK I/O US NESS. 1 195
variations, and unquestionably also to many other cosmic varia-
tions as yet unknown to us. Some forecast and feel changes in
the weather, sharp changes of barometric pressure, shifting of
the direction of the wind, the precipitation of mist, etc., with
extreme accuracy and under such conditions as exclude all pos-
sibility of fraud. The author has often had occasion to witness
a rheumatic, neuralgic patient, sitting in the evening in a closed
room with the shutters drawn and curtains pulled together, shut
off from any direct or indirect contact with the outer air, an-
nounce with infallible precision a rise or fall of barometric pres-
sure of moderate extent (5 to 10 millimeters) or a shift in the
direction of the wind or the onset of snowfall, etc. Every one
may readily observe phenomena of this type among his associates.
The events are such as would suggest that the majority of meteoro-
logic changes cause a disturbance of balance of the body fluids,
objectively manifested in various physical effects and subject-
ively in pain.
Whatever explanation be conceived as to the intimate causation
of these disturbances, it is hard not to think of them as being de-
pendent upon an unusually unstable electrochemical balance in the
body fluids, a species of supersaturated state on the threshold of
precipitation and in relation to which the least shock or perturbation
suffices to bring on an intra-organic reaction involving the precipita-
tion of some noxious agent either at the nerve-terminals (neuralgia),
the joints (arthralgia) , or certain internal organs (visceralgia). In
this way may be roughly described the relationships existing be-
tween the as yet rather poorly defined groups of patients with "a
tendency to" rheumatism or neuralgia, at present loosely combined
under the term "neuro-arthritism."
III. Psychic nervousness is perhaps a commoner condition.
Its outstanding feature, on the whole, is mental instability in all
its different expressions. The subject is emotional, and the least
untoward event causes him to lose his self-possession ; he is not
"master of his own acts." Often periods of enthusiastic excite-
ment and exaggerated optimism alternate with periods of depres-
sion and unwarranted pessimism.
In the condition characterized by excitement the subject is
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1196 SYMPTOMS.
irritable and even impulsive ; he quickly becomes angry and even
violent.
In the depressed condition, he is morose, anxious, aboulic, and
is readily seized with apprehension or actual fear.
The question of the "neuroses" and "psychoneuroses" might
appropriately be taken up here. We shall not do so, however,
merely reminding the reader that in these cases the chief aim of
the practitioner should, seemingly, be to ascertain :
1. Whether the existing psychopathic disorder is not the ex-
pression of a concrete somatic condition, the most important dis-
ease in this connection being general paralysis, as well as some
common, latent or overlooked morbid state such as diabetes, ar-
teriosclerosis, intoxication (as by alcohol, etc.), tuberculosis in
its insidious stage, malaria, etc.
2. Whether the psychopathic disorder is not the necessary
and perhaps inevitable consequence of some conscious mental
stress, such as secret sorrow, frequently present in young girls
and women, or professional difficulties or disappointments, which
are responsible for a high percentage of embittered, anxious,
nervous individuals, etc. Political, literary, and even medical
pursuits yield a host of such cases.
3. Whether the psychic nervousness is not, properly speaking,
a constitutional, congenital, and frequently inherited state.
Nothing could be more illuminating in this connection than the
simultaneous examination of a mother and her daughter, the
latter showing the same psychopathic manifestations as the
former, but with twofold or even threefold intensity.
The highly suggestive psychologic conception of hysteria
considered as a disorder characterized essentially by a contrac-
tion of the "field of consciousness" which allows the subject to
group together at a given moment only an extremely restricted
number of sensations and recollections accounts satisfactorily
for this variety of "psychic nervousness," with its expressions
in the form of instability, impulsiveness, psychic and moral in-
coordination, suggestibility, etc., a single idea, image, or sensa-
tion sufficing to overcrowd the field of consciousness, so that
one idea drives out another.
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NERVO USNESS. 1 197
IV. Visceral and vasomotor nervousness. — The ''spasmodic"
and ''paretic" manifestations predominate in this group, whether
the spasmophilia be chiefly visceral, and capable of causing very
various phenomena such as spasm of the esophagus, meteorism, re-
gurgitation of food, dyspepsia, constipation, retention of urine, etc.,
or cardiovascular, being represented by the anginal symptom-group,
neurocardiac erethism, the tachycardiac neurosis, spasm of the ves-
sels, hyperidrosis, dermographism, acrocyanosis, disturbances of
skin temperature, etc. In these cases sympathetic disturbances
predominate.
In some subjects there is observed an actual vasomotor ataxia
characterized by evidences either of vasodilation or vasocon-
striction or of a mixture of these two varieties of vascular dis-
order. Graves's disease represents the extreme vasodilator type,
and Raynaud's disease, the extreme vasoconstrictor type. Be-
tween these two are found many intervening varieties, of vary-
ing intensity and location, such as simple urticaria, dermograph-
ism, nervous edema, drug idiosyncrasies, hay fever, intermittent
albuminuria, a tendency to purpura and petechiae, multiple angio-
mata of the skin, and paroxysmal tachycardia. The disturbances
at the menopause present essentially this condition of vasomotor
ataxia.
Clinical tests. — There are available, indeed, certain elementary
clinical tests which enable the practitioner to detect such exces-
sive irritability of the sympathetic system :
(a) The vasomotor skin reactions induced by rubbing or by the
application of heat or cold. When exaggerated, these lead to der-
mographism, as in the "meningeal line"; when perverted, to re-
actions in the opposite sense, vis., redness after the application of
cold and pallor following the application of heat.
(b) The reactions as to heart frequency induced by the respira-
tion. Normally, the influence of the respiration on the pulse is prac-
tically nil. Under abnormal conditions, however, the pulse becomes
irregular and arhythmic during respiration; this constitutes the so-
called "respiratory arhythmia" met with in young subjects and
many neuropathic patients.
(c) The trigemino-cardiac reactions, the one most investigated
so far being the oculocardiac reflex. Normally, slowing of the
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1198 SYMPTOMS,
pulse rate results from pressure upon the eyeballs. Under abnor-
mal conditions, the pulse-rate is unchanged or even accelerated.
These tests are of exceedingly great importance in the frequently
difficult diagnosis of the cardiac neuroses (tachycardiac neuroses).
Whether present singly or in combination, the various nervous
symptoms above referred to, sometimes associated with insomnia,
paretic or convulsive disturbances, headache, asthenia, mental cloud-
ing, various disorders of the tendon- and skin- reflexes, and some-
times even states of mental confusion with amnesia, delirium, and
hallucinatory restlessness, constitute the main factors in the neuroses
and psychoneuroses — hysteria, neurasthenia, Krishaber's cerebro-
cardiac neuropathy, Dupre's emotive constitution, the anxiety neu-
rosis, cardiac neurosis, and Grasset*s psychosplanchnic neuropathy.
Sometimes the clinical symptom-groups given in text-books as
characteristic of these various neuroses and psychoneuroses are
sufficiently well marked and differentiated as to permit of actually
applying to the case a fairly precise designation, such as neuras-
thenia (with its stigmata: type of special headache, amyosthenia,
brain depression, etc.) ; hysteria (with its characteristic pithiatism) ;
neuropathy (with its stigmata: special type of headache, amyos-
thenia, brain depression, etc.) ; psychosplanchnic neuropathy (with
its debility of the higher mental processes, hyperkinesthesia, and
psychosplanchnic interdependence) ; the emotive constitution, and
the anxiety neurosis; but the symptoms of these disorders are
dovetailed and superimposed, with the result that differentiation is
often a very difficult task.
* * *
Somewhat recent investigations have drawn the attention of
the profession to two types of nervousness — which, as a matter
of fact, overlap — the emotive or emotional constitution and the
anxiety neurosis. Both of these are of marked clinical import-
ance ; hence it is deemed advisable to present a short account of
each, the first as described by Dupre, and the second, by Heckel.
I.— THE EMOTIVE CONSTITUTION.
Dupre^ proposed some years ago to set apart, under the appel-
lation emotive constitution, a special type of imbalance of the
1 DupRf: : Acad, de med., Apr. 2, 1918.
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NERVO USNESS, 1 199
nervous system, characterized by diffuse erethism of general,
special sense, and psychic sensitiveness; by inadequacy of motor
inhibition, reflex as well as voluntary, and clinically manifested by
responses abnormal in degree, diffusion, duration, and lack of pro-
portion to their exciting causes.
Hyperemotivity, a normal condition in infants and very fre-
quently present in older children (infantile nervousness) dis-
appears in the adult owing to the gradual development of the
inhibitory nerve paths, which insure balance and stability of the
nervous system. Abnormal emotivity, usually constitutionally
inherent and inherited, may be an acquired state and be the re-
sult of infectious, toxic, and especially traumatic factors, such
as intense or repeated body commotions or emotions.
Emotion, indeed, often sensitizes the nervous system to subse-
quent emotional stresses, and through a species of emotive ana-
phylaxis may bring about a constitutional emotivity. In contrast
to such cases one may, on the other hand, observe in well balanced
subjects a gradual habituation to an entire group of emotions, a
rather remarkable emotive immunity being thus conferred through
repetition of like emotional stresses.
The emotive constitution is characterized by two groups of
permanent signs, the physical and the mental:
Physical signs. — Exaggerated reflex action, diffuse and involv-
ing both the tendon, skin, and pupillary reflexes. Sensory hyper-
esthesia, with sharp, extensive, and protracted motor responses,
principally as regards gestures and speech. Loss of motor equi-
Ubritim, manifested in spasm of viscera, as in pharyngo-esophageal
spasm, gastroenterospasm, bladder spasm with frequent urination,
and palpitations. Emotive tremor in all its numerous expressions,
such as tremor of the extremities, shuddering, quivering, shivering,
chattering of the teeth, stammering, transient myoclonic move-
ments, tics, etc. Functional inhibition and loss of power of motor
structures, of a transient nature, as in sudden giving way of the
knees, inability to speak, or relaxation of the sphincters. Loss of
circulatory equilibrium, manifested in tachycardia, sometimes occa-
sional but often permanent and paroxysmal; instability of the
pulse. Alternate peripheral vasoconstriction and vasodilation ;
dermographism. The relationship of these circulatory disturb-
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1200 SYMPTOMS.
ances, chiefly permanent tachycardia, with certain types of high
blood-pressure remains to be ascertained, especially in the subjects
free of arteriosclerosis and renal disease. Loss of thermal equi-
librium, as shown in objective variations of temperature, detected
by local thermometric tests, and subjective sensations of heat and
cold, chiefly in the extremities. Loss of glandular equilibrium,
with spontaneous or emotionally induced variations of the sweat,
salivary, lacrymal, gastrointestinal, urinary, genital, and biliary
secretions. Disturbances of intennsceral reflex action, taking
place, in the major systems of the body, through association of
spasmodic conditions, secretory disorders, and functional stimula-
tion or inhibition, brought about through abnormal reflex eflFects
exerted upon one organ by another along the vagosympathetic or
cerebrospinal nerve paths.
Mental signs. — Undue impressionability, a distraught condi-
tion, apprehensiveness, anxiety, irritability, and impulsiveness.
More or less constant or remittent, and frequently paroxysmal,
these morbid conditions appear in alternation or combination and
form a permanent basis or soil upon which appear and develop
the emotive symptom-groups, timidity, scruples, doubts, obses-
sions, phobias, simple or delirious states of anxiety, and psycho-
sexual emotive abnormalities. In the more severe cases there
appear attacks of anxious melancholia, and chronic states of ob-
session with ultimate development of incurable delusions of self-
accusation, hypochondria, or negation.
Constitutional emotivity, which, to be sure, is not incom-
patible with normal or unusual intellectual attainments and af-
fectivity, is frequently combined with other neuro-psychopathic
states, notably neurasthenia and hysteria, with which it exhibits
certain interesting relationships as regards combination or se-
quence, but from which it should be clearly distinguished.
II.— THE ANXIETY NEUROSIS.
The following data concerning the semeiology of anxiety and
more particularly of the anxiety neurosis are based on Heckel's
monograph on this subject^ :
Pathologic physiology. — Anxiety and angor (angoisse) occur
1 H ECKEL : Ncvrosc d* angoisse, Masson, pub!., 1917.
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NERVOUSNESS, 1201
normally as physiologic, functional manifestations. The former,
anxiety, characterized by disquiet, restlessness, and mental disturb-
ance of varying degree, is produced normally and casually under the
influence of emotional stresses, fear, and under all circumstances
in which life and the preservation of the individual are menaced.
It is ordinarily accompanied by certain xoncomitant manifesta-
tions, physical, organic, or somatic. It is these concomitant
manifestations which characterize angor, i.e., a distressful sensa-
tion of constriction (from the Greek word, ayyeiv, to choke)
involving various systems of the body. We thus have:
(a) Respiratory angor, consisting of a feeling of thoracic dis-
comfort, of pressure on the sternum, of tightening of the inner
and outer musculature of the chest, and of tightening of the
bronchi; whence, oppression, fear of asphyxiation, terror, respira-
tory spasms, sighing, aphonia, and cough — all of emotive and
anxious origin.
(b) Cardiovascular angor, simulating angina pectoris in all
its grades of intensity (emotive or anxious pseudoangina pectoris),
manifested in sensations of gripping at the heart, of constricted
heart, or of unduly large heart, by subjectively noticeable heart-
beats, palpitation, arhythmia, faintness preceded by vertigo, vas-
cular phenomena, resulting in coldness of the extremities, beating
arteries, and flushing or pallor of the face or body.
(r) Digestive angor, characterized by interference with swal-
lowing, the emotive '^globus," epigastric discomfort with a feeling
of weight on the stomach, anxious gastralgia with or without
pyrosis, nausea and even vomiting, colicky pains, tenesmus, consti-
pation or diarrhea, arrest or excess of bile secretion, white or un-
duly colored stools, and cholemia or sometimes jaundice.
(d) Cerebral angor, associated with a feeling of constriction of
the temples, of narrowing of the skull, and of emptiness in the
head with consequent inability to maintain thought. There is also
a typical facial expression. The facies of anxious emotivity is
characterized by a transversely wrinkled forehead with two vertical
folds due to the muscles of the supraorbital ridges and by accen-
tuation of the nasolabial folds, descent of the labial and palpebral
commissures, and sometimes, in the presence of marked terror,
protrusion of the eyeballs. The expression of preoccupied con-
76
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1202 SYMPTOMS,
centration, of g^ief , or of fear and the preoccupied or tragic facics
of the anxious patient are due to constriction of the nasal, ocular,
and oral orifices by the contracted muscles, to a narrowing of the
face as a whole, and to the vertical traction exerted along the
facial lines and muscular furrows, as well as to the subject's shift-
ing, worried, distracted glances and at times to dilatation of the
pupils. This anxious facies is most striking under marked emo-
tional stress or in the presence of abject fear.
Lastly, cerebral angor or anxiety is associated with a psychic
state expressed in manifestations which are:
1. Mental, inz., worry, disordered thought, incoherence of men-
tal association or even marked mental impairment with amnesia
and delirium.
2. Such anxiety is also expressed in motor phenomena, such as
restlessness of the body as a whole, inability to remain in one
place; sudden, purposeless, contradictory, jerky, discontinuous
movements ; stamping on the floor ; sometimes limited or exuberant
gesticulations; at other times headlong flight or, on the contrary,
motionlessness, stupor, and retirement; there may also be exclama-
tions, complaints, and sobs.
Motor reactions may also be manifested in spasm or contrac-
ture of smooth as well as striped muscles, local or general tremor
with chattering of the teeth, and even tonic and clonic convulsions,
constituting the spasmodic attack of anxious emotivity, which is
nothing other than the well-known nervous ^pell formerly con-
founded with hysterical seizures.
3. The attack of anxiety also exhibits a secretory manifestation
in the form of lacrymation, profuse sweats, emission of ordinary
or colorless urine, salivation, and diarrhea, where there is secre-
tory stimulation, or, on the other hand, inhibition of secretion as
shown by dryness of the mouth, constipation, acholia, anorexia,
apepsia, etc.
All these motor and secretory manifestations, which are an
expression of the lowest ebb of anxious depression, lead to ces-
sation of the latter through an actual process of "release."
4. Lastly, the sensory manifestations of anxiety are neuralgic
pains along the thoracic nerve-trunks, intercostals, sciatics. tri-
geminals, etc., headache, and rheumatoid pains, which, when
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NERVOUSNESS. 1203
present alone, in incipient forms, cannot be specifically recognized
and lead to numerous diagnostic errors.
It will have been noted, then, that anxiety is an emotive state,
especially of a conscious sort, made up of mental distress, worry,
and doubt, together with a senscUion of physical constriction to
which the term angor is particularly applied. The essential fea-
tures of the latter are, in the first place, a feeling of contracture or
spasmodic condition not only of the voluntary muscles but more
especially of the visceral involuntary muscles, and secondly, of
a distressful modification of the internal sensibility or cenesthesia.
Under normal conditions anxiety follows any sort of emo-
tional stress brought about by external or internal conflicts, to
which it remains sufficient and proportionate.
Under abnormal conditions the reactions from morbid emo-
tions are excessive and unduly prolonged, whereas the causes
responsible for them are futile and seemingly absent; in the
latter instance, anxious emotivity or anxiety would appear, then,
to be spontaneous, but this is not actually the case, as the mech-
anism of emotive sensibility is always set in motion by stimuli,
often reflex and unconscious, some of which are of psychic and
others of organic origin.
In short, angor is a condition of bulbar origin, manifested in
reactions of the body dependent upon disturbance of the nuclei
of the vagus or, more exactly, the bulbar origin of the vagus
and of the sympathetic. This disturbance may reach the
medulla by descent from the cerebrum where it orig^inated in
the psychic sphere — in which event the condition is a descend-
ing angor of psychic origin ; — or it may ascend from the depths
of the organism toward the bulbar center of angor along the
visceral branches of the vagus and of the sympathetic — in which
event the condition is an ascending angor of organic (visceral)
origin. Often both routes of ascending, vagosympathetic trans-
mission are simultaneously stimulated by the group of slight
visceral commotions the knowledge of which as a whole by the
brain constitutes cenesthesia (obscure consciousness of favor-
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1204 SYMPTOMS.
able or unfavorable conditions of intimate functioning of the
body organs).
Yet, while bulbar angor of psychic origin is dependent upon
a brain primarily disturbed through some external emotion
causing cerebral anxiety, it may also be initiated through the
transmission to the brain of an organic ascending angor. In
most instances, psychic cerebral angor or anxiety is so closely
combined with bulbar angor of somatic and visceral origin that
it is sometimes hard to distinguish the origin of these manifes-
tations.
Anxiety and angor are symptoms of marked clinical interest
from which every physician should be able to obtain diagnos-
tic and therapeutic indications of prime importance in practice.
Clinical conclusions. — Heckers investigations lead to the
conclusion that the physician should, for purposes of diagnostic
guidance, recognize three main classes of angor and anxious
states: 1. Angor consequent upon functional disturbances or
pathologic conditions of internal organs. 2. Angor present in
disturbances of general nutrition. 3. Essential angor or the
angor neurosis.
Etiologic resume. — Aside from the favoring influence of
heredity (Dupre's emotive constitution) and of race (Semitics
and Latins of the Mediterranean division), symptomatic angor
and anxiety, in common with the anxiety neurosis, may be conse-
quent upon inherited tendencies of the metabolic type (gout,
diabetes, obesity, etc. ; hereditary arthritism) and upon all fac-
tors causing emotion (sentimental emotion or ungratified sexual
desire). Emotional shocks, traumatism, nervous impressions,
overwork, and fatigue are the usual causes of acquired angor
and anxiety, certain infectious diseases or intoxications are pre-
disposing factors. Heckel has demonstrated the relationship of
tuberculosis and the metabolic diseases to angor. Casual slight
causes, such as anger and changes in the weather suffice to bring
on attacks in those predisposed.
Let it be repeated, in conclusion, and even more earnestly than
in earlier sections, that a diagnosis of neurosis or of psychoneur-
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NERyOUSNESS. 1205
osis, even with a special symptom-group attached, but without
etiologic qualification, is a diagnosis *'by exclusion" or "makeshift"
diagnosis with which one cannot rest satisfied. The physician should
always make a systematic attempt to ascertain the casual, provoca-
tive or exciting cause of the "psychoneuropathic" syndrome.
The methodical examination to which the patient is subjected
should, as always, be thoroughgoing, though dealing more par-
ticularly with the nervous system, blood-pressure, urine (always an
indispensable procedure), blood (urea and Wassermann), thyroid
gland, etc.
In patients below forty the practitioner should think especially
of anemia, latent tuberculosis, syphilis, exophthalmic goiter, sex-
ual excesses, and nutritional disturbances.
In patients past forty he should think especially of arterio-
sclerosis, diabetes, the menopause, and general paralysis.
Both before and after forty years a careful inquiry should
be made for psycho-emotive causes, such as overwork, psycho-
venereal excesses, and emotional shocks.^
* Regarding the war neuroses and psychoneuroses and the anxiety neu-
rosis, the following works may be consulted :
Grasset: "Les grands types cliniques des psychon^vroses de guerre
{Reunion medico-chir. de la XF/« region, Jan. 22, 1917; abstracted in Presse
mid,, Aug. 22, 1917, p. 495).
DuPRfe: Constitution ^motive {Acad, de med., Apr. 2, 1918).
J. Babinski and J. Froment: Hysteria, pithiatisme, et troubles nerveux
d'ordre rcflexe en neurologie de guerre (Masson, pub!.. 1916).
F. Heckel: La nevrose d'angoisse (Masson, 1917).
Devaux and Logre: Les anxieux (Masson, 1916).
Roussy: Traitement des psychonevroses de guerre (Masson, 1918).
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OBEiSITY. [Obesus, stout; ovemourished.]
Obesity is derived from the Latin word obesus, meaning an
ovemourished individual. It is a poor term, since obesity is not
always due to an excessive intake of food.
Obesity is essentially characterized by a general overgrowth
of adipose tissue as compared to the other kinds of tissue (espe-
cially the muscles).
It will not be inappropriate to note that there exists a cer-
tain affinity between the processes of fat accumulation in the
system and the processes of sugar accumulation, as in diabetes,
or of protein accumulation, as in gout. All these metabolic
changes are effected through the agency of special ferments.
Three oxidizing ferments or oxidases preside over the chemical
transformations to which sugar, fat, and proteins are subjected.
If one of these is lacking or becomes insufficient, there results
a disturbance of nutrition featured by the appearance of dia-
betes, gout, or obesity. Thus, gout, diabetes, and obesity may
be ascribed to such causes as react upon the production of fer-
ments by the internal organs and to conflicts between the fer-
ments and the substances they transform. In truth, however,
the anaerobic life of cells and the conception of the endocrin hor-
mones and hormozones has in late years lent a considerable
added complexity to the question. The etiology and pathogenesis
of obesity seem in some respects analogous to those of diabetes and
of gout ; one is led to ascribe the disorder partly to the endocrin or
ductless glands and in a larger measure to the nervous system.
As Heckel has very clearly shown, obesity is a progressively
developing symptom-group, easily corrected in its initial stage
(minor obesity), which is due to exogenous and endogenous dis-
turbances of fat regulation and is characterized by :
(a) Fatty infiltration and degeneration, more or less pro-
nounced, of the connective and even other tissues.
(1206)
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OBESITY, 1207
(b) Concomitant . functional disturbances (with or without
pathologic changes) in the nervous system, digestive tract, en-
docrin glands, cardiovascular system, kidneys, etc.
(c) A rise in the adipomuscular coefficient, i.e,, of the ratio
fat which is normally 1 : 10.
muscle ''
The prognostic significance of obesity is dependent upon the
importance, progression, and seriousness of the concomitant
functional disturbances.
Obesity is a clinical s3n(idrome and not a disease, since it is
dependent upon no single cause and has no constant patho-
genesis.
There may occur a temporary or permanent obesity :
1. From superalimentation, through hyperphagia or overeating,
since fat may accumulate in the tissues after excessive ingestion of
food rich in proteins and carbohydrates.
Through hypolipolysis in the muscles and blood : Insufficient ex-
ercise in sedentary or invalid persons, etc. — insufficient oxygenation
and anoxemia among hyposphyxics, anemics, sedentary individuals
confined in rooms, etc.
2. From disturbances in various organs:
(a) Inadequacy of the digestive functions and gastrointestinal
dyspepsia. The fats, in this event, being insufficiently or not at all
converted, remain in the form of neutral fats which are less readily
oxidizable and accumulate more readily in the tissues.
(b) Insufficiency of the endocrin glands as a group, though
principally of the thyroid, thus unequal to their r61e as oxidizing or
fat-splitting glands.
The role of thyroid insufficiency in obesity is unquestionable, as
exemplified in the obesity of thyroidectomized animals, the obesity
of the earlier stages of myxedema, and the sometimes marked loss
of weight caused by thyroid administration.
The role of the reproductible glands is even more obvious, as in
the obesity of castrated animals (capons and hogs), the obesity of
eunuchs, and the obesity associated with ovarian insufficiency (Der-
cum's disease, obesity of the menopause, obesity after ovariectomy,
obesity of puberty in chlorotics with irregular menstruation, obesity
of the early months of pregnancy, etc.).
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1208 SYMPTOMS,
3. From disturbances of the nervous system. — This cause is
obvious at least in certain localized adipose states, such as Grasset's
nen'ous adiposis (Duchenne's pseudohypertrophic paralysis, sym-
metric lipomatosis, adiposis dolorosa or Dercum's disease, etc.).
It is probably present in certain forms of obesity associated
with other nervous symptoms (herpes zoster, joint disorders,
scleroderma, exophthalmic goiter, etc.).
4. From disturbed general nutrition:
(a) Neuro-arthriiic obesity, dependent upon a chronic general
nutritional disorder, usually inherited and associated or variously
combined with the several morbid states termed arthritis, with gout,
diabetes, lithiasis, etc. The word "neuroarthritic" is here used as an
accepted makeshift, without attempting to conceal the fact that, to
the author, arthritism is merely a nutritional symptom-group devoid
of specificity.
(6) Intoxications. — Certain intoxications, particularly of the
mild but repeated variety, lead to obesity. First place may here be
given to alcoholism, and after it come, in the order of decreasing
frequency, arsenic, phosphorus, and lead,
(c) Infections, — Those of greatest interest are the typhoid and
tuberculous infections. The increase of weight, sometimes exces-
sive, witnessed during convalescence of typhoid cases is a matter of
common observation. Tuberculous obesity — a less, exceptional con-
dition than is generally thought — is due to three factors, vis,, irra-
tional overfeeding (when it is readily curable, at least at first),
neuroarthritic heredity, and the complex action of the tubercle
bacillus itself or its toxins in certain forms of the disease and in
certain predisposed individuals (Carnot's experimental tuberculous
obesity).
If all clinical and experimental data are taken into account, it
becomes necessary, broadening our earlier conceptions of the patho-
genesis, to recognize that obesity is the outward expression of the
organic response to a lesion or functional disturbance at some point
in the lipotrophic nutritional system.
This lipotrophic nutritional system, which is extremely complex,
is governed and coordinated by the cerebrospinal and sympathetic
nervous system, which insures functional cooperation in this system ;
whence the possibility of a hyperadiposis of nervous origin through
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OBESITY. 1209
lipotrophic incoordination (the fact is clinically certain as regards
localized or symmetric hyperadiposes, and probable as regards
obesity). The system is mainly constituted of a group of glandular
organs, vis., the gastrointestinal mucosa, liver, pancreas, thyroid,
reproductive glands, etc., which are charged with the task of elab-
orating the fats and governing their conservation (lipogenesis) and
destruction (lipolysis), and overactivity or insufficiency of which,
constituting a lipodystrophy, induces obesity of glandular origin.
This lipolytic activity, however, though devolving especially on
certain organs or tissues, appears to be a functional attribute of
living cells in general, so that any general disturbance of cell nutri-
tion, while usually combined, indeed, with the above mentioned
glandular disturbances, may induce obesity: dystrophic obesity of
neuroarthritic or toxic-infectious origin.
Sometimes obesity is obvious. The most casual inspection
shows that the individual is too stout for his height. Such a
diagnosis, however, brings in too much of the subjective ele-
ment. A person is obese when his weight exceeds the normal
as compared to hi^ height. What is this normal weight? To
find out, one may turn to the tables prepared by Quetelet and
by Bouchard.
It is more convenient, however, to adopt the following
simple, elementary rule : The normal weight of an adult equals
in kilograms the number of centimeters by which his height ex-
ceeds one meter. Thus, 154 centimeter? = 54 kilograms; 165
centimeters = 65 kilograms; 172 centimeters ^^ 72 kilograms.
This rule and the tables mentioned are quite sufficient for
clinical purposes provided the following corrections required
because of individual peculiarities of physique are taken into
account. Human subjects may be roughly classed in three
groups :
Mediolinear: The average type, in which the transverse and
vertical measurements exhibit a mean, normal ratio:
Height
Biaxillary diameter
= 5.6 to 6.
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1210
SYMPTOMS.
Longilinear: An unusually elongated type, in which the vertical
measurements are manifestly excessive as compared to the
transverse :
Fig. 835. — Longilinear subject.
Height
>6.
Biaxillary diameter
Brezilinear: An unusually short type, in which the transverse
measurements are relatively excessive as compared to 'the vertical :
Height
Biaxillary diameter
<5.6.
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OBESITY.
1211
In medioHnear subjects the rule that the weight in kilograms
equals the number of centimeters over one meter is quite suffi-
cient in practical work. Example: 169 centimeters; normal
weight, 69 kilograms.
Fig. 836. — MedioHnear subject.
Fig. 837. — Brevilinear subject.
In longilinear subjects one should allow, in calculating the
normal weight, a reduction which may reach -\. Example : 169
centimeters (longilinear) ; normal weight, from 69 kilograms to
69 — -J|- = 62.1 kilograms.
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1212 SYMPTOMS,
In brevilinear subjects one should allow, on the other hand,
an excess which may reach JL. Example: 169 centimeters
(brevilinear); normal weight, from 69 kilograms to 69 +-^ =
75.9 kilograms.
After these corrections have been deliberately introduced, if
the subject's weight is distinctly above the theoretic weight, the
diagnosis of obesity may be rendered.
The only features that are of actual importance from the
practical standpoint are :
1. The type of obesity (plethoric or anemic).
2. Its association with some allied symptom-group:
(a) Gout, diabetes, or lithiasis.
{b) Hyposphyxia, polyglandular insufficiency, or dysthyroidia.
(c) Asthma, emphysema, or hay fever.
3. The presence of some complication which, as a matter of fact,
is a natural consequence in the course of the disorder.
(a) Cardiac or cardiovascular.
{b) Pulmonary or cardiopulmonary.
(c) Renal or zxisculorenal,
(d) Hepatic.
These are the data upon which the treatment of the case depends.
Clinical classification. — From the purely clinical standpoint
the following classification appears to be the best because it auto-
matically specifies the therapeutic indications — ^which is, after all,
the essential point Obese subjects may be divided into two dia-
metrically opposed groups:
Florid, plethoric, ftdl-blooded obese subjects.
Atonic, asthenic, anemic obese subjects.
In either of these two groups, obesity may exist in the pure
state, i,e,, without any associated morbid state or complication,
or it may occur in combination with the morbid syndromes
affiliated with it, or with complications. Thus, with all possi-
bilities taken into account, the following classification is offered
the clinician:
I. Simple plethoric obesity.
Plethoric obesity associated with gout, diabetes, lithiasis, etc.
II. Simple atonic obesity.
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OBESITY,
1213
1. Table Showing the Average Height and Weight at
Different Ages (after Quitelet)A
Age.
Males.
A.
Females.
Height.
Weight.
Height.
Weight.
0 year
1 year
2 years
3 .....
4 "
5 "
6 "
7 "
8 "
9 "
10 "
11 "
12 "
13 "
14 "
15 "
16 "
17 "
18 " .....
20 "
25 "
30 "
40 "
50 "
60 "
70 "
meters.
0.500
0.698
0.771
0.864
0.928
0.988
1.047
1.105
1.162
1.219
1.275
1.330
1.385
1.439
1.493
1.546
1.594
1.634
1.658
1.674
1.6»}
1.684
1.684
1.674
1.6,39
1.623
kilograms.
3.20
9.45
11.34
12.47
14.23
15.77
17.24
19.10
20.76
22.65
24.52
27.10
29.82
34.38
38.76
43.62
49.67
52.85
57.85
60.06
62.93
63.65
63.67
63.46
62.94
59.52
meters.
0.490
0.690
0.780
0.852
0.915
0.974
1.103
1.146
1.181
1.195
1.248
1.299
1.353
1.403
1.453
1.499
1.535
1.555
1.564
1.572
1.577
1.579
1.579
1.536
1.516
1.514
kilograms.
2.91
8.99
10.67
11.79
13.00
14.36
16.01
17.54
19.08
21.36
23.52
25.65
29.82
32.94
36.70
40.39
43.57
47.31
51.83
52.28
53.28
54.33
55.23
56.16 •
54.30
51.51
Atonic obesity associated with polyglandular insufficiency or
hyposphyxia.
III. Complicated plethoric or atonic obesity (with cardiac,
pulmonary, renal, or other complications).
It is true, to be sure, that the majority of these "complica-
tions" are absolutely certain to set in at some stage in the
course of obesity, if the latter is not corrected in time.
I. Simple plethoric obesity is characterized by a simple, ua-
complicated plethora. The plethoric is a supernormal individual all
of whose functions or other features are of the "hyper" variety,
but preserve a normal mutual balance. Thus, he exhibits over-
weight, hypertension, hyperviscosity, polyphagia, polydipsia, and
1 One meter = 39.370 inches. One kilogram = 2.20462 pounds Avoirdupois.
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1214 SYMPTOMS,
polyuria. He is a florid-complexioned, full-blooded, obese subject
whose digestive, nutritive, circulatory, urinary, and other functions
are of an exaggerated type but nevertheless very satisfactorily car-
ried out ; bodily vigor and the mental faculties are unimpaired.
It cannot be too often repeated, how^ever, that such a subject
is predisposed to the so-called neuro-arthritic disorders, z*ic^
gout, diabetes, lithiasis, etc., and a likely victim of connective
tissue deposit in the viscera, especially the arteries and kidneys.
This fact should be duly borne in mind when the diagnosis
is made, and the necessary precautions taken, even in the **minor
obesity" stressed by Heckel, for, as this observer correctly
writes: "It is ridiculous to wait, in order to obtain a suitable
label, until a person is deformed with fatty accumulations be-
fore warning him of the risk he is running."
Ovemutrition and an arthritic family tendency are generally
met with as etiologic factors in these cases.
Plethoric obesity is very frequently associated with gout, dia-
betes, and lithiasis, the pathogenesis of which seems to be closely
related to plethora. All plethoric obese subjects should therefore be
gone over carefully in this connection, being examined for evidences
of gout in the joints or internal organs, of diabetes (glycosuria),
and of lithiasis (high specific gravity, acidity, and uric acid con-
tent of the urine ) , and warned against these possible complications.
IL Anemic, atonic, asthenic obesity, on the other hand, is
manifested in a pale complexion and at times a waxy appear-
ance; the appetite is often poor, the digestive functions are im-
paired, constipation is frequent, bodily vigor is below normal,
indolence and apathy are habitual, the circulation is deficient,
hyposphyxia frequent, and the elimination of chlorides often
disturbed. All test features are of the "hypo" variety, Wr., hy-
potension, hypopepsia, etc., with the exception of the body
weight and viscosity, which are increased.
' In these cases the etiologic factors most often met with are
dyspepsia, anoxemia, intoxications, infections, and degeneration
of glandular organs, such as the thyroid and testicles. Typhoid
and tuberculous obesity belong in this category.
Anemic, atonic obesity, usually attended with slowed and vitiated
nutritive processes and circulation, is very frequently, if not always,
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OBESITY. 1215
combined with polyglandular insufficiency and hyposphyxia, for evi-
dences of which a systernatic search should always be made (goiter,
genital dystrophies, myxedema, etc., on the one hand; low blood-
pressure, high viscosity, lividity, cryesthesia, and dyspnea on exer-
tion, on the other). Highly serviceable indications concerning the
pathogenesis and hence also as to the treatment are thus obtained
III. Cardiac, renal, and pulmonary complications. — Either
one of the foregoing types of obesity may, and frequently does, be-
come complicated with other disorders. The heart, kidneys, and
lungs are the organs most frequently affected, and investigation of
these organs is therefore particularly necessary in all obese patients.
(a) Cardiorenal Disturbances. — Subjects with plethoric
obesity are, as already pointed out, likely victims of cardio-arterio-
renal fibrosis (arteriosclerosis and interstitial nephritis), which is
detected through blood-pressure determinations (hypertension) and
examination of the urine (albuminuria and lowering of the hydruric
coefficient — ) and the heart (hypertrophy, gallop rhythm).
Atonic obese cases are predisposed to venous stasis (varicose
veins and edema), to dilatation of the heart and cardiac insuffi-
ciency (tachycardia, low blood-pressure, dyspnea on exertion,
cyanosis, and reduced urinary output), and to chlorine retention.
Both types terminate in heart failure and uremia the result of
progressive cardiorenal inadequacy.
Heckel, in his book on obesity, was the first to lay stress on
the marked frequency of the chronic nephritides among the
obese, stating that "nearly all the obese are incipient uremics."
Marcel Labbe reached the following conclusions : "The ratio of
interstitial nephritis among the obese is 22 per cent, before the
age of fifty years and 77 per cent, after fifty years. This means
that in all old obese subjects renal sclerosis is almost inevitable."
The author of the present work has demonstrated the above-
mentioned relationship of the plethora of obese cases to chronic
hydremic (hypertensive) and azotemic (uremigenous) nephritis,
and has formulated rules, based on observation of the blood-
pressure, blood viscosity, and daily output of urine which en-
able the physician to discern the moment when patients are
passing from the sta^e of simple plethora to that of chronic
nephritis (see High blood-pressure).
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1216
SYMPTOMS.
(b) Pulmonary Disturbances. — Obese persons are exposed to
numerous complications:
Respiratory insufficiency, anoxemia, asthma, and emphysema
— almost constant features at a certain stage of obesity.
Active hyperemia, congestive attacks, and acute edema of the
lungs in plethorics, and more especially in the cardiorenal stage.
Passive hyperemia, edema of the bases of the lungs, and hy-
drothorax in the atonic cases and more especially in the stage
of cardiac insufficiency. In this group, as a matter of fact, a
cardiopulmonary trend of the disease is much commoner than
cardiorenal complication.
This diagnosis of the complications of obesity constitutes,
on the whole, in conjunction with the causal diagnosis, the essen-
tial feature in the diagnosis of obesity, and one should not wait,
to render it, until irreparable tissue lesions have set in. To wait
for the appearance of gallop rhythm before rendering a diagno-
sis of interstitial nephritis is like waiting for the police before
cutting down a man who has just been hung. As Heckel writes :
"It is not the amount of fat accumulated which allows of the
prognosis being made, but the intensity of the functional disturb-
ances accompanying the obesity, whether the latter be of the
major or minor variety."^
2. Height, Weight, Average Anthropometric Segments, Fat per
Segment, Fat in the Whole Body (after Bouchard).^
Height in
Weight of
Centim-
Weight in
THE Segment
Fat per
Fat in
eters
Kilograms
w.
Segment
THE Whole
H.
W.
H
in Grams.
Body.
140
45.81
3.27
425
5.955
141
46.66
3.31
430
6.066
142
47.50
3.35
435
6.175
143
48.36
3.38
440
6.292
144
49.18
3.42
444
6.394
145
50.05
3.45
449
6.506
146
50.88
3.49
453
6.614
147
51.73
3.52
462
6.725
148
52.58
3.55
462
6.835
1 For additional data on this question, see F. Heckel : Grandes et petites
ohesith, Masson, 2d Ed., 1920.
2 One hundred centimeters = 39.370 inches. One kilogram = 220462
pounds Avoirdupois.
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OBESITY.
1217
2. Height, Weight, Average Anthropometric Segments, Fat per
Segment, Fat in the Whole Body (after Bouchard), continued.
Height in
Weight of
Centim-
Weight in
the Segment
Fat per
Fat in
eters
Kilograms
W
Segment
THE Whole
H.
W.
H*
in Grams.
Body.
149
53.45
3.59
466
6.948
150
54.32
3.62
471
7.062
151
55.21
3.66
475
7.173
152
56.09
3.69
480
7292
153
56.93
3.72
483
7.401
154
57.78
3.75
488
7.511
155
58.64
3.78
492
7.623
156
59.50
3.81
496
7.735
157
60.38
3.85
500
7.849
158
6126
3.88
504
7.964
159
62.15
3.91
508
8.080
160
62.91
3.93
511
8.178
161
63.76
3.96
515 .
8291
162
64.61
3.99
518
8.392
163
65.46
4.02
522
8.509
164
66.26
4.04
525
8.610
165
67.06
4.06
528
8.712
166
67.79
4.08
531
8.815
167
68.55
4.11
534
8.912
168
69.30
4.13
536
9.005
169
69.98
4.14
538
9.092
170
70.69
4.16
541
9.197
171
71.38
4.17
543
9.285
172
72.07
4.19
545
9.374
173
72.78
4.21
547
9.463
174
73.48
4.22
549
9.552
175
74.11
424
551
9.642
176
74.77
4.25
552
9.715
177
75.40
4.26
554
9.806
178
76.04
427
555
9.879
179
76.77
4.29
558
9.988
180
77.42
4.30
559
10,062
181
78.08
4.31
561
10.150
182
78.73
4.33
562
10228
183
79.40
4.34
564
10.321
184
80.06
4.35
566
10.414
185
80.73
4.36
567
10.489
186
81.39
4.38
569
10.583
187
82.07
4.39
571
10.678
188
82.76
4.40
572
10.759
189
83.43
4.41
574
10.849
190
84.11
4.43
576 .
10.944
191
84.79
4.44
577
11,021
192
85.48
4.45
579
11.117
193
86.17
4.47
581
11213
194
86.85
4.48
582
11.291
195
87.48
4.49
583
11.372
196
88.06
4.49
584
11.446
197
88.81
4.51
586
11.544
198
89.32
4.51
586
11.603
199
89.87
4.52
587
11.681
200
90.40
4.52
588
11.752
77
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OLIGURIA r ^^^' scanty; oiJpor, wine; ]
' [diminished secretion of urine.]
In a normal adult person on a normal diet, the average daily
output of urine is from 1250 to 1500 cubic centimeters, the out-
put in the daytime, from 9 a.m. to 9 p.m. (750 to 1000 cubic cen-
timeters), being always distinctly greater than the nocturnal out-
put, from 9 P.M. to 9 a.m. (500 to 400 cubic centimeters).
Oliguria is present when the amounts excreted are distinctly
below the above mentioned average figures. Oliguria is said to
be total, diurnal, or nocturnal according as the reduction affects
the daily output or only that in the daytime or at night.
Diuresis being closely and obviously dependent both upon the
amount of water ingested either in beverages or in solid food and
upon the various excretions other than the urine (cutaneous, intes-
tinal, and pulmonary), many factors may, singly or in combination,
induce under physiologic circumstances a definite diminution of the
output of urine. Such factors should be thought of from the start,
in order that they may be excluded : Habitual restriction of fluids,
whether spontaneous or under the physician's direction (dry
regime) ; one should always ascertain approximately the intake as
well as the output of fluid ; spontaneous free szveats, as from violent
and sustained exertion or from summer temperatures (oliguria in
the summer is almost constant in normal individuals) ; free evacua-
tions of the bowels, spontaneous (transient diarrhea) or induced
(purgation), etc.
The foregoing brief and elementary inquiry having been gone
through, there remain:
1. Oliguria of a transient, temporary, accidental type.
2. Oliguria of a lasting, permanent, habitual type.
(1218)
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OUGURIA. 1219
TRANSIENT, TEMPORARY, ACCIDENTAL OLIGURIA.
After evacuation of an extensive collection of fluid, as in
cysts, ascites, or pleurisy, it is the rule to observe a distinct re-
duction in the amount of urine. An actual drainage of water
occurs toward the affected structures. The oliguria is less
marked at the time of spontaneous reabsorption of an exudate,
which process may instead be associated with a relative
polyuria.
In cholera, amebic and bacillary dysentery, infantile enteritis,
yellow fetter, cholera morbus, etc., intense oliguria may occur on
account of repeated, copious bowel movements, and the usual
presence of albumin in the urine indicates that even apart from
the withdrawal of water through the intestine the kidneys are
more or less affected by the existing toxic-infectious disorder.
In another group of cases, oliguria appears to be the consequence
of a reflex inhibition of diuresis, which may originate either in
the urinary system itself or elsewhere. Reference may here be made
to the reflex oliguria of renal colic, which involves not only the dis-
eased but also the opposite kidney ; to calculous anuria, which passes
off upon catheterization on the affected side, and to the oliguria fre-
quently induced by urethral and ureteral catheterization.
Peripheral stimuli, burns, traumatic injuries, neuroses such as
hysteria and neurasthenia, painful conditions {hepatic colic), peri-
tonitis, appendicitis, and laparotomy may, as is well known, like-
wise induce a temporary oliguria, with excretion of clear urine of
high specific gravity, of good concentration, and free of any ab-
normal constituents.
In a final group of cases, oliguria appears in the presence of
some infectious process, and this type of oliguria forms part, in
conjunction with the temperature and the quality and rate of
the pulse, of the most characteristic symptomatic triad giving
information as to the course of the infection. A moderate de-
gree of oliguria, with a full, regular, and moderately accelerated
pulse, and a temperature of varying height, but with good morn-
ing remissions, points to a favorable course and termination.
Excessive oliguria, with a frequent, small, irregular pulse and
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1220 SYMPTOMS.
sustained hyperthermia with but slight or no remissions, points
to the necessity of a very guarded prognosis.
Upon defervescence one observes a more or less marked out-
burst of polyuria, with emission of urine of high specific gravity,
poor in chlorides but rich in urates, phosphates, urea, urobilin,
pigments, etc., imparting to the highly colored urine, with its
abundant brick dust sediment, a highly characteristic appearance.
LASTING, HABITUAL, PERMANENT, OR AT LEAST
EASILY RECURRING OLIGURIA.
Of far greater import from the standpoints of semeiology
and treatment are the lasting, habitual or recurring forms of
oliguria. The major systems most frequently responsible are
the circulatory and renal systems. Oliguria is one of the cardi-
nal evidences of cardiorenal inadequacy, and the heart and kid-
neys are always the organs to be investigated above all else in
these cases.
Cardiac insufficiency. — Reduced urinary output is, mith dyspnea
on exertion, one of the earliest signs of incipient cardiac inadequacy,
hyposystoly, or circulatory decompensation. One cannot emphasize
too strongly the following fundamental features: The output of
urine is dependent upon renal permeability (and more probably,
glomerular permeability) and upon the blood-pressure (especially
the differential or pulse pressure). Where compensation for the
cardiac or renal or cardiorenal disorder has been lost; when the
cardiac fiber, no longer equal to its task, shows signs of becoming
fatigued, the kidney, no longer receiving blood under the required
degree of pressure, becomes oliguric ; if, however, the heart is alone
at fault, the urine is more markedly reduced in amount, but is of
high specific gravity, well concentrated, and free of foreign con-
stituents.
For a long time, as a matter of fact, oliguria is manifest only
when the patient is in the standing posture {orthostatic oliguria),
and is counterbalanced by the relative polyuria existing when he is
recumbent (clinostatic relative polyuria, or nycturia), so that in the
earliest stages, diurnal oliguria is compensated for by nocturnal
polyuria, and the daily intake and outgo of fluid are in equilibrium.
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OLIGURIA. 1221
Gradually cardiac decompensation becomes more marked, and
with it appear continuous total oliguria, permanent and paroxysmal
dyspnea, edema, hypostatic congestion of viscera, cardiac insuffi-
ciency, and cardiac failure. The importance of watching the out-
put of urine in heart disease and its value in connection with the
prognosis and treatment are well known; the urine graduate
serves in such cases as does the thermometer elsewhere.
Oliguria of cardiopulmonary origin. — Whether primary or
Secondary, decompensation or cardiac insufficiency is sooner or
later complicated with stasis in the pulmonary circulation, anox-
emia, hyposphyxia, and even asphyxia; the viscosity of the blood
rises in the absence of any compensatory ascent of blood-pres-
sure, renal stasis becomes more mark^ on this account, and
consequently, oliguria increases.
As is well known, an opposite sequence of events may occur
instead, some respiratory disorder, such as chronic bronchitis,
emphysema, capillary bronchitis, etc., bringing on cardiac in-
sufficiency and the syndrome of cardiopulmonary insufficiency
causing oliguria.
So long as the kidneys remain uninvolved, the urine remains
scanty, of high specific gravity, deeply colored, and highly con-
centrated.
Oliguria of cardiorenal origin. — Participation of the kidneys
in the reduction of urinary secretion is shown by a definite, pathog-
nomonic sign: The ratio of the absolute daily output of urine to
the number of centimeters of mercury of differential or pulse pres-
sure, as determined with the Pachon instrument, shows a reduction.
In a normal subject this ratio (of the daily output of urine, H, to
the differential pressure, p) is equal to or exceeds 250. In a subject
with interstitial or congestive renal involvement it is below 200 (law
of Martinet).
Simultaneously there are observed to appear more or less
rapidly :
Either the evidences of hydremic, hypertensive nephritis —
high blood-pressure, low viscosity, hydremia, gallop rhythm,
hemorrhages, false polyuria with elimination of urine of low
specific gravity, a slight degree of albuminuria, etc.
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1222 SYMPTOMS.
Or those of uremigenous nephritis — headache, dyspnea, som-
nolence, excess of blood urea, etc.
Or those of hydropigenous nephritis— ed^ma, serous exu-
dates, diminished chlorides in the urine, etc.
Or the combined indications of a pan-nephritis, combining
in greater or less degree the above several deficiencies of renal
functioning.
In some instances — in fact, generally — this primary renal im-
pairment, relatively well compensated for a varying period of
time through compensatory cardiac hypertrophy, becomes as-
sociated with evidences of heart weakness only in a relatively
late stage.
In other instances the heart weakness is primary and the
renal inadequacy secondary.
Present methods of determining the functional capacities of
the heart and kidneys ordinarily yield sufficient information as
to the comparative parts played by the two symptoms, and such
information is of far more than mere academic interest, since it
gives a clue to an efficient line of treatment.
Oliguria of cardiopneumorenal origin. — In the final stage of
cardiac, pulmonary, or renal disease, the disorder is no longer
limited to the heart, lungs, or kidneys. A combined insufficiency
of these major systems, closely united as they are through the
circulation, exists. There is present a cardiopneumorenal in-
sufficiency : Heart failure, asphyxia, and uremia are conjointly
operative, each engendering and aggravating the others, and an
extreme degree of oliguria is produced. But however serious —
and frequent — such a condition may be, it is not necessarily
fatal, at least at the outset. Active, energetic, and judicious treat-
ment often insures to sucb patients an additional more or less
prolonged lease of life.
Oliguria of hepatic origin. — Hepatic obstruction is likewise a
factor in the production of lowered urinary excretion, and in diflfer-
ent ways, vie, through high pressure in the portal circulation and
abdominal venous stasis, and through pressure upon the vena cava
above the renal veins and passive hyperemia of the kidneys.
Oliguria of hepatic origin is known sometimes to show the char-
acteristic feature termed opsiuria, or delayed excretion of ingested
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OUGURIA. 1223
fluid, of which clinostatic polyuria (nocturnal polyuria or nycturia)
is, as a matter of fact, merely one variety.
Oliguria of renal origin is also deserving of some considera-
tion.
The oliguria of rend congestion, constantly present in acute
nephritis, is generally accompanied, at least in the more serious
cases, by severe lumbago with dense, highly-colored, albuminous,
and acid urine, yielding a sediment containing more or less dis-
organized red blood cells and exhibiting renal epithelia, granular
and blood casts, etc. It may be the result of poisoning by a drug,
typically cantharides, of an infection, as in beginning grippe with
backache, or of an autointoxication, as exemplified in gout.
In gouty nephritis, the marked accumulation of urates along the
uriniferous tubules checks diuresis and may induce renal congestion
and oliguria, which may in turn progress to complete anuria.
Hyperemia of the kidneys may find its expression in the course
of chronic renal disorders in the appearance of a more pronounced
oliguria.
A separate place in the classification should be made -for
oliguria with cloudy urine, whether the latter contains an excess
of readily deposited crystalloid compounds, such as phosphates
and carbophosphates, blood cells that have passed out from the
vessels during acute hyperemia, or pus.
Oliguria with cloudy urine containing pus may follow or even
alternate with cloudy polyuria. Polyuria is, as is well known, a
customary reaction of the kidney to extrarenal urinary infection, as
in prostatic hypertrophy, cystitis, or pyelonephritis; in these cases
the urine is of low specific gravity and low in urea and chlorides.
Cloudy oliguria following cloudy polyuria indicates that extension
of the infectious process to the kidney itself has occurred, nephritis
following pyelonephritis.
At times, in some cases of nephritis, the urine becomes
cloudy owing to the passage of pus and blood cells into it; un-
der these circumstances, either the kidney has undergone certain
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1224 SYMPTOMS.
changes owing to the toxic effect of faulty metabolism, or the
changes in it are of infectious origin. In the former event, the
urine is readily rendered clear by dietetic measures; in the
latter, its cloudy condition is harder to overcome.
Bacteria may harm the kidneys either directly (in situ), or in-
directly through the action of their toxins and altered metabolism.
Tuberculous infection affords many instances of this kind ; outside of
what is properly termed tuberculous nephritis, there are many cases
in which tuberculous disease of the lungs, intestine, or even the
joints leads to the appearance of the signs of nephritis with reduced
output of cloudy urine — and sometimes slight hematuria— even
though no tubercle bacilli can be found at the time by the most
advanced methods ; tuberculosis of the kidneys often sets in in this
manner.
Later, the urine, reduced in amount, becomes .increasingly
cloudy through secondary development of many varieties of
germs, especially the colon bacillus, in a kidney with lowered
powers of resistance.
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PAIN IN THE SIDE.
The expression "pain in the side" is not infrequently used to
designate acute pains in the region of the chest which may be
compared to those induced by the impact of a pointed instru^
ment in this vicinity. This is a common symptom in many
thoracic affections, yet one which may be practically pathogno-
monic in pleurisy and pneumonia.
For practical purposes it is convenient to group such "pains
in the side" into those of visceral origin and those of parietal
origin.
Thoracic pain of visceral origin is typically referable to the
pleura or lung.
Pleurisy is a common cause of such pain.
Acute serofibrinous pleurisy induces, in general, a rather diffuse
pain, sometimes extending over an entire half of the thorax, of
variable intensity, and increased by cough, deep inspiration, sneez-
ing, and often by motion and lying on the affected side. It inter-
feres with the breathing, which becomes more superficial. The
usual signs of pleurisy should be examined for, vis., dulness, loss
of fremitus, muffled breath-sounds, egophony, etc. ; in the event of
doubt, exploratory puncture will settle the diagnosis.
Suppurative pleurisy, aside from the usual signs of pyemia, in-
cluding the severe constitutional disturbance and the special charac-
teristics of the temperature curve, is sometimes marked by a more
superficial location of the pain and greater sensitiveness to digital
pressure. Here again exploratory puncture will eliminate all un-
certainty.
The advent of pneumothorax is generally marked by a sharp,
intense, sudden pain, almost causing syncope and attended with ex-
treme dyspnea.
Pain is most violent, however, in diaphragmatic pleurisy, caus-
ing the patient to cry out and literally cutting short his respiration.
(1225)
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1226 SYMPTOMS,
Figs. 838 to 841. — Anterior, posterior, and lateral topographic fea-
tures of the chest, showing the pleural culs-de-sac and the interlobar
fissures.
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PAIN IN THE SIDE. 1227
The pain is situated lower down than in ordinary pleurisy. The
five cardinal points of tenderness emphasized by Peter and Gueneau
de Mussy should be investigated in these cases:
1. Between the two heads of the sternocleidomastoid.
Fig. 842. — Relations of the heart as shown in a horizontal section
through the chest of a new-born infant (Poirier). a. Right auricle, b.
Left auricle, c. Right ventricle, d. Left ventricle, e. Phrenic nerve. /.
Elsophagus. g. Aorta, h. Vena azygos.
2. Along the border of the sternum in the upper costal in-
terspaces.
3. The diaphragmatic point, at the junction of the sternal
line (right or left sternal margin) and the line of prolongation
of the bony portion of the tenth rib.
4. The insertions of the diaphragm at the base of the thorax.
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1228 SYMPTOMS.
5. The spinous processes of the upper cervical vertebrae.
These points, which constitute, 'as a matter of fact, the
points for stimulation of the, phrenic nerve, are of service, ac-
cording to Peter, not only to ascertain the condition of the dia-
phragmatic pleura but also that of the peritoneal covering of
the diaphragm.
Interlobar pleurisy is marked in particular by "fissured points"
which Sabourin describes as follows : "On either side, at the level
where the third and fourth ribs mark the beginning of the chief
Fig. 843. — Anatomic relations of the intercostal nerves.
fissure, is the vertebral point; at the anterior end of the chief fissure,
at about the sixth rib, is the antero-inferior point. In addition, on
the right side, owing to the differentiation of the middle lobe, there
is a post-axillary point corresponding to the beginning of the hori-
zontal secondary fissure and an antero-superior point corresponding
to the axillary end of this secondary fissure. These are actually the
only marginal foci of clinical interest."
At these points there is spontaneous pain, which is accentu-
ated by motion, deep inspiration, coughing spells, etc.; pain is
also induced by digital pressure.
Special mention should be made of localised dry pleurisy in the
precordial cul-de-sac, giving rise to a precordial painful point and
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PAIN IN THE SIDE. 1229
frequently attended with angor, dyspnea, and premature beats — in
short, with pseudocardiac neighborhood manifestations. Careful
and accurately directed auscultation elicits characteristic friction
sounds corresponding with the respiratory movements; one might
at times be in doubt as to the possible presence of dry pericarditis,
Figs. 844 and 845.— Head's zones.
which may, indeed, be combined with the pleural disturbance (see
Precordial pain).
Inflammatory conditions of the lung likewise induce pain in
the side. Whether the disturbance present is pneumonia or tuber-
culosis, these inflammatory states are very often in the nature of a
pleuropulmonary "corticalitis," and the pleura participates, as al-
ready mentioned, in the production of the pain.
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1230 SYMPTOMS,
Acute frank lobar pneumonia represents the type of the diseases
attended, with pain in the side. The pain is generally more violent
and situated more anteriorly (often in the nipple line), more
"stabbing," and hence more intolerable than that of pleurisy. It is
Figs. 846 and 847. — Head's zones.
usually accompanied with a marked chill, followed by a rapid rise
of temperature, which lead the physician to look for the usual local
evidences of pneumonia (dulness, exaggerated fremitus, bronchial
breathing, crepitant rales, and characteristic sputum), the appear-
ance of which is, however, often postponed until much later, par-
ticularly in central pneumonia. In the latter form, the disease
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PAIN IN THE SIDE.
1231
;CS.
;*^
sometimes takes several days to reach the cortex and to become
objectively noticeable through manifest auscultatory signs.
As is well known, however, this "dra-
matic" onset is lacking in aged subjects,
in whom one should arbitrarily look for
the signs of pneumonia, often practically
latent; the same is true, but for opposite
reasons, in children.
Congestion of the lungs and broncho-
pneumonia may, in a varying degree, give
rise to variously situated pains in the
chest.
The old-fashioned notion of a "chest
flux" (fluxion de poitrine) had to do with
an inflammatory condition in the chest
involving both the muscles (pleurodynia),
the nerves (neuralgia), the pleura (pleu-
risy), and the lung (pneumonia, inflam-
matory congestion). While this syn-
drome is not specifically dealt with in our
text-books, it certainly occurs clinically.
An investigation of "pains in the side"
is especially indicated in pulmonary tuber-
culosis. Such pains occur under two
entirely different circumstances: 1. In
connection with acute pneumonic and bron-
chopneumonic attacks (with especial in-
volvement of the apex), in which they are
not notably different from the pains of
ordinary pneumonia and bronchopneu-
monia.
2. In a practically permanent and chrOnic
form, in any stage of the disease, even
when latent. The pain is sometimes spon-
taneous and intermittent, but is nearly
always induced or augmented by pressure
upon or percussion over the supraclavicular and supraspinous
regions, corresponding to the apex of the lung. It is undoubtedly
./i"
\
\
,\
Fig. 848.— Sesni^ental
cutaneous distributions
of the nerves of the
trunk (after Head).
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1232 SYMPTOMS.
due to a plcuro pulmonary corticalitis or apical plctiritis, which is
practically a constant accompaniment of tuberculosis.
Lastly, pneumothorax likewise begins with a sudden, severe pain
in the side, generally starting in a coughing spell or upon exertion,
situated in the vicinity of the inferior angle of the scapula or the
I ntercostohumeral
cut. br. of II N.
Lat. cut. br. of II N cut. br. of I N.
Lat cut br. of III N.
N. to serratus magnua
\.nt. cut br. of VI N.
Int cut br. of X N.
Lat. cut br. of XII N.
I lumbar N.
nguinal
Fig. 849. — Cutaneous branches of the intercostal nerves (after Poirier).
nipple, and accompanied by severe dyspnea with marked accelera-
tion of the respiration. Tympany, loss of vocal fremitus, disap-
pearance of the vesicular murmur, sometimes amphoric breathing,
the coin test, metallic tinkle, and the usual history of tuberculosis or
emphysema (though sometimes wholly negative in this respect),
generally permit of a rapid diagnostic decision in these cases.
Various abdominal affections, especially subdiaphragmatic
disorders, may give rise to pain in the side. Mention need here
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PAIN IN THE SIDE, 1233
only be made of the right scapular point in gaJl-stones, the left in-
ferior thoracic and precordial points in flatulence and especially in
aerophagia, and the right or left inferior thoracic points encountered
in the different varieties of subdiaphragmatic abscess.
Thoracic pain of parietal origin may arise from any one of
the several layers of tissue constituting the thoracic wall :
1. The skin, in which herpes zoster may occur as an outward
expression of a deep-seated nervous disturbance.
2. The muscles, inflammation of which causes pleurodynia, or
pains accentuated particularly by motion or palpation of the muscles
concerned; pains diffuse in distribution, involving muscular rather
than nervous structures, or at least exhibiting neither the character-
istics nor the distribution of intercostal neuralgia.
3. The bones — ribs and spinal column : Osteitis, osteoperiostitis
(generally tuberculous or specific), or chondrostemal or costoverte-
bral osteoarthritis, actually giving rise rather to a locali/ed area of
painful exacerbation on pressure than to a true "pain in the side."
Involvements of the spinal column will be briefly considered below.
4. The nerves. — (a) Intercostal neuralgia, outlining a costal
interspace with the three classic Valleix's points of hyperesthesia:
1. Posterior, just lateral to the corresponding spinous process. 2.
Intermediate, in the axillary line. 3. Anterior, slightly lateral to
the sternum.
(&) Herpes zoster (zona; shingles), referred to above as a skin
manifestation, is as a matter of fact **a neuralgia-neuritis with neur-
itid or nervous (nerve), radicular (ganglion), or segmental (hori-
zontal zone) distribution, and with herpetic vesicles forming a burn-
ing half-girdle" (Grasset).
(c) The pseudoneuralgia (neuritis) of Pott's disease, of verte-
bral cancer, of vertebral spondylitis, of aneurysm of the abdominal
aorta, and of cancer cases uithout spinal involvement, is generally
bilateral and associated with hyperesthesia and accentuation of the
pain by percussion of a definite vertebral zone.
5. Lastly, in the spinal cord, tabes and dorsal meningomyelitis
may give rise to girdle pains or to thoracic constriction with or
without lightning pains, gastric crises, and the usual signs of tabes
(Argyll-Robertson pupil, ataxia, astasia, loss of knee-jerks, etc.).
78
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1234
SYMPTOMS.
Exceptional cases. — One cannot conclude a discussion of the
symptom, "pain in the side/' without referring to Head's cones of
cutaneous hyperesthesia. Head showed that in many disorders of
internal organs investigation of skin sensitiveness demonstrates the
existence of corresponding, well-defined hyperesthetic (hyperal-
gesic) zones, and on the basis of natural sequence and reciprocity,
concluded that the observation of such a zone erf hyperalgesia in
any given case definitely means the existence of some disturbance
of the underlying deep organ. His conceptions do account for
many otherwise inexplicable pains and are of considerable service
in the clinical study of many more or less latent affections of
viscera. It seems advisable, therefore, to recall here the various
associations of skin regions to the viscera of the chest and ab-
domen, as established by Head. Through their agency the author
has frequently been enabled to announce the existence of other-
wise completely latent foci of inflammation in the pleura and lung.
The subject appears of sufficient practical importance to war-
rant the reproduction in extenso from Head of a complete table
showing the areas of pain referred to the skin surface from vis-
ceral disease.
Table Showing the Relationships Between the Thoracic and Abdominal
Viscera, the Spinal Segments, and the Peripheral Nerves of the
Trunk. (After Head, in Poirier's "Anatomy.'*)
[The question marks following certain pairs of nerves in the table are
intended to call attention to the fact that the transmission of pain does
not occur constantly in the field of distribution of these nerves].
nbrye8 along which pain is
Orqans. rbfbrrbd to the pabibtes in
VISCERAL DISEASE.
Remarks.
Heart and aorta
Lungs
In angina pectoris the referred pain
extends down the arm to the area of dis-
tribution of Di, D2, and D3, and also in
the thoracic region in the segments D5,
De. D7, Dg, and D9.
The pain in pneumonia is more •espe-
cially localized in the 4th and 5th costal
interspaces; collaterally the area of re-
ferred pain may extend into the segmen-
tal distributions De and D7.
Esophagus
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PAIN IN THE SIDE.
1235
NERVES ALONG WHICH PAIN 18
OBOANS. RBrEUBED TO THE PARIETES IN
VISCERAL DISEASE.
REMARKS.
I Cardiac
p;.rc"
region
Small and large in*
testine
Xiphoid point and spinal point in gas-
tric ulcer.
Dorsolumbar pain in cancer of the in-
testine or mesentery.
Rectum
Liver
Gall-bladder
Kidney and renal
pelvis
Ureter
Muscular
layer . .
Bladder
Mucous
layer .
In gall-stones pain is referred mainly
in the 8th and 9th costal interspaces, less
frequently in the 9th and 10th.
Girdle pains in malignant disease of
the kidney.
Girdle pains and pain referred toward
the nerves of the lumbar plexus in neph-
ritic colic.
Y Dorsolumbar pain in cystitis.
I Pain the result of irritation by foreign
f bodies (stones, etc.).
Uterus
Body .
Cervix
Testicle or ovary
Dorsolumbar pain in parturient women.
Dio
}Pain due to inflammatory states and
tumors of the cervix.
(Dorsolumbar pain in tumors or tuber-
culosis of the reproductive glands.
Referred girdle-pain in cysts of the
ovary.
Epididymis | ^^ I Dorsolumbar pain in orchitis, epididy-
Fallopian tube | V^^ f mitis, or suppurative salpingitis.
f ^" f sf ?
Prostate j D12 and j ^
^ ^^ I S3
r>i^„^o- o«^ ^«^; f Referred pains extend along the course of the
fnn^Tim \ Peripheral nerves, and are associated with deep-
loneum ^ seated pain confined to the area actually involved.
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PLETHORA. InXrideLv, to be full]
The terms "plethora" and "plethoric," freely used in the clin-
ical medicine of olden times, are not to be found in the standard
treatises and text-books published in the course of the last forty
years. In this fact lies one of the inevitable weaknesses of the
prevailing nosology, which, soundly based as it was upon the
pathologic conception of a certain clinical picture corresponding
exactly to a certain definite organic lesion, found itself com-
pletely at a loss when required to classify correctly the func-
tional symptom-complexes attendant upon morbid physiology.
It was obliged to yield, unwillingly, in some instances, and at-
tempted to associate a symptom-group with a definite lesion — not
always, nor even frequently, succeeding in its endeavor. One
need merely recall the countless "lestonal" theories of angor pec-
toris, such as the neuritis theory and the theories of coronary
arteritis, of aortitis, of myocarditis, etc. As for certain other
conceptions, such as the morbid temperaments, constitutional
morbid predispositions, the "preorganic" stages of various dis-
eases, and the "boundaries of the disease," according to Heri-
court's very justifiable expression they were deliberately jetti-
soned from the nosological field as it was formerly accepted.
This opposition between that which the author has deliber-
ately— and without overlooking the inaccuracy of the terms
when taken in the strict sense— designated as functional nos-
ology and the realm of lesional or organic nosology accounts in
part for the frequently recorded lack of harmony between hos-
pital practice and private practice. Hospital practice deals al-
most exclusively with lesional cases suflFering either from acute
disorders or from chronic, long-standing, lesional, inveterate, in-
curable disorders that have reached the stage of organic decom-
pensation, such as advanced tuberculosis, arteriosclerosis, inter-
stitial nephritis, cirrhosis of the liver, tumors, etc. Private prac-
(1236)
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PLETHORA, 1237
tice, on the other hand, deals chiefly with functional cases suf-
fering from morbid affections. or tendencies of relatively recent
advent and generally curable, such as pretuberculosis, hypo-
sphyxia, plethora, transient or mild forms of cardiorenal insuffi-
ciency, active or passive congestion of the liver, etc. Hospital
medicine, which hitherto has afforded the most clearcut material
utilized in standard systems, deals mainly with extreme forms
of disease, very often perfectly established and with highly de-
finite outlines. Private practice generally supplies for the physi-
cian's observation incipient clinical types, an infinitely greater
range of abnormal conditions, and morbid tendencies sometimes
as yet barely outlined; yet any one can see that it is precisely
upon the detection of these premonitory stages of presclerosis,
of pretuberculosis, of cardiac, renal, or hepatic insufficiency, etc.,
latent or incipient, that the efficacy of our therapeutic endeavors
depends.
A concise consideration of plethora will illustrate this assertion
as a concrete clinical example.
Plethora {Tdkri^is^^ from TtXyjOeiv, to be full) constitutes a
very distinct and common clinical type. In its simple, uncompli-
cated form, it strikes the eye by virtue of the subject's flourishing,
often ruddy, supernormal, "overfilled,*' "plethoric" appearance^
The plethoric subject is, in truth, by no means a sick person in
the ordinary sense of the term ; on the contrary, apart from certain
minor, intermittent ailments such as skia disturbances, hemor-
rhoids, etc., he enjoys a flourishing, seemingly perfect state of
health ; he even shows an unusual functional activity character-
istic of more intense vitality ; he is polyphagic and his digestive
functions are admirably carried out (as, indeed, they are in dia-
betic, gouty, and obese subjects) ; he is polydipsic and polyuric
(like the diabetic and gouty) ; his skin is ruddy and his general
appearance robust ; without his being actually obese, his weight
is nevertheless above the normal (96 kilograms with a height
of 187 centimeters, 74 kilograms to 166 centimeters, etc.) ; his
powers of endurance are great; he is unusually active and the
amount of work he does may be far above the average (as in
many gouty and diabetic individuals).
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1238 SYMPTOMS.
In short, in the absence of any sort of illness on his part,
one would almost be apt to state that the plethoric is a super-
normal person or "superman" from the standpoint of body
physiology. His more powerful, hypertrophied heart contracts
more forcibly, leading to an unusually high systolic and differ-
ential blood-pressure. His blood, more rich and less dilute,
exhibits a higher viscosity and frequently an enhanced number
of blood cells. His kidneys, adapted to more active circulation
and nutrition, excrete unusually large amounts of water, salt,
urea, uric acid, etc., and of urine, which often shows high acidity
and high specific gravity. His digestive glands, copiously sup-
plied with blood, produce unusually laxge amounts of secretion,
causing polyphagia, polydipsia, polyuria, plethora, etc.
The plethoric subject is thus not, strictly speaking, an abnor-
mal, but rather a supernormal individual, clinically characterized
by his flourishing appearance, his supernormal body weight, and
his high blood-pressure and blood viscosity.
He is predisposed, however, to obesity, to diabetes, to gout,
and to urinary lithiasis, of which he already presents certain typ-
ical features as regards body conformation and functionation.
He is predisposed to the development, sooner or later, of cardio-
vascular-renal fibrosis. The chief advantage, indeed, of 'a diag-
nosis of true plethora founded on the symptomatic triad, over-
weight, high blood-pressure, and high viscosity (with their corol-
laries, high urinary acidity and specific gravity), is that it points,
long before any recognized and ordinarily listed morbid mani-
festation has appeared, to the presence of an abnormal tendency
which, at the time, is still susceptible of relatively easy correc-
tion before any irreparable organic change has become estab-
lished (see High blood- pressure).
In over one-half of all cases of plethora duly substantiated by
the presence of overweight and high blood-pressure and viscosity,
the plethoric state will be found associated with a recognized
metabolic disease, inc., diabetes (see Glycosuria), obesity (q.v.),
gout (see Joint pains), or urinary lithiasis (see Lumbar region,
pain in).
Plethora constitutes, furthermore, a premonitory stage in
arteriorenal fibrosis or arteriosclerosis, which it precedes, heralds.
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PLETHORA, 1239
and elaborates. When the, plethoric subject has exhausted the
cardio-arterio-renal reserve powers which have up to that time
maintained and insured his abnormally high level of physiologic
performance, he passes gradually into a stage of angiospastic pre-
sclerosis, during which he experiences intermittent attacks of renal
insufficiency with retention, clinically expressed in paroxysmal high
blood-pressure, hydremia, and their consequences — anginose
pains, suffocative sensations, pseudoasthma, transient reduction of
urinary output, etc. If this condition of presclerosis, which is
still in large measure a reducible condition, is not set right, a
definitive and practically irremediable arteriorenal sclerosis becomes
established. The subject is no longer merely a patient, but a per-
manent invalid.
The foregoing concise account will have set before the reader
the prime importance of the syndrome, plethora, which, correctly
interpreted and treated, will obviate in many instances an other-
wise refractory condition of general tissue deterioration. ^
ipor further details, see Martinet: Pressions artirielUs et viscositi
sanguine, Masson, 1912 ; Clinique et thSrapeutique circulatoires, Masson, 1914,
and in the present work, the section on High blood-pressure.
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POLYURIA. [7toXi;$, much; oipov, urine.]
The first thing to do in a patient who states that he passes
much urine or in whose case there is reason to believe that
polyuria exists is to make sure that the condition is actually
present. Many patients confuse the terms frequent urination (pol-
lakuria) and free urination (polyuria). As a matter of fact, no
necessary and intimate relationship exists between these two mani-
festations. The practitioner should therefore have the patient
carefully and systematically collect the twenty-four hour urine in
one or more two-liter (or two-quart) containers. Polyuria can-
not be said to exist unless the twenty- four hour output (e,g., from
8 A.M. to the following 8 a.m.) materially exceeds 1.5 liters, which
is the normal average amount in an adult on a normal diet. The
average degree of polyuria which is by far the most frequently
met with is that ranging between 1.750 and 3 liters. In exceptional
instances, such amounts as 4 to 6, 8, 10 liters, or even more, have
been and are encountered.
Little space will be devoted to the subject of induced polyuria,
whether of physiologic origin and due to spontaneous ingestion of
fluid in large amounts, as in polydipsic subjects, or of therapeutic
origin, in conformity with the physician's orders. Where this form
of polyuria exists care should be taken at least to ascertain s^proxi-
mately the total amounts of fluid ingested and of urine excreted.
Only by a comparison of these two amounts can a reliable conclu-
sion be reached as to the eliminatory power of the kidneys as
regards water (see Functional examination of the kidneys: In-
duced diuresis).
This applies to plethoric subjects ; they eat much food and drink
much fluid and consequently pass a large volume of urine, and if a
careful comparison of their ingesta and excreta is made, a satis-
(1240)
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POLYURIA. 1241
factory balance between the two is noted. Their urinary output
per centimeter of differential or pulse pressure is, moreover, nor-
mal, zfis., 250 cubic centimeters (see High blood-pressure).
Polyuria following injections of saline or glucose solutions, the
administration of diuretic agents, or the institution of other
diuretic measures likewise presents an obvious exciting cause, but
should stimulate the physician to record accurate and carefully
made observations such as will ultimately permit of our formulat-
ing a practical and rational system of pharmacodynamics as related
to the diuretic agents.
♦ ♦ ♦
Spontaneous, accidental, temporary polyuria is met with par-
ticularly under two well-defined conditions :
1. After paroxysmal nervous attacks, especially among hys-
teric subjects, epileptics, and exophthalmic goiter (post-hysteric,
post-epileptic, and hyperthyroid polyuria), and even after ordi-
nary spells of nervous excitement among naturally "nervous"
subjects, ue., persons with unusual, excessive nervous reactions
to stimuli.
2. In the critical stage of febrile diseases and more particu-
larly in the stage of resolution in pneumonia, influenza, broncho-
pneumonia, pleurisy, etc. In these it constitutes, as a rule, a
favorable prognostic sign of the greatest importance and which
generally marks the change of trend of the disease from a fatal
to a favorable termination.
The foregoing types of polyuria are, as will have been noticed, of
considerable practical importance, but those to follow are far
more significant still.
Spontaneons, habitnal, chronic, or at least recurring, polyuria.
— The most commonly encountered forms are those of renal fibro-
sis (interstitial nephritis), diabetes, and chronic diseases of the
urinary tract. The several different forms may be intermingled,
but ordinarily they are completely dissociated and their recogni-
tion is easy, rapid, and elementary.
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1242 SYMPTOMS,
1. Polyuria in renal fibrosis (interstitial nephritis). — ^The
patient is of ripe or advanced age. Usually he has a moderate
degree of polyuria (1800 to 2000 cubic centimeters), with pol-
lakuria and nycturia. The urine passed is light colored, of low
specific gravity (1014 or less), with small proportions of urea and
chlorides, and traces of albumin, frequently so small as to pre-
clude determination, or even entire absence of albumin.
Sometimes, and even often, the polyuria is accompanied by
the ordinary signs of arteriosclerosis : Cardiac hypertrophy, ac-
centuation of the second sound at the base, or even gallop rhythm,
together with sinuous or sometimes actually hardened peripheral
arteries; at a more advanced stage: Hemorrhages in various
situations, as in the retina, from the nose (epistaxis), etc.
There exists, furthermore, a sign which in the author's view
is pathc^nomonic of renal fibrosis in the stage of eusystoly, i.e,,
of adequate cardiac compensation. In this stage there is always a
high systolic pressure, a high pulse pressure, and also frequently a
high diastolic pressure. Determination of the quotient ^ of the
actual twenty-four hour output of urine, H, over the pulse pressure,
p, as estimated with the Pachon instrument in the sitting patient
in the later morning hours or in the afternoon, yieldst in the
normal subject a^ result equal or superior to 250 cubic centim-
eters. In the patient with interstitial nephritis the same cal-
culation yields constantly and permanently a result more or less
inferior to 250 cubic centimeters, and the lower the figure, the
more pronounced the process of sclerosis. By accident and in a
strictly transient m.anner, such a figure may be recorded in an
angio-spastic case, but- never lastingly and permanently.
2. Polyuria in diabetics. — The patient is generally in middle
adult life and presents a flourishing appearance. The pol3ruria is
usually more marked than in interstitial nephritis, amounting to 2
liters or more. The urine is more highly colored, and at times even
deeply tinted; it is always of high specific gravity, viz,, 1020 or
above, 1030, 1034, etc. Whether glycosuria is present or absent,
this feature alone is almost sufficient to differentiate the polyuria
of low specific gravity of nephritis from the diabetic polyuria
with high specific gravity.
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POLYURIA. 1243
(a) In 9 cases out of 10 there is glycosuria, signifying diabetes
mellitus, the cause of which is thereupon to be sought.
(b) In 1 case out of 10 glycosuria is absent, but there is excess
of nitrogen, of chlorides, of phosphates, etc. In this event the
condition is termed diabetes insipidus, and in this connection one
is confronted with one of the more complex aspects of polyuria,
since it borders on the condition known as renal hyperpermeability
— a syndrome exactly opposite to the hypopermeability which re-
sults from renal fibrosis^ — as well as on amyloid degeneration of
the kidney, on idiopathic (or cryptogenic) polyuria, sometimes of
hysteric origin (and what now remains of hysteria?), and on poly-
uria symptomatic of nervous disorders, especially bulbar, tumors
of the medulla, disseminated sclerosis, general paralysis, hemor-
rhage, softening, tumors of the pituitary, etc. Discussion of all
these allied and varied conditions would lead us too far afield ; let
the mere mention of their possible clinical occurrence here suffice.
3. Polyuria in "urinary" cases. — In this group are included
the instances of polyuria almost constantly met with in the
course of the chronic diseases of the urinary tract, such as hyper-
trophied prostate, stone in the bladder, chronic cystitis, pyelo-
nephritis (especially of calculous origin), etc.
Its mode of production is undoubtedly complex, the symptom
being the result of a reflex stimulation (possibly vasodilator), of
secondary interstitial changes in the kidney with secondary high
blood-pressure, and probably of other as yet poorly understood
factors.
At all events, such a polyuria seldom exceeds 2 or 2^^ liters.
Only very exceptionally is the urine passed clear as in the pre-
ceding categories. The associated infection of the urinary tract
makes of it a cloudy polyuria, in which the turbidity is due to pus
in the urine and sometimes, likewise, to alkalinity (or hypoacidity)
and phosphaturia. In relatively recent cases the urine clears up on
standing, the pus and other solid substances forming a voluminous
deposit at the bottom of the receptacle ; in inveterate cases, on the
other hand, with more advanced renal lesions, the urine remains
cloudy, with a much less abundant sediment.
1 See Martinet : *'Clinique et therapeutique circulatoires" section on
Renal hyperpermeability.
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1244 SYMPTOMS.
This cloudy form of polyuria may be met with in renal tuber-
culosis, especially when in an advanced stage. At the beginning a
copious, clear polyuria is more frequently observed, with traces of
albumin, phosphaturia, and quite frequently with slight, mani-
fest or occult hematuria, the latter being examined for by centrifu-
gation and examination of the sediment for red blood cells.
Such are, for practical purposes, the three main varieties of
chronic, persistent, lasting polyuria. Yet, as in all other clinical
groupings, there remains, in last analysis, a residue of cases still
obscure and which lend themselves poorly to any satisfactory
didactic description. This is the g^oup alluded to above in con-
nection with the polyuria of diabetes insipidus, vis., the essential
or idiopathic polyurias, or better, the cryptogenic polyurias, the
latter term being more in accord with our present state of knowl-
edge, since we are ignorant of their cause and even of their prob-
able mode of production. Most of the case reports refer to young
subjects, twenty to forty years of age, frequently alcoholic, and
nearly always hysteric. The onset is almost abrupt, with frequent
urination. The amounts reported by many of the authors are so
amazing, e.g,, 10 liters, 15 liters, or even 30 liters, that they in-
evitably suggest the "Tales of Hoffmann" and that it is difficult
to believe that there are not among them some instances of "colos-
sal" faking. Personally, the author has never observed any
amount approaching the above figures. The highest amount recorded
has been 7 liters, already a remarkable figure, and even in this case
the circumstances as regards supervision of the patient, although a
rather close watch was kept, were not such as to exclude all pos-
sibility of faking on the part of the patient — an irresistible tendency
in such subjects, who are always going after that which is excessive
and extraordinary and seeking mainly, like the members of certain
schools of art, to "astound the physician." "The spider," said Mar-
cus Aurelius, "takes pride in catching a fly ; another creature takes
pride in catching a hare ; another, in catching a sardine ; another, in
destroying a wild boar; another, in killing Sarmatians." Another,
we may add, in . . .
Where will pride not seek its outlet !
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PRECORDIAL PAIN.
There are many patients who complain of pains in the region
of the heart and believe, therefore, that their heart must be af-
fected.' As a matter of fact, precordial pain, while sometimes
of cardiac origin, is far more frequently of extracardiac origin.
The commonest among these extra-cardiac causes are dyspepsia,
aerophagia, neuroses, and more particularly the so-called "psy-
chosplanchnic neurosis;'* in addition, a host of other factors may
on occasion be operative.
The fact is that the precordial region is anatomically highly
complex.
The precordial parietes comprisie, from before backward :
1. The skin, subcutaneous cellular tissue, mammary gland, and
subjacent muscles, in particular the pectoralis major,
2. The chest wall proper, consisting of muscle, bone, and car-
tilage, and including the sternum, ribs, costal cartilages, together with
the costal interspaces and their vessels and nerves,
3. The pericardium and heart.
4. Anteriorly, the tongue-like projections of the pleurcc and lungs
between the pericardium and the thoracic wall.
5. Posteriorly, the heart is ensconced in its medic^tinal recess
in more or less direct relationship zvith the esophc^us, the descend-
ing aorta, and the mediastinal lymph-glands.
6. Above, it is prolonged by the great vessels at the base, viz,,
the aorta and the pulmonary vessels,
7. Below, it rests on the thin diaphragm, which alone separates
it from the fundus of the stomach.
8. Laterally, it is in relationship with the mediastinal pleura, the
lungs, the phrenic nerves, and the vessels to the diaphragm.
There is not one of these structures which may not be the
source of pain in the precordial region, some commonly, like the
stomach, others exceptionally, like the mammary glands.
(1245)
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1246 SYMPTOMS.
Clinically, a correct dia^osis can, as a rule, be quickly
reached on the basis of three circumstances, viz., the nature of the
pain, the time at which it appears, and the associated signs.
Vena azygoB Aorta ISsophagus Phrenic nerve
Right auricle Left auricle Right ventricle Left ventricle
Fig. 850. — Horizontal cross-section of the chest of a new-born infant
through the eighth dorsal vertebra (Poirier).
(a) NATURE OF THE PAIN.
This may, for practical convenience, be divided into the fol-
lowing six varieties :
1. A sensation as of a '"misstep" or momentary arrest of the
heart, frequently accompanied by a precordial thump with a
slight feeling of constriction at the apex of the heart and of
transient faintness, and sometimes preceded by a sensation of
constriction in the esophagus.
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PRECORDIAL PAIN, / 1247
This is the ordinary extra-systole or premature beat, a condi-
tion frequently encountered and recorded. It is rather a transitory
discomfort than an actual pain. For its clinical interpretation the
reader is referred to the section on Arhythmia.
2. Pain localized about the apex of the heart, recrudescent
with each cardiac contraction, and with an exacerbation at the
same point when a rather deep inspiration is taken. This is the
typical pain of pleurisy involving the precordial cul-de-sac, often
leadily detected by auscultation (localized rub during inspira-
tion and expiration, ceasing during the periods of apnea).
The pain of pericarditis sicca, sometimes rather similar, is, as a
rule, easily differentiated by the persistence of the friction sounds
even during apnea and their synchronism with the heart beats.
They may be accompanied by local tenderness.
3. Pain more or less localized at the apex, with superficial
darts and radiation toward the left lateral "^nd posterior portion
of the chest. This is the typical pain of intercostal neuralgia.
The three characteristic points of tenderness should be examined
for.
The various possible causes of the pain should be sought, vis.,
rheumatic fever, Pott's disease, beginning meningomyelitis,
osteoperiostitis, etc.
4. Pain as of a surface bruise or muscle cramp in the left side
of the thorax, accompanied by tenderness on pressure or pinch-
ing of the muscles, accentuated by movements of the left arm,
and allayed by rest of the extremity. This may be a myalgia of
the pectoral muscles due to overuse of these muscles, trauma-
tism, or exposure to cold.
5. A sensation of intrathoracic distention, of a **large heart," of
a too narrow chest, frequently accompanied by some degree of
anginose discomfort and by dyspnea increasing upon exertion,
walking, and climbing. All grades may be encountered, from a
slight, transient pain behind the sternum coming on upon marked
exertion and ceasing upon termination of the, latter, to a continued
pain with persistent anginose discomfort and increasing dyspnea.
In these cases the physician's attention should be definitely directed
tcl the myocardium; the condition is probably a myocardialgia ; the
well-known dyspnea on exertion is present ; only a concrete clinical
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1248 SYMPTOMS. ,
study and the use of appropriate tests will, however, permit of
estimation of its degree, significance, and seriousness. It may just
as well be the result of aerophagia, interfering by direct pressure
with expansion of the myocardium, as the result of cardiac neurosis,
bringing about an angiospastic attack with excess of work imposed
upon the heart, or as the result of true myocardial degeneration
leading to progressive cardiac insufficiency.
6. A sensation of violent constriction of the thorax, of squeez-
ing of the chest as in a vice, with a constricting pain, clawing
sensation, spasm, or strangling extending from the post-sternal
area to the upper part of the chest, sometimes with radiation to
the left arm on its ulnar aspect, more rarely along both, arms or
only on the right, paroxysmal, and accompanied by anginose dis-
tress o£ varying degree which may go so far as to yield a sub-
jective impression as of imminent death. This is the typical pain
of angina pectoris, which may be encountered in varying degrees.
As in the preceding type, its significance, degree and seriousness
can be determined only by accurate clinical analysis. Angina
pectoris, or better the anginose syndrome, is, indeed, not only
witnessed in all grades but may be brought on by the most
varied causes, f com the mildest kind of aerophagia to the most seri-
ous aortitis with coronary disease and myocarditis. Hence the
much criticized classification of olden times into pseudoangina
pectoris which does not threaten life and true angina pectoris
which kills the patient. This simple conception is incorrect in
that such a clean-cut division is a practical impossibility and by
no means harmonizes with clinically observed facts. What is
true, however, is that it is the physician's duty to a.scertain, by-
painstaking clinical analysis, that which underlies the anginose
syndrome and, together with its intensity and its cause, its mild-
ness or seriousness, to estimate its gravity in the individual case
— an extremely variable quantity.
The diagnosis of angina pectoris is often made with discon-
certing freedom. One cannot sufficiently warn the practitioner
of the twofold moral responsibility he undertakes either in over-
looking the seriousness of an singinose syndrome which is the
clinical expression of a lethal cardioaortic disease or in holding
the terrible sword of Damocles of sudden death over the head
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PRECORDIAL PAIN. 1249
of a neurotic or aerophagic patient Hence, he should carefully
analyze the symptom before making, even merely in his own
mind, a diagnosis of angina, and should avoid expressing any
sort of a prognosis imtil after painstaking, repeated, and pro-
longed examination. The author has seen patients with exten-
sive aortic lesions and subject to apparently alarming anginose
attacks live ten, twelve, fifteen years or longer, in some instances
evert with complete intermissions of several years' duration.
The reader may have noted) how difficult it has been to dis-
sociate in a clear-cut manner the pains of the myocardialgic type
from those of the type of angina pectoris. Indeed, the relation-
ship between the two is very close and there are insensible gra-
dations. This has been well and forcefully expressed by Esmein
as follows:
"There now appears the cardinal symptom of insufficiency of the
left ventricle, painful dyspnea. This term, which certain methodical
minds might be tempted to criticize, is the one most appropriate for
designating the underlying functional disturbance existing in these
subjects. From the beginning, the dyspnea on exertion (manifest
upon climbing stairs, hilly streets, etc.) is accompanied by painful
sensations behind the sternum and in the epigastrium, and these
painful sensations are, from the start, of a subjectively alarming
character, although ephemeral and rapidly allayed by rest.
"Then, there appears the dyspnea of recumbency, coming on ab-
ruptly on the approach of or during sleep, and likewise accompanied
by subjectively alarming precordial pains, frequently radiating to
the back, shoulders, and arms. Sometimes the dyspneic factor dis-
tinctly predominates over the pain factor; there exists then an
asthmatoid dyspnea or, employing the questionable term which is
nevertheless consecrated by usage, a cardiac pseudoasthma.
"When the main features of these painful manifestations are re-
flected upon, a single word at once comes to mind, viz,, angina pec-
toris: Shall we, on the basis of slight symptomatic variations relat-
ing to the duration and intensity of a symptom, perpetuate former
errors and separate these anginose pains, this alleged angina minor
(from which one is not expected to succumb!), from true angina
pectoris, which causes death ? The clinical course of the disturbance,
here again, will bring us back to the truth. It is not rare, indeed, to
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1250 SYMPTOMS,
find appearing, in subjects who had previously presented merely this
rather attenuated syndrome, the major disturbances of insufficiency
of the left ventricle: Angina pectoris, the most characteristic, and
also pulmonary edema, a description of which need not here be given.
Since the investigations of Merklen, it is no longer possible to over-
look the bond which unites the painful dyspnea of high pressure
cases, angina pectoris, and pulmonary edema, as well as the relation-
ship of these symptom-groups to left ventricular insufficiency/*
Yet, in the anginose syndrome, while it appears that one may
ordinarily attribute the anxiety, dyspnea, and sensation of thoracic
constriction to left ventricular insufficiency with dilatation or a
tendency to dilatation, the clawing sensation beneath the sternum,
the strangling, and the interscapular pain radiating to the trachea
seem rather dependent upon traction on the nerve plexuses around
the aorta. The anginose syndrome, as a rule, does actually result
from a combination of these two factors, vis,, the aorticonervous
factor and the myocardial factor.
(b) TIME OP APPEARANCE OF THE PAIN.
The time relations of the pain, and the circumstances under
which it occurs, sometimes supply extremely valuable diagnostic
indications.
Precordial pain accompanied by dyspnea, appearing only upon
exertion (walking up inclines, carrying heavy weights, etc.) and dis-
appearing upon rest, nearly always indicates an at least relative in-
sufficiency of the myocardium. The same is frequently true of con-
tinuous dyspnea with a sensation of pressure in the chest, increased
by exertion; this is the form regularly met with in the advanced
stages of decompensation in cardiopulmonary disorders, such as
emphysema, tuberculosis, chronic bronchitis, chronic endocarditis,
cardiorenal fibrosis, etc. This long accepted conception of a
"dyspnea on exertion" is of the greatest clinical service provided it
is accurately observed, seen, and even measured (see Functional
heart tests),
A hearty meal acts in the same way as marked exertion, and
may lead to the appearance, in cases of cardiac insufficiency, of
dyspnea, a sensation of pressure in the chest, subjective alarm, and
even an attack of angina. Thus, post-prandial dyspnea may have
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PRECORDIAL PAIN, 1251
the same meaning as dyspnea on exertion. Much oftener, however,
it is merely the symptomatic expression of a neurotic dyspepsia in
which contact of food with- a hyperesthetic mucous membrane re-
flexly brings on various cardiac disturbances, such as palpitation,
painful tachycardia, premature beats, angor, dyspnea, and anginose
attacks, or of a'erophagia giving rise, through pressure on the heart
through the diaphragm, to a mechanical hindrance to relaxation of
the heart in diastole.
Emotional factors act similarly through angiospasm, which
is one of their essential manifestations. The sensation as of a
bubble.
Fig. 851.— Case 1279. H., 1900; 178 cm.; 80.5 kilogr. Pulse rate, 92.
Pressures, i*%o. Aerophagia. Dyspnea on exertion. Precordialgia.
*4arge heart'* or of a "constricted heart" is one of the constant
attributes of depressing emotions such as worry, apprehension,
grief, and pain. Painful tachycardia, with the heart "palpita-
ting" and "driven," is one of the constant attributes of abrupt,
violent emotions such as surprise, emotional shock, fear, etc.
The angina syndrome and mental anguish often form a reversible
couple. This amounts to saying that painful emotional dyspnea is
a common, physiologic occurrence devoid of any marked pathologic
meaning. Yet, upon analysis, it may reveal itself as meaning
myocardial asthenia, in common with dyspnea on exertion, or as
meaning a neurotic visceral pain. It is only upon supplementary
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1252 SYMPTOMS.
clinical analysis and by bringing together the coexisting morbid
signs, however, that such a distinction can be made.
Finally, there remains the highly important subject of pains
occurring mainly in the daytime or at night This question is
often rather hard to interpret. While, in its earlier stages, the
painful dyspnea of incipient cardiac insufficiency is relieved
by rest and recumbency, at a later period one may, on the
contrary, observe the appearance, especially in cardiorenal cases,
of a decubital dyspnea coming on abruptly at the approach of or
during sleep and sometimes accompanied by subjective alarm
and asthmatoid attacks.
Again, these nocturnal manifestations, insomnia, subjective
alarm, dyspnea, or even angina and cardiac pseudoasthma are
ordinarily far more frequent, striking and dramatic in neurotics
(cardiac neuroses) than in organic heart cases. Such psycho-
somatic nocturnal disturbances are especially characteristic in
neurocardiac patients (see below).
Consequently, this analysis of the subjective aspects of precor-
dial pain and its several modalities, however valuable it may be and
however systematically it should be carried out, must, from the
standpoints of diagnosis, prognosis, and treatment, give place to the
concrete, objective examination of the case, and to the search for
coexisting signs, observation and correlation of which can alone
permit of a well-founded and firm conclusion.
(c) ASSOCIATED SIGNS ALONG WITH PRECORDIAL PAIN.
The three least distressing varieties of precordial pain,
myalgic, neuralgic, and pleuropericardial, having been rapidly,
and as a rule very readily, excluded, there remain the three
standard forms previously described: 1. Extra-systoles. 2.
Dyspnea on exertion. 3. Anginose syndrome. Taken singly
these conditions sometimes, in fact frequently, offer marked dif-
ficulties as regards a causal diagnosis.
The associated signs alone will permit of making such a
diagnosis, the symptoms themselves possessing only a very re-
stricted meaning.
Extra-systoles are of no definite diagnostic significance; all
depends upon the circulatory symptoms accompanying them.
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PRECORDIAL PAIN, 1253
In practice the following varieties are more or less readily
distinguished :
Functional extra-systoles, reflex (aerophagia, dyspepsia, or
neurosis) or toxic (gout), intermittent temporary extra-systoles,
unaccompanied by any general circulatory disturbance, are
devoid of any significance as regards the heart and circulation.
They diminish or even disappear upon exercise. They are
generally the symptomatic expression of a cardiac neurosis or
dyspepsia, or of both. They constitute one of the most frequent
attributes of the psychosplanchnic neurosis.
Organic extra-systoles, as a rule practically permanent, are
the outward expression of myocardial disease and are accom-
panied by the ordinary signs of myocardial and vascular de-
generation already repeatedly enumerated (changes in blood
pressure, stasis symptoms, dyspnea on exertion, evidences of
aortic degeneration, orthostatic oliguria, nycturia, stasis edema,
etc.). They are increased or brought on by exercise and exer-
tion. In this event the extra-systole is an evidence of myocardial
degeneration which, taken in conjunction with other evidences,
points toward the customary prognosis of myocarditis.
Dyspnea on exertion, from the very fact of being so common,
is of significance only by reason of the objective signs with
which it is accompanied. It may be and frequently is the sub-
jective manifestation of an organic cardiopulmonary insufficiency
due, e.g., to an endocardial lesion (valvular disease), myocardial
disturbance (fibrous degeneration), or pulmonary disorder (em-
physema, chronic bronchitis, etc.) ; it may, however, be merely
the outward expression of aerophagia or of a neurosis.
A care'ful search should therefore be made for:
1. The usual signs of valvular disorders, particularly mitroaortic
(se^ Circulatory procedures).
2. The usual signs of pulmonary disorders, such as emphysema,
chronic bronchitis, and lung congestion (see Respiratory procedures).
3. The usual signs of cardiac decompensation, zia., vesperal
edema, latent edema at the bases of the lungs, ortho§tatic tachy-
cardia, and orthostatic oliguria. In this investigation one should,
if need be, seek assistance from the circulatory functional test (see
Circulatory procedures) .
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1254 SYMPTOMS.
As in the case of the extra-systoles, this systematic and necessary
investigation will lead to the differentiation of :
Functional dyspnea on exertion, in the absence of organic disease
of the heart or lungs (as in aerophagia, dyspepsia, and neurosis),
the result of mechanical pressure on the heart (gastric air bubble),
of reflex excitation (dyspepsia), or of an erethistic psychosplanchnic
predisposition (psychosplanchnic neurosis).
Organic dyspnea on exertion, due to cardiopulmonary insuffi-
ciency, the result, in turn, of an appreciable, tangible lesion in the
cardiopulmonary system, associated with the hyposphyxic syndrome
(see Low blood-pressure).
The previously emphasized relationship of dyspnea on exertion
and the anginose syndrome suggests a priori that the same con-
siderations shall apply to angor, and at bottom this is in all likeli-
hood what the older authors understood without actually expressing
it in their much-criticized division into the pseudoanginas and the
true anginas. The author will take good care not to enter into any
doctrinal discussion in this purely practical work.
The following exclusively clinical classification seems ad-
vantageous :
1. Angina pectoris dependent upon an aortic lesion (aortic
aneurysm, aortic valvular disease, interstitial or specific aortitis,
arteriosclerotic degeneration, or cardiorenal sclerosis), very fre-
quently combined with chronic degeneration of the myocardium,
yields a first rather homogeneous group of cases — cases of serious
angina which may prove fatal, and always necessitating a very
guarded prognosis, although the author has witnessed survival for
ten, fifteen, or more years, even in the presence of very advanced
aortic lesions (see High blood-pressure),
2. Angina pectoris occurring in plethora, presclerosis, angio-
spasm, nicotinism, or gout, generally much less serious than the
preceding type, and very often curable provided the patient will
submit to appropriate hygienic regulation (see Plethora, High blood-
pressure, etc.).
3. Angina pectoris in aerophagia, well described by Robin
and Fiessinger, and actually rather often encountered by the
author. While occurring alone, such angina rarely assumes the
form of true major angina.
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PRECORDIAL PAIN. 1255
4. Angina pectoris in neuroses and psychoneuroses, eminently
benign as regards the heart, but of such practical importance that it
seems advisable to devote considerable space in this section to its
discussion and to reproduce in extenso an article on the cardiac
neuroses published by the author some years ago (Presse tned.,
Nov. 4, 1915).
id) THE CARDIAC NEUROSES.
Special significance! was lent to the question of the cardiac
neuroses by the late war. More than two-thirds of the hospital
cases labelled **heart disorder" belonged in this category.
And first of all, what is meant by the term cardiac neurosis?
The practical, clinical definition of thq condition seems simple:
Cardiac neurotics are those subjects who, in the absence of any acute
or chronic organic lesion of the heart or its coverings (endocarditis,
pericarditis, or myocarditis)^ in the absence even of any true myo-
cardial weakness, e,g., congenital or constitutional weakness, or of
any recognized lesion of the nervous system, suffer from a symp-
tom-complex involving mainly the heart. This definition excludes
all the organic disorders of the heart, all cardiac manifestations de-
pendent upon some organic nervous disorder, central or peripheral,
and all temporary and evanescent cardiac manifestations of reflex
origin and extra-systoles, e.g., of digestive origin.
With the ground thus cleared by a relatively easy process of
clinical elimination, there yet remains an extensive, rather homo-
geneous group of cases — although further study of the cause
may easily resolve it into sub-groups very variable in their
pathogenesis and clinical course (cardiac neurasthenia, Graves's
disease, etc.). All these subjects have in common the fact of
suffering from severe, manifold, and refractory manifestations in
the cardiac region, and more generally, of disturbances of a cir-
culatory nature, while nevertheless presenting upon examina-
tion an apparently complete integrity of the system referred to.
As a matter of fact, it is these self-same cardiac neuroses which
are accompanied by the most numerous and distressing cardiac or
pseudocardiac symptoms: Squeezing or constriction of the heart, a
distressful sensation of beatmg arteries or of "missteps" of the
heart, an anginose feeling with pains radiating in the arm and neck
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1256 SYMPTOMS.
(nervous angor, dyspnea, constriction of the esophagus and neck,
choking sensations, etc.), as well as by equally numerous, if not
alarming, objective signs, such as tachycardia, tachy-arhythmia,
extra-systoles, marked vasomotor instability (involving both the
pulse frequency and the blood-pressure), fainting spells, profuse
sweats, frequently cardiac hypertrophy, with a special vibrant
quality of the first sound, at times even an intermittent systolic
apical murmur transmitted toward the axilla and the left sternal
border, and frequently accentuation, sometimes reduplication, of
the second pulmonic sound, etc.
Finally, these conditions are ordinarily combined with unques-
tionable neuropathic manifestations, such as insomnia, nervousness,
exaggeration of emotive reactions and of the reflexes, cenesthesic
instability, headache or actual migraine, asthenia and abnormal ex-
citability (irritable weakness of the nervous system, etc.), and
sometimes manifestations of asthenic nervous overexcitability of
other systems, as evidenced, e,g,, by gastrointestinal dyspepsia,
asthmatoid phenomena, dermographia, and paroxysmal sweating.
This clinical picture, which is of exceedingly frequent occur-
rence, whether existing merely in faint outline or with its salient
features pushed to their ultimate conclusion as in exophthalmic
goiter, betokens and outwardly manifests better than could the
most perfect experiment in physiology the intimate relationship
existing between the nervous and circulatory systems. In the
present state of our knowledge, this neurocirculatory interde-
pendence may be outlined as follows:
Cardiovascular activity is controlled and regulated as a whole
by the so-called vegetative nervous system, which consists, as is
well known, of the vagus and the sympathetic with their bulbar
centers. The vagus and the sympathetic are in a large measure
mutually antagonistic. Stimulation of the sympathetic causes
acceleration of the pulse (tachycardia), elevation of the systolic
blood-pressure, and shortening of cardiac systole; when very
marked it is capable of inducing an excessive, or even extra-
systolic, pulse acceleration of the type of paroxysmal tachycardia.
Stimulation of the vagus causes, on the other hand, slowing of the
pulse (bradycardia); reduction of the systolic blood-pressure,
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PRECORDIAL PAIN.
1257
and lengthening of both ventricular diastole and systole; when
very marked it is capable of inducing a pronounced slowing of
intracardiac conduction or even auriculoventricular dissociation
through inhibition of the bundle of His, aa in the bradycardia
and dissociation produced by digitalis. Inhibition of the centers
referred to leads to opposite results — a fact which by no means
tends to facilitate, in clinical studies, inquiries as to that portion
of the eflFects relating to each one of these nerves.
ryng. nerve.
Pneumog.
Recurrent
Middle ai
cardiac i
Phrenic nei
•yng. nerve,
g. nerve.
iCUSSCDii.
rdiac nerve.
nt nerve,
plexus.
irenic nerve.
ronch. plexus.
at. cardiac
plexus.
Fig. 852.— The nerves of the heart (Hirschfeld) .
It should be added that the actions of both nerves extend
to the peripheral circulatory structures, giving rise, as the case
may be, to vasoconstrictor phenomena (or even angiospasm) or
to vasodilator phenomena (or even vagoparesis), reacting, in
turn, upon the heart either in a direct mechanical manner or
indirectly and reflexly.
The medullary centers, on the one hand, and the myelogang-
lionic nerve paths, on the other, are manifestly influenced alike
by stimuli of psychic and special sensory origin (special sen-
sory stimuli and concepts, images, recollections, emotions, etc.)
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1258
SYMPTOMS.
and by cenesthesic stimuli arising through visceral sensation,
which may be pleasant or unpleasant, or even painful.
The result of all this is an exceedingly close interdependence
of the nervous and circulatory systems, which leads the circu-
lation to react with extreme sensitiveness to any nervous stimu-
lus, whether latent or manifest, conscious or unconscious.
Clearly, the circulation reacts, perhaps more than any other
system, to such incessant nervous traumatism as characterized
the late war. How does it react under such conditions? Actual-
ly, in very diverse fashion, according to the individual.
Heart
Fig. 853. — The nervous system as related
to the circulation. Connections of the vag^us
nerve and the sympathetic system.
In most ostensibly normal persons the neurocardiac, or bet-
ter, neurocirculatory reaction does not extend beyond a condi-
tion of temporary insomnia with accelerated pulse rate, nervous
overexcitability with exaggerated reflexes, transient subjective
alarm and tremor, and a few evanescent vasomotor and secre-
tory manifestations, such as pallor or hot flushes, "goose flesh,"
sweats, temporary diarrhea, etc. Within a few days a more or
less complete tolerance becomes established, the vegetative nerv-
ous system adapts itself to the new conditions, and the cardiac
and vasomotor reactions are reduced to a physiologic minimum.
In others the emotional shock persists, leading to a pro-
tracted or permanent loss of neurocirculatory balance charac-
terized by appearance of the symptoms already mentioned as
constituting the cardiac neurosis.
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PRECORDIAL PAIN. 1259
As in the case of the reserve power of the heart-muscle itself,
so the reserve power of the nervous system in these cases, in-
cluding the capacity of resisting without collapse or even adapt-
ing itself to certain psychophysiologic stresses, varies exceedingly
in different individuals. Some nervous systems resist and adapt
themselves even to the most severe trials, as in the case of the
peasant who was buried for twenty-five days among the debris
in a landslide and whose first words when finally set free were :
"Have the animals been saved?" In other instances the mere
fact of entering the barracks is enough to upset the nervous
system completely.
As a matter of fact, the author saw just as many, if not more
cases of cardiac neurosis among subjects on duty far from the
scenes of military action than among those who had actually
been subjected to the gruelling life at the front.
Huchard used to remark that "the physical heart is lined with
a mental heart." The author some years ago read in an Italian
periodical^ the following naive yet truthful statement concerning
subjects suffering from organic heart disorders and fully conscious
of their infirmity: "Sustained by small doses of digitalis and more
particularly by their valorous spirits, they were able to perform long
and fatiguing missions, even as aviators."
This statement serves as a good paraphrase of Turenne's
sublime remark to his own "beast" or body. "You are trembling,
carcass ; 5'ou would be trembling much more if you knew where
I am going to take you." A penetrating statement this was
from the standpoint of body physiology : We are powerless to
restrain the reflexes of our medullary and spinal vegetative
system, but an "energetic, valorous spirit" can always make its
"beast" of a body advance, even if it is "shivering" and "palpita-
ting" at the time.
Cases even occur in which the stimulus afforded by constant
danger exerts a favorable effect on a preexisting cardiac neurosis.
Such is the personal case of Longhi, the Italian translator of
Stokes's^ classic work, which he describes as follows in his trans-
lation :
1 Mendes : Manuale di medicina chirurgia di guerra, Rome, 1915.
2 Stokes : Malattie del cuore c delV aorta. Prima traduzione italiana del
dott. A. Longhi, Turin, 1858, p. 223.
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1260 SYMPTOMS,
**In the course of the winter of 1848, I was constantly troubled
with palpitations and with the dejection of spirits which neariy
always occurs in heart disorders. Tired of suflFering, I went to
see a distinguished colleague, a specialist in chest disorders,
who told me that I had a hypertrophied heart — not a very serious
condition in itself, but one which is incurable like any other
dependent upon an organic lesion. He prescribed for me a line
of treatment calculated to moderate the heart action and advised
me not to give way to melancholia, as the disorder was not
serious and would allow me to continue living a long time, even
though I might experience slight discomforts from it.
**On the very next day after my visit the revolution broke out
in Milan, and in it I took a rather active part. At the first
gunshots that I saw and heard, my heart began to beat so
strongly that I almost fell to the ground and feared lest I might
be obliged to retire from the fight, not through cowardice, but
from physical weakness. Shortly after, my heart became more
quiet and I found myself drawn into a skirmish in the course
of which I had no opportunity to think of it. Subsequent to
that day I led a very active life at the camp, at first as a volun-
teer and later as a Piedmontese officer of the bersaglieri, without
ever being conscious of my heart action. During the last nine
years I have been in excellent health and have had no precordial
pain. I am convinced that . in 1848 my discomforts were due
principally to a temporary engorgement of the heart resulting"
from the sedentary life I led at tl\at time, spending eight or ten
hours at my desk each day, whereas in my youth I had been
accustomed to a very active life."
The author knows of many neuro-cardiac subjects who no
longer "felt their hearts" after the mobilization, as exemplified
by an artillery officer aged forty-eight who, afflicted with palpita-
tion, precordial pain, and angor, had been living since 1908
obsessed with the fear of aneurysm or angina pectoris and had,
to the author's own knowledge, consulted about ten physicians
in Paris, none of whom had found anything more than neurocardiac
erethism and a moderate degree of hypertrophy. The author
saw him again after he had been one year at the front, including
three months in the trenches with the infantry, at which time he
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PRECORDIAL PAIN, 1261
had entirely forgotten his cardiac discomforts and experienced
merely slight dyspnea on running.
Such a turn of affairs is not exceptional, although, as a mat-
ter of fact, much less common than the converse sequence of
events.
Considering only the heart S3miptoms, the diagnosis between car-
diac neurosis and organic disease is not always easy. Auscultation
may be puzzling and misleading, and various forms of arhythmia
(extrasystoles, sinus arhythmia, etc.) may be observed in either
instance; the same consideration applies to the customary hyper-
trophy of the left ventricle and even more strikingly to the sub-
jective manifestations, vis,, dyspnea on exertion, sensation of con-
striction or actual angina, palpitation, phrenocardia, etc. Yet there
are a number of differential signs:
(a) The first and most important, perhaps, is the neurotic sub-
strate upon which the cardiac neurosis always develops. The car-
diac symptom-group above referred to merely forms part of an
always more or less pronounced neuropathic clinical picture, which
is confirmed, in turn, by the family history and by extracardiac neur-
opathic manifestations, digestive and mental in particular.
(&) The second is the relative frequency and importance of
nocturnal symptoms, such as insomnia, subjective alarm, dyspnea,
and even anginose discomfort and cardiac pseudoasthma, which are
far more common and striking and generally more dramatic than in
subjects with organic heart disease. These characteristic and inter-
esting nocturnal psychosomatic disturbances among neurocardiacs
are in themselves deserving of a thorough study.
(r) The neurocardiovascular instability and lability constituting
an outward expression of abnormal emotivity. The pulse frequency
and blood-pressure exhibit surprising variations from the slightest
disturbing causes. This is often true likewise even of the ausculta-
tory signs which are far from presenting the relatively high degree
of permanency and constancy of those of organic lesions. The
changeableness as regards arhythmias is perhaps even more char-
acteristic (Fig. 854).
(d) There may frequently be noted an absence of the usual
etiologic factors of organic heart conditions, such as rheumatic.
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1262 SYMPTOMS,
typhoid, syphilitic, diphtheritic, and other infections ; plethora and
autointoxication, gout, uricemia, etc.
m e If e9 m
- ♦ -
•
9
■• "♦""
•
H15.17 8 IS
Rr 96 17 4
11
RJ
Rr
Fig. 854.— Cardiac neurosis. H., 1885; 174 cm.; 73.6 kilogr.;
pulse, %; pressures, *'^91oo; viscosity, 4.
The two above tracings were taken about V/i minutes apart. The
first shows premature contractions imparting to the pulse tracing a bi-
geminal , aspect. In the second, all premature contractions have dis-
appeared.
{e) High blood-pressure, systolic as well as diastolic, is noted in
the great majority of cases, in spite of the widely held view to the
S S SItUng
^^••■M Recumbent
I I I Standing
L L L Dipping exercises
1*2*3'. Time in minutes
Blood-pressures
■>■■■■■» Pulse frequency
Fig. 855.— Normal individual. H., 1893; 173 cm.; 70 kilogr.
(Mx = systolic pressure; Mn = diastolic pressure; pressures
given in centimeters of mercury).
contrary. There do occur, however, a few cases of cardiac neurosis
with low blood-pressure; thefee are of two varieties, as the author
proposes to show elsewhere.
(/) Lastly, the functional test of the circulation, which consists
in recording the changes in pulse frequency and systolic and dias-
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PRECORDIAL PAIN. 1263
tolic blood-pressure occurring when the subject rises from recum-
bency to the standing posture as well as after a series of carefully
standardized exercises (20 dips with flexion of the lower extremi-
Fig. 856. — Normal subject as re- Fig. 857. — Heart weakness,
gards the circulation. H., 1893, 165 cm.; 60 kilogr.
H., 1875; 169 cm.; 7:^ kilogr.
ties), demonstrates clearly the exaggerated vasomotor reactions
(reflex overexcitability) in well-marked cases, as well as the con-
Fig. 858. — Cardiac neurosis. Fig. 859. — Cardiac neurosis.
H., 1878, 169 cm.; 67 kilogr. H., 1895, 169 cm.; 64^ kilogr.
siderable margin of reserve myocardial power usually present, as
exemplified in the five annexed illustrations, two of which are from
normal subjects, one from a case of weak heart, and two from car-
diac neurotics (Figs. 855-859).
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1264 SYMPTOMS.
In short, the true, organic heart case, when well compensated,
reacts like a normal individual; when poorly compensated, he
reacts like a case of heart weakness and yields a typical curve de-
noting cardiac insufficiency, vis., a weak blood-pressure reaction, or
even a reversed reaction, with slow return to the original state of
equilibrium.
The cardiac neurotic reacts to an exaggerated extent both as
regards pulse rate and rise of blood-pressure, thereby affording an
outward manifestation of his reflex cardiac and vasomotor over-
excitability; on the other hand, his blood-pressure test shows no
tendency toward myocardial insufficiency.
To be sure, an organic heart ca^e may also be neurotic, and a
true neurotic may be found suffering from cardiac debility, plethora,
or even organic heart disease. In such cases the functional test
alone is frequently sufficient to demonstrate the simultaneous pres-
ence of the two disorders; when used in conjunction with the other
methods of clinical investigation it nearly always enables the ob-
server to distinguish that which attaches to the nervous system from
that which is referable to the circulation, and thus to render a well-
founded prognosis and institute a rational line of treatment based
on a reliable physiopathologic conception of the case.
As far as the patient's availability for military service is con-
cerned, it is not, as will readily be seen, the reserve power of
the heart which is the criterion in the matter, ample reserve
power being, as a rule, available. It is rather the power of
nervous resistance and reaction that should be investigated by
appropriate methods.
The cardiovascular symptom-complex here constitutes but a
single outward manifestation, albeit a highly important one, of
an abnormal psychoneurotic state which dominates and governs
the entire symptomatology as well as the prognosis.
From the foregoing description the reader will, it is hoped,
have been led to realize both the complexity and the relative
simplicity of the diagnostic problem which arises in connection
with the precordial pains. Its solution may, on the whole, be
concretely stated as follows :
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PRECORDIAL PAIN, 1265
1. One should make a careful analysis of the characteristics and
nature of the precordial pain present. This initial procedure will
orient the investigation a priori in some particular direction, but
however searching the analysis may have been, it will never lead to
a sound diagnosis, which can only be established by objective exami-
nation of the patient.
2. Only a complete objective examination (carried out as des-
cribed in the section on Systematized clinical examination) zvill per-
mit of obtaining a more or less prompt solution of the diagnostic
puzzle presented.
In concluding this section it seems advisable to go over the sub-
ject of precordial pain summarily from a different aspect, viz.^ by
starting with the clinical conditions themselves and correlating with
them the various forms of pain.
DISORDERS OF THE HEART AND AORTA.
1. DiBorders of the Cardiac Orifices. Endocarditis.— (a) Dur-
ing the stage of adequate compensation, endocarditis can hardly
be said to cause pain. The frequency with which patients are
unaware of their condition apart from periods of lost compensa-
tion is well known. Yet the possibility must be recognized that
among some nervous and hyperesthetic subjects there may
eventually occur extra-systoles and a sensation as of cardiac
distention, precordial hyperesthesia, or chronic precordialgia.
Mackenzie doubtless had these cases in mind when he wrote:
"Many subjects suffering from an actual heart lesion, such as
may involve the mitral or aortic valve, exhibit evidences of ex-
aggerated precordial sensitiveness. This sort of thing is witnessed
more particularly in women Attacks of very severe
pain in the chest may be experienced. . . . More frequently
there is an unpleasant dull sensation The hyperalgesia
may extend over a very large area and is sometimes very marked.
.... The pain may not be as distressing as in the more severe
instances of angina pectoris, but it persists a longer time.
.... It is often associated with extreme tenderness of the
tissues of the neck or left side of the chest, especially the left
breast. Where the condition of tenderness of the skin and
80
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1266 SYMPTOMS.
muscles has been tested by pinching them ^between the thumb
and forefinger, the part remains sensitive for several hours."
As a niatter of fact, this type of chronic precordialgia has
seemed to the author quite exceptional among well compensated and
non-neurotic cases of endocarditis. It is the rule, on the other hand,
in the cardiac neuroses (see above), hyposphyxia (see Low blood-
pressure), and cardiac insufficiency of whatever cause. In the latter
type of case, the mechanical factor, distention of the heart, seems
to be more particularly concerned in its causation.
(&) During the stage of lost compensation, ranging from a
mere reduction in the reserve power of the heart to actual heart
failure, the picture witnessed is mainly that of the dyspneic
syndrome, from dyspnea on exertion to continuous dyspnea with
more or less pronounced anginoid phenomena and with the usual
signs of impaired heart action, such as orthostatic oliguria,
cyanosis, edema, etc.
2. MyocarditiB. — Here the signs of lost compensation and
cardiac insufficiency already enumerated constitute the main
feature, sometimes with extra-systoles and attaicks of angina.
3. Pericarditis. — Pericarditis may either be completely latent
or be accompanied by pain so slight and evanescent that some pa-
tients pay no attention to it. In the majority of cases pericarditis,
especially when of the "dry*' variety, induces precordial pain which is
localized in the region about the apex or the sternum and is some-
times recurrent with the successive heart-beats. Examination may
demonstrate the presence of tender points the result of radiation
along the phrenic nerve (Gueneau de Musses points), vis., the
lower point, between the ensiform appendix and the border of the
costal cartilages on the left side; the intermediate points, at the
anterointemal portion of the left costal interspaces, along the sternal
border, and the upper point, between the sternal and clavicular heads
of the sternocleidomastoid muscle.
4. Aortitis. — Dilated Aorta. — ^AneiUTsm.— This disorder may
be accompanied by three sorts of pain :
(a) Pain behind the sternum and in the chest, with or with-
out radiation, either, as is most often the case, toward the axilla and
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Precordial pain, 1267
left arm, or toward the right axilla and arm, or toward both arms,
in accordance with the location and size of the aortic deformation.
This pain appears to be mainly of periaortic, neurovascular origin,
being related to an inflammatory condition and distention of the
nerve plexuses around the aorta. ■
(b) Pain as of constriction of the chest, with a squeezing sen-
sation, subjective alarm, a sensation as of impending death, the
whole constituting the essential factor in the syndrome, known as
angina pectoris, while the preceding type, which so often accom-
Fig. 860. — Aortic aneurysm resulting in an elevated pulsating tumor
on the left side.
panics it, is merely an auxiliary factor. This pain seems to be de-
pendent upon deficient functioning of the heart muscle, or more
specifically, an cu:ute insufficiency of the left ventricle, which is
painfully striving to overcome a resistance so marked as to exhaust
its reserve power.
Dyspnea on exertion necessarily accompanies this t^'pe of
pain. The author has noted its absence, however, with the pre-
ceding type, in particular in a case of aneurysm of the ascending
aorta which had eaten away the sternum, formed a pulsating
tumor of the size of a hen's egg, and induced pain on the right
side of the chest radiating to the right axilla and arm.
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1268 SYMPTOMS,
(c) In the stage of lost compensation are added permanent
paroxysmal dyspnea and the usual signs of heart failure.
5. Arteriosclerosis. Disorders Attended with High Blood-
Pressure. — ^The forms of pain experienced in these cases are
very similar "to those referred to in connection with diseases of
the aorta, which, indeed, is itself often involved in the process.
Thus, there occur:
Fig. 861.— Aortic aneurysm with precordial pulsating tumor.
(a) Pain of the type of dyspnea on exertion, which is the
first to appear.
(b) Pain of the type of permanent paroxysmal precordialgia
with dyspnea, subjective alarm, etc., of myocardial origin.
(r) Clawing pains behind the sternum, radiating to the
periaortic region.
Interstitial nephritis and uremia are frequently accompanied
by similar manifestations.
6. Vasomotor Angiospastic Attacks. — The attacks of high
blood-pressure from vasoconstriction induced in some subjects
by overwork, emotional impressions^ or abuse of tobacco may
eventually be accompanied by manifestations of precordial pain
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PRECORDIAL PAIN, 1269
and angina in all respects similar to those already described.
Again it should be emphasized that it is only through the
anamnesis and especially by systematic and thorough clinical
examination that these subjective disturbances can be traced to
their actual causes.
7. Cardiac Neuroses. — This subject has already been referred
to at such length that it seems unnecessary to discuss it again
here. Any form of disturbance may be witnessed, from dyspnea
on exertion to the anginal attack and from extra-systoles to
permanent paroxysmal dyspnea.
DISORDERS OF STRUCTURES ADJACENT TO THE HEART.
1. Pleurisy of the Precordial Diverticulum of the Pleura. —
In this condition there is pain localized at the cardiac apex,
recurring with each heart beat and increased by rather deep
breathing.
In nervous subjects it may lead to the production of reflex
extra-systoles.
2. Aerophagia and Dyspepsia with Gastric Distention. — This is
one of the commonest and yet one of the most frequently over-
looked causes of precordial pain, the individuals concerned often
being neurotic.
Dyspnea on exertion, most marked after meals, feelings of
painful distention in the vicinity of the cardiac apex, extra-
systoles, and attacks of pseudo-angina (angina pectoris of
aerophagics), may be observed. The time of occurrence of the
pain (after meals), the tympany and increased size of Traube*s
space, actual observation of the aerophagia, and the absence of
objective heart signs easily lead to the correct diagnosis if they
are merely thought of.
The orthoradioscopic view shown in Fig. 851 gives a good
idea of the extent to which the heart can be pushed aside by the
air content of the stomach.
3. Gaseous Distention of the Colon. — The rather frequently
encountered accumulation of gas in the splenic flexure brings
about the same symptoms as have already been enumerated, and
through the same process of mechanical displacement of the
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1270 SYMPTOMS,
diaphragm. The patients concerned suffer from spastic constipa-
tion; percussion elicits exaggerated resonance over the colon,
and fluoroscopy sometimes yields an actual view of the gaseous
accumulations. Liquid petrolatum and extract of belladonna are,
as a rule, both diagnostically and therapeutically su<:cessful in
these cases.
4. Mastodynia, when localized in the left breast, may suggest,
albeit only approximately, precordial pain. Any possibility of a
mistake is readily obviated by the most superficial examination,
including palpation of the breast and the observation of diffuse
induration or of small scattered nodules, in conjunction with the
absence of all true cardiac manifestations.
5. Intercostal neuralgia is usually distinguished by virtue of
the three characteristic points of Valleix : Anterior, by the side of
the sternum ; lateral, in the axillary line, and posterior or paraverte-
bral. The neuralgia, moreover, would hardly tend to mislead unless
located exactly in the precordial region. It should be borne in mind
that the term intercostal neuralgia, purely an anatomic expression,
implies nothing as to the cause, which should be sought and may
be either toxic, as in lead fK)isoning, gout, etc.; infectious, as in
rheumatism, typhoid fever, etc.; osseous, as in osteoperiostitis,
Pott's disease, etc. ; pleuro pulmonary, as in pleurisy, pneumonia, etc.,
or even cardiomedic^tinal, as in aortic aneurysm, hypertrophy of the
heart, mediastinal tumor, etc. One should never hesitate to resort
to fluoroscopy in obscure cases.
6. As an exceptional cause, mention should be made of
tabetic pains. Tabes dorsalis is frequently associated, as is well
known, with more or less pronounced pathologic changes in the
aorta, and some tabetics, quite naturally, may experience attacks
of angina pectoris definitely of aortic origin. In at least two
tabetic cases, however, the author has observed paroxysmal and
transient attacks of precordial pain which, since they occurred
in alternation with other paroxysmal attacks of pain referred to
the gastric region and lower extremities, were necessarily con-
sidered of tabetic origin.
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SLEEP, MORBID.
To die, to sleep;
To sleep: perchance to dream,
(Shakespeare, Hamlet,
Act III, Scene I.)
The crude analogy existing between sleep and death is
obvious. It would lend itself most readily to a fascinating meta-
physico-poetic discourse, most concisely and suggestively ex-
pressed in the Shakespearean epigram at the head of this sec-
tion. Such a discourse would, however, far transcend the definite
purposes underlying the present work, and we shall have to
preserve due limitations in this connection.
Sleep may occur in very variable degrees and modalities.
It may be divided, according to its intensity, into somnolence, light
sleep, profound sleep, and coma, the latter, on the whole, being
diflferent from profound sleep only in a more complete loss of
sensibility, in the impossibility of rousing the subject by artificial
stimulation, and frequently in paralysis of the sphincters. The
differential diagnosis of the several forms of coma has already been
dealt with in a special section (see Coma).
To base conclusions on the degree of sleep present is not of
great clinical value, for in general one sees no definite lines of de-
marcation between the different grades of sleep and the same
morbid cause — e.g., toxic — may, according to the individual and the
extent of the morbid influence present, yield any degree of hyper-
somnia, from simple somnolence to the most profound coma. This
is true, for example, in the case of alcohol, opium, and azotemia.
It seems more in keeping with clinical conditions and even cur-
sory observation to base our interpretation of the hypersomnias upon
their clinical features, and to divide them as follows :
Hypersomnia presenting the appearances of normal sleep and
differing from it only in its time relations, duration, or depth.
(1271)
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1272 SYMPTOMS.
Hypersomnia of the lethargic type, prolonged and profound,
with pronounced slowing of the circulatory and respiratory
functions.
Hypersomnia accompanied by more or less definite symptom-
groups :
Infectious states.
Meningeal conditions.
Toxic states.
Hypersomnia accompanied by motor manifestations.
I. — ^Hypersomnia presenting the appearances of normal sleep
and differing from it only in the depth or duration of sleep may
be due to such a variety of causes — exhaustion, intoxications,
infections — that its diagnostic significance is thereby greatly re-
duced.
The semeiology of profound sleep partially merges with that of
the lethargic states (see below) and that of coma (see Coma). It
will, therefore, be necessary here only to recall briefly that of
morbid somnolence or narcolepsy, manifested in an abnormal and
practically irresistible tendency to sleep, sometimes only of short
duration, but at others almost permanent, as, e.g., in the sleeping
sickness.
This variety is met with in most of the meningoenccphalic states
(sleeping sickness, lethargic encephalitis, various meningeal disturb-
ances, and brain tumor) (see below).
It is certainly caused oftenest by toxic-infectious conditions,
which may be enumerated for purposes of memorization as follows :
Heterotoxic hypnogenotis intoxications: Opium, chloral hydrate,
alcohol, cannabis, chloroform, ether, and various h)rpnotics (barbital,
sulphonethylmethane, etc.).
Autotoxic hypnogenous intoxications: Acetonemia (diabetes),
azotemia (uremia), ill-defined autointoxications due to hepatorenal
insufficiency, intestinal fermentations, or slowing of tissue oxida-
tion (hyposphyxic states; cardiopulmonary insufficiency).
Less frequently, these narcoleptic states are witnessed during the
period of decline in general infections; some of them, such as the
narcolepsies of convalescence, are actually of the nature of repara-
tive sleep.
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SLEEP, MORBID. 1273
Hysteria and epilepsy claim a large proportion of these hypnotic
conditions.
Lastly, after, as in the comas, careful, systematic clinical inquiry
(history, physical examination, uranalysis, and investigations of the
blood and cerebrospinal fluid) has been carried out and one of the
foregoing hypnotic factors discovered, there remains a small num-
ber of unclassable cases for which must be preserved, until further
light is shed on the subject, the term essential or idiopathic narco-
lepsy, probably of constitutional origin, encountered most often in
neuropsychopathic families, and the most characteristic feature of
which is that of being chronic, wholly incurable, and not accounted
for by any clinically expressible cause.
II. — ^The lethargic states, in the commonly accepted sense
of the term, i,e,, states featured by morbidly prolonged sleep
(persisting for days, weeks, months, or even years), and at-
tended with pronotinced slowing of the circulation and of nutri-
tion, impose upon the practitioner two serious tasks :
1. In the presence of an actual lethargic state, to ascertain its
nature.
2. In the presence of an actual state of death, to distinguish
it from a lethargic state, and vice versa.
Only exceptionally is a lethargic state attended with inhibi-
tion of the circulatory and respiratory functions to such an
extent as to lead actually to apparent death as seen by a careful
and trained observer. Ordinarily, indeed, an obscure grade of
consciousness is still present and the taking of food is frequently
possible. The lethal appearance, however, is the thing that proves
striking to bystanders and is expressed in Ambrose Fare's defini-
tion : **Sleep by virtue of which the faculties and powers of the
mind lare buried, in such wise that it seems as if one were dead."
Death having been excluded by the findings later to be men-
tioned, the nature of the lethargic condition remains to be ascer-
tained. Singular complications have been injected into the ques-
tion by the doctrinal discussions concerning hysteria. Lethargy
has been and is still considered by a few authors as a specific
manifestation of hysteria; it has been termed, comatose hysteria.
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1274 SYMPTOMS.
attacks of hysteric sleep, and hysteric apoplexy. While due
account has to be taken of the possibility of simulation; while
one sTiould be on his guard, and while it is prudent to question,
with Dupre and Meige, whether certain cases recorded and ad-
vertised in the public press are not "simply fantasies of my-
thomaniacs desirous of drawing attention to themselves/' there
seems to be no doubt but that "hysteric sleep" probably comprises
the majority of the true lethargic states.
Yet it does not appear to the author that lethargy is exclusively
an attribute of hysteria. Lethargic states may seemingly be brought
on by many other causes, in particular through intoxication by
hypnotics, the resulting lethargic state being sometimes sufficiently
profound even to induce a state of apparent death, as illustrated in
the following case, recorded in the Deutsche medizinische Wochen-
schrift for November 13, 1919, page 1277. A nurse aged 23
took, on October 27, 1919, 1.7 grams of morphine and 5 grams of
veronal. She was found the next day in a park, life being almost
extinct. In the ambulance she was thought to be dead. The exist-
ing signs of death were, rigidity, extreme pallor, and absence of
reflexes, of the pulse, of breathing, and of the heart-beats. Appli-
cation of hot sealing wax over the skin caused no reaction. After
she had been in the Morgue for fourteen hours, the coffin was
opened on October 29, a medical official wishing to identify the
body. The cheeks were seen to be slightly roseate and slight move-
ments of the larynx were observed. No respiratory movements
nor pulse beats were noted, but obscure heart sounds were audible.
At 10 o'clock in the morning the i>atient was taken to the hospital ;
hypodermic injections of caffeine and camphor in oil were adminis-
tered and the stomach washed out. A hot bath was then given,
with vigorous rubbing, followed by artificial respiration and oxygen
inhalation. At 11 o'clock the pulse was perceptible and a few brief
inspiratory movements were noted; the rigidity of tlie limbs was
passing off. At noon the pulse was distinctly noticeable, with a
rate of 50 per minute. On October 30, the patient regained con-
sciousness and made short verbal statements. She gradually re-
covered, but exhibited a persistent leucopenia.
In this case the arrest of the circulation and respiration with
continuance of life appears to have lasted over twenty-four hours.
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SLEEP, MORBID, 1275
Perhaps the explanation of this anomalous occurrence is to be
found in the combined action of cold and of the narcotic causing
general vasomotor paralysis with marked reduction in the organic
demand for oxygen — a condition similar to that of hibernation
in certain animal species.
Was this a hysteric subject? The history does not mention
it, but it is plain that the condition of lethargy and even appar-
ent death was here brought about through the combined action
of intoxication by a hypnotic and of exposure to cold.
While undue weight is not to be laid on literary documenta-
tion, the case of Juliet — which is naturally brought to mind —
seems to show that these toxicolethargic states were well known and
had been accurately observed even before* Shakespeare's time. At
all events, a more precise description of them would be hard to find :
. . . out, alas! she*s cold;
Her blood is settled, and her joints are stiff.
(Romeo and Juliet, Act IV, Sc. V).
• Take thou this vial, being then in bed,
And this distilled liquor drink thou off;
When presently through all thy veins shall run
A cold and drowsy humour, for no pulse
Shall keep his native progress, but surcease:
No warmth, no breath, shall testify thou livest;
The roses in thy lips and cheeks shall fade
To paly ashes, thy eyes* windows fall.
Like death, when he shuts up the day of life.
Each part, deprived of subtle government.
Shall, stiff and stark and cold, appear like death:
And in this borrow'd likeness of shrunk death
Thou shalt continue two and forty hours.
And then awake as from a pleasant sleep,
{Romeo and Juliet, Act IV, Sc. I).
Incidentally and without further discussion, the mysterious
and disturbing spirit of Lazarus may here be alluded to.
The deep sleep of convalescents and of the depressive form of
melancholic stupor rarely assumes actual lethargic characteristics,
though a marked similarity may exist.
In all such instances the diagnosis is indicated by the history
far more than by direct observation of the case.
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1276
SYMPTOMS.
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SLEEP, MORBID, 1277
Mors certa, mors incerta,
Moriendum esse certutn omnino,
Mortum esse incertum aliquando,
(WiNSLOw, 1740).
Thus, profound sleep, and especially certain morbid forms
of sleep, may be confused, at least by hasty observers, with
actual death. A few instances of unwarranted burial have been
recorded, but the number of such cases has been singularly
amplified through popular imagination. While such occurrences
have doubtless been rather frequent in backward and some-
what savage countries, it should be repeatedly emphasized that
very few authentic instances exist in civilized nations and that
in Paris not a single case of this kind in the last thirty years has
come to the author's notice. Yet the instance above referred to
shows that such an occurrence is not an absolute impossibility.
The fact remains, therefore, that in the case of the practi-
tioner and more particularly the coroner's physician, professional
conscience and the anxiety of relatives often place before him
with singular force the question of apparent death and actual
death. It is therefore appropriate to recall here the definite signs
of death.
These indications are, on the whole, drawn just as they were
a century ago, from the direct or indirect observation of perma-
nent cessation of circulation, respiration, heat production, and
the functions of the nervous system. Modem observers have
merely devised a few improved procedures which permit of as-
certaining more accurately or more promptly the cessation of
function of the systems referred to.
A concise summary of these procedures, with brief descrip-
tions of the technic, is given in the annexed table.
♦ ♦ ♦
III. Hypersomnia Associated With Definite Clinical Syn-
dromes.— Meningeal disturbances in which somnolence or sleep
of varying depth and obstinacy is one of the chief features are
extremely common. Coma is a usual ultimate manifestation.
Special mention must be made, however, of three meningo-
encephalic conditions, now rather well-defined clinically, and
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1278 SYMPTOMS.
constituting actual examples of a narcoleptic meningo-encepha-
litis, vis., the sleeping sickness, lethargic encephalitis, and post-
influenzal meningeal disorders with narcolepsy.
The true sleeping sickness is, as is well known, endemic in
the African territories near the equator, and is specifically caused
by primary development in the blood and secondary development in
the cerebrospinal fluid of the parasite known as Trypanosoma gam-
biense. In its primary stage of blood infection, clinically manifested
in trypanosomic fever and glandular enlargement, somnolence is
absent or slight, and the disturbance might be mistaken for malaria
or filariasis ; under these conditions blood examination is necessary,
and will remove all doubt by revealing either the trypanosome,
Plasmodium, or filaria.
In its secondary or cerebrospinal stage, somnolence becomes
pronounced. In the waking state the patient is confused, sleepy,
with drooping lids, a dull expression, sluggish, benumbed men-
tality, and an unsteady gait. Somnolence is invincible, irresistible,
and permanent; sleep is constant or nearly so, but is relatively
light, the patient being easily roused by the slightest sound.
Fever, weakness, tremor, asthenia, emaciation, and progressive
cachexia complete the clinical picture. If the diagnosis was not
confirmed by blood examination in the preceding stage, examina-
tion of the cerebrospinal fluid now clinches it by revealing the
trypanosome.
Lethargic encephalitis has been the subject of a large mass of
literature in the last few years, whence it appears that the con-
dition is characterized by three main symptoms :
1. Fever, 39** to 40** C, associated with weakness and loss of
weight.
2. Dissociated ocular paralyses, sometimes combined with facial
paralysis. This would appear to be, perhaps, the most constant and
striking manifestation of the disease, the patients frequently seek-
ing medical advice because of seeing double (diplopia), because of
squint (strabismus), or because the lids fail to stay open (ptosis).
Upon examination there may be observed inequality of the pupils,
paralysis of accommodation, ptosis, and dissociated paralyses of the
motor nerves resulting in disturbed movements of the eyeballs.
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SLEEP, MORBID. 1279
3. A condition of sleep, a hypersomnia, ranging, as in trypano-
somiasis, from simple somnolence to constant, deep, lethargic sleep,
— without actual coma, however, as it is nearly always possible to
rouse the patient.
As subsidiary manifestations one may note depressive states,
paralysis of the extremities of hemiplegic type, sensory disturb-
ances, pain, mental disturbances, or signs of excitement, such as
muttering delirium, tremor, contractures, convulsions, and vaso-
motor disturbances.
Examination of the cerebrospinal fluid yields two important
signs:
1. Low cell content or absence of cells.
2. High sugar content, 0.7 to 1 gram to the liter, probably due to
stimulation of Claude Bernard's glycobulbar center.
3. Exceptionally the cerebrospinal fluid may be hemorrhagic.
In truth, the pathogenic agent in lethargic encephalitis is as
yet unknown, and its specificity not wholly demonstrated. While
the diagnosis is clinically obvious in cases combining typically
the triad of symptoms already mentioned, it is far more difficult
in the atypical, incomplete forms. It seems wise, therefore, tem-
porarily to maintain, with Claude, a clihical subdivision for :
Meningeal conditions with narcolepsy, in which the chief symp-
tom is somnolence, present in association with fever, spinal
rigidity, Kemig^s sign, retention of urine, diminished reflexes,
excess of albumin and lymphocytes in the cerebrospinal fluid, and
sometimes headache, squint, and inequality of the pupils.
Claude cautiously concludes: "The concurrence of these
narcolepsies attended by very pronounced meningeal reactions
with an epidemic of influenza would seem to justify the view of
some etiologic relationship between the two conditions."
As a matter of fact, narcolepsy may be met with in the majority
of meningeal disorders, including tuberculous meningitis in par-
ticular.
Brain tumor is associated with insomnia much more frequent-
ly than w^ith narcolepsy, which, in any case, is here of but slight
diagnostic service and of no localizing value.
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1280 SYMPTOMS.
IV. Morbid Sleep Associated With Motor Manifestations.
— This subject is highly complex and covers a singularly large
field, as it brings up the question of ambulatory automatism,
somnambulism, and the cataleptic states; leads, without undue
extension, to the interpretation of insane delusions and wander-
ing tendencies, to which it bears an obvious connection, and
brings up in last analysis the vexing problems of hypnotic sug-
gestion, dual personality, and responsibility of the human indi-
vidual.
One need here merely point out the interrelationship of these
questions and briefly recall the clinical significance of somnam-
bulism, which is obviously inseparable from ambulatory automatism.
The definition, limits, and meaning of the term somnambulism have
been rendered singularly vague through- the conflicts between dif-
ferent schools of thought concerning the nature and even the exist-
ence of hysteria. From the standfK)int of elementary clinical com-
mon sense, somnambulism is constituted of the fact that a sleeping
person may carry out more or less complex motor acts of which
he loses all remembrance upon awakening.
The MINOR SOMNAMBULISTIC STATES are commonly observed
conditions and may be witnessed in practically normal subjects under
the influence of some ratfier compelling thought or mild intoxica-
tion ; constitutional neuropsychopathic states predispose to these
manifestations. Their frequency is surprising if they are looked
for at all carefully. A person with simple nervousness, not des-
cribed by any definite clinical term, after a rather strenuous and
difficult voyage, during which a single obsessive thought had kept
him almost awake for a whole week, and in which, as he bore
with him a rather large sum of money, he h^d naturally had to
take certain precautions against being robbed, was led for months
to brief somnambulistic practices which consisted in his getting up
to see that the door of his room was closed and his wallet safe in his
inner coat pocket. The obsessive thought by which he had been
dominated for a whole week left an impression that wore off only
after several months.
Alcoholic somnambulism, met with especially m persons with
inherited psychopathic taint, is to be compared with the alcoholic
delusional state known as delirium tremens. In these minor somn-
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SLEEP, MORBID, 1281
ambulistic conditions inquiry should be made for some obsession,
hitoxication, or a neuropsychopathic predisposition. It seems diffi-
cult to set up an absolute line of demarcation between true somn-
ambulism and the clear-cut, active dream-states in which insane
illusion, continuing for a time "after the awakening," leads the
subject to carry out unconscious, absurd motor acts.
Attacks of MAJOR SOMNAMBULISM, featured by the duration
and complexity of the motor acts carried out, or by their repetition,
are of more definite clinical significance. They are hardly met with
in any conditions other than epilepsy and hysteria, and according to
some authors in neurasthenia and alcoholism. The forms en-
countered are sometimes sufficiently distinct to permit of the making
of a differential diagnosis.
Epileptic somnambulism (and fugue, or wandering tendencies)
is characterized sometimes by sudden onset, imperious, blind im-
pulses, the absence of any definite purpose, and complete amnesia.
Hysteric somnambulism (and fugue) frequently reflects the un-
conscious influence of a previous idea, whence there results some
degree of logical coherence of motor acts directed to some more or
less definite purpose, a vague consciousness of which may persist
after awakening.
Neurasthenic, or better, psychasthenic somnambulism (and
fugue), the occurrence of which is doubted by some writers, is
claimed to be associated with relative consciousness of the obsessive
idea, logical sequence in the motor acts carried out, and almost
complete remembrance upon awakening.
Alcoholic somnambulism is described as usually occurring only
among congenitally psychopathic subjects, and as exhibiting the
features of epileptic or neurasthenic somnambulism, according to
the individual case.
Brief mention may here be made of a condition of limited clin-
ical diagnostic interest, zns,, somnambulism indited during hyp-
nosis, which has been and still is the subject of acrimonious discus^
sions. This practice obviously serves the purposes of therapeusis
rather than of diagnosis.
♦ ♦ ♦
It has always been a matter of surprise to the author, and par-
ticularly so while writing this section, that most of the terms
81
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1282 SYMPTOMS.
relating to sleep, and especially its abnormal forms, are so vague
and ill-defined in their meanings. Thus, the terms catalepsy,
lethargy, and somnambulism each have two entirely different ac-
cepted meanings, popular and scientific, and even the latter is far
from being uniform as used by different writers. It has seemed in-
dispensable, therefore, to prepare a short glossary of hypnotic
terms:
Catalepsy.
1. A disorder featured by the ability of the limbs, and even the trunk,
to maintain throughout the attack positions which they had previously occu-
pied or had been placed in.
2. A condition in the presence of which the subject is unable to move, al-
though consciousness and sensation are retained.
[Historical (16th century) : "And if said vapors ascend to the brain,
they cause epilepsy or catalepsy, which is when the whole body remains stiflF
and cold and in the same attitude which it was in before the illness, the eyes
being open without seeing and without hearing." (Ambrose Pare, xviii, 52.)].
Derivation: KordXiT^tt, from Kard, down, and X^tt, seizure.
Dream.
An involuntary combination of images or ideas, generally without sequence,
sometimes very distinct and well co-ordinated, occurring during sleep.
Hjrpnosis.
Commonly: Artificial sleep. Example: Chloroform hjrpnosis. [Also
abnormal sleep, and the approach or production of sleep.]
Derivation: *Tirivj, sleep.
Hsrpnagogue.
Something which leads to sleep. Hypnagogue hallucinations: Visions
experienced when half asleep.
Derivation: "TirpoSf sleep, and dywyitt leading.
Hjrpnology.
The study of sleep. Xcfyot, treatise.
Hsrpnophobia.
Fear of sleeping: <f>6^s, fear or terror during sleep.
Derivative words: Hypnotic, hypnotism, and hypnolepsy.
Lethargy.
Deep and continued sleep in which the patient will talk if awakened but
does not know what he says, forgets what he has said, and sinks again into
slumber.
Derivation: X^a/ryto, TutOapyos, see Lethargus.
Lethargus.
A term applied by the old Greek physicians to a remittent type of fever
featured by drowsiness.
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SLEEP, MORBID, 1283
\ifiafnfoty as adjective, one who is somnolent ; as noun, the desire to sleep ;
from XiJ^, forgetfulness, without exact knowledge of the mode of derivation.
Common acceptance of the term :
1. A state of apparent death characterized by almost complete suspension
of respiration and circulation.
2. Profound, irresistible, uninterrupted sleep, lasting several hours or days.
Narcosis.
Stupor due to the action of a narcotic.
Derivation: lSiapx<»fTix6s, from i^pxv» stupor.
Narcotic
That which produces stupor, like opium, hyoscyamus, belladonna, etc.
Narcotism.
The aggregate of the effects caused by narcotic substances. Same deriva-
tion.
Narcotin.
A chemical term. An alkaloid discovered in opium by Derosne in 1803;
also known as Derosne's salt.
Derivation : N arpptic.
Narcotico-acrid.
An adjective and toxicologic term. A word applied to the poisons which,
like aconite, helleborus, etc., induce both narcotism and inflammatory effects
in the intestine.
Derivative words: Narcolepsy, narcomania, etc.
Oneiric.
From 6p€tpos, a dream. Something in the nature of a dream. Oneiric de-
lirium : Dream-like delirium.
Derivative words: Oneirocritia (the art of interpreting dreams) ; onei-
romancy (divination or diagnosis through dreams).
Sleepw
Complete stupor of the senses, or, in physiologic terms, a temporary cess-
ation of the activity inherent in animal life.
Somnifacient
Something which induces sleep.
Derivation: From the Latin, somnus, sleep, and facere, to make.
Sonmiloquy (somniloquence).
The habit of talking during sleep.
Derivation: From the Latin, somnus, sleep, and loqui, to speak.
Somnolence.
Slight drowsiness which is unpleasant but irresistible.
Derivation: Latin, somnolentia, from somnus.
Somnolent
Affected with somnolence.
Derivation: Latin, somnolcntus, from somnus.
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1284 SYMPTOMS,
Somnambulism.
i. A disorder of the cerebral functions featured by a tendency to repeat
during sleep acts that have become customary, or of walking and carrying
out various motor acts without retaining any memory of them on awakening.
2. Magnetic somnambulism : A special nervous state into which highly
susceptible persons, especially hysteric women, can be thrown by a species
of psychic influence.
3. Commonly accepted meaning : A nervous state during which a sleeping
person rises from bed and carries out certain motor acts which he fails to
remember on awakening.
Derivation: Latin, somnus, sleep, and ambulare, to walk.
Soporific.
Something which induces profound sleep.
Derivation: Latin, soporificus, from sopor, sleep.
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SLOW PULSE r/?pa5i5$, alow, ^ap^w^t, heart;!
L slowing of the heart. J
(BRADYCARDIA).
True bradycardia is attended by a slowing of the rate of car-
diac contraction to 56 per minute or lower. Palpation of the
/5 1 I I f I I I I I I I I I ( I I I , I , I
A
F
^ normal
Fig. 862.— Normal heart-rhythm.
^J\jjJ\;r^AjJ\}j^
Fig. 863. — Tendency to auriculoventricular dissociation. Delayed
conduction. Prolongation of the a-c period.
pulse in combination with auscultation of the heart is essential
for the recognition of true bradycardia. Pseudo-bradycardia, or
bradysphygmia, i.e., slowing of the pulse rate without actual
(1285)
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1286
SYMPTOMS.
- slowing of the heart rate, may occur in the alternating pulse and
in the bigeminal pulse of extra-systole when the second pulsation
is too weak to be perceptible at the wrist; under these conditions
I I I I I I I I I I I • I I I I a I I I I I I I I I I.
II II
II II
Fig. 864. — Partial heart-block. Incomplete auriculoven-
tricular dissociation.
only one pulsation is felt for every two beats of the heart (see
Arhythmia).
• I I I I I I I I f f I » I I I I I I I I 1 1 I I I I I t 1
\ \ \ \ \ \ \
\ \ \ \
Fig. 865. — Complete auriculoventricular dissociation. Co-ordination be-
tween the contractions of the auricles and ventricles is wholly lost.
Although recent investigations, such as those of Daniel
Routier, of Frederiq, and Petzetakis, in particular, have shown
that the accepted division of bradycardia into several varieties is
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SLOW PULSE (BRADYCARDIA),
1287
not literally valid and that rather numerous ambiguous or
transitional conditions occur, the subjoined synoptic table is
available for practical purposes.
DIFFERENT TYPES OF BRADYCARDIA.
Clinical
Graphic
Various.
Features.
Features.
Reactions.
History.
Due to Intracardiac Disease.
Disease of the bundle of His (gumma). Ventricular myocardial
disease (uncommon) (fibrous or rheumatic myocarditis).
Bradycardia.
Complete indepen-
No reaction to Specific history most |
1. Very pro-
nounced (30
dence of the
atropine.
frequently.
auricular beats,
No reaction to
Sometimes com-
or 40 beats
the rate of which
the respiratory
bined jaundice and
per minute, or
remains practic-
movements, to
uremia.
less).
ally normal, from
exertion and
During the initial
2. Continuous
the ventricular
posture, nor to
period (paroxys-
or paroxys-
beats, with their
fever.
mal bradycardia),
mal.
markedly reduced
severe and pro-
rate.
longed epileptoid
(Heart-block.
seizures (Stokes-
Auriculo- ventric-
Adams disease).
ular dissociation.)
Due to Pathologic Change or Functional Defect in the Vagus.
Bradjrcardia.
Usually a total Marked reac-
Nervous depression :
1. Moderate:
bradycardia with-
tion (accelera-
Lassitude, exhaus-
56 to 40.
out auriculo-ven-
tion) to atro-
tion, shock, neuras-
2. Transient
tricular dissocia-
pine.
thenia, and psy-
tion.
Positive reac-
choses.
tion (acceler-
Hepatic: Jaundice.
ation) to mo-
Pharmaceutic:
tion, posture,
Strophanthus, digi-
respiration,
talis.
exertion, and
Autointoxication :
fever.
Uremia.
Nervous lesions in-
volving :
Medullary center:
Hemorrhages, soft-
ening, arterioscle-
rosis, etc.
Points of emer-
gence : Meningitis.
Nerve - trunk : En-
larged tracheo-
bronchial glands,
mediastinal turn-
ors, or aneurysm. 1
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1288
SYMPTOMS.
The above schematic classification is clinically convenient, but
the fact that there are still many obscure and as yet incompletely
elucidated points should be kept in mind.
"■vnr^^^r-^rv^ ^r'v^nr-
r^r^'Vy v^»'V''^>-7r'^^^^p'v^'
Fig. 866.— Delayed conduction (RouHer),
1. Anatomic: There exist auriculo- ventricular bundles inde-
pendent of the bundle of His (Stanley Kent).
Fig. 867.— Partial heart-block (Routier),
2. Physiologic : Persistence of auriculo-ventricular conduction
after section of the bundle of His (Stanley Kent).
i.5J3.DiSioc complete
Fig. 868. — Complete dissociation (Routier).
3. Physiopathologic : (a) Removal of block from some hearts
by adrenalin (D. Routier).
Fig. 869.— Total bradycardia (Routier).
(b) Block in some hearts upon compression of the eyeballs
(Petzetakis).
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SLOPy PULSE (BRADYCARDIA),
1289
The atrc^ine test consists in injecting- into the bradycardic
subject 0.001 gram of atropine sulphate (1 cubic centimeter of
a 1:1000 solution), and later, in the succeeding days, 2 cubic
centimeters if the first test was negative and well borne by
the patient.
• c
Fig. 870. — Bradycardia due to auriculoventricular dissociation the
result of a gumma of the bundle of His.
Case 1257. H., 1855 ; pulse, 27 ; pressures, 25%o. Former
specific infection. Wassermann +.
The test is considered negative if, in the hour following the
injection, acceleration occurs to the extent of less than ten beats
per minute.
The test is considered positive if, in the hour following injec-
tion, acceleration greater than twenty beats per minute occurs.
The test is considered doubtful if, in the hour following in-
jection, an acceleration ranging between ten and twenty beats
per minute takes place.
|M
19l7.2t.1f
Fig. 871.— Total bradycardia due to depressive psychoneurosis.
It is held that any bradycardia which is not changed in the
atropine test cannot be considered a nenous bradycardia. Atro-
pine, termed by Frangois-Franck *'the curare of the nerves of
the heart," prevents the inhibitory, bradycardic action of the
vagus. This rule, however, is still under widespread discussion,
and can be accepted only provisionally and as being subject to
change upon further investigation.
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SORE THROAT FAngina, frcm angere,]
(ANGINA). L to mffocate. J
No classification of sore throat (angina) that is both rational
and clinically serviceable can as yet be presented. A classifica-
tion based on bacteriologic grounds alone, while theoretically at-
tractive, is soon found inadequate for practical needs, i.e., for the
securing of well-founded indications for rational treatment; pre-
cisely the same is true of a purely clinical classification, although
such a division is practically simple of attainment. None of the
outlines based on but a single feature will stand the test of
clinical usa^e, all being at fault in more than one respect ; all one
can do is to combine in the least objectionable manner the
clinical and bacteriologic data as well as those relating to the
course of the disease. The plan of division hereinafter followed,
which is in rather general use, is one of the least defective in
the present state of our knowledge.
Acute angina may be primary, ue., occur as the outward
evidence of an infection involving the pharynx first, or secondary,
i,e,, occur as the pharyngeal manifestation of a more general infec-
tion, whether constituting its first or its last symptom.
Whether primary or secondary, sore throat appears to the ob-
server either in the form of a red throat (red angina), attended with
more or less diffuse and intense redness of the tonsils and pharynx,
without white patches;
Or in the form of a white throat (white angina), attended
with the presence of whitish or grayish exudates, which vary in
conspicuousness according to the degree of contrast with the
red background of inflamed pharyngeal mucous membrane.
Such white anginas occur in the following four types :
(a) Pultaceous. — The tonsil shows disseminated white points
or is covered with a grayish, creamy, puriform, friable, non-
adherent exudate which can be detached merely by contact of
the tongue depressor or of cotton on an applicator.
(1290)
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SORE THROAT (ANGINA). 1291
(&) Vesicular. — The pharynx, soft palate, and tonsils are at
first the seat of a more or less extensive and confluent vesicular
eruption, rupture of which results in the formation of small cir-
cular ulcerations or small patches of false membrane
(c) Pseudomembranous. — Thfe pharynx, red and swollen, is
covered with grayish yellow false membrane which is adherent
tOj the mucous membrane, thick, detached only with difficulty,
causing the mucous membrane to bleed, and recurring more or
less rapidly after removal.
(d) Ulceromembranous. — This type runs a two-stage course :
First stage: False membrane on the tonsil, whitish, only
slightly adherent, and readily reproduced.
Second stage: Ulcers with punched-out margins encroach-
ing upon the pillar and digging into the tonsil, the base contain-
ing a pseudomembranous exudate; no induration.
(1) Bacteriologic examination, especially necessary in the
pseudomembranous and ulceromembranous forms (see Bacteriol-
ogy) ; (2) the associated clinical signs, and (3) the visible features
, just referred to, allow, as shown in the subjoined table, of a rather
thorough and clinically serviceable discrimination between the vari-
ous forms of acute angina.
Lastly, reference may be made to the probably unsuspected
frequency of chronic or subacute pharyngeal infections as the
underlying cause of '*cr>^ptogenic" fevers, refractory rheumatoid
manifestations of undetermined nature, and of inveterate, vague
deficiencies in the general condition of the body. The pharynx
and nasopharynx certainly constitute one of the great foci of
systemic infection. They should always be subjected to ex-
amination, especially in the presence of subacute or chronic
febrile states and erratic joint manifestations the true source of
which has not previously been revealed.
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1292
SYMPTOMS.
C9 I
O 1
"rt 6
S «
w C
CO
ill >
J"-
b:2
P to "M
«5
.. to
^ m ^
♦3 « 5 oj
!3 55 4^ a
IS
i: o
s
o
s
I!
Hot
CO p
In o
^^ ^
c« p O
6 ^ i^ '
be
rj_cic6
.s
CO
<
O ^« fl 3 5 ^
A ffi . a; !: A U4 . 9
si
So--
S .2 aligns. 2 p ^^^
a. -S a'^Bh g-c -s .gS^g
Q ^ c< Q ,
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SORE THROAT (ANGINA),
1293
9 £ .
.PI I
III 1 1
■ssg |5«
<0 " . • a 3
0) 0) I, « 9 w O
^111 c I
Hill
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TINNITUS AURIUM. [Tinnitus, "a tinkling:']
"De minimis non curat praetor" is a well known adage. It would
be unwise, however, to apply it to the minor symptom known as
tinnitus aurium, or ringing in the ears. While sometimes really of
negligible clinical significance, it may, on the other hand, be an
indication of previously unsuspected morbid conditions. When
persistent, it becomes to the patient an unbearable obsession,
which may lead to what amounts practically to a delirium.
In a patient who comes complaining of distressing and obstinate
tinnitus, whether in the form of whistling sounds, cockle-shell
sounds, or buzzing sounds, the proper procedure is to examine
first of all the ear and make a systematic search for any lesion
of the external, middle, or internal ear which might be the cause
of the tinnitus.
Tinnitus due to quinine, subjectively resembling the ringing
of bells and accompanied \>y hardness of hearing and a heavy feel-
ing in the head is practically a normal condition which passes oflF
completely in a few hours. It occurs so constantly after quinine
that it serves, in a measure, as a control of quinine exhibition.
Where it is lacking the physician should carefully inquire: 1. As
to whether the patient has actually taken the dose prescribed. 2.
Whether the salt supplied was actually the salt ordered, 3. Whether
the medicine was taken in the manner specified (with an acid
beverage).
When intense, these aimcular disturbances may become
abnormal and alarming, or even progress toward a highly severe
vertigo comparable to that of Meniere's disease. According to
Lermoyez, "all depends on the condition of the labyrinth, and
if there is the least labyrinthine lesion, the least dose of drug is
sufficient to produce manifestations of vertigo," and the adminis-
tration of quinine is contraindicated.
Such marked disturbances are seldom induced by sodium sali-
cylate; yet one should take into account the possibility of a tem-
(1294)
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TINNITUS AURIUM. 1295
porary brain congestion with tinnitus, transient deafness, slight
dizziness, flushing of the face, and even epistaxis. i
The frequency of tinnitus aurium in chronic aortitis and
arteriosclerosis is well known; it may even induce giddiness or
fainting spells. It is often, a preliminary indication of further
trouble to come. In any elderly patient complaining of tinnitus
and dizziness a careful examination of the cardiovascular system
and kidneys should be made, including auscultation, blood-pres-
sure determinations, and uranalysis. The pathogenesis is com-
4
3
Fig. 872. — Mode of production of tinnitus aurium (G, Laurens),
Tinnitus is the result of irritation of the internal ear. The latter may
be due, in turn, to a disturbance: (o) Of the external ear (wax), ex-
erting pressure on the drumhead, ossicles, and endolabyrinthine fluid (1).
(b) Of the middle ear (3), eg., otitis or catarrh or disease of the
Eustachian tube (2), in the same way as the preceding condition, (c)
Of the internal ear (4), e.g^, disturbed circulation, anemia, congestion,
constitutional disorders, arteriosclerosis, etc
plex, but the condition is probably dependent largely upon reflex
spasm of the capillaries in the brain, probably due, in turn, to
the irritation to which the intima of the aorta is subjected
through changes in the blood-pressure caused in aortic and
arteriosclerotic cases by changes of posture, locomotion, and
exertion.
Tinnitus aurium and vertigo are very closely allied (see
Vertigo).
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1296 SYMPTOMS.
Usual Causes of Tinnitus Aurium.
External car: Impacted cerumen or a foreign body.
Middle ear: Otitis media, especially with exudation and pressure on
the stapes, or obstruction of the Eustachian tube.
Internal ear: The exciting cause of tinnitus is always actually some
form of irritation of the internal ear, some disturbance in its circu-
lation (hyperemia or ischemia) , or an increase or decrease of in-
tralabyrinthine pressure.
In the absence of any apparent disease of the internal or middle ear:
An examination should be made for degeneration of vessels, dia-
thetic disorders, and pharmaceutic or autogenous toxic states. These
conditions induce tinnitus through the hyperemia or ischemia, or
the rise or fall of pressure which they cause in the internal ear.
The following conditions should be looked for :
Arteriorenal degenerative changes: Arteriosclerosis or Bright's dis-
ease.
Diathetic disorders of the neuroarthritic type: Gout or diabetes.
Drug intoxications: Quinine or sodium salicylate.
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TONGUE, DIAGNOSTIC FEATURES
RELATING TO THE.
The tongue has been aptly said to "mirror the stomach ;*' but
it also supplies a clue to the fimctional state of many other
structures, when inspected by a practised eye.
I. Examination of the Tongue Reveals Neither Ulcerations
nor Tumor-like Formations. — Aside from all malformations,
ulcerations, and tumors of the tongue, to which brief reference
will be made later, the appearance of the lingual mucous mem-
brane is in itself highly informative. The normal roseate and moist
appearance, with the characteristic leaf-like oblique striations and
the posteriorly situated V-shaped angle, are too familiar to require
mention. It may be pointed out, however, that even under physio-
logic conditions the lingual mucous membrane is frequently covered
with a light grayish normal coating resulting from the continuous
desquamation of the superficial epithelia. This coating accumulates
as the interval since the preceding meal increases ; mastication of
solid food, on the other hand, is generally sufficient to cause it to dis-
appear. One may therefore expect to find this coating thicker and
more persistent in persons on a diet, taking liquid food, as well as in
the morning on awakening. The presence of such a coating in the
morning obsesses some patients to such an extent that they scrape
their tongues every morning with some scraping instrument.
On the other hand, in sialorrhea the tongue is red, moist, and
glistening; it is, in fact, too clean-looking, and should lead to the
discovery of excessive salivation, the cause of which is thereupon to
be inquired into.
With the practically normal coating is combined an almost rasp-
like dryness in heavy smokers and especially in mouth-breathers
(coryza or adenoid vegetations).
The whitish or grayish color of the coating may be changed as a
result of the ingestion of certain foods or drugs. It may turn to a
82 (1297)
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1298 SYMPTOMS.
color ranging from purplish red to dark brown upon ingestion of
red wine, of blackberries, of chocolate, of extract of licorice, of
catechu, of cinchona, of fresh nuts, of tobacco, etc.; it becomes
saffron yellow upon ingestion of laudanum or rhubarb, and creamy
white in persons on a milk diet.
Epiglottis
Median glosso-
epiglotUc fold
Faucial tonsil
Lingual follicle
Foramen
ClrcumTallate
papilla.
Fungiform
papilla
Median
Fig. 873.— Dorsal surface of the relaxed tongue (Poirier),
Certain peculiarities the result of defective functioning of the
digestive tract are universally known, in particular the dirty yel-
low brown coating of dyspepsia and indigestion. In gastric dis-
orders the brown coating is thick and the tongue flattened out,
with its margins sho\ying imprints of the teeth, sometimes with
small red elevations, consisting of the papillae, when clearing
begins.
Some infectious diseases affect the tongue in almost patho-
gnomonic fashion:
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TONGUE, DIAGNOSTIC FEATURES. 1299
The "strawberry'' or "raspberry/* scarlet red, bare tongue of
scarlet fever.
The varnished, porcelain-like tongue, with a red band at its
margins, of grippe at its height.
The parched, dry, fissured tongue, covered with dry and black-
ened mucus, of the typhoid patient (when poorly cared for, one
might add, i.e,, where the ordinary measures of oral hygiene are not
carried out).
The "sooty," dry, black, rough, "parrot tongue'' of grave infec-
tions of the typhoid type and of certain varieties of uremia.
The phrase "certain varieties" is used in reference to uremia be-
cause in some other forms, in particular in certain instances of acute
azotemia, the author has had occasion to observe a thick, **viscou^'
tongue, with excessive flow of viscid saliva containing a large
amount of urea.
II. True glossitis is reached by insensible gradations from the
preceding group.
1. Thrush is the most frequent disorder in infancy, being a re-
sult of poor quality of the milk or unclean bottles. In the adult and
elderly, it may occur as a complication of grave infectious states and
of cachexias, as in advanced tuberculosis, severe typhoid fever,
infections of the urinary tract, etc. The tongue, at first red and
"varnished," becomes covered with small grayish masses like milk
curds, which thereupon draw together, fuse, and expand into creamy
patches which can be detached rather easily by rubbing.
2. In the mercurial stomatitis of patients intolerant of mer-
cury and ignorant of oral hygiene, the tongue is swollen, viscous,
of a dirty gray color, and bearing imprints of the teeth on its
margins. The malodorous breath, the ptyalism, the coexisting
stomatitis, and the history of having taken liiercury lead directly
to the diagnosis.
3. Aphthous fever is, as a rule, rather discretely manifested on
the tongue. Aphthw may be noted at the tip and along the margins
of the tongue in the form of vesicles similar to those of skin herpes
or of a circle of swollen mucous membrane; the vesicles rupture
after a few days, leaving small circular ulcers of the size of a pin-
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1300 SYMPTOMS.
head up to that of a lentil, with grayish bases and irregular
margins.
4. Marginal exfoliative glossitis is a chronic, recurrent affec-
tion of the tongue characterized by desquamation of plate-like
scales with circinate, ^'geographic" margins, usually with their
convexity directed outward.
The very multiplicity of the terms applied, vis,, pityriasis
linguae (Rayer), geographic tongue (Bergeron), marginal ex-
foliative glossitis (Fournier), eczema desquamatif lingual en
aires, margine (Besnier), psoriasis linguae, etc., is sufficient proof
of our ignorance of its nature — which may perhaps be variable
and complex. It does not seem to be of syphilitic origin; at
least it is not amenable to specific treatment. Yet, as in the
case of leukoplakia, to be next discussed, the distinction to be
made from syphilitic glossitis is most difficult, and how many derma-
tologists have — as of yore in connection with tabes and general
paralysis — used the phrase **parasyphilitic manifestation" in this
connection? The "What do I know?" attitude of Montaigne is
alone justifiable at the present time.
5. Leukoplakia buccalis appears in the form of amorphous,
pearl-white, patches on the tongue, without any special marginal
band; the patches are irregularly dispersed, thin, bluish, trans-
lucent, discrete at first, and show an almost invincible tendency
to extend, thicken, and undergo hardening, with resulting for-
mation of whitish, thick, adherent patches, which become fissured
and cracked through desquamation. Such patches may also be
observed on the mucous membrane of the lips and on the inner
surface of the cheeks.
Syphilis is noted in a very grtat many of these cases, and it
seems likely that a large number of leukoplakias are of syphilitic
origin. Yet such exciting, provocative, or predisposing causes as
tobacco (nicotinic leukoplakia), traumatism (dental leukoplakia,
with dental caries or poorly made dentures), neuroarthritism
(irritative neuroarthritic leukoplakia of Brocq), etc., play a role
in their production which is not negligible.
The marked clinical interest of leukoplakia resides in its rela-
tionship to syphilitic glossitis and the possibility of the occur-
rence in it of epitheliomatous degeneration.
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TONGUE, DIAGNOSTIC FEATURES. 1301
Brocq, with his usual ability, discussed this question, which
is of prime clinical importance, in 1919.^ The following three
points are worth quoting here:
(a) There occurs a buccal lichen planus which is sometimes
hard to distinguish from other conditions. It is marked by the
presence, on the inner aspect of the cheeks, of white striae exhibiting
occasional small nodular elevations; on the tongue one observes
instead opalescent spots, which coalesce to form more extensive
patches.
(&) Leukoplakia nearly always develops on a syphilitic substrate,
but not always. Non-syphilitic leukoplakic^ do occur.
These two propositions are of marked practical import, for
while they justify antisyphilitic treatment in the majority of
cases, they condemn the blind tendency to institute intensive and
repeated antisyphilitic treatments in all persons with ordinary
white patches. In playing the part of the wise and well-versed
clinician, it is well to make a careful diagnosis in these cases
(discrimination from lichen planus, or syphilis — manifest, prob-
able, or non-existent) and to act accordingly as regards treat-
ment.
(c) It is certain that many leukoplakias undergo epitheliomatous
degeneration. "Yet, many subjects harboring leukoplakial patches
do not show degeneration of the disorder into cancer; such degener-
ation of the disorder is even relatively rare when the patients,
warned in good time, carry out and persistently continue all the
required hygienic measures." (Brocq, loc. cit.)
6. Syphilitic glossitis is of greater importance in the adult
than any of the preceding varieties. It is well established, to be
sure, that the majority of instances of leukoplakia and a few in-
stances of marginal exfoliative glossitis are syphilitic.
Syphilis may yield lingual manifestations in any of its stages :
Primary (chantre of the tongue) ; secondary (various forms of
secondary glossitis, mucous patches) ; tertiary (gummas, tertiary
syphilomas).
Some varieties are merely exudative and exfoliative, like the
majority of the secondary manifestations; others are tumor-
1 Brocq : Presse mid., May 22, 1919.
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1302 SYMPTOMS.
producing and ulcer-forming (gummas). They consequently oc-
cupy a border-line position in the didactic classification herein
followed. Yet they will be placed in the present group. They
serve for purposes of transition to the clinical cases of glossitis
associated with ulcers or tumor-formations.
Chancre of the tongue is relatively uncommon, representing
hardly more than 10 per cent, of the cephalic chancres. It is gen-
erally located at the tip of the tongue, and exhibits either an erosive,
papulo-erosive, or ulcerative character with diffuse induration. The
submaxillary lymph-glands are always and the sternoid mastoid
glands sometimes involved, and exhibit the usual features of pri-
Fig. 874. — Extensive gummatous Fig. 875. — Tertiary syphilitic scle-
ulceratiou of the tongue (Musee de rosis of the tongue (Musce de Saint-
Saint-Louis). Louis).
mary syphilitic glandular enlargements (one large node with sur-
rounding smaller nodes, practically painless; see Neck, glandular
enlargements in). The history of infectious contact, the examina-
tion for the spirochete, and eventually the appearance of the roseola
constitute, as always, the chief diagnostic factors.
Secondary lingual syphilides (mucous patches) are usually
discrete and demand a careful search. They occur in the form of
round or elliptical patches, of smooth "depapillated" appearance,
contrasting with the normal granular background of the lingual
mucous membrane.
Tertiary syphilides occur in two main clinical forms, 7^'c., the
sclerous and the gummatous, which in exceptional instances arc
combined in a mixed sclero-gummatous form.
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TONGUE, DIAGNOSTIC FEATURES. 1303
Gumma of the tongue may be superficial or deep. When
superficial, it causes local elevations of the dorsum in the form of
multiple small nodosities varying in size from a leaden shot to a
pea, and sometimes arranged in a horse-shoe-shaped figure. If
tuitreated, it softens and ulcerates, leaving a relatively deep, cyclic
or polycyclic ulcer with clear-cut margins. When deep, it is situated
in the midst of the muscles of the tongue, forming there a hard
node, nearly spheric or ovoid in shape, of hazelnut to walnut size,
painless, and unaccompanied by any glandular reaction. If allowed
to progress unopposed, it enlarges and involves the dorsal surface of
the tongue, softens, and ulcerates, discharging a characteristic
gummy fluid. This constitutes the deep tertiary syphilitic ulcer, with
punched out margins, discharging base, not bleeding, and unattended
with any glandular reaction unless infection or secondary degenera-
tion sets in.
Fibrous glossitis, like gumma, may be either superficial or
deep-seated.
When superficial, the cords and patches of fibrous tissue form
irregular islets of superficial induration, sometimes smooth, at
other times leucoplastic, the tongue at times assuming a stringy-
appearance owing to the presence of a network of shallow fissures
lined with fibrous tissue.
When deep-seated, they infiltrate the major portion of the
tongue, especially its anterior region, imparting to it a hard,
wood-like consistency. The simultaneous presence of large and
small knob-like elevations, lobulated, smooth, and devoid of papillae,
gives to the tongue an absolutely pathognomonic aspect (lingual
cirrhosis). Like gummatous glossitis, fibrous glossitis is not
accompanied by any secondary glandular enlargement and is
practically painless. These two features should never be over-
looked, as they are of capital diagnostic import.
III. A Tumor-like Enlargement is Present— In most instances
the patient first notices that certain movements of the tongiie are
somewhat hard to execute. Clinical examination thereupon re-
veals some abnormality in the size and consistency of the organ.
Brief reference may be made, as an altogether exceptional pos-
sibility, to cysts (either parasitic, glandular, or congenital), which
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1304 SYMPTOMS.
are very hard to diagnose. Unless an exploratory puncture is made,
there can be nothing more than a mere presumption of the presence
of a cyst, based on its fluid consistency — ^which is, however, not easy
to detect — and on the history. The same is true of the connective
tissue tumors, viz,, lipoma, fibroma, fibrosarcoma, and chondroma.
In the presence of a tumor-like enlargement of the tongue, the
chief possibilities which should come to the physician's mind are
syphiloma, epithelioma, tuberculoma, and actinomycosis.
Nothing more need be said concerning the syphilomas, the
customary features of which have already been briefly referred to
— gumma and fibrous glossitis, characterized by painlessness and
the absence o4 glandular enlargement.
The condition which has most often to be differentiated is
epithelioma. In theory such differentiation is easy. The epi-
thelial induration present shows a special consistency; it is
imperfectly circumscribed, having a tendency to infiltrate the
neighboring tissues ; it is attended with a varying degree of ten-
derness, or may cause actual pain ; the accompanying glandular
enlargement consists at first of small separate nodes, which roll
beneath the finger and coalesce only at a late stage of the dis-
order; finally, the condition occurs only in elderly subjects and
its tendency toward progressive extension to surrounding tissues
is manifest and obstinate. Nevertheless, the actual distinction of
certain hypertrophic forms of epithelioma of the tongue from
fibrous glossitis is sometimes a matter of great difficulty and
baffles even the most astute clinicians, particularly in view of
the fact that there occur mixed forms giving rise to a hybrid
cancerosyphilitic glossitis — a condition which has been carefully-
studied by Verneuil. The physician is thus easily induced to
institute the therapeutic test by brief but active administration
of potassium iodide and mercury or potassium iodide and arsenic-
als — a procedure which rapidly dissipates the disease if it is
syphilitic or, on the other hand, stimulates it temporarily to
greater activity if epithelioma is present
Tuberculomas, which are very uncommon in the tongue as
compared to the syphilomas and epitheliomas, appear usually
on the upper surface of the organ. They are sensitive or pain-
ful on pressure, engorgement of lymph-nodes is exceptional, the
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TONGUE, DIAGNOSTIC FEATURES. 1305
patient is always a tuberculous individual, and, if necessary, ex-
cision of a bit of the tumor tissue for examination and injection
of the diseased tissue into a guinea-pig will lead to recognition
of the presence of the tubercle bacillus.
Lingual actinomycosis may so resemble fibrogummatous
syphilis or a deep tuberculoma as to be readily mistaken for it.
If the condition is only thought of, however, the diagnosis may
be settled by exploratory puncture and examination on a slide
(with cover-slip) of the characteristic small yellow granules, sug-
Fig4 876. — Actinomycosis.
gesting powdered iodoform, which the fluid withdrawn allows
to settle on the walls of the tube into which it has been ex-
pressed. When stained with picrpcarmin they appear as if
made up of a central felt-like central mass consisting of mycelial
filaments and surrounded by a radiating zone of ovoid bodies
disposed like petals, the whole resembling to some extent a
daisy.
Lastly, mention may be made of a congenital anomaly, for-
tunately very rare, constituting a real pathologic curiosity, viz,,
macroglossia, which, undergoing development during later child-
hood and even the period of puberty, may lead to permanent
prolapse of the tongue, which has become too large for the buccal
cavity.
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1306 SYMPTOM!^',
IV. Ulcerations are Present. — Small ulcers on the tongue may
be observed :
1. During an attack of whooping-cough; there is ulceration
of the lower surface of the tongue and its frenum, due to forcible
projection of the tongue against the teeth during cough.
2. As a result of biting of the tongue ; there is present a cut-
like ulceration along the margins of the organ, e,g., in epilepsy.
3. As a result of dental traumatism, the ulcer being situated
opposite a badly decayed, broken, or deviated tooth.
Fig. 877. — Macroglossia {Mikulicz and Kiimmel),
The more extensive ulcerations of the tongue are due to the four
following major causes of tumor formation :
Syphilitic ulcers. Tuberculous ulcers.
Neoplastic ulcers. Actinomycotic ulcers.
Syphilitic ulcers are represented mainly by ulcerated gum-
mas; mention need here be made only of their characteristic
depth, perpendicular margins, sloughing base, absence of bleed-
ing, and relative painlessness, as well as the usual absence of
glandular enlargements and the history. In the event of doubt
the therapeutic test will settle the diagnosis.
Neoplastic ulcers, or epitheliomatous ulcers, show lacerated,
irregular margins, with suppurating bases, and oozing of blood,
and are superimposed on an indurated mass which infiltrates the
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TONGUE, DIAGNOSTIC FEATURES, 1307
neighboring tissues. There is copious salivation and a malodorous
breath. Such ulcers give .rise to pain, sometimes of marked
severity, radiating toward the ears. The submaxillary lymphatic
ganglia are involved.
Tuberculous ulcers are generally broad and superficial, multi-
ple, writh clear-cut, but only slightly elevated margins, with a
Fig. 878.— Tuberculosis of the tongue.
pale, grayish base, not prone to bleed, but causing much pain.
Sometimes they are surrounded by discrete yellowish points or
granulations resembling millet seeds, constituting actual small
tuberculomas, which would be pathognomonic were similar mani-
festations not sometimes observed in actinomycosis.
Actinomycotic ulcers may present an appearance similar to
that of the preceding type of ukers ; they exude serous pus, in
which the characteristic yellow granules already referred to
should be sought.
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TREMOR. [Tremulare, to tremble.^
Tremor consists of regular oscillatory movements taking
^ place at a varying rate and with varying amplitude, involving the
entire body or an extremity, and symmetric in both directions
from the resting position. The mode of production of tremor
is still obscure and a mooted subject.
Tremor may be either accidental (transitory) or essential
(permanent).
I. Accidental (transitory) tremor is chiefly :
(a) Emotional, in which it is easily traced to its cause, e.g.,
fear or other emotional stress.
(fc) Pyrexial, frequently marking the onset of an acute infec-
tion (see Chills).
The initial chill of pneumonia and that occurring in the first
stage of the malarial paroxysm are well-known examples, both
of which are as a rule traceable to their cause.
(r) Cryogenic, or brought on by cold, and in the initial stage
of fevers. "You are trembling, Bailly? — Yes, but it's because
Tmcold!"
II. Permanent tremor occurs in two forms :
Tremor during the execution of volitional movements (kinetic
or intention tremor), typically exemplified in disseminated sclerosis.
Tremor at rest (static tremor), exemplified in paralysis agitans.
A. Tremor during voluntary motion. — Charcot ascribed this
form of tremor to the usual persistence of the axis cylinder de-
prived of its myelin sheath in the midst of the areas of sclerosis.
Pierre Marie compares such an axis cylinder to an electric wire
from which the insulation has been removed and along which
an escape of electricity occurs causing the tremor.
(a) This type of tremor is illustrated in the highest degree and
in the utmost state of purity in disseminated sclerosis. While
(1308)
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TREMOR. 1309
absent during rest, it starts up when movements are undertaken. It
quickens, develops, and exhibits increased amplitude during the
execution or repetition of the motor act. The rate of vibration is
always moderate, vi::., six or seven vibrations per second. The
amplitude, which increases during the performance of the motor act,
may become very great — 5, 10, or even 30 or 40 centimeters.
In this disease the tremor is accompanied by vertigo or apoplecti-
form seizures, by ocular disturbances and nystagmus, by exaggerated
reflexes, and sometimes by spastic paralysis and slow, scanning
speech.
(b) Hereditary tremor (with a similar tremor or merely a neu-
rotic tendency in the parents) may be considered to be present when
the tremor is absent during complete rest, exhibits a rapid rate of
vibration, develops with movements but does not increase during
their execution, involves particularly the upper extremities, eyelids,
lips, and face, and set in slowly during childhood or adult life. It is
sometimes present to a slight extent during rest.
(c) -Toxic tremor, due to alcohol, coflFee, tea, lead, mercury, etc.,
is remittent and of the intentional type, of intermediate rate, and
but slightly marked or absent during rest. A brief inquiry as to the
subject's past history will generally settle the diagnosis. This is by
far the commonest kind of tremor.
(d) Tremor is said to have been observed sometimes in the
secondary stage of malaria,
B. Tremor during rest (static tremor) is but slightly or not
at all aflFected by voluntary movements.
(a) This variety of tremor is most characteristically exempli-
fied in paralysis agitans (Parkinson's disease). In contrast with
the preceding variety, it is continuously present during rest and
ceases — at least in the earlier stage of the disease — during the
performance of voluntary movements. It is a slow tremor, ex-
hibiting four or five vibrations per second, of slight amplitude,
and coordinated, simulating the endless repetition of voluntary
movements — pill rolling, thread winding, crumbling of bread,
masturbation, etc.
It involves chiefly the uppei^ extremities, the head and neck
being relatively free. It is accompanied by a special kind of
muscular rigidity (waxy flexibility) and a slowness in starting
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1310 SYMPTOMS.
locomotion which impart to the act of walking a very typical
slow and scanning appearance. There are also noted a subjec-
tive sensation of heat and a morbid desire for locomotion.
Grasset called attention to two anatomic regions often found
the seat of morbid changes in this disease:
1. The region of peri-ependymal myelitis, with obliteration
of the central canal.
2. The automatic pontobulbar centers and the capsulotha-
lamic region.
(fc) The commonest form in this class of tremors is perhaps
senile tremor, which, as the term implies, occurs particularly in
old persons, is of comparatively slow rate and, affecting mainly
the head and neck, imparts to the tremor the peculiar suggestion
of an indefinitely repeated nod of affirmation or shake of nega-
tion.
(r) Graves's (Basedow's) disease. — Here the tremor shows a
rapid rate. It generally occurs in conjunction with the sympto-
matic triad, tachycardia, goiter, and exophthalmos. This triad
may, however, be absent or only partially represented, in which
event one should look for the other signs of hyperthyroidia —
frequent pulse, tremor, hyperidrosis, exaggerated reflexes, and
diarrhea.
(d) Tumors of the cerebral peduncle. — In tumors of the cms,
the tremor presents the same features as in Parkinson's disease,
but is generally unilateral.
(e) Post-hemiplegic tremor is sufficiently characterized by
the history of hemiplegia and exaggeration of the reflexes.
(/) The tremor of progressive general paralysis exhibits a
rapid rate; it is accompanied by a special difficulty of speech,
by pupillary disturbances (Argyll-Robertson pupil), and by
special, characteristic changes of mentality.
(g) Meige has called attention to the occurrence of tremor of
the type of paralysis agitans in wound cases.
III. Hysteric Tremor. — A special division is required for hysteric
tremors. These do not belong in any of the foregoing categories.
Their various modalities closely imitate most of the other forms of
tremor. How are they to be differentiated, then, from such tremors,
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TREMOR. 1311
and in particular, from toxic, exophthalmic, Parkinsonian tremors,
etc.? Such differentiation is" often rendered all the more difficult
in that hysteria is frequently combined with most varied forms of
intoxication and neurosis.
On the whole, the diagnosis of hysteric tremor is founded on
two groups of symptomatic features :
1. Positive indications: Sudden onset, following convulsive
seizures, in a subject exhibiting sensory and special sense stigmata
of hysteria; possibility of change in the type of tremor present;
curative influence of suggestion.
2. Negative indications: Absence of the usual signs of hyper-
thyroidia, of disseminated sclerosis, of exaggeration of the
reflexes, etc.
* * *
The clinical course exhibited by the tremor may also be of
diagnostic assistance :
1. Progressive tremor, at first localized in one limb or portion of
a limb, progressively extends to one or more other limbs. Such
is the case in the tremor of paralysis agitans.
2. Retrogressive tremor, generalized at the start, tends gradu-
ally to become localized in one limb or portion of a limb. This kind
of a clinical course obtains particularly in tremor of neuropathic
origin.
3. Migratory tremor, exhibiting variable localizations both as
regards space and time. Such changes in the situation of the
tremor may come on spontaneously; they are rendered more dis-
tinct by changing the positions of the limbs or immobilizing one or
more portions of the limbs. This is frequently the case in hysteric
tremor.
4c 4t 4t
The relative order of frequency of the various types of tremor
as encountered in practice appears to be as follows :
1. Toxic tremor (alcohol, tea,
and coffee).
2. Tremor of Graves's disease.
3. Neurotic, hysteric tremor.
4. Senile tremor.
5. Hereditary tremor.
6. Tremor of paralysis agitans.
7. Sclerotic tremor (dissemi-
nated sclerosis).
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1312
SYMPTOMS.
TREMOR.
I. — Accidental.
Readily referred to its cause:
(a) Elmotional: Fear, pleasure, or other pronounced emotion.
(b) Febrile: (See Chills.)
(c) A frigore: Shivering.
II. — Permanent
A. During motion (as typified in Disseminated sclerosis).
(a) Disseminated
sclerosis.
(b) Hereditary
tremor.
(c) Toxic tremor
(tea, coffee, akohol,
etc.) (by far the
most frequent
form).
1. Tremor absent during rest; sets in and in-
creases with voluntary motion.
2. Dizziness, apoplectiform attacks, nystagmus,
exaggerated reflexes, and scanning speech.
1. Absent or slight during rest; sets in, with-
out accentuation, during voluntary motion.
2. None of the above associated signs; often
sets in in childhood.
1. Less extensive, but more rapid tremor than
in the preceding disorders.
2. History of toxic poisoning.
B. During rest (as typified in Paralysis agitans).
(a) Paralysis agi-
tans.
(b) Graves's dis-
ease.
(r) Post-hemiplegic
tremor.
(d) Progressive
general paralysis.
1. Persistent during rest ; lessens or disappears
during voluntary motion.
2. Special kinds of muscular rigidity ; slow,
jerky locomotion; characteristic facies and
posture.
Tremor associated with frequent pulse, goiter,
and exophthalmos.
History of hemiplegia; exaggerated reflexes.
Special speech disorder; pupillary disturbances
(Argyll-Robertson pupil) ; special and char-
acteristic mental changes ; history of syphilis.
in. — Hysteric.
(a) Abrupt onset after a convulsive seizure; sensory and
special sense stigmata; variability of the type of tremor.
(5) Absence of concrete somatic evidences,
(f) Mythomania.
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UPPER EXTREMITIES, PAIN IN.
This section on pains in the upper extremities is undertaken by
the author with some degree of trepidation, as such pains have
seemingly little to do with "internal medicine." Yet the author
has frequently found him3elf embarrassed in the interpretation
of some of these pains. While often of obvious causation, as in
herpes zoster or acute articular rheumatism, they are at times
In the succeeding illustra-
tions, borrowed from the writ-
ings of Mme. Benisty, and
showing diagrammatically the
innervation of the upper ex-
tremity, the fields of distribu-
tions of the different nerves
are to be recognized by the
kind of shading, as follows:
Median nerve,
Musculospiral nerve.
Musculocutaneous nerve.
^^H Ulnar nerve.
^^^ Circumflex nerve.
Fig. 879.
very obscure, as in many vasomotor disturbances concerning
which little is as yet known.
In such cases, it is necessary to carry out a careful, syste-
matic anatomo-clinical analysis, which, while indispensable, un-
fortunately does not always yield clear-cut information..
Any of the tissues forming part of the upper limb may be
the source of painful disturbances ; many brachialgias constitute
the outward manifestations of some spinal or deep visceral dis-
order, ordinarily mediastinal and in the majority of instances
aortic or peri-aortic.
Aside from the post-traumatic affections (fractures, luxations,
sprains, wounds, and contusions), the diagnosis of which is gen-
erally obvious, the joint disorders greatly predominate as causes of
pain in the upper extremity, whether localized in the shoulder,
«3 (1313)
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1314 SYMPTOMS.
elbow, the joints of the carpus or metacarpus, or the phalanges.
Reference need not here be made to all the possible causes of
articular pains, a special section having been devoted to the subject
(see Joint pains). Systematic examination by inspection, palpation,
Supraclavicular
Circumflex
MuBculoapiral
Musculocuta-
neous
Radial
Median
Fig. 880. — Peripheral sensory dis- Fig. 881. — Peripheral sensory dis-
tribution in the upper extremity tribution in the upper extremity
(posterior aspect). (lateral aspect).
and passive motion will first of all localize the pain in one of the
above mentioned joints. The special features of the joint disturb-
ance, the history, the mode of onset, and the subsequent course will,
as a rule, enable the observer quickly to class the condition under
one of the following heads, viz,, acute articular rheumatism, gonor-
rheal rheumatism, tuberculous rheumatism, post-infectious {e.g,,
post-typhoid) rheumatism, gout, arthritis deformans, etc. One can-
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UPPER EXTREMITIES, PAIN IN.
1315
not too earnestly recommend to the practitioner, as in other dis-
orders, to examine the painful region carefully and by actual in-
spection, to palpate and mobilize it; in short, to localize with care
the pain and the actual local condition present, to determine its
nature if possible, and especially, not to rest content with the in-
definite term "rheumatism," — a temi just as devoid of true diag-
nostic meaning as "headache" or "pain in the side."
The examiner should not forget the possibility of tabetic joint
disease, which, while an exceptional disorder, presents characteristic
Figs. 882 and 883. — Two common types of distribution of the sensory
disturbances in complete section of the radial nerve. Black area:
Anesthesia to all stimuli except deep pricking, which is often felt as a
mere contact with the tissues. Gray area: Marked hyperesthesia to
pricking, anesthesia to heat, cold, and very superficial tactile stimuli.
Dotted area : Slight hypoesthesia to tactile stimuli and to heat and cold.
(Mtne. Benisty).
features consisting of a striking degree of deformity, extreme re-
laxation of the joint, and painlessness. If only the condition is kept
in mind, the diagnosis can be made by observation of the other
signs of tabes, vis., specific history, reflex disturbances (Argyll-
Robertson pupils and loss of knee-jerks), astasia, ataxia, lightning
pains, sphincter disturbances, etc.
Disorders of bones — osteitis, osteoperiostitis, osteoarthritis,
and osteomyelitis — are, in the order of their frequency :
Tuberculous: Periostitis and osteoarthritis (white swelling).
Syphilitic: Osteoperiostitis and gumma.
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1316 SYMPTOMS.
Post-infectious: Staphylococcic (osteomyelitis) .
Neoplastic : Osteosarcoma.
The following features will insure a proper diagnosis:
1. The history : Lymphatic diathesis, specific taint, infection
(typhoid fever or staphylococcic infection).
Superficial cenrlcal plexus
Circumflex
Intercostal branches*
External cutaneous/
Intercostohumeral .
Internal cutaneous]
Musculocutaneous/
Ulnar
Radial (external branch)
Median (palmar cutaneous branch)
Median (digital branches)
Ulnar (terminal superficial branch) •
Fig. 884. — Peripheral sensory distribution in the upper
extremity (anterior aspect).
2. Fever (generally wanting in syphilis and neoplasms).
3. Localization particularly around the joint in tuberculous
disease.
4. A rather sluggish clinical course in tuberculosis and
syphilis.
5. The nature of the pain, with nocturnal exacerbations in
syphilis.
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UPPER EXTREMITIES, PAIN IN,
1317
6. special tests such as the Wassermann reaction and the
successful therapeutic test (mercury and iodide) in syphilis.
Disorders of the muscles and serous surfaces, viz., myositis,
subacromial bursitis, and deltoid rheumatism, are possible localiza-
tions of rather poorly defined painful manifestations, the origin of
which, however, seems actually to be that mentioned by Le Gendre:
"Deficient functioning of the locomotor apparatus, either through
lack of exercise (sedentary mode of life) or through excessive mus-
cular labor." Such a deficiency through loss of functional balance.
Fig. 885.— Palm of the hand. ^ig. 886.— Dorsum of the hand.
EWstribution of the disturbances of sensation in severe injuries of
the median nerve. Black area: Complete anesthesia of all types. Gray
area: Hypoesthesia to pricking and anesthesia to heat and cold. Dot-
ted area: Less marked hypoesthesia.
''when it has been present in patients, necessarily places the various
component parts of the locomotor apparatus in a weakened state in
which it becomes susceptible to influences ordinarily not noticed by
well persons; these are the influences to which we are constantly
exposed, inc., the cosmic influences. Among these influences, the
best studied has been that of cold, which is even considered an
etiologic factor — especially damp cold and long-continued cold or
exposure.'*
The upper extremity may be, and manifestly is, the seat of
neuralgia and neuritis variously situated (e.g., ulnar, radial, or
median) and of varying cause: Traumatic (contusions, open sur-
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1318 SYMPTOMS.
faces and wounds), toxic (lead poisoning, alcohol, etc.), pressure
(osteoperiostitis, osteosarcoma, or defective callus of the humerus,
radial paralysis of lovers, etc.), and infections. Careful examina-
tion for local sensitiveness (see illustration showing the distribu-
tion of the sensory nerves), as well as of mobility (paralysis; see
illustration showing distribution of the motor nerve fibers) will
soon lead to discovery of the site of the lesion. The history and
even the location of the neuritis will frequently permit of tracing
the cause of the disturbance.
Lastly, mention may be made of vasomotor disturbances,
represented in the highest degree by Raynaud's disease (local
asphyxia of the extremities), and seemingly often of specific
origin, whether acquired, inherited, or secondary to a mitral
malformation.
Exceptionally, in particular among the Senegalese, there may be
noted evidences of leprosy of the nervous or anesthetic types, the
nerve symptoms being manifest in a prodromal stage by a monili-
form enlargement, frequently of considerable size, of the nerve
trunks, which are very sensitive to pressure; later, the pain, of
neuralgic t3rpe, is constant and spontaneous,* with repeated violent
paroxysms; it is accompanied by dysesthesias (itching, etc.) and by
vasomotor disturbances ("dead finger" sign), and ends in anes-
thesia, with trophic disorders, atrophy of muscles, and deformity.
These manifestations of leprosy exhibit great clinical analogy with
syringomyelia and with ''Morgan's disease'* or panaritium analgicum.
Pain in the arm occurring in the absence of any local lesion,
whether muscular, articular, 'osseous, nervous, or vascular, may
constitute the outward expression of remote lesions, the most im-
portant of which are :
(a) Aortic and periaortic lesions (radiation of the pains of
angina pectoris and aneurysm to the arm).
(fc) Certain *'high" forms of degeneration of the posterior
columns (lightning pains of cervical tabes).
(c) Lesions of the brachial plexus.
(d) Certain mediastinal tumors.
(a) The pain of angina and of aortic and periaortic disorders in
general is, as a rule, felt in the area of distribution of the fourth
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UPPER EXTREMITIES, PAIN IN. 1319
left dorsal nerve over the chest and arm. It may descend and
radiate as far as the epigastrium in the areas of distribution of the
fiftband sixth dorsal nerves. More often, however, it ascends and
radiates along the first, second, and third dorsal or even the seventh
and eighth cervical nerves, being felt, therefore, along the ulnar
Muscles Nerves Roots
Deltoid Circumflex C,* C.«
Fectoralls major Circumflex C,* C,« C.^
Triceps Musculosplr. C," CJ
Biceps MuBculocut. C,^ C*
Bracbialis ant Musculocut. C,' C."
Pronator teres Median C,« C'
Supinator longus Musculosplr. C,*^ C*
Ext. carpi rad. Musculosplr. C,* C
long, and brev.
Flexor carpi
rad.
Median
C c,» d:
Palmaris longus
Median
C,8 D.i
Flexor sublim.
dig.
Median
C,8 D.i
Flexor carpi
uln.
Ulnar
0,8 D.i
Thenar muscles
Median
c.« c.f
Hypothenar
muscles
Ulnar
C,« D.i
Fig. 887. — Nerve-supply of the muscles of the upper extremity
(anterior aspect).
border of the forearm and hand. This constitutes the typical area
of distribution of anginose pain, vie., precordial (mammillary), left
upper thoracic (axillary), and ulnar.
Exceptionally, the pain extends to the corresponding areas
on the right side (chiefly in cases with aortic dilatation) and to
the neck, including its posterior aspect (nuchal region).
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1320 SYMPTOMS.
Such pain is, as is well known, when present in conjunction with
a feeling of constriction of the chest (squeezing sensation or suffo-
cation) and a fear of impending death, the cardinal indication of
angina pectoris. It should always be borne in mind, however, that
many neuropathic states, whether or not based on some cardioaortic
disease, may lead to a syndrome of "anxiety neurosis" similar in all
respects to the anginose syndrome, yet far more favorable from the
standpoint of prognosis. For a discussion of the differential diag-
Fig. 888. — Distribution of the pain and cutaneous hyperalgesia after
repeated attacks of angina pectoris.
nosis in this connection the reader is referred to the section on
Precordial pain.
(b) Aortic aneurysm may cause pain in the arm of threefold
origin : \
1. Anginose pain of the type above described.
2. Neuralgic or neuritic pressure pain.
3. Pain due to stasis on account of pressure on venous trunks.
These pains may be of unbearable intensity and necessitate
the use of morphine. Oftea the clinical evidences, such as
aneurysmal swelling and signs of pressure on the veins (visible
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UPPER EXTREMITIES, PAIN IN. 1321
venous network in the superior caval area, swelling of the neck,
edema of the face, and inequality of the pulse on the two sides,
etc.), are obvious; fluoroscopic examination will remove all
doubt as to the condition present.
(c) The same is true in tumors of the medidstinum. The coex-
istence of pain in one or both upper extremities with evidences of
interference with the return circulation in the superior caval area
(cyanosis, visible superficial venous circulation, swelling of the neck
and face, prominence of the eyeballs, and facial edema) is almost
pathognomonic of mediastinal tumor, e.g., dilatation of the aorta,
pericarditis with effusion, enlarged lymphatic glands, etc.
((/) The pains of tabes, although much less common in the upper
than in the lower extremities — the latter constituting the site of
election — ^may occur as the usual "lightning pains," sharp, abrupt,
and fulgurant, like lightning. Sometimes they occur singly, at
others grouped in paroxysmal attacks of varying duration — from
one to several days. They are felt more particularly along the inner
border of the forearm and the fifth and fourth fingers. They may
be of the piercing, burning, lancinating type ; at times, however,
they are of the nature of a constriction, squeezing, or ring-like pain.
This special characteristic of the pains of tabes — ^though not an
exclusive attribute, since it may be met with likewise in peripheral
neuritis (due, e.g., to alcoholism or leprosy) and in pressure on
nerve-roots — is nevertheless, as a rule, highly suggestive. Let the
observer merely recollect the possibility of tabes — and how could he
fail to think of it in such cases? — and the diagnosis will bo quickly
confirmed by examination for the typical tabetic indications (specific
history, reflex disturbances, motor disturbances, visceral disturb-
ances, particularly genitourinary, etc.).
The foregoing review by no means exhausts the possibilities as
regards pain in the upper limbs. Various exceptional clinical con-
ditions, such as supernumerary cervical rib, poliomyelitis, etc., have
been designedly omitted in order not to make the present section too
unwieldy.
The same applies to abscesses, felons, lymphangitis, phlegmonous
inflammations, and the attendant glandular enlargements — all con-
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1322 SYMPTOMS.
ditions met with in everyday practice, but the diagnosis of which is
ordinarily devoid of difficulty and to which reference is here made
merely to call them to the reader's mind.
In conclusion, the hope may be expressed that the reader will
find lessi difficulty in reading and reflecting on this section than
the author experienced in writing it.
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VERTIGO. [Vertigo, frcm vertere, to ium.'\
Vertigo is characterized by a mistaken subjective sensation in
virtue of which the patient believes himself to be rotating al-
though he is motionless, or sees surrounding objects turning
about him although they are at rest. When vertigo is persistent
or very marked, it may induce loss of equilibrium and a fall to
the ground if the subject is in the standing position at the time.
It may be, and frequently is, attended with nausea, or even
vomiting, and by nystagmus or even deviation of the eyes.
The highly complex pathogenesis of this symptom seems, at the
present time, to be rather well condensed in the following definition
formulated by Grasset: Vertigo is the symptom of functional in-
sufficiency (intermittent claudication) of the automatic centers
(mesencephalic and cerebellar) of equilibration. Bonnier, as is well
known, has made a profound study of vertigo from the physio-
pathologic, clinical, and therapeutic standpoints.
These automatic mesencephalic and cerebellar centers of
equilibration:
1. Receive:
(a) Vestibular fibers coming from the semicircular canals
through the auditory nerve.
(b) Visual fibers coming from the retina through the optic
nerve.
(c) Muscle-sense fibers from Clarke's columns and the posterior
columns.
2. Send:
(a) Fibers terminating in the Rolandic area on the opposite side
and acting on the motor centers.
(b) Fibers terminating in the nucleus of Deiters, which is con-
nected with the oculomotor nerves, these in turn governing the
ocular muscles.
(c) Fibers terminating in the anterior horns of the spinal cord,
whence radiate motor fibers to the voluntary muscles.
(1323)
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1324 SYMPTOMS.
(rf) Fibers to other bulbar centers (glossopharyngeal and pneu-
mogastric).
These anatomic and physiologic connections of the mesen-
cephalic and cerebellar centers account for the following:
(a) The clinical combination of vertigo, disturbances of equilib-
rium, nausea, and ocular disturbances (nystagmus and deviation of
the eyeballs). (Normal equilibrium is the result of harmony of the
retinal, labyrinthine, and muscular impressions).
AflFerent paths.
EflFerent paths.
1. Vestibular fibers.
2. Semicircular canals.
3. Acoustic nuclei of Bech-
terew and Deiters.
4. Visual fibers.
5. Corpora quadrigemina.
6. Sensory fibers.
7. Columns of Clarke.
8. Cerebello-rolandic commis-
sural fibers.
9. Cerebello-auditory fibers.
10. Cerebello-oculomotor fibers.
11. Cerebello-spinal fibers.
12. Cerebello-bulbar fibers.
13. Muscles.
14. Retina.
Fig. 889.— -Pathogenesis of vertigo (Bonnier), The cerebellum ap-
pears as the "vertigo center," whence the frequency, if not the uniform
presence, of vertigo in cerebellar disorders.
(fc) The factors generally causative in vertigo:
1. Disorders and pathologic changes in the centers of equili-
bration (cerebellum and crura).
2. Wrong or disharmonious impressions supplied from the
receptive structures (retina, labyrinth, and muscle-sense).
3. Morbid stimuli in the field of the pneumogastric nerve
(gastric disorders, helminthiasis, etc).
From the foregoing brief and synoptic enumeration the
reader will readily conceive how common vertigx) may be and
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VERTIGO. 1325
in how many different varieties it may occur, and what powers
of clinical analysis will frequently have to be brought to bear
in seeking its causes (auricular vertigo, arteriosclerotic vertigo,
cerebral vertigo, neurotic vertigo, migrainous vertigo, ocular
vertigo, epileptic vertigo, toxic vertigo, etc.)
Under physiologic conditions, vertigo may be brought on by
abrupt change in the position of the body, e.g,, rising from re-
cumbency to the standing posture, by an abrupt change of di-
rection or motion, by rapid rotation, by an ascent, and by looking
down from a high place. Travelling in a railway or trolley car
suffices, as is well known, to induce vertigo in some persons.
Vertigo is an essential component of seasickness. • The electric
current, in particular the application of the galvanic current to
the head, or sharp percussion of the middle ear by use of the
aural syringe, will induce vertigo in predisposed individuals.
Clinically, one cannot here do more than recall in a concise
table the more usual causes of vertigo, which investigation of
the concomitant symptoms will alone identify :
L— CENTRAL VERTIGO.
Central vertigo occurs mainly when the position of the body is
changed, e.g., upon passage from the horizontal to the vertical
position.
Arteriosclerosis. — ^The highest degree of importance should
be attached to vertigo coming on without apparent cause in
elderly individuals previously never afHicted with it. Old age,
vertigo and high blood-pressure, present in combination, nearly
always mean arteriosclerosis. The vertigo may be of mild de-
gree, even in this type of case, and remain so for years ; some-
times— too often — it is an alarm signal betokening an approach-
ing and threatening attack of apoplexy.
Cerebral tumor. — Vertigo is observed in the majority of
cases of frontal tumor and in over one-third of cases of tumor in
other regions of the cerebrum ; the attacks of vertigo seem to
correspond to the periods of enlargement of the tumor. Examin-
ation of the eyegrounds for choked disc should never be neglected
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1326 SYMPTOMS.
in suspected cases, and other signs of brain tumor, such as
vomiting, etc., should be inquired for.
Cerebellar tumor. — Vertigo is almost constant in tumors of
the cerebellum; in nearly all instances it is associated with dis-
turbances of equilibriiun which lead to a staggering gait, latero-
pulsion, a gait as of "pseudo-intoxication" — ^the cerebellar gait,
which is highly significant to a practised eye.
Disseminated sclerosis. — Vertigo is one of the most frequent
signs of disseminated sclerosis, being combined with nystagmus
and the intention tremor characteristic of this disorder.
Paretic dementia. — Vertigo occurs in two stages of this in-
curable affection, zis,, at the start, in the preliminary stage, and
in the advanced stage, as a precursor of some acute complicatibn,
such as coma, convulsions, or hemiplegia.
Disturbed circulation in the centers, whether of hyperemic or
anemic type, and whether dependent upon actual congestion,
actual anemia, or vasomotor disturbances, may be an exciting
cause of vertigo. Such is the vertigo of syncope (in its premoni-
tory stage), of the menopause, of chloroneurosis, of the anemias,
of hemorrhage, of heart disorders, etc.
II.— AURAL VERTIGO.
M6nidre*8 verti^^o. — Labyrinthine vertigo.!
(By G. Laurens, M.D.)
What is meant by aural vertigo? — One portion of the
ear, as is well known, is concerned in audition, and the other in
equilibration, i.e., in orientation of the head, which plays an im-
portant role in the maintenance of bcdy balance. These two por-
tions are independent:
Disease of the one causes deafness and .tinnitus.
Disease of the other causes vertigo.
What is M6niire's disease? — About fifty years ago Meniere
described a disorder characterized by the following three symptoms:
vertigo, deafness, and tinnitus, and on post-mortem examination of
the few cases upon which his contribution was based, observed
1 From Laurens : Loc. cit., p. 132 ff.
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VERTIGO. 1327
hemorrhage into the internal ear.^ Thus, only a very small number
of cases served in the earliest description of this disease.
Since then, the meaning of the term has been expanded, and
whenever a patient presents aural vertigo he is said to be
suffering from Meniere's disease. This is a mistake, however, for
while the symptom is the samie, the underlying pathologic con-
dition is entirely different, and it is well to bear in mind that
any disease of the ear (external, middle, internal, Eustachian
tube, tympanic membrane, and tympanic cavity, . . . e.g., an
ordinary impaction of earwax, or suppurative otitis) is capable
of bringing on vertigo with deafness and tinnitus. This occurs
through irritation of the labyrinth. Thus, given a plug of wax in
contact with the tympanic membrane and forcing in the latter,
and consequently also the chain of ossicles, irritation of the
labyrinth results; and the same is true when there is increased
tension of the labyrinthine fluid from the presence of pus in
otitis, and where there is anemia, congestions or infection of the
internal ear in certain constitutional disorders or through poison-
ing by drug^ such as quinine and sodium salicylate.
To recapitulate:
1. The term Meniere's disease should be exclusively set apart for
vertigo induced by an actual hemorrhage into the labyrinth. This
condition is very uncommon.
1 Meniere's initial case is deserving of reproduction ; he studied it in
Chomers service, being at that time on the staflF of the Hotel-Dieu.
"A young girl, having travelled at night on the top of a stage-coach dur-
ing her menstrual period, was seized, after considerable exposure to cold,
with sudden and complete deafness. Upon admission in Qiomer's service
she showed constant vertigo as the chief symptom ; the least attempt to move
brought on vomiting, and death took place on the fifth day.
"The necropsy showed the cerebrum, cerebellum, and spinal cord to be
completely free of any patholbgio change; but inasmuch as the patient had
become suddenly deaf after having always enjoyed good hearing, I removed
the temporal bones in order to make a careful inquiry into what might be
the cause of this complete deafness of such sudden advent. I found nothing
in the way of a pathologic change save the filling of the semicircular canals
with a plastic red material, a species of bloody exudation, of which only
traces could be seen in the vestibule and which was entirely absent from the
cochlea. Careful investigation enabled me to establish with all necessary
accuracy that the semicircular canals were the only structures exhibiting an
abnormal condition in this case.''
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1328
SYMPTOMS.
2. There occurs also a syndrome of Miniere, or, more com-
monly, aural vertigo, when there is irritation of the internal ear
from any cause.
How is one to recognize the existence of aural vertigo?
1. From the nature of the disturbances complained of by the
patient.
2. By otoscopic examination.
Cerebral cortex
I
2
6
Fig. 890. — Diagram illustrating aural vertigo.
The two portions of the internal ear: 1. The auditory portion, rep-
resented by the cochlea and related to the cochlear nerve. 2. The organ
of equilibration or of the spacial sense, represented by the vestibule and
semicircular canals and related to the vestibular nerve.
1. From the Nature of the Disturbances Complained of by
the Patient..
(a) Sometimes he will tell you that while in perfect health,
without any noticeable cause, he felt a sort of explosion or intense
sound in the ear. At the same moment, there was tinnitus, dizziness,
sometimes an actual fall to the floor, with or without nausea and
vomiting. This attack lasted from a few minutes to a few hours;
as soon as it ended, the patient noticed that he was deaf. This
major attack sometimes recurs, but in a much less pronounced form.
Such is a typical case of Meniere's disease.
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VERTIGO, 1329
(&) In some instances, the subject is a person in good health in
whom vertigo appears without the least apparent cause — and this
is frequently the case ; — in other instances he is already deaf, suffer-
ing from otosclerosis, or acute or chronic suppurative otitis; or,
again, in the course of some general infectious disease, or some-
times following ingestion of drugs, such as quinine and salicylates,
he was seized with the symptoms already mentioned, ins,:
Vertigo, causing staggering, failing to disappear in recumbency
or upon closure of the eyes, drawing the patient toward the side
of the affected ear, and lasting a few hours ; sometimes inducing
a continuous state of malaise with dizziness; acute tinnitus, with
8.^
Fig. 891.— The causes of aural vertigo. Aural vertigo may be the
result of a disorder of the external ear (/) (foreign body, wax in con-
tact with the drum, etc.) ; of otitis media (2) ; of hemorrhage in the
labyrinth (Meniere's disease), or of anemia, hyperemia, or suppuration
of the labyrinth, intoxication by drugs, or general, infectious diseases.
This is the common form of aural vertigo.
loud whistling soimds; increasing deafness. This symptom-
group is at times supplemented by bilious vomiting, appearing
spontaneously, without the least exertion, and which the physi-
cian is led to ascribe to dyspepsia.
Such is the ordinary type of aural vertigo. Its existence must
be confirmed :
2. By Otoscopic Examination.
The observer finds in some instances a plug of wax, sometimes
an otitis, and in still others an absolutely normal tympanic memr-
brane: this last means that the vertigo is of labyrinthine origin.
S4
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1330 SYMPTOMS.
IIL— NEUROPATHIC VERTIGO.
1. In a first group should be plax:ed neurasthenia, psychoneu-
roses, and the neuroses of congenital origin, in which there seems
to be operative a congenital or acquired hypersensitiveness to
stimuli and impressions of all kinds, sometimes with an added
autosuggestibility which, for example, may automatically start
an attack of vertigo in the presence of some factor — such as an
odor, railway travel, riding in a carriage, etc. — ^which had already
been previously associated with vertigo.
2. In a second group we shall place epilepsy, in which vertigo
may be encountered either as a premonitory aura or as an equiv-
alent of the epileptic seizure.
IV.— TOXIC VERTIGO.
This may be due to. alcohol, tobacco, carbon monoxide, qui-
nine, sodium salicylate, or cannabis. The pathogenesis seems to
be complex — angiospastic conditions in the brain, congestion of
the internal ear, transient cerebral anemia, etc.
The influence of renal disease has been clearly shown by Bonnier,
who called attention to the frequent occurrence of vertigo in renal
cases and proposed as a suitable term in this connection the word
otobrightism. Here is another circumstance showing how impor-
tant it is to test the blood-pressure and examine the urine (and the
renal functions more generally) in all patients, and in cases of
vertigo in particular. The practitioner should keep in mind, at
least, that vertigo may be dependent upon high blood-pressure,
arteriosclerosis, and uremia.
v.— REFLEX VERTIGO.
Perhaps it is best to place under this heading the so-called
"gastric vertigo" or 'Vertigo a stomacho laeso" of older authors.
These cases have been rather overlooked of late. One should,
however, bear in mind — in general practice — that vertigo, what-
ever be its precise mode of production, is with exceeding fre-
quency, if not constantly, associated with nausea and vomiting;
that it is often manifested in "gastric upsets" of varying cause
and origin, and that it frequently yields in these cases to treat-
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VERTIGO. 1331
ment directed toward the alimentary tract, vis., diet, purgation,
and stomach washing.
It is a fact that vertigo and vomiting or nausea, present in
combination, may be obviously dependent upon a single cause
which brings them on at the same time and is associated with
and regulates them, as in seasickness, mountain sickness, car
sickness, and, as we have already seen, brain tumors.
VL— VERTIGO WHICH RESTORES THE SENSE
OF *H EARING.
In a well-grounded and highly suggestive article entitled
"Vertigo which restores the sense of hearing; — labyrinthine an-
giospasm,'' Lermoyez^ described a curious vertiginous symptom-
group characterized by abrupt and violent onset with recovery
within a few hours of hearing in subjects whose auditory func-
tion had previously seemed hopelessly lost.
"It appears to me," he wrote, "that one has to deal in these cases
with local angiospasms in neuroarthritic (or, as I would rather put
it, gouty) subjects possessed of exaggerated sensitiveness of the
internal ear, both as regards external stimuli (clattering sounds,
violent and prolonged movements) and internal irritants (various
intoxications and especially gastric autointoxications) — which ex-
cuses Trousseau for having conceived his celebrated vertigo a stotn-
acho laeso!"
Lermoyez compares the condition to the local asphyxia of the
extremities with the characteristic painful numbness (onglee)
which precedes restoration of circulation through the tissues.
"Similar phenomena occur in the ears, and it would not be
an exaggeration to speak of a 'painful numbness of the laby-
rinth.' The closure of the internal auditory artery, which took
place slowly, induced gradual anesthesia of the ear, i.e., deafness.
But now the spasm abruptly relaxes; the blood rushes anew
into the labyrinth, which it stuns; and this excessively sudden
influx, which, in the fingers, causes the well-known pain, here
induces simultaneously the special pain of the cochlear organ,
which is tinnitus, and the suffering of the vestibular organ,
which is vertigo ; in addition, it causes disappearance of the an-
esthesia of the ear, i.e., of the deafness."
1 Presse mSd., Jan. 2, 1919.
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VOMITING. [From vomere, to vomit.]
Vomiting consists of the evacuation of the stomach contents
by way of the esophagus and mouth. It constitutes a "reversed
deglutition" during which, as in deglutition, the openings of the
larynx and nasal cavities into the pharynx are closed. As a
matter of fact, esophageal vomiting is also a possibility. In con-
trast with the preceding variety, it is not generally accompanied
by nausea and always results in the ejection of food, though
sometimes also of varying amounts of blood.
True (gastric) vomiting is a reflex of which :
The center is in the medulla, in the vicinity of the respiratory
center.
The afferent, sensory nerve-paths arise mainly:
From the pneumogastric (abdominal stimuli).
From the glossopharyngeal (pharyngeal stimuli).
From the trigeminal (nasal stimuli).
From the cerebral cortex (cerebral stimuli, inflammatory, toxic,
or psychic).
The efferent, motor nerve-paths follow chiefly:
The phrenic nerve (diaphragm).
The pneumogastric nerve (stomach).
The spinal nerves (muscles of the abdominal parietes, recti, etc.).
The above anatomic and physiologic features account for the
fact that vomiting may be either of central origin (meningitis,
apomorphine, or revolting impressions) or of peripheral origin
(appendicitis, indigestion, pregnancy, or tickling of the uvula).
The vomited material may be either:
1. Alimentary. It is extremely important to note the degree of
previous digestion of the food vomited, its more or less acid or
alcoholic odor, its nature, and especially the greater or less interval
between its ingestion and evacuation. The mere fact of the pres-
ence of food ingested on the preceding day, and especially on the
(1332)
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VOMITING. 1333
second preceding day, is a serious indication of stasis with marked
probability of pyloric stenosis.
2. Bilious.
3. Mucous, as in the morning vomiting of alcoholics.
4. Bloody (see Hematemesis),
VOMITING
Efferent Vomiting center in meduUa Afferent paths of
motor paths xt *u • . . stimulation
^^^, . Near the respiratory center.
SI
;Musc
lAbdoi
•oUiqi
! vers
Fig. 892.— Pathogenesis of vomiting.
5. Fecal Old, detected at once by the odor, or if necessary by the
pigment tests. Such vomitus is of grave portent. It is nearly
always an evidence of intestinal obstruction or occlusion (peritonitis,
strangulated hernia, etc.).
The history is always of great importance :
In some subjects, vomiting (rangirfg from simple regurgitation
to true vomiting) is an ordinary, habitual event, which occurs
almost without effort and with the greatest ease. This is the case
in many children, in many alcoholics, in some hearty eaters, and in
many gastric neuroses. It is important to record the symptom, but
it is usually devoid of any serious significance.
In others, on the contrary, vomiting is diflficult, distressing, and
unusual. Its significance is much greater ; the physician must know
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1334
SYMPTOMS.
that he is not to rest content with the superficial and common-
place explanation of indigestion, but is to make a careful examina-
tion for the obscure and serious causes of certain cases of vomiting,
such as uremia, acetonemia, brain tumor, etc.
In other words, there are some persons in whom quasi-habit-
ual vomiting is almost a negligible event; there are others, how-
ever, in whom vomiting is exceptional and of marked clinical
significance.
In regard to the approximate relative frequency of the com-
moner causes of vomiting, Cabot g^ves the following table :
Toxemia of pregnancy.
"Acute dyspepsia'* (indigestion).
Alcoholism.
Seasickness.
Onset of infectious diseases.
Postoperative shock.
"Gastritis."
Gastric neurosis.
Acute appendicitis.
Cardiac disease.
Peptic ulcer.
Cases too many and too vaguely
enumerable for accurate estima-
tion.
Intestinal obstruction.
Gastric cancer.
Uremia.
Tabes.
Diseases of the brain (meningitis, abscess, tumor) are not in-
cluded; as a matter of fact, the percentage of such cases in the
total number of instances of vomiting is very low. The foregoing
list, moreover, is by no means complete; it is well, at all events, to
mention the vomiting of meningitis, of acetonemia (precursor of
diabetic coma), and of hepatic and renal colic.
It is not in the scope of this work to review all the possible
causes of vomiting and analyze their "diflferential clinical feat-
ures ; it w^ill be sufficient to present a synoptic table of the more
common causes with their diagnostic signs.
Some space will, however, be devoted to certain facts chiefly
culled from an article by Professor Marfan,* relating to a peculi-
arly difficult task of diflferential diagnosis, in::., that of dis-
tinguishing the periodic acetonemic vomiting of children and
the vomiting symptomatic of acute appendicitis.
^Presse med., Sept. 11, 1916.
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VOMITING. 1335
Periodic Vomiting with Acetonemia is not a Form of Appen-
dicitis.— The phrase **periodic vomiting with acetonemia" is ap-
plied to a disorder of childhood characterized by attacks of
vomiting, accompanied from the start with pronounced elimina-
tion of acetone with the urine and expired air, such attacks gen-
erally coming on during apparently satisfactory general health,
lasting from a few hours to a few days, and stopping abruptly,
being replaced by a state of perfect tolerance of food.
They occur almost exclusively in the children of neuroar-
thritic parents (migrainous, asthmatic, eczematous, lithiasic,
obese, gouty, diabetic, and hemorrhoidal). Their occurrence is
favored by a diet rich in fats.
Some have asserted that such periodic vomiting with aceton-
emia is due to an acute attack of appendicitis, constituting an
exacerbation of chronic appendicitis. The falsity of this view is
shown by the fact that the periodic vomiting may occur in chil-
dren whose appendix has already been removed.
Marfan has long been emphasizing the differential features of
these two disorders. The following discussion is borrowed from
his writings on the subject:
"Is the diagnosis between an attack of periodic vomiting and
one of appendicitis a matter of great difficulty? In many cases
it is not difficult; in a few, it is; occasionally, it is impossible.
This is what the writer now wishes to prove by a consideration
of the various features on which the diagnosis may be based.
"In distinguishing periodic vomiting from the vomiting
caused by acute appendicitis, chief stress is laid on the results
of examination of the ileocecal region. One should not, however,
neglect any of the other symptoms, although they are of less
value.
"In acute 'appendicitis the temperature is, in general, higher
than in the attacks of periodic vomiting, in which it is often
normal and in which it is high only under exceptional circum-
stances and for a short time. In acute appendicitis, acetonemia
is inconstant, late in appearing, and often slight, as it is due to
the inanition resulting from the vomiting or from the diet or-
dered by the physician ; in periodic vomiting, acetonemia is con-
stant and pronounced, and appears early; it may even be ob-
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1336 SYMPTOMS,
served before the attax:k. In acute appendicitis the vomiting and
nausea are generally less marked than in the attack of aceton-
emia. In acute appendicitis, the abdomen is frequently dis-
tended; in periodic vomiting, very seldom; on the contrary, in
the latter disorder it is usually flat and sometimes scaphoid as
in meningitis. It should not be forgotten that below the age of
five years appendicitis is a comparatively rare aflfection, being
more uncommon in that period of life than periodic vomiting.
**The decisive factors in the diagnosis are, however, supplied
by examination of the ileocecal region. If superficial touch
elicits cutaneous hyperesthesia of this entire region ; if forcible,
deep palpation reveals a painful contracture of the muscles of
the abdominal wall, and if it induces a well localized or dis-
tinctly more pronounced pain at McBumey's point (the middle
point of a line joining the umbilicus and the anterior superior
spine of the ilium, or slightly outside this point), the disorder
present is acute appendicitis. We are not referring to the cases
in which the diagnosis is rendered still more obvious by the pres-
ence of a swelling in the ileocecal region or by symptoms of
diffuse peritonitis. Of the foregoing signs, cutaneous hyperes-
thesia and rigidity are the most important ; they are possessed,
to my mind, of greater significance even than pain on deep pal-
pation, which is often hard to localize at McBurney's point on
account of the resistance oflfered by the abdominal muscles.
"In the attack of periodic vomiting, the abdomen is not pain-
ful at any point ; it is only after the attack has lasted some days
that the muscles of the abdominal wall, having been repeatedly
dragged upon by attempts at vomiting, may become the seat, not of
actual pain, but of a feeling of soreness, especially at their points
of insertion on the ribs.
"As a rule, the examination of the abdomen permits of readily
making a diagnosis between periodic vomiting and appendicitis.
But such is not always the case. There are cases in which one
is in doubt, and in which one has a right to be in doubt. Following
is an example of such a case : A child is seized with vomiting and
slight fever, hardly exceeding 38** C. ; the ileocecal region is ex-
amined ; cutaneous hyperesthesia is absent, and rigidity is lacking or
is very slight and diffused over the entire abdomen ; deep palpation
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VOMITING, 1337
elicits only trifling pain, without distinct localization, so that the phy-
sician questions whether the sensitiveness elicited is not merely due
to the pressure exerted by the examining finger; finally, aceton-
emia appears early and is pronounced. In a case of this sort
it is very hard to come to any definite diagnostic decision.
**True, sometimes rectal palpation will remove the doubt; if
such palpation leads the examiner to feel a tender infiltrated area
at the upper portion of the wall of the pelvic cavity on the right
side, a decision in favor of the presence of appendicitis should be
made. But this sign is frequently lacking, and if it cannot be
elicited, the original doubts persist.
**There is another class of cases in which the diagnosis re-
mains in suspense; these are the cases in which the results
of examination of the ileocecal region change from one attack
to the next: In one attack there is nothing wrong in the ileo-
cecal region, acetonemia appears early, and a diagnosis of peri-
odic vomiting is made. In the next succeeding attack, there are
found abdominal evidences pointing to inflammation of the ap-
pendix.
"These cases are readily explained. The same subject may
be suffering both from periodic vomiting and from appendicitis.
An appendicular attack in a predisposed subject may, like any
other acute febrile disorder, bring on an attack of periodic vomit-
ing with pronounced acetonemia.
"To recapitulate, in the majority of cases periodic vomiting
and acute appendicitis appear in a typical form and are rather
easily distinguished. Sometimes, however, such diflferentiation
is very difficult, and occasionally it is impossible. The common-
est cause of such difficulties consists in the possible coexistence
of the two affections in the same subject. In the event of doubt,
the case should be dealt with as though appendicitis were known
to exist, i.e., if the patient is a child, one should nearly always
recommend subsequent removal of the appendix.
"In the foregoing presentation, we have referred to cases in
which the physician is called upon to settle the question of diag-
nosis during the attack of vomiting. But it may happen that he
must make a retrospective diagnosis, i.e., one made a variable
time after the occurrence of an attack which he did not witness.
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1338 SYMPTOMS,
We believe that it is often very hazardous to make a decision
under such circumstances. No doubt there are cases in which
examination of the ileocecal region will yield unmistakable evi-
dences ; where, the attack of vomiting having terminated a vari-
able time before, deep palpation nevertheless reveals distinct
tenderness clearly localized at McBurney's point, and where
such palpation also reveals the presence of some degree of mus-
cular contracture strkrrty confined to the abdominal wall in the
right iliac fossa aniT^cking in the left iliac fossa, one may con-
clude that^^lbere ha& ^^urred an attack of acute appendicitis
which has left behiad it some degree of subacute or chronic in-
liammation of the appendix. But such cases are rather uncom-
mon. Usually examination of the right iliac fossa after the at-
tack shows no abnormal condition, or else, examination for
tenderness at McBumey's point or for rigidity gives such
indefinite and inconclusive results that they cannot be inter-
preted without risk of error. Hence, where the practitioner has
not actually seen the attack, he should leave to the physician
who may have seen it the responsibility of reaching a definite
decision. If, however, circumstances are such that a decision
must be made even under the conditions already described, the
family should be carefully apprised of the fact that the decision
made can be based only upon conjecture."
It seems impracticable to conclude an article on the semeiology
of vomiting without a brief additional consideration of the subject of
"Vomica." By the term vomica is meant the evacuation through
the respiratory tract of an accumulation of pus in such amount
that it suggests vomiting {vomere, to vomit).
The condition is entirely different from vomiting, inasmuch
as the evacuation of fluid takes place through the respiratory
tract. A vomica is, strictly speaking, an expectoration of pus
in large amount. But from the standpoint of gross symptoma-
tology the occurrence is a vomiting of pus — a sudden ejection
through the mouth of a considerable amount of purulent fluid,
generally accompanied by paroxysmal cough and a degree of
suflFocation sometimes bordering on complete asphyxia.
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VOMITING. 1339
By far the commonest kind of vomica is the pleural vomica,
which constitutes a possible termination of suppurative pleurisy,
interlobar, mediastinal, diaphragmatic, or encysted, sometimes
with formation of a pyopneumothorax.
The pulmonary vomica, much less common, follows, as the
term implies, abscess of the lung or gray hepatization (suppurative
pneumonia) ; the germ found in the evacuated pus is nearly always
the pneumococcus. Some cavities in fA^liteiifijaildiSQme bronchiec-
tatic cavities may lead to purulent expectaration in ^uch amount as
to suggest a vomica.
As an exceptional condition, reference may be imade to the
hydatid pulmonary vomica, or suppurative pulmonary hydatids,
which simulate the pleural vomica and can be differentiated from
it only by the finding of pieces of hydatid membrane and of
echinococcic booklets in the ejected material.
Finally, any variety of subdiaphragmatic abscess, whether of
hepatic, renal, gastric, or splenic origin, may under exceptional cir-
cumstances burrow through the diaphragm and pleura and appear
externally in the form of a vomica.
In all these disturbances the history of the case arid systematic
examination will, as a rule, enable the physician very easily to
trace back from the symptom, vomica, to its pleural, pulmonary, or
subdiaphragmatic (hepatic, gastric, renal, or splenic) source.
Digitized by
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1340
SYMPTOMS.
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1342
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INDEX OF THE PRINCIPAL CLINICAL
SIGNS.^
ARRANGED ACCORDING TO THE NAMES OF THE
AUTHORS CONCERNED.
Abderhalden Reaction.
Biochemistry,
A reaction having for its purpose
to demonstrate the proteolytic fer-
ments set free in the blood upon in-
troduction into the system of incom-
pletely elaborated organic products.
Has been used for the diagnosis of
pregnancy. Technic difficult. Re-
sults questionable.
Abrams's Reflexes. Physiology.
Cardiopulmonary reflexes awakened
by peripheral stimulation (skin, mus-
cles, and mucous membranes). Per-
cussion over the precordium causes a
reduction of the area of heart dull-
ness through dilatation of the lungs
and contraction of the heart.
Adams-Stokes Disease. Syndrome.
Featured by a marked slowing of
the pulse rate (to 30 or 40) with diz-
ziness, epileptoid seizures, and some-
times actual syncope. Due to auricu-
loventricular dissociation, and is be-
lieved usually the result of disease of
the bundle of His.
Addison's Disease. Endocrinology.
Characterized by a variable degree
of asthenia, brown pigmentation of
the skin and mucous membranes, and
low blood-pressure. It is due to dis-
ease of the adrenal glands.
Anui-Duchenne Type. Neurology,
Progressive muscular atrophy be-
ginning with the muscles of the
hands.
Argyll-Robertson PupiL Neurology.
An early sign of tabes dorsalis, con-
sisting of disappearance of the pupil-
lary light reflex with conservation of
the accommodation reflex.
Arthus's Phenomenon. Serology.
Local skin disturbances (eruptions,
erythema, edema) following repeated
injections of foreign serums.
Aschner's Sign. Neurology.
The oculocardiac reflex, consisting
of a slowing of the pulse rate by 5
to 15 or 20 beats per minute upon
compression of the eyeball. The re-
flex is enhanced in vagotonic states.
Acceleration of the pulse rate (inver-
sion of the reflex) occurs in sym-
patheticotonic states.
Avellis's Ssmdrome. Neurology.
Hemiplegia of the soft palate and
paralysis of the recurrent nerve on
the same side.
B
Babinski's Sign. Neurology.
This sign of disease of the spinal
cord (pyramidal tract) consists in
extension of the big toe when the
sole of the foot is mechanically stim-
ulated by drawing the point of a pin
over it.
Baccelli's Sign. Lungs.
Whispering pectoriloquy. Distinct
transmission of the whispered voice
to the ausculting ear on the side of
a pleural eflusion.
Baccelli's Anguloscapular Sign.
Lungs.
Reduced motion of the scapula
during deep inspiration in tubercu-
losis of the apex.
Balfour's Disease;
Osseous sarcomatosis aflecting
chiefly the bones of the cranium and
face and attended with greenish dis-
coloration (chloroma ) .
1 Prepared with the assistance of Dr. Prevel.
(1343)
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1344
PRINCIPAL CLINICAL SIGNS.
Bamberger's Sign. Neurology,
A disturbance of sensation in ta-
betics. Stimulation of a restricted
area of skin is referred by the pa-
tient to the opposite side of the
body (allochiria).
Banti's Disease. Liver.
Hepatic cirrhosis with ascites, pro-
gressive anemia, and enlargement of
the spleen.
Baranjr's Sign. Otology,
Disappearance of hydro-caloric ves-
tibular nystagmus in severe disease
of the internal ear.
Bard and Pic's Syndrome.
Pancreas,
In cancer of the head of the pan-
creas the following conditions are
present in combination: Chronic,
progressive jaundice, cachectic ema-
ciation, and dilatation of the gall-
bladder.
Bard's Sign. Neurology.
Serves to distinguish organic from
congenital nystagmus. In the first
instance, the oscillations of the we
increase as the patient follows the
physician's finger moved before his
eye from right to left and then from
left to right. In the second instance,
the oscillations disappear.
Barlow's Disease. Pediatrics,
A disease of early childhood char-
acterized by anemia with bone pains
(subperiosteal hemorrhages).
Basedow's Disease. Endocrinology,
Thyroid enlargement with tachy-
cardia, exophthalmos, and tremor.
Baum^s, Law of. Syphilography,
A S3^hilitic father may procreate
a syphilitic child without the appear-
ance of specific manifestations in
the mother and without risk to her
in nursing her infant.
Beard's Disease. Neurology,
Neurasthenia. A neuropathic symp-
tom-complex consisting of a variable
degree of insufficiency of the muscu-
lar, circulatory, secretory, and digest-
ive functions, with insomnia and gen-
eral asthenia. Met with in over-
worked individuals.
BeU's Sign. Neurology.
Displacement of the eyeball upward
and outward when the patient at-
tempts to lower the paralyzed upper
eyelid (peripheral facial paralysis).
Bence- Jones's Disease. Sarcoma.
Concomitant albumosuria and sar-
coma.
Benedikfs Syndrome; Neurology,
Hemiplegia with paralysis of the
oculomotor nerve of the opposite side
(disease of the cerebral peduncle).
Bergeron's Disease. Pediatrics.
Infantile chorea with rhythmic
movements in more or less rapid rep-
etition.
Besredka's Method.
Vaccine therapy.
Antianaphylactic vaccination car-
ried out by administering an injection
of 0.1 cubic centimeter of scrum two
hours before the therapeutic injec-
tion.
Bier^s Method. Therapeutics,
Use, in the treatment of inflamma-
tory conditions, of venous hyperemia
induced by elastic constriction of
the veins (in the extremities) or by
application of suction cups of vary-
ing shape and size.
Biett's Ring. Dermatology.
A small ring of white epidermis
frequently present about the skin
lesions of secondary syphilis.
Bird's Disease. Metabolism.
The sum of the digestive, urinary,
circulatory, and nervous disturbances
resulting from the oxalic diathesis.
Bockhart's Impetigo. Dermatology,
Vesiculopustules always developing
about a hair follicle. A skin disorder
of childhood.
Bonfils's Disease. Blood.
Proliferation of the lymphoid tissue
without increase in the white blood
cells (aleukemic or simple lympha-
denia).
Bordet and Gengou Reaction.
Serology,
A complete specific serum (contain-
ing antibodies following injection of
an antigen : bacteria, cells, or toxins)
yields a specific reaction (hemolysis,
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PRINCIPAL CLINICAL SIGNS,
1345
bacteriolysis, etc.) with the corres-
ponding antigen.
When heated to 55° C. the specific
serum loses its specific reacting power.
Brought in contact with the antigen,
it is inactivated.
It is reactivated by the addition of
normal serum, which supplies to it
what it lacks, Tnsf,, complement.
Brought in contact with the antigen,
it now again yields the specific re-
action.
The complement of the normal
serum thus utilized is permanently
fixed in the reaction, i.e., it is deviated
and cannot serve again for further
reactivation.
Bouchard's Nodes. Metabolism.
Thickening of the second joints of
the fingers in certain subjects with
dilatation of the stomach.
Boudin's Law. Tuberculosis.
Antagonism of malaria and tuber-
culosis, possibly dependent upon hy-
pertrophy of the liver.
Bouillaud's Laws. Rheumatism.
Endocarditis and joint inflamma-
tion are usually concomitant in acute
articular rheumatism with severe and
multiple manifestations.
They are not concomitant in cases
with only partial or mild manifesta-
tions.
Bouveret's Disease. Cardiology.
Marked tachycardia (180, 200, or
higher) accompanied by low blood-
pressure and elevation of 'tempera-
ture, coming on in sudden attacks of
variable duration, from a few
minutes to several days (heart fail-
ure). Paroxysmal tachycardia.
Bozzolo's Siga Cardiology.
Visible pulsations of the nostrils
in some cases of thoracic aneurysm.
Brandt's Method. Therapeutics.
Treatment of typhoid fever by the
systematic use of cold baths.
Bright's Disease. Kidneys.
Chronic nephritis with albuminuria,
high blood-pressure, and terminal
edema.
Bright's Siga Peritonitis.
Peritoneal friction sounds.
85
Briquet's Gangrene. Lungs.
Gangrene of the bronchi in the
course of bronchiectasis.
Brissaud and Sicard, Syndrome of.
Neurology.
Motor disturbances on one side of
the body with facial hemispasm on
the opposite side.
Broadbent's Siga Cardiology.
Systolic retraction of the left pos-
terior aspect of the chest at the level
of the diaphragm; a sign of peri-
cardial adhesion.
Broca's Aphasia. Neurology.
Motor aphasia resulting from dis-
ease of the lower portion of the left
third frontal convolution.
Brown-S6quard'8 Mediod.
Endocrinology.
Opotherapy. The administratic«i of
extracts of organs in disease of the
identical organs to make up for their
deficiencies or to stimulate them. A
procedure based on the fact that the
vascular glands produce an internal
secretion.
Brown-S6quard's Sjoidrome.
Neurology.
Unilateral disease of the spinal cord
causing hemiparaplegia with hemi-
anesthesia on the opposite side.
Brudzinski's Signs. Neurology.
Signs of meningitis. A reflex
movement of flexion or extension of
the lower extremity is obtained by
strongly flexing the limb of the op-
posite side (contralateral reflex).
Flexion of the lower extremities is
obtained upon flexing the neck.
Bryson's Siga Graves^s disease.
Deficient chest expansion during
inspiration in cases of Graves's dis-
ease.
Charcot's Disease. Neurology.
Spastic paralysis in conjunction
with progressive muscular atrophy.
Charcot-Marie's Siga Neurology.
The rapid tremor of exophthalmic
goiter.
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1346
PRINCIPAL CLINICAL SIGNS.
Chesme-Stokes Breathing. Lungs.
A type of breathing comprising a
series of respirations of increasing
amplitude, then of decreasing ampli-
tude, followed by a varying period of
apnea and resumption of the increas-
ing respirations.
Chvostek, Jr.'s Sign. Tetany.
Increased mechanical irritability of
the motor nerves in tetany.
Clapton's Sign, Copper poisoning.
A greenish line on the gums in
copper poisoning.
A sympathetic ocular syndrome
characterized by enophthalmos, my-
osis, and vasomotor disturbances on
the same side of the face (elevation
of local temperature and sweating).
Colrafs Test Liver.
Alfmentary glycosuria, demon-
strated by having the patient take
150 grams of glucose on an empty
stomach and tracing the sugar in the
urine on the same dav (an indica-
tion of insufficiency of the liver).
Conigan's Disease. Cardiology.
Aortic insufficiency of rheumatic
origin.
Corrigan Pulse. Cardiology.
A bounding and brief pulse. Ab-
rupt ascent, rapid turn, and quick
descent of the pulse tracing. Aortic
insufficiency due to endocarditis.
Courvoisier and .Terrier,
Law of.
Liver.
Atrophy of the gall-bladder in the
presence of obstruction of the com-
mon bile-duct by a stone; dilatation
of the gall-bladder in other kinds of
obstruction.
Cruveilhier's Disease.
Gastric ulcer.
Stomach.
Damoiseau's Curve. Pleura.
A curve with its convexity upper-
most, formed by the surface of
pleural effusions.
Dehio's Test. Cardiology.
Testing for cardiac acceleration in
bradycardia upon injection of 1 mil-
ligram of atropine sulphate. If the
test is positive, the bradycardia is of
nervous origin ; if negative, of car-
diac origin.
Dejerine-Klumpke, Sjoidrome of.
Neurology.
Paralysis of the lower nerve-roots
of the brachial plexus, accompanied
by myosis and enophthalmos.
Dubini's Chorea. Neurology.
Chorea marked by convulsive at-
tacks which are followed by para-
lysis and coma.
Duchenne's Disease.
Tabes dorsalis.
Neurology.
Duguet's Sign. Cardiology.
Ulcers on the pillars of the soft
palate in typhoid fever.
Duroziez's Disease. Cardiology.
Uncomplicated mitral stenosis.
Duroziez's Sign. Typhoid fever,
A double murmur heard with a
stethoscope exerting gentle pressure
over the femoral artery.
A sign of aortic regurgitation.
Auscultation.
the whispered
D'EsfHne's Siga
Bronchophony of
voice elicited by auscultation over
the spinal column between the scap-
ulae (a sign of intertracheobronchial
glandular enlargement).
Erb's Siga Neurology.
Enhanced electric excitability of
the muscles and nerves in tetany.
Disappearance of the pupillary re-
sponse to pain in tabes.
Fallot's Disease. Cardiology.
Congenital malformations of the
heart in "blue babies:" Stenosis of
the pulmonary artery, interventricu-
lar communication, hypertrophied
right ventricle, and displacement of
the aorta to the right.
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PRINCIPAL CLINICAL SIGNS,
1347
Finsen's Method. Therapeutics,
Treatment of skin disorders by
means of selected light rays.
Fochier*8 Method. Therapeutics.
Treatment by means of artificial
aseptic abscesses (fixation abscesses).
Friedreich's Disease. Neurology.
Hereditary locomotor ataxia ap-
pearing in childhood and persisting
indefinitely.
Frdhlich's Sjmdrome.
Endocrinology,
Obesity associated with an infan-
tile condition of the sexual organs,
due to pituitary insufficiency.
Fiirbringer's Siga
Subphrenic abscess.
Serves to differentiate subdia-
phragmatic abscess from abscess in
the chest. A needle passed into the
abscess cavity is displaced with the
respiratory movements in the former
case and not in the latter.
Gaucher's Disease. Spleen.
Primary epithelioma of the spleen.
Gerhardt's Test Urine.
Portwine color of the urine upon
addition of ferric chloride, pointing
to the presence of diacetic acid.
Gmelin's Test Urine.
An emerald green rinu: formed at
the surface of contact between urine
and nitric acid without application of
heat; points to the presence of bile
pigments in the urine.
Godelier's Law. Tuberculosis.
Tuberculization of the pleura al-
ways occurs when tuberculosis of the
peritoneum exists.
Gordon's Siga Neurology.
Extension of the great toe upon
compression of the muscles of the
calf; points to disease of the pyra-
midal tract.
Gradenigo's Sjmdrome. Otology.
Paralysis of the sixth cranial nerve
(abducens) during acute otitis media.
Graefe's Sign. Endocrinology.
Dissociation of the movements of
the upper lid and eyeball when the
eye glances downward. A sign of
exophthalmic goiter.
Grancher's Disease. Lungs.
Massive congestion of the lung
without pleural effusion, but )nelding
clinical signs similar to those of
pleurisy.
Graves's Disease. Gaiter.
Exophthalmic goiter or Basedow's
disease.
Graves's Sign. Gout.
Abnormal sensitiveness of the
dental nerves in gouty individuals,
causing them to grind the teeth.
Grocco's Triangle. Percussion.
A triangular area of paravertebral
dullness at the base of the thorax on
the side opposite that of pleurisy.
Ascribed to displacement of the
mediastinal structures.
Gu6rin's Law. Rachitis.
Rachitic deformities begin in the
lower portions of the body.
H
Hahnemann's Method. Therapeutics.
Homeopathy.
Hanot's Disease. Liver.
Hypertrophic cirrhosis with chronic
jaundice.
Harley's Disease. Blood.
Paroxysmal hemoglobinuria com-
ing on on account of exposure to
cold.
Harrison's Groove. Rickets.
Observed in rachitic Subjects dur-
ing deep inspiration, between the
chest and the upper portion of the
abdomen, at the level of insertion
of the diaphragm.
Head's Zones. Neurology.
Innervation of the visceral struc-
tures and skin surface in correspond-
ing zones. Cutaneous hyperesthesia
in definite zones points to disease of
the corresponding deep-seated or-
gans.
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1348
PRINCIPAL CLINICAL SIGNS.
Heberden's Nodes. Rheumatism.
Nodes about the terminal phalan-
geal joint in chronic rheumatism.
Heine-Kreysig's Sign.
Pericardial adhesion.
Systolic depression of the inter-
costal spaces indicating pericardial
adhesion (cardiac symphysis).
Heine-Medin's Disease. Infections.
An infectious, epidemic disorder
resembling infantile paralysis.
Heine-Sanders' Sign.
Pericardial adhesion.
Wave-like motion of the chest-
wall extending beyond the bound-
aries of cardiac dullness and most
marked in the epigastric region.
Characteristic of pericardial adhesion.
Herxheimer's Reaction. Syphilis.
Temporary accentuation of syphi-
litic manifestations as a result of
mercurial or arsenical treatment.
Hirschsprung's Disease. Colon,
Congenital megacolon accompanied
by constipation and abdominal en-
largement in young children.
Hodgson's Disease. Cardiology.
Aortic insufficiency of arterial
origin.
Hutchinson Teeth. Teeth.
Dental deformity characterized by
semicircular notches in the free
margins of the median upper incisors
with narrowing of the necks of the
teeth. A sign of congenital syphilis.
Jaccoud's Siga Cardiology.
A sign of pericardial adhesion con-
sisting of a rolling movement in the
precordial region,
Jellineck's Siga Dermatology.
Discoloration of the eyelids in
Basedow or nervous subjects.
Karell's Treatment Therapeutics.
Marked reduction in the intake of
fiolid and liquid food (800 grams of
milk per diem) ; used in certain
cases of heart weakness.
Kemig's Sign. Neurology.
l^lexion of the legs on the thighs
when the lower limbs are placed at
a right angle with the trunk (sit-
ting posture in bed). A sign of
spinal meningitis.
Kienbock's Siga Pleura.
Fluoroscopy showing a rise of the
diaphragm at the time of inspiration
on the side of an effusion of fluid
and air in the pleura.
Klippel's Disease. Neurology.
A species of rapidly progressive
general paralysis occurring in old
men (dementia, stroke, and paralytic
phenomena).
Kussmaul Breathing. Respiration.
A kind of breathing characterized
by a prolonged inspiration followed
by a pause and a brief expiration,
followed by a second pause. Met
with in diabetic coma.
Laennec's Cirrhosis. Liver.
Atrophic cirrhosis.
Landouzy-Dejerine Tsrpc. Myology.
A form of progressive muscular
atrophy of childhood beginning with
the face, shoulders, and arms.
Landry's Disease. Neurology.
Paralysis of the lower extremities
of an acute t)rpe, soon involving the
trunk and causing death within a
few days.
Lasdgue's Siga Neurology.
A sharp pain elicited in the but-
tock by flexion of the thigh on the
pelvis with the lower extremity
extended. An indication of sciatica.
Leyden-Mobius Typt. Myology.
Muscular atrophy beginning in the
lower limbs and later gradually in-
volving the upper extremities.
Litten's Siga Lungs.
Reduced mobility of the diaphragm
on the affected side in pulmonary
tuberculosis.
Little^s Disease. Neurology.
Congenital spastic paraplegia oc-
curring in premature infants or fol-
lowing unusually difficult labor.
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PRINCIPAL CLINICAL SIGNS.
1349
Ludwig's Angina. Mouth,
Infectious cellulitis of the floor of
the mouth.
M
Madelung's Disease.
Hand in the valgus position, with
prominence of the head of the ulna
and palmar subluxation of the hand.
Marejr's Law.
Tachycardia generally
low blood-pressure and
high blood-pressure.
Marie's Disease.
Enlargement of the
and face.
Cardiology.
accompanies
bradycardia
Dystrophy.
hands, feet,
Martinet's Laws. Circulation.
Dividing the daily output of urine
by the mean differential (pulse)
pressure gives a result equal to or
exceeding one-fourth liter in the
healthy subject on a normal diet.
Persistence of the result below
0.200 liter is characteristic of renal
sclerosis.
Martinet's Ssmdrome. Circulation.
Hyposphyxia, characterized by low
blood-pressure and an absolutely or
relatively high blood viscosity, with
small pulse and slowed circulation.
Menetrier's Ssmdrome.
Thoracic duct.
Signs of pressure upon the thor-
acic duct: Firm edema of the lower
portion of the body, the chest and
the left arm, with peritoneal and
pleural effusions on the left side.
M6nidre's Sjmdromc. Otology.
Vertigo, with various sounds heard
by the patient. Reduction of audi-
tory acuity. An indication of in-
ternal ear disease.
Mikulicz's Disease. Glands.
Enlargement of the lacrymal and
salivary glands on both sides, with
suppression of their secretion but
without local pain; believed fre-
quently due to leukemia.
Millard-Gubler Ssmdrome.
Neurology.
Hemiplegia on one side with facial
paralysis on the other.
Mbbius's Disease. Neurology.
Ophthalmoplegic migraine.
Mobius's Sign. Endocrinology.
Difficulty of convergence of the
eyes in exophthalmic goiter.
Morton's Disease. Feet.
Metatarsalgia frequently following
fatigue.
Morvan's Disease. Leprosy.
Felon accompanied by anesthesia
of the fingers; considered of leprous
nature.
Murphy's Method. Therapeutics.
Rectal administration, drop by
drop, of glucose or saline solution
in high fever or after surgical oper-
ations.
Musset's Sign, Cardiology.
Rhythmic jerking movements of
the head, synchronous with the heart
beats, in patients with aortic regur-
gitation. [Alfred de Musset is said
to have exemplified this sign.]
N
Negri Bodies. Rabies.
Found in the central nerve cells of
animals that have succumbed to
rabies. Considered specifically re-
lated to the disease.
Negro's Sign. Neurology,
A sign of peripheral facial paral-
ysis : Elevation of the eyeball is
more marked on the paralyzed side
when the patient looks upward with
the head motionless.
Ocrtcl's Method. Therapeutics.
Treatment by graded exercise
(walking on level ground or in-
clines) in chronic heart disorders.
Oliver's Sign. Aortic aneurysm.
Movements of the larynx from
below upward, synchronous with car-
diac systole, in subjects suffering
from aneurysm of the arch of the
aorta.
Oppenheim's Sign. Neurology.
A sign of disease of the pyramidal
tracts. Ascent of the great toe when
pression is exerted from above down-
ward over the muscles of the antero-
external aspect of the leg.
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1350
PRINCIPAL CLINICAL SIGNS.
Paget's Disease of the Bones.
Bones.
Marked thickening of the bones of
the skull and extremities. Believed
an indication of inherited syphilis.
Paget's Disease of the Nipple.
Breast.
A malignant tumor starting at the
nipple, in old women.
Parkinson's Disease. Neurology.
A disease characterized by rigid
posture of the body, a facies as of
surprise, and a peculiar (pill-rolling)
tremor of the fingers.
Parrot's Disease. Bones.
Syphilitic epiphyseal detachment.
Parrot's Law. Tuberculosis.
A tuberculous lesion of the bron-
chial lymph-nodes is always accom-
panied by a pulmonary lesion of the
same nature.
Parrot's Siga Meningitis.
Dilatation of the pupil when the
skin is pinched in meningitis.
Pavy's Disease. Albuminuria.
Intermittent cyclic albuminuria in
young subjects, occurring in the day-
time.
Perret and Devic, Signs of. Pleura.
Signs of pleurisy at the base of the
left lung, posteriorly; they disappear
in the knee-chest posture, and are
met with particularly in children
suffering from pericarditis with
effusion.
Pettenkoffer's Test Urine.
Purple violet color of the urine
when treated with sulphuric acid in
the presence of sugar; points to the
presence of bile acids.
Pfuhl's Sign. Pleura.
Shows whether an effusion is
above or below the diaphragm. In
the first instance the pressure in the
manometer connected with the trocar
rises during inspiration; in the sec-
ond instance, it falls.
Porgds's Reaction. Serology.
Precipitation of serum in the pres-
ence of a solution of sodium glyco-
cholate. Claimed to indicate syphilis.
Pott's Disease. Bones.
Tuberculosis of the vertebrae.
Profeta, Law of. Syphilis.
A syphilitic mother may nurse her
healthy infant without risk of in-
fecting it.
Q
Quincke's Disease. Dermatology.
Hereditary acute paroxysmal ede-
ma, unattended with constitutional
disturbance.
R
Raynaud's Disease. Circulation.
Disturbances of the circulation in
the extremities (cyanosis, local as-
phyxia, "dead finger"), which may
lead to dry gangrene.
Recklinghausen's Disease.
Dermatology.
Cutaneous and nervous tumors
(neurofibromata) accompanied by
pigmentation of the skin.
Reclus's Disease. Breast.
Presence of many small shot-like
cysts in the breast.
Revilliod's Phenomenon.
Hemiplegia.
Inability, in organic hemiplegia, to
close the eye on the paralyzed side
without at the same time closing
that on the well side.
Rinn^'s Test Otology.
Rinne positive when the sound of
the tuning-fork is heard better by
air conduction than by mastoid
(bone) conduction. Rinne negative
when the sound is better conducted
by bone than by air.
Rivalta's Test Serology.
A few drops of effused fluid cause
a turbidity when dropped in water
acidulated with acetic acid if the ef-
fusion is of inflammatory nature.
Roger's Disease. Cardiology.
Congenital communication between
the ventricles of the heart, unat-
tended with dyspnea nor cyanosis
when the subject is at rest.
Romberg's Sign. Neurology.
An indication of tabes dorsalis :
Loss of equilibrium when, with the
eyes closed, the heels are brought
together.
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PRINCIPAL CLINICAL SIGNS.
1351
Rosenbach's Sign. Neurology,
Persistence of the abdominal reflex
in hysteric hemiplegia, in spite of
the anesthesia of the skin.
Rosenheim's Siga Perigastritis,
Friction sounds heard on auscul-
tation over the left hypochondrium
in cases of fibrous perigastritis.
Ruault's Siga Respiration,
Diminished amplitude of respira-
tion on the affected side in incipient
pulmonary tuberculosis.
Sahli's Test Pancreas,
Where the pancreas is functionat-
ing normally, iodine appears in the
urine six hours after ingestion of a
gluten-coated iodoform pill.
Sicard's Method. Neurology,
Treatment of certain disorders by
the introduction of solutions of
drugs into the epidural space.
Sieur's Siga Pleurisy.
A ringing, metallic sound elicited
in pleural effusion by percussing the
opposite point with two coins, the
one placed against the thorax and
the other used as pleximeter.
Souques's Siga Neurology,
Spreading of the fingers when a
patient with organic hemiplegia at-
tempts to raise the paralyzed arm
(incomplete flaccid hemiplegia).
Stellwag's Siga Endocrinology,
Incomplete closure of the eyes in
exophthalmic goiter.
Stokes-Chopart, Law of.
Inflammation,
The muscles underlying an in-
flamed mucous membrane or serous
surface are in a paralyzed state.
Straus's Siga Neurology.
In severe peripheral facial paral-
ysis the sweating induced by pilocar-
pine is delayed.
Thomsen's Disease. Myology,
Spastic contraction of the muscles
when voluntary movements are at-
tempted.
Thure-Brandt Posture. Abdomen,
Posture in which the abdominal
wall is relaxed. Dorsal decubitus,
lower extremities flexed, and but-
tocks raised, the patient taking deep
inspirations.
Traube's Law. Circulation,
Interstitial nephritis always tends
to bring about hypertrophy of the
left ventricle.
Troisier's Ganglioa Lymphatics,
Glandular enlargement above the
clavicle on the left side in cancer of
the stomach.
Trousseau's Siga Neurology,
Contracture obtained by exerting
pressure on nerves or vessels in
tetany.
V
Valleix's Laws. Neurology,
Governing the location of pain in
neuralgia: The painful areas are to
be found at the points of emergence
and in regions where the nerve rami-
fications become superficial.
Valsalva Test Otology.
By attempting to blow out air with
the mouth and nose closed the pa-
tient inflates the t)rmpanic cavity.
Vaquez's Disease. Blood.
A disorder characterized by a
marked increase in the number of
red cells, together with cyanosis and
splenic enlargement.
Vincent's Angina. Tonsils,
Subacute tonsillitis with a diph-
theroid exudate and associated with
the presence of fusiform bacilli.
Vulpian's Law. Neurology.
In hemiplegia the patient turns his
head and eyes toward the side of the
lesion, which he appears to look at.
W
Wassermann Reactioa Serology,
The Bordet and Gengou reaction
of fixation applied in the diagnosis
of syphilis.
Weber's Test Blood.
A test for traces of blood in the
feces or in vomitus. Acetic acid,
ether, fresh tincture of guaiac, and
hydrogen peroxide solution yield a
blue color.
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1352
PRINCIPAL CLINICAL SIGNS.
Weber's Test Otology,
A test of the hearinpr carried out
by applying a tuning-fork over the
forehead. If conduction is better on
the affected side, there is middle ear
disease. If conduction is better on
the opposite side, there is internal
ear disease.
Werlhoff's Disease. Blood.
Cryptogenic purpura and hemor-
rhages, unattended with fever and
prognostically favorable.
Wernicke's Siga Neurology.
Consists in that, in a subject with
bilateral homonymous hemianopsia,
pupillary response when a beam of
light strikes the blind half of the
retina occurs only when the lesion
involves the optic fibers beyond the
thalamus. In the opposite event, a
response is obtained only by stimu-
lating the normal half of the retina.
Westphall's Sign. Neurology,
An early sign of tabes dorsalis :
Loss of the patellar reflex.
Woillex's Disease. Lungs.
Acute pulmonary congestion giv-
ing rise to symptoms similar to those
of pneumonia.
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INDEX TO VOLUMES I AND II.
Abderhalden test, 1343
Abdomen, 80; sec also the various
organs.
fluoroscopy of, 81
inspection of, 80, IZl, 1089
palpation of. 81, 738, 1091
percussion of, 81, 738, 1094
prominent, 80
rigid, 1093
scaphoid, 81
succussion of, 81
Abdominal angina, 835, 841
ptosis, lumbar pain of, 1180
reflex, 475
wall, edema of, 739
Abdominocardiac reflex, 281
Abducens paralysis in otitis media,
1347
Abortion of syphilitic origin, 856
Abrams's reflexes, 1343
Abscess, brain, headache of. 983
of the liver, 1069, 1082, 1120, 1127
ossifluent, 1188
perinephric, 1061, 1066, 1070, 1072
subdiaphragmatic, 1062, 1074, 1339,
1347
Accentuated aortic second sound, 208
Accommodation, paralysis of, in en-
cephalitis, 1278
Acetonemia, dyspnea of, 810, 823
sleep of, 1272
vomiting of, 1334
Acetonuria, 425
Achilles reflex, 468
Achondroplasia, 604, 606
Achorion Schcenleinii, 504
Achylia gastrica, 793
Acidosis, convulsions of, 771, 772
dyspnea of, 824
itching of, 1116
Acrocyanosis, 1197
Acromegaly, 605, 606, 912
Actinomycosis, 586
of the skin, 956
of the tongue, 1305, 1307
Adams-Stokes disease, 2, 722, 776,
927, 1343
Addison's disease, 1343
asthenia of, 754
loss of weight in, 1142
low blood-pressure of, 1147
Adenoid vegetations, 150
coated tongue in, 1297
Adhesion, pericardial, 1348
Adhesions, jaundice due to, 1120
Adiposis dolorosa, 1208
nervous, 1208
Adrenal diabetes, 970
insufficiency, 754, 928, 1145, 1147,
1152
Aerophagia, 805, 1039, 1058, 1233,
1251, 1254, 1269
Agglutination test for typhoid fever,
548
Agraphia, 484
Agrypnia, 1101
Albumin, qualitative tests for, 409
quantitative determination of, 411
test (sputum), 196
Albuminuria, 649
acute, 650
artificial, 412
cardiac, 655
chronic, 652
cryptogenic, 658
cyclic, 658, 1350
diabetic, 655
digestive, 658
functional, 658
gouty, 655
intermittent, 659
neuromotor, 658
of autointoxications, 655
of chronic infections, 654
(1353)
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1354
INDEX TO yOLUMES I AND II.
Albuminuria of intoxications, 654
of pregnancy, 655
of fatigue, 658
orthostatic, 659
simulated, 659
Tabular Synopsis, 656-657
Alcoholism, convulsions of, 773, 774,
776
cough of, 784
edema of, 830
eye disturbances of, 922
gastritis of, 803, 1000
loss of weight of, 1143
nervousness of, 1193
neuritis of, 1318
obesity of, 1208
sleep of, 1271
somnambulism of, 1281
tremor of, 1309
vertigo of, 1330
vomiting of, 1334, 1340
Alimentary chloriduria, 440
enterocolitis, 791
glycosuria. 125, 970, 1346
pruritus, 1106
tract, 41
ulceration in, topographic diag
nosis of, 102
Allochiria, 1344
Alopecia, 661
areata, 661
cicatricial, 668, 673
congenital, 661, 668
in the adult, 669
in the child, 661
in the elderly, 673
in the nursling, 669
infectious, 668
occipital, 661
pityrodcs, 670
senile. 673
syphilitic, 672
temporal, 668
x-ray, 668
Alternating pulse, 726, 1286
Amaurosis, 915, 919
Ambard's coefficient, 443
ureometer, 293
Amblyopia, 913
Ambulatory automatism, 1280
Ambulatory case examination, 627
Amebae in stools, 108, 541
Amebic dysentery, diarrhea of, 790
Amphoric breathing, 166
voice, 166
Anemia, 675
asthenia of, 754
epistaxis of, 845
low systolic pressure of, 1145
vertigo of, 1326
aplastic, 676
. autotoxic, 677
by spoliation, 676
cancerous, 677
cholemic, 679 ,
infections, 677
pernicious, 676, 793
edema of, 828
plastic, 676
toxic, 678
Aneurysm, 1189
aortic, 226, 228, 237, 685
arm pain of, 1318, 1320
bradycardia of, 1287
cough of. 783
edema of, 830
hematemesis of, 1035
hemoptysis of, 1035
hiccough of, 1040
intercostal pain of, 1270
lumbar pain of, 1180
Oliver's sign of, 1349
precordial pain of, 1266
pulsation of nostrils in, 1345
recurrent nerve paralysis in. 685
arteriovenous,, 1189
carotid, 1189
innominate, 1189
of abdominal aorta, 842, 1120
pain in side in, 1233
subclavian. 1189
Angina (sore throat), 1290
abdominalis, 835, 841
pectoris, 840, 1248
arm pain of, 1318
dyspnea of, 817
epigastric pain of, 800
pseudo-, 1201
phlegmonous, 1184
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INDEX TO VOLUMES I AND II.
1355
Anginoid syndrome, 1065, 1254
Angiocholitis, 937
Angiomata, multiple, 1197
Angioneurotic edema, 831
Angiospasm, 237, 238, 1051, 1056,
1257, 1268
angina pectoris in, 1254
labyrinthine, 1331
Angiospastic presclerosis, 1239
Angor, 1201
Anguillula intestinalis, 117
Aniline violet, 517
Ankylostoma, 112, 113
Anthrax bacillus, 534
Anthropomorphic measurements, 596
Antianaphylactic vaccination, 1344
Antiformin method for sputum, 521
Antipyrin in urine, 427
Anuria, 651
calculous, 1219
Anxiety neurosis, 1200, 1320
Aorta, atheroma of, 208
dilatation of, 225, 227. 237, 1266,
1319
diseases of. 237
relations of, to body morphology,
600
Aortic insufficiency, 201, 202, 204
chronologic diagrams of, 202, 204
Corrigan pulse in, 1346
epistaxis of, 844
low diastolic pressure of, 1146
Musset's sign of, 1349
stenosis, 203, 204
chronologic diagrams of, 203, 204
Aortitis, 237, 238, 1040
angina pectoris in. 1254
hiccough of, 1040
pain of, 1266
tinnitus of, 1295
Aphasia, 484, 803
bundle, 1017
Aphonia, 680
acute. 680
chronic, 680
hysterical, 692
simulated, 692
Tabular Synopsis, 686-690
Aphtha, 1299
Aphthous fever, 1299
Apical pleuritis, 1232
systolic murmurs, 209
Apomorphine, vomiting due to, 1332
Apoplexy, see Coma, 759, and Hemi-
plegia, 1014
Appendicitis, dyspepsia of, 804
epigastric pain of, 842
left hypochondriac pain of, 1059
right hypochondriac pain of, 1070,
1084
ilac pain of, 1089
yomiting of, 1332, 1334, 1335, 1340
Aran-Duchenne type of muscular
atrophy, 1343
Argyll-Robertson pupil, 481, 1343
Arhsrthjnia, 693
perpetual, 728
respiratory (sinus), 710. 1197
Tabular Synopsis, 732-733
Arm, see Upper extremities.
Ameth's neutrophilic blood-picture,
175, 315
Arsenic,^diarrhea due to, 791
hematemesis due to, 996
obesity due to, 1208
Arsphenamin, jaundice due to, 1124
Arterial stupor, traumatic, 245
Arteries, 239, 1159
Arteriosclerosis, 927, 1024, 1146
asthenia of, 755
dyspepsia of, 803
epistaxis of, 844
high bIo6d-pressure of, 1053
in obesity, 1215
itching of, 1106
loss of weight of, 1143
plethora preceding, 1238
precordial pain of, 1268
tinnitus of, 1295
vertigo of, 1325
vomiting of, 1342
Arteritis, 1159
syphilitic, 1025. 1026
Arthralgia, 1128. 1157
Arthritides, acute, 1129
chronic, 1130
traumatic, 1130
trophoneurotic, 1130
Digitized by
Google
1356
INDEX TO VOLUMES I AND II.
Arthritis, coxo femoral, 1164
deformans, 1130
eye disorders of, 915
gonorrheal, 1156
tuberculous, 1156
Arthus's phenomenon, 1343
Ascaris, 112, 117
Aschner's sign, 1343
Ascites, 324. 737, 1071
Tabular Synopsis, 748, 749
Ascitic fluid, 743
Astasia, 458
Asphyxia, local, of the extremities,
1318
Asphyxiating gases, 824
Asthenia, 751
humoral, 754
infectious, 755
myocardial, 281
nervous. 752
vasomotor, 281
Tabular Synopsis, 753
Asthma, bronchial, 189, 809, 811, 815
cardiac, 819
Astigmatism, 879, 904, 985
Ataxia, 458
differentiation of, 498
locomotor, see Tabes dorsalis.
Atheroma of aorta, 208
Atrophy, progressive muscular, 1343
Atropine test, 1289. 1346
Aura, vertigo as, 1330
Aural vertigo, 1326
Auricular fibrillation, 728
Auriculoventricular conduction, 1288
dissociation, 714, 1286
Auscultation of bronchi and lungs,
166-190
of heart. 199-215
Avellis's syndrome, 1343
Azotemia, 442, 755, 823. 980, 1116,
1151, 1271, 1299
Babinski sign, 474, 1343
induced vertigo sign, 494
Baccelli*s sign, 1343
anguloscapular sign, 1343
Bacillus anthracis, 534
coli, 543
Bacillus cholerae Asiaticae, 540
diphtheriae, 535
dysenteriae, 541
influenzas, 526
of Ducrey, 534
of Hoffmann, 545
tetani, 535
tuberculosis, 525
Backache, 1170, 1180
with fever, 1176
Bacteria, classification of, 524
in urine, 434
Bacteriology, 513
Balanitis, 955
Baldness, 669
Balfour's disease, 1343
Bamberger's sign in tabes, 1344
Bands, jaundice due to, 1120
Banti's disease, 1071, 1344
Barany sign, 496, 1344
Bard and Pic's syndrome, 1344
Barlow's disease, 1344
Barraquer-Simons's disease, 1144
Bartholin's glands, 385
Basedow's disease, see Goiter, ex-
ophthalmic.
Baumes, law of, in syphilis, 1344
Beard's disease, 1344
Bedside case examination, 619
Bell's sign in facial paralysis, 1344
Belladonna, itching due to, 1107
Bence-Jones's disease, 1344
Benedikt's syndrome, 1344
Bergeron's disease, 1344
Besredka's method, 1344
Bier's method, 1344
Biett's ring in secondary syphilis,
1344
Bile acids in urine, 420
in blood, 124
pigments, albumin reaction, 101
in blood, 299
in urine, 417
Triboulet's reaction, 100
Bilharzia, 113, 1010
Bilioseptic fever, 937, 940
Bilious headache, 980
Bilirubin in blood, 299
in urine, 418
Digitized by
Google
INDEX TO VOLUMES I AND II.
1357
Bird's disease, 1344
Biting of the tongue, 1306
Bladder, 351
capacity, 353
cystoscopic appearances in disease,
360
hematuria, 1006. 1013
stone in, 353, 361
tumors of, 361
ulcerations of, 360
Blastocystis hominis, 111
Bleeding time, 289
Blepharitis, 919
Blistering test of death, 1276
Blood, 282, 963
bacteriologic examination, 520
bile, 124
chemical examination, 292
bile pigments, 299
chlorides, 298
picric acid, 301
urea, 292, 442, 764
cultures, 318, 543, 552
cytologic examination, 301
collecting blood samples, 301
cell counts, 305
red cells, 308
white cells, 310
differential, 312
dry blood smear, 311
filarial larvae, 320
malarial parasite, 319
hemoglobin, 310
in alimentary canal, 102
stools, 101, 330
urine, 330, 424, 433
physical examination, 282
coagulability, 288
resistance of red cells, 290
spectroscopy, 282, 588
viscosity, 282, 1148, 1238
plasma, collection of, 303
serum, collection of, 303
stains, detection of, 589
Blood-presure estimation, 239
auscultatory method, 243
oscillatory (Pachon) method, 240
palpatory method, 239
high, 1043
Blood-pressure, high, in nephritis, 653
low, 981, 1145
relationship of, to body-weight,
1141
Blurred vision, 904
Bockhart's impetigo, 1344
Body weight, 1138
Bones, disorders of, in upper ex-
tremity, 1315
Bonfils's disease, 1344
Bordet-Gengou complement fixation
test, 551, 565, 1344
Bothriocephalus, 113, 115
Botulism, 791, 793, 923
Bouchard's nodes in dilatation of the
stomach, 1345
Boudin's law concerning malaria and
tuberculosis, 1345
Bouillaud's laws concerning rheu-
matism, 1345
Bouveret's disease, 1345
Bozzolo's sign in aneurysm, 1345
Brachial plexus, pain in disease of,
1318
Brachyalgia, 1313
Bradycardia, 717, 718, 776, 927, 1256,
1285
Bradysphygmia, 1285
Bradytrophic diathesis, 1133
Brain abscess, headache of, 983
congestion, 1295
diseases, eye disturbances in, 921
vomiting in, 1344
softening, 484. 1014 .
tumor, 984, 991, 1279, 1325
Brandt's method, 1345
Brass sound, 166
Breast, pain in, 1270
Breathing capacity, 193
Bright's disease, see Nephritis,
sign in peritonitis, 1345
Briquet's gangrene, 1345
Brissaud and Sicard, syndrome of,
1345
Broadbent's sign in pericardial ad-
hesion, 1345
Broca's aphasia. 1345
Brocq's pseudopelade variety of fol-
liculitis decalvans, 673
Digitized by
Google
1358
INDEX TO VOLUMES I AXD II.
Bromides in urine, 427
Bronchial breathing, 166
glands, enlarged, 170, 171
Bronchiectasis, 184, 783, 784, 1339,
1345
Bronchitis, 170, 868, 869, 872, 1151,
1250
capillary, 171
chronic, 868, 869
dyspnea of, 812
hemoptysis of, 1033
hemorrhagic, 866
Bronchophony, 166, 1346
Bronchopneumonia, 186
pain of, 1231
Bronchopulmonary infections, cough
of. 782
Bronchospirochetosis, hemorrhagic,
866
Brown-Sequard's method, 1345
syndrome, 1021, 1023, 1345
Bnidzinski's signs, 1345
Bruit, aneurysmal, 1189
d'airain, 166
Bryson's sign in Graves's disease,
1345
Bubo. 953
Bulbar hemiplegia, 1020, 1022
Bullous eruptions, 849
Bundle of His, gumma of, 1287, 1289
Bursitis, subacromial, 1317
Cachexia, ascites of, 746
edema of, 828, 832
low blood-pressure of, 1145
Cadaveric cooling, 1276
hypostasis, 1276
putrefaction, 1276
rigidity, 1276
Calculi, urinary, 350, 353, 361 ; see
also Nephrolithiasis and
Stone in bladder and ureter.
Calmette's tuberculin test, 557
Caloric test, 496
Cancer of esophagus, 685
of gall-bladder, 1080
of intestine, diarrhea of, 791, 793
dyspepsia of, 802
of kidney, 1008
Cancer of larynx, 681, 689, 1190
of liver, 1069, 1071, 1083, 1120, 1127
of pancreas, 1071. 1120
of prostate, 380
of splenic flexure, 1063
of stomach, 106. 807
edema of, 826, 838
epigastric pain of, 837
hematemesis of, 997, 1000
vomiting of, 1334, 1341
of tongue, 1304
of vertebrae, 1233
Cannabis, vertigo due to, 1330
Cantharis poisoning, hematuria of,
1010
Car sickness, vertigo of, 1331
Carbol-fuchsin, 517
-thionin, 517
Carbon monoxide anemia, 678
vertigo, 1330
Cardiac asthma, 819
disorders (see also Heart), etio-
logic diagnosis, 236
edema, 827
hypertrophy, 1270
neuroses, 821, 1252, 1255
differentiation from organic dis-
ease, 1261
high blood-pressure in. 1262
Cardiography, 261
Cardiorenal sclerosis, 1055, 1057, 1139
in obesity, 1215
Casts in urine, 430
Catalepsy, 1282
Cataract, 902. 923
Catheterization, of bladder, 362, 1219
ureteral, 340, 1010, 1219
Causalgia. 1115
Cavernous breathing, 166
Cavities in lung, 1339
Cell counts, blood, 305
Cells in exudates, 320
Cellulitis, diffuse, of the neck, 1184
suprahyoid, 1183
Cephalalgia, 976
Cerebellar tumor, vertigo of, 1326
Cerebral abscess, headache of, 983
arteritis, 484
embolism, 1014-1026
Digitized by
Google
INDEX TO VOLUMES I AND II.
1359
Cerebral hemorrhage, see Hemi-
plegia,
eye disturbances of, 921
peduncle, disease of, 1344
tremor in tumor of, 1310
softening, 1014
tumor, Babinski sign in, 475
vertigo of, 1325
Cerebrocardiac neuropathy, 983
Cerebrospinal fluid, 324, 492
bacteriologic and biologic examina-
tion, 330
chemical examination, 327
cytologic examination, 329
in lethargic encephalitis, 1279
physical features, 324
Cerumen, impacted, tinnitus' due to,
1296
vertigo due to, 1327
Cervical glands, enlarged, 960
rib. 1321
tabes, 1318
Chancre, 885, 952, 953, 960
of tongue, 1302
Chancroid, 952, 953
bacillus of, 534, 952
Charcot joint, 1156, 1315
Charcot's disease, 1345
Charcot-Marie*s sign in exophthalmic
goiter, 1345
Chauflfard's congenital icterus, 1123
Chest circumference, 191
constriction, 1267
expansion, 192
Cheyne-Stokes breathing, 167, 714,
813, 1346
Chicken-pox, 861, 916
Chills, 757
Chloral hydrate, hypnotic use of, 1103
Chloride balance, 441
retention, 440
Chlorides in blood, determination of,
298
in urine, 406, 439
Chloroform syncope, 927
Chloroma, 1343
Chlorosis, 679
Cholelithiasis, 1069, 1082 (see also
Gall-stones).
Cholelithiasis, epigastric pain of, 799,
835,838
gaseous distention of, 1059
jaundice of, 1120
lumbar pain of, 1180
Cholemia, familial, 1123
Cholera, bacillus of, 540
diarrhea of, 790, 794
oliguria of, 1219
Choleroid state, 791
Choluria, 419
Chvostek, Jr.'s, sign in tetany, 1346
Chylous ascites, 746
Circulatory system, 199
functional tests, 270, 1262
relationship to nervous system,
1258
Cirrhosis of liver; see Liver, cir-
rhosis of.
Clapton's sign in copper poisoning,
1346
Claude Bernard-Homer syndrome,
918, 919, 1346
Clinical examination, guiding prin-
ciples of, 609
signs, index of, 1343
Coagulability of blood, 288
Coenurosis, 507
Coffee intoxication, 950, 1102, 1107
tremor of, 1309
Cogwheel breathing, 167
Coin test, 167
Cold abscess, 959
Colitis, mucous, 1086
Colon bacilluria, 1224
bacillus diarrhea, 790
gaseous distention of, 1269
tumors of, 1063, 1087, 1271
Color vision, disturbances of, 906
Colrat's test, 1346
Coma, 759
Tabular Synopsis, 762-763
Comma bacillus, 540
Complement deviation, 565
in hydatid disease, 511
fixation test, 551
Congenital alopecia, 661
heart defects, 1346
syphilis, 856
Digitized by
Google
1360
INDEX TO VOLUMES I AND II.
Conjunctiva, diseases of, 896
Conjunctival tuberculin test, 557
Conjunctivopalpebral reflex, 476
Constipation, 766, 804
headache of, 980
itching of, 1106
right iliac pain of, 1100
Contusions, neuritis due to, 1317
Convalescence, narcolepsy of, 1272
Convulsions, 770
acute, 771
chronic, 774
simulated, 770
Copaiba in urine, 427
Copper poisoning, 1346
Cornea, 886, 898, 920
Corneal reflex, 476
Corrigan pulse, 1346
Corrigan's disease, 1346
Cosmic influences, 1317
Cough, 777
clinical features, 778
mode of production, 779
therapeutic indications, 780
varieties, 782
Courvoisier's law, 1080, 1346
Cowper's glands, 381
Coxalgia, 1156
Cracked pot sound, 167
Crackling sounds, 167
Cremasteric reflex. 475
Croup, see Diphtheria.
false, 783
Cruveilhier's disease, 1346
Culs-de-sac, pelvic, 388
Culture media, 541
inoculation, 543
preparation, 542
Cultures, 544
blood, 318, 543, 552
Cupping, wet, 302
Cutaneomuscular reflexes, 474
symptomatic significance, 475
Cutaneovasomotor reflexes, 476
Cuti-reaction, 556
Cyclic albuminuria, 658, 1350
vomiting in children, 1334
Cylindroids, 433
Cvrtometric mensuration, 192
Cyst, cervical, 1190
hydatid, 508, 1071, 1079, 1107
ovarian, 740, 832, 1088, 1098
sebaceous, 956, 1190
Cysticercosis, 506
Cystitis, 1007, 1012
polyuria of, 1223, 1243
Cystocele, 385
Cystoscopy, 340, 355
Cytologic examination of blood, 301
of cerebrospinal fluid, 329
of exudates, 320
of gastric fluids, 64
Damoiseau's curve in pleural effu-
sion, 1346
Dandruff, 504
Dark-ground illumination, 513
Dead finger sign, 1318, 1350
Death, signs of, 923, 1276
apparent, 1277
Dehio's test in bradycardia, 1346
Dejerine-Klumpke, syndrome of, 1346
Delirium, 785
autotoxic, 789
cordis, 728
dream-like, 785
infectious, 786, 789
of interpretation, 788
oniric, 785
systematized, 786
toxic, 786, 789
tremens, 1280
Delusional interpretations, 788
Delusions, 785
Deltoid rheumatism, 1317
Dementia, 787
Deplasmatized red cell method, 292
Depressive psychoneuroses. 752
Dercum's disease, 1207, 1208
Dermatitis herpetiformis, 1110
multiformis, 1110
Dermographism, 478, 1197, 1256
D'Espine*s sign of tracheobronchial
adenopathy, 1346
Diabetes insipidus, 1243
mellitus, 969, 1191
acetonemia of, 823
albuminuria of, 655
Digitized by
Google
INDEX TO VOLUMES I AND II.
1361
Diabetes mellitus, asthenia of, 754
coma of, 764
convulsions of, 773, 775
diarrhea of, 791
dyspnea of, 823
eye disorders of, 915
high blood-pressure of, 1045
itching of, 1106, 1116, 1117
loss of weight of, 1143
obesity with, 1214
polyuria of, 1242
specific gravity of urine in, 395
tinnitus of, 1296
vomiting of, 1342
Diabetides, 955
Diacetic acid in urine, 426
Diagnosis, causal, 4
clinical, 4
errors of judgment in, 25
functional, 4
lesional, 4
Diagnostic science, evolution of, 1
Diaphanoscopy, 889
Diaphragmatic pleurisy, hiccough of,
1040
pain of, 1225
Diarrhea, 790
circulatory. 792, 1258
digestive, 793
emotional, 792
infectious, 790
nervous, 791
toxic, 791
vasomotor, 791
Diastolic blood-pressure, 1043
low, 1146
murmurs, 202, 204, 206, 207
Diathetic disorders, tinnitus in, 1296
Differential leucocyte count, 312, 963
pressure, 1043, 1146
Digestive albuminuria, 658
activity in stomach, 67
residues, 57
tract, 41
Digitalis, bradycardia due to, 1287
Dionin test of death, 924, 1276
Diphtheria, 1293
bacillus, 535, 545
bacteriologic procedures, 545
Diphtheria, cough of, 783
eye disturbances of, 916
Diplopia, 906
in encephalitis, 1278
Disseminated sclerosis, 472, 475, 484
eye disturbances of, 922
polyuria of, 1243
tremor of, 1308
vertigo of, 1326
Dissociation, auriculoventricular, see
Heart-block.
thermo-analgesic, 458
Distention of colon, gaseous, 1269
Diuresis, induced, 434, 1240
Dizziness, see Vertigo.
Double vision, 906
Dream states, 1281, 1282
Drug intoxications, discolored tongue
of, 1297
dyspepsia of, 798
edema of, 831
eruptions of, 848, 849
eye disturbances of, 922
hematuria of, 1011
insomnia of, 1102
itching of, 1107
nervousness of, 1193
oliguria of, 1223
sleep due to, 1272
tinnitus of. 1296
tremor of, 1309
vertigo of, 1329, 1330
Dry blood smear, 311
Dubini's chorea, 1346
Duchenne's disease, 1346
Ducrey, bacillus of, 534, 952
Ductless glands, eye disturbances in
disorders of, 919
Duguet's sign in typhoid fever, 1346
Duodenal kink, 1073
ulcer, 75, 77, 82, 105, 998
fluoroscopy in, 77, 82
jaundice of, 1120
right hypochondriac pain of,
1070, 1083
topographic diagnosis in, 105
Duodenum, 75
Duroziez's disease, 1346
80
Digitized by
Google
1362
INDEX TO VOLUMES I AND II.
Durozicz's signs in typhoid fever
and aortic regurgitation,
1346
Dwarfs. 604, 606
Dyschromia, 850
Dysentery, ameba of, 106, 541
bacillus of, 541
diarrhea of, 790
oliguria of, 1219
Dysesthesia, 457
Dysidrosis, 1108
Dysmenorrhea, 1088
Dyspepsia, 796, 837
atonic, constipation of, 768
coated tongue of, 1298
cough of, 778
neurotic, dyspnea of, 1250
precordial pain of, 1269
vomiting of. 1334, 1340
Dysphagia, 1292
Dyspnea, 809
cardiac, 817
decubital, 817, 1252
dyscrasic, 822
emotional, 1251
neurotic, 810, 824
of respiratory origin. 815
on exertion, 811, 1250, 1253, 1267
paroxysmal, 1268
p09t-prandial, 1250
toxic, 810 .
Ear, external, foreign body in, 1296
internal, 493
hemorrhage into, 1327
tinnitus in disorders of, 1296
middle, tinnitus in disorders of,
1296
Echinococcosis, 507, 508
Eclampsia, infantile, 771
puerperal, 773
Ectropion, 895
Eczema, 830, 848, 1109
marginatum, 504
seborrheicum, 504
Edema, 825
angioneurotic, 831
cardiac, 827
dyscrasic, 828
Edema, dystrophic, 829
hemic, 828
hepatic, 829
in nephritis, 651
nervous, 829
of abdominal wall, 739
of face, 830, 1321
of lids, 830
of lower extremities, 831
of upper extremities, 831
paroxysmal, 1350
preascitic, 829
renal, 651, 827
Effort cough, 783
Egg albumin in urine, 412
Egophony, 167
Einhorn's bead method, 131
Electrocardiography, 264, 721, 729
Electrodiagnosis, 460
Embolism, 998, 1014
pulmonary, 190
Emotional angiospasm, 1268
chill, 758
Emotive constitution, 1198
Emphysema, pulmonary, 188, 189,
1151
dyspnea of, 811, 812, 1250
pseudolipoma of, 1189
Empyema, 181, 182
pain of, 1225
Encephalitis, lethargic. 328, 921, 1278
Endocarditis, 236, 934, 943, 1025.
1040. 1250, 1253
pain of, 1265
Endocrine glands in diabetes, 971
Endostethoscopy, 43
Enophthalmus, 896, 918
Enteritis, 793
Enterocolitis, infectious. 790
mucomembranous, 1086
toxic, 791
Enteroptosis, constipation of, 767,
804
Enuresis, 775
Eosin, 517
Eosinophilia, 506, 509
Epidermal scales, 500
Epidermophyton, 504
Epididymis, 382
Digitized by
Google
INDEX TO VOLUMES 1 AMD 11.
1363
Epidural treatment, Sicard's method
of, 1351
Epigastric pain, 833
Tabular Synopsis. 840-841
reflex, 475
Epilepsy, 773, 775, 926
biting of tongue in, 1306
eye disturbances of, 921
narcolepsy of, 1273
polyuria of, 1241
somnambulism of, 1281
vertigo of, 1330
Epistaxis, 843, 1029, 1055
Tabular Synopsis, 846
Epithelioma of tongue, 1304
Equilibration, disturbances of, 1323
Erb*s signs in tetany and tabes, 1346
Eruptions, skin, 847
Erysipelas, 849, 863
edema of, 830
eye disturbances of, 917
insomnia of, 1103
of the newborn, 863
of throat, 1292
Erythema multiforme in eyeball, 919
Erythematous eruptions, 849
throat, 1292
Erythrasma, 503, 504
Erythrocyte count, 308
Erythrocytes in urine, 433
Erythrodermias, 849
Esbach's albuminometer, 412
Esophagoscopy, 46
contraindications, 50
Esophagus, 41
anatomical considerations, 41
auscultation of, 42
bleeding from, 994, 999
cancer of, 685
disorders of, 999
diverticulum of, 46
examination of, with sounds, 43
fluoroscopy of, 43
palpation of, 42
stenosis of, 42
stricture of, 46
varicose vessels of. 999
Ether pearl method, 67
Ethylmorphine hydrochloride test of
death, 1276
Eustachian tube, tinnitus^ in obstruc-
tion of, 1296
Examination, medical, guiding prin-
ciples in, 609
Exanthemata, 847
Tabular Synopses, 848-850, 855-
863
Exhaustion, 751
Exophthalmic goiter, see Goiter, ex-
ophthalmic.
Exophthalmus, 896, 918, 920
Expectoration, 865
of pus, 1339
Tabular Synopses, 868-869, 872-
873
Expression sound in esophagus, 42
Extra-uterine pregnancy, 1088, 1099
Exudate, pharyngeal, 544, 1290
pleural, 182
Exudates, cells in, 320
differentiation of, by Rivalta's test,
331
Eyeball, compression of (oculocar-
diac reflex), 213
prominence of, 896, 918, 920, 1321
retraction of, 896
Eyelids, discoloration of, 1348
disorders of, 895
eversion of, 883
Eyes, disorders of, 894
headache in, 984
in general disease^, 913
examination and symptomatology,
876, 893
pain in, 903
Facial neuralgia, 982
paralysis, 1025
in encephalitis, 1278
peripheral, Straus's sign of, 1351
Fainting, 925
Fallot's disease, 1346
Fats in stools, 99, 130, 794
intolerance of, 793
normal assimilation of, 100
Fatigue, 751
humoral, 754
Digitized by
Google
1364
INDEX TO VOLUMES I AND II.
Fatigue, infectious, 754
nervous, 752
Favus, 5()4, 666
Febricula, 936
Fecal obstruction, 802
Fecaloid vomiting, 1333
Feces, examination of, 91 ; see also
Stools.
Fehling's solution, 415
Female reproductive organs, 384
Fever, 929, 948
Tabular Synopsis, 938-939
Fibrillation, auricular, 728
Fibrous glossitis, 1303
Field of vision, 891, 910
Filaria, 320
Filiform bougies, 365
Finsen's method, 1347
Fissural points in interlobar pleurisy,
1228
Fixation abscess, 1347
methods of, 522
Flask bacillus, 503, 504
Flat foot, 1153, 1154
Flatulence, 1058, 1065, 1066, 1233
Flatulent dyspepsia, 804
Flexor reflex of forearm, 469
Flint murmur, 201
Fluorescin death test, 923, 1276
Fochier's method, 1347
Folliculitis decalvans, Brocq's, 673
Food intoxication, 793, 848
residue in stomach, 59
Forcipressure test of death, 1276
Fosse method of urea determination,
296
Fracture of skull, hemiplegia of,
1027
Frequent pulse, 942
Tabular Synopsis, 950
Fresh blood preparation, 304
Friction, pericardial, 212
pleural, 168
Friedreich's ataxia, 1347
eye disturbances of, 922
Frohlich's syndrome, 1347
Frontal tumor, vertigo of, 1325
Functional capacity of kidneys. 346
tests of circulation, 270, 1262
Funiculitis, vertebral, 1167, 1168
Mirbringer's sign, 1347
Fusiform bacillus, 538, 1351
Future of medicine, 640
Gall-bladder, cancer of. 1080
perforation of, 1075
point, 117
Gall-stones, 1068, 1080, 1082 (see also
Cholelithiasis),
dyspepsia of, 799
epigastric pain of, 835
hypochondriac pain of, 1068, 1082
jaundice of, 1120
Gallop rhythm, 201
Gaseous distention of colon, 1269
Gastralgic crises of tabes, 801, 842
Gastric analyses, 61
atony, 55
cancer (see Cancer of stomach),
contents, examination of, 58
acid, 62
bile, 64
blood, 64
cells, 64
fatty acids, 64
free HCl, 63
lactic acid, 64
protein substances, 64
removal of, 55
cough, 778
distention, precordial pain of, 1269
esthesiometer, 54
neuroses, 836, 837, 1340
points of tenderness, 54
residues, 57
secretion, study of, without stom-
ach tube, 65
ulcer, 6, 104, 837
differentiation from cancer, 106,
807, 808, 837
from duodenal ulcer, 105
hematemesis of, 997, 1000
right hypochondriac pain of, 1083
topographic diagnosis, 104
vomiting of, 1341
Gastritis, alcoholic, 803
vomiting of, 1334. 1340
medicamentosa. 798
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Google
INDEX TO VOLUMES I AND II.
1365
Gastrointestinal disorders, loss of
weight in, 1142
Gaucher's disease, 1347
Gel reaction in syphilis, 579
General considerations, 1
paralysis, see Paralysis, progres-
sive general.
Genital ulcerations, 951
Tabular Synopses, 953, 955
Genitourinary tract, 332
Geographic tongue. 1300
Gerhardt's test, 426, 1347
German measles, 860
Giddiness, see Vertigo.
Giemsa stain, 518
Gigantism, 605, 606
Gilbert's familial cholemia, 1123
Gilbert and Herscher method for
urobilin in blood, 301
Glandular enlargements, 956
chancroidal, 953
in the neck, 960, 1184
neoplastic, 961
syphilitic, 855, 953. 958. 960
Glaucoma, 899, 900, 908, 910, 983
Glenard's procedure in kidney palpa-
tion, 338
test, 52
Glossitis, 1299
cancerosyphilitic, 1204
fibrous. 1303
marginal exfoliative, 13(X), 1301
syphilitic, 1301, 1303
Glucose solution, polyuria following
administration of, 1241
Glycosuria, 969, 1191
alimentary, 125, 970, 1346
and loss of weight, 1143
traumatic, 974
Gmelin's test, 300, 417, 1347
Godelier's law in tuberculous peri-
tonitis, 1347
Goetsch's test, 1192
Goiter, exophthalmic, 5, 896, 1191,
1197, 1344
chief clinical signs of, 1192
diarrhea of, 792
eye disturbances of, 919
fever of, 936
Goiter, exophthalmic, itching of,
1115
loss of weight of, 1142
polyuria of, 1241
tachycardia of, 944
tremor of, 1310
simple, 1191
cough of, 783
dyspnea of, 810
Gonococcus, 527
Gonorrhea, 375, 939
urethrovaginal, 384
Gonorrheal arthritis, 1156
urethritis, 378
Goose flesh, 1258
Gordon's sign in pyramidal disease,
1347
Gout, albuminuria of. 655
angina pectoris of, 1254
arthritis of, 1130, 1156
diarrhea of, 791
edema of, 831, 832
extra-systoles of, 1253
eye disorders of, 915
grinding of teeth in, 1347
hemoptysis of, 1035
high blood-pressure of, 1045
intercostal neuralgia of, 1270
itching of, 1106
obesity in, 1214
tinnitus of, 1296
Gradenigo's syndrome, 1347
Graefe's sign, 919, 1347
Gram's method, 523
solution, 518
Gram-negative germs, 524
-positive germs, 524
Grancher's disease, 1347
Graphic methods, 249
Grave icterus, 1121
Graves's disease, see Goiter, ex-
ophthalmic,
sign in gout, 1347
Grimbert method for albumin in
urine, 411
test for bile in urine. 418
Grocco's triangle of dulness, 1347
Guaiac test for blood in urine, 424
Gueneau de Mussy's points, 1266
Digitized by
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1366
INDEX TO VOLUMES I AND II,
Guerin's law in rickets, 1347
Gumma, 852, 856, 953
of bone, 1154, 1315
of bundle of His, 1287, 1289
of tongue, 1301, 1303
Gums, bleeding from, 1030
Guyon's procedure of kidney palpa-
tion, 336
reno-renal reflex pain, 1179
Habit cough, 783
Hair, diseases of, 499
Hallucinations, 786
Hanot's disease, 1347
Harley's disease, 1347*
Harrison's groove, 1347
Hay fever, 1197
Hay's test, 420
Hayem's hematinieter, 306
hemochromometer, 310
solution, 306
Head's cranial zones, 977, 978, 986,
1347
zones of cutaneous hyperesthesia,
1234
Headache, 976, 989
alcohol, 981
bilious, 980
muscular, 987
nasal, 986
nervous, 981, 1256 •
ocular, 984
of constipation, 980
pressure, 983
prodromal, 979
syphilitic, 984
tobacco, 981
toxic, 979
uremic, 980
utero-ovarian, 987
winter, 981
Tabular Synopsis, 990-991
Heart action, weak, 274, 278
arhythmia, 693
block, 714, 1286
cough, 783
defects, congenital, 1346
disorders, anginose syndrome of,
1250
Heart disorders, blood-pressure in,
1046, 1047
dyspnea of, 812, 1250
edema of, 826, 827
epigastric pain of, 836
etiologic diagnosis, 236
eye disorders of, 915
frequent pulse of, 942
hemoptysis of, 1031
oliguria of. 1220
vertigo of. 1326
vomiting of, 1334, 1341
distention, 1266
failure, ascites of, 745
bradycardia of, 1287
hematemesis of, 1001
hypochondriac pain of, 1069
insomnia of, 1103
low pulse pressure of, 1146
irregularities, 693
landmarks on chest wall, 211
murmurs, 201-207, 209
pains in region of, 1245
percussion, 215
. relations to body morphology, 600
sounds, 200, 208
underdeveloped, 1150
weakness, 187, 274, 812, 817, 827,
1220
x-ray examination of, 219
fluoroscopy, 220
orthodiagraphy, 222
orthofluoroscopy, 225
teleradiography. 230
Heberden's nodes, 1348
Height, 596
Heinc-Kreysig's sign in pericardial
adhesion, 1348
Heine-Medin's disease, 1348
Heine-Sanders's sign in pericardial
adhesion, 1348
Helminthiasis, 506, 1039
vertigo of, 1324
Hematemesis, 993, 1030, 1055
Tabular Synopsis, 1000-1001
Hematin, 588
Hematology, 282
Hematoxylin, 518, 519
Hematuria, 1003
Digitized by
Google
INDEX TO VOLUMES I AND II.
1367
Hematuria, cryptogenic, 1010, 1013
false (drugs). 1011
hemic. 1009
parasitic, 1010
prostatic, 1005
renal, 1007
toxic, 1010
ureteral, 1007
urethral, 1005
vesical, 1006
Tabular Synopsis, 1012-1013
Hemeralopia, 905
Hemianopsia, 911
Wernicke's sign in, 1352
Hemiplegia, 761, 1014, 1343
organic, Revilliod s phenomenon in,
1350
Souques's sign of, 1351
Vulpian's law in, 1351
Tabular Synopsis, 1026-1027
Hemoconia, 125
Hemoglobin estimation, 310
spectroscopic determination, 594
examination, 588
Hemoglobinuria, paroxysmal, 1347
Hemolysis, 290
Hemolytic jaundice, 1123, 1126
reaction, 565
Hemophilia, cpistaxis of, 845
hematuria of, 1009
hemoptysis of, 1035
Hemoptysis, 994, 1029, 1055
Hemorrhage, anemia due to, 676
cerebral, 765, 1015.
eye disorders in, 915
hematemesis. 993
hematuria. 1003
hemoptysis, 1029
syncope in, 928
vertigo of. 1326
Hemorrhagic bronchospirochetosis.
866
Hemorrhoids, blood from, 105
lumbago in, 1176
pelvic pain in, 1163
Hepatic colic, see Cholelithiasis,
oliguria of, 1219
vomiting of, 1334, 1340
diabetes, 970
Hepatic obstruction, oliguria of, 1222
Hepatitis, 742
Hepatization, gray, pulmonary vom-
ica in, 1339
Hepatoptosis, 1071
Hereditary tremor, 1309
Hernia, inguinal, left iliac pain in,
1088
right iliac pain in, 1089, 1099
scrotal, 382
strangulated, hematemesis of, 997
vomiting of, 1333, 1341
Herpes, genital, 954, 955
zoster, 1078, 1172, 1233, 1313
of pharynx, 1292
Herpetic angina, 1292
Herxheimer's reaction, 1348
Hesperanopia. 905, 919
Hiccough, 1039
High blood-pressure, 1043
diseases attended with, 844
epistaxis of, 844
vertigo of, 1330
Tabular Synopsis, 1056-1057
portal pressure, 436. 742, 1000, 1046
Hip disease, 1156
Hippocratic succussion sound, 167
Hirschsprung's disease, 1348
Hoarseness, ^80
Hodgkin's disease, 961, 962
edema of, 830
Hodgson's disease, 1348
Hookworm (ankylostoma), 112, 113
Hot flushes, 1258
Hourglass stomach, 801
Hunger pain, 76
Hutchinson teeth, 1348
Hydatid disease, 508. 1107
of liver, 1071, 1079
pulmonary vomica, 1339
Hydremia, 653
Hydrocele, 324. 326, 73H
Hydrocephalus, eye disturbances of,
921
Hydronephrosis, 1060. 1066
Hydruria, 436
Hydrurimetric coefficient, 439
Hydrurimetry, 390, 434
Digitized by
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1368
INDEX TO VOLUMES I AND II.
Hyperchlorhydria, epigastric pain of.
836
Hyperesthesia, 1194
lumbar, 1178
Hyperidrosis, 1177
Hyperopia, 904, 985
Hypersomnia, 1271
Hypertension, 1043
intraocular, 899
portal, 436, 742. 1000, 1046
Hypertensive diseases, 844
Hyperthermia, 929
Hyperthyroidia, 1193, 1310; see also
Goiter, exophthalmic.
Hypertrophy of heart, pain of, 1270
of prostate, 380, 1223, 1243
Hyphema, 898
Hypnophobia, 1282
Hypnosis, 1282
somnambulism during, 1281
Hypnotics, sleep due to, 1274
Hypoadrenia, 1147
Hypochondria, dyspepsia in, 806
Hjrpochondrium, left, pain in, 1058
Tabular Synopsis, 1066-1067
right, pain in, 1068
points of tenderness in, 1076
Tabular Synopsio, 1082-1084
Hypopyon, 898
Hyposphyxia, 227, 1140, 1148
asthenia of, 754
dyspnea of, 823
headache of, 981
low systolic pressure of, 1145
obesity and, 1215
sleep of, 1272
Hypotension, see Low blood-pres-
sure.
Hypothyroidia, chief clinical signs of,
1192, 1207
Hysteria, 1198
differentiation of, from epilepsy,
475
Hysterical aphonia, 692
coma, 928
convulsions, 774. 775
cough, 780
headache, 982
hematemesis, 996
Hysterical hemiplegia, 1023, 1026
Rosenbach's sign of, 1351
hiccough, 1040
pain, 1091
polypnea, 824
polyuria, 1241
sleep. 759, 1273
somnambulism, 1281
tremor, 1310
Hysterometry, 389
Hysteropithiatism, eye disturbances
of, 920
Icard*s fluorescein formula, 1276
Icterohemorrhagic spirochetosis, 1121,
1157
Icterus, 998, 1119
grave, 1121, 1126
hematic, 1122
hepatic, 1119
infectious, 1121, 1126
picric, 1123
Idiocy, eye disturbances of, 921
Iliac fossa, left, pain in, 1085
Tabular Synopsis, 1088
Iliac fossa, right, pain in, 1089
Tabular Synopsis, 1098-1099
Illuminating gas, glycosuria due to,
971
Impetigo, Bockhart's, 1344
bullosa, 504
Inanition, dyspepsia due to, 798
Incubators, 543
India-ink method; 519
Indican in urine, 421
Indigestion, 796 (see also Dyspepsia).
coated tongue in, 1298
diarrhea in, 795
vomiting in, 1332, 1340
Indurative muscular headache, 988,
991
Inequality of pulse in aortic aneu-
rysm, 1321
of pupils, 915, 1278
Infantile eclampsia, convulsions of,
771
giants, 606
Infarction of lung, 190
Digitized by
Google
INDEX TO i OLUMES I AND 11.
1369
Infectious diseases, see articles on
Asthenia, Delirium, Fever,
Frequent pulse, Headache,
Lumbar pain, and Oliguria,
jaundice, 1120, 1126
Influenza, 935, 938
bacillus, 526
headache of, 979
loss of weight in, 1142
tongue of, 1299
Inoculation test for tubercle infec-
tion, 558, 561
Insanity, see Delirium, 785
eye disturbances of, 921
Insomnia, 1101, 1258
due to circulatory disturbances,
1103
due to nervous overexcitability,
1102
due to pain, 1101
due to respiratory disturbances,
1103
Intercostal neuralgia, 1270
Intermittent albuminuria, 1197
claudication, 1160
fevers, 940
hepatic fever, 937, 940
pulse, see Premature beats and
Sinus arhythmia.
Internal ear, 493
hemorrhage into, 1327
Intestinal fermentations, sleep due
to, 1272
obstruction, vomiting of, 1333, 1341
parasites, 111-117
Intestine, 80, 105
cancer of, 791, 793, 802
x-ray examination of, 82
Intoxication (see also Drug intox-
ications), delirium of, 789
Intraocular tension, 887, 899
Iodides in urine, 428
Iridonesis, 901
Iris, diseases of, 899
examination of, 886
Irregularities of heart action, 693
Israel's procedure of kidney palpa-
tion, 337
Isuria, 434
Itch, 1112
Itching, 1106
dermatosic, 1107
neurotic, 1115
parasitic, 1112
toxic, 1106
Tabular Synopsis, 1106
Jaccoud's sign in pericardial ad-
hesion, 1348
Jaundice, 1119
bradycardia of, 1287
catarrhal, 1120
due to arsphenamin, 1124
hematic, 1122
hemolytic, 1123, 1126
hepatic, 1119
infectious, 1120, 1126, 1157
hemoptysis of, 1034
itching of, lll6
picric, 1123
relapsing, temperature curve in,
937
syphilitic, 1124
Tabular Synopsis, 1126-1127
Jejunum, 75
Jellineck's sign, 1348
Joint pains, 1128
in lower extremities, 1155
in upper extremities, 1313
KarelFs treatment, 1348
Keratitis, 898
Kerion of Celsus, 667, 668
Kemig's sign, 485, 1279, 1348
Kidney, amyloid degeneration, poly-
uria of, 1243
anatomic relations of, 1073
eye involvement in disorders of,
914
functional tests of, 434, 452
inspection of, 334
pain, 1172, 1178
painful enlargements of, 1179
palpation of, 336
percussion of, 339
permeability of, 448, 651
physiologic laws relating to, 446
points of tenderness, 335
Digitized by
Google
1370
INDEX TO VOLUMES I AND II.
Kidney stone, 350, 1008, 1060, 1066;
see also Nephrolithiasis,
tuberculosis of, see Tuberculosis,
renal,
tumor of, 1012 -
x-ray examination of, 344, 349
Kienbock's sign in hydropneumo-
thorax, 1348
Killian's tracheoscope, 47
Kink, 767
Kiva method for urobilin in blood,
300
Klebs-Loffler bacillus, 545
Klippel's disease, 1348
Knee-jerk. 467 .
Koplik's spots, 859
Kraurosis vulvae, 385
Kussmaul breathing, 1348
Kyphosis, hyposphyxia in, 1151
Labioglossolaryngeal paralysis, 10^2
Labyrinth. 493
Labyrinthine angiospasm, 1331
vertigo, 493, 1326
Lacrymal duct, 885
Lacrymation, 894
Laennec's cirrhosis, 1348
Lamblia intestinalis, 111
Landouzy-Dejerine type of muscular
atrophy, 1348
Landry's disease, 1348
Lanz's point, 1097
Larval worms, parasitic, 506
Laryngismus stridulus, 783
Laryngitis, acute, 680, 686
chronic, 680, 686
Laryngoscopic picture. 160
Larynx, cancer of, 681, 689, 1190
diseases of, 680
examination of, 155
hemorrhage into, 1030
paralyses of, 6^2, 689
syphilis of, 681, 688
tuberculosis of, 681, 687
tumors of, 680, 688
Lasegue's sign in sciatica, 1162, 1177,
1348
Lead acetate as test of death, 1276
anemia, 678
Lead colic, 1096
constipation, 766
convulsions, 773
dyspepsia, 801
eye disturbances, 923
gastralgia. 801
hemiplegia, 1027
intercostal neuralgia, 1270
nervousness, 1193
neuritis, 1318
right iliac pain, 1096
tremor* 1309
Left ventricle, acute insufficiency of,
1267
Leg, see Lower extremities.
Lematte*s test of renal activity, 452
Lens, crystalline, 888
Leprosy, anesthetic, 1318
eye disturbances of, 917
nervous, 1318
Lethargic encephalitis, 328, 1278
states, 1273
Lethargus, 1283
Lethargy, 1283
Leucocyte count, 310
differential, 312
Leucocytes in urine, 434
Leucoma, 898
Leucopenia, 676
Leukemia, 939, 964
epistaxis of, 845
hematuria of, 1009
Leukoplakia buccalis, 1300
epitheliomatous degeneration of,
.1301
Lcyden-Mobius type of muscular
atrophy, 1348
Lichen planus, buccal, 1301
Lichenification, 1108
Lids, edema of, 830, 831
Lieben's test, 425
Lingual syphilides, 1302
Lipemia, alimentary, 125
Lipodystrophy, progressive, 1144
Lipoma, 956. 1189, 1190
Litten's sign in pulmonary tuber-
culosis, 1348
Little's disease, 1348
eye disturbances of, 922
Digitized by
Google
INDEX TO VOLUMES I AND II,
1371
Liver, 117, 742, 1068
abscess of, 1069, 1082, 1120. 1127
cancer of, 1069, 1083, 1120, 1127
cirrhosis of, atrophic, 742, 1071,
1127, 1150, 1348
edema of, 829
epistaxis of, 846
hematemesis of, 998
tympanites of, 792
hypertrophic, 1071
disorders, epistaxis in, 845
eye disturbances in, 919
fluoroscopy of, 124
hydatid disease of, 1079
inspection of, 117
outline of, 117
overactivity of, 793*
palpation of, 120
ChaufFard's procedure, 120
Gilbert's procedure, 121
Glenard's thumb procedure, 121
Mathieu's procedure, 121
two-thumb procedure, 122
passive congestion, pain of, 835,
1068, 1082
percussion of, 118
suprahepatic ballottement, 119
transthoracic hydatid fremitus,
119
wave, 119
points of tenderness, 124
radiography of, 124
syphilis of, 1069, 1083, 1127
Locomotor ataxia, see Tabes dor-
salis.
Loss of weight, 1137
Lovers, radial paralysis of, 1318
Low blood-pressure, 1145
headache of, 981
in adrenal insufficiency, 1147
in hyposphyxia, 1148
in tuberculosis, 1147
Tabular Synorsis, 1152
Lower extremities, pain in, 1153
Ludwig's angina, 1349
dyspnea of, 810
edema of, 830
Lumbago, 1168, 1172, 1176, 1180
Lumbar pain, 1170
Lumbar plexus, 1165
puncture, 487
Lumbarthritis, 1175
Lung, abscess of, 184, 1033
pulmonary vomica in, 1339
congestion of, 1352
massive, 1347
pain in the side in, 1231
passive, 187
emphysema of, 188
fibrosis, dyspnea of, 812, 818
gangrene of, 184, 1034
hydatid cysts of, 184
infarction, hemoptysis of, 1031
inflammation, pain of, 1229
syphilis of, 1034
tuberculosis of, see Tuberculosis,
pulmonary.
tumors of, 184, 1034
Lymphadenitis, 956
cervical, 960, 1184
tuberculous, 959, 1185
Lymphadenoma, 1186
Lymphangitis, 1321
edema of, 826
Lymphatic temperament, 967
Lymphosarcoma, 967, 1188
MacDonagh reaction in syphilis, 579
Macroglossia, 1305
Macular eruptions, 849
Madelung's disease, 1349
Malaria, eye disturbances of, 917
headache of, 979
hemoptysis of, 1034
temperature curve in, 935
tremor of, 1309
Malarial parasite, 319
Malum coxae senilis, 1156
Marey's law, 1349
Marie's disease, 1349
Martinet's laws, 1349
syndrome, 1349
Masseter reflex, 472
Mastodynia, 1270
Maurel's reagent for egg albumin in
urine, 413
McBurney's point, 1094, 1097
Measles, 858
Digitized by
Google
1372
INDEX TO VOLUMES I AND II,
Measles, epistaxis of, 846
eye disturbances of, 916
German, 860
sore throat of, 1292
Median nerve, sensory disturbances
in injuries of, 1317
Mediastinal tumors, arm pain of,
1318, 1321
bradycardia of, 1287
cough of, 783
edema of, 830
intercostal pain of, 1270
Medical organization, 640
Megacolon, congenital, 1348
Melancholic stupor, 1275
Menetrier's syndrome, 1349
Meniere's disease, 1326
syndrome, 1328, 1349
vertigo, 1326
Meningeal hemorrhage, hemiplegia
of, 1027
hyperemia, 486
states, 328
cell findings in, 329
convulsions of, 771
eye disturbances of, 921
headache of, 983, 991
hiccough of, 1040
hypersomnia of, 1277, 1279
insomnia of, 1102
tache cerebrale of, 478
vomiting of, 1332, 1342
Meningitic line, 478
Meningitis, cerebrospinal, 4, 528, 939,
948, 1176
Brudzinski's signs of, 1345
Parrot's sign of, 1350
tuberculous, 326, 1027. 1279
Meningococcus, 528
Meningomyelitis, acute, 1176
girdle pains of, 1233
Menopause, vasomotor disturbances
of, 1197
vertigo of, 1326
Menstruation, vicarious, 844, 1036
Mensuration, 597
of chest, 191
Mercurial anemia, 678
diarrhea, 791
Mercurial stomatitis, 1299
tremor, 1309
Mercury ureometer, 294
Metabolic disturbances in exophthal-
mic goiter, 1191
Metallic tinkle, 167
Metatarsalgia. 1349
Meteorism, 739, 1058
Meteorologic hyperesthesia, 1194
Methemoglobin, 588
Methylene blue, 517. 523
test for renal permeability, 448
Meyer's test for blood in urine, 424
Microsporia, 502, 663
Microsporon Audouini, 504
furfur, 503, 504
minutissimum, 503, 504
Migraine, 981, 988
ophthalmic, 903
ophthalmoplegic, 909
vomiting of, 1342
Mikulicz's disease, 1349
Millard-Gubler syndrome, 909, 1017,
1019, 1349
Mistaken diagnoses, causes of, 15
Mitral insufficiency, 205, 207, 238
chronologic diagrams of, 205,
207
stenosis, 201, 206, 207, 238, 735,
1151
chronologic diagrams of, 206,
207
dyspnea of, 818
hemoptysis of, 1031
Mobius's disease, 1349
sign in exophthalmic goiter, 1349
Morbid sleep, 1271
Morphine and veronal intoxication.
1274
hypnotic use of, 1103
in urine, 428
intoxication, chronic, loss of weight
in, 1143
Morphologic indices, 599
Morris's point, 1097
Morton's disease, 1349
Morvan's disease, 1318, 1349
Motion, examination of, 458
Mountain sickness, vertigo of, 1331
Digitized by VjOOQIC
INDEX TO VOLUMES I AND II.
1373
Mouth breathers, coated tongue of,
1297
Mucous enteritis, 792
patches, 855, 1302
Mumps, eye disturbances of, 917
Murmurs, heart, 201-207, 209
features differentiating organic and
functional, 212
ocular compression in, 213
Murphy's method, 1349
Muscae volitantes, 905
Muscles of lower extremities, pain-
ful disturbances of, 1157
of upper extremities, painful dis-
turbances of, 1317
Muscular power, testing, 459
Musset's sign in aortic regurgita-
tion, 1349
Myalgia, 1157
pectoral, 1247
Mycoses, 584, 918
Mydriasis, 901, 918
Myelitis, 1024
eye disturbances in, 922
peri-ependymal, 1310
Myocardial asthenia, 281, 1250
Myocardialgia, 1247
Myocarditis. 274, 275, 942, 1040, 1266,
1287
Myopia, 904, 985
Myosis, 901, 918
Myositis, 1157, 1317
Myxedema, asthenia in, 754
Myxedematous dwarfs, 604, 606
Nanism, 606
Narcolepsy, 1272, 1279
idiopathic, 1273
Narcosis, 1283
Narcotin, 1283
Nasal cough, 778
fossae, 136
headache, 986
Nasopharynx, digital examination of,
149
Nausea in aural vertigo, 1328
Neck, swellings in the, 1182
acute, 1183
chronic, 1184
Neck, swellings in the, in aortic
aneurysm, 1321
Negri bodies, 1349
Negro's sign of peripheral facial
paralysis, 1349
Nephritis, anemia of, 678
ascites of, 746
edema of, 826, 827
epis taxis of, 844
eye disorders of, 914
hemiplegia of, 1024
high blood-pressure of, 1053,
1056
oliguria of, 1221, 1223
polyuria of, 1242
precordial pain of, 1268
tinnitus of, 1296
vertigo of, 1330
acute, 650
azotemic, 653
chloridemic, 653
chronic, 653
gouty, 1223
hematuric, 1008, 1012
hydremic, 653
hyperacute, 651
in obesity, 1215
interstitial, 439, 1045, 1242
Traube's law in, 1351
Nephrolithiasis, 350, 1008, 1060, 1070,
1083, 1238
oliguria of, 1219
polyuria of, 1243
x-ray examination in, 350
Nephroptosis, 1073
Nervous angiospastic cases, high
blood -pressure of, 1051
cough, 783
diabetes, 974
diarrhea, 792
disorders, dyspepsia of, 803
eye disturbances of, 920
edema, 829
erethism, 1053, 1056
fatigue, 752
headache, 981
insomnia, 1102
system, 457
Nenrousness, 1193
Digitized by
Google
1374
INDEX TO VOLUMES I ANITIL
Nervousness, motor, 1193
psychic, 1195
sensory, 1194
vasomotor, 1197
visceral, 1197
Neuralgia, 988, 1164, 1317
anterior crural, 1166
external cutaneous, 1166
facial, 982
in lower extremities, 1164, 1168
in upper extremities, 1317
intercostal, 1233, 1247, 127D
lumboabdominal, 1165
sciatic, 1168
Valleix's laws in, 1351
Neurasthenia, 755, 1344
constipation of, 769
eye disturbances of, 921
headache of, 982
low systolic pressure of, 1145
somnambulism of, 1281
vertigo of, 1330
Neuritis, 1317
lead, 1318
multiple, 458
pressure, 1318
Neuroarthritism, 1195
Neurodocitis, 1167
Neurosis, 1196
angina pectoris of, 1255
anxiety, 1200
cardiac, 279, 821, 944, 1198, 1255
gastric, 836, 837, 1340
intestinal, 791, 793
• tachycardic, 944, 950
vertigo of, 1330
Neurotic dyspnea, 810
itching, 1116. 1118
lumbago, 11?3
vomiting, 1340
Nicotinism, angina pectoris of, 1254
leukoplakia of, 1300
Night terrors, 775
Nitrogen retention, 442
Nose, 135
Nosebleed, 843
Nosology, 6
Nostrils, 136
Nutritive balance, 455
Nyctalopia, 904
Nycturia, 435, 1220
Nystagmus, 493, 917, 1309, 1324
induced, 496
Obesity, 1206, 1347
anemic, 1214
asthenia of, 754
high blood-pressure of, 1045
ovarian, 1207
plethoric, 1213
with cardiorenal or other compli-
cations, 1215
Obstruction, fecal, 802
intestinal, vomiting of, 1333, 1341
Ocular functions, examination of,
890
headache, 984
paralyses in encephalitis, 1278
Oculocardiac reflex, 213, 482
Oculomotor paralysis. 907, 1016
Odors, vertigo due to, 1330
Oertel's method in chronic heart dis-
orders, 1349
Office equipment, special, 630
Oil of santal in urine, 427
Oliguria, 435, 1218
lasting, 1220
orthostatic, 435, 1220
transient, 1219
Olive-tipped sound, 43
Oliver's sign in aortic aneurysm, 1349
Oneiric states, 1283
Opacity, 898
Opaque enema, 86
meal, 82
Ophthalmic disorders, 894
migraine, 903
Ophthalmoplegia, 909
Ophthalmo-reaction in tuberculosis,
557
Opium, hypnotic use of, 1105
sleep from, 1271
Opotherapy, 1345
Oppenheim's sign of pyramidal dis-
ease, 1349
Opsiuria, 126, 434, 1222
Orbitoscopy, 890
Orthodiagraphy of heart, 222 .
Digitized by
Google
INDEX TO VOLUMES I AND II.
1375
Orthofluoroscopy of heart, 225
Orthopnea, 809
Orthostatic albuminuria, 659
oliguria, 435
tachycardia, 281
Ossifluent abscesses, 1188
Osteoarthritis, iliac, 1175
sacroiliac, 1175
vertebral, 1175
Osteomalacia, 1155
Osteomyelitis, 1154, 1316
Osteoperiostitis, 1153, 1315
intercostal, 1270
post-infectious, 1154, 1316
staphylococcic, 1154
syphilitic, 1153, 1315
Osteosarcoma, 1154, 1315
Otitis media, abducens paralysis in,
1347
convulsions of, 771
eye disturbances in, 918
headache of, 991
suppurative, vertigo of, 1327, 1329
Otobrightism. 1330
Otosclerosis, 1329
Otoscopic examination in vertigo,
1329
Ova, parasitic, in stools, 112
Ovarian cyst, 740
edema in, 832
left iliac pain of, 1088
right iliac pain of, 1098
obesity, 1207
Overeating, 793, 798
Overwork, angiospastic attacks due
to, 1268
dyspepsia due to. 806
Oxalic diathesis, 1344
Oxyuris vermicularis, 113, 116
Pachon's sphygmomanometer, 240
Pachymeningitis, 1025
Paget's disease of the bones, 1350
of the nipples, 1350
Pain, epigastric, 833
in duodenal ulcer, 76
in the hypochondrium, left, 1058
right, 1068
in the iliac fossa, left, 1085
Pain, in the iliac fossa, right, 1089
in the joints, 1128
in the lower extremities, 1153
in the lumbar region, 1170
in the side, 1225
in the upper extremities, 1313
interlobar, 185
precordial, 1245
(See also Neuralgia).
Pallor, 1258
anemic, 675
Palpitations, 1059, 1251
Panaritium analgicum, 1318
Pancreas, 126
cancer of, 1071, 1120
inspection of, 126
palpation of, 126
tenderness, 127
percussion of, 128
Pancreatic diabetes, 970
disorders, epigastric pain of, 838
stools in, 130
chemical analysis, 130
Einhorn*s bead method, 131
Schmidt's nucleus test, 130
function, Sahli's test of, 1351
point of tenderness, 127
Pancreaticobiliary syndrome, 838
Pancreatitis, 839
Pannus, 898
Papular skin affections, 848
Paracentesis pericardii, 231
Paralysis, 459
abducens, 1347
agitans, tremor of, 1309
facial, 1025, 1278, 1349
hemiplegic. 1014
laryngeal, 681
ocular, 907, 1016, 1278
progressive general, 776, 787, 856,
922, 927, 1243
tremor of, 1310
vertigo of, 1326
radial, 1318
Paranoia, 786
Paraphasic disturbances, 484
Paraplegia, spastic, 472, 475
Parasites, intestinal, 111-117
Parasitic fungi, 584
Digitized by
Google
1376
INDEX TO VOLUMES I AND II.
Parasitology, 505
Paratyphoid infections, 549, 552
Paresthesias in arteriosclerosis, 803
Parkinson's disease, 1350
tremor of, 1309
Parotid glands, 131
Paroxysmal cough, 778
hemoglobinuria, 1347
tachycardia, 260, 707, 946
Parrot's disease, 1350
law in tuberculous bronchial lymph-
adenitis, 1350
sign in meningitis, 1350
Passive congestion of lungs, 187
Patellar reflex, 467
Pavy's disease, 1350
Pectoriloquy, 167
whispering, 168
Pediculosis, 1115
Pelvic pain, sciatic, 1163
suppuration, pain of, 1088
Pemphigoid eruptions, 849, 919
Penis, 375, 952, 954
Percussion, see the various separate
organs or structures.
Pericardial friction, 212
puncture, 231
Pericarditis, 933, 943, 948, 1040, 1266
arm pain of, 1321
diagnostic considerations, 235, 238
edema of, 830
posterior. 226
sicca, 212. 235
pain of, 1247
with effusion, 235
Perigastritis, Rosenheim's sign of,
1351
Perinephric abscess, 1061, 1066, 1070,
1072
Peristalsis, visible, 81
Peritoneum, ascites in cancer of, 744
Peritonitis, 948, 1039
tuberculous, ascites in, 581, 745
vomiting of, 1333, 1341
Permeability of kidneys, 448
Pernicious anemia, 676
Perret and Devic, signs of, in peri-
carditis, 1350
Pettenkoffer's test for bile acids,
420, 1350
Pezzer catheter, 27Z
Pfeiffer bacillus, 526
Pfuhl's sign in effusion, 1350
Pharyngeal cough, 778, 784
exudate, 544
infections, 1291
Pharynx, examination of, 150
Phenols in urine, 428
Phenolsulphonephthalein test, 452
Phlebitis, 827, 831, 832, 1031, 1158
puerperal, edema of, 826, 832
Phlegmasia alba dolens, 827, 832
Phosphates in urine, 395, 409
Phosphaturia, 1243
Phosphenes, 905
Phosphorus poisoning, 996, 1010
Photophobia, 895, 906
Phthiriasis, 1115
Physical examination, systematic, 621,
629, 634
Picric acid in blood, test for, 301
jaundice, 1123
Pignet's index, 603
Pill-rolling movements, 1309
Pituitary disease, eye disturbances of,
912, 920
headache of, 982
tumors, polyuria of, 1243
Pityriasis linguae, 1300
Plague bacillus, 539
Plantar reflex, 474
Plethora, 1213, 1236, 1254
epistaxis of, 844
high blood-pressure of, 1049
Pleura, diseases of, 180
exploratory puncture of, 194
Pleural effusion, 181, 322
syncope of, 928
exudates, cells in, 322, 323
fluid, cells in, 182
friction, 168
vomica, 1339
Pleurisy, 181, 322, 1065, 1084, 1339
cough of, 778
dry, 183
encysted, 184
fainting in, 928
Digitized by
Google
INDEX TO VOLUMES I AND 11.
1377
Pleurisy, hiccough of, 1040
interlobar, 184, 1228
pain of, 1225
painful points in, 185
precordial, 1228, 1247, 1269
right hypochondriac pain of, 1072,
1074
suppurative, see Emphysema.
Pleuritis, adhesive, dyspnea of, 818
apical, 1232
Pleurodynia, 1231, 1233
Pluriglandular insufficiency, 1149,
1215
Pneumococcus, 526
Pneumonia, 172
expectoration in, 872
hemoptysis of, 1033
left hypochondriac pain of, 1065
right hypochondriac pain of,
1072, 1084
bronchial, 186
lobar, 4, 872
pain of, 1230
vomiting of, 1341
Pneumonokonioses, 873
Pneumothorax, 179
pain of, 1225, 1232
Polarimeter, for sugar in urine, 417
Polioencephalomyelitis, 1022
Poliomyelitis, arm pain of, 1321
Pollakuria, 1240
Polyglandular insufficiency, 1149
in obesity, 1215
Polygrams, 695, 731 •
Polygraph, Jacquet's, 252
Mackenzie's, 256
Polypnea, 809
hysterical, 824
Polyuria, 435, 1223, 1240
clinostatic, 1220 ,
cryptogenic, 1244
experimental, 347
induced, 1240
of diabetes, 1242
of nephritis, 1242
of urinary cases, 1243
Popliteal space, painful disturbances
in, 1164
Porges's reaction in syphilis, 1350
Portal hypertension, 436, 742, 1000,-
1046
Post-hemiplegic tremor, 1310
Potain on heart percussion, 215
Pott's disease, 1154, 1175, 1233, 1270
Precordial pain, 1245
Pregnancy, 740
albuminuria of, 655
edema of, 830
extra-uterine, 1088. 1099
indigestion of, 797
obesity of, 1207
pyelonephritis of, 655
vomiting of, 1340
Premature beats, 700, 1247
Presclerosis, 1051, 1254
angiospastic, 1239
Presystolic murmur. 201, 206, 207
Proctoscopy, 88
Prodromal headache, 979
Profeta, law of, 1350
Projection sound in esophagus, 43
Prolonged expiration, 168
Proportions of the human body, 597
Prostate, 378
abnormal findings on palpation of,
380
blood from, 1005
cancer of, 380
expression of, 380
massage of, 380
Prostatic catheter, 368
hypertrophy, 380
polyuria of, 1223, 1243
Prostatitis, 377, 380
Protozoa in the stools, 108, 111
Prurigo, 848, 1109
Pruritus, 1106, 1107
insomnia of, 1101
Pseudoangina of aerophagics, 1269
Pseudocasts, 433
Pseudodiptheria organisms, 545
Pseudomembranous sore throat, 1291,
1293
Psoas inflammation, 1166
Psoriasiform parakeratoses, 1111
Psoriasis, 6
linguae, 1300
Psychoneuroses, depressive, 752, 1142
87
Digitized byV^OOQlC
1378
INDEX TO VOLUMES I AND II.
Psychoneuroses, dyspepsia of, 806
headache of, 990
insomnia of, 1102
loss of weight of, 1142
lumbago of, 1173
slow pulse of, 1287
vertigo of, 1330
Psychoneurosis. 1196, 1204
appendiceal, 1099
Psychosplanchnic neuropathy, 1198,
1253
Pterygium, 896
Ptomain poisoning, 793
Ptosis, 895, 1278
abdominal, 1180
Puberty, epistaxis of, 845
Puerile breathing, 168
Pulmonary abscess, 184, 1033
apoplexy, 190
complications in obesity, 1216
congestion, 187, 1347, 1352
disturbances in obesity, 1216
embolism, 190
emphysema, 188
fibrosis, dyspnea of, 812, 818
gangrene, 184, 1034
infarction, 1031
syphilis, 1034
thrombosis, 190
tuberculosis, see Tuberculosis,
pulmonary.
tumors, 184, 1034
valve lesions, 2^
vomica, 1339
Pulse, 1043
alternating, 726
bigeminal, 704
Corrigan, 1346
frequent, 942
intermittent, 702
pressure, 1146
records, 249
slow, see Bradycardia.
Puncture, lumbar, 487
of finger-tip, 301
of pericardium, 231
of pleura, 194
venous. 248, 302
Pupil, Argyll-Robertson. 481, 901
Pupil, abnormalities of, 900
Pupillary reflexes. 479, 887
Pupils, inequality of, 915, 1278
Purpura, 849, 1352
epistaxis of, 845
hematuria of, 1009
hemoptysis of, 1034
Pus, 521
Pustular skin affections, 849
Pyelography, 344
Pyelonephritis, polyuria of, 1223
calculous, hematuria of, 1012
Pylephlebitis, ascites In, 743. 750
Pyonephrosis, 1050, 1066, 1070. 1072
Pyopneumothorax, 178, 1339
Pyramidon in urine, 427
Pyuria, 333, 394, 394 1223
Quincke's disease, 831, 1350
Quinine, eye disturbances due to, 923
in urine, 4?8
tinnitus due to, 1294
vertigo due to, 1329, 1330
Rabies, 772, 1349
Rachitic dwarfs, 604, 606
Rachitis, 1347
Radial nerve, sensory disturbances in
section of, 1315
Radiculitis, 1168
Radioscopy, see X-ray examination.
Railway travel, vertigo in, 1330
Rales, bubbling, 166
crepitant, 167
sibilant, 168
sonorous, 168
subcrepitant. 168
Rapid eating, 805
pulse, 942
Raynaud's disease, 1197, 1318, 1350
Reaction of degeneration, 462
Recklinghausen's disease, 1350
Reclus's disease, 1350
Rectocele, 385
Rectum, 87
endoscopy of, 90
fluoroscopy of, 90
palpation of, 87
proctoscopy, 88
Digitized by
Google
INDEX TO VOLUMES I AND II.
1379
Rectum, radiography of, 90
Recurrent nerve paralyses, 683, 689
Red blood cells, count of, 308
in anemias, 675
in urine, 433
resistance of, 290
Reflex convulsions, 771
cough, 777
dyspepsia, 804
headache, 978, 984
Reflexes, 462
circulatory, 482
cutaneomuscular, 474
cutaneovasomotor, 476
oculocardiac, 213, 482
pupillary, 479
tendinomuscular, 466
Refraction, disorders of, 904
headache of, 984
Regurgitation of food, 803
Renal ballottement, 336
calculus, 1008 (see also Nephro-
lithiasis).
cancer, 1008
colic, oliguria of. 1219
vomiting of, 1334, 1340
congestion, oliguria of, 1223
diabetes. 970
disease, see Nephritis.
function, tests of. 434, 452
hematuria, 1007, 1012
hyperpermeability, 1243
pain, 1172, 1178
permeability, 448, 651
points of tenderness, 335
stone, 350, 1008, 1060, 1066; see also
Nephrolithiasis.
tub e r c u 1 o s i s , see Tuberculosis,
renal.
tumor, 1012
Renault's test for indican, 421
Reproductive system, eye disturb-
ances in disorders of, 920
role of, in obesity, 1207
Respiratory arhythmia, 710
tract, 133
extrathoracic (upper), 133
intrathoracic (lower), 164
physical signs. 164
Respiratory tract, x-ray examination
of, 170, 172, 176, 178, 182,
184, 187, 188, 191
Retained catheter, 373
Retention of urine, 352, 740
Retinitis pigmentosa, 905, 910
prealbuminuric, 914
Retropharyngeal abscess, dyspnea of,
810
Revolting impressions, vomiting due
to, 1332
Revilliod's phenomenon in organic
hemiplegia, 1350
Rheumatic pleurisy, 181
Rheumatism, 236, 938, 1128, 1156,
1174
chronic vertebral, 1175
cryptogenic, 1136
eye disturbances of, 917
gonorrheal, 1130
Heberden's nodes in, 1348
insomnia of, 1103
intercostal neuralgia of. 1270
pain in upper extremities in, 1313,
1317
tuberculous, 1130
Rhinitis, 986
Rhinoscopy, anterior, 136. 147
posterior, 141, 147
Rhizomelic spondylosis, 1175
Rhonchi, 168
Ribs, pain in, 1233
Rigidity, abdominal, 1093
muscular, in paralysis agitans, 1309
Ringing in the ears, 1294
Ringworm, 501, 502, 663
Rinne's test in otology, 1350
Rivalta's test of effused fluids. 331,
1350
Roger's disease, 227, 1350
Romberg's sign, 438, 494, 1350
Rosenbach's sign of hysterical hemi-
plegia, 1351
Rosenheim's sign of fibrous perigas-
tritis, 1351
Roseola, syphilitic, 855
Rotation test, 497
Rough breathing, 168
Roux's stain, 518
Digitized by
Google
1380
INDEX TO VOLUMES I AND II.
Ruault's sigii of incipient tuber-
culosis, 1351
Rubella, 860
Sacroiliac osteoarthritis, 1175
Sacrolumbar pain, 1172
Sahli's test of pancreatic function,
1351
Salicylates in urine, 428
tinnitus due to, 1294
vertigo due to, 1329
Saliva, 132
Salivary glands, 131
Salol in urine, 428
Salpingitis, pain of. 1088, 1098
and appendicitis, 1093
Sarcomatosis, osseous, 1343
Sarcoptes scabiei, 1113
Scabies, 954, 955, 1112
Scanning speech, 1309
Scarlet fever, 858
eye disturbances in, 916
sore throat of, 1292, 1293
tongue of, 1299
vomiting of, 1341
Schick test, 547
Sciatica, 1160, 1177
Sclera, diseases of, 898
Scleroderma, 850
Scoliosis, pain in, 1177
Scotoma, 892, 912
scintillating, 905
Scrofula, 960
Scrotum, 382
Scurvy, hematuria of, 1009
Seasickness, vertigo of, 1331
vomiting of, 1334
Sebaceous cyst, 956, 1190
Seborrhea, 503
decalvans, 669
Seborrheic psoriasiform eczema, 1111
Segregation, urinary, 340
Seminal vesicles, 380
Senile alopecia, 673
tremor, 1310
Sensation, 457
Septic affections, 934, 938
edema of, 831, 832
Sergent's white line, 478, 754
Serous surfaces in upper extremity,
disorders of, 1317
Shingles, see Herpes zoster.
Shock, post-operative, vomiting of,
1334
traumatic, 1146
Shreds in urine, 376
Sialorrhea, 1059
tongue in, 1297
Sicard's raised knee sign in sciatica,
1162
method of epidural treatment, 1351
Sieur's sign of pleural effusion, 1351
Sigmoid, tumors of, 1087, 1088
Sigmoiditis, left iliac pain in, 1068
Sigmoidoscopy, 88
Signs, index of clinical, 1343
Silent breathing, 168
Singultus, 1039
Sinus arhythmia, 710
Sinusitis, eye involvement in, 918
headache of, 986
Skene's glands, 384
Skin discolorations, 850
eruptions, 847
artificial,. 851
reflexes, 474
tumors, 850
Skodaic resonance, 168
Skull fracture, hemiplegia of, 1027
Sleep, morbid, 1271
Sleeping sickness, lethargic enceph-
alitis, 328, 1278
trjrpanosomiasis, 1278
Slow iNilse, 1285
Small-pox, 860
eye disturbances of, 916
sore throat of, 1293
vomiting of, 1341
Smokers* tongue, 1297
Softening of brain, 484, 1014
Solar plexus, hyperesthesia of, 837
Somnambulism, 1280
Somniloquy, 1283
Somnolence, morbid, 1272
Sore throat, 1290
erythematous, 1292
pseudomembranous, 1291, 1293
pultaceous, 1290, 1292
Digitized by
Google
INDEX TO VOLUMES I AND IL
1381
Sore throat, streptococcic, 1293
ulceromembranous, 1291, 1293
vesicular, 1291, 1292
Souques's sign of organic hemiplegia,
1351
Spasmophilia, 771
Spastic contraction of muscles in
Thomsen*s disease, 1351
paraplegia, 472, 475
Special medical diagnostic proced-
ures, 41
Spectroscopy, 587
of blood, 424
Speech disturbances, 484
Spermatic cord, 382
Sphygmography, 249, 1043
Sphygmohydruric coefficient, 437
Sphygmomanometer, 239, 621
Spinal cancer, 1233 '
hemiplegia, 1021, 1023
localizations of skin reflexes, 475
of tendon reflexes, 473
pains, 1163, 1167, 1174, 1176
Spirochaeta bronchialis, 527, 875
pallida, 528, 563
Spirochetosis, icterohemorrhagic, 1121,
1157
Spirometry, 193
Spiroscope, 193
Spleen, enlargements of, 1062, 1067,
1071
primary epithelioma of, 1347
topographic features of, 1059
Splenic flexure, 1063. 1067
Splenomegaly with chronic polycyth-
emia, see Vaquez's disease,
1351
Spondylitis, 1174, 1233
Spondylosis, rhizomelic, 1175
Sporotrichosis, 584
Sputum, albumin test, 196
examination of, 196, 521
semeiologic significance of, 865
Squamous skin affections, 848
Staining methods, 523
Stains, bacteriologic, 515
blood, 589
Stammering, 484
Staphylococcic osteomyelitis, 1316
Staphylococcus, 538
Steatorrhea, 95, 129, 794
Stellwag's sign of exophthalmic
goiter, 1351
Sternum, pain behind the, 1266, 1268
Stethoscopic glossary, 166
Stokes-Adams disease, 2, 722, 764,
776, 927, 1343
Stokes-Chopart, law of, 1351
Stomach, 50
anatomical considerations, 50
auscultation of, 54
cancer of, see Cancer of stomach.
contents, 57
digestive activity, estimation of, 67
dilatation of, Bouchard's nodes in,
1345
eye disturbances in affections of,
919
fluoroscopy of, 69
gaseous distention of, 1058, 1065
hematemesis in affections of, 997
hiccough in affections of, 1039
hourglass, 801
inflation of, 54
inspection of, 55
introduction of stomach tube, 55
pains, 836
palpation of, 52
percussion of, 54
radiography of, 75
residues, 57
succussion. sounds, 52
test meal, 57
tube, 55
ulcer of, see Gastric ulcer.
x-ray examination of, 69
Stomatitis, mercurial, tongue of, 1299
Stone in bladder, 353, 361
in kidney, see Nephrolithiasis.
in ureter, 1088, 1099
Stools, examination of, 91, 126, 129,
794
bacteriologic, 106
bacillus of dysentery, 106
cholera bacillus, 107
chemical, 99, 130
bile pigments, 100
blood. 101, 330, 794, 795
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1382
INDEX TO VOLUMES I AND II,
Stools, examination of, chemical,
fats, 99, 130, 794
mucus, 794
ratio of dry to moist constit-
uents, 99
reaction, 99, 795
macroscopic, 94, 794
amount, 794
color, 94, 794
concretions, 95
consistency, 794
food remnants, 94
odor, 95, 794
rice bodies, 795
sand, 795
tapewonn, 114
microscopic, 95
amebse, 108
connective tissue, 97
crystals, 98
debris, 98
elastic fibers, 98
fats, 98
muscle fibers, 96
Nothnagel's yellow granules, 97
parasitic cysts, 110
ova, 112
pus, 794, 795
starch, 95
vegetable cells, 95
Strabismus, 907, 920, 985
in encephalitis, 1278
Strangulated hernia, vomiting of,
1333, 1341
Straus's sign of peripheral facial
paralysis, 1351
Streptococcic sore throat, 1293
Streptococcus, 538
Stricture of esophagus, 46
of urethra, 364, 378
Strongyloides stercorals, 116, 117
Strophanthus, bradycardia due to,
1287
Strychnine poisoning, 772
Subacromial bursitis, 1317
Subcutaneous tuberculin test, 555
Subdiaphragmatic abscess, 1062, 1074,
1339, 1347
disorders, pain of, 1232
Sublingual glands, 132
Submaxillary glands, 132
lymphadenitis, 960, 1183
Succussion sound, Hippocratic, 167
splash, in abdomen, 81
in stomach, 52
Sugar in cerebrospinal fluid, 328
in urine, 415
Supraclavicular glands, 957
Suprarenal, see Adrenal.
Sweating, paroxysmal, 1256
Symblepharon, 895, 919
Sympathetic disturbances, 1197
excessive irritability, clinical tests
of, 1197
excitation, 945
Symptoms, analysis of, 647
Syncope, 722, 760, 925
vertigo of, 1326
Synechia, 899, 900
Syphilis, 853, 953
alopecia of, 672
backache of, 1176
bacteriologic diagnosis of, 528, 563
bone pains of, 1153
chancre of, 885, 952, 953, 960. 1302
clinical features of, 855-857
congenital, 856, 1151
Wassermann reaction in, 575
eruptions of, 855, 8^6, 857
eye disorders of, 916, 917
gland enlargements of, 855, 953.
958, 960
headache of, 984, 991
heart disorders of, 237
jaundice of, 1124
leukoplakia of, 1300
lingual manifestations of. 1300,
1301, 1302
lumbar pain of, 1176
MacDonagh reaction in, 579
mucous patches of, 855, 1302
Porges's reaction in, 1350
of larynx, 681, 688
of liver. 1069, 1083, 1127
of lungs, 1034
secondary meningeal reaction of,
1176
skin manifestations of, 855
Digitized by
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INDEX TO VOLUMES I AND IL
1383
Syphilis, sore throat of, 1292, 1293
spirochete of. 528, 563
Vernes phenomenon in, 582
Wassermann reaction in, 563, 583
Syphilitic epiphyseal detachment, 1350
osteoperiostitis, 1315
sclerosis of tongue, 1302
urethritis, 377
Syphilometry, 583 ,
Syringomyelia, 1318
Systematic medical examination, 609
Systolic blood-pressure, 1043
low, 1145
murmurs, 203, 205, 207
Tabes dorsalis, 458, 481
arm pains of, 1321
cervical, 1318
Erb's sign of, 1346
eye disturbances of, 481, 922, 1343
gastralgic crises of, 801, 835, 842
girdle pains of, 1233
hemiplegia of, 1027
lightning pains of, 1167
precordial pain of, 1270
right hypochondriac pain of, 1078
Romberg's sign in, 494
vomiting of, 1334, 1342
Tabetic joints, 1156, 1315
Tache cerebrale, 478
Tachycardia, 942, 950, 1200, 1256
emotional, 949
orthostatic, 281, 949
painful, 1251
paroxysmal, 260, 707. 946
Taenia saginata, 114, 505
solium, 114, 505
Tallqvist's hemoglobin scale, 311
Tanret's reagent for albuminuria, 410
Tapeworm, 114, 505
itching of, 115
Taylor principle, 610
Tea intoxication, tremor of, 1309
Teleradiography, 230
Temperature, 929
Tendinomuscular reflexes, 466
symptomatic significance of, 472
Tertiary syphilides of the tongue,
1302
Test chart for eye examination, 879,
890
Test diet for renal function, 452
Test meal, 57, 93
Testicles, 381, 920
tumor of, 382
Tetanus, 772
bacillus, 535
Tetany, Trousseau's sign in, 1351
Tetramitus mesnili. 111
Theobrominism, 950
Thermo-analgesic dissociation, 458
Thionin, 518, 523
Thomsen's disease, 1351
Thoracentesis, 194
Thoracic duct, compression of, 1349
fluctuation, 168
mensuration, 191
pain, 1233
Throat exudates. 522, 543, 544
sore, see Sore throat
Thrombosis, pulmonary, 190
with hemiplegia, 1014, 1026
Thrush, 1299
Thure-Brandt posture, 1351
Thyroid, congestion of, 1191
disorders, eye disturbances in. 919
enlargement, 685, 1191 (see also
Goiter),
recurrent laryngeal paralysis
due to, 685
glycosuria, 970
insufliciency, 1192, 1207
obesity, 1207
Thyroiditis, 1184, 1191
Tic cough, 783
hiccough, 1040
Tinea, 499
favosa, 504, 666
tonsurans, 501, 502, 663
versicolor, 503, 504
Tinnitus aurium, 1294
in Meniere's disease, 1326, 1328
mode of production of, 1295
Tobacco abuse, angiospastic attacks
of, 1268
eye disturbances of, 922
headache of, 981
sore throat of, 1292
Digitized by
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1384
INDEX TO VOLUMES I AND II.
Tobacxro abuse, vertigo of, 1330
Toison's fluid, 306
Tongue, diagnostic features relating
to, 1297
actinomycosis of» 1305
chancre of, 1302
cysts of, 1303
discolorations of, 1297
epithelioma of, 1304
gumma of, 1301, 1303
tuberculoma of, 1304, 1307
tumors of, 1304
Tonsil, tuberculosis of, 1293
Tonsillitis, 1290
Torticollis, symptomatic, 1184
Toxemic dyspnea, 813
Toxic glycosuria, 970
hematuria, 1010
insomnia, 1102
neuritis, 1318
sleep, 1272
tinnitus, 1296
tremor, 1309
Tracheobronchial adenopathy, 170,
171, 685
bradycardia of, 1287
recurrent laryngeal paralysis of,
685 .
Transudates, Rivalta*s test for, 331
Traube's law in nephritis. 1351
Traumatic diabetes, 974
neuralgia and neuritis, 1317
shock, 1146
Tremor, 1308
accidental, 1308
hereditary, 1309
hysteric, 1310
intention, 1308
migratory, 1311
permanent, 1308
post-hemiplegic, 1310
progressive, 1311
regressive, 1311
senile, 1310
Tabular Synopsis, 1312
Treponema pallidum, 528, 563
Triacid stain, 518
Triceps reflex, 469
Trichiasis, 895
Trichocephalus, 113
Trichomonas, diarrhea due to, 791
Trichophyton, 502, 665
Tricuspid lesions, 238, 735, 1150
Troisier's ganglion in gastric cancer,
1351
Trophedema, 829
Trousseau's sign in tetany, 1351
Trypanosomiasis, 1278
Tube casts, 430
Tubercle bacillus, 525, 558
in urinary sediment, 558
Tuberculin, 555
tests, 555
Tuberculoma of the tongue, 1304
Tuberculosis, 934, 938
diagnostic bacteriologic procedures
in, 555
lingual, 1304, 1307
of joints, 1156
of tonsils, 1293
pericecal, right iliac pain of, 1098
pulmonary, 174, 869, 872
alarm zone in, 175
Ameth's neutrophilic blood pic-
ture in, 175
asthenia of, 755
dyspepsia of, 798
dyspnea of, 1250
eye disorders in, 917
fluoroscopy in, 176
hemoptysis of, 1031
hyposphyxia in, 1151
loss of weight of, 1142
low systolic pressure of, 1145,
1147
pain of, 1231
physical signs of, 174-179
renal, bacteriologic diagnosis of,
558
hematuria of 1008
hypochondriac pain in, 1060, 1066
urine in, 333, 346, 558, 1008, 1012,
1224, 1244
tests for, 555
Tuberculous diarrhea, 791
laryngitis, 681, 687
lymphadenitis, 959, 1185
meningitis, 326, 1027, 1279
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Google
INDEX TO rOLUMES I AND II.
1385
Tuberculous obesity, 1208
osteoarthritis, 1315
periostitis, 1315
peritonitis, ascites of, 581, 745
pleural involvement in, 1347
prostatitis, 380
urethritis, 377
Tubular breathing, 168
Tumors, see various structures con-
cerned.
loss of weight in, 1143
Tunica vaginalis, 382
Tuning-fork test, Weber's, 1352
Tympanic cavity, Valsalva inflation
of, 1351
Tympanites in hepatic cirrhosis, 792
Typhlocolitis, 1098
Typhoid fever, 936, 938
agglutination test f^, 548
blood cultures in, 552
delirium of, 786
diarrhea of, 790
Duguet*s sign of, 1346
Duroziez's sign of, 1346
epistaxis of, 846
eye disturbances of, 917
fever of, 934, 936, 938
headache of, 979
hemolytic tests for, 550
hemoptysis of, 1034
insomnia of, 1103
intercostal neuralgia of, 1270
temperature curve in, 934
tongue of, 1299
Widal test for, 548
Uffelmann's reagent, 64
Ulcer, duodenal, see Duodenal ulcer.
gastric, see Gastric ulcer.
Ulcerations, genital, 951
lingual, 1306
Ulnopronator reflex, 472
Ultra-microscope, 513
Upper extremities, pain in, 1313
post-traumatic, 1313
nerve-supply to muscles of, 1319
peripheral sensory disturbances
in, 1314, 1316
Uranalysis, 390, 429
Urea in blood, 292, 442
in urine, 398
Uremia, 653
asthenia of, 755
bradycardia of, 1287
coma of, 764
convulsions of, 773y 775
diarrhea of, 791
dyspepsia of, 797
dyspnea of, 810, 813, 823
headache of, 980
hematemesis of, 997
hemoptysis of, 1035
high diastolic pressure of, 1046
hyposphyxia of, 1151
in obesity, 1215
itching of, 1106
precordial pain of, 1267
tongue of, 1299
vertigo of, 1330
vomiting of, 1334, 1342
Ureter, blood from, 1007
stone in, 1068, 1099
x-ray examination of, 349
Ureteral catheterization, 340
cytologic and bacteriologic ex-
amination of urine, 345
points of tenderness, 1179
Urethra, female, 383
male, 362
catheterization of, 362
spasm of, 367
stricture of, 364
urethritis. 365, 375, 377
Urethral discharge, varieties of, 377
hematuria, 1005
Urethrorrhagia, 1006
Urinary secretion, rhythm of, 126
segregation, 340
tract, 332
Urine, abnormalities of, 333
chemical analysis of, 396
acetone, 425
acidity, 396, 425
albumin, 409
quantitative determination, 411
bile acids, 420
pigments, 410, 417
blood, 330, 424, 1003
Digitized by VjOOQIC
1386
INDEX TO VOLUMES I AND II.
Urine, chemical analysis of, chlorides,
406,439
diacetic acid, 426
indican, 421
phosphates, 395, 409
sugar, 415, 969
urates, 395
urea, 398
uric acid, 395
urobilin, 420
drugs in, 427
antipyrin, 427
bromine (bromides), 427
copaiba, 427
iodine (iodides), 428
morphine, 428
oil of santal, 427
phenols, 428
pyramidon, 427
quinine, 428
salicylates, 428
salols, 428
macroscopic examination of, 390
amount, 390, 434, 1218
color, 394
odor, 394
pus, 333, 394, 395, 1223
sediment, 395
shreds, 376
specific gravity, 395
microscopic examination of, 430
bacteria, 434
casts, 430
cylindroids, 433
erythrocytes, 433
leucocytes, 434
parasites, 434
pseudo-casts, 433
red cells, 433
tubercle bacilli, 558
retention of, 352
Urobilin in blood, 300
in urine, 420
Uroseptic fever, 940
Urticaria, 848, 849, 1108
bullosa, 11C8
papulosa, 1108
Uterus, 386
displacements of, 387
Uterus, examination of, with specu-
lum, 388
with retractors, 389
hysterometry, 389
Uvula, vomiting due to tickling of,
1332
Vaccine, 862 »
Vagina, 385
Vaginismus, 385
Vaginitis, 385
Vagus nerve, disease of, 1287
Valleix's laws in neuralgia, 1351
points, 1162, 1270
Valsalva's test, 1351
Vaquez's disease, 1351
Varicella, 861, 916
Varicocele, 382
Varicose eden^, 832
veins, 1150, 1158
Variola, 860
eye disturbances of, 916
sore throat of, 1293
vomiting of, 1341
Vas deferens, 3S2
Vasomotor angiospastic attacks, 1268
asthenia, 281
ataxia, 1197
disturbances, 1318
instability, 1256
nervousness, 1197
reflexes, 476, 1263
Vegetations, adenoid, 150
on penis, 954, 955
Vegetative nervous system, 1256
Veins, 248
inflammation of. 1157 (sec also
Phlebitis).
Venous network, visible, 1321
pressure, 248
high, 1150
puncture, 248. 302
Ventricle, acute insufficiency of left,
1267
Vernes phenomenon in syphilis, 582
Veronal and morphine intoxication,
1274
Vertebral cancer, pain of, 1233
Digitized by
Google
INDEX TO VOLUMES I AND 11,
1387
Vertebral column, inflammatory con-
ditions of, 1176
funiculitis, 1167, 1168
Vertigo, 493, 1323
a stomacho laeso, 1330
arteriosclerotic, 1325
aural, 1326
central, 1325
cerebral, 1325
gastric, 1330
induced, 494
labyrinthine, 1326
neuropathic, 1330
ocular, 906
pathogenesis of, 1323
reflex, 1330
toxic, 1329, 1330
which restores the sense of hear-
ing, 1331
Vesical disorders, see Bladder.
Vesicular skin affections, 848
Vicarious menstruation, 844, 1036
Vincent's angina, 538, 1293, 1351
Visceralgia, 1195
Visceroptosis, 949
Viscosity of blood, 282
in hyposphyxia, 1148
Cuvier viscosimeter, 287, 288
Hess viscosimeter, 284
Vision, colored, 906
double, 906
iridescent, 906
Visual acuity, 890
field, 891, 910
Vitreous body, 888
Voice disturbances, 484
Vomica, 1338
pleural, 1339
pulmonary, 1339
Vomitiiig, 1332
alimentary, 1332
bilious, 1333
bloody, see Hematemesis.
central, 1332
fecaloid, 1333
habitual, 1333
in aural vertigo, 1328
in children, 1333, 1334
periodic acetonemic, 1334
Vomiting, mechanism of, 1332
mucous, 1333
pathogenesis of, 1333
peripheral, 1332
Von Graefe's sign, 919, 1347
Von Pirquet's test, 556
Vulpian's law in hemiplegia, 1351
Vulva, 384
kraurosis of, 385
Vulvitis, 385
Wassermann reaction, 564, 764, 855,
1351
Weber's syndrome, 909, 1016, 1019
test for blood in stools or vomitus,
101, 1351
in otology, 1352
Weight, 590, 1209
relationship to blood-pressure, 1141
Weil-Mathieu's disease, 937
Wen, 956, 1190
Werlhoff's disease, 1352
Wernicke's sign in bilateral homo-
nymous hemianopsia, 1325
Westphal's sign of tabes, 498, 1352
Whistling sounds in the ears, 1329
White line, 479
Whooping-cough, ulceration of tongue
in, 1306
Widal test in typhoid fever, 548
Woillez's disease, 1352
Word blindness, 484
deafness, 484
Worm cough, 778
parasites, 114, 505
Wounds, tremor in, 1310
Xanthelasma, 1123
X-ray alopecia, 668
examination in duodenal ulcer, 77,
82
in gastric cancer, 807
ulcer, 807
in nephrolithiasis, 350
in pulmonary tuberculosis, 176
of abdomen, 81
of duodenum, 77, 82
of esophagus, 43
of heart, 220
Digitized by
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1388
INDEX TO VOLUMES I AND II.
X-ray examination of kidney, 344,
349
of liver, 124
of rectum, 90
of respiratory tract, 170-191
of stomach, 69, 75
of ureter, 349
opaque enema in, 86
meal in, 82
Yeasts, 504
Ynnurigaro's esophageal sounds,
43
Ziehrs carbol-fuchsin, 517, 521, 525,
531, 559
Zona, see Herpes zoster.
Zuber's sign of simulated aphonia,
692
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