Skip to main content

Full text of "An introduction to the study of the diseases of the nervous system : being lectures delivered in the University of Edinburgh during the tercentenary year"

See other formats


AN 



INTRODUCTION TO THE STUDY 



OF THE 



DISEASES OF THE NERVOUS SYSTEM : 



LECTURES DELIVERED IN THE UNIVERSITY OF EDINBURGH 



F.R.C.P.E., F.R.S.E., 

PHYSICIAN IN ORDINARY TO HBR MAJESTY THE QUEEN, TOR SCOTLAND ; 
PROFESSOR OF THE PRACTICE OF PHYSIC AND OF CLINICAL MEDICINE, UNIVERSITY OF EDINBURGH 
CONSULTING PHYSICIAN TO THE ROYAL HOSPITAL FOR SICK CHILDREN ; 
HONOBABT AND CORRESPONDING MEMBER OF VARIOUS LEARNED SOCIETIES IN 
/"^^T^v LONDON, BERLIN, ABERDEEN, ETC. 



BEING 



DURING THE TERCENTENARY YEAR. 



BY 



THOMAS GEAINGETl STEWART, M.D., 




EDINBURGH: 
BELL & BEADFUTE, .12 BANK STREET. 
LONDON : SIMPKIN, MARSHALL & CO., and 
HAMILTON, ADAMS & CO. 



MDCCCLXXXIV. 



EDINBURGH : 
HKINIED BY LORIMER AND GILLIES, 
31 ST. ANDREW SQUARE. 



TO 

FREDERICK J. MOUAT, M.D., 

A DISTINGUISHED GRADUATE AND A GENEROUS BENEFACTOR OF THE 
UNIVERSITY OF EDINBURGH, 

C^jjsc |;ccturcs 

ARE DEDICATED. 



PEEFACE. 



"PvURING the last winter session I delivered a short 
^ course of lectures introductory to the systematic 
description of the diseases of the nervous system, and I 
promised the members of the class that they should be 
published. 

They were accordingly taken down in shorthand by 
my friend, Dr. Maciver, and have been carefully revised, 
re-arranged, and expanded where, on consideration, it seemed 
desirable. 

I could not have accomplished the revision, and got them 
through the press, without the co-operation of my friend. 
Dr. Philip, to whom I am deeply indebted for his valuable 
assistance. I have also to thank my colleague, Dr. Argyll 
Robertson, for advice in regard to Lectures Y. and VI. ; 
and Drs. Graham Brown, Ireland, and Barlow, who have 
favoured me with many valuable suggestions. I am indebted 
to many of my professional brethren for illustrations, which 
they have kindly permitted me to use in this work ; and, 
above all, to Mr. Liebreich, who has allowed me to repro- 
duce a number of the exquisite representations of morbid 
ophthalmoscopic conditions originally published in his 
"Atlas;" and to Professors Flower and Hamilton for other 
illustrations. 

Those who are familiar with my systematic and clinical 



vi 



PREFACE. 



teaching, will observe that the lectures from the fourth 
to the twelfth constitute a commentary upon, and illustra- 
tions of, the method of examining and describing nervous 
symptoms which I have for many years employed in the 
hospital and the lecture-room ; while the first three lectures 
treat of the foundation upon which all accurate knowledge 
of nervous diseases must be built, and the last two bring out 
certain important points bearing upon the pathology of the 
nervous system, and some general considerations as to treat- 
ment. Those who are not acquainted with this method of 
investigating the nervous functions, will find it appended on 
the succeeding page. Of its utility I ca,n. speak from an 
experience now extending over many years. 

I hope that the lectures may prove useful to students and 
practitioners, by aiding them in their study and treatment 
of nervous diseases. 

T. GRAINGER STEWART. 

19 Charlotte Square, 
Edinburgh, 2lst Novcmher, 1884. 



METHOD OF INVESTIGATING THE NERVOUS 
EUNGTIONS. 



Sensory Functions. — Sensations (Pain — Heat — Cold — Formica- 
tion — Numbness — Tingling) — Sensibility to Touch. — Heat — Tickliug 
— Paia. Muscular Sense. Sight {Ophthalmoscopic Examination, if 
necessary). Condition of PupU. Hearing (Otoscopic Examination, if 
necessary). Taste. Smell. 

Motor Functions. — Organic Keflex {Swallowing — Breathing — 
Micturition — Defcecaiion, &c.) — Skin Reflex — Tendon Reflex — 
Voluntary {Systematic Examinations of Groups of Muscles, if neces- 
sary). Co-ordination — Electric Irritability {Faradic — Voltaic). 

Vasomotor and Nutritive Functions. — {Local Congestions — 
Pallor — (Edema — Perspiration, d:c. — Inflammation — Sloughing — 
Wasting). 

Cerebral and Mental Functions. — Consciousness {Exaltation of 
— Diminution of — Sleep — Trcmce, — Torpor — Coma — Perversions of — 
Delirium — Hallucinations — Hlusions — Delusions) — Attention — 
Memory — Judgment — Will — Emotions — Moral Sense — Speech 
{Comprehension of Language, Heard, Seen — Utterance of Language, 
Spoken, Written). 

Cranium {Peculiarities) — Spine {Form and Appearance — Percus- 
sion — Hot Sponge Test), 

Locomotory System. — Bones — Joints {Pain — Swelling — Effusion 
— Mobility) — Muscles {Rigidity — Flaccidity — Cramp — Twitching, 
General or Fibrillary — Hypertrophy — Atrophy). 



7 



CONTENTS. 



LECTURE I. 
Medical Anatomy of Nervous System. 

PAGES 

Introduction — Necessity for Preliminary Study of certain Sub- 
jects — Medical Anatomy of Nervous System — Lines of Sensory 
Conduction — Nerve-Endings in Skin — Course of Fibres into 
Spiaal Cord — Distribution in Cord — Decussation — Passage 
tbroiigb Medulla, Pons, and Crusta to Internal Capsule — Its 
Posterior Third — Passage to Posterior Convolutions — Olfactory 
Nerve : Peripheral Structures, Course and Deep Connections — 
Optic Nerve : Peripheral Structures, Course and Deep Connec- 
tions — Centre for Vision — Sensory Part of Fifth Nerve : Course 
and Deep Connections — Auditory Nerve : Peripheral Struc- 
tures, Course and Deep Connections — Sensory Part of Glosso- 
pharyngeal Nerve : Peripheral Structures, Course and Deep 
Connections — Sensory Part of Vagus : Course and Deep 
. Connections, 1 — 20 

LECTUEE II. 

Medical Anatomy op Nervous System — (Continued). 

Lines of Motor Conduction from Cortex Cerebri outwards — 
Psycho-motor Area — Its Histological Peculiarities — Corona 
Eadiata and Internal Capsule — Motor Fibres in Crura Cerebri, 
Pons, Medulla Oblongata, and Spinal Cord — Direct and 
Crossed Pyramidal Fibres — Origin of Spinal Motor Nerves — 
Motor Nerve-Endings in Muscle — The Cranial Motor Nerves — 
Third, or Oculo-Motor— Fourth, or Trochlear— Motor Division 
of Fifth— Sixth, or Abducens — Seventh, or Facial — Motor 
Part of Glosso-Pharyngeal— Motor Part of Vagus — Spinal 
Accessory — Hypoglossal, 21 — 32 

LECTUEE III. 
Medical Anatomy op Nervous System— (Co ?i<wmcrf)- 
Fibres Afferent to Cerebellum— Histological Arrangement in 
Cerebellum— Fibres Efferent from Cerebellum— Ganglia on 
Nerves, in Cord, Medulla, Pons, Crura Cerebri, Cerebrum, and 



X 



CONTENTS. 



Cerebellum— Commissural Fibres connecting different Parts 
of Nervous System— Diagrammatic Resumd of Anatomy of 
Cord, Medulla, Pons, and Cerebrum— Relationship of Con- 
volutions to the Surface of the Cranium— Sympathetic System, 33—56 



LECTURE IV. 

Sensory Functions. 

Subjective Phenomena — Pain — Girdle-Pain- Feelings of Heat or 
Cold — Cold with Pressure — Formication — Numbness — Ting- 
ling — Globus Hystericus — Giddiness — Sensibility to Impres- 
sions — Various Kinds — Contact — Pressure — Temperature — 
Tickling — Pain — Rate of Conduction — Hypersesthesia and 
Hyperalgesia — Anaesthesia and Analgesia — Dyssesthesia — 
Allochiria — Polysesthesia — Retarded Conduction — Muscular 
Sense, 57 — 72 

LECTURE V. 

Sensory Functions — (Continued). 

Eye Symptoms in Nervous Diseases — Subjective Phenomena — 
Flashes of Light — Muscse VoHtantes — Eye Symptoms in 
Megrim — Colour-Hearing — Blindness — Area of Vision — Tests 
— Perimeter — Central Scotoma — Marginal Scotoma — Partial 
Scotoma — Hemianopsia, Homonymous and Heteronymous, 
General Dimness — Snellen's Types — Colour Blindness, . 73 — 86 



LECTURE VI. 
Sensory Functions — (Continued). 

Eye Symptoms — Alterations of Pupil — Irregular Form — Myosis 
— Mydriasis — Argyll Robertson Symptom — Headache and 
Neuralgia due to Hypermetropia, Myopia, and Astigmatism 
— Ophthalmoscopic Examination — The Normal Fundus — 
Optic Neuritis — Not necessarily attended by Loss of Sight 
— Primary Optic Atrophy — Embolism — Retinal and 
Choroidal Changes. 

Ear Symptoms — Subjective — Hearing Increased, Diminished, or 
Prevented. 

Smell — Subj ective Symptoms — Increase — Diminution — Perver- 
sion of Smell. 

Taste — Subjective Symptoms — Increase — Diminution — Perver- 
sion of Taste, 87—106 



CONTENTS. 



PAGES 

LECTUEE VII. 

Motor Functions. 

Keflex Action— Organic Keflexes— Micturition— Respiration — 
Rapid and Slow — Cerebral — Cheyne-Stokes— Skin Reflexes 
— Plantar— Cremasteric — Gluteal — Abdominal— Epigastric 
—Lumbar and Dorsal— Scapular— Modifications — Tendon 
Reflexes— Patellar— Ankle Clonus— Spinal ;Epilepsy— Modi- 
fications— Paradoxical Contraction, 107 — 115 

LECTURE VIII. 

Motor Functions — (Continued). 

Voluntary Movement — Dynamometer — Paralysis — Paresis — 
Weakness from Disease of Muscles — Clioreic Movements — 
Clonic Spasms — Tonic Spasms — Athetosis — Saltatory Spasms 
and Eclampsia Nutans — Cramp— Cataleptic Rigidity — Con- 
tracture — Co-ordination — Definition — Inborn — Acquired — 
Mechanism subserving it — Failure from Sensory, Central, 
and Efferent Disease— Trade Spasms — Conjugate Deviation 
—Cough, 116—131 

LECTURE IX. 

Electricity in Diagnosis. 

Varieties of Electricity — Application — Direct Method — Indirect 
Method — Motor Points for Muscles — Galvanism — -Weak, 
Moderate, and Strong Currents — Symbols — The Galvanometer 
— Faradism — Electric Irritability Undisturbed, Increased, 
Diminished, Altered in Quality — Reaction of Degeneration — 
Electricity in Feigned Disease — Distinction between Trance 
and Death — Precautions necessary in using Electricity, . 132 — 145 

LECTURE X. 

Vaso-Motor, Secretory, and Trophic Functions. 

Vaso-Motor Functions— Neuro-Paralysis — Neuro-Spasm — Tache 
Cerebrale, &c. — Body Heat — Secretory Changes not Vaso- 
Motor— Saliva — Gastric Juice — Bile, &c. — Glycosuria — 
Trophic Changes— Nervous Olldema — Inflammation — Changes 
in Hair and Nails— Glossy Skin — Myxoedema — Lepra Anaes- 
thetica— Gangrene— Bed-Sores— With and Without Pressure 
—Muscular Atrophy— In Polio-myelitis Anterior— In In- 
fantile Paralysis— Wasting Palsy— Not Vaso-Motor— Changes 
in Joints— Changes in Bones— Facial Hemiatrophia, . .146—169 



xii 



CONTENTS. 



PAGES 

LECTURE XT. 

Cerebral and Mental Functions. 

Consciousness — E.valtation — Diminution — Sleep — Trance— Hyp- 
notism — Torpor — Coma — Perversion of Consciousness — 
Delirium — Hallucinations— Illusions — Delusions — Attention 
— Memory— Judgment— Will— Emotions— Moral Sense, . 170 — 179 

LECTUEE XII. 
Language. 

Diagrammatic Scheme of Speech. Eelationship — Peripheral Struc- 
tures — Seeing Centre — Hearing Centre — "Word - Seeing 
Centre — Word-Hearing Centre — Illustration — Automatic 
Language — Its Development — Organic and Functional Changes 
— Loss of Voluntary Speech — Varieties — Loss of Spoken 
Language — Aphasia — Loss of Written Language — Agraphia — 
Delayed Conduction — Scanning Utterance— Motor Paralysis — 
Aphonia — Interference Avith Co-ordinating Function — Stam- 
mering — Functional Aphasia— Anatomical Changes in such 
Cases —Definition of Terms, 180—195 

LECTURE XIII. 
Some Points bearing on the Pathology of Nervous Diseases. 

The Structures which are the Seat of Lesion in Nervous Disease — 
Histological Elements of the Nervous System — Lesions occur- 
ing in the Nervous System — Vascular Distribution in Relation 
to Nervous Disease — Observations of Duret and Heubner — 
Vascular Supply of Basal Ganglia and Neighbouring Parts — 
Vascular Supply of Cortex— Of Cerebellum, .... 196—205 

LECTURE XIV. 
The General Treatment of Nervous Diseases. 

Prevention — Treatment — General Management and Diet — Inter- 
nal Medicines — Nutrients and Tonics — Stimulants — Sedatives 
— Specific Remedies — Electricity — Faradisation — Galvanisa- 
tion — Other External Applications — Massage — Sedative Lini- 
ments— Counter-irritants— Blood-Letting— Regulated Mus- 
cular Exercise— Ling and Zander's Methods— Spinal Supports 
— Elastic Contrivances— Surgical Methods— Nerve-Section 
— Nerve - Stretching — Removal of Tumour — Tapping the 
Cranium—Trephining for Local Injuries— To relieve Tension, 206—220 



LIST OF ILLUSTEATIONS. 



FIG. PAGE 

1. Nerves of finger, witL. Pacinian corpuscles (KoUilcer), . . 3 

2. Pacinian corpuscle x 350 (KoUiker), ... .3 

3. Section of skin, showing touch papilla (Biesiadecki), . . 4 

4. End organ of Krause, from conjunctiva (Key and Eetzius), . 4 

5. Nerve-ending from cornea (Schultze), .... 5 

6. Semi-diagrammatic representation of the constitution of tlie 

posterior nerve-roots (after Dr. Ai'thur Thomson), . . 6 

7. Semi-diagrammatic representation of brain and spinal cord, show- 

ing lines of sensory and motor conduction (after Dr. Jas. Eitchie), 8 

8. Sensory band of fibres, radiating to. posterior part of cortex 

(Huguenin), ....... 9 

9. Median aspect of human brain (Ecker), ... . .10 

10. Section through olfactory mucous membrane (Schultze), . . 11 

11. Dissection to show general relation of cranial nerves (Quain), . 11 

12. Layers of retina (Schultze), . .... . . .12 

13. Diagrammatic representation of course, decussation, and distribu- 

tion of optic nerve-fibres, ... . . .13 

14. Lateral view of skull, with convolutions outlined, and cortical 

visual centre shaded, . . . . . .14 

15. Nuclei of cranial nerves (Erb), . . . . .15 

16. Vertical transverse section through basilar membrane and organ 

of Corti (after Waldeyer), . . . . .16 

17. Ending of auditory nerve in vestibule (after Eiidinger), . .17 

18. Nuclei of cranial nerves (Erb), . . . . .17 

19. Lateral view of skull, with convolutions outlined and cortical 

auditory centre shaded, . . . . . .18 

20. Section through rabbit's tongue, showing gustatory bulbs (Turner, 

after preparation by A. B. Stirling), . . . .19 

21. Nuclei of cranial nerves (Erb), . . . . .20 

22. Lateral view of skull, with the names of the chief convolutions 

marked, .... . . . . .22 

23. Lateral view of skull, showing convolutions and Ferrier's motor 

areas, . ... . . , .23 



xiv 



IJST OF ILLUSTRATIONS. 



24. Microscopic section of grey matter of frontal region (after 

Meynerl), 24 

25. Semi-diagrammatic dissection of medulla and pons to show course 

of fibres (after Quain), . . . . . ,25 

26. Decussation of pyramids (Quain), . . . . .25 

27. Transverse section of cord at different levels (Quain), . . 26 

28. Semi-diagrammatic representation of brain and spinal cord, to 

show the different lines of sensory and motor conduction, . 27 

29. Semi-diagrammatic section of spinal cord, showing composition 

of anterior nerve-roots, . . . . . .28 

30. Nerve-ending in muscle of lizard (after Kiihne), . , .29 

31. Nuclei of cranial nerves (Erb), , , . . .30 

32. Diagrammatic transverse section of cord, showiag fibres passing 

from cells of Clarke's column to the direct cerebellar tract, . 33 

33. Transverse section of cord at different levels (Quain), . . 34 

34. Microscopic section of the cortical portion of cerebellum (Saukey), 35 

35. Diagrammatic transverse section of cord, with groups of nerve- 

cells in grey matter, . . . . . .37 

36. Section through basal ganglia and island of Eeil (Quain), . . 39 

37. Diagrammatic transverse section of cord, showing groups of cells 

and chief tracts, . . . . . . .41 

38. Vertical transverse section of brain (after preparation by Professor 

Hamilton), . . . . . . .44 

39. Horizontal section of brain (after preparation by Prof. Hamilton), 47 

40. Vertical antero-posterior section of brain (after preparation by 

Professor Hamilton), . . . . . .50 

41. Lateral view of skull, showing relations of convolutions and sulci 

to sutures of skull, . . . . . .52 

42. Sympathetic nervous system (Flower), . . . .55 

43. ^stliesimeter, ....... 64 

44. M'Hardy's perimeter, . . . . . .76 

45. Perimetric record of normal field of vision, . . .78 

46. Perimetric record of visual field in central scotoma, . . 78 

47. Perimetric record of slight marginal scotoma, . . .79 

48. Perimetric record of marginal scotoma in advanced case, . . 79 

49. Perimetric record of scotoma in patches, . . . .80 

50. Perimetric record in case of hemianopsia (homonymous), . . 81 

51. Diagrammatic representation of course and decussation ol oplic 

nerve-fibres, showing effect of lesions, . . . .82 

52. Perimetric record of normal field of vision for colour, . . 85 

53. Perimetric record of field of vision for colom", as altered in case of 

tobacco colour-blindness, . . . . .85 

54. Ophthalmoscopic appearance of normal fundus (Liebreich), . 92 

55. Ophthalmoscopic appearance of optic neuritis (1st stage), (Liebricli), 95 



LIST OF ILLUSTRATIONS. 



XV 



FIG. 



PAGE 

56. Ophtlialnioscopic appearance of optic neuritis (2nd stage), 

(Liebreicli), . . • • • • .95 

57. Oplitlialmoscopic appearance of optic neuritis (3rcl or atrophic 

stage), (Liebreicli), . . • • • .95 

58. Ophthalmoscopic appearance of primary optic atrophy (Liebreich), 95 

59. Ophthalmoscopic appearance in case of embolism of retinal vessels 

(Liebreich), .... . . .98 

60. Ophthalmoscopic appearance in case of embolism of retinal vessels 

(later, atrophic stage), (Liebreich), . . . .98 

61. Ophthalmoscopic appearance in case of tubercle of the choroid 

(modified from Bouchi;t), ..... 101 

62. Tracing of cerebral breathing, . . . . .110 

63. I. Tracing of Cheyne-Stokes breathing ; II. Eelation of the differ- 

ent elements in Cheyne-Stokes breathing to action of the heart, 110 

64. Dynamometer (Collin), . . . . . .116 

65. Microscopic section of radial nerve, from case of peripheral paralysis, 118 

66. Contracture of muscles of arm, . . . . .127 

67. Motor points of forearm (Ziemssen), .... 133 

68. Motor points of forearm (Ziemssen), . . ... 134 

69. Motor points of head and neck (Ziemssen), . . .135 

70. Motor points of lower limb (Ziemssen), . . . .136 

71. Motor points of lower limb (Ziemssen), .... 136 

72. Motor points of leg (Ziemssen), ..... 137 

73. Motor points of leg (Ziemssen), . . , . .138 

74. Diagram illustrating reaction of degeneration (rapid recovery), 

(Erb), 143 

75. Diagram illustrating reaction of degeneration (slow recovery), 

(Erb), 143 

76. Diagram illustrating reaction of degeneration (no recovery), (Erb), 144 

77. Altered physiognomy in exophthalmic goitre, . . .147 

78. Gangrene of hand from nerve disease, . . . .159 

79. Gangrene of foot from nerve disease, .... 159 

80. Acute bed -sore on gluteal region of paralysed side in case of 

cerebral apoplexy (Charcot), . . , , .161 

81. Acute bed-sore of sacral region in case of partial spinal myelitis 

(Charcot), . . . . . . ,161 

82. Ill-developed arm in adult, resulting from attack of poliomyelitis 

anterior acuta in infancy, . . . . .164 

83. Advanced case of progressive muscidar atrophy, . . . 165 

84. Case of pseudo-hypertrophic paralysis, . . . . .166 

85. Altered os innominatum from case of locomotor ataxia (after 

Charcot), 1(37 

86. Altered head of femur from case of locomotor ataxia (after 

Charcot), 



xvi 



LIST OF ILLUSTRATIONS. 



FIG. PAGE 

87. Altered physiognomy in facial heniiatrophia, . . . 169 

88. Diagrammatic scheme of speech relationships, . . . 181 

89. Similar diagrammatic scheme modified, to illustrate automatic 

speech, ......... 186 

90. Multipolar nerve-cell (after Quain), .... 197 

91. Nerve-fibre (Quain), ...... 198 

92. Non-medullated nerve-fibres (Quain), .... 198 

93. Neuroglia (Quain), . . . . . . .199 

94. Arterial distribution at bas6 of brain (Charcot), . . . 201 

95. Cortical arterial supply (Duret), ..... 203 

96. Apparatus for regulated muscular movement of arms, shoulders, 

and chest, ....... 215 

97. Apparatus for regulated miiscular movement of legs and back, . 216 

98. Distortion of vertebral column after recovery from caries of 

cervical vertebra, . . . . . .217 



AN 

INTEODUCTION TO THE STUDY 

OF THE 

DISEASES OF THE NERVOUS SYSTEM. 



LECTURE I. 

Introduction. — Fecessity for Preliminary study of certain Subjects. — 
Medical Anatomy of Nervous System. — Lines of Sensory Conduc- 
tion. — Nerve-Endings in Skin. — Course of Fibres into Spinal 
Cord. — Distribution in Cord. — Decussation. — Passage through 
Medulla, Pons and Grusta to Internal Capsitle. — Its Posterior 
Third. — Passage to Posterior Convolutions. — Olfactory Nerve: 
Peripheral Structures, Course and Deep Connections. — Optic 
Nerve : Peripheral Structures, Course and Deep Connections. — 
Centre for Vision. — Sensory Part of Fifth Nerve : Course and 
Deep Connections. — Auditory Nerve: Perip)heral Structures, 
Course and Deep Connections. — Sensory Part of Glosso-pharyn- 
geal Nerve : Peripheral Structures, Course and Deep Connections. 
— Sensory Part of Vagus : Course and Deep Connections. 

n ENTLEMEN — You will find that your study of the 
^ individual diseases of the nervous system becomes 
much easier if you first master certain general facts regard- 
ing its anatomy and physiology in health and in disease, 
and I purpose to give you this session a series of lectures 
on these points before I take up the diseases individually. 
These preliminary topics divide themselves into four groups 
(1.) The medical anatomy of the nervous system — that is 
to say, the structure of the nervous system in its relation to 

B 



2 



LINES OF SENSORY CONDUCTION. 



practical medicine, and ttie localisation of nervous diseases. 
(2.) The functions of the nervous system, with the various 
methods of determining their condition, the alterations which 
they undergo in disease, and the clinical significance of these 
alterations. (3.) The morbid processes Avhich occur in the 
nervous system, with a consideration of anatomical condi- 
tions which influence the development of the various lesions. 
(4.) General considerations regarding the treatment of nervous 
diseases. 

I. Medical Anatomy of the Nervous System. 

I shall speak first of the cerebro-spinal system, and aftei'- 
wards of the sympathetic. In describing the cerebro-spinal 
system, I shall ask you to notice (1) the line of the sensory 
fibres from the periphery inwards to the sensory centres in 
the cerebral convolutions ; (2) the line of the motor fibres, 
from the motor cerebral convolutions outwards ; (3) the line 
of the afferent fibres to the cerebellum inwards ; (4) the 
line of the efferent fibres from the cerebellum outwards ; 

(5) the superadded ganglia on nerves, in the spinal cord, 
and the medulla oblongata, and at the base of the brain ; 

(6) the commissural fibres connecting different parts of the 
nervous system together ; and (7) some general statements 
as to localisation. 

We shall consider first the Line of the Sensory Fibres 
from the Periphery inwards to the Sensory Centres in the 
Cerebral Convolutions. You are familiar, from your previous 
studies, with the various forms of nerve-endings which 
receive sensory impressions. You observe in the drawings 
the features of some of those which are best recognised. 
In fig. 1 you perceive the general arrangement of the 
Pacinian bodies on the nerves of the finger, and you will 
remember that they occur also in the toes, the arms, the 
neck, the thorax, the genital organs, the joints, the peri- 
osteum, and the mesentery. 

In fig. 2 you see the appearance of a Pacinian body 
magnified 350 diameters. 

In the papillfB of the skin, there are other end-organs 



SENSORY NERVE-ENDINGS. 3 

known as toiicli corpuscles, and first described by E. Wagner 




Fia. 1. — Serves of finger, with Pacinian corpuscles (Kolliker). 
Flo. 2. — Pacinian corpuscle x 350 ; a, peduncle ; !), nerve-flbre ; c and d, con- 
nective tissue capsule ; e, axis cylinder, with/, branching terminal end (KSlliker). 



and Meissner. Their position and general character is shown 
in fig. 3. 



4 



SENSORY NERVE-ENDINGS. 




Fio, 3. 

Section of skin, showing a, vascular papilla ; 6, touch papilla : 
c, blood-vessel; d, nerve-fibre going to touch corpuscle (e); 
f, transversely-cut nerve-fibre (Biesiadecki). 




l<"lo. 4. 

End organ of Krauso, from conjunctiva ; axis cylinder 
breaking up into a number of branches (Key and Retzius). 



LINES OF SENSORY CONDUCTION. 



5 



In the conjunctiva there are end-organs which, were first 
described by Krause, In 
fig. 4 you perceive the 
appearance of these 
bodies with the nerve- 
fibre entering them, the 
axis cyhnder dividing 
into several branches, 
which become convol- 
uted and lost in the 
matrix. 

Besides these definite 
end - organs there are 

other arrangements of ^ , . 

° Nerve-ending in cornea. Axis cylinder breaking up 

nerve-PerilDherSe as, for into branches, wMch ramify among tlie tissue elements 

T F I (Ma.\; Schultze). 

example, m the cornea, 

where fine ramifications of the axis cylinder are distributed 
among the elements of the tissue (fig. 5). 

From these nerve-endings the sensory fibres start, and 
gathering, along with other fibres, into nerve-branches and 
nerve-trunks, they make their way to the spinal cord, entering 
it by the posterior nerve-roots. They pass into the cord in a 
somewhat oblique manner. The distribution, so far as it is at 
present ascertained, may be traced in this diagram (fig. 6). 

Two difierent courses are followed by the fibres of the pos- 
terior root on entering the cord. 

1. The external set (A) — rather the smaller — passes directly 
towards the grey matter, their course being upwards in a 
sHghtly oblique direction through the substantia gelatinosa 
of Eolando. In this structure the fibres spread out, the 
substance itself acting as a kind of support for them. The 
further distribution is even more complicated. The greater 
number of the fibres (a) apparently do not go beyond 
the substance, but bend on themselves and come to run 
vertically, both in an upward and a downward direction, 
close to the junction of the gelatinous substance with the 
grey matter proper ; possibly they pass in horizontally higher 
up. Some of the fibres (b) pass horizontally into the pos- 
terior horns of grey matter, where they are lost, possibly 




6 



SENSORY FIBRES IN CORD. 



ending in the spindle-shaped colls there. Some fibrils (c), 
however, pass to the anterior cornua, while others can be 
traced to the posterior commissure, by which they cross to 
the other side. 




Fig. 6. 

Semi-diagrammatic representation of the constitution of the posterior nerve-roots 
(Dr. Arthur Thomson). For explanation of lettering, see text. 

2. The internal (B) or median set of fibres passes first into 
the external division of the posterior column, the fibres then 
bend on themselves and pass (/) for some distance upwards, 
and, according to Stilling, also downwards. They then 
penetrate the grey matter almost horizontally. It is not 
certain whether all of these fibres make this second bend into 
the grey matter, or whether some are not continued up directly 
through the posterior column to the brain. On reaching the 
grey matter, the fibres spread out, some entering the cells of 
the posterior horn ; some (g) ajaparently joining the lateral 
cells of the anterior cornua ; others (h) passing to the cells 
of Clarke's column ; and others (i) winding through the 
anterior commissure to the other side, reaching the cells of 
the anterior horn. 

From these structures fibres proceed which form the 



LINES OF SENSORY CONDUCTION. 



7 



postero-meclian column, which is composed of long fibres, 
and are believed by some to convey sensory impressions from 
the legs. In the cervical region the postero-lateral columns 
come to contain similar afferent fibres, which probably convey 
sensory impressions from the arms.. 

There is reason to think that the sensory fibres subserving 
different kinds of impressions are distinct from one another, 
and occupy different parts of the cord. It appears, for, 
example, that impressions of pain and of temperature are trans- 
mitted by deeper portions of the cord than are the ordinary 
tactile impressions. But it seems as if while ordinary sen- 
sory impressions are usually conducted along the posterior 
column, they may be, under certain conditions, transmitted 
through the grey matter. You observe that these relation- 
ships are very complicated, and by no means definitely 
ascertained ; but the fact of the decussation of the sensory 
fibres near their point of entrance to the cord has been known 
for many years, and is of the utmost clinical importance. The 
fibres for impressions of pain and temperature decussate on 
entering the cord, those for tactile impressions a little higher 
up, while those subserving the muscular sense cross at the 
medulla oblongata. Some of the most important of these 
relationshijDS may be seen in the accompanying drawing 
(fig- 7). 

The course of the sensory fibres in the medulla oblongata, 
pons varolii, and crura, is very complicated, and not yet 
fully ascertained. It is certain that the funiculus gracihs 
is the upward continuation of the postero-median column, 
and the funiculus cuneatus of the postero-external. These 
contain nuclei, into which the fibres enter. The posterior 
horns pass up, and spreading outwards are further continued 
in the formatio reticularis. From the nuclei of the funiculus 
gracilis and funiculus cuneatus, fibres pass upwards in the 
inter-olivary fibres, and also into the formatio reticularis. In 
the pons these tracts are continued in the formatio reticularis 
and the fiUet. In the crura cerebri the tracts pass upwards 
in the outer part of the tegmentum external to the red 
nuclei. The fibres then pass into the posterior third of the 
internal capsule. Its fibres, on reaching the level of the 



O LINES OF SENSORY CONDUCTION. 

upper middle part of the optic thalamus, radiate towards the 
cortex (fig. 8). 

The most recent researches of Terrier indicate that 




Fio. 7. 

Semi-diagrammatic representation of brain and spinal cord, to sliow the different lines of 
sensory and motor conduction, founded upon a schema by Dr. James Uitchie. 

C.CAL., corpus callosum ; NC, caudate nucleus; NL, lenticular nucleus; CL, claustrium ; 
OT, optic tlialamua ; Cr, crusta ; Teg, Tegmentum ; CQ, corpora quadrigemina ; CD, corpus 
dentatum ; SP, superior peduncle ; MP, middle peduncle ; IP, inferior peduncle ; 0, olivary 
body; TuN, Triangular nucleus; CL.N, clavate nucleus; M, muscle; S and T, sensory end 
organs. 

entire destruction of the hippocampal region (the hippocam- 
pus major and gyrus hippocampi) and the neighbouring inferior 



CENTRES FOE GENERAL SENSORY IMPRESSIONS, 



9 



temporo-splienoidal region (fig. 9, H, TS), causes complete 
anaesthesia — cutaneous, mucous and muscular — of the opposite 
side of the body. Thus it appears that in this region the 
centres for general sensory impressions are situated. That it is 
so localised is further shown by the same authority, who finds 
that no other cortical lesion interferes with tactile sensibility, 
and moreover that, in proportion to the amount of destruction 
ia the hippocampal region, touch is impaired. These con- 




i'lu. 8. 

Sensory band of fibres (6) radiating backwards to posterior part of cortex (Huguenin). 

elusions are opposed to those arrived at by Munk, Tripier, Molle, 
and others, but I have much confidence in the accuracy of 
Professor Ferrier. Further experimental and pathological 
mvestigations will soon test the correctness of his opinion. 

Now, when you consider the very large number of afferent 
fibres derived from the whole cutaneous surface, as well as 
from internal parts, it becomes apparent that nothing like 
the whole of these fibres reaches the cerebral convolutions. 



10 



OLFACTORY NERVE. 



Many of tliem, no doubt, subserve reflex functions, and 
terminate in lower ganglia ; and we do not at present know 
liow it is that the fibres are arranged so that structures so 
small as the cervical portion of the cord and the medulla 
oblongata are capable of conveying distinct and separate 
impressions derived from so many parts. It is supposed by 
some that the conduction of these impressions in the cord is 
not direct by fibres, but that there are loops and communica- 
tions with nerve -cells on the way. 




Fig. 9. 

Median aspect of human brain ; Gf, gyrus fornicatus ; U, sulcus hippocampi : iT, gyrus hippo- 
campi ; U, subiculum cornu ammoni ; I'.S, inferior temporo-sphenoidal convolution (Ecker). 



Besides the sensory fibres of the skin, the muscles, and 
other internal parts of the body, there is a large number of 
special sensory fibres with whose course you must also be 
acquainted. 

Tlie olfactory nerves have their point of origin in the 
Schneiderian membrane. In this drawing (fig. 10), you 
see the form of the nerve-ending as seen in man. It 
consists of slender processes (e) projecting slightly beyond 
the general surface of the membrane, between the ordmary 
columnar cells (a) of the region, and continuous below with 



OLFACTORY NERVE. 



11 



peculiar spindle-shaped cells (b), containing large prominent 
nuclei, wliich in all probability pass into the fibrils (cZ) of the 
olfactory nerve. The fibres pass from the Schneiderian mem- 
brane to the olfactory bulb, which is lodged in the olfactory 
sulcus. From this the tract j)roceeds and divides as it passes 





Fio. 10. 

Section through 
olfactory mucous 
membrane, a, epi- 
thelium cell ; b, ol- 
factory nerve ceU, 
with (c, e) its peri- 
pheral termination, Fia. li. 

™°i'!l'«I'rf ?l!li''*il''^'v" Dissection to show general relation of cranial nerves. Nerves are 

mwation (Schultze). indicated in order with Roman numerals (Quain). 

backwards into three lines (fig. 11 L), formerly described as 
the three roots of the olfactory nerve. A more correct view, 
according to the most eminent anatomists, is that the so-called 
central grey root is not really a root, but a portion of grey 
matter, the tuber olfactorium, representing the forward pro- 



12 



OPTIC NERVE, 



jection of the anterior cerebral vesicle in the embryo. The 
outer root passes outwards and backwards along the anterior 
margin of the perforated space towards the Sylvian fissure, 
Avhere it disappears from the surface. The inner root passes 
obliquely inward to the side of the great longitudinal fissure 
between the hemispheres. Of the further 
course and deeper relations of these fibres 
there is no definite knowledge at present. 
Neither are the precise limits of the centre 
for smell as yet ascertained. But there can 
be no reasonable doubt that it is situated 
towards the tip of the temporo-sphenoidal 
lobe. 

The nerve- endings for vision are very 
complicated. They consist of (fig. 12) — 
First, the internal limiting membrane (1) ; 
second, the layer of optic nerve-fibres (2) ; 
third, layer of large gangHon cells (3) ; 
fourth, the internal molecular layer (4) ; 
fifth, the internal granule layer (5) ; sixth, 
the outer granulated or molecular layer 

(6) ; seventh, the external granule layer 

(7) ; eighth, the outer limiting membrane 

(8) ; and ninth, the layer of the rods and 
cones (9). Originating thus in the retinal 
structures, the nerve-fibres pass along the 

Different layers of tlie ■,. r ,^ ,• , .^ • 

retina. For explanation linCS 01 tnC OptlC UCrVCS tO tbe COmmiS- 
of numbers see text. i , i , • i • c , t 

(Schuitze). sure, and there a partial crossing oi the 

fibres takes place. In fig. 13 you can trace the lines of the 
different fibres. You perceive that those originating in the 
corresponding halves of the two retina3 meet behind the com- 
missure in the optic tract. Each optic tract divides into two 
processes, as you can easily make out with the naked eye (fig. 1 1). 
One of these — the externcd — passes backwards to the external 
geniculate body (fig. lie) and appears to terminate in it. Some 
of its fibres really do so, but some proceed to the pulvinar, 
some over the external geniculate body to the stratum zonale, 
— that is, the superficial layer of white matter, — Avhile others 
pass under the external geniculate body and penetrate deeply 




OPTIC NERVE. 



13 



into the pulvinar. On examination of tlie parts with the 
naked eye, one cannot overlook the distinct band of fibres 
which proceeds from the external geniculate body, or from its 
immediate neighbourhood, towards the anterior cor^^us quad- 
rigeminum, constituting what is known as the brachium of 
that body. The internal passes to the corpus geniculatum 
internum (fig. 1 1 i), where some fibres end, others are described 
as passing over its surface to the anterior corpus quadri- 
geminum of its own side. Experiments seem to show that 



LEFT EYE RIGHT EVE 




Fig. 13. 

Diagrammatic representation of course, decussation, and 
distribution of optic nerve-fibres. 



the relation of the internal geniculate body to sight is not 
nearly so intimate as is that of the external. From these 
gangUa, fibres proceed backwards to join those connected' with 
the^ other sensory fibres in the posterior part of the corona 
radiata, and make then- way to the cortical centre for vision. 
We have, as yet, no demonstration of decussation further 
back than the chiasma ; though it is supposed by some that 
further decussation takes place at the corpora quadrigemina 
in such a way that both lateral halves of each eye stand 



14 



VISUAL CENTRE. 



related exclusively to the sight centre in the opposite hemi- 
sphere. ^ We shall see later on that clinical facts are opposed 
to this view. The optic nerve is said also to derive fibres 
from the medulla oblongata and the spinal cord. These 
connections are probably related to the movements of the 
eyeballs, the iris, and other parts. 

Munk's observations and experiments indicate that the 
cortical centre for vision is on the outer convex surface 
of the occipital lobe ; while those of Terrier lead us to 
conclude that the function resides also in the angular 
gyrus. He has found that lesions of the occipital lobes 




Fig. 14. 

Lateral view of skull,* with convolutions outlined and cortical visual centre shaded. 



and angular gyri cause affections of vision, without inter- 
ference with other kinds of sensation or of motion ; that 
the only lesion which causes complete and permanent loss 
of vision in both eyes is total destruction of the occipital 
lobes and angular gyri on both sides. Destruction of both 
angular gyri alone does not suffice to produce this effect. It 
causes temporary total bhndness, succeeded by lasting visual 

* In preparing tlie various figures illustrating tlie convolutions on the 
external surface of the brain, I have made use of a skull, with the sulci 
outlined, presented to me by my friend, Dr. Alex. Bruce. Tlie outlines 
were revised by Professor Charcot. 



SENSORY PORTION OF FIFTH. 



15 



liv 



defect. If the cortical portion of the angular gyrus of one 
side be destroyed, there is temporary abolition or impairment 
of sight of the opposite eye, not hemiopic. He finds, further, 
that destruction of the occipital lobe and angular gjnrus on 
one side causes temporary amblyopia of the opposite eye, and 
homonymous hemianopsia towards the side opposite the lesion ; 
but, on the other hand, he failed to produce hemianopsia by 
removing the greater portion of one occipital lobe, or even 
both. A monkey, with both occipital lobes removed, gave 
unmistakeable evidence of vision within two or three hours. 
We are thus entitled to believe that the centre for vision is 
in the occipito-angular region, and that each eye is related 
to these regions of both sides of the brain. 

In fig. 1 4 the deeply-shaded part corresponds to the centre for 
vision, involving the supra- marginal lobule, the angular gyrus, 
and the occipital lobe. 

The next afferent 
nerve that we have to 
consider is the sensory 
2Jortion of the fifth. 
Its nerve-endings pre- 
sent no peculiarity, 
and, with regard to its 
course, we have only 
to note that it passes 
through the Gasserian 
ganglion and becomes 
connected with the 
nerve-centre by seve- 
ral roots. Its nuclear 
connections are dia- 
grammatically repre- 
sented in fig. 15. 
Some fibres proceed to 
a nucleus analogous to 
those in the posterior 
hornofthegreymatter fio. 15. 

nf ihp. or>r-A T+ °{ nerves. Roman figures indicate the 

Ui bue OOra. it con- numberofthenorve; i'l/./cr., decussation of pyramids (Erb). 

tains only small ganglionic cells, and is situated on a level 




16 



AUDITORY NERVE. 



with the point of exit of the fifth nerve from the pons, 
towards the outer part of the anterior segment of the floor 
of the fourth ventricle. Other fibres proceed to a nucleus 
in the posterior column of the cord, some of the fibres 
passing as far down as the middle of the neck. There 
are also connections with the crura cerebri and Avith the 
cerebellum. The further course of fibres from these nuclei 
to the cortical sensory centres is not ascertained ; but it 
appears that the fibres pass upwards to the junction .of the 
upper and middle thirds of the pons, where they decussate. 
They then pass upwards in the outer part of the teg- 
mentum, to reach the posterior third of the internal capsule, 
and into the corona radiata in its lowest part. It is 
worthy of remark how intimate the connections are between 
them and the various motor nerve -nuclei in the neigh- 
bourhood. 

The next avenue into the sensory centres is the auditory. 
The drawing (fig. 16) represents the endings of the auditory 




Fig. 16. 



Vertical transverse section through basilar membrane 
i innpr liiir cell • ir inner, and or, outer rod of corti, o, outei nair ceii. 
c« cochlear nerve; sjrsupporting' cells; SV, scala vestibu i ; «!Zf mem 
hm^rTRk^nex ; DC, dukus cochlearis ; ST, scala tympani ; basiUr 
membraner niem'brana tectoria; rm, reticular membrane (after 
Waldeyer). 

nerve-fibres within the cochlea. You remember the arrange- 
ment of the organ of Corti, consisting of a series of cells 



AUDITOEY NERVE. 



17 



ranged along the basilar membrane (6m) in two groups, an 
outer (o) and an inner (i), these cells, armed with hairs, which 
project through the processes in the reticular membrane (rm) 
into the endolymph, occupying the cavity of the ductus coch- 
learis (DC). In the vestibule there are auditory cells with 
hairs (fig. 1 7, p) projecting into the endolymph beyond the 
plane of the endothelial surface, and continuous with the 
auditory nerve-fibres (fig. 17, n). The arrangement in the 
semi-circular canals is similar to that in the vestibule. 




Fig. 17. 

Ending of auditory 
nerve in vestibule, n, 
nerve fibres ; p, peri- 
pheral, and c, central 
termination of auditory 
cells ; cl, ordinary col- 
umnar cells (after 
Kiidinger). 



-Fig. 18. 

Nuclei of cranial nerves. Roman numerals indicate nerves 
in succession (Erb). 



The nerve passing through its canal reaches the surface of 
the encephalon at the lower edge of the pons (fig. 11, viii.) on 
the outer side of and close to the facial nerve, and its fibres 
pass to four nuclei, all of which are situated in or close to 
the floor of the fourth ventricle. The position of these nuclei 
is shown m the drawing (fig. 18, viii.) — the anterior median 
nucleus, the posterior median nucleus, the anterior lateral 
nucleus, and the posterior lateral nucleus. The course 

c 



18 



AUDITORY CENTRE. 



of fibres from these nuclei to the sensory centre in the 
convolutions is not at present clearly made out, but no 
doubt decussation takes place, and fibres pass upwards in 
the internal capsule. We know that some of the fibres 
from the anterior nuclei pass by the cerebellar peduncles 
to the cerebellum, and it is very probable that these fibres in 
some way subserve the function of equilibration. 

The researches of Terrier have rendered it certain that the 
superior temporo-sphenoidal convolutions are the cortical 
centres for hearing. He finds that destruction of these con- 
volutions on both sides causes complete and permanent deaf- 




FiG. 19. 



Lateral view of skull, -with convolutions outlined and cortical auditory centre shaded. 

ness, without other sensory or motor defect. In fig. 19 
I have marked the centre for hearing the superior temporo- 
sphenoidal convolution. 

The next set of sensory fibres that we have to consider 
are those of the glosso-pharyngeal. Its nerve- endings 
are very characteristic. They consist of the taste bulbs, 
situated mostly in the circumvallate papillse of the tongue, 
but also at its point and along its margins, as also on 
the soft palate and the palatal arches, perhaps also in 



GUSTATOKY NERVE. 



19 



the beard palate and about tbe entrance of the larynx. 
In fig. 20 you perceive tbe characters of these bulbs or 




Ej3 G 



Fig. 20. 

Section through rabbit 's tongue, showing (G) gustatory bulbs in relation to V, 
capillary bloofl-vessels, and Ep, epithelial layer of mucous membrane (Turner, 
after preparation by A. B. Stirling). 

goblets. The drawing is from the tongue of a rabbit, and 
shows at several points tbe external openings of tbe bulbs. 
The nerve passes by a series of five or six roots arranged 
vertically into the medulla close to the auditory nerve (fig. 
11, ix.). They proceed upwards and inwards into a nucleus 
adjacent to that of the vagus in the lower half of the floor 
of the fourth ventricle (fig. 21), and this nucleus, again, is 
probably connected by fibres with which we are not acquainted 
with the sensory centre in the convolutions. 

The fact of the existence of such a connection is, however, 
established by tbe occurrence of loss of taste on one side of 
the tongue in certain cases of hemiplegia due to lesion of the 
internal capsule. The cortical centre for taste, though not 
yet positively ascertained, appears to be situated about the 
region of the subiculum cornu ammonis (fig. 9, p. 10, IT). 

The last set of sensory fibres are those of the imeumogastric 
or vagus, which conveys sensory impressions from the larynx, 
the lungs, the oesophagus, the stomach, and the heart. Its 
endings present, so far as we know, no special peculiarity, 
and the fibres pass upwards and enter the medulla by a long 
series of bundles in line with those of the glosso-pharyngeal 
nerve (fig. 11, x.). Its nucleus, partially divided into a 
greater central and a smaller lateral part by the so-called 



20 SENSORY FIBRES OF VAGUS. 

solitary or respiratory bundle, is situated in the medulla 
oblongata in the lower part of the floor of the fourth 
ventricle, just external to the nucleus of the hypoglossal 




Fig. 21. 

Nuclei of cranial nerves. Koman numerals indicate nerves in succession (Erb). 

nerve (fig. 21). It may be assumed, although we have as 
yet no demonstration of the fact, that fibres pass upwards 
from the nuclei to the sensory centres in the convolutions. 

Such is in outline the medical anatomy of the sensory 
structures so far as it is at present ascertained. 



LECTUKE 11. 



Medical Anatomy of Nervous System (continued). — Lines of Motor 
Conduction from Cortex Cerebri outwards. — Psycho-motor Area. 
— Its Histological Peculiarities. — Corona Radiata and Internal 
Capside. — Motor Fibres in Crura Cerebri, Pons, Medulla 
Oblongata, and Spinal Cord. — Direct and Crossed Pyramided 
Fibres. — Origin of Spinal Motor Nerves. — Motor Nerve-endings 
in Muscle. — The Cranial Motor Nerves. — Third, or Oculo- 
motor. — Fourth, or Trochlear. — Motor Division of Fifth. — Sixth, 
or Abducens. — Seventh, or Facial. — Motor Part of Glosso- 
pharyngeal. — Motor Part of Vagus. — Spinal Accessory. — Hypo- 
glossal. 

ENTLEMEN, — We now proceed to consider the second 
point in the medical anatomy of the nervous system, — 
the lines of conduction of motor impulse from the psycho- 
motor centres in the cerebral convolutions to the muscular 
fibres throughout the body. These convolutions have been 
definitely made out within the past few years, mainly by the 
experimental researches of Fritsch and Hitzig in Germany, and 
of Ferrier in this country, and by the clinical observations of 
Hughlings Jackson, Broadbent, Charcot, and many others. If 
you refer to the drawing of the surface of the brain, you per- 
ceive that on many of the convolutions there are marks indicat- 
ing the motor function proper to the part. You observe that 
the motor area extends from about the posterior end of 
the horizontal frontal convolutions to the postero-parietal 
lobule, following the line of the ascending parietal convolu- 
tions, and that the function does not appear closely to 
correspond to the anatomical folds and fissures. 

I am inclined to think that the balance of evidence is in 
favour of the belief that in the primates this grey matter is 
the starting point of voluntary motor impulse, for it has been 

21 




22 



LINES 01'' MOTOR CONDUCTION. 



proved that irritation of such parts leads to spasm in certain 
groups of muscles, while destruction leads to paralysis. It is 
true that the results obtained by Professor Goltz, with respect 
to the dog, tend to controvert this view, but on the whole the 
balance of evidence seems to me to confirm it. 

For convenience of reference, I put fig. 22 to remind you 
of the names of the different convolutions and sulci, and 
fig. 23, in which I have marked Dr. Terrier's motor centres. 

The motor area, you observe, occupies most part of the 
parietal region, and the posterior part of the frontal. 




C 



Fsa. 22. 

Lateral view of skull, with tbe names of chief cerebral convolutions marked. 



Commencing above the fissure of Sylvius, and behind its 
ascending ramus, — occupying, therefore, the lower part of the 
ascending frontal and the inferior frontal convolution, and 
including a little of the ascending parietal convolution, — is the 
centre for the movement of the lips and tongue, as in articula- 
tion (9 and 10). This includes what has been named Broca's 
convolution, from his having made out its relation to aphasia. 

Immediately behind this centre, above the fissure of 
Sylvius, — occupying, therefore, the lower part of the ascend- 



PSYCHO-MOTOR CENTRES. 



23 



ing parietal convolution, — is tlie centre for movement of the 
platysma myoides and retraction of the angle of the mouth 

Extending in series along the ascending parietal convolu- 
tion, are the centres for movements of the hand and wrist 
(a, h, c, and d). 




Fig. 23. 

Lateral view of skull, showing convolutions and Ferrier's motor areas. 



1. Centre for movements of opposite leg and foot — e.g., in walking. 
2-) 

3. V Centres for complex movements of arms and legs — e.g., m swimming. 
i.) 

B. Centre for extension forward of arm and hand. 

6. Centre for movements of hand and forearm where biceps is implicated. 

7. Centre for elevators. 

8. Centre for depressors of angle of mouth. 

j- Centre for movements of lips and tongue, as in articulation. 

11. Centre for retraction of angle of mouth (platysma). 

12. Centre for lateral movements of head and eyes, with elevation of eyelids and 

dilatation of pupils. 
a, h, c, and d, Centres for movements of hand and wrist. 

At the upper and posterior extremity of this, occupying 
the postero-parietal lobule, is the centre for movements of the 
leg and foot, as in locomotion (1). 

In the ascending frontal convolution, there are situated 
above the area first described, the centres for the depression 
(8) and the elevation (7) of the angles of the mouth. 

Above this, in the same convolution, and coming near to 



24 



PSYCHO-MOTOK CENTRES AND 



the supero-frontal sulcus, is the centre for movements of hand 
and forearm, in which the biceps is particularly engaged (6). 
Above this, at the upper end of the ascending frontal 

convolution, reaching also backwards 
into the ascending parietal and for- 
wards into the posterior extremity of 
the first frontal, are centres for com- 
plex movements of arms and legs, such 
as are concerned in climbing and 
swimming (2, 3, and 4). 

In front of this centre, occupying 
mainly the posterior extremity of the 
superior frontal convolution, but 
impinging somewhat upon the second 
and upon the ascending frontal con- 
volution, is the centre for extension 
forward of the arm and hand, as in 
putting forth the hand to touch some- 
thing in front (5). 

In front of this, and occupying a 
wide area in the middle and in the 
superior frontal convolutions, is a 
centre for lateral movements of the 
head and eyes, with elevation of the 
eyelids and dilatation of the pupils 
(12). 

The minute structure of these 
motor convolutions has been described 
as differing from that of the rest of 
the brain. The prevailing type of 
structure in the cerebral convolutions 
is what is described as the five-layer 
type. If you refer to fig. 24 you 
perceive that there is, first, nearest 
the surface a layer containing few 
ordinary nerve-structures, and mostly 
composed of fibrous tissue (1) ; second, a grey layer rich in 
small pyramidal nerve-cells (2) ; third, a thicker grey layer 
containing numerous longer pyramidal cells, the longest being 




Fig. S4. 

Microscopic section of grey 
matter of frontal convolution 
(x 100). For explanation of 
numbers see text (after Meynert). 



THEIR HISTOLOGICAL STRUCTURE. 



25 



generally those situated towards tlie deepest part (3) ; fourth, a 
layer containing ill-defined globular cells (4) ; fifth, a layer in 
which we find fusiform cells, which are generally arranged in a 
transverse manner, and appear to be connected with commis- 
sural structures, of which I have to speak afterwards (5). Now, 
Betz beHeves that the pyramidal giant-cells are most abundant 
in the anterior lobes ; that in the dog they exist only in 
Ferrier's psycho-motor area ; and that in man they are 
certainly most numerous in the parts corresponding to Ferrier's 
motor convolutions, and that they send out processes, some 
of which pass downwards through the centrum ovale as 
nerve-fibres. While mentioning this view of Betz, I must 
also inform you that Professor Golgi of Pavia denies the 
accuracy of these statements. He is very sceptical even as 
to the correctness of the division of the grey matter into the 
five layers, and states that there is no solid foundation in fact 
for the assertion of Betz with regard to the distribution of 
the giant pjo-amidal cells. Further research will enable 
us to decide which observer is really correct. In the mean- 
time the question must be left open. These fibres converge 
as they pass downwards in the corona radiata, and form, when 
they reach the level of the corpora striata and optic thalami, 
an important part of the internal capsule. It is especially in 
the anterior two-thirds of the posterior segment of the capsule 
that the motor fibres are placed. From the capsule they 
pass down in the crura cerebri, occupying the crusta. In 
the pons they lie rather towards the lower surface, covered 
up and intersected by transverse fibres (fig. 25). In the 
medulla oblongata, the majority of the fibres which go to 
form the crossed pyramidal tracts in the cord, decussate 
(fig. 26), while a smaller bundle, without decussation, passes 
directly to the cord (fig. 28). There are thus formed in 
the spinal cord two strands of motor fibres, one of which is 
known as the crossed, the other as the direct pyramidal 
tract (fig. 27). In the transverse section of the cord (fig. 27), 
you see that the crossed pyramidal tract occupies a position 
in the interior and towards the back part of the antero-lateral 
columns, while the direct pyramidal tract occupies a position 
on the other half of the cord, beside the anterior fissure. 



26 



LINES OF 



With regard to the relationship of these strands or tracts 
to the grey matter of the spinal cord and the anterior or 
motor nerve-roots, it is somewhat difficult to speak precisely. 
But as they pass downwards in the cord we find that the size 

I. dqxt. 




Fig. 25. 

■ Semi-diagrammatic dissection of medulla 
and pons to show the course of the fibres 
(after Quain). 




Fkj. 20. 

Decussation of the pyramids (a) (Quain). 



jr. 



JK. 



JV. 





ri8. 27. 

Transverse section of cord at 
different levels. 
I. At level of sixth cervical nerve ; 
II. At level of third dorsal ; 

III. At level of sixth dorsal ; 

IV. At level of twelfth dorsal ; 
V. At level of fourth lumbar. 

dpt, direct pyramidal tract ; 
cpt, crossed pyramidal tract ; ct, 
direct cerebellar tract ; g, postero- 
internal column (Quain). 



of these tracts diminishes, until at last they disappear. The 
direct tract ceases between the middle and lower end of the 
dorsal region, while the crossed tract continues as low down 



MOTOR CONDUCTION. 



27 



as the origin of the third or fourth pair of sacral nerves (see 
fic^. 27). "There is reason to believe that the direct pyramidal 
tracts decussate all along their course in the cord, their fibres 




Fia. 28. 

Semi-diagrammatic representation of brain and spinal cord, to show the different lines of 
sensory and motor conduction, founded upon a schema by Dr. James Ritchie. 

C.CAL., corpus callosum ; NC, caudate nucleus ; NL, lenticular nucleus ; CL, claustrium ; 
OT, optic thalamus ; Cr, crusta ; Teg, Tegmentum ; CQ, corpora quadrigemina ; CD, corpus 
dentatiim ; SP, superior peduncle ; MP, middle peduncle ; IP, inferior peduncle ; O, olivary 
body; TbN, Triangular nucleus; CL.N, clavate nucleus; M, muscle; S and T, sensory end 
organs. 

passing through the anterior commissure, and through the 
grey matter of the opposite side, to reach the lateral pyra- 



28 



MOTOR FIBRES IN COED. 



midal tract of the other side of the cord. The proportionate 
size of the direct pyramidal tracts varies greatly, sometimes 
they are altogether wanting. 

The fibres of the crossed pyramidal tracts pass, some of them 
(fig. 29 a), directly into the grey matter, and thence directly out- 
wards as anterior nerve-roots, while other fibres (b) in the passage 
through the grey matter become connected with the nerve- 
cells of the anterior cornua. The anterior roots also contain, 




Tio. 29. 

Semi-diagrammatic section of spinal cord, showing composition of anterior neiTe-roots. 
For explanation of lettering, see text. 

no doubt, fibres which subserve reflex action, and fibres (c) may 
be traced proceeding to them from the posterior cornua, and (d) 
from the other side through the anterior commissure. 

The motor fibres pass outward from the grey matter in several 
bundles, and leave the cord by the anterior roots of the spinal 
nerves, and are distributed mainly to the muscles, the fibres 
presenting no peculiarity of structure, but the nerve-endings 
showing such an appearance as you see in fig. 30, which 
show the nerve-endings in the voluntary muscles of the lizard. 

Passing now to the cranial motor nerves, I shall first 



MOTOE-OCULI. 



29 



speak of the Mrcl or motor-oculi. We know little as yet of 
the fibres which connect its motor convolutions with its nuclei 
of origin, and although some of Ferrier's results point to a 
localisation of the function in the posterior end of the two 
upper frontal convolutions, we cannot for certain determine 
its position. We know that it is most abundantly related to 
what we may regard as its nucleus proper, which is situated 
beneath the floor of the aqueduct of Sylvius in the upward 
prolongation of the anterior cornua of the cord. But this 
probably proceeds in part from the lenticular nucleus, 
through fibres coming from the raphe, in part from the 
anterior corpora quadrigemina. The nerve passes through 
the tegmentum and sub- 
stantia nigra, and emerges 
(see p. 11, fig. 11 iii.) on 
the inner surface of the 
crus, near the pons. It 
supplies the levator palpe- 
brse superioris, and all the 
muscles of the eye-ball, 
except the superior oblique 
and external rectus. It 
supphes also the con- 
strictor muscle of the 
pupil. 

The fourth or trochlear 
nerve has not as yet been 
traced to its source in the convolutions, but, like the oculo- 
motor, it derives fibres from the corpora quadrigemina (Mey- 
nert), but mainly from a nucleus close to, indeed constituting 
a downward prolongation of, that of the third. Its fibres pass 
downwards and backwards in the wall of the aqueduct, at the 
commencement of which in the anterior medullary velum 
they cross to the other side, and emerge from the velum close 
to the middle line. Hence they bend round (see p. 11, 
fig. 11 iv.) the crus cerebri, and reach the base of the brain. 
The nerve supphes the superior oblique muscle. 

With regard to the motor division of the fifth, it appears 
from cases recorded by Lupine that it has cortical origin 




Fig. 30. 

Nerve-ending in muscle of lizard (after Kuhne). 



30 



MOTOR PART OF FIFTH, 



in tlie inferior third of the ascending frontal convolution. 
From this district fibres proceed to the internal capsule, and 
thence through the cms and pons. But a relationship has 
been traced between it and several nuclei. Most of its 
fibres proceed from a nucleus (see fig. 31 v.) situated under 
the lateral angle of the fourth ventricle, immediately in 
advance of the anterior end of the nucleus of the facial, 
and to the inner side of the larger sensory nucleus of the 

fifth. Other fibres'"^ 
spring from the large 
cells of the grey 
matter of the aque- 
duct of Sylvius, com- 
mencing high up in 
the region of the 
anterior corpora 
quadrigemina, and 
receiving accessory 
fibres in their passage 
down to the place of 
emergence of the 
nerve. This set of 
fibres forms the so- 
caUed descending root 
of the fifth. StiU 
other fibres can be 
traced to the central 
raphe, where they 
probably decussate 
with fibres of the 
opj)osite side. 

The nerve passes 
through the substance of the pons varolii, and emerges on 
the lateral surface of the pons, nearer to the upper than the 
lower border (see p. 11, fig. 11 v.). It then passes out of 
the skull by the foramen ovale, joining the third or inferior 
maxillary division of the fifth (sensory), and supplies the 

* Some (vide Scliwalbe, p. 679) regard these as possibly sensory, 
others as partly sensory, others as trophic. 




FACIAL, GLOSSO-PHARYNGEAL, AND VAGUS. 



31 



masse ter, temporal, external and internal pterygoids, tlie 
mylo-hyoid and the anterior belly of tlie digastric, but not 
the buccinator, as was formerly supposed. 

With regard to the sixth or abducens, we have as yet no 
evidence as to its cortical source. But its point of origin is 
distinctly made out in a large-celled nucleus at the bottom 
of the groove in the anterior part of the floor of the fourth 
ventricle, slightly anterior to the strise-medullares (fig. 31 vi.). 
The fibres make theu' way forwards and downwards through 
the pons, and emerge (fig. 11 vi., p. 11), between the pons and 
medulla. It supphes the external rectus muscle. 

The seventh or facial nerve would seem, from the results 
of Ferrier's experiments, and the observations of Charcot 
and Pitres, to have cortical origin in the lower part of the 
ascending frontal convolution and its junction with the ascend- 
ing parietal. The course of fibres from that point is, no doubt, 
by the corona radiata and internal capsule, and thence by the 
raphe to the other side ; but certamly we know that it derives 
fibres from a nucleus similar to that of the sixth, situated about 
the same level, though deeper in the substance of the pons (fig. 
3 1 vii.). But fibres have also been traced to this nerve through 
the raphe from the lenticular nucleus of the opposite side. 
The nerve, after several bends (fig. 11 vii., p. 11), emerges from 
the medulla between the olivary and restiform bodies, and is 
distributed to the facial muscles, with the exception of the 
levator palpebrse superioris, and to the levator palati, azygos 
uvulae, hngualis, occipito-frontalis, retrahens aurem, posterior 
belly of digastric, stylo-hoid, and the platysma. 

Of the motor part of the glosso-pharyngeal we also do 
not know the origin, but it has a nucleus in the medulla 
oblongata occupying a position continuous posteriorly with 
that of the vagus, as is shown in fig. 31 ix. It emerges 
(fig. 1 1 viii., p. 1 1) by five or six roots arranged in vertical series 
downwards from the place of emergence of the auditory 
nerve, and supplies the stylo-pharyngeus and, perhaps, the 
constrictor muscles of the pharynx. 

The cortical connection of the motor part of the vagus is 
not ascertained. Its fibres proceed from a nucleus in the 
lower half of the floor of the fourth ventricle, and in part 



32 



SPINAL ACCESSOEY AND HYPO-GLOSSAL. 



from one in the medulla oblongata near the olivary body. 
The position of these nuclei is shown in fig, 31. The nerve 
emerges by twelve roots arranged in series with those of the 
glosso-pharyngeal, and is distributed to the muscles of the 
pharynx, of the larynx, of the oesophagus, and of the stomach 
and the heart. 

The spinal accessory nerve originates in two divisions, one 
from a nucleus in the lower part of the medulla, continuous 
at its upper end with the nucleus of the vagus (fig. 31 xi.) ; 
and the other from the cervical portion of the cord as low 
down as the sixth or seventh cervical nerve. The nerve 
emerges from the medulla by a long series of roots, con- 
tinuous with the posterior roots of the spinal nerves. It 
divides into an external and an internal half of which the 
former supplies the sterno-mastoid and the trapezius, while 
the latter joins the upper ganglion of the vagus, to which it 
becomes accessory. 

The hypo-glossal nerve must have very intimate relations 
with the cortex cerebri. Its cortical centre appears from 
Ferrier's researches to be situated at the extreme lower 
end of the ascending frontal convolution, at its junction 
with the ascending parietal ; and Kaymond and Artaud bring 
together six cases in which a lesion in that position produced 
paralysis of the tongue on the side opposite to the lesion. 
From this cortical district fibres proceed in the inferior frontal 
fasciculus of Pitres, and the authors above referred to 
cite a series of cases, showing that lesion of these fibres 
induces paralysis of the tongue, the lips, and velum 
palati. The fibres then proceed downwards in the internal 
capsule, crura cerebri, and pons, in the last part occupying 
a place internal to and behind the motor pyramids. It 
derives fibres from the nuclei composed of large nerve-cells, 
which extend as low down in the medulla as the decussation of 
the pyramids (fig. 31 xii.). Some fibres seem also to proceed 
from the olivary body. It emerges from the medulla, between 
the olive and the pyramid, by a series of five roots (see fig. 11, 
p. 11), and is distributed to both the extrinsic and the intrinsic 
muscles of the tongue, and also to the omo-hyoid, sterno-hyoid, 
sterno-thyroid, thyro-hyoid, and genio-hyoid muscles. 



LECTURE III 



Medical Anatomy of N'ervous System [continued). — Fibres Afferent to 
Cerebellum. — Histological arrangement in Cerebellum. — Fibres 
Efferent from Cerebellum. — Ganglia on Nerves, in Cord, 
Medulla, Pons, Crura Cerebri, Cerebrum, and Cerebellum. — 
Commissural Fibres connecting different parts of Nervous- 
System. — Diagrammatic resume of Anatomy of Cord, Medulla, 
Pons, and Cerebrum. — Belationship of Convolutions to the 
Surface of the Cranium. — Sympathetic System, 

ENTLEMEN, — "We now proceed to consider our third 
point in the medical anatomy of the nervous system 
— the fibres afferent to the cerebellum. I wish that our 




P 

Fio. 3i?. 

Diagrammatic transverse section ot cord, showing fibres (o) passing from the cells of the 
column of Clarke (0) to the direct cerebellar tract ot the cord. 

knowledge were such as would enable me to describe 
minutely the relationships of the cerebellum with the 

33 D 




34 



CEEEBELLAE FIBRES. 



jr. 



periphery, but upon this subject it is impossible at present to 
speak definitely. The existence of direct cerebellar fibres 
in the spinal cord is well known. They occupy a position at 
the surface of the posterior part of the antero-lateral columns. 
You see in the diagram (fig. 32, ct) their position marked by 

shaded lines. 

By reference to figure 33, you will 
see that these fibres are distinct as low 
as the origin of the twelfth dorsal nerve, 
but have disappeared at the level of 
origin of the second or third lumbar 
nerve. It is believed that some of the 
fibres (fig. 32 a), are connected by axis- 
cyhnder processes with the cells of 
the column of Clarke (c), and cer- 
tainly they issue from the central 
grey matter just at the point of 
junction of the anterior and poste- 
rior horns. Passing into the region 
of the cord I have mentioned, they 
pursue their course upwards, and 
without decussating constitute the 
restiform bodies in the meduUa ob- 
longata and enter the cerebellum by 
its inferior peduncles. We know that 
these are afferent structures, because 
we find that ascending degeneration 
occurs in them, but we know nothing 
of the source of these fibres beyond 
what I have indicated. Another set 
of ascending cerebellar fibres passes 
up the posterior column, a group in 
the internal and one in the external 
division. The internal becomes con- 
nected with the clavate nucleus, and 
the external with the triangular 
nucleus in the medulla oblongata. 
From each of these nuclei fibres pass towards the oHvary 
body of the same side, and it is probable that from the 



jy. 




Fig. 33. 

Transverse section of cord at 
different levels. 
I. Atlevelof sixthoervicalnerve; 
II. At level of third dorsal ; 

III. At level of sixth dorsal ; 

IV. At level of twelfth dorsal ; 
V. At level of fourth lumbar. 

dpt, direct pyramidal tract ; 
cpt, crossed pyramidal tract ; ct, 
direct cerebellar tract ; g, postero- 
internal column (Quain). 



HISTOLOGICAL STEUCTUEE OF CEEEBELLUM. 



35 



olivary bodies some fibres pass after decussation to the 
cerebellum (see fig. 28). 

It may be well here to refer to the histological arrange- 
ment of the elements in the cerebellum. In fig. 34, you 
perceive that at the sur- 
face there is a layer of 
pia mater (a) ; an external 
layer composed of a deli- 
cate matrix, apparently of 
the nature of neuroglia 
(b) ; a layer containing 
the large flask-like cells 
of Purkinjd (c) ; a layer, 
known as the inner ox 
granular layer, consisting 
of granule-Hke corpuscles 
in a gelatinous matrix, 
among which ramifies a 
plexus of fine nerve-fibres 
(d) ; and the medullary 
or white centre of each 
lamina consisting of par- 
allel and interlacing nerve 
fibres (e). Of the rela- 
tionships of these parts 
individually to afferent or 
efferent nerves we know 
nothinsi". 

o 

Fourthly, with regard 
to efferent nerves from the 
cerebellum, it is true that 
there are many efferent 
fibres proceeding from the 
organ to connect it with 
ganglia, particularly with 
the olivary bodies, the anterior grey substance of the pons 
and with the red nuclei. It is probable that these fibres 
pass into the anterior white columns of the cord, and in that 
way descend, perhaps becoming connected with motor cells 




Fig. 34. 

Microscopical section of cortical portion of 
cerebellum. For explanation of lettering see 
text (after Sankey). 



36 



GANGLIA IN CORD. 



in the grey matter of the cord, or possibly passing out into 
the motor nerves. Of the connections between the cere- 
bellum and the cerebrum, I shall speak when describing the 
commissural fibres of the nervous system. 

I have next, fifthly, to take up a subject on which we have 
already touched at many points — viz., the ganglia which 
exist in connection with nerves, the spinal cord, the medulla, 
and the encephalon. 

On the posterior roots of each of the spinal nerves there 
are small gangha, and similar accumulations of nerve-cells 
are to be found on the trigeminal, the vagus, the facial, and 
also on the third nerve. It is possible that some of these 
may have functions corresponding to that of the sympathetic 
gangha, of which I have to speak afterwards ; but we must 
acknowledge, that although various suggestions have been 
made, we have no data on which to found definite statements. 
In the spinal cord itself you will find great numbers of gang- 
lionic centres. In fact, you may most accurately conceive of 
the spinal cord, if you add to your idea of it as a conducting 
structure, that it also consists of a series of seg-ments^ con- 
taining ganglia, run together and made continuous. If you 
refer to this section of the cord (fig. 3 5), you will observe that 
there are groups of nerve-ceUs distributed throughout the 
grey matter. In the anterior part of the anterior horn the 
largest and most prominent cells are found, and they are 
often described as constituting the motor- ganghonic column, 
or the vesicular column of the anterior cornu. They receive 
the name " column," because the successive gangha are 
welded together into a continuous mass. In some parts, 
the cells are separated into groups, — a lateral (a), which 
is nearer the lateral ; and a mesial group (6), which is nearer 
the anterior column. In the lumbar enlargement you can 
also see a posterior group (c), more deeply seated. A 
second great ganglionic column occupies an area at the 
inner angle of the base of the posterior horn (d). It is 
cut off from the rest of the grey matter by fibres which 
proceed from the posterior root. This is commonly Imown 
as Clarke's column. Lockhart Clarke himself called it tlie 
posterior vesicular column. It is chiefly developed in the 



GANGLIA IN MEDULLA AND PONS. 



37 



lower dorsal region, but traces of it are found as low as 
the third sacral nerve, and as high as the origin of the third 
and fourth cervical. The third great ganglionic column (e) 
is Icnown as the column of the intermedio-lateral tract, and, 
like tliat tract, is distinct only in the dorsal region. In 
other parts it is blended with the anterior cornu. Its cells 
are larger than those of Clarke's column, but not so large 
as those of the anterior horn. There are also, in addition 
to these great ganglionic columns, groups of cells scattered 




Fig. 35. 

Diagrammatic transverse section of cord, with groups of nerve cells in grev matter. 
For explanation of lettering, see text. 

throughout the posterior horn (/). They are of smaller size, 
mostly spindle-shaped, and they extend into the substantia 
gelatinosa of Kolando. There can be no reasonable doubt 
that these various groups of cells subserve the reflex func- 
tions of the cord, and perhaps some of them are connected 
With the transmission of impressions upwards and down- 
wards. 

In the medulla oblongata and pons varolii many of the 
nuclei which I have already described as the nuclei of origin 
of cranial nerves are situated. The diagrams (figs. 15 and 18) 



38 



BASAL GANGLIA. 



will indicate to you tlie relative position of these. You observe 
that the nuclei of the spinal accessory, the hypo-glossal, the 
vagus, the glosso-pharyngeal, the auditory, the facial, the 
fifth, and the sixth, occupy the positions which have been 
already pointed out. But besides these there are special 
nuclei — the olivary bodies, each with its contained corpus 
dentatum, and the smaller nuclei, known as the outer 
and inner accessory olivary nuclei — whose relationships to 
the nerve-fibres are not yet known. In the formatio 
reticularis also there are numerous scattered accumulations 
of grey matter. Within the pons, the superior olivary nuclei 
and the locus cseruleus are found, the latter being in the 
anterior part of the floor of the fourth ventricle. The medulla 
oblongata and the pons are thus, you see, very rich in nuclei, 
although the functions performed by these nuclei are at 
present unknown. 

In the crura cerebri are the upward continuations of the 
formatio reticularis in the tegmentum. At a higher level is 
situated the tract of grey matter containing large pigmented 
ceUs, called the nucleus of the tegmentum, or red nucleus. 
Separating the crusta from the tegmentum is a mass of grey 
matter containing darkly pigmented irregular cells, loiown as 
the substantia nigra. In this part also you find the nuclei 
of the third and fourth cranial nerves. 

At the base of the cerebrum there are important accumu- 
lations of grey matter. To the corpora quadrigemina I have 
already referred when speaking of the optic nerves. The optic 
thalami (fig. 86, th), including the external and internal geni- 
culate bodies, the pulvinar, the outer, the inner, and the anterior 
nuclei, have also been mentioned in the same connection, 
but they have, doubtless, functions beyond those of sight. 
The corpora striata, which include the lenticular (nl) and 
the caudate nuclei {nc), are intimately connected with the 
strands of motor- fibres ; but of the influence which they exert 
we are, unfortunately, at present ignorant. Another layer 
of grey matter, the claustrum {d), lies to the outside of the 
lenticular nucleus, separated from it by the external capsule, 
and from the grey matter of the convolutions of the island 
of Keil by the white fibres of the island. In the diagram 



BASAL GANGLIA. 



39 



(fig, 36), you perceive the arrangement of the different 
structures. 

In the cerebellum, the most prominent grey nuclei are the 
corpora dentata, which closely resemble the ohvary bodies ; 
but recent writers have described three others in the white 
substance of the cerebellum — viz., the nucleus emboliformis, 
nucleus globosus, and 
nucleus fastigii. Of 
their functions we also 
know nothing. You 
thus perceive that all 
through the nervous 
system ganglia or nuclei 
of grey matter occur, 
but that our knowledge 
of their relationships 
and functions is most 
imperfect. 

It is difficult to say 
what the functions of 
these numerous ganglia 
may be. It is obvious 
that they must be 
centres, and may sub- 
serve sensation, motion, 
or nutrition. Some 
must be reckoned reflex 
centres ; some inter- 
mediary motor ; some, 
perhaps, intermediary 
sensory ; and some, 
probably, trophic. 

We next proceed to consider, sixthly, the commissural 
fibres connecting different parts of the nervous system together. 
The first set of commissural fibres with which we meet in 
passing inward from the periphery, are those which connect 
the anterior and posterior roots of the spinal nerves. The 
second series are the various commissural fibres within the 
cord. Some of these are transverse, some longitudinal, and 




Fia. 36. 

Section through basal ganglia and island of BeU. 

nc, caudate nucleus ; nl, lenticular nucleus ; cl. 
claxistrum ; th, optic thalamus ; ic, internal capsule, 
with its knee (g) ; vl, lateral ventricle ; cc, corpus 
caUosum ; ch, choroid plexus ; !, island of Eeil (Quain). 



40 



COMMISSUKAL FIBBES. 



the length of the longitudinal varies, some of them connect- 
ing neighbouring segments, others more distant segments. 
Longitudinal fibres also connect the cord with the medulla 
oblongata, and it appears that within the medulla there are 
commissural fibres connecting the two lateral halves and 
different nuclei with one another. The pons varolii is to a 
large extent composed of fibres connecting the two sides of 
the cerebellum, although, of course, many fibres proceeding 
from the cerebellum through its substance are not merely 
commissural. Within its substance, also, there are commis- 
sural fibres connecting its two lateral halves and the various 
nuclei within it. Commissural fibres also connect the basal 
ganglia with those of the opposite side and with one another. 
The two lateral halves of the cerebrum are connected by the 
great commissures, the corpus callosum, the anterior com- 
missure, the middle or soft commissure, and the posterior 
commissure. There are also fibres of a commissural char- 
acter connecting the anterior with the posterior parts of the 
cerebrum, the fornix. And, further, there are fibres con- 
necting neighbouring convolutions together, either adjoining 
convolutions or more distant ones. There are also commis- 
sural fibres connecting the medulla with the cerebellum, 
passing by the inferior peduncles, the cerebellum with the 
cerebrum and with its basal ganglia, the two lateral halves of 
the cerebellum and its nuclei (fig. 28). 

The last point to be taken up in connection with the 
medical anatomy of the cerebro-spinal nervous system is the 
localisation of nervous lesions. What I have already said 
might sujffice for this ; but I think that by now taking the 
nerve-centres as a whole, I may be better able to bring out 
what you require in practice. 

If disease be localised in a nerve, we find the functions of 
the nerve interfered with, while other parts remain normal. 
If the nerve be motor, we find generally paralysis or paresis ; 
if sensory, we find hypersesthesia or auEesthesia ; and if it 
be trophic, we find various alterations of nutrition. If the 
disease affect a mixed nerve, we find all the functions 
involved to a greater or less extent. The reaction of degener- 
ation is also usually present. In cases of paralysis of hands 



LOCALISATION IN COED. 



41 



and feet from disease of the nerves, I have seen the symptoms 
very pronounced. 

With regard to the spinal cord and localisation of lesions 
in it, .you have to consider it as seen in transverse section, 
and in its length. Look first at a transverse section of the 
cord (fig. 37). 

Commencing with the grey matter, we know that the 
groups of ganglion cells {ac and aci), in the anterior ; horns 
are related to motor and trophic functions, and that lesions 
in these parts induce paralysis, with alteration of nutrition 




Diagrammatic transverse section of the cord, showing groups of cells and chief tracts. 

of the corresponding districts. We do not know what special 
functions are subserved by the vesicular column of Clarke (cc), 
nor the spindle-shaped cells (pc) of the posterior cornua. 
Turning now to the white matter on each side of the 
anterior fissure, we find the direct pyramidal tracts {clpt), 
whose lesions induce motor paralysis. In the antero-lateral 
columns, near the anterior horn, is the bundle of fibres 
described by Dr. Gowers as sensory ; lesion of these must 
lead to sensory changes. Farther back in the antero-lateral 
columns is the considerable area of the crossed pyramidal 



42 



LOCALISATION IN CORD. 



tracts (cpt), whicli also when diseased induce paralysis ; and 
to the posterior and external side of these are the direct 
cerebellar tracts {dot). Within the posterior column, next 
to the nerve-roots, we find the posterior root zone (pec), which 
is so constantly the seat of change in locomotor ataxia. To 
the inner side of this, on each side of the posterior fissure, is 
the postero-internal column {pic), whose function is probably 
connected with sensation, seeing that in ascending degenera- 
tion changes occur in it. 

Turning now to the localisation of diseases along the 
length of the cord, we find that the cord extends from the 
foramen magnum to the lower border of the first lumbar 
vertebra, and contains centres for various reflex move- 
ments, by means of which we are able pretty accurately 
to determine the position of a lesion. The lumbar 
enlargement contains many centres, such as that for the 
plantar, cremasteric, and gluteal reflexes ; for micturition, 
defeecation, and parturition and sexual action ; and for 
movements of lower limbs. Somewhat higher in the cord 
is the centre for the abdominal and epigastric reflexes. In 
the upper dorsal and lower cervical region are the centres for 
the scapular reflex and for the dilator movements of the 
pupil (the cilio- spinal region). Within the dorsal region there 
are centres also connected with the stomach and intestine. 
In the cervical region, the centres are situated for move- 
ments of the arms and upper part of the trunk. 

Within the medulla oblongata, besides the motor and 
sensory conducting fibres, we find the respiratory centre, the 
vaso-motor centre, the cardio-inhibitory centre, the centres 
for deglutition, for swallowing, for vomiting. There is also 
the salivary centre, centres connected with glycosuria and 
polyuria. There are centres also for movements of the face 
and the tongue, and nuclei connected with hearing. 

With regard to the pons varolii, it is to be noted that as 
some of the cranial nerves decussate in that region, crossed 
paralysis of various kinds depend upon its lesions. 

With regard to the brain itself, I show you sections of it 
made in various directions, as prepared by my friend, 
Professor Hamilton of Aberdeen. 



LOCALISATION IN BRAIN. 



45 



Notice first a vertical transverse section of the brain (fig. 
38). It passes through the middle of the basal ganglia 
through the ascending frontal (AF), part of the ascending 
parietal convolution (AP), and through part of the temporo- 
sphenoidal lobe (TS). You observe in it the corpus callosum 
(cc), the fornix (J), the fifth ventricle {v), the lateral ventricles 
(LV), a small part of the optic thalamus (th), a considerable 
part of the internal capsule (^c) cut across close to its genu, 
the caudate nucleus (cn) the lenticular nucleus {In), the 
external capsule (ec), the claustrum {cl), the white and grey- 
matter of the island of Reil (R). 



46 



LOCALISATION IN BEAIN. 



I show you next a horizontal section (fig. 39), in which you 
perceive the frontal (F), temporo-sphenoidal (TS), and occi- 
pital lobes (0), with their grey and white matter, the island of 
Eeil(R), its grey and white substance, the claustrum {cl), the 
external capsule (ec), the lenticular nucleus (Ln), the caudate 
nucleus {cn), the internal capsule {ic), the optic thalamus (th) 
and pulvinar (p), the corpus callosum (cc), the anterior and 
posterior commissures (ac) and (jpc), the lateral ventricle (LV), 
with the choroid plexus (cli). 



LOCALISATION IN BRAIN. 



51 



I show you next a vertical antero-posterior section (fig. 40), 
showing the lenticular (Ln) and caudate nuclei (cn), separated 
by the internal capsule {ic), the corpus callosum (cc), the 
anterior commissure (ac), the optic tract (II), the optic thala- 
mus (th), the corpora geniculata (g), and the pulvinar (p), the 
crusta (cr), the tegmentum (tg), pons (P), and cerebellum (C). 



52 



RELATIONS OF BRAIN TO SKULL, 



With the view of helping you to realise the relation which 
subsists between the surface of the cranium and the under- 
lying convolutions and sulci, a subject on which Professor 
Turner has made the most important observations, I show 
you again the drawing of a skull, on which have been traced 
the outlines of the various convolutions and sulci, with the 
name of ^each of the chief convolutions marked upon it 
(fig. 41). Before entering on the detailed description, let 
me ask you to note two fundamental points, viz. : — 




C 



Fui. 41. 



Lateral view of skull, showing relation of convolutions and sulci to sutures of skull. 

1. That the fissure of Sylvius (B), which separates the 
frontal and the parietal from the temporo-sphenoidal lobes, 
corresponds to a line starting from a little in front of the 
upper anterior part of the squamous portion of the temporal 
bone, and running obliquely through the parietal bone to a 
little beyond the parietal eminence. 

2. That the fissure of Rolando (A), which separates the 
frontal from the parietal lobe, commences at the vertex, 
nearly half-way back in the parietal bone, and slants slightly 



RELATIONS OF BRAIN TO SKULL. 



53 



forwards, so that at its lower anterior extremity it is about 
one-fourth from the front of the parietal bone. 

You observe that the frontal lobe, which is bounded 
posteriorly by the fissure of Kolando (A), underlies the whole 
frontal and fully one-third of the parietal bone ; that its 
lower margin is formed by the fissure of Sylvius (B), and 
that in it you can make out the ascending, first, second, and 
third convolutions. You perceive that the parietal lobe, 
which extends from the fissure of Eolando to the parieto- 
occipital fissure, and is bounded below in part by the upper 
part of the fissure of Sylvius, corresponds to only a small 
portion of the parietal bone. It includes its ascending con- 
volution, which corresponds to the middle part of the parietal 
bone, the postero-parietal convolution which lies between this 
and the parie to-occipital fissure (C), the supra-marginal con- 
volution, which corresponds to the most prominent part of 
the parietal bone, and is, therefore, sometimes called the con- 
volution of the parietal eminence, and above it the angular 
gyrus, which forms a curve round the extremity of the Sylvian 
fissure. 

The occipital lobe, which extends backwards from the 
parieto-occipital fissure (C) to the lower margin of the cere- 
brum, and corresponds to the lower part of the parietal bone 
and the occipital as far down as the protuberance, consists 
of three parallel convolutions, named respectively superior, 
middle, and inferior convolutions. The temporo-sphenoidal 
lobe includes the portion of the cerebrum lying below the 
Sylvian fissure, and extends backwards to the parietal and 
occipital lobes. It is composed of superior, middle, and 
inferior convolutions. It corresponds to the squamous part 
of the temporal bone and a considerable part of the parietal bone. 

Having thus recalled to you the general anatomical relation- 
ship, let me now say a few words as to the localisation of the 
lesions. The great conducting fibres, both motor and sensory, 
are to be found in the internal capsule and corona radiata, 
the sensory occupying the posterior, the motor the anterior 
portions. Lesions in these produce symptoms corresponding 
to the exact point injured. We cannot at present say what 
precise effects follow lesions confined to the basal ganglia. 



54 



SYMPATHETIC SYSTEM. 



Lesions of the cortex are attended by changes in the districts 
connected with the various convolutions ; and what I have 
said will enable you to make out the seat of lesion in 
individual cases. You will meet in practice with examples 
both of paralytic and of irritative results ; injury or disease of 
a convolution leading to paralysis or to convulsive movement 
in the corresponding district when the motor area is in- 
volved. The very interesting phenomena known as Jacksonian 
epilepsy, from having been first well described by Hughlings 
Jackson, are among the most striking of these phenomena. 
The lesions of sensory areas you will find also of great 
clinical interest, although much more rare. 



Sympathetic System. 

The sympathetic is a complicated system of ganglia and 
fibres, with numerous plexuses. It is usually described by 
anatomists as composed of two portions — viz., the great 
gangliated cords and the great pre-vertebral plexuses, with 
the nerves proceeding from them. The great gangliated cords 
are two, each consisting of a series of ganglia united by nerves. 
They are placed symmetrically, partly in front and partly at 
the side of the vertebral column, and extend from the base 
of the skull to the coccyx. There are divisions which are 
known as cervical, dorsal, lumbar, and sacral, corresponding to 
the vertebrae by the side of which they are placed ; and, 
except in the neck, the number of the gangha corresponds to 
that of the vertebrae. The ganglia are connected with the 
anterior primary divisions of the spinal nerves, some of the 
fibres coming from the spinal cord by anterior, others by 
posterior roots. Each connecting filament consists of a white 
and grey portion, the white portion of the filament being 
that derived from the spinal nerve, and the grey being that 
passing from the sympathetic ganglion to the spinal nerve. 
The cords which connect the different ganglia together are 
also grey and white, the white fibres being, again, the 
spinal fibres, the grey those proper to the structure. Fig. 
42 will recall to your minds the general plan of this s3'-stem. 
The cervical ganglia are three — the upper, the middle, and the 



SYMPATHETIC SYSTEM. 



ji *-.^4« '*•^*^'^ 



LUKBAA C.VKCUA < 



tArUAL CaNClIA 



COCCVFCAL V (^VCLION KII'Ari 




/■■ — J"* <iui^ /Art' 



Fio. 42. 

Sympathetic nervous system (Flower). 



E 



56 



SYMPATHETIC SYSTEM. 



lower. The upper receives communicating branches from 
the four highest cervical nerves, the middle from the fifth 
and sixth, and the lower from the seventh and eighth. The 
pre- vertebral plexuses are great aggregations of ganglia and 
nerves, and are named — in the thorax, the cardiac ; in the 
abdomen, the solar ; and in the pelvis, the hypogastric 
plexus. From these, fibres proceed to supply the vascular 
system and the viscera ; and it appears that the function 
which they subserve is the regulation of blood-supply and of 
nutritive processes. 



LECTURE IV. 



Sensory Functions. 



Subjective Phenomena. — Fain. — Girdle-pain. — Feelings of Heat or 
Cold. — Cold with Pressure. — Formication. — Numbness. — Ting- 
ling. — Globus Hystericus. — Giddiness. — Sensibility to Impres- 
sions. — Various Kinds. — Contact. — Pressure. — Temperati(,re. — 
Tickling. — Pain. — Pate of Conduction. — Hyper CBsthesia and 
Hyperalgesia. — Ancesthesia and Analgesia. — Dyscesthesia. — 
Allochiria. — Polycesthesia. — Retarded Conduction. — Muscular 



ENTLEMEN, — We enter to-day upon the consideration 



^ of tlie second part of our programme, — viz. the 
functions of tlie nervous system, with the various methods 
of determining their conditions, the alterations which they 
undergo in disease, and the cHnical significance of these 
alterations. We consider first the sensory functions, and 
shall commence with the subjective phenomena. This 
term includes the various sensations experienced by patients 
in the absence of the external causes ordinarily producing 
such sensations. It is to be observed that they do not 
constitute a weU-defined group, seeing that in many instances 
the cause, although not external, is distinctly recognisable. 

One of the commonest of the subjective phenomena is 
pain. Pain is the representation in consciousness of certain 
impressions or of an excessive degree of any kind of sensory 
impression. You are all familiar with pain as produced by 
irritants, but it is not of this that I have to speak at present : 
it is of subjective pain, — pain occurring independently of 
external irritation. Such pain may originate in any part of 
the sensory tract. The cause may be in the nerve-endings, 
in the nerves themselves, in the cord, or in the sensory 



Sense. 




67 



58 



SUBJECTIVE PAIN. 



centres. But it is always referred to the peripheral area of 
the sensory nerve. Subjective pain is not necessarily 
associated either with anjESthesia or hyperaBsthesia ; it may 
exist along with either, or occur independently of both. If, 
for example, you examine some cases of neuralgia closely, 
you will find that there is often at first an increase of sensi- 
bility, while later on there is a distinct diminution. 

There are many kinds of subjective pain. It may be like 
cutting, or tearing, or burning, or boring ; it may be darting or 
like a strong electric shock. It may be confined to a limited 
area, or widely distributed, may occur in a single nerve-fibre 
or affect all the branches of a nerve, or a whole plexus. The 
situation of the pain also varies greatly. It may be in the 
head, the limbs, or the trunk. It may be near the surface, 
or it may be deep. Some of the most agonising pains 
that I have heard described in cases of locomotor ataxia, 
have been seated deeply within the abdomen or the chest. 
Pain may also be constant, paroxysmal, or periodic ; 
and the periodicity may vary in different cases. It may 
occur at night or by day, or at some special hour or season. 
It may also last for a longer or shorter time. It may be 
only momentary but oft recurring as in the lightning pains 
of locomotor ataxia, or the sudden agony in some of the 
branches of the fifth cranial nerve in epileptiform neuralgia. 
You will meet with pain resulting from pressure on nerves. 
I have known a minute growth pressing upon one of the 
nerves of a toe cause the most intense pain for a long period. 
I have known an exostosis pressing upon the great sciatic 
produce sciatica which yielded only when the exostosis was 
removed. And you wiU frequently see fibrous and other 
growths producing pain in this way. You may already 
have had opportunity of observing what great pain often 
accompanies aneurism, this pain is the result of pressure upon 
nerves. You wiU find also that pain is often associated 
with congestion and inflammation in nerve, whether it 
involves primarily the sheath and the fibrous tissue binding 
the nerve-fibres, or the nerve-tissue proper. Diseases of 
the membranes of the cord, and of the cord itself, particu- 
larly its posterior columns, are attended with much pain in 



GIKDLE SENSATION. 



59 



many instances, as Ave see so often in cases of spinal 
meningitis, and of locomotor ataxia. Morbid conditions also 
of the brain may give rise to pains in the head, but not, so 
far as I have seen, to pains referred to the sensory nerves 
of the body. You will often find that irritation at the end of 
a nerve induces pain in some other branch of the same 
nerve, or in other nerves. For example, caries of a tooth may 
not only induce pain in the dental branch of the fifth, but 
in the infra-orbital or supra-orbital branches, or even in 
other nerves. As an illustration of the fact that irritation 
of an organ may induce pain in a distant part of the body, I 
shall mention a case Avhich Avas under the care of my friend, 
Professor Hay, of Aberdeen. The patient had for tAvo and 
a-half years, once a month at the menstrual period, been 
attacked Avith ear-ache so agonising that she screamed aloud, 
and had to be held in bed ; while, in the intervals, she Avas 
perfectly Avell. Professor Hay surmised that the pain might 
be due to irritation proceeding from the ovaries, and, re- 
membering Charcot's success in checking the paroxysm of 
hystero-epilepsy by pressure on those organs, tried the effect 
of firm pressure in that region. Immediate relief followed, 
and blistering over the ovary completed the cure. Commonly 
also you Avill find that pains are due to constitutional con- 
ditions, such as anaemia, gout, or rheumatism. Often also 
they are due to exposure to currents of cold air. But in a 
large number of instances it is impossible to trace the cause 
of subjective pains. 

A subjective feeling far less common than that of pain 
is knoAvn as girdle-pain or the girdle-sensation — a feeHng 
as if a belt were tightly bound round the thorax, abdomen, 
or other part. Usually the tightness is not felt straight round 
the body, but it passes from the back obliquely downwards 
and forwards in the line of the distribution of the nerve. It 
is evident that in such cases it results from irritation of the 
sensory roots. I have Imown it to be confined to one side, 
only one of the sensory roots being affected. But occasion- 
ally you Avill find that it is felt as if going straight round the 
body, and not corresponding to particular nerves. Moreover, 
a corresponding sense of constriction is sometimes felt in the 



60 



FEELINGS OF HEAT AND COLD. 



limbs, — round a thigh or an anlde, for example. Obviously 
irritation of a nerve-root could not account for this, and we 
cannot at present explain it, unless the hypothesis that there is 
irritation of the nerve-endings in a certain zone be accepted 
as an explanation. Girdle-pain is sometimes associated with 
hypersesthesia of the district in which the constriction is felt, 
but sometimes there is anaesthesia, and sometimes the sensi- 
bihty is natural. It is a very common symptom in locomotor 
ataxia, — often an early symptom, sometimes persisting for 
years, and sometimes, as I have seen, coming and going in 
the same and in different situations. It is also markedly 
present in cases of myelitis and of meningitis, usually at the 
upper limit of the lesion. 

You will occasionally meet with patients who complain of 
subjective feelings of heat or of cold. You examine Avith the 
hand or with the surface thermometer, and find that the tem- 
perature is natural. You may demonstrate the fact to the 
patient, but still he feels the sensation. The feeUng of heat 
may be constant, or at least persistent for a considerable time, 
or it may pass like a wind ripple on the surface of a pool. It 
may be situated in the limbs, or in a single limb, or in the 
head, or what I thinlc is its most common seat, in the abdomen. 
The patient will tell you that a stream of some hot substance 
seems to pass through the abdomen and the thorax. I have seen 
this very distinctly in cases of paralysis agitans. A sensation 
of great coldness is felt more frequently in the legs. It may be 
unconnected Avith any other lesion. I have known it persist 
for many months without any other symptom being developed, 
and without any other alteration of the sensory nerves or of 
the nutritive functions. You wiU meet with it also sometimes 
in cases of disease of the spinal cord, such as spastic 
paralysis, and locomotor ataxia. Patients sometime describe 
a feeling which combines coldness with pressure ; they 
feel as if a cold wet towel Avere being drawn over their leg, 
or a part of the leg. I have known this combination of 
subjective phenomena in several cases, and have seen it per- 
sist for a long time. I am unable to offer any satisfactory 
explanation of these phenomena. 

Another sensation sometimes complained of is formication 



FOEMICATION, NUMBNESS, TINGLING. 



61 



an uneasy feeling like the itcliing produced by ants creeping 

over the skin. This is an effect of irritation short of that 
which produces pain ; and while the irritation is less in 
degree, it evidently passes from nerve-fibre to nerve-fibre. 
In some cases it is so pronounced as to amount to a 
distinct tickling or itching sensation. These symptoms are 
probably sometimes due to affections of the nerve-endings, 
as is most likely the case in the itching often felt by 
patients suffering from jaundice, from long standing 
renal disease, from diabetes mellitus, and from the use of 
certain drugs, particularly morphia, aconite, and ergot. 
They may also result from compression of the nerve-fibres, 
either from changes within the nerve itself or from pressure 
on it, and are often induced by accidental pressure on a nerve. 
Changes in the spinal cord are also found to induce it, as 
we see in cases of locomotor ataxia. I have seen in a case 
of that disease the symptom present for a long time in a 
minor degree, and at once brought to great severity if a small 
dose of morphia was administered. It is probable that in 
certain cases cerebral irritation produces the feeling as in 
some hemiplegias. It is possible that the morphia and ergot 
act through the central nervous system, although I incline 
to think that they act like aconite on the nerve-endings. A 
very distinct and constant itching sensation in the nose often 
accompanies the presence of worms in the small intestines. 
I was lately consulted by a lady who had become affected with 
ascaris lumbricoides while residing in the south of France. 
She complained greatly of itching at the point of her nose, 
and whenever the worm was discharged the itching dis- 
appeared. I do not Imow how this is to be explained, but it 
essentially corresponds to many other morbid phenomena, 
which we meet with in the nervous system. 

Closely connected with these sensations are the feelings 
described as numbness, tingling, pins and needles, sleeping 
of a limb, and such like. They also occur probably from 
changes in the nerve-endings, certainly from disease of 
nerves, as I have seen in well-marked cases of paralysis of 
hands and feet from nerve disease, or as we see constantly as 
a result of temporary compression of nerve-trunks. Cord and 



62 



GIDDINESS. 



brain diseases also sometime induce them. They may be 
associated with hypersesthesia or with anjBsthesia, and it is 
worthy of note that muscular action often increases the 
uneasy sensation. From this it is clear that irritation of the 
sensory nerve-fibres in the muscles goes along with the more 
superficial symptoms. It is to be noted, also, that feelings of 
numbness are not unfrequently a result of some functional 
derangement of the liver and stomach, many people having 
numb feelings in the fingers when they become what is 
popularly termed "bilious," and that such feelings are 
increased by fatigue of body or mind. 

A sense of pressure on or weight of the limbs is often 
complained of — a feeling as if the limbs were loaded with 
a heavy weight. This is sometimes seen in cases of acute 
disease, sometimes in mere dyspeptic conditions ; and it 
seems to be mainly a result of abnormal conditions of the 
nerve structures which subserve the muscular sense. 

This leads me to speak of various peculiar visceral sensa- 
tions, which are often of a vague and undefined character, 
such as a feeling as if the abdominal cavity were a vacuum, 
a feeling of sinking, a feeling of internal movement, a feeling 
of universal pulsation, the feelings which lead to a craving for 
food, or for particular and often unsuitable articles of diet. 

Along with these, I must draw your attention to a common 
subjective symptom known as globus hystericus — a condition 
in which hypercesthesia of the nerves of the throat induces a 
feeling as if it were distended by a globular mass. It is very 
common during the hysterical paroxysm, and I have heard a 
similar condition described by men suffering from profound 
emotional excitement. 

The last subjective sensation to which I shall refer is one 
of the most important — vertigo or giddiness. It is a feeling 
of uncertainty in regard to our position relatively to surround- 
ing objects. Sometimes the body is felt as if turning 
round a vertical, or much more rarely, round a hori- 
zontal axis, and sometimes objects appear to be whirling 
round either definitely in some direction, or indefinitely 
in a tumultuous manner. Giddiness may arise from a great 
variety of causes. It may be a result of external conditions. 



SENSOKY IMPEESSIONS. 



63 



as in the case of cliff or tower giddiness, and jDcrliaps in 
agoraphobia. It may be a result of morbid conditions of cer- 
tain peripheral organs, as in miners' nystagmus and Meniere's 
disease ; or of the contradictoriness of impressions, as in the 
giddiness which attends upon sea-sickness, swinging, or upon 
double vision from squint. It results from diseases of the 
spinal cord, as we sometimes see in locomotor ataxia, from 
disease of the cerebellum, of the cerebellar peduncles, of the 
pons varolii, of the crura cerebri, and of the cerebrum itself, 
— also from general changes in the cerebrum, such as conges- 
tion, or anaemia, or the pressure of tumours. It may also be 
produced by toxic materials, such as alcohol, tobacco, and 
stramonium. It is often a result of gastric and hepatic 
derangement — the so-called gastric or dyspeptic vertigo. It 
occurs also in fevers and in influenza, and occasionally from 
intestinal irritation, from coughing, sneezing, and other actions. 
You see, then, that giddiness may depend upon an extraor- 
dinary variety of causes — causes too numerous to be adequately 
discussed in this course, but which I have described and 
illustrated in a series of clinical lectures recently published. 

The subjective phenomena connected with the special 
senses, I shall take along with the other points connected 
with these senses. 

We now pass from the study of the subjective phenomena 
to that of the sensibility of the sensory structures. We take 
first the cutaneous. In studying this, you must note — (1st) 
the various kinds of sensory impressions ; (2nd) the methods 
by which we determine their acuteness ; (3rd) the altera- 
tions which they undergo in disease, and the explanation of 
these alterations. 

1. The Various Kinds of Sensory Impressions. — There 
is a sensibility to touch or contact ; to pressure, which is 
scarcely to be distinguished from touch ; to temperature, 
to tickling, and to pain, the last being experienced also when 
any of the other kinds of impression is sufficiently intensified. 
In investigating cases of disease of the spinal cord, you will 
find it to be true, as Dr. Brown-Sequard pointed out more 
than twenty years ago, that sensibility to some kinds of 
impressions may be lost while others are retained. For 



TOUCH. 



example, there may be loss of sensibility to touch, pressure 
and pain, and retention of it to thermic impressions and 
tickling ; or there may be no sensibility to touch or tickling, 
and distinct perception of pain, as by pricking or pinching ; 
or there may be diminished sensibility to touch, and exagger- 
ated sensibility to pain. It is probable that there are distinct 
structures for each of these kinds of impressions. At all events, 
it may be held as proved that the lines of conduction for some 
of them in the spinal cord are different from those for others. 

2. The Methods hy ivhich we determine their Aeuteness. 
Contact. In some measure we can determine the sensi- 
bility by touching the skin at any point, the patient's eyes 
being closed. For a more accurate determination it is necessary 

to touch the skin at two points 
simultanously, and make out the 
distances at which two simultane- 
ous impressions are recognised as 
distinct. This differs normally in 
various parts of the skin. Accurate 
observation may be conveniently 
made by the help of the eesthesi- 
meter shown in the figure. The 
points are somewhat blunt, and the 
index is marked so that one can 
read ofi' the distance of the two points 
from one another. Perception of 
contact is, according to Weber, most acute in the tip of the 
tongue. His tabular statement may make this more distinct : — 




Fig. 43. 
jEstliesiraeter. 



Tip of tongue, two points on, perceived at 


. 1-1 


mm. 


Palm or surface of last phalanx of linger 


. 2-2 


J) 


„ second ,, 


4-4 


)> 


Tip of nose ...... 


. 6-6 


)> 


Skin of lips 


. 8-8 


)) 


Back of second phalanx of finger 


. 11-10 


>j 


Skin over malar hone .... 


. 15-4 


1) 


Back of hand ..... 


. 29-8 


)) 


Forearm 


. 39-6 


)) 


Sternum 


. 44-0 


)j 


Back 


. 66-0 


!> 



PEESSURE, TEMPERATURE. 



65 



But I must warn you that unless great care is exercised, and 
repeated examination made, ttie results obtained may be 
very untrustworthy. 

It is sometimes important to test the patient's power of 
making out the precise position of a tactile impression. 
His eyes being closed, you direct the patient to tell you 
Avhere you are touching him, or to touch the point with his 
finger, and you judge of his sense of locality by the correct- 
ness of his answer. 

Pressure. In testing the sense of pressure, it is best to 
lay the affected part — e.g., the hand — upon some support, 
and then place coins or weights of different kinds upon 
it. In health, the weight of a sovereign is easily distinguished 
from that of a shilling ; but sometimes, in disease, differences 
far more marked remain unperceived. In the wards we have 
a series of balls all having the same external appearance, 
but weighted differently, and sometimes a patient proves 
unable to distinguish between one weighing above a pound and 
one weighing less than an ounoe. There is, in my opinion, 
no need for more elaborate instruments for testing pressure, 
such as those devised by Goltz and Eulenburg. 

Tenvperature. There are many simple plans by which 
we may roughly determine the perception of temperature. 
Among the best is that of asldng the patient to judge 
whether one hand laid upon his skin is warmer or colder 
than another. A second method is to see whether he can 
distinguish between a breath of hot air and a breath of cold 
air blown upon the surface. Or, in cases where there is 
a distinct deficiency, one may adopt the method usually 
employed in the Avards, touching the patient's skin with a 
cold test-tube, and then with one more or less heated. As 
the test-tubes present the same appearance and produce the 
same tactile impression, they usually afford us definite and 
satisfactory information. You will find that in health one 
can distinguish a difference so slight as half a degree Fahren- 
heit, within what we may call the middle range of temperature ; 
but below about 80°F., and above 90°F., the perception is 
much less acute, — may be absolutely unreliable. Different 
parts of the surface have different thermic sensibility. The 



60 



TICKLING, PAIN. 



face and tho elbow are more sensitive than the hand, the 
back of the hand more than the front. And of internal 
parts, some have no perception of heat. The mouth feels 
heat acutely ; the resophagus only as pain, or, at all events, 
much less distinctly. 

Ticlcling. This kind of sensibility normally exists only in 
certain parts, particularly the soles of the feet and the 
flanks, and it is best elicited by very slight contact. It 
varies much in different individuals, and may be increased or 
diminished in disease. You may find that it is lost when the 
reflex movements usually induced by it are retained. A 
physician one day asked a paraplegic patient, " Do you feel 
me tickling your soles ?" " No," said the patient, " but 
my legs do." 

Pain. For the development of painful impressions, it is 
most convenient to prick or to pinch the skin. By such a 
plan you may generally satisfy yourselves as to the degree of 
sensibility. For more accurate and minute determination, 
you may pass a Faradic current of determined strength 
through the parts under investigation, and note exactly at 
what strength the impression becomes painful. I do not 
think that it is necessary in practice to adopt this method, 
the simpler plans being, as a rule, sufiiciently reliable. 

Rate of Conduction of Impressions. The rate of conduc- 
tion of different kinds of impressions differs somewhat in 
health. Touch is perceived almost instantaneously ; heat or 
tickling somewhat more slowly. In disease, the rate of con- 
duction of aU kinds may become very slow. For ordinary 
clinical purposes it is sufficient to touch or pinch the patient 
and see what interval elapses before he perceives it ; but for 
more accurate scientific inquiry, special instruments may be 
employed, by which it may be ascertained whether the rate 
falls below the normal forty-two metres per second. 

3. The alterations which sensory im-pressions undergo in 
disease, and the explanation of these alterations : — 

Perception may be increased, diminished, or altered. 

Hypercesthesia. Increase of sensibility to touch is a con- 
dition which you can scarcely recognise in practice. When 
there is an increase in sensibility, it very generally amounts 



HYPERESTHESIA, AN/ESTHESIA. 



67 



to hyperalgesia, ordinary impressions being felt as painful, and 
painful impressions being felt with undue intensity. This 
condition may be a result of change in the nerve-endings, 
and in the skin and mucous membrane. Inflammatory or 
other irritation supplies the most famihar example. It may 
be in the nerves, or in the spinal cord or its membranes, that 
the undue excitability originates, as we see often in inflam- 
matory and congestive conditions. There is often a zone of 
hypersesthesia corresponding to the upper margin of a spinal 
inflammatory lesion. The fault may lie in the sensory 
centres themselves. We see it very commonly in hysteria, 
and in hypochondriasis, and in insanity, and it occurs in 
hydrophobia and tetanus. It occurs as a temporary symptom 
in some cases of megrim, the whole head or one side of the 
head becoming, during the attack, extremely sensitive, so that 
the patient cannot bear to be touched even in the gentlest 
way. It is described as resulting from certain drugs, in parti- 
cular cannabis indica, and is sometimes, no doubt, congenital. 

Ancesthesia. Diminution of sensibility may result from 
changes in the nerve-endings, or in the nerves. Local 
auEesthesia may be artificially produced by means of great 
cold, or by aconite, and it probably sometimes results from 
disease in the end-organs. It is also frequently a result of 
injuries of nerves or pressure upon nerves, sometimes such an 
injury leading to permanent local anaesthesia. I remember a 
patient who suffered much from neuralgia, and required 
frequent subcutaneous injections. He always liked to have 
the needle introduced into one side of' his forehead, because it 
chanced that as the result of an old injury he had permanent 
anaesthesia of the district supplied by the supra-orbital nerve. 
It also frequently results from disease of the spinal cord, par- 
ticularly disease of its posterior part. When of spinal origin, 
it may affect the legs only, or the trunk and arms also. It 
may be confined to one leg, or to a part of the leg. I have 
known a little patch in the thigh retain sensibility when the 
rest of the limb had lost it ; and I have known, in locomotor 
ataxia, anaesthesia varying in degree, sometimes getting 
better, and then again growing worse. Sometimes it appears 
as a zone or belt around the body, or one half of the body. 



68 



DYSESTHESIA. 



The belt may be so broad as to corresiDond to several nerve 
districts, or may correspond to one only, Anrestbesia may 
be confined to the skin, or it may affect mucous membranes 
as well. Sometimes the skin may retain at least some kinds 
of sensibility, wbile tlie bladder and uretbra have none. One 
of my patients, suffering from locomotor ataxia, had such a 
degree of ansesthesia of the bladder and urethra, that he never 
knew when there was a call to micturition, or that micturition 
had taken place, until he felt the warm urine touching his 
thigh. The lesion causing the anassthesia may be farther up. 
It may be in the medulla, in the pons, the crura cerebri, the 
posterior part of the internal capsule, or in the sensory centres 
about the hippocampus. AuEesthesia originating in these parts 
is commonly a result of organic disease, but you must remember 
that purely functional conditions suffice in some cases to pro- 
duce it. The cerebral ansesthesise are very often unilateral, and 
even the functional ones frequently present this distribution. 
The typical hysterical hemi-aneesthesia, involving cutaneous 
and special sensibility in one half of the body, seems to be 
much more common in France than it is here, but we meet 
with it occasionally in the hospital and private practice. It 
is very striking to observe in some of these cases the anaesthesia 
pass from the one side of the body to the other, the side which 
a few minutes before had been so torpid as to be indifferent 
to formidable injuries becoming quite sensitive, while the other 
side, which had been normal, has passed into the torpid 
condition. My friend, Dr. Ireland, informs me that he has 
observed spots in the skin of some idiots, which were 
congenitally insensible to pricking or other irritation. 

Byscesthesia. There is a curious condition, first described 
by Charcot, and which he has termed dysesthesia. It con- 
sists of a sensation of a peculiar kind, produced in various 
ways. For example, when a foot is touched with somethmg 
cold, the patient feels a distressing trembling sensation 
running up the interior of the leg. Then the sensation seems 
to pass down the leg and may persist for a quarter of an hour. 
In this condition, there is manifestly irritability of the nerve- 
centre, so that a slight impression produces a powerful, wide- 
spread, and prolonged effect. 



KATE OF CONDUCTION OF IMPRESSIONS. 



69 



Allochiria. Another sensory abnormality is that known as 
allocliiria. The sensation is perceived not on the side 
touched, but on the other side of the body. If you prick 
one Hmb, a patient feels pain in the other. I Icnow no satis- 
factory explanation of this rare peculiarity. 

Polycesthesia. Sometimes a patient, when touched at one 
point, feels as if he were touched at two, three, four, or five. 
To this condition the name polysesthesia has been applied. 
It may be explained on the hypothesis, that a certain radiation 
of the impression takes place, so that more than one central 
point becomes affected. I have lately had an opportunity of 
demonstrating a case of this kind to members of the clinical 
class. The patient had sustained an injury to the head, and 
presented several obscure nervous symptoms. If I touched 
him with one finger, he said that he felt two, three, or four 
— and this especially when I touched one particular part of 
his leg. 

Retarded Conduction of Impressions. In disease the 
rate of conduction may become very slow. Sometimes an 
interval of twenty or more seconds may elapse before touch 
may be perceived. I remember that a patient, whose case 
I used often to demonstrate to some of your predecessors, 
was so slow in perceiving touch that we had sometimes gone 
on to another point when he would say, " I feel it now." 
It is also remarkable how much slower the conduction of 
painful impressions may become in cases of this kind. You 
may blindfold a patient, and ask him to teU you whenever 
he feels himself touched. Prick him with a needle, or touch 
him with a very warm test-tube, he may say, " Now," and 
then, a little afterwards, cry out " Oh ! " as the painful 
impression reaches his sensorium. This slowness of 
conduction I have seen mainly in cases of locomotor 
ataxia ; and in such cases you will sometimes find that it 
varies from time to time, the conduction being now slower, 
and now again more rapid. When one kind of sensory 
perception is affected, as to its rate of conduction, it is 
usually found that all are. But as I have abeady shown you, 
one or other may be specially involved. 

Passing now from the cutaneous sensibility, we proceed 



70 



MUSCULAR SENSE, 



to consider the Muscular Sense and its abnormalities. 
By means of the muscular sense, wo are informed of the 
condition of contraction in the muscles, and guide ourselves 
in motion and co-ordination. It is true that we do not 
usually realise in our consciousness the impressions derived 
from this source. It is doubtful whether it would be 
possible to realise them in many instances. Certainly the 
ordinary process is for the motor and co-ordinating move- 
ments to respond to the muscular sense, without the 
intervention of consciousness, and in an automatic way. 
Subjective changes connected with the muscular sense are 
by no means well-defined ; but I think that the peculiar 
sensation known as " fidgets," a feeling of uneasiness within 
the muscles which leads to an irresistible desire for movement, 
is to be classed as such. Possibly some other feelings, 
such as great weight in the limbs, may be dependent on it 
also. 

The acuteness of the sense may be tested in various ways. 
We may ask the patient to judge of the weight of different 
coins placed in his hands, or of weights slung over his feet 
or legs. In health one can distinguish easily with the hand 
between the weight of a sovereign and of a shilling ; and 
although the perception through the legs is less acute, yet 
comparatively slight differences may be appreciated. Another 
method is to let the patient stand with closed eyes, the feet 
being placed close together. A healthy person stands 
steadily under these conditions, but if the muscular sense is 
impaired, the patient sways about or sometimes even falls. 
Such unsteadiness may occur in other conditions — for 
example, in slight paraplegia — unattended by impairment of 
muscular sense. But, on the whole, it is fairly characteristic. 
Another plan is to direct a patient, his eyes being closed, to 
touch rapidly with the tip of his finger some part of his body, 
such as the point of his nose or the lobe of his ear. In health 
the movement is usually performed with precision and rapidity. 
When the muscular sense is impaired, the movement is 
hesitating and the result inaccurate. Another method 
which is commonly employed, but which is less a test of the 
muscular sensibility than of the cutaneous and articular, is 



MUSCULAR SENSE. 



71 



putting the patient's limbs in different positions and asking 
him to tell you where they are. 

The muscular sense may be increased. It seems to be so in 
soronambulists and in the hypnotic state, for it appears 
probable that it is mainly by the muscular sense that the 
somnambulist with closed eyes, or the hypnotised patient, 
Sfuides his movements. In certain of the eccentric forms of 
epilepsy, the same may be held to occur ; for a patient may, 
in that condition, be seen to guide his movements with the 
eyes closed, or without attending to visual impressions. 
Dr. Carpenter has speculated in an interesting way upon the 
suggestion of ideas through the muscular sense, remarking 
that when the subject of a mesmeric experiment is put into 
one position he becomes combative, in another assumes the 
air of pride or arrogance. 

We very frequently find muscular sense diminished. You 
have probably heard of the case of a patient whose muscular 
sense had become lost, and who found that if she removed 
her eyes from the baby which she was accustomed to carry 
in her arms, she was sure to let it drop. Sometimes it is 
affected without other impaument of sensory functions ; far 
more frequently cutaneous sensibility is impaired along with 
it. I have often demonstrated the case of a man whose 
muscular sense was so much impaired that he could not 
distinguish between the weight of a few ounces swung over 
his legs and one of many pounds. Ultimately he lost 
cutaneous sensibility ; but at one time he could so far distin- 
guish by the sense of pressure, and we had to take special 
precautions in determining the facts. It is very common, in 
cases of locomotor ataxia, to find the muscular sense markedly 
impaired ; and I once had under my care a patient who, 
whenever she closed her eyes for more than a second, used to 
drop down, falling all of a heap. One of the most extra- 
ordinary cases that I know of is described by Professor 
Niemeyer, It was that of a peasant, who lived a few 
miles from Tubingen, where Niemeyer was at one time 
professor. He had a profound anaesthesia of the skin 
and the muscles. On his extremities being loaded with a 
weight of twenty-five pounds, no difference was perceived. 



72 



MUSCULAR SENSE. 



On being requested to estimate weights by lifting them, 
be failed to distinguish between one pound and one 
hundred pounds. When he stood or sat up, if he closed 
the eyes, he immediately fell. "With his eyes closed, 
he could not tell whether his limbs were flexed or straight- 
ened out by strong electric currents. The severest injury 
could not hurt him. He could not distinguish between 
cold and warm water ; and not only did he fail to feel the 
ground under his feet, but, when lying in bed, he felt as if 
cushioned on air. It is worthy of remark that this patient 
could walk very considerable distances, and exhibited, when 
his eyes were open, ver}'- slight tokens of imperfect co- 
ordination. 

It is conceivable that such loss of muscular sense as I have 
described may result from lesions of the nerves, but I have not 
yet seen proof of this. It is usually seen in disease of the 
spinal cord, and especially in disease of the posterior root-zone 
in locomotor ataxia. Whether it is ever connected with brain 
disease of an organic kind, as one would naturally suppose to 
be the case, is not at present known ; but the fact that it 
often occurs in hysteria makes it probable that its cause may 
be situated in the cerebrum as weU as in lower parts of the 
nerve-centres. 



LECTUEE V. 



Sensory Functions — (Continued). 

Eye Symptoms in Nervous Diseases. — Subjective Phenomena. — 
Flashes of Light. — Muscce Volitantes. — Eye Symptoms in Megrim. 
— Colour-hearing. — Blindness. — Area of Vision-Tests. — Peri- 
meter. — Central Scotoma. — Marginal Scotoma. — Partial Scotoma. 
Hemianopsia (Homonymous and Heteronymous.) — General 
Dimness. — Snellen's Types. — Colour Blindness. 

ri ENTLEMEN, — We now proceed to consider the nerve 
^ symptoms connected with sight. I shall speak first of 
the subjective phenomena. 

Flashes of Light. Patients often complain of seeing bright 
flashes of light before their eyes, like those produced in 
healthy people by pressure on the eyeball. Such appear- 
ances occur frequently in disease, and not only in cases of 
inflammatory and degenerative changes of the retina or optic 
nerve, but in hypersesthetic conditions of the retina connected 
with affections of the brain. As you might expect, such 
patients often find the condition increased by very sHght 
muscular movements or trivial pressure on the eyeball. 

Muscce Volitantes. The spectrum of black or grey fly- 
like objects before the eyes, sometimes with definite and some- 
times with indefinite forms, sometimes motionless, at others 
following one another in definite lines, or moving irregularly, 
constitutes what are known as muscse, and muscse volitantes. 
They are said to be due to shadows thrown on the retina by 
connective tissue corpuscles in the vitreous humour. They 
are often seen in connection with disease of the eye itself, and 
frequently with affections of the aUmentary system, particu- 
larly functional diseases of the liver. But they also occur as an 
accompaniment of cerebral disease. When you meet with 
them you must conclude either that the retina is unduly 
sensitive, so as to perceive what would not be perceptible 



74 



SUBJECTIVE EYE SYMPTOMS. 



in health, or that the connective tissue corpuscles are increased 
in size and throw shadows more distinctly than they ought 
to do. But you will find that they are most distinct when the 
pupil is contracted, and I think that most of you will succeed 
in demonstrating them to yourselves if you look at a bright 
light through a pin-hole in a piece of cardboard. Now it 
is obvious that hypermetropic individuals, having as a rule 
contracted pupils and suffering from congestion, due to strain- 
ing of the accommodation, with enlargement of the connective 
tissue-corpuscles as a consequence, must be specially liable 
to this symptom. In cases of myosis you may expect to find 
this symptom present, but remember that it is rare when the 
myosis is of spinal origin. It is evident that if enlarged 
connective-tissue corpuscles suffice to produce the symptom, 
blood or inflammatory products in the vitreous humour may 
also suffice. 

Eye Symptoms in Megrim. In connection with megrim, 
various subjective phenomena occur. One of the commonest 
is the spectrum of fixed or moving lines of bright colour. 
The lines are uneven, presenting a Vandyked appearance, 
with acute angular projections and recesses. They are often 
best seen when the eyes are closed, and are modified by 
firm closure of the lids. Sometimes there is only one 
colour at each point, as is shown in Dr. Airey's well- 
known drawing ; at others there is play of colours in 
parallel lines. Another common feature of megrim is 
the partial dimness or actual blankness of the field of 
vision. The blank area may be bounded by a Vandyked 
line, or occur without it. Sometimes there is central scotoma, 
often unilateral or partial. Sometimes, again, there is a 
distinct hemianopsia. These symptoms often usher in the 
attack of hemicrania. And many patients say that the eye 
symptoms disappear when the headache sets in, while others 
have the dimness of vision all through the attack. 

Colour-hearing. A curious eye-symptom which has only 
recently been described is known as colour-hearing. People 
who are affected with it see some particular colour in the field 
of vision when certain musical notes are heard, with higher notes 
brighter colours, with deeper notes colours less vivid. I may 



FIELD OF VISION. 



75 



mention in this connection a somewhat analogous phenomenon 
which once came under my observation. I was remarking 
on a beautiful combination of colours to a gentleman, when 
he turned to me and said, "Whenever I see such colours 
as these, a sweet taste fills my mouth." One may suppose 
that in such cases the commissural links connecting different 
sensory centres are highly developed, so that excitation of one 
produces a corresponding change in the other. 

Blindness. Sight may be interfered with in respect either 
of area, or acuteness, or of both. 

I. Area or Field of Vision. The normal field of vision 
is limited only by the position of the eye and the prominence 
of the nose and forehead. You will find that not unfre- 
quently this area becomes diminished. The limitation may 
be in the centre, while the edges remain distinct. It may be 
at the edges. It may affect half the eye or irregular patches. 
In order to determine the field of vision each eye must be 
separately tested. You may do this in a rough way — accu- 
rately enough, however, for most clinical purposes — by asking 
the patient to fix his eye on some point right in front of him, 
and ascertaining when he catches sight of objects brought into 
the margin of the field. In cases in which it is desirable 
more accurately to determine and record the area of vision, 
one or other of the various perimeters should be employed. 
The best is that of Mr. M'Hardy. 

This perimeter consists essentially of two uprights (C and D), 
which rise perpendicularly from opposite ends of a flat, heavy 
bed-plate (A) The first of these (C) is for the support of the 
patient's head, while the other (D) carries the automatic 
arrangement for the perimetric record. Both have telescopic 
fittings, to allow of vertical adjustment, fixation at any parti- 
cular height being obtained by the locking-screws (G and h.) 
The patient's head is supported by means of the double 
chin-rest (E), and the bit arrangement (L, M). Alteration in 
the relative position of these is permitted by the sliding of 
the horizontal bar of L on the upright F, fixation in any special 
position being produced by the milled screw (0). The bent 
stem (H), also borne by the upright (C), and terminating in the 
porcelain button (I), serves in the adjustment of the "fixation- 



76 



PERIMETER. 



point " (see below) on a level with the patient's eye. It is 
attached by a sliding-collar (J) to the upright, and a hinge 
arrangement allows of its being turned aside after the adjust- 
ment has been made. The automatic arrangement for 
obtaining the perimetric record is rather more com- 
pHcated. It consists essentially of a revolving quadrant, 
which is attached to the front end of a hollow male 




Fig. 44. 



M'Hardy's perimeter. For explanation of lettering and method of use, see text 

axle, which turns in the female upper expanded end of a, 
supported by the upright D. The quadrant describes a 
hemisphere around a horizontal axis, and may be fixed at 
any angle by the slightest turn of the screw-head (g). The 
anterior concave surface of the quadrant bears a carriage 
(i), which is made to move rapidly from one end to the other 
by means of an endless band with pulley arrangement. The 
moving carriage bears the test objects. The strong endless 



PEKIMETER. 



77 



band is connected with a large groove-wheel, which, in its 
turn, is connected with three different-sized pinion- wheels. 
Of these, the largest gears with a toothed wheel, driven by 
the large milled-head (J). Eotation of this milled-head 
moves the carriage, by means of the large grooved wheel and 
the endless band, and, at the same time, drives the two 
smaller pinion-wheels. These wheels, of which one is twice 
the other in diameter, gear with two racks attached to two 
slides (k and I), travelling at the relative rate of 2 to 1. 
The mechanical arrangements are such, that when the large 
milled-head is moved, the carriage goes ten times as fast as 
the slow slide, and five times as fast as the other. Each 
slide has a cyhndrical projection, to which a hollow cylinder 
terminating in a pointer (p) can be fixed. To the lower end 
of the upright (D) is hinged the movable limb (c), terminating 
in the square socket (d), fitted for the reception of the stem 
of a double-faced frame (e), which carries the record- charts 
(right and left eye). When the limb (c) is upright, it is 
so placed in relation to the slide with the pointer, that 
the pointer can just pierce a chart held in the frame. 
In the position of the axis of the imaginary hemisphere, a 
circular piece of white ivory is let into the vulcanite forming 
the anterior concave surface of the quadrant midway between 
its edges. This is the " fixation point " of the instrument. 
If a more conspicuous fixation point is desired, a piece of 
white paper can be attached to a needle-point, which projects 
from the surface of the ivory. Both edges of the quadrant 
are graduated, commencing with zero at the fixation point up 
to 90°. 

The arrangement is such that, if everything is in proper 
order, with the carriage eclipsing zero, the point ought to 
pierce the chart paper exactly in the centre. This point must 
always be ascertained before making a record. The fixation 
point being arranged on a level with the patient's eye 
by the mechanism previously referred to and by the Vernier 
scale on a and K, the patient looks intently at it, and the 
can-iage is moved along the quadrant until it passes from the 
field of vision. Exactly where it does so, the pointer is made 
to pierce the chart. The angle of the quadrant is then 



78 



CENTEAL SCOTOMA. 



altered, and a second observation made, and so on. By this 
means a complete graphic representation of the patient's 
field of vision is obtained. Of course, each eye must be 




FlO. 45. 

Perimetric record of normil field of vision. 



tested separately, the other eye being closed, and the position 
of the chin altered. By changing the colour of the test 
object in the carriage, the perimetric representation of the 




Fio. 46. 

Perimetric record of visual field in central scotoma. 



patient's colour field may also be obtained. In the 
drawing (fig. 45), you see the perimetric record of the field of 
vision in normal eyes. 

Central Scotoma is the condition in which the central part 



JIARGINAL SCOTOMA. 



79 



of the field of vision is dim or blind. In the drawing (fig. 46) 
you see the field of vision in a case of organic disease at the 
macula lutea. It may result from organic causes, such as 
inflammation, degeneration, or hemorrhagic extravasations, 
or may be merely toxic, as from tobacco or alcohol. You 
Avill find in practice, that among the commoner causes of 
central scotoma is the excessive use of tobacco. The organic 
cases are often unilateral — the toxic affect both eyes. In 
the organic, there is often a sharp line of demarcation 
between the blind and the sensitive part. In the toxic, the 
transition is gradual. The organic changes often lead to 
complete blindness, while in the toxic there is only dimness 




Pig. 47. 

Perimetric record of slight marginal scotomtu 



Fill. 48. 

l erimetric record of marginal scotoma in 
advanced case. 



as a rule. You will find, for example, that the centre of 
vision in cases of tobacco amblyopia is reduced in sensitive- 
ness to about the standard natural to the periphery. You 
will notice that such patients direct their eyes straight 
towards the object at which they are looking, which implies 
that the centre is not blinder than the periphery. 

Marginal Scotoma is that form in which the dimness or 
blindness is at the margin of the field, the centre being 
clear. The degree of contraction of the field of vision 
varies greatly in different instances. In fig. 47 you see 
the field of vision in a slight case. In fig. 48 you see it in 
one more advanced. The condition is almost invariably 



80 



SCOTOMA IN PATCHES. 



a result of organic changes in the optic nerve and its 
expansion in the retina. It is most common in optic 
atrophy, whether following upon optic neuritis, from local 
or from intra-cranial disease, or a process confined to 
the nerve or associated with spinal affections. Such con- 
ditions also arise in glaucoma and in other diseases of the 
eye proper. 

Scotoma in Patches is a condition frequently seen in 
practice, and one which is not unfrequently overlooked by the 
patient, as it may come on gradually and is often confined 
to one eye. In the chart (fig. 49), you observe that a well- 
defined blindness exists in one eye. In the particular case 




J'IG. 49. 

Perimetric record of scotoma in patches. 



from which this was taken, the patient suffered about twenty 
years ago from acute rheumatism, and, during convalescence, 
was suddenly seized with dimness at first in the whole field 
of vision. In a few minutes the field cleared up to one 
half, and soon after to a quarter. On ophthalmoscopic 
examination, it was found that emboHsm had taken place 
in one of the branches of the retinal artery. An extrava- 
sation followed, and the portion of the retina correspond- 
ing to the drawing remains to the present day blind. 
The condition may result from other causes besides embohsm, 
as from retinal hcemorrhages, inflammations, or degenera- 
tions. 



HEMIANOPSIA. 



81 



Hemianopsia, or Hemiopia, is a condition of great interest, 
half of one or of both eyes being bHnd. In fig. 50 you see the 
perimetric record of such a case. You observe that the line 
passes almost straight down the middle of the field of vision, 
diverging slightly to one side at the central spot. Hemian- 
opsia may be homonymous — i.e., may occur in the correspond- 
ing halves of the two retinse, the inner half of one and the 
outer half of the other. It may be heteronymous — i.e., 
occurring in the inner or the outer half of both eyes. 
The latter is extremely rare. The explanation of these 
various conditions is to be found in the arrangement of the 
optic nerves within the cranium, which I have already 
described. 



Fro. 50. 

Perimetric record in case of hemianopsia (homonymous). 

Homonymous hemianopsia is apt to be overlooked. 
I have known a patient make no complaint about it, and 
remain unconscious of its existence till he was carefully 
tested. In one case, for example, suspecting that there was 
something wrong with the sight, I asked the patient to read 
a text which hung upon the wall of the ward. The man 
was a bill-sticker and familiar with placards, and instead of 
the text, which contained the words : 



CAN A WOMAN 
FORGET HER 
SUCKING CHILD ? 



He read — 



WOMAN 
HER 
CHILD ? 



82 



HEMIANOPSIA. 



If you refer to fig. 51, you will at once perceive how 
homonymous hemianopsia results from injury (A) of the optic 
tract on either side, or from destruction of the radiating 
fibres or of the cortical visual centre. In the case of internal 
heteronymous hemianopsia, the figure also .shows how the 
lesion (B) must be situated at the anterior part of the optic 
commissure ; while in the case of external heteronymous 
hemianopsia there must be a double lesion (CC) so situated as 
to command exclusively the fibres going to the external half 
of each retina. 



LEFT EYE R/CHT EVE 




Fig. 51. 

Diagrammatic representation of course and decussation of optic 
nerve-tibres, showing eflect of lesions (see text). 



While opinion may be said to be unanimous upon these 
points, there has been much discussion as to whether lesion 
at the roots of the optic nerve on either side of the brain 
may induce the symptom. Dr. Allen Starr, of New York, in 
a valuable paper recently published, argues that anatomical 
research, physiological experiment, and pathological obser- 
vation unite in assigning to the occipital lobes the function 
of sight, the right occipital lobe receiving impressions from 



AMBLYOPIA. 



83 



the right half of both eyes, and the left occipital lobe from 
the left half of both eyes. Ferrier's most recent experiments 
have satisfied him that destruction of the whole occipital lobe 
and angular gyrus on one side produces temporary amblyopia 
of the opposite eye, and homonymous hemianopsia (of both 
eyes) of the side opposite the lesion. But he finally con- 
cludes that, as these changes are temporary, vision is possible 
with both eyes, if only portions of the visual centres remain 
intact on both sides. 

Hemianopsia of central origin may result from organic 
lesions, as softening, tumour ; but it may also be purely 
functional. Along with other hysterical manifestations the 
most pronounced hemianopsia sometimes occurs. In megrim, 
as I have already told you, short attacks of hemianopsia 
sometimes are not uncommon. 

II. Dimness of Vision. Besides blindness in areas more or 
less extensive, brain disease may give rise to general dimness 
of vision. You see this resulting from toxic causes, as in 
some cases of uraemia ; sometimes also in diabetes mellitus. 
The uraemic amblyopia may amount to actual blindness or 
may be a mere misty dimness. It may come and go with 
considerable rapidity, and is unattended by any ophthalmos- 
copic change or lesion of the optic tract, so far as we know 
at present. Sometimes similar dimness occurs in oxaluria, 
in hysteria, and in cases of nervous exhaustion. 

The modes of determining the degree of acuteness of 
vision are — (1) in ordinary cases, asking the patient to 
count fingers or to describe any object in the room in which 
you may happen to be examining him ; but (2) in more 
special cases, the use of the various type tests, such as are 
employed by oculists for determining the condition of the eyes. 
Snellen's types are those most generally recommended. They 
are of different sizes, so arranged that at certain distances the 
normal eye is able to read them. According to the degree of 
visual acuteness, they are more or less distinctly seen. You 
will find that in ordinary physician's practice such a set of 
tests as has been arranged by Mr. Ncttleship is very suitable. 
The number above each of the types shows the greatest 
distance (in feet) at which it can be read by a normal eye 



84 



COLOUR VISION. 



in good dayliglit, the distance being of course considerably 
less by bad daylight or artificial light. 

Di'plopia, or double vision, is often met with in cases of 
nervous disease. It is usually binocular and a result of 
squint, sometimes of a misdirection too slight to be observed. 
It of course disappears when one eye is closed. Sometimes 
we meet with double vision in one eye, as in commencing 
cataract, and in some cases of cerebral disease. I cannot 
explain the mechanism of its production in the latter class 
of cases, and have not myself met with an example of it. 

Hemeralopia and Nyctalopia are rare alterations of sight. 
The former may be described as a condition in which vision 
is imperfect during the day or in bright Hght, and much 
better in dim light. It is found associated with incipient 
cataract. The latter, nyctalopia, may be described as a 
disorder of vision in which sight is good by day or by bright 
light, but unduly defective in dim light. It is a result of 
temporary exhaustion of the retina from prolonged exposure 
to bright light, and occurs especially in people in a low state of 
health. It is not a result of central change, but of change in the 
eye itself, and is often associated with retinitis pigmentosa. 

Colour Vision. The perception of colour is often interfered 
with in disease. The colour perception may be tested by 
showing articles of different colours, and seeing how far they 
are distinctly recognised. Holmgren introduced a plan which 
is very convenient. The patient is directed to match a skein 
of coloured wool or silk with other skeins of different tints. 
Or you may adopt Stilling's method, which consists in show- 
ing the patient plates of coloured letters printed on a ground- 
work of complementary colours. Mr. Nettleship has also 
arranged a set of tests, which are sold along with the types 
to which I have above referred. The colours are planned 
chiefly for the detection of well-marked defect for green and 
red. It is best, showing the patient a series of the colours, 
to ask him to point out those which resemble one another. 
The area of colour-vision may be conveniently determined 
by means of M 'Hardy's perimeter wafers of different tints, 
replacing the ivory knob in the carriage. All colours are 
not equally well perceived in the different areas of the eye. 



COLOUR BLINDNESS. 



85 



Thus in health, at the margins blue is best seen. Next to 
blue comes yellow, then red, and then green. Fig. 52 
shows the normal area of colour-perception. 

Colour-blindness is sometimes slight, sometimes very pro- 
nounced. I have heard of the case of two tradesmen in 
Edinburgh, one of whom was so colour-blind that he would 
offer an article of one colour when asked for another ; while 
his neighbour, who worked in metals, used to carry a small 
pocket file with him, as it was only by their degrees of hard- 
ness that he was able to distinguish them. Red and green 
are often confused, blue and yellow much more rarely. 
Bonders states that a red -green-blind person sees in the 




Fig. 52. Fig. 53. 

Perimetric record of normal field of vision The lines surround the blind area. 

for colour. Perimetric record of field of vision for colour, 

as altered in case of tobacco colour-blindness. 



spectrum only two colours, separated by a neutral stripe, 
placed somewhere in the greenish blue. All the reds are 
confounded, and all the violets, but he finds the red and 
violet never confused. Colour-blindness is often congenital, 
and occurs far more frequently in the male than in the 
female sex. I have noticed that colour-blind people are 
frequently mentally acute, but have a peculiarity of manner, 
and some angularity of character. But it also occurs as a 
result of disease, particularly with inflammatory and degene- 
rative changes in the optic nerve, such as we see so often in 
cases of cerebral tumour and locomotor ataxia, less commonly 
in diseases of the retma and in glaucoma. Dr. Brill has 
recorded an interesting case in which, along with other 



86 



COLOUR BLINDNESS. 



symptoms, colour-bKndness occurred without limitation of 
tlie visual field, and in which the autopsy revealed a 
patch of softening in the left side of the brain, involving 
the cortex of the occipital lobe where it borders on the 
calcarine fissure, the upper edge of the uncinate gyrus, and 
the lower half of the cuneus. It . may be diffused over 
the whole field of vision, or may be localised in patches. 

Colour-blindness may also result from mere functional con- 
ditions, affecting one eye, as in cases of hysterial hemianses- 
thesia, or both eyes, in other hysterical conditions. In certain 
toxic conditions, also, functional colour-blindness arises. It 
attends upon tobacco amaurosis, and also sometimes arises 
from excessive indulgence in alcohol. In these cases the 
colour perception is often- most markedly interfered with in 
the centre of the field of vision. 

Fig. 53 shows the record of a case of tobacco colour- 
blindness. Within the red line there was no perception of 
red, within the green line no perception of green. It is 
these colours that are most markedly interfered with in 
such cases. The perception of blue and yellow is frequently 
more acute at the periphery than at the centre, but generally 
it is not lost. 



LECTURE VL 



Sensoey Functions — (Continued). 

Eye Syinptoms. — Alterations of Pupil. — Irregular Form. — Myosis. 
— Mydriasis. — Argyll Kohertson Symptom. — Headache and 
Neuralgia due to Hypermetropia, Myopia, and Astigmatism. — 
Ophthalmoscopic Examination. — The Normal Fundus. — Optic 
Neuritis. — Not necessarily attended hy Loss of Sight. — Primary 
Optic Atrophy. — Embolism. — Retinal and Choroidal Changes. 

Ear Symptoms. — Subjective. — Hearing increased, diminished, or pre- 
vented. 

Smell. — Subjective Symptoms. — Increase. — Diminution. — Perversion 
of Smell. 

Taste. — Subjective Symptoms. — Increase. — Diminution. — Perversion 
of Taste. 

GENTLEMEN, — In continuing the account of the rela- 
tionship of eye symptoms to nervous diseases, we 
proceed to consider the important indications afforded by 
alterations of the pupil. You remember that the movements 
of the iris are regulated by two distinct nerves. The 
sympathetic fibres which proceed from the cilio-spinal region 
of the cord induce dilatation, while the ciliary branches 
of the third nerve, which pass through the lenticular 
ganglion, produce contraction. You remember also that the 
size of the pupil varies in health with the intensity of light, 
impressions being received by the optic nerve, conducted to 
the corpora quadrigemina, and thence, probably by fibres 
described by Meynert, to the nuclei of the third nerve in the 
floor of the fourth ventricle. Alteration of size also occurs 
with the accommodation of the eye to near and distant 
objects, these movements, along with convergence, being prob- 
ably regulated by a centre towards the posterior part of the 
floor of the fourth ventricle. You will find it convenient in 

87 a 



88 



MYOSIS, MYDRIASIS. 



practice to have a handy means of estimating and recording 
the size of the pupil, and Mr. Nettleship has supphed this 
also in his pocket-case for testing the eyes. The card should 
be held flat with the iris and close to the outer canthus. 
The number near each circle on the card shows its diameter 
in millimetres. 

Irregular Form of Pupil. The pupil may be irregular in 
its form, as we see often in iritis, whether of syphilitic or 
non-syphihtic origin, adhesions binding portions of the 
curtain in abnormal positions. In general paralysis of the 
insane the pupil often becomes somewhat angular, presumably 
from altered nerve influence, and you will occasionally notice 
congenital peculiarities of the form of the pupil. 

Contraction of the Pupil or Myosis arises under a great 
variety of conditions. 1. It occurs in hypermetropia or far- 
sightedness, and in certain trades, such as watchmaking, 
the patient being always under the necessity of straining 
his power of accommodation, associated myosis being 
thereby produced. 2. In cases of photophobia, from the 
excessive sensitiveness of the retina. 3. It occurs also in 
conditions which paralyse the sympathetic fibres. These are, 
so far as I know, three in number : (a) disease of the cord 
itself in the ciHo-spinal region, as we see so frequently in 
locomotor ataxia ; (h) pressure upon the sympathetic, as by 
tumour, seen often in aneurism of the aorta ; (c) paralysis of 
the sixth nerve, from involvement of the accompanying fibres 
of the sympathetic. 4. It occurs, in association with cerebral 
irritation, as from concussion of the brain, from meningitis, 
from typhus fever, and is sometimes associated with hysteria 
and with epileptic convulsions. 5. Lesions of the pons and of 
the medulla may induce myosis. 6. It has been found associ- 
ated with progressive muscular atrophy. 7. It is produced 
by the local application of certain substances, such as 
Calabar bean and pilocarpin. 8. It may be produced by 
the internal use of remedies, particularly opium and chloral 
hydrate. 

Dilatation of the Pupil or Mydriasis is also often met 
with in disease. 1. It is seen in cases of myopia or short- 
sightedness, the relaxation of the structures for accommoda- 



ARGYLL ROBERTSON SYMPTOM. 



89 



tion being associated witli relaxation also of the pupillary 
contractor fibres. 2. It occurs in amaurotic affections, such 
as blindness from disease of the optic nerve. 3. In cases 
where the sympathetic nerve is irritated, as we sometimes see 
in tlie earlier stage of aneurismal pressure on the nerve. 4. 
It occurs in cases of paralysis of the third nerve. 5. You 
often see it in connection with paralysis of the ciliary 
branches of the third. 6. It is present in cases of glaucoma, 
the lens being pushed forward and mechanically dilating the 
pupil ; but this scarcely belongs to our present subject. 7. 
It occurs in consequence of compression of the brain, either 
from external injury or from apoplectic extravasation. 8. It 
is very commonly associated with chlorosis, cerebral anaemia, 
hysteria, and typhoid fever. 9. It sometimes results from 
peripheral irritation, such as rubbing the skin of the forehead 
or the back of the neck. 1 0. It results from the local appli- 
cation of various substances, particularly atropine, to the eye. 
11, It foUows the use of certain internal medicines, such as 
belladonna. 

Argyll Robertson Symptom. Besides the alterations in 
the size or form of the pupil, you must remember that its 
movements vary under certain morbid conditions. The 
most interesting of these is the occasional failure of the 
pupil to react to light, while it still alters with accom- 
modation. This symptom, to which we have given the 
name, the " Argyll Robertson symptom," was discovered by 
Dr. Argyll Robertson, and is now universally recognised as 
of common occurrence in locomotor ataxia. It is interesting 
to notice that it may exist, either with or without spinal 
myosis ; and the explanation of the symptom obviously lies 
in this, that whereas in locomotor ataxia the structures 
subserving the reflex contractions with light are diseased, 
those which have to do with accommodation rarely, if ever, 
become involved. 

Headache and Neuralgia from Eye Defects. Among 
the other eye-changes with which you should, as physicians, 
be acquainted, are hypermetropia, myopia, and astigmatism. 
Patients often complain of headache, coming on especially 
when they have been reading small print, or working in 



90 



HEADACHE FROM EYE DEFECTS. 



dim light, or otherwise straining their eyes. Such symptoms 
are often due to one or other of the conditions I have 
named. In hypermetropia, or far-sightedness, the eye is flat- 
tened, shortened in its antero-posterior axis, so that refractive 
media of natural power bring the rays to a convergence at a 
point beyond the retina. This, of course, makes the sight 
indistinct. The patient instinctively makes an effort to over- 
come the defect, by altering the accommodation, and thereby 
strains the eye. From this straining, perhaps also from the 
indistinctness of vision which still remains, headache arises. 
Myopia, or near-sightedness, in which the eyeball is elongated, 
interferes with vision by requiring the object to be close to 
the eye. It thus demands great convergence of the eyes, 
and this involves effort and fatigue, often inducing headache 
and neuralgia. There are two other more recondite factors 
— the alteration in the shape of the eyeball, which constitutes 
a mechanical hindrance to its movements, and the want of 
correspondence between two sets of muscular movements. 
In normal vision the effort for convergence corresponds to 
the effort for accommodation. Wherever these do not 
correspond, uneasiness results. Now, in the case of myopia, 
the interior of the eye is already arranged for near vision. 
Muscular effort is required for convergence and not for 
accommodation, — fatigue, therefore, results. Astigmatism, 
again, a condition which is commonly a result of an altered 
shape of the cornea, sometimes of the lens, leads to peculiar 
deficiency of sight. The cornea, instead of representing, as in 
health, a segment of a sphere, represents the segment of an 
ellipsoid. The existence of astigmatism is readily discovered 
if the patient looks at parallel groujDS of straight lines, the 
position of the lines being varied, some vertical, some hori- 
zontal, and some oblique. Those running in certain directions 
are seen by the astigmatic more sharply and clearly defined. 
Along with the other tests for vision, Mr. Nettleship has 
provided some for astigmatism, which you will find very useful 
in practice, . It may also be discovered by means of the 
ophthalmoscope. Such irregular curvings of the media 
necessarily interfere with the accurate convergence of rays 
upon the retina, and, when the eyes are used for any length 



OPHTHALMOSCOPY. 



93 



of time, headache and neuralgia ensue. It is also to be 
noticed that combinations of two of these causes often 
co-operate to produce headache. 

Ophthalvioscopic ExaminaMon. The last point to which 
you have to attend in examining the eye is the ophthalmos- 
copic examination. It is unnecessary for me to say anything 
of the nature of the instrument or of its employment by the 
direct and indirect methods. You will remember that by its 
use we are enabled to make out the state of the optic nerve, 
the retina, the choroid, the vitreous humour, the lens, and 
the condition of refraction. 

It is difficult to render in a satisfactory manner the 
appearances seen with the ophthalmoscope ; but, on the 
whole, there are no representations of these appearances 
equal to those contained in the atlas of ophthalmoscopy 
published by Mr. Liebreich. By his kind permission, I am 
enabled to reproduce such of his plates as seem to come 
within the scope of these lectures. 

With regard to the fundus of the eye, you are familiar 
with the appearance seen in health. In fig. 54 you see 
the optic disc occupying a position rather to the nasal side 
of the middle line, and of a circular or slightly oval shape. 
Its margin is sharply defined from the surrounding fundus 
by colour as well as texture. Its surface, mostly on a level 
with the fundus, has in its centre a depression — the physio- 
logical cupping. Its colour is of a pinkish-yeUow, except 
the centre, which is whiter. You observe that the vessels 
pass upwards and downwards and to the inner side, very few 
to the outer. The vein is easily distinguished from the artery 
by its larger size, its deeper colour, and its single outline. 
The retinal stand out in bold relief as compared with the 
choroidal vessels, and are terminal, not anastomosing, while 
the choroidal vessels branch and anastomose freely. You 
observe also the macula lutea lying to the inner side of the 
optic disc. It is not always well marked. 

The fundus may be altered in many ways. A large number 
of its morbid changes do not come within the range proper 
to these lectures. It were out of place for me to" describe 
detachment of the retina, albuminuric and leucocytha^mic 



94 



OPTIC NEURITIS. 



retinitis, the extravasations which occur so commonly in 
pernicious anasmia, and sometimes after injuries ; or to 
describe morbid states of the choroid, or of the vitreous 
humour or the lens. Even the syphilitic inflammations do 
not seem to me to be within our province. I shall speak 
only of the morbid conditions which are symptomatic of or 
usually associated with diseases of the nervous system. 
Some of these affect specially the optic nerve, others the 
retinal expansion, and yet others the choroid. We shall 
speak first of the changes in the optic nerve. 

Optic Neuritis {Papillitis). Inflammation of the optic 
nerve, with the tissues immediately adjoining its entrance to 
the retina, often attends upon nervous disease, and almost 
invariably affects both eyes. It may be described as pass- 
ing through three stages, in the first of which there is a 
cloudy opacity with marked congestion of the disc (fig. 55); 
in the second (fig. 5 6) the congestion is even more pro- 
nounced, the outline of the disc is quite obscured, and the 
disc itself is swollen. In consequence of this swelling the 
veins become over -distended, and the arteries relatively 
smaller. Haemorrhages also are not unfrequent. The swell- 
ing is sometimes so considerable as to obscure or conceal 
the vessels on the disc. The process may terminate in 
resolution or may pass to a third stage, that of atrophy 
(fig. 57). In this stage the disc has a dull and some- 
what flattened look, and is white. The arteries are seen to 
become in many cases much diminished, while the veins 
return to their normal size. 

The causes of optic neuritis are numerous. The process 
may originate in and be confined to the nerve itself. Much 
more commonly it results from intra-cranial changes. It 
may be said, generally, that conditions which increase the 
intra-cranial pressure produce it. Among these are tumour, 
aneurism, abscess, hydatid growth, haemorrhagic effusion, and 
such like. Some have supposed that the effect is produced 
by accumulation in the lymphatic sheath, and at one time 
" choked disc " was regarded as a result of this, and as 
essentially distinct from optic neuritis. In Edinburgh this 
distinction was never admitted, and it appears now to be 



OPTIC ATROPHY, EMBOLISM. 



99 



generally held that extension of inflammatory change is the 
one cause. If one studies the encephalitis which so often 
occurs in connection with cerebral tumour, it is not difficult 
to understand how an optic neuritis may also arise. Optic 
neuritis attending upon meningitis may be explained in the 
same way. 

Optic neuritis may be well marked without perceptible 
impairment of vision. But it is only in very rare cases that 
this condition persists long without the sight suffering 
more or less. 

Optic atrophy arising apart from inflammation, is termed 
primary. The process advances very insidiously and is 
recognised by the slowly progressing alteration of the 
disc. It becomes slightly excavated and paler, the pallor 
having a greyish tinge. There is also less alteration of 
vessels than we see in atrophy following upon inflammation. 
In fig. 58 you see the appearance of primary atrophy. 

This process is often seen as an accompaniment of spinal 
disease, presumably due to a lesion occuiTing in the nerve 
corresponding to what is going on in other nerve structures. 
It is said also sometimes to result from excessive use of 
tobacco and alcohol. 

Embolism occasionally affects the retinal vessels. It 
may occur along with embolic processes in other parts pro- 
ducing distinct symptoms, or it may be the only one which 
attracts attention. I have already incidentally referred to 
the symptoms which attend its formation (p. 80). The 
appearances as seen by the ophthalmoscope are very charac- 
teristic (fig. 59). At first the arteries beyond the obstruction 
become attenuated, sometimes even lose their normal colour. 
The veins are also narrowed, but to a less extent than the 
arteries. The optic disc is usually pale. The retina generally 
shows a greyish white opacity, most marked about the macula 
lutea and around the disc. The fovea centraHs usually retains 
a bright red colour like an extravasation. Haemorrhages 
sometime occur in the retina, usually when only one of the 
branches has been blocked. Later on the optic disc may 
become clouded and obscure. Often it remams clear, the 
pallor passing gradually into the whiteness of atrophy (fig. 60). 



100 



HEARING. 



In such cases the vessels remain small. The process usually 
results from the impaction of a minute fragment of fibrin 
derived from the heart. Similar changes may result from 
thrombosis of retinal vessels. 

The Retina may show various alterations, such as 
albuminuric and leucocytliEemic retinitis, extravasation as in 
pernicious ansemia, and after injuries, and syphiHtic inflam- 
mations ; but these are, as I have said, less closely connected 
with the subject at present under discussion. 

The Choroid also may show inflammatory changes with 
pigmentation. But the most . important change is the 
formation of tubercular nodules, which sometimes accompany 
tubercular meningitis, and sometimes occur in general tuber- 
culosis, even when the pia mater is not involved. The 
nodules vary in size from a very minute point to a spot 
about half the size of the disc, generally of a rounded or oval 
form, pretty sharply defined, of a greyish, sometimes greyish- 
yellow, colour, usually situated near the posterior pole of the 
eye, generally only two or three in number, resembling small 
spots of choroidal exudation, but unattended by adjacent 
haziness. The appearance is shown in fig. 61. 

It is unnecessary in this connection to say anything of the 
changes in the vitreous humour, the lens, or the refraction, 
which may also be made out by means of the ophthalmo- 
scope. 

Hearing. Subjective symptoms connected Avith hearing 
are very common. Indeed, it may be said that tinnitus 
aurium is among the most frequent of all the subjective 
phenomena. The character of the noise varies. It may be 
like a humming or a buzzing sound, or like whispering, 
whistling, or like the ringing of bells. It may be constant 
or intermittent. It may also be of a pulsating character, the 
noise being increased with each cardiac systole. In a great 
majority of cases, these subjective sounds are due to diseases 
of the ear itself, with which, in the present connection, we 
have nothing to do. But sometimes they result from or 
accompany congestion of the brain, sometimes antemia, either 
• general or local ; sometimes, again, it results from intra- 
cranial aneurism. It is also produced by the use of certain 



HEARING. 



103 



mediciues, pear tic vJarly quiuine and salicylate of soda. Both 
of these exert a direct influence on the ear, as is manifest 
from the deafness which they are apt to produce. 

Patients suffering from brain disease sometimes have 
auditory illusions, — not merely vague noises, but distinct 
sounds, as of various animals or of speech. Especially in cases 
of alcoholic affection of the brain you will find this symptom 
present. 

Then, again, you have to note the degree of perception of 
sounds. There may be hyperesthesia. This may result 
from disease in the ear itself, or from congestive and inflam- 
matory changes in the brain. There may also be dyssesthesia, 
usually, I believe, a result of disease in the ear. I have 
known a patient complain that he could no longer enjoy 
music, seeing that it produced a very disagreeable impression 
on his ear, however beautiful it might really be. There 
is further anaesthesia, commonly produced from changes 
in the mechanism of the ear itself, but also, no doubt, from 
disease of the nerve or the nerve-centres. I have at the 
present time under my care a patient who is deaf in both 
ears, and to whose case I shall again refer. His deafness 
resulted from an accident, with fracture of the base of the 
skull. Deafness followed immediately on the accident, and 
has now persisted for upwards of two years. This appears to 
be a typical case of nervous deafness. He can feel vibrations, 
but hears nothing. Deafness also sometimes occurs as a 
functional affection in cases of hysterical hemi-ansesthesia, 
and sometimes in organic diseases affecting the centre or in 
the conducting fibres. 

The acuteness of hearing is ordinarily tested by the ticking 
of a watch or the sounding of a tuning-fork, the condition 
being judged of according to the distance at which the sound 
may be heard. Special instruments have been devised for the 
purpose of more accurate determination ; but they are more 
useful to the aurist than to the physician. You are familiar with 
the process of testing by the tuning-fork as appHed to the skull 
or the teeth, the sounds often being conducted to a healthy 
cochlea through these structures when the air vibrations are 
prevented from passing. If no soimd is heard when the 



104 



SMELL. 



tuning-fork is applied in this way, you may conclude that 
you have to do with a case of nervous deafness. After the 
age of fifty this test is less rehable, because then frequently 
the tuning-fork is not heard when so applied, either because 
of changes in the bone or in the nerve. In acute inflamma- 
tions, and in marked indrawing of the tympanic membrane, 
you must not absolutely rely upon the tuning-fork. There 
are other peculiarities of hearing regarding the perception 
of high notes or low notes, but these belong rather to the 
department of the specialist, being due to disease of the 
media and not of the nerve structures. My friend. Dr. 
M'Bride, however, tells me of a case reported by Professor 
Moos of Heidelberg, in which there was deafness to high notes, 
and on examination after death it was found that there was 
atrophy of the filaments of the auditory nerve supplying the 
first or lowest turn of the cochlea. 

Smell. With regard to the sense of smell, subjective pheno- 
mena are occasionally met with. They may be persistent, or 
may occur only from time to time. They constitute a variety of 
aura in some epileptics, and are said to be not unfrequent in the 
insane. Such subjective changes are probably due to irrita- 
tion of the olfactory centre in the temporo-sphenoidal lobe. 
Post-mortem examinations have in some cases confirmed this 
opinion. In one, for example, a tumour was found in that 
I'egion. Occasionally you meet with subjective perversion of 
smell, especially in the insane. Patients may tell you that 
every object seems tainted with a disagreeable odour. You 
will often notice that some perversion of smell accompanies 
coryza. 

Hyyercesthesia of the olfactory nerve (hyperosmia) is 
observed in certain cases of general hypersesthesia in 
hysterical conditions, but diminution (hyposmia) or loss 
of sensibility (anosmia) is far more common. It may 
be congenital. I know an individual who has no sense 
of smell, and says that he has not the slightest idea of 
Avhat the nature of the sensation may be. It may be 
lost as the result of disease or injury. Loss may be 
caused by catarrh of the olfactory mucous membrane, 
by the presence of polypi or other growths, and by paralysis 



TASTE. 



105 



of the fifth, as was shown by Majendie. It is said to result 
from paralysis of the seventh, inducing deficient entrance of 
air, or preventing its direction into the olfactory region. 
Rupture of the olfactory nerve, of the olfactory fibrils, and 
disease of the olfactory bulbs, as also of the olfactory centre, 
may give rise to the symptom. It occurs in some cases of 
locomotor ataxia, probably from disease of the nerve itself. 
When it is associated with other paralysis, it is sometimes on 
the same side, or sometimes on the side opposite to that on 
which the paralysis exists. Thus, if associated with aphasia 
and right-sided hemiplegia, the anosmia affects the left nostril. 
It may be explained, as Dr. Ogle suggests, by the fact that 
the loss of smell is due to softening of the external root 
of the olfactory nerve, which is supplied by the middle 
cerebral artery, as are Broca's convolution and the motor 
area of the cortex. When the anosmia is on the same side 
as the paralysis, as we see in lesions of the posterior third 
of the internal capsule, and in hysterical anesthesia, the con- 
dition may be due to lesion of the fibres of the fifth, or, what 
seems to me more likely, to involvement of olfactory fibres 
proceeding, along with other sensory structures, to the 
centre in the opposite hemisphere. In many cases, the 
anosmia is bilateral, and a result of blows on the occiput. 
One can readily understand how the counterstroke should 
bring this about. Perhaps rupture of the olfactory fibres, 
perhaps injury of the olfactory bulbs, perhaps the impinging 
of the temporo-sphenoidal lobes upon the great wings of the 
sphenoid bone, with consequent disorganisation, may bring 
about the result. 

Taste. With regard to taste, subjective phenomena are also 
not uncommon. Very generally they are unpleasant and are 
associated with hysteria, with insanity, and with the epileptic 
aura. They may be peristent or occasional. The passage of 
a galvanic current through the head produces a metallic 
taste. Perversion of taste is occasionally seen in nervous 
cases, sweet things being regarded as bitter, bitter things as 
salt, and so on. Among hysterical patients you will find 
these most frequent. 

Hyperaesthesia of taste (hypergeusia) is met with in excit- 



106 



TASTE. 



able states of the nervous system, in hysterical and insane 
people, and along with general hypcr<jesthesia. Diminution 
(hypogeusia) or loss of taste (ageusia) is sometimes dependent 
upon changes in the mucous membrane of the tongue, on dry- 
ness of the surface, on changes in the taste bulbs, on alteration 
of the sensory nerves of the tongue, the fifth and the glosso- 
pharyngeal, also of the chorda tympani, from changes also 
within the cranium, either in the taste-centre situated in the 
temporo-sphenoidal lobe of the opposite side, or the fibres 
connecting it with the nerve. It may be unilateral, as in 
some cases of hysterical hemi-ansesthesia, and of lesion of the 
internal capsule or of the centre. It may be bilateral from 
peripheral changes or from lesions of centres on both sides. 

Alterations of smell and taste very often go together, both 
as results of accident and otherwise. Some incline to con- 
found the two functions. But, Avhile in the perception of 
flavour, we have the result of the conjoined action, the tAvo are 
essentially distinct. Dr. Ferrier records the case of a patient 
of his who had entirely lost taste and smell in consequence 
of an injury to the head. When the case came under his 
care, all the symptoms had disapj)eared, excepting the 
anosmia and ageusia. Acetic acid was not smelt, and sweet 
and bitter could not be distinguished. Under treatment taste 
was restored, so that the patient could not only distinguish 
sweet from bitter, but beef from mutton, and yet complete 
anosmia remained. Such an observation as this shows how 
acute is the sense of taste apart from all perception of smeU. 



LECTURE VII 



Motor Functions. 

Reflex Action. — Organic Rejlexes. — Micturition. — Respiration. — Rapid 
and Slow. — Cerebral. — Cheyne-Stokes. — Skin Reflexes. — Plantar. 
— Cremasteric. — Gluteal. — Abdominal. — Epigastric. — Lumbar 
and Dorsal. — Scapular. — Modifications. — Tendon Reflexes. — 
Patellar. — Ankle Clonus. — Spinal Epilepsy. — Modifications. — 
Paradoxical Contraction. 

ENTLEMEN, — Having completed our survey of the 
sensory functions, we now proceed to consider the 
motor. I shall speak (1) of the reflexes, (2) of voluntary 
motion, (3) of co-ordination, and shall show you how each of 
them is liable to be modified in disease. 

The reflex actions themselves may be grouped in three 
divisions : (a) the organic reflexes ; (6) the skin or super- 
ficial reflexes ; (c) the tendon or deep reflexes, 

(a) Organic Reflexes. The most important of the organic 
reflexes are those connected with respiration, circulation, 
digestion, micturition, and defsecation. It may suffice if we 
consider one or two of them, and let them stand as types of 
all the others. We shall select first micturition. For the 
performance of this function there are required sensory struc- 
tures, connected with the bladder and the urethra ; a centre 
capable of receiving and transmitting to motor structures, or 
transforming into motor power, these sensory changes ; efferent 
motor structures distributed to muscles : and a co-ordinatinsr 
structure, whereby certain muscles shall be made to relax at 
the time that others are brought into contraction. When 
the appropriate stimulus is applied, changes are set up in 
the reflex centre, which result under normal conditions in the 

107 




108 



ORGANIC REFLEXES. 



performance of the act. This reflex chain is, however, under 
the influence of higher inhibitory centres. Within certain 
limits the will may keep the sphincters in action, or may 
bring the expelling muscles into play. In disease the 
mechanism may be altered at any part of its course. The 
sensory structures may be at fault. Sensibility may be 
either abnormally acute or impaired. The afferent impression 
may fail to reach the spinal cord, and consequently no reflex 
action be performed. Or the impressions may be cut off 
above the reflex centre, and the patient may be unconscious 
of the state of the bladder. In such cases, the inhibitory 
influence is lost. The reflex centre may be diseased. It 
may be irritated so that its functional activity is excessive, 
or it may be cut off from its inhibitory centre. It may have 
its power diminished or abrogated in consequence of disease, 
such as myelitis, involving its substance. Perhaps the motor 
influence may be interfered with in consequence of disease 
of efferent nerves. Certainly co-ordination may be affected, 
so- that there is a failure of the harmonious action of different 
sets of muscles. The muscular structures themselves may be 
at fault, and thereby the function disturbed. In seeking to 
analyse any abnormality of the bladder functions, you should 
proceed upon the lines that I have indicated. 

I shaU now direct your attention to the respiratory reflex 
and its modifications in disease. It seems definitely ascer- 
tained that the respiratory process, although influenced in 
various ways by peripheral impressions from the lungs, from 
the skin and other sources, is mainly determined by 
influences exerted directly on the centre itself The circu- 
lation of venous blood within it induces the, movement, and 
the more venous the blood, the greater is the activity of the 
respiratory centre. Moreover, it is the want of oxygen and 
not the excess of carbonic acid, that constitutes the resj)iratory 
stimulus. But although the respiration is mainly set in 
action by the centre, peripheral influences do affect it in various 
ways. It is frequently modified by changes both in afferent 
and efferent nerve -structures. There may be excessive 
irritation of vagi, which results in increased rapidity of 
respiration. There may be irritation of cutaneous nerves of 



ORGANIC REFLEXES. 



109 



the chest, and consequent acceleration ; there may be irritation 
of the superior laryngeal nerve, and consequent inhibition 
of the respiratory movement. There may, on the other 
hand, be interference with the motor nerves. The dia- 
phragm may fail to play, or may play excessively, from 
changes in the phrenic : as may also the scaleni, supplied 
by branches from the brachial plexus ; the intercostal 
muscles, supplied by the intercostal nerves ; the abdominal 
muscles, supplied by the lower intercostal and first lumbar 
nerves. Besides these ordinary muscles of respiration, 
you may find abnormal action of the extraordinary muscles 
under circumstances of laboured breathing, the serrati, sup- 
plied from the brachial plexus and the posterior divisions of 
the spinal nerves ; the sterno-mastoid and trapezius, supplied 
by the spinal accessory, and by deep branches of the cervical 
plexus ; the levator anguli scapulae, and rhomboidei, supplied 
by branches from the upper part of the brachial plexus. 
Besides these thoracic and abdominal movements, there are 
respiratory movements in the face and larynx, the nostrils being 
expanded, and the glottis opened up for the admission of air. 
It is thus obvious that disease situated in the medulla 
oblongata, in the spinal cord, or in a considerable number 
of the cranial or spinal nerves, may interfere with the 
respiratory process. 

You will find that the breathing is at times quickened, 
as in some cases of hysteria and uremia ; is sometimes 
slowed, as in some inflammations at the base of the brain ; 
is sometimes irregular, as in what is called cerebral breath- 
ing (fig. 62), which often follows injury to the encephalon ; 
is imperfect, in one or more respects, from interference, 
say, with the play of the diaphragm, when the phrenic 
is involved, or of the intercostals, when the intercostal 
nerves are affected. A very peculiar alteration exists, 
which is known as Cheyne-Stokes breathing, or the ascend- 
ing and descending respiration (fig. 63 1). In fig. 03 II. you 
see a tracing of the respiratory movement and of the cardiac 
movement in a case of this kind. You observe that the 
respiration rises and falls in a regular rhythmical manner ; 
and, when you refer to the cardiogram, you observe 



ORGANIC REFLEXES. 

that, during tlie long respiratory pause, there is extremely 
rapid but slight movement of the heart, while, with the 



Fio. 62. 

Tracing of cerebral breatliinj. 

return o£ the respiration, the cardiac movement also becomes 
slower and fuller. This condition is found generally associ- 
ated with fatty degeneration of the heart, but sometimes also 



Fig. 63 I. 
Tracing of Cheyne-Stokos breathing. 




( respira- 
, - tory 
(, curve. 



t cirdio- 
^ irraiiliic 



Fio. e.'? n. 

Relation of the different elements in Clieyne-Stokes breatMng to action of heart. 

with valvular disease. Its explanation is not very easy. It 
seems most reasonable to refer it to the condition of the 



SKIN REFLEXES. 



Ill 



respiratory centre. The blood supply may be of such a kind 
as fails to excite the respiratory movements, or the respiratory 
centre itself may be defectively nourished, and incapable of 
continued action. 

A similar method of analysis will help you in your study 
of other organic reflexes. Each organic reflex, doubtless, has 
a well-defined centre in the spinal cord ; but their exact 
positions are scarcely as yet definitely ascertained. We 
may say, however, that in the lumbar enlargement are 
situated the micturition, the defeecation, and the sexual and 
parturition centres ; that in the medulla oblongata are 
situated the respiratory, the circulatory, the vaso-motor, the 
centre for coughing, for sneezing, for swallowing, for vomiting, 
and for articulation, and that in the lower cervical and upper 
dorsal region are the centres connected with the pupil, so 
far as its dilating functions are concerned, while throughout 
the whole cord vaso-motor centres exist. It is probable that 
in the lower dorsal regions there are centres connected with 
the stomach and intestine, which are related to these organs 
through the sympathetic fibres. 

Skin Reflexes. The skin reflexes may be evoked by 
titillation of the skin. The most familiar is the plantar. 
By tickling the sole one produces movement of the corres- 
ponding leg, or sometimes of both legs. The centre for 
this reflex is in the lumbar enlargement of the cord. The 
cremasteric reflex is easily demonstrated, especially in 
boys, when one touches the inner side of the thigh. So 
soon as that part is touched a contraction of the cremaster 
on the same side occurs, and the testicle is drawn up. The 
centre for this reflex is also situated in the lumbar enlarge- 
ment. You may frequently elicit by drawing a pencil 
firmly over the buttock a contraction of the gluteal muscles. 
This is termed the gluteal reflex, and has its centre also 
in the lower part of the cord. The abdominal reflex is 
produced by touching the side of the abdomen, and consists 
in contraction of the abdominal muscles. Its centre is rather 
higher in the cord. The epigastric reflex is often more 
distmct than the gluteal or abdominal. It consists in a 
contraction of the upper part of the rectus abdominis, and is 

H 



112 



SKIN EEFLEXES. 



induced by touching the side of the chest in the fourth, 
fifth, or sixth interspaces. Its centre is in the dorsal region 
of the cord. Sometimes stroking along the margin of the 
erectors of the spine induces contraction of these muscles. 
The scapular reflex is far more important, consisting in a 
contraction of many of the muscles attached to the scapula. 
It is produced by irritation of the skin in the inter-scapular 
region. Its centre is situated in the upper dorsal and lower 
cervical part of the cord. There are other skin reflexes, 
such as deep inspiration caused by cold applied to the skin 
of the chest, and the laughter produced by tickling. The 
centres for these reflexes are higher in the cord. We are 
indebted to Dr. Gowers for having systematised our know- 
ledge of these different conditions. It is obvious, as I have 
shown in a previous lecture, that an investigation of these 
reflexes affords us the means of determining the condition 
of almost any portion of the cord. 

The skin reflexes may be increased or diminished in disease. 
Their increase is most marked in cases of irritation of the cord, 
either from functional or from commencing organic disease, 
or from poisons, such as strychnia; also in diseases 
which cut off the inhibitory influence of the brain 
from the spinal centres, as in transverse myelitis above 
the lumbar enlargement, and in antero-lateral sclerosis. 
Where such increase exists, the movement extends to other 
groups of muscles besides those ordinarily brought into play. 
The skin reflexes are diminished in myelitis, softening, 
diphtheritic paralysis, and other diseases of cord, when the 
lesion involves the centres for reflex action. Sometimes, 
also, you will find the skin reflexes diminished on the 
paralysed side in cases of cerebral disease, probably from 
irritation of the inhibitory centre in the encephalon. Professor 
Ferrier has recorded a very interesting fact as occurring in 
a patient who exhibited the symptoms which I have already 
described as allochiria. In this case the reflex movements 
occurred on the opposite side of the body to that which was 
tickled. If one tickled the sole of one foot, it remained still 
while the other moved. 

Tendon Reflexes. These reflexes have also been spoken 



TENDON EEFLEXES. 



113 



of as deep reflexes, and as myotatic contractions. The 
phenomena excited great interest when first described a few 
years ago by Professor Westphal of Berlin, and Professor Erb 
of Heidelberg. Erb called them tendon reflexes, Westphal 
spoke of them as the knee phenomenon and foot phenomenon. 
It is most easily studied in the knee, and most of you 
will at once understand what it is when I recall to you 
a favourite trick of boys, of sharply tapping on the liga- 
mentum patellse and thereby producing a jerking forwards 
of the foot. The jerk is best seen when the leg is bent at 
about a right angle and the foot unsupported, as when one 
is sitting with one knee crossed over the other, or upon a 
high seat with the feet dangling. When the ligamentum 
patellae has been struck, almost instantaneously the foot is 
jerked forwards. This results from a sudden contraction of 
the quadriceps extensor femoris. The blow may be admini- 
stered with a thin book or with the side of a hand, but best 
of all with a Bennett's percussion hammer. Brief observation 
will satisfy you that it is not a mere mechanical result of a 
momentary indentation of the tendon, for the jerk follows 
the tap after an appreciable interval and is always associated 
with contraction of the muscle. All parts of the tendon are 
not equally sensitive, and sometimes it is necessary to try 
different parts before the result is obtained. 

It is almost invariably present in healthy people, but its 
intensity varies in different individuals. It is lost in the 
great majority of cases of locomotor ataxia, often early in the 
disease. It is frequently lost also in diphtheritic paralysis, 
in paralysis of legs from disease of nerves, in myelitis, and 
other destructive diseases of the cord; sometimes also for a 
time after a convulsion, and it has been found absent in both 
legs in cases of unilateral cerebral tumours. 

Often we find exaggeration, especially in cases of lateral 
sclerosis and of descending degeneration. Yon will find that 
a tap in such a case leads to a violent jerk forwards, and 
then to a sudden retraction of the leg when the flexor 
tendons have been stretched, and if you tap gently many 
times upon the ligamentum patellas you may succeed in 
extending the leg and keeping it fixed for a time. I once 



114 



ANKLE- CLONUS. 



knew a patient who had learned to overcome some of the 
disadvantages of the spastic rigidity of his legs, by tapping 
upon the tendons and muscles in different places, and could 
thereby accomplish movements which he could not make by 
an effort of the will. 

Phenomena essentially corresponding to these are met with 
in other muscles. I have seen them often in the biceps and 
triceps of the arm, and in some morbid conditions, such 
as old hemiplegia with descending degeneration, I have been 
able to trace them in every muscle of the paralysed side. 

Pressure upon the tendon is not the sole cause, for some- 
times tapping the body of the muscle, sometimes tapping the 
bone in the neighbourhood of the muscle, suffices to produce 
the movement. Various views have been maintained as to how 
these movements are brought about. When we consider that 
the phenomena cease when sensory or motor nerves are cut, 
and when the central structures are destroyed, surely no diffi- 
culties should suffice to preclude a reflex theory. Dr. Gowers 
has come to the conclusion, as have certain other observers, 
that the time elapsing between the tap and the jerk is too 
short for the accomplishment of a reflex movement. It is 
obviously much shorter than that required for a skin reflex, 
but if one considers the function of muscles, one may well 
understand how likely it is that their reflexes may be very 
rapid. That irritation of tendon is not the only thing is 
obvious enough, and it is possible that by traction on the 
muscle by the tendon the contraction is produced. Of the 
clinical significance of the phenomena you will be satisfied 
from what I have said with regard to individual points 
already. Let me add only this, that a comparison of the 
condition on the two sides of the body sometimes suffices to 
throw great light upon difficult nervous cases. 

The second of these tendon reflexes is what is known as 
ankle-clonus. It is not present in healthy people, but is 
very characteristic of certain diseases. In order to bring 
it out, the patient should be reclining or sitting with the 
leg stretched out, the knee nearly but not quite extended. 
Sudden pressure should be made upwards upon the ball of 
the toes. Immediately a series of clonic spasms is set up. 



PAEADOXICAL CONTRACTION. 



115 



tlie toe being pressed downwards, and then raised up by a 
succession of rapid movements. This condition is well seen 
in cases of spastic paralysis, and in descending degeneration 
of the crossed pyramidal tracts. It is also frequently excessive, 
as is also the patellar reflex, during epileptic coma, and 
that while the plantar reflex is in abeyance. It is apt to be 
present when the nervous system or the muscles are exhausted. 
The essential condition for its production is the sudden 
traction upon the tendo Achillis by the abrupt depression 
of the calcaneum. Similar movements are sometimes seen 
in connection with inversion and eversion of the foot, and 
sometimes they are marked in these muscles when they are 
absent in those of the calf. 

A condition obviously closely related to this tendon 
reflex, which you will often meet with in practice, is that 
jerking of the foot, formerly called by some spinal epilepsy. 
It is a result of an undue irritability of the muscles, and 
frequently comes on when the patient attempts to stand, 
especially if he is tired, or when he sits with the ball of the 
foot touching the ground and the heels raised, or with the 
heels on the ground and the toes raised. Sometimes, too, this 
clonic jerking of the limbs occurs when the person is in bed. 

Paradoxical Contraction. There is another condition 
which Professor Westphal has described as 'paradoxical 
contraction. You see it, perhaps, best in the tibialis anticus. 
When the foot is passively bent forward, it sometimes 
happens that this muscle, which then becomes greatly relaxed, 
gets into a state of contraction, and continues so for a con- 
siderable time. I know one individual in whom, when his 
foot is placed in a particular position, so as to relax the 
tibialis anticus, contraction at once results. It is not con- 
fined to the tibialis anticus, but may occur in the muscles of 
the wrist and finger-joints, and the supinator longus, as 
well as in the flexors of the knee-joint. You will some- 
times see it in locomotor ataxia, and sometimes it occurs in 
people who are apparently quite healthy, and sometimes in 
connection with paralysis agitans, and sometimes, again, in 
paralysis of the muscles. We very seldom see examples of 
this condition, and I cannot at present explain it. 



LECTURE VIII. 



Motor Functions — (Continued). 

Voluntary Movement. — Dynamometer. — Paralysis. — Paresis. — 
Weakness from Disease of Muscles. — Choreic Movements. — 
Clonic Spasms. — Tonic Spasms. — Athetosis. — Saltatory SjMsms 
and Eclampsia Nutans. — Cramp. — Cataleptic Rigidity. — Con- 
tracture. — Co-ordination. — Definition. — Inborn, — Acquired. — 
Mechanism subserving it. — Failure from Sensory, Central, and 
Efferent Disease. — Trade Spasms. — Conjugate Deviation. — Cough. 

r\ ENTLEMEN, — We commence to-day with the study of 
" voluntary movements and their modifications. In 
testing the power of movement possessed by the muscles, it 
is necessary to advert both to the power of movement 
proper, and to the power of co-ordination. The former 
may be determined by systematically testing the move- 
ments at the different joints. The amount of strength in 




Fig. 64. 
Dynamometer (Collin). 

the arms and legs may be estimated in a rough way by 
asking the patient to squeeze the hand, or to step up upon a 
chair, or to execute similar movements. But for accurate 
determination it is necessary to use special instruments, the 
most convenient of which for the hand is the dynamometer 
116 



PARALYSIS. 



117 



(fig. 64). But in the use of all these instruments you must 
remember that there is a good deal of knack, some people 
managing with less actual power to produce more effect than 
others. In the case of the leg, it is difficult to get a good 
dynamometer, and you may judge well enough by such tests 
as I have already mentioned, or by directing the patient to 
He down upon the side and then get up, or asking him, with 
the leg flexed on the abdomen, to extend it in opposition to 
your pressure in the opposite direction. 

In some cases you find that the patient is quite unable to 
make any movement, and if you lift the limb from the bed. it 
falls back like a dead mass. You may find merely a certain 
feebleness — a lesser degree of paralysis, which we term paresis. 
You may find the motor power normal. You may find it 
unduly excitable, so that actions are in excess of the purpose. 
You may find that other muscles come into play in a fitful and 
irregular way, besides those which the patient desires to use, 
and the movement is, consequently, vacillating and irregular. 
Or you may find that the motor impulse produces firm and 
persistent contraction of antagonistic muscles, as well as those 
which the patient desires to employ, so that the limb becomes 
rigid and locked. You may further find that in the muscles, 
apart from voluntary effort, various morbid actions exist. 
There may be clonic spasms, contractions of short dura- 
tion ; tonic spasms, contractions of more prolonged type ; 
there may be cramp — that is, sudden and painful contrac- 
tion of the muscle ; or there may be contracture, persistent 
rigidity of the muscles. The muscular substance itself 
may also be found in abnormal conditions. It may be 
atrophied ; it may be hypertrophied ; it may be in a state of 
pseudo-hypertrophy, an increase of bulk by growth of fibrous 
or fatty, not of sarcous elements. 

Paralysis may result from disease in the nerve supplying 
the paralysed part. If so, you will find that there are, in 
the case of mixed nerves, alterations in the sensory and trophic 
functions as weU as in the motor, and the reaction of degenera- 
tion will be distinct. The changes may be a result of inflam- 
matory alteration of the nerve substance or of pressure upon 
the nerve, destroying its conducting power. In the drawing 



118 



PAEALTSIS. 



(fig. 65) you see the appearance which I found in the radial 
nerve of a well-marked case of paralysis from nerve disease. 
You perceive that the medullary sheath is Ijroken up at many 

points. Paralysis may 
also result from disease 
in the spinal cord, so 
situated as to cut off the 
communication down- 
wards from the brain, 
as we see in cases of 
paraplegia. In such 
cases the paralysis is, in 
the great majority of 
cases, bilateral; and not 
unfrequently the reflexes 
are exaggerated in the 
portions of cord below 
the lesion. If, in a case 
of spinal cord disease, 
only one side is par- 
alysed, you will gener- 
ally find that sensation 
is affected in the corres- 
ponding part of the 
opposite side. Paraly- 
sis may be due to lesion in the line of the fibres through 
the structures at the base of the brain. If the lesion 
be in the medulla oblongata, you may expect an afiec- 
tion of the arms and legs, — sometimes of all four, some- 
times two only, — conjoined with difiiculty of articulation, 
swallowing, abnormal respiration, and cardiac action, from 
involvement of bulbar nerves. Coughing and vomiting are 
also sometimes prominent symptoms. If the lesion be in the 
lower part of the pons varolii, you will find alternate paralysis 
— usually the face paralysed on the side of the lesion, the 
body on the other side. In addition to the paralysis of the 
facial, you may find paralysis of the abducens on the same 
or the opposite side. There may also be paralysis of the 
fifth nerve, and defective articulation. There is generally a 




Microscopical section of radial nerve, from case of 
peripheral paralysis. 



PARESIS. 



119 



degree of vaso-motor paralysis, and an elevation of the 
temperature of the affected side. If it be further up in the 
pons, you will find paralysis of both the face and the body 
on the side opposite to the lesion. If the lesion be in one of 
the crura cerebri, you may expect to find another well-marked 
form of alternate paralysis, there being paralysis of motion 
and sensation on the side opposite to the lesion, and paralysis 
of the third nerve on the side of the lesion, easily explained by 
reference to the relation of the third nerve to the crus. The 
temperature also rises markedly on the paralysed side, accom- 
panying marked vaso-motor paralysis. Paralysis may also 
result from disease involving the internal capsule, as we see 
in so many cases of hemiplegia. In such cases the face is 
paralysed on the same side as the body. Insensibility may or 
may not occur. In hemiplegia, you will find that paralysis 
is much more severe in some muscles than it is in others. 
Those of the arm and leg are quite motionless, while those 
of the thorax, larynx, and upper part of the face continue 
to act. This has been explained by Broadbent on the 
theory that, when the muscles of the two sides act habitu- 
ally together, they have a bilateral innervation, and con- 
sequently a lesion of one side does not paralyse them. 
Now, the muscles of the two hands or the two legs do not 
habitually act together, while those of the larynx, the 
thorax, and the upper part of the face do. Paralysis may 
be due to lesions of individual portions of the convolutions, 
as we see characteristically in monoplegic cases. 

Paresis. The lesser degree of paralysis, known as paresis, 
may be produced by lesions in the structures to which I have 
referred, the lesions being less profound than those which 
result in actual paralysis. But it occurs frequently in mere 
functional conditions, and is aggravated by ill-health or by 
bodily fatigue. I know a gentleman who suffers from 
occasional paresis of some of the muscles of the eye. I 
notice him often put his hand over one eye to get rid of the 
double vision, when he hais been in some way fatigued, or is 
a little out of health — perhaps merely constipated. I Imow 
a lady in whom there is a slight tendency to ptosis of one 
eyehd. Any little disturbance of her system suffices to make 



120 



WEAKNESS FROM MUSCULAR DISEASE. 



the ptosis quite distinct. You will in practice meet with many 
cases essentially corresponding to these. 

Weakness from Disease of Muscle. With regard to the 
abnormalities of the muscular tissue itself, you will find 
that they often play an important part in interfering 
with voluntary motion. One of the most common of 
these conditions is muscular atrophy. It is characterised 
by diminution in the bulk of the muscle, and often by 
the spontaneous or easily induced occurrence of fibrillary 
twitchings in its substance. Such wasting of muscles 
may occur from many causes — firstly, from mere disuse, as 
you have often seen in the case of fractured limbs, which 
have been in splints for weeks, and of stiffened joints when 
muscular movement had become imperfect ; secondly, from 
motor paralysis and consequent disuse, as you see so constantly 
in ordinary paralytic cases ; thirdly, it occurs specially as a 
trophic change, as I shall point out when speaking of the 
trophic functions. The muscular fibre may be enlarged, either 
with true hypertrophy or with a pseudo-hypertrophic change. 
The latter gives rise to extreme weakness of the muscles. 
I shall describe it also along with the trophic changes. 

Belayed Movement In some cases we find that a voluntary 
effort at movement does not at first succeed, but afterwards 
goes on all right. A patient of mine, who suffered from loco- 
motor ataxia, used sometimes to fail to speak or to make other 
movement when he desired, but, when once he began, went 
on easily. A similar peculiarity, but much more pronounced, 
is met with in what is known as Thomsen's disease ; having 
been well described by Dr. Thomsen, of Schleswig. If a 
patient, suffering from this malady, has been for some time 
at rest, great effort is necessary before he can initiate a volun- 
tary movement. If he attempts to rise from his seat, a 
considerable time elapses before he is able to do it. If he 
attempts to walk, he appears at first rooted to the ground. 
At last he accomplishes the movement, and from being stiff 
and awkward, as he goes on the motion becomes easy and 
natural. The pathology of this condition is as yet unascer- 
tained, but the fact that the muscles are sometimes tender to 
touch, points to some peripheral irritation. A condition of 



INCREASED IRRITABILITY. 



121 



temporary tetanic rigidity is produced when the voluntary 
effort is made. 

Irradiation of Impulse. The curious condition,^ in 
which the impulse seems to be irradiated to antagonistic 
groups of muscles, is seen most typically in spastic paralysis. 
In such cases, I have often seen the patient quite able by 
voluntary effort to bring the muscles which produce any 
particular movement into play, but unable to use them, 
because other antagonistic muscles came simultaneously into 
action. 

Increased irritability may be seen in connection with 
central changes, whether in the spinal cord or in the brain. 
In cases of tetanus and strychnia poisoning, movement is in 
excess of what is intended, and in certain excited conditions 
of the brain, as in hysterical states, the same result occurs. 
With regard to the irregular and vacillating movements, we 
see them typically in cases of chorea and of multiple cerebro- 
spinal sclerosis ; but in the former this occurs apart from, as 
well as with, voluntary effort, the patient being unable to keep 
still ; while in the latter the irregular movements only occur 
when a voluntary effort is made. You have seen these con- 
ditions illustrated in the hospital wards. You have seen the 
choreic patient unable to keep still in consequence of an 
irresistible tendency to twitching of his muscles, the tendency 
being more pronounced the longer he remained in one posi- 
tion. You have seen that the patient with multiple sclerosis, 
on the contrary, remains quite free from jerking, while he is 
sitting or standing in an easy position ; but when you ask 
him to turn his eyes to one side, you see a jerking movement 
— nystagmus — at once developed. If you ask him to lift a 
cup to his lips, you see his hand and arm jerking, the agitation 
increasing as it nears his head, then the head itself beginning 
to jerk as he tries to make the neck-muscles co-operate in the 
difficult task of drinking. It is not necessary here to enter 
into the pathology of chorea or of multiple sclerosis, more than 
to remind you that choreic movements may probably originate 
either in the cord or in the brain, and that in multiple 
sclerosis the sclerotic patches are met with in both these 
structures. 



122 



CONVULSIONS. 



Tremor. Short of actual spasm, thero often occurs a 
tremulous movement of muscles, wliich is aggravated by 
emotional excitement, and sometimes by voluntary effort. 
It is common in the intemperate, occurs in mercurial poisoning, 
sometimes in lead-poisoning, and in conditions of general 
debility. It is also seen in some cases of hemiplegia, in 
connection with — according to Nothnagel — lesions in the 
posterior part of the internal capsule, the optic thalamus, 
and the foot of the corona radiata. Tremor may result from 
debility of the muscles, or of the motor nerve-structures, or 
from irregular discharge of motor nerve-force during or apart 
from voluntary effort. 

Fibrillary Twitching. Besides the coarser tremor, result- 
ing from the fitful action of individual muscles, or groups 
of muscles, you have to recognise the contractions of portions 
of muscle — fibrillary twitching — usually without movement 
of the tendon or limb, but marked simply by a tremulous 
movement beneath the skin in the superficial muscles. 
These movements may often be induced by blowing upon 
or gently tapping upon the skin. They are most charac- 
teristically seen in progressive muscular atrophy. 

Myoidema. In connection with this, I may refer to a 
local irritability of the muscular fibre, often seen in phthisical 
patients, where by tapping firmly over a muscle, say the 
great pectoral, contraction of the tapped portion of the 
muscle takes place, so that a little swelling suddenly rises 
and may persist for a considerable time. 

Convulsive Contractions may be of many kinds, from the 
slightest local spasm up to general convulsions of the whole 
muscular system. They may or may not be attended by loss 
of consciousness. They always result from sudden discharge 
of nerve-force from motor centres, and may be due to primary 
irritation of the centre, or to irritation propagated from the 
sensory peripherse. Convulsions are usually classified as tonic 
and clonic, the tonic being regular and the clonic being 
irregular in character. 

Clonic Spasms may be rhythmical, as we see in ordinary 
cases of paralysis agitans, when the patient has constantly 
or frequently a tendency to rhythmical movements. The 



CLONIC SPASMS. 



123 



movements may be rapidly alternating pronation and supina- 
tion of one or both hands. It may be a movement of the 
thumb upon the fingers, which has been compared to 
the rolling of a cigarette. One of the most striking peculi- 
arities of these movements is that they are in the earlier 
stages often under control, and that the patient can by 
voluntary effort check the movement for a longer or shorter 
time. You often see this illustrated in hospital practice, 
and I have heard of an artist affected with the disease, who 
could so control the spasms that he was able to use his brush 
for a little and then had to yield for a time to the movement, 
then again recovered the power of control. In later stages 
the jerking is no longer under control, and the movements 
are constant during the waking hours. We do not yet know 
what the lesion is in this disease, but I have reason to suspect 
that it is sometimes situated in the nerves. 

Clonic spasms are, however, not necessarily rhythmical. If 
you watch the convulsive movements in the later stages of an 
epileptic fit, or in an ordinary convulsion of infancy, you 
observe a succession of jerks by no means rhythmical in 
character. The force of the contractions varies, as does 
also the seat of the contraction, from moment to moment. 
Such clonic convulsions are often due to disease of brain, 
often also to peripheral irritation, leading to central changes 
and to discharges of motor force. Clonic spasms are often 
of a less formidable character. Hiccough, for example, is the 
result of clonic spasm of the diaphragm. It is usually due to 
peripheral irritation of sensory nerves in the stomach or in 
the pharynx, and sometimes may be produced by irritation of 
other parts. A very accomplished member of the profession 
sometimes amused me in his student days by producing 
hiccough by simply stroking his chin. Cough may also be 
described as a clonic spasm, but it is of a peculiarly co-ordi- 
nated kind, to which I shall refer later on. Another form of 
clonic spasm lately came under my notice. A patient com- 
plaining of giddiness was brought to me by his doctor. The 
attacks came on occasionally without warning, and lasted only 
for a few seconds. I had the opportunity of seeing him in 
one of them. "Now," he said, "it is coming on." He 



124 



TONIC SPASMS. 



became pale, and his left eyeball began to rotate in a 
peculiar manner. It seemed to turn upon its antero-posterior 
axis. The seizure continued for a short time, and was 
attended by no other convulsive movement. While it 
lasted the patient felt giddy and uneasy. Within a few 
weeks of the commencement of these symptoms, I was called 
to see him suffering from well-marked left-sided hemiplegia. 
The spasm in that case was probably a result of irritation at 
the root of the fourth cranial nerve. 

Facial, Histrionic, or Mimic Spasm is a condition not 
unfrequently met with in practice. It consists in a clonic 
or more rarely a tonic contraction of some of the facial 
muscles. It may be unilateral or bilateral, may affect the 
cheek, the eyelids, the angle of the mouth, or the forehead. 
Sometimes it is associated with movement of the muscles of 
the neck, the platysma, or of the eyeball. It is met with 
frequently in different members of a neurotic family. It is 
aggravated by emotion, fatigue, or bodily debility. I may 
refer as an illustration to the case of a gentleman, upwards 
of seventy years of age, who has suffered from this for many 
years. Till lately he showed nothing beyond a drawing-up 
of the left angle of the mouth, a jerking closure of the 
orbicularis palpebrarum, and an elevation of the cheek, but 
now these are accompanied by spasms of the external rectus 
of the left eye, and the internal rectus of the right, which 
adds greatly both to the discomfort he feels and the disagree- 
able appearance of the face. Such spasms may result from 
peripheral irritation, or from central changes about the origin 
of the seventh nerve. 

Tonic Spasms are characterised by their longer continu- 
ance, the muscles appearing to remain in firm contraction for 
a considerable time. This kind of spasm is well seen 
in the commencement of an epileptic seizure. There is a 
continued distortion of certain parts — say, for example, a 
conjugate deviation of the head and eyes ; that is to say, a 
turning of the head and the eyes to one side. There is a spasm 
of the respiratory muscles, a locking of the limbs — all these 
lasting for a considerable period and preceding the occurrence 
of the clonic spasms, to which I have already referred. It 



SPASMS. 



125 



may be even more typically seen in tlie disease known as 
tetany, in which there are spasmodic movements of the 
hands and feet, with spasms lasting for a few minutes, or 
sometimes even for several hours. 

Athetosis. Dr. Hammond, of New York, was the first to 
describe this condition. It affects the hand and the foot, 
and is characterised by slow, irregular movements which the 
patient is unable to resist. It is, as a rule, unilateral, and 
unattended by paralysis. Slowly and deliberately the fingers 
and hands are twisted about, the foot is inverted, . the toes 
flexed and extended. It is sometimes painful, sometimes pain- 
less, and may cease during sleep, or continue in a modified way. 
It is sometimes a sequel of hemiplegia, or of a convulsion, 
sometimes it arises independently. Dr. Hammond concludes 
that it must be due to lesion in the corpus striatum or optic 
thalamus — a lesion of an irritative but not destructive kind. 

Saltatory Spasm and Eclampsia Nutans. These two 
conditions may serve as types of special forms of spasm 
which are occasionally met with in practice. The former 
was described by Bamberger, and has been ably discussed by 
Dr. Gowers and others. The symptoms appear only when 
the patient attempts to stand, or, rather, only when pressure 
is exerted upon the soles of the ieet. As soon as such 
pressure is made, violent contraction of the muscles of the 
leg occurs, so that the patient leaps into the air, and, when- 
ever he touches the ground, again bounds up. Eclampsia 
nutans is a condition commonly met with in infants, which 
has been admirably described by certain writers, among others 
by Dr. Barnes of Carlisle. It is characterised by a peculiar 
nodding or salaam movement, the patient bending the head 
and body forward, sometimes slowly, sometimes with great 
rapidity, for a period ranging from a few seconds up to 
several minutes at a time, the attacks recurring sometimes 
rarely, sometimes frequently in the course of a single day. 
Besides these pretty definite types, you may meet occasion- 
ally in practice a great variety of convulsive movements 
occurring in patients of very nervous constitution. I had, 
some years ago, under my care a lady between twenty and 
thirty years of age, who went on for weeks or months 



126 



CRAMP. 



constantly nodding the head to one side or the other alter- 
nately, these more constant movements occasionally becoming 
replaced by more general spasms, sometimes by convulsive 
movements, in which she would leap like a frog from one 
end of her bed to the other, sometimes with opisthotonos, 
and sometimes with dancing movements fitted to recall those 
of the dancing mania of the Middle Ages, or of Madagascar 
in recent times, as described by Dr. Davidson. One also 
meets occasionally with cases of spasmodic rhythmical con- 
tractions of diaphragm, recti, and other muscles. I have seen 
such spasms in a neurotic patient, and known them persist 
for weeks. Among the most violent of the spasmodic attacks 
which you will meet with in practice, are those seen in hystero- 
epilepsy. In such a case the patient may be suddenly 
seized with tonic spasm, the features fixed, the back arched, 
the head thrown back, the limbs rigid, the eyes fixed and 
markedly turned up. After a few seconds the most violent 
contractions set in, the patient tosses about in bed, lying on 
his back, and springing from the bed ; from this condition 
she passes into a quiescent state. 

Cramp. Closely allied to tonic spasm, is the condition of 
cramp in the muscle. It consists in powerful contraction of 
the muscular fibres of a single muscle or group of muscles, and 
is attended by very severe pain. It commonly occurs when 
the muscle is fatigued, and is apt to be induced when volun- 
tary effort is made under such circumstances. But it occurs 
also when the muscles are at rest, as during sleep. It is 
often complained of by pregnant women, by gouty people, 
and by those somewhat advanced in life. It is a distressing 
accompaniment of cholera and severe diarrhoea, and occurs 
occasionally in other diseases. You wiU find that it may be 
generally undone by mechanical effort. If the cramp be in 
the gastrocnemius and soleus, pressing the toes on the ground 
will often suffice, by drawing out the muscular fibre on the 
back of the leg, to remove the cramp. If it be in the 
muscles extending the toes, so that they are turned up, 
pressing them downwards wiU often cure it. It appears to 
me probable that cramp is usually produced by alteration of 
the muscle itself, rather than of its nerve supply. 



CATALEPSY, CONTRACTURE. 



127 



Cataleptic Rigidity. Prolonged rigidity of muscles charac- 
terises catalepsy. Quite suddenly, and perhaps without any 
warning, a patient is seized with rigidity, and in whatever 
position the limbs may have chanced to be at the commence- 
ment of the seizure, they remain. It may be only for a few 
minutes, it may be for hours. I have seen it subside within 
half a minute or a minute of the commencement ; and I know 
of an asylum patient who, having been left by his attendant at 
night in the act of emptying his bladder, was found in the 
morning standing with 
the chamber utensil in 
his hand, cataleptic 
rigidity having fixed 
him in the position all 
night. The rigidity is 
of a very peculiar land. 
It keeps the parts fixed, 
and yet scarcely resists 
passive motion. In a 
case of catalepsy you 
will find no difficulty 
in moving the arm and 
leg into any position 
you wish, and, when 
they are so placed, they 
remain fixed until the 
fit is over. We know 
nothing at present of 
the nature of the nerve- 
influence which pro- 
duces catalepsy, but it 
is manifestly functional, and is apt to be associated with 
other functional manifestations, such as hysteria. 

Contracture. The last morbid mode of action of muscle 
to which I shall refer is contracture. By this term we under- 
stand a state of permanent or persistent contraction, some- 
times a result of functional, sometimes of organic changes. 
The affected part, most commonly an arm, remains fixed in 
some position, and no effort on the patient's part suffices to 




Fio. 66. 
Contracture of left arm. 



128 



CO-OEDINATION. 



alter it materially, whilst there is also the most marked resist- 
ance to passive movement. The condition is typically seen in 
old cases of hemiplegia, but may also occur at an early stage 
of the same disease. It is seen also in spastic paralysis. It 
is difficult to explain with certainty the occurrence in recent 
hemiplegia ; but in long-standing hemiplegia, and in spastic 
paralysis, it is due to descending degeneration or primary 
change in the lateral columns of the cord (fig. 60). It 
occurs also in functional conditions, especially in hysteria. 
Some years ago I treated, in a side-room in the wards of the 
Old Infirmary, a patient who had been obliged to relinquish 
her work as a governess, in consequence of various hysterical 
symptoms, of which one of the most prominent was con- 
tracture of the arm. For weeks and months it remained 
fixed and rigid, not closely pressed against the chest, but 
held out at a little distance. 

Go-ordination. Co-ordination is the harmonious action 
of muscles, or groups of muscles, whereby precise and definite 
movements are accomplished. Certain co-ordinations are 
inborn. Breathing, sucking, swallowing, micturition, and 
defsecation, all require co-ordination of numerous muscles, 
and from the moment of birth each of them is perfectly 
performed. Occasionally you find some of them imperfectly 
developed in idiots. But a large number of co-ordinated 
movements are slowly acquired during childhood. Physical 
education consists in learning to co-ordinate. Among the 
first acquired co-ordinate actions is that of the muscles of the 
eye, whereby a chUd learns to look at an object. Another 
is the power of definitely grasping and holding objects. By 
degrees the child learns to stand, to run and walk, to speak, 
to write, to draw, to dance, to play musical instruments, to 
use special implements, and in each of these there is a 
laborious process to be gone through ; the co-ordination 
becoming, however, by degrees more and more easy, until at 
last it becomes automatic. 

The mechanism which subserves co-ordination is somewhat 
complicated. It is uncertain whether it is subserved by 
separate nerve-structures or not. I incline to think that it is. 
It requires sensory structures for the reception, conduction. 



FAILUKE OF CO-OEDINATION, 



129 



and perception of impressions. It requires central gangli- 
onic structures, which are thought by some distinct from 
the motor centres ; and it requires efferent nerves, by which 
the impulse from the centre is conducted to the motor 
structures. 

Failure of Go-ordination. This mechanism may fail at 
any point. We often find co-ordination diminished or lost 
This may be from sensory changes, as you see most typically 
in cases of muscular anaesthesia. When I spoke to you of 
the muscular sense, I referred to cases of the kind. I may 
mention one in which there was loss of muscular sense, and 
of cutaneous sensibility in an extraordinary degree, and 
although the patient could walk well with open eyes, he 
fell at once if they were closed. It is not essential for 
all co-ordinated actions that the sensory impressions should 
be recognised in the consciousness. I have seen a patient 
who was quite unaware of the condition of his bladder, and 
Imew nothing of the fact that micturition was going on, who 
3^et used to evacuate the contents in an ordinary way from 
time to time. His brain did not receive the sensory impres- 
sion, but a co-ordinating centre in his spinal cord did. And 
even higher co-ordination may be accomplished without the 
intervention of consciousness. It is important for you 
to observe that co-ordination may fail, in consequence of 
central changes without any failure of motor power. You 
see this constantly illustrated in the wards in consequence 
of locomotor ataxia and of cerebellar disease. You have 
noticed how strong the muscles are in many cases of 
locomotor ataxia, how the patient can grasp with great 
force, although he cannot accomplish any movement accur- 
ately, how he can kick out with his legs or carry a heavy 
weight on his shoulders, although his gait is so staggering 
and unsteady. And this, you will remember, is sometimes 
well^ seen where there is little or no impairment of the 
sensibihty. In cerebellar disease, again, you frequently see 
no weakness of muscles, notwithstanding the unsteadiness of 
the gait. In these cases, also, there is not necessarily any 
sensory change. These, then, are examples of impairment 
or of failure of co-ordination from central disease. With 



130 



FAILUEE OF CO-ORDINATION. 



regard to failure from lesions in the efferent structures, it is 
more difficult to speak positively. Perhaps multiple sclerosis 
may in some cases illustrate this. 

Defects of co-ordination sometimes appear only when 
the co-ordinating effort is made, other co-ordinations of the 
same groups of muscles remaining intact. One of the 
best illustrations of this is afforded by writers' cramp, but 
other trade spasms are essentially of the same nature. If 
you investigate closely the changes which occur from exces- 
sive use of certain muscles, you will find that there are 
at least three varieties. Sometimes there is muscular atrophy, 
with consequent weakness of movement. Sometimes there is 
true paralysis of muscle, due to change in the nerve, or in the 
nerve-centres. But more frequently than either there is simple 
failure of co-ordination. A patient Avas under my care who 
had been employed in a lawyer's office during an eagerly- 
contested parliamentary election. For several days he had 
gone on addressing circulars throughout almost the whole 
twenty-four hours. But before the work was complete his 
power of co-ordination for writing failed him. Although he 
could button his coat, or put in a pin perfectly well, when- 
ever he attempted to write, his hand would jerk away in the 
wrong direction. It may be thus suddenly developed, or it 
may come on gradually, varying in severity according to the 
general condition of the patient. A patient suffering from 
writers' cramp lately told me that he could write best when 
he was not attending to the act, but writing mechanically. 
This fact points to the conclusion that the fault is in some 
of these cases situated in the highest centres. Similar 
failures of co-ordination are met with in tailors, shoemakers, 
violinists, pianists, telegraphists — particularly those who use 
the Morse instrument, I showed to some of your predeces- 
sors a girl who had been employed in a factory, and whose 
duty had been to watch the passage of a spindle as it was 
cast from side to side in weaving. This required her to 
move the head from side to side many thousand times 
in every hour. Gradually she became unable to keep the 
head still, but moved it from side to side, a permanent 
co-ordinative spasm having been developed in connection 



CO-ORDINATIVE SPASM. 



131 



with certain of the muscles of the neck. I have seen 
many cases strictly analogous to this, — cases, for example, 
of miners' nystagmus, and of backward jerking of the head 
in people who had been accustomed to carry heavy weights 
on the head. Another example of co-ordinated spasm is 
afforded by the commencement of many epileptic seizures. 
You find the patient's head turned upwards and away to one 
side, the eyes turned as far as possible in the direction in 
which the head has been turned — the conjugate deviation. 
When I speak of the changes of the function of speech, 
I shall have occasion to refer to certain co-ordinated spasms, 
when a patient suddenly feels himself impelled in the midst 
of a sentence, or before he has commenced to speak, to utter 
spasmodically some form of words. 

Cough. An important co-ordinated action which often 
constitutes a symptom in disease is cough. It consists in a 
deep inspiration, a sudden closure of the glottis, followed by 
a spasmodic contraction of the expiratory muscles, with 
sudden relaxation of the glottis. For its performance, as 
for other organic reflexes, there are required sensory and 
afferent nerves, reflex centre and efferent motor, with co- 
ordinating structures. In the great majority of cases, the 
act of coughing is beneficial, removing materials from the 
respiratory tract ; but, from failure of the sensory imjjression, 
it may be awanting, the appropriate stimulus not being 
supplied. From central disease, or from paralysis of motor 
nerves, it may also disappear. On the other hand, it may 
be present in excess, as from peripheral irritation during the 
second dentition, or from undue irritability of the centres, as 
in some cases of malarious poisoning. In cases of locomotor 
ataxia you sometimes find paroxysms of coughing a prominent 
symptom. The patient is seized with a fit of coughing like 
that which occurs in whooping cough ; this is often attended 
by whistling inspiration, sometimes by headache, nausea, 
vomiting, or even epileptic convulsions. This is apt when it 
occurs to be one of the early symptoms of locomotor ataxia. 
It may serve as a typical illustration of other co-ordinated 
movements. 



LECTUKE IX. 



ELECTRICITY IN DIAGNOSIS, 

Varieties of Electricity. — .Application, — Direct Method. — Indirect 
Method. — Motor Faints for Muscles. — Galvanism. — Weak, Moder- 
ate, aoid Strong Currents. — Symbols. — The Galvanometer. — 
Faradism. — Electric Irritability Undisturbed, Increased, Dimin- 
ished, Altered in Quality. — Reaction of Degeneration. — Electricity 
in Feigned Disease. — Distinction between Trance and Death. — 
Precautions necessary in Using Electricity. 

r\ ENTLEMEN, — I shall to-day briefly explain to you the 
^ uses of electricity in diagnosis, speaking of the varieties 
of electricity, their modes of application, the effects which 
they produce in health, and the modifications of these effects 
in disease. 

The forms of electricity which are of practical importance 
in medicine are Galvanism or Voltaism, or the constant 
current, and Faradism or the interrupted current. The 
Galvanic owes its existence to chemical action, and is 
continuously evolved, flowing always in the same direction 
from the positive to the negative pole. The Faradic current 
is generated by induction from voltaic or magnetic source, 
is momentary in duration, and its direction is constantly 
changing. 

Electricity is applied by means of rheophores, which may 
be sponge-holders, or metallic discs covered with wash-leather 
— oval or pointed, or of round form. In order that the current 
may penetrate the skin, the rheophore and the cutaneous 
surface must be well moistened with salt and water. Localised 
electrisation alone is of importance in diagnosis, and it gives 
us information as to the state of the nerves and muscles. 
Examination of the latter is effected in either of two ways — 
the direct method (of Duchenne), both rheophores being 
applied over the muscle which is the subject of examination ; 
132 



ELECTRO-MOTOR POINTS. 



133 



and the indirect method (of Ziemssen), one rheophore being 
applied over the nerve, the other on some indifferent part of 
the body. Each mode of apjplication has its advantages. 

It is important to keep in mind the motor points for the 
nerves supplying different muscles, and I show you diagrams 
copied from Ziemssen, -which correctly indicate them. In 



Branch of median nerve to 
Pronator teres 



Palmaris longus . 



Flexor carpi ulnaris 



Flexor aublimis digitorum . . — 



Ulnar nerve _ 

Flexor sublimis digitorum . . . . 
(Index and little finger). 

Deep branch of ulnar nerve., 
Pulmaris brevis ^ 

Abductor minimi digiti ^ 

Flexor brevis minimi digiti 

Opponens minimi digiti 

Lumbricales (2, 3, and 4). . | ■- 



^—fj/- Flexor sublimis digitorum. 




— . Flexor carpi radial is. 

- Flexor profundus digitorum. 



|Jl Flexor longus poUicls. 

' Median nerve. 



Abductor pollicis. 

Opponens pollicis. 

Flexor brevis pollicis. 

.idductor pollicis. 

— Lumbricalis (1st). 



Fig. 67. 

Motor points of forearm (Ziemssen). 

order to test individual muscles or groups of muscles, you 
apply the one pole at some neutral part, the other at the 
point marked. 



134 



ELECTRO-MOTOR POINTS. 



Supinator longus 

Extensor carpi radialis longior . . 



Extensor carpi radialis brevier 



Extensor communis digitorum 



Extensor indicia 

Extensor indicia et extensor) 

ossis metacarpi pollicis f 

Extensor ossis metacarpi pollicis. 



Extensor primi internodii pollicis 
Flexor longus pollicis 



Dorsal interossii < 2 




— Extensor carpi ulnaris. 



— Extensor minimi digiti. 



Extensor indicis. 



( Extensor secundi 
t internodii poUicls. 



Abductor minimi digiti. 
Dorsal interosseus (4). 



Fig. 68. 

Motor points of the forearm (Ziemssen). 



135 




Flo. 69. — Motor points of head and neck (Ziemssen). 



1. Frontalis muscles. 

2. Attrahens and attollens auriculam muscles. 

3. Eetrahens and attollens auriculam muscles. 

4. Occipitalis muscle. 

5. Facial nerve. 

6. Posterior auricular branch of facial nerve. 

7. Stylohyoid muscle. 

8. Digastric muscle. 

9. Buccal branch of facial nerve. 

10. Splenius capitis muscle. 

11. Subcutaneous branches of inferior maxillary 

nerve. 

12. External branch of spinal accessory nerve. 

13. Sterno-mastoid muscle. 

14. CucuUaris muscle. 

15. Sterno-mastoid muscle. 

16. Levator auguli scapulse muscle. 

17. Posterior thoracic nerve (rhomboidei 

muscles). 

18. Phrenic nerve. 

19. Omohyoid muscle. 

20. Lateral thoracic nerve (serratus magnus). 

21. Axillary nerve. 



22. Branch of brachial plexus (musculo- 

cutaneous and part of median). 

23. Anterior thoracic nerve (pectoral muscles). 

24. Corrugator supercilii muscles. 

25. Compressor nasi and pyramidalisnasi muscles. 

26. Orbicularis palpebrarum muscle. 

27. Levator labii superioris alfeque nasi muscle. 
2S. Levator labii superioris muscle. 

29. Zygomaticus minor muscle. 

30. Dilatator naris. 

31. Zygomaticus major.* 

32. Orbicularis oris. 

33. Branch to triangularis and levator meuti 

muscles. 

34. Levator menti muscle. 

35. Quadratus menti muscle. 
30, Triangularis menti muscles. 

37. Cervical branch of facial nerve. 

38. Branch to platysma muscle. 

39. Sterno-hyoid muscle. 

40. Omohyoid muscle. 

41. Sternothyroid muscle. 
I 42. Sternohyoid muscle. 



• The upper of the two lines that converge on 31 should have been directed to 30, as it applies to 
the dilatator naris posterior muscle. 



136 



ELECTRO-MOTOR POINTS. 




ELECTEO-MOTOR POINTS. 



137 




rio. 72. 
Motor points of leg (Ziernssen). 



138 



ELECTEO-MOTOR POINTS. 




GALVANISATION. 



139 



You are aware that both Galvanic and Faradic electricity 
act on the nerves, and that normally both of them produce 
muscular contraction as a result of nerve-stimulation, while 
only one of them acts upon muscular fibre itself. The 
interrupted current influences muscle by acting on the nerve 
structures within its substance, while the Galvanic acts both 
upon them and directly upon the muscular tissue. If an 
animal is brought under the influence of curara, which 
paralyses the nerve-endings within the muscles, there is no 
response to Faradic stimulation, but contraction very dis- 
tinctly follows the application of the Galvanic current. 

Galvanisation. When healthy muscles are acted upon by 
Galvanisation, muscular contraction occurs at the moment of 
opening or of closing of the current, and the effects are observed 
to differ in accordance with the strength of the current. At 
each pole there are characteristic changes. With a weak cur- 
rent, we get contraction at the negative pole on closing; with 
a medium current, we get strong contraction at the negative 
pole on closing the current, slight contraction at the positive 
pole on closing the current, and slight contraction at the 
positive pole on opening the current. With a strong current, 
we get tetanic contraction at the negative pole on closing, 
contraction at the positive pole on closing, contraction at 
the positive pole on opening, and perceptible contraction at 
the negative pole on opening. This is troublesome to express 
without the use of symbols. Let me explain the symbols 
commonly employed : — 



An.= 


Anode, the positive pole. 


Ca.= 


Cathode, the negative pole. 


C. = 


Contraction. 


c. = 


Feeble contraction. 


C\ = 


Strong contraction. 


Te.= 


Tetanic contraction. 


CI. = 


Closure of current.* 


0. = 


Opening of current. 



* In many of the English books, such as Dr. Eoss's work on the Diseases 
of the Nervous System, and Dr. Buzzard's Clinical Lectures, the letter S. is 
used instead of CI., thus adopting the initial letter of the word " Schliess- 
ung" instead of the initial letter of the word " closure." 



140 



GALVANISATION. 



Stating tho normal result of the Galvanic stimulation of 
muscles by the symbols, we find : — 

1. With a weak current we get contrac- = Ca. CI. C. 

tion at the negative pole on closing 
the current. 

2. With a medium current we get strong 

contraction at the negative pole on 

closing the current, slight contrac- = Ca. CI. C \ 

tion at the positive pole on closing 

the current, and slight contraction = An. CI. c. 

at the positive pole on opening 

the current. = An. 0. c. 

3. With a strong current we get tetanic 

contraction at the negative pole on 

closing the current, contraction at = Ca. CL Te. 

the positive pole on closing, con- = An. CI, C, 

traction at the positive pole on = An. O. C. 

opening, and contraction at the 

negative pole on opening. = Ca. 0. c. 

In ordinary practice, it is usually held sufficient if we 
compare the contraction produced on the diseased part with 
that on the healthy side, or, if the disease be bilateral, in a 
healthy individual. But such a method is far from satis- 
factory. In using Galvanism, you will find that clinical 
observers often say that contraction Avas produced in a given 
case with a certain number of cells, but considering the 
variableness of the activity of cells, and of the resistance of 
the tissues in different parts of the body, this is insufficient. 
The true way is to use the galvanometer. By its apjDhca- 
tion we are able to read off, according to a definite standard, 
the strength of a current circulating in any given circuit. 
It sometimes happens that a current which suffices to pro- 
duce a movement on one side fails to do it on the other, 
and this may be due either to change in nerve and muscle, 
or to increase of resistance in tissues. Without the galvan- 
ometer you could not distinguish between these. But when 
it is used you find the record of the full but inefficient 



MODIFICATIONS OF ELECTRICAL REACTIONS. 141 

current when the nerve and muscle are at fault, and of a 
diminished because obstructed current when the tissues offer 
a resistance. . Further, in recording results it is essential, if 
we would exclude all fallacies, that we make an accurate 
note of the character and size of the electrode, and the mode 
and points of application. 

Faradisation. When a healthy muscle is acted upon by 
Faradisation, it is brought into a rapidly alternating state of 
contraction and relaxation, so long as the rheophores are in 
contact with the skin. 

In the use of Faradism we are able to obtain and record 
definite results by making use of an apparatus with a move- 
able secondary coil, provided with a scale giving the strength 
of current in terms of the distance between the primary and 
secondary coils. 

In disease we may find the electric irritability undis- 
turbed, increased, diminished, or altered in quality. 

The reaction to both forms of stimuli may be undisturbed, 
as we see in the majority of paralyses resulting from cerebral 
lesions, where secondary degeneration has not occurred ; in 
paralysis due to the cutting off of cerebral influence by 
transverse spinal lesion (the parts suppHed by the actively- 
diseased portion manifesting the reaction of degenera- 
tion, to be presently described) ; in spinal diseases 
affecting only the white substance as in the early stages 
of locomotor ataxia ; and in some mild cases of peripheral 
paralysis. 

Increased irritability (without qualitative change) is the 
rarest of all conditions. It is described as occurring in the 
first stages of a certain number of cases of hemiplegia, of 
locomotor ataxia, and of facial paralysis, and it is very dis- 
tinct in cases of tetany. 

Diminished irritability is present in all paralyses of cerebral 
and spinal origin, where secondary degenerative processes 
have ensued, in atrophy from disuse, in pseudo-hypertrophic 
paralysis, in peripheral paralysis, and in some cases of slowly- 
progressing muscular atrophy. 

Qualitative changes consist in alteration of the normal 
reactions, both in respect to time (serial alteration) and 



142 



EEACTION OF DEGENERATION. 



character (modal alteration), and they never occur without 
quantitative. 

Reaction of Degeneration. "When qualitative and quanti- 
tative changes are present together, they form the most 
important modification in the electrical conditions, the 
reaction of degeneration. Wherever it occurs, we are entitled 
to conclude that the nerve-supply to the muscle is interfered 
with, either from alteration in the nerve-fibres, or in the 
trophic cells connected with the nerves. But it is not 
necessarily attended by paralysis. In lead-poisoning, for 
example, it may be demonstrated before the muscles are 
paralysed. The following changes characterise the reaction : 
— (1.) Stimulation of the nerve supplying the affected muscles 
(either by the Faradic or the Galvanic current) gives negative 
results. (2.) Direct stimulation of the muscle by the Faradic 
current also gives negative results. But (3.) direct stimulation 
of the muscle by the (galvanic current produces, in fully de- 
veloped cases, contraction more easily, — that is, with a weaker 
current than in health. This contraction is, however, more 
sluggish in character, and tends to last longer. Further, 
the normal order of polar reactions is disturbed, in so far 
that An. takes the place of Ca. ; so that whereas in 



health- 



Ca. CI. C. An. CI. C, and 
An. 0. C. Ca. 0. C. 



Now— An. CI. C. = or => Ca. CI. C, and 
Ca. 0. C. = or An. 0. C. 

You may find it difficult to remember these facts, but you 
will have opportunity of seeing them demonstrated in this 
class-room and in the wards of the Infirmary; and when you 
have once seen them for yourselves, you wiU have no difficulty 
in recalling them. Meanwhile, remember that the main 
features are the loss of Faradic excitability, and the fact that 
with Galvanisation contraction takes place at the positive 
more readily than at the negative pole. 

By reference to the diagrams devised by Professor Erb of 
Heidelberg, you may readily make out the points just referred 



]iKA('T[C)N OF DEGENKRATIOX. I'i:! 



to, with certain others whicli I think it worth while to bring 
under your notice. 

0 1 2 3 4 f) 0 7 8 !) 10 11 12 weeks. 




Fig. 74. 

Diagram illustrating reaction of degeneration, with rapid recovery (Eib). 

In fig. 74 you see stated the facts in a case of paralysis ter- 
minating speedily in recovery. You observe that motility 
totally disappears at once ; that the reaction of the muscle to 
the Faradic current, and of the nerve to both kinds of stimula- 
tion, diminishes rapidly during the first fortnight and then 
disappears, reappearing again at the end of the seventh week, 
and gradually returning to a normal standard. Before they 
begin to return, motility reappears, and you see that in the 
diagram it is shown as appearing a week before. With 
regard to the reaction of the muscles to Galvanism, you 
observe that during the first ten days it shows a gradual 
diminution, which in the course of the succeeding four or 

0 1 2 4 6 10 1."^ 20 25 30 So 40 4". 50 weeks. 




Fui. 75. 

Diagram illustrating reaction of degeneration, witli slow recovery (I5ib). 

five days is replaced by an increase whicli continues at a 
maximum till the fourth or fifth week, and then gradually 
falls to the normal, reaching it about the tenth week. 

In fig. 75 you have the conditions in a case where recoveiy 

K 



144 



J{EACTION Of DEGENERATION. 



is slow. As before, motility is lost at once, and the reaction 
of the nerve and of the muscle to the two currents is affected 
in a similar manner to that Avhich we have just described. 
The return to the normal is considerably later than in the 
case rejDresented in the last figure. Motihty begins to re-assert 
itself about the thirteenth week, and this is followed in a 
week or two by a gradual reappearance of Galvanic and Faradic 
excitability on the part of the nerve, and of Faradic excita- 
bility on the part of the muscle. Galvanic excitability 
on the part of the muscle, after being diminished in the first 
ten days, and increased beyond the normal during the 
succeeding three weeks, slowly returns to the level of 
health. 

In fig. 76 is shown the course of a case where recovery does 
not take place. Motility is lost at once, and for ever. The 
excitability of the nerve to the Galvanic and to the Faradic 

0 1 n in -20 30 40 so on 70 sn no 100 weeks. 




Fid. 76. 

Diagram illustrating reaction of degeneration, where recovery does not occur (Erb). 

current, and of the muscle to the Faradic current, disappear 
as before, and do not return. With regard to the reaction 
of the muscle to the Galvanic current, there is, as before, an 
early diminution, rapidly followed by an increase beyond the 
normal, and then by a steady decline, till about the end of 
the second year the muscle finally loses its excitability to the 
Galvanic current. 

Another diagnostic use of electricity which you must keep 
in view is its power of distinguishing in some cases between 
real and feigned disease. You may find in a case otherwise 
uncertain that in one limb, or in a group of muscles, there 
is no response to Faradic irritation, while elsewhere normal 



ELECTRICITY IN CASES OF TRANCE. 



145 



irritability exists. In such a case you know at once that 
there is real disease. 

In cases also in which the question of diagnosis is, whether 
the patient is dead or in a state of profound trance, 
electricity will solve the question, as the electric irritability 
persists in the latter and disappears within an hour or two 
after death. 

Lastly, in using electricity, especially Galvanism, and when 
you are about to apply it to the face or head, always try the 
current upon yourselves to begin with. Duchenne, one of the 
greatest medical electricians that has ever lived, once pro- 
duced permanent injury by a too bold application to the 
head. 

If you wish to study more minutely the questions con- 
nected with electricity, I should recommend you to read 
the works of De Watteville, Hughes Bennett, Tibbits, of 
Duchenne, Erb, and Ziemssen. 



LECTURE X. 



Vaso-motoe, Secretory, and Trophic Functions. 

Vaso-Motor Functions. — Neuro-Paralysis. — Neuro-Spasm. — Tache 
Cerebrale, &c. — Body Heat. — Secretory Changes not Vaso-Motor. 
— Saliva. — Gastric Juice. — Bile, <&c. — Glycosuria. — Trophic 
Changes. — Nervous (Edema. — Haimorrhages. — Hoematoma 
Aurium. — Inflammation. — Changes in Hair and Rails. — Glossy 
Skin. — Myxoedema. — Lepra Ancesthetica. — Gangrene. — Bed- 
Sores. — With and Without Pressure. — Muscular Atrophy. — In 
Polio-myelitis Anterior. — Near Rheumatic Joints. — In Infantile 
Paralysis. — Wasting Palsy. — Not Vaso-Motor. — Changes in 
Joints. — Changes in Bones. — Facial Hemiatrop)hia. 

r^ENTLEMEN, — The action of the nervous system upon 
^ vascular supply, upon the body heat, and upon secretory 
and nutritive processes, has been definitely made out only 
of recent years. I shall speak first of its influence upon the 
blood-vessels, and on temperature ; secondly, on secreting 
glands ; and, third, upon nutritive processes in the tissues. 

1. Vaso-Motor Function. You are all familiar with the 
physiological neuro-paralytic processes, whereby the skin be- 
comes suffused from vascular congestion. You are familiar, 
also, with the experiments on the cervical sympathetic, which 
induce extraordinary congestion of the vessels in the neck, 
head, and face. Similar effects are sometimes met with in 
disease. In hemiplegia, for example, the paralysed limbs 
sometimes present well-marked congestion, due to neuro- 
paralytic changes. And occasionally, in functional nervous 
disease, you may notice districts of the sldn extremely 
congested and contrasting with the pallor in other parts. 
Among the effects of vascular dilatation of nervous origin, 
none is more striking than that met with in exophthalmic 
goitre. You are familiar with the features of this malady. 
146 



VASO-MOTOR FUNCTION. 



147 



The drawing shows you the protrusion of the eyeballs and 
the peculiar nervous expression, and you can easily satisfy 
yourselves, when you examine a patient, of the symptom 
first described by Von Grsefe — the delayed descent of the 
upper eyelid. In health, as the eye is directed from a 
higher object to a lower, the eyelid descends coincidently 
with the movement of the eyeball ; but in this disease the 
eyeball moves first, and the lid follows after an interval. 
This delay is not a mere mechanical result of the exophthalmos, 




Fig. 77. 

Altered physiognomy in exophtlialinic goitre. 



but depends upon irritation of the muscular fibres of Muller, 
which are suppUed by the sympathetic. With these you 
observe the characteristic rapid action of the heart. It ranges 
from one to two hundred in the minute, and its rapidity is 
probably due to irritation of the sympathetic. In typical 
cases one of the most outstanding features is the dilatation 
of the vessels, not in the enlarged thyroid gland alone, but 
in the whole neck and head, sometimes in the body generally. 
The dilatation is not to be ascribed to the excited cardiac 



148 



VASO-MOTOll FUNCTION. 



action nor to any change in the tissues, but probably to an 
influence exerted on the walls of the vessels. Although m this 
disease, as after section of the sympathetic, the congestion 
is well marked, there is no tendency to inflammatory changes 
nor to hypertrophy of the congested tissues. The disease 
may persist for years, and the nutrition remain unchanged. 

Another disease in which neuro-paralytic vascular symptoms 
appear is megrim. In that, sometimes it is very pronounced. 
With every return of the paroxysm thevessels become distended, 
the affected half of the face is congested, while painful 
throbbing is a symptom of which the patients very frequently 
complain. 

You are aware, also, that the very opposite condition 
occurs ; that, under stimulation of the sympathetic, the vessels 
may be made to contract. We meet with similar conditions 
in disease. The vascular contraction may be so great that 
the skin becomes pale and extremely cold, and may even be 
pricked with a needle, or cut with a knife, without bleed- 
ing. This results from spasm of the small arteries. It 
is often met with in cases of hysterical disease, and most 
typically in hysterical hemi-ansesthesia, in which I have 
seen pins driven through between the metacarpal bones 
without producing ha3morrhage. In cases of hemiplegia, 
this condition is also occasionally seen, the paralysed parts 
being extremely pale, the pallor not being confined to the 
skin, but affecting the deeper structures also. 

Taclie cerebrale is a result of altered innervation of the 
vessels. It consists of a marked and somewhat persistent line 
of congestion following upon touching the skin, or stroking 
it with a pencil or the finger-nail. It comes out some- 
what gradually, and persists for a considerable time. It is 
met with very generally in cases of tubercular meningitis, but 
it also occurs in other brain diseases, and in fevers. It has, 
therefore, less diagnostic significance than Trousseau was at 
one time inclined to suppose. In this connection I may 
refer also to other vascular changes, such as those in factitious 
urticaria and similar conditions, in which, by irritating the 
skin, congestive and urticaria-like patches may be induced ; 
and when after writing with a blunt point on the skin the 



TEMPERATURE. 



149 



letters come out and persist for a long period — a change 
corresponding to the tache cerebrale. 

The vaso-motor function lias its chief centre in the medulla 
oblongata, but there are subsidiary centres throughout the 
cord, and the cerebral convolutions themselves exert an 
influence upon the vessels of certain districts on the opposite 
side of the body — districts apparently corresponding pretty 
closely to those whose muscles are brought into play by irrita- 
tion of the psycho-motor areas. 

With the vascular alteration we often find alterations of 
the temperature. When a greater supply of blood is sent to 
a part the temperature rises. We see that in many cases of 
cerebral paralysis, such as hemiplegia from haemorrhage, there 
is at first congestion of the paralysed side, with elevation of 
temperature, and afterwards a fall to the normal or to sub- 
normal. Occasionally you will find the temperature rapidly 
mounting to a high point — 104°, 106° F. — within a few 
hours of the commencement of the attack. This is a very 
ominous feature. 

In cases of injury to great nerves, such as the sciatic, you 
sometimes find vascular congestion and elevation of the tem- 
perature of the affected limb at the beginning of the attack, 
giving place to depression of temperature when the nerve has 
undergone the degenerative changes. 

It is certain that the temperature of the body and of 
individual parts may be influenced in other ways than through 
the vaso-motor function, for sometimes the elevation of tem- 
perature is out of aU proportion to the vascular congestion. 
Then it is clear that the heat-regulating centre is itself dis- 
turbed. This is seen in some apoplectic cases, such as 
those we have referred to. Charlton Bastian concurs with 
Bourneville in recognising four categories of cerebral hsemor- 
rhages in relation to temperature ; and I shall mention them 
to you, though I have not yet been able to verify them in 
my own experience. 

1st. Cases with very large haemorrhage, death occurring 
within an hour or two ; temperature lower throughout. 

2nd. Cases fatal in from ten to twenty-four hours ; tem- 
perature at first lowered, then rapidly rising. 



150 



SI'X'RETION. 



3rd Cases proving fatal at the end of a few days, where 
there is first a lowering, then a stationary period at about 
the normal standard, then a rise. 

4ith. Cases ending in recovery ; first a lowering, then a 
temporary rise, and then a return to the healthy standard. 

Still more strikingly is alteration of temperature shown 
in the case of hysterical hyperpyrexia, of which several 
instances are on record. In these cases the temperature has 
reached 110°, 115°, or even 122° F. without any per- 
manent mischief followinsf. 

2. Secretory Changes. Secretion is affected to some extent, 
no doubt, through the vaso-motor action ; but nerve influence 
upon glands is not exclusively of that kind, — it acts directly 
upon the secreting structures. It has been demonstrated 
that nerve-fibres are distributed to glands, and pass to and 
terminate in the secreting cells. It has been proved also 
(particularly by the beautiful experiments of Ludwig) that, 
when an excessive flow of sahva is brought about by stimula- 
tion of the nerves supplying the salivary glands, the pressure 
in the gland-duct exceeds that in the blood-vessels. This 
fact can only be explained on the hypothesis that the gland- 
cells are stimulated directly by the nerve. In this we find 
sxn explanation of many famihar facts as to increased activity, 
diminished activity, and perversion of function of glands 
under various nerve influences. The influence of the nervous 
system upon the secretion of milk and of urine has long been 
recognised, and every one is familiar with the effect of excite- 
ment in producing dryness of the mouth, and of other condi- 
tions producing excessive secretion. The rule aj)phes to all 
the secreting glands of the body. 

The salivary secretion varies much under the influence of 
the nervous system. I have seen a patient of hysterical con- 
stitution, and apart from any local cause that I could discover, 
pour forth saliva as freely as a patient fully under the influ- 
ence of mercury ; and I have seen an arrest of the secretion 
almost equally pronounced. Increase or diminution is also 
found to attend upon facial neuralgia, just as in that disease 
you sometimes meet with excess or diminution of the 
lachrymal and nasal secretions. Claude Bernard found that 



SECRETION. 



151 



the prick of a needle in the neighbourhood of the pons, close 
behind the origin of the fifth nerve, produced salivation. 

On the receipt of bad news, the secretion of the gastric 
juice often becomes arrested, and, in states of nervous 
exhaustion, impaired secretion is constantly seen. Under 
favourable mental conditions, and in good states of the 
nervous system, the secretion is abundant, and in some mor- 
bid states may be found to be excessive. The secretion of 
the liver also is largely determined by nerve influence It 
has been remarked that animals with artificial biliary fistulse 
are noticed, when caressed, to secrete bile more rapidly, and, 
when threatened or struck, to secrete less. 

But perhaps it is in the skin and kidneys that you see the 
effect most distinctly. Under mental effort, you often see the 
brow and face suffused with perspiration, and corresponding 
conditions are sometimes met with in disease. The excessive 
sweating may be constant, occasional, or intermittent. It may 
be limited to the distribution of some particular nerve, or 
may affect one lateral half of the body. My friend, Dr. Ogilvie 
AVill of Aberdeen, once showed me a patient who had, six or 
eight years before, had a slight attack of diphtheria, and 
from that time had been subject to well-marked unilateral 
perspiration. On the other hand, the secretion of the skin 
may be diminished or entirely absent, and that even when 
its vessels generally are congested. Under nerve influence, 
coloured perspiration sometimes appears. 

Excessive secretion from the kidneys is often seen as a 
result of nerve influence, mere excitement leading not only to 
frequent calls to micturition, but also to excessive secretion. 
After attacks of hysteria, asthma, epilepsy, and other affections, 
polyuria is frequent, and some cases of diabetes insipidus are, 
no doubt, referable to nerve influence. Nervous causes also 
may induce great diminution or total suppression of urine, 
and ischuria may exist for many days, or even for weeks, 
from this cause. Alterations of the secretion, almost certainly 
referable to nerve influence, are also met with — albumin- 
uria, for example, following upon epileptic seizures, being 
more properly referable to this than to other possible causes. 
The experiments of Claude Bernard, by which he showed 



152 



SECRETION, 



that puncture at a certain part of the floor of the fourth 
ventricle led to glycosuria, cannot, of course, be referred to 
an influence exerted on the kidney, but the albuminuria, 
which he found to result from puncture at a neighbouring- 
point, must undoubtedly be so ; and this observation is of 
interest in connection with the post-epileptic albuminuria. 
Not less important than this is the change in the urine- 
occurring in myelitis. Within a few days of the commence- 
ment of an acute inflammation of the cord, the urine becomes 
alkaline, and that not as a result of catarrhal changes in the 
urinary tract, but from an influence upon the urinary secre- 
tion, or the chemical processes in the system. I am not 
aware of any evidence to show that the amount of urea varies 
according to nerve-influence ; and, in the case of the Iddney, 
you will observe that the effect is rather produced through 
the vascular system than through action on the secreting 
elements proper. It is an increased transudation of water 
rather than a true increase of the urinary constituents. You 
remember that Claude Bernard showed that slight irritation 
in a particular part of the floor of the fourth ventricle induces 
polyuria, and that apart from the conditions capable of 
producing glycosuria and albuminuria. 

In connection with the secretory changes, I must direct 
your attention to the conditions known as gastric crises in 
nervous disease. They are sometimes of short duration, 
lasting only for a few hours, at other times for one day or 
several days. Perhaps I shall give you the best idea if 
I describe a case which I demonstrated to many of your pre- 
decessors in the clinical wards. The patient, who was suffering 
from locomotor ataxia, was occasionally seized with violent 
internal pain — pain which seemed to be more distressing than 
the lightning pains in the limbs from which he often suffered. 
Coincidently with this, his skin became very pale and of a 
greyish colour. His pupils contracted, his speech became 
slow, his pulse feeble, and he began to vomit. The vomited 
matter was of a greenish or brown colour, very watery, and it 
welled up in large quantity. Solution-pan after solution-pan 
was filled. There was neither furring of tongue nor other 
token of gastric catarrh, and gradually the sj'mptoms 



TROPHIC CHANGES. 



153 



subsided. The only thing which reheved the patient was 
morphia. When administered subcutaneously, it diminished 
his pain, but produced an exaggerated itching or stinging 
feeling in the skin. Although by no means the only feature, 
the excessive secretion poured out into the stomach was a 
very distressing element in the case. 

,The influence of the nervous system upon the chemical 
processes going on within the body is well illustrated in 
glycosuria. We caimot at present say how the nervous 
system operates, but certain facts are well ascertained. Claude 
Bernard demonstrated that injury of a point in the floor of 
the fourth ventricle induces it. Schiff and Eckhard showed 
that section of the cord anywhere down to the level of the 
first lumbar vertebra also does so. Eckhard and Cyon 
demonstrated that it also follows destruction of the upper 
and lower cervical, and of the upper thoracic sympathetic 
ganglia ; and Schiff found that after section of one of the great 
peripheral nerves, such as the sciatic, the same results appear. 
It is probable that these results are brought about through 
vaso-motor influences. In connection with nervous diseases 
we occasionally see diabetes developed, and it often occurs in 
people of neurotic constitution. It is possible that in all 
cases it is of nervous origin. 

Jaundice occasionally results from nerve influence. A 
friend of mine told me that, as he was riding home one 
evening, he was suddenly startled, and, in a very short time, 
jaundice became developed. Many such cases are on record, 
but the precise explanation of them is as yet unknown. 

3. Trophic Changes. Besides the vascular changes which 
induce congestion and pallor of the skin, a great variety of 
nutritive changes result from diseases of the nervous system. 
I shall speak, first, of nervous oedema — a condition the more 
interesting to us from having been first described by my 
predecessor. Professor Laycock. He observed that in some 
cases of hemiplegia the paralysed side became dropsical, and 
that not only when there was co-existent renal or cardiac 
disease, although with such complications the change was 
more pronounced. It seems probable that the purely nervous 
hemiplegic oedema is brought about by blood stasis, which 



154 



TROPHIC CHANGES. 



results in part from dilatation of the arterioles, and in part 
from the want of muscular action, -which is so important an 
agent in connection with the flow of blood in the veins. It 
is possible, also, that mechanical conditions connected with 
the attitude of the patient may contribute to the result, there 
being pressure upon veins hindering outflow, due to the 
patient's decubitus on the paralysed side. But I think it 
very probable that there may be a direct influence upon 
the tissues, which favours the occurrence of cedematous 
infiltration. 

Hcemorrhages into the subcutaneous tissue sometimes 
appear in cases of locomotor ataxia after violent attacks of 
pain. They are irregular in shape and size, and undergo 
the series of transformations proper to ecchymoses. 

Hcematoma aurium, which is Imown as the insane ear, 
seeing that it occurs almost exclusively in the insane, and 
especially in general paralytics, consists in a swelling of the 
external ear, of a bluish-red colour, tending to spread, and 
leading ultimately to a cicatricial contraction. If cut through, 
it is found to contain a bloody and gelatinous material, 
evidently a result of extravasation, originating in arterial 
degeneration and local injury. 

Inflammation of the skin results from nerve influence. 
Herpes zoster is recognised as a typical instance. The fact 
of its being so constantly developed in the distribution of 
one particular nerve, or of two nerves, and of its associa- 
tion with neuralgia of the same part, and sometimes with 
paralysis, naturally suggested this theory of the nature of 
the disease. It sometimes results from injury to a nerve. 
I had a patient who, as the result of a slight accident con- 
tasing the small sciatic nerve, got a well-marked herpetic 
eruption in the area of its distribution. Many such cases 
are on record. Disease of the ganglia on the posterior roots 
has been suggested as the starting point of the herpetic 
process, but the evidence in favour of this view is not 
conclusive. Some recent observers have found inflammation 
of the nerves supplying the herpetic district. Dubler found 
this change in one case due to irritation by a caseous perios- 
titis, and in another a spontaneous process. It may, how- 



TROPHrC CHANGES. 



155 



ever, be due to disease of the cord, and we may infer that 
herpes may have a cerebral origin, from the fact that it has 
been known to occur in a limb simultaneously with a sudden 
attack of hemiplegia. 

Other inflammations of skin, such as urticaria and pemphi- 
gus of various forms, are often found due to nerve influence ; 
erythema, lichen, and eczema have sometimes been ascribed to 
it, and chilblains are probably as much dependent on the 
nerves as upon changes originating in the tissues themselves. 
Ichthyotic thickening of the skin is in some cases produced 
by this cause. A condition of pseudo-phlegmon, closely 
resembling ordinary boils, is also described as resulting from 
nerve influence. All these varieties may probably result from 
changes in the nerves, the spinal cord, or the brain. 

Nerve influence may affect the colour of the skin, as is 
probably the case in Addison's disease, in localised pigmenta- 
tions, and in localised leucoderma. You know how often 
in pregnancy and in uterine and ovarian disease patches of 
brown discoloration appear on the face. Nervous disease 
may also change the colour of the hair. You are familiar with 
stories of people whose hair passed from dark to white in a few 
hours under the influence of mental emotion. I believe that 
there are well-authenticated cases of the kind. Landois, for 
example, records a case of delirium tremens in which the hair of 
the head and beard became grey in a single night as the result 
of excessive fright. In neuralgia, the hair of the neuralgic part 
has been observed to become grey or white during the attack, 
the normal colour returning when the neuralgia disappeared. 
I once watched a curious change of colour of the hair in a 
patient suffering from syphilitic cerebral tumour. When the 
cerebral symptoms were at their worst, his hair changed from 
its natural dark colour to an auburn red, and, when after- 
wards the symptoms subsided, leaving behind them only 
blindness from permanent optic atrophy, the hair gradually 
resumed its natural tint. ' 

The structure of the hair often becomes modified under 
nervous influence, tending to split at the ends, and growing 
much more feebly than in health. Sometimes more rapid 
changes occur. I know a member of a very neurotic family 



15G 



TROPHIC CHANGES. 



who occasionally, on awaking of a morning, finds that she 
has a degree of pain or uneasiness in some part of the scalp, 
and that a quantity of hair has been shed, so as to leave a 
bald patch. This recurs from time to time, the hair grad- 
ually growing on the patches which had been bald, and new 
portions becoming affected. Many such cases are on record, 
and there are others in which the hair of the affected parts has 
become thicker and stronger during the occurrence of 
neuralgia. 

The nails are often altered in cases of nervous disease. 
In locomotor ataxia, for example, the toe-nails, and especiallj'- 
those of the great toes, are apt to drop off, and then to grow 
again in a very imperfect fashion. The nails also present 
various abnormalities of shape — being sometimes friable and 
broken, sometimes thickened, crumpled, and furrowed. It 
is worthy of notice that these changes are generally associated 
with lightning pains, or signs of change in nerves. In cases 
of injury of the nerves, also, changes often appear in the nails. 

In some cases of locomotor ataxia, the teeth have become 
loose and dropped out. 

Glossy shin is a condition well described by Sir James 
Paget and by Dr. Weir Mitchell as occurring in nerve disease. 
The wrinkles and folds are less marked, while the whole 
surface acquires a smooth and glossy appearance. It is often 
well seen in cases of injury of nerve : but I have seen it 
in cases of spinal disease, particularly in locomotor ataxia. 
Moreover, I have observed it come and go ; sometimes very 
distinct, at others disappearing. 

Important nerve changes exist in cases of myxoedema, and 
it is possible that the trophic changes are primarily due 
to morbid influence of the nervous system. The character- 
istic change consists in the development in the subcutaneous 
tissue and in other parts of a mucoid substance, which gives 
to the sldn an appearance resembling anasarca. The lesion 
occurs also in internal organs, such as the kidney, and through- 
out the nervous system. It is to the latter changes that the 
general blunting of the sensibility, slowness of articulation 
and other movements, and impairment of the mental powers 
are to be ascribed. 



TEOPHIC (JHANGES. 



157 



Ancesthetic leprosy may also be regarded as due to nerve- 
disease. Certainly, many of its features are to be explained 
by reference to this. The infiltration of the nerve-tissues with 
new formation interferes with sensory motor and trophic 
functions, as is manifested by the anaesthesia, the paralysis, 
the pigmentation, and the ulceration which so constantly 
attend upon it. 

Pellagra is another disease which is probably of nervous 
origin, and due to the use of bad Indian corn. The nervous 
symptoms are pain, muscular weakness, sometimes with 
spasms, melancholia, apathy, and stupor. 

Another reported trophic condition of great importance, 
and very suggestive in regard to the pathology of the nervous 
system, is the series of changes described as following upon 
extirpation of the thyroid gland. If the organ is wholly 
extirpated from dogs, a pecuHar state of system sets in, 
which results speedily in death, and which various observers 
refer to changes in the central nervous system, probably 
acting through the sympathetic. Remarkable nervous 
phenomena have also been observed in patients who have 
undergone extirpation of the thyroid. Out of twenty-four 
cases observed by Dr. Kocher, sixteen exhibited a group of 
symptoms very similar to those which characterise myx- 
cedema, in particular, a swelling of the limbs and a condition 
of mental dulness, with slowness of speech. Should further 
examination confirm the correctness of these statements, the 
importance of the observations wiU be great, both in its 
bearing on the functions of the thyroid gland and on the 
nutritive processes. 

The most formidable change affecting the skin is gangrene. 
1 have seen, not the skin alone, but the deeper structures, 
iDecome gangrenous from nerve disease, and fingers and toes 
■drop off in consequence of the gangrenous process. The case 
was so remarkable that I must tell you about it somewhat in 
•detail. The patient, when he came under my care, was 
between fifty and sixty. He was a man of nervous constitu- • 
tion, of strong nature, and of excellent character. He told 
me that early in life he had served as a soldier, and experi- 
enced considerable privations, and that during that period. 



158 



TROPHIC CHANGES. 



and afterwards, the tendency to gangrene had manifested 
itself. When he came under my care, he had lost the toes 
of both feet by spontaneous gangrene, and was complaining 
very much of pains in the fingers, especially in the district 
supplied by the ulnar nerves. The skin on these parts was 
glossy, but was not pale, rather congested, and of a bluish 
tint. The nails tended to drop off. I found that by rest in 
hospital, the use of nourishing diet, and electrisation in the 
line of the nerves which were the seat of pain, the symptoms 
were speedily relieved, the circulation improving, and the 
fingers becoming more mobile. There was no muscidar para- 
lysis, but a certain stiffness from the trophic changes. The 
heart and blood-vessels were quite normal, and there was no 
disease discoverable, except the severe neuralgic pains, and 
the trophic changes in the extremities. For many months 
the man continued under observation, returning to the 
Infirmary from time to time as he got worse. At length, after 
being absent for some time, he returned in a condition of 
extreme distress. He was utterly dispirited, in consequence 
of having, during one of his paroxysms of neuralgia, lost his 
temper, and committed some act of violence for which he was 
arrested and sentenced to a period of imprisonment. Up to 
that time there had been no blot upon his character, and he 
felt the degradation very acutely. Before his term of imprison- 
ment had expired, intense neuralgia set in in both hands and 
feet. The glossiness and blueness passed into a black gangren- 
ous condition. Lines of demarcation formed, and separation 
set in, as is shown in the drawings (figs. 78 and 79) made for me 
at the time by my friend, Dr. Caton, now of Liverpool. The 
post-mortem examination, which was made by Dr. Ferrier 
and myself under great difficulties, enabled us to make sure 
of the absence of any of the ordinary vascular causes, but we 
were unable to secure specimens of the nerve-centres or to 
satisfy ourselves of the condition of the nerves. The evi- 
dence with regard to the case is thus incomplete, but a 
consideration of the facts leaves, in my mind, no doubt that 
the gangrene was of nervous origin. 

No one doubts the importance of nerve influence in rela- 
tion to the formation of bed-sores; and Avhile there is one 



TROPHIC CHANGES. 



161 



variety in wliich the nerve influence only contributes towards 
the production — the bed-sore from pressure and from care- 
less nursing — there is another variety which results directly 
from nerve influence. Within a few days, or even hours of 
the occurrence of a nervous lesion, extensive inflammation and 
sloughing of the surface appears in the buttock. The lesion 
may be situated in the brain, or in the spinal cord. In the 
former case, the sore lies towards the centre of the gluteal 
region on the paralysed side. It commences usually on the third 
or fourth day after the attack of apoplexy as an erythematous 




S'IG. 80. Fig. 81. 

Acute bed-sore on gluteal region of paralysed side Acute bed-sore of sacnd region iu a case of 
in a case of cerebral apoplexy (after Charcot). partial spinal myelitis (after Charcot). 



patch, which rapidly becomes bullous, ecchymotic, and gan- 
grenous. In fig. 80, the appearances are represented. This 
acute bed-sore is of very ominous import. When the bed- 
sore is due to disease of the spinal cord, as in an acute 
transverse myelitis, it occupies a different position, lying 
above and internal to that of the cerebral sore. It is 
placed over the sacral region, and extends symmetrically 
to either side, as is shown in fig. 81. 

Another trophic change, closely related to this, I watched 
lately in the case of a patient who suffered from extensive 

L 



1G2 



TROPHIC CHANGES. 



sclerosis of the brain and cord. In that case, when he first 
came under my care there was a deep ulceration of the heel, 
which was very difficult of cure, but ultimately closed. Soon 
afterwards, on various parts of the toes patches appeared 
of a deep livid colour. These speedily underwent further 
changes. The cuticle was raised to form a bleb, whose con- 
tents were a sanious-looking, reddish fluid. The bleb burst, 
and it was with great difficulty that the formation of an ulcer 
was prevented. We did not succeed in every case in pre- 
venting ulceration. They arose apart from all violence of 
pressure, and in a patient who was attended to in every 
respect with extraordinary care. 

Perforating ulcer of the foot is another effect of nerve 
disease. It resembles a sinus rather than an ulcer — 
the orifice surrounded by thickened and insensible skin. 
The skin around the ulcer is cold, but prone to attacks 
of congestion, erythema, and eczema. The sinus extends 
downwards to bone, and there are frequently changes 
in the bones and in the joints beyond the points to 
which the sinus extends. You will see ulcers of this kind 
in connection with true leprosy, but also in locomotor ataxia. 

Before leaving these forms of gangrene, I ought to point 
out to you certain of the dangers which they entail upon the 
patient. They arise chiefly from the absorption of septic 
materials, inducing pyaemia. Thrombi forming in the vessels 
of the part become loaded with micro-organisms, and are con- 
veyed with the circulation into different organs, where they 
set up inflammatory changes. Pyasmic and septicsemic pro- 
cesses may thus be induced, in addition to the dangers and 
discomforts of the local inflammatory process. 

A condition has been described by Raynaud, of which 
I have not seen an example, unless the case of which I have 
shown you drawings was a somewhat anomalous example of 
it. Occurring rarely in children and in old people, it tends 
to affect the fingers, the toes, the tip of the nose, and the 
ears. It begins with a deadness of the part ; with shrinking, 
pallor, coldness, and a degree of stiffness. These usually 
come on pretty rapidly. They are followed by congestion, 
the parts becoming livid, usually painful, and sometimes 



TROPHIC CHANGES. 



163 



itchy. Inflammatory changes then set in with excoriation, 
and not unfrequently a mummifying process follows, and 
portions of the affected part drop off. Even after the stage 
of lividity has been reached, improvement may set in. 

The muscles become altered in various ways under nerve 
influence. The commonest change is muscular atrophy. 
You are aware that muscular fibre, when not used, is liable 
to become wasted, and that, consequently, in cases of para- 
lysis of all kinds, wasting is apt to occur ; but in some cases 
of paralysis wasting proceeds with very great rapidity, and 
in others the weakness of the muscle is manifestly due to the 
Avasting rather than to loss of motor influence. In such 
cases the muscular fibres may be found simply wasted, or 
there may be increase of nuclei and of connective tissue, in 
addition to the atrophy of the sarcous elements. It is in 
<3onnection with inflammation of the anterior horns of the 
grey matter of the cord that you see this most markedly. 
The disease is not a common one. I may refer to an 
instance of it which was under my care a few years ago. 
The patient, who was a gardener, began to complain of 
debility. He had febrile symptoms, so weU marked as to 
lead a very acute practitioner, under whose care he was, to 
suspect that typhoid fever might be commencing. Very 
speedily it became apparent that there was special muscular 
weakness, affecting the legs, and to a less extent the arms. 
But almost immediately rapid wasting of the muscles set in, 
and in the course of a week or two the limbs had become 
extremely attenuated. By slow degrees improvement set in. 
The muscular power returned to some extent, the muscles 
recovering some of their former volume. 

A very acute observer, Dr. Ord, of St. Thomas's Hospital 
in London, has lately drawn attention to the fact that nutri- 
tive changes in the muscles around joints occasionally accom- 
pany rheumatic disease of the joints. This might be explained 
ia either of two ways. On the one hand, the muscle may 
be held to be affected with an inflammatory process corre- 
sponding to, and an extension of, what is going on in the 
neighbouring joint, and thereby to be weakened and atro- 
phied. On the other hand, the muscle may be supposed to 



1G4 



TllOPHIC CHANGES. 



be altered in consequence of nerve influence. That the 
latter view is probably the more correct is shown by such 



cases as the 
opportunities 



following, Avhich I had exceptionally good 
of wa,tching in the case of a medical man. 
He was recovering from an attack of acute rheumatism, and, 
on awakening one morning, was distressed to find that he 
seemed to have lost the power of movement of the shoulder- 
joints. He at once expressed the fear that he had been 
attacked with polio-myelitis anterior, and that it might 
spread to other muscles besides those first attacked. It was 
certainly clear that the muscles were paralysed, and they 
underwent rapid atrophy. They were gradually restored, 
but six months elapsed before they recovered their natural 

volume or power. Circum- 
stances made it impossible to 
try the electric tests, but be- 
tween three and four months 
after the attack, the muscles 
responded only to very power- 
ful galvanisation. 

You will often meet in 
practice with cases of in- 
fantile paralysis, in which 
the little patient is suddenly 
seized with febrile symptoms 
and with paralysis more 
or less extensive. The area 
of paralysis generally becomes speedily limited, but 
where it persists is very intense. A rapid wasting of the 
muscles occurs, and it is found that afterwards there is 
little or no growth of the affected part, so that the child 
may grow up with ill-developed arm or arms, one hand small 
like an infant's, the other, it may be, fully grown. In this 
case you observe that the disease affects the bones as well 
as the muscles (fig. 82). A similar condition to that in 
spinal infantile paralysis may be produced as a result of 
cerebral lesion. I may refer, in illustration of the fact, to a 
case recorded by my friend, Dr. M. D. Macleod, in which. 




I'IG. 82. 

Ill-developed right arm in adult, resulting 
from au attack of poliomyelitis anterior acuta in 
infancy. 



along 



Avith 



wasting 



on one side, extensive atrophy of the 



TEOPHIC CHANGES. 



165 



corresponding motor areas on the opposite side of the cere- 
brum was found. 

Progressive viuscular atrophy or wasting palsy is another 
of the trophic diseases of muscle. Individual muscles 
or groups of muscles are attacked with a slowly advancing 
atrophy- course of months or years the disease 

spreads (fig. 83), and, at last, a fatal result may arise from 
atrophy of muscles of respiration or from some intercurrent 
disease. In this disease, also, the 
lesion is situated in the anterior 
horns of the grey matter. 

It may be proved very definitely 
by experiment that muscular atrophy 
is not a mere result of vaso-motor 
influence, but is a directly trophic 
change. If you cut the sciatic nerve 
of an animal, you produce a rapidly 
advancing atrophy of the muscles, to 
which the branches of that nerve 
are distributed. This is due to the 
fact that by the section of the nerve 
these muscles have been cut off from 
the spinal mechanism by which their 
nutrition as well as motion is con- 
trolled. But as it contains vaso- 
motor fibres, one might conclude 
that it was through them that the 
result was brought about. But the 

facial nerve affords the opportunity 

of testing this, for it receives its 

vaso-motor fibres between its point 

of origin and its reaching the edge 

of the masseter muscle. Cut it 

or below that point, and you find 




Fig. S3. 

Advanced caae of progressive 
muscular atrophy. 



through either above 
rapid atrophy of the 
facial muscles follow, and just as definitely where it has 
no vaso-motor fibres as lower down where it has. Such 
experiments seem to me abundantly to justify the opinion 
that muscular atrophy is not of vaso-motor origin. Patho- 
logical observation justifies our referring this trophic influence 



166 



TROPHIC CHANGES. 



to the large ganglion cells in the anterior horns of the grey 
matter of the cord, and the corresponding structures in the 
medulla, pons, and crura. 

Pseudo -hypertrophic 'paralyais is a condition in which 
there is increase of bulk of muscle, with a diminution of 
power ; the increase being due to excess of fibrous or adipose 
tissue and not increase of sarcous elements. It has been 
supposed by some to result from changes in the central 

nervous system ; but the balance 
of evidence seems to me at present 
to be opposed to this view. In 
fig. 84 you see the appearance 
presented by a child suffering from 
this disease. 

Joints also undergo changes 
from nerve disease. The disease 
- in the joints pursues a somewhat 
chronic course, and at first mani- 
fests itself by painless swelling of 
the joint, with copious effusion of 
synovial fluid. Following on this 
is an atrophic process of the end 
of the bone, very similar to that 
which occurs in osteo-arthritis, 
but without the outgrowth of bony 
tissue which is so characteristic of 
it. As the disease advances, 
movement becomes more or less 
Case of psendo-hypertrophic paraiysia. interfered with, ultimately the joint 

becomes useless. Dislocations very 
readily occur. I believe that such joint-affection may become 
arrested, either temporarily or permanently, and that even 
where the nervous disease is not checked. These arthropathies 
occur from nerve injury, but most frequently in connection 
with locomotor ataxia, and they are to be recognised clinicalh^ 
by their sudden onset, by the rapid progress of the altera- 
tions in. the articular surfaces, and by the fact that their 
appearance is co-incident with one particular stage of the 
spinal affection — namely, that during which the motor 




Fig. 84. 



TKOPHIC CHANGES. 



167 



inco-ordination is setting in. Tiiis fact leads us to suppose 
that the trophic centres for the joints are situated in the 
posterior part of the grey matter of the cord. 

Dr. Seeligmliller describes, under the name of hydrops 
articulorum intermittens, a peculiar condition, in which an 
otherwise healthy adult becomes affected at regular intervals, 
generally suddenly and without discernible cause, by an 
intense swelling of one or both knee-joints, unattended by 
inflammation or fever. After reaching its maximum, it 
gradually subsides, and it usually recurs with perfect 
regularity both as to day and hour. It may also affect 
other joints. These swellings are probably induced through 
the nervous system. 




Fig. 85. 

Altered os innominatum from case of locomotor ataxia (after Charcot). 



Bones may become changed in nervous diseases, — a certain 
softening of the bones, a rendering of them more porous 
or friable, — in consequence of which fracture readily occurs. 
A fall or a slight muscular effort may suffice to induce 
formidable injury. The process appears to commence with 
an absorption of the mineral matter, so that the phosphates 
in the bony tissue are reduced to one half or even one fourth 
of the normal amount. The Haversian canals become widened 
out, the fatty matter within the bone greatly increased, and 



168 



TROPHIC CHANGES. 



the tissue often presents a fleshy appearance from increase of 
the vascular elements within the canals. The bone thus 
becomes much lighter, more porous ; and you can readily 
understand how so slight a cause as muscular effort may 
suffice to produce fracture. It is in locomotor ataxia and 
in insanity that bone changes are most frequently seen. In 
figures 85 and 86 are seen the appearances presented by 
the innominate bone and the femur in a case of this kind, 
and they illustrate both the articular and the osseous 
changes. 




Fig. 86. 

Altered head of femur from case of loco- 
motor ataxia (after Charcot). 

I 



The last of the trophic changes to which I shall refer is 
facial hemiatrophia. In that disease the two sides of the 
face are seen to be markedly different in size. The skin of 
the affected side is sunken and hollow, often shrivelled and 
atrophied. The hair and the glands are distinctly wasted, 
as compared with those on the opposite side. It is 
said that the sebaceous secretion is more affected than the 
perspiration. Subjective pain is often felt in the nerves of 
the affected side. The muscles are in some cases unaltered, 
in others they are distinctly diminished. The bones of the 



TKOPHIC CHANGES. 



169 



face are sometimes very decidedly atrophied — the lower jaw, 
the upper jaw, the malar bone. The teeth also may be 
altered. The course of the disease is slow and protracted. 




Fia. 87. 

Altered physiognomy iu facial hemiatrophia. 



The general health is not interfered with. The drawing 
(fig. 87) shows you the appearance of the face in this 
disease. 



LECTURE XL 



Cerebkal and Mental Functions. 

C onsciousness. — Exaltation. — Diminution. — Sleep. — Trance, — Hyp- 
notism. — Torpor. — Coma. — Perversion of Consciousness. — 
Delirium. — Hallucinations. — Hhosions. — Delusions. — Attention. 
— Meviory. — Judgment. — Will. — Emotions. — Moral Sense. 

ENTLEMEN, — In considering the cerebral and mental 
functions, I shall speak first of consciousness and its 
various modifications. I shall not, however, attempt to 
define what it is, for very high authorities have declared it 
to be incapable of accurate definition. It is most important 
for the medical man to understand its modifications. The 
consciousness may be exalted, it may be diminished or lost, 
it may be perverted. 

1. Exaltation of Consciousness. In this condition all the 
mental processes, or some of them, are exaggerated. There 
is more perceptive power, better memory, more vigour of 
judgment, more strength of will, more capacity for emotional 
excitement, than the individual usually possesses, or it may 
be that one or other of these is especially predominant. In 
normal conditions, you may see a certain degree of these 
determined by the states of the weather, the companionship, 
and other surroundings of the individual. In conditions 
less physiological, you see it after the use of moderate doses 
of alcohol or opium. It is often seen in its most formidable 
condition in the early stages of some forms of insanity, and 
in the commencement of delirium. I think, however, that 
if you look closely at any of these cases, you will find that 
there is not a true elevation of all the functions, rather that 
there is a loss of inhibitory power, so that phenomena are 
manifested which would otherwise not appear. 
170 




CONSCIOUSNESS, SLEEP. 



171 



2. Diminution and Temporary Suspension of Conscious- 
ness. This occurs periodically as a physiological change. 

Sleep. In ordinary deep sleep there is complete uncon- 
sciousness to external impressions, and, according to its 
profundity, a greater or less impression is required for 
disturbing it. Some are light sleepers, easily disturbed ; 
others sleep deeply, and are difficult to rouse. This varies 
also in the same individual from time to time, and even 
differs during a single night. It has been abundantly proved 
that during sleep the brain is anaemic, the calibre of arteries 
is smaller, that of the veins somewhat larger, and the tissues 
generally are paler than in the waking state. But it does 
not follow that this anaemia is the cause of sleep ; it may 
be a mere result of diminished cerebral activity. 

The function may be altered in various ways. It may be 
deficient, as in insomnia. You will meet with insomnia in 
many morbid conditions. Under great mental emotion, after 
prolonged mental effort, in the course of delirium tremens, 
in fevers and in insanity, it is very common. Sometimes 
it results from perijoheral irritation, as in disturbance of 
stomach, duodenum, and bowels, and sometimes appears to 
be a result of central causes. In individual cases of sleep- 
lessness you must carefully search for the cause — for, without 
attention to it, you will find that you cannot give relief 

The patient may obtain sleep, but it may be of an unsatis- 
factory kind, the sleep being disturbed and restless. The 
same set of causes which induces the other induces also 
this. In particular, you will find the taking of indigest- 
ible food, the use of such articles as tea and coffee, 
not long before going to bed, great mental excitement, — 
either from emotion or from overwork, — debility from exces- 
sive bodily fatigue or from haemorrhage, feverish conditions, 
painful diseases, gouty states of the system, undue cold or 
warmth of the room, among the common causes. 

Sleep may be excessive. Sometimes patients tell you 
they can sleep for twenty-four or even thirty-six hours. I 
was lately consulted by a young lady, whose pupils were so 
dilated as to suggest that belladonna had been used, and 
who said that she was never satisfied with sleep, could easily 



172 



SLEEP, TRANCE. 



sleep for twelve or fifteen hours at a time. I have heard 
of the case of a nobleman, who was so good a sleeper that 
sometimes when his valet called him of a morning, if he was 
told that the weather was disagreeable, he would simply turn 
round on his side and bid his valet call him again next day. 
I had, some years ago, the opportunity of studymg, along 
with my friend, Dr. Underbill, a remarkable case. A girl of 
six was observed to get out of health, with poor appetite, 
occasional sleepiness during the day, and a tendency to sleep 
for twelve or thirteen hours when she was put to bed. 
Gradually the tendency to sleep during the day increased, 
and when I saw her it manifested itself in an extraordinary 
way. Her general health was fairly good, and between 
her attacks she seemed to play like a healthy child. But 
many times in the course of the day she would suddenly 
fall asleep, and remain so for a period varying from ten 
minutes to half-an-hour. It was then impossible to awaken 
her, and at first she lay in a quite passive condition. After 
a time, the sleepiness became complicated with a tendency 
to cataleptic rigidity. She was often found asleep standing, 
her arms generally half-folded and half-upraised. Still later, 
it was found that during her attacks she became very sensi- 
tive to touch, and ultimately there were slight spasmodic 
movements. The condition gradually improved, and for at 
least a year the health remained perfectly good. 

You will often notice abnormal drowsiness in people of 
weak brain-power, but it is not confined to such. It occurs 
sometimes in organic brain disease, and is sometimes toxic 
in its origin. It may pass, by insensible gradations, into the 
condition of trance and stupor. A very extraordinary malady 
is described as occurring on the West Coast of Africa. It 
is known as the sleeping sickness, and is characterised by 
swelling of cervical glands and extraordinary drowsiness. 
As the disease advances, the somnolence becomes more pro- 
nounced. The patient can at last scarcely be roused to take 
food, and dies after illness prolonged through many months. 

Trance. Occasionally true cases of trance are met with, in 
which the patient, for a longer or shorter period, remains in a 
state of torpor, as if deeply asleep, for days or even 



HYPNOTISM. 



173 



weeks. I liave only seen one well-marked case of the kind. 
It occurred in a girl who had been greatly excited. She lay 
for weeks, taking no notice of anything, and, when I 
examined her, she remained completely passive. It is very 
closely allied to hysteria, and is often associated with great 
pallor. Occasionally the reflexes are lost, the conjunctivas 
or corneoe may be touched without producing winking, and 
snuff blown into the nostrils produces no sneezing. Some- 
times the patient is conscious, and simply has no power of 
movement. A remarkable case is recorded of a patient whose 
state of trance so closely simulated death, that she was about 
to be put into a coffin. She was quite aware of what was 
going on, but unable to express herself in any way ; fortun- 
ately, a violent perspiration came on under the excitement, 
and the attendants thereby discovered that life was not extinct. 
In managing such cases, you have of course to feed the 
patient by the stomach-tube. Generally in the long run 
recovery takes place somewhat suddenly. If any of you 
should ever be in difficulty as to whether a patient be dead 
or not, the test on which I should advise you to rely is the 
loss of excitability of the muscles by electrisation. It does 
not occur in trance, but does occur within an hour or two 
after death. 

Hypnotism. Closely allied to the condition of trance, is 
that of hypnotism or mesmerism. It is capable of being 
produced in most individuals, but especially in people of 
nervous constitution. It is induced by continued monotonous 
impression made upon the sight, the touch, or the hearing. 
The commonest plan for producing it is to direct the patient 
to stare intently at a disc of metal or a coin held in his hand. 
After a time, the hypnotic condition results. The state of the 
nervous system is very peculiar, combining torpor and indiffer- 
ence to most kinds of impressions, with great acuteness to 
some, the attention being all the while, to a large extent, under 
the control of the mesmeriser. Under his influence the 
special senses are often preternaturally acute, but on the 
other hand there may be complete anoesthesia or hemi- 
an£Bsthesia. The patient may be made to perform extra- 
ordinary movements, and is readily induced to entertain 



LOSS OF CONSCIOUSNESS. 



hallucinations of all kinds. We know nothing at present of 
the explanation of these phenomena. 

Somnambulism and Somniloquy are also well worthy of 
your attention. In the first of these conditions, the patient, 
while in all other respects asleep, is able to walk about, and 
often to pass along perilous ledges, and to accomplish 
arduous feats which, in the waking condition, he could not 
venture to undertake. His muscular sense appears greatly 
elevated ; and while he is regardless of most kinds of impres- 
sions, he can guide his movements with admirable precision. 
In the latter, the patient speaks during sleep, and may even 
hold a conversation, of which, however, he has no recollection 
when he returns to the waking state. 

3. Loss of Consciousness. The consciousness may be lost, 
as we see frequently in syncope, in coma, and in asphyxia. 
In syncope, there is deficient supply of blood to the brain, 
and consequent arrest of its functions. This may depend 
upon organic affection of heart, or on merely functional 
failure. It is very common as a result of emotional excite- 
ment, terror, grief, or joy ; of shock to the nervous system, 
painful or otherwise. It is also apt to be connected with 
impurity of atmosphere, and with morbid conditions of the 
stomach and intestine. It is markedly associated with 
antemia, whether due to causes of a chronic kind or as a 
result of copious haemorrhage. Coma may dejDcnd upon a 
great variety of causes. It may be a result of injury to 
the head, either mechanical or by sunstroke ; of extravasa- 
tion of blood within the cranium, necessarily compressing the 
brain ; of effusion of inflammatory products or of dropsical 
fluid, also compressing the brain substance ; or of obstruction 
of the cerebral vessels. Sometimes it is a result of a poison 
introduced from without, such as alcohol or opium ; or of 
blood-poisoning, some substance being retained which ought 
to be eliminated, as in uraemia. Sometimes it is due to 
epilepsy. A less degree of coma is known as torijor or 
stupor. You see this often in fevers and in cerebral diseases, 
and when you come to study insanity you will meet with it 
in various forms of imbecility and dementia. Asphyxia does 
not itself imply, but may lead to loss of consciousness. 



HALLUCINATIONS. 



175 



Although the term literally signifies pulselessness, it has 
come to be applied to interference with respiration. If this 
interference be carried sufiiciently far, unconsciousness results, 
the brain being poisoned with carbonic acid. 

Apoplectiform attacks are not uncommon in the course of 
nervous maladies, such as general paralysis of the insane, 
alcohoHsm, senile dementia, multiple sclerosis, and locomotor 
ataxia. They come on suddenly, and last perhaps for an 
hour, perhaps for several days. Very often there is loss of 
consciousness, and when this has passed off, weakness or 
actual paralysis of one side, or a limb, or of the whole body. 
Often also there is aphasia, and sometimes ashy pallor of the 
countenance. We cannot, at present, explain these seizures ; 
but from their transitory character we are entitled to con- 
clude that they do not result from serious brain lesion. 

4, Perversion of Consciousness is very common. Deliriv/in 
is its most frequent variety. Delirium may be low or mutter- 
ing in character, the patient heedlessly rambling on and 
muttering to himself on the subjects of his incoherent 
thoughts. It may be raving or maniacal, the patient shout- 
ing or yelling, and conducting himself with the greatest 
violence. Either of these conditions, but especially the 
latter, may be associated with a tremulousness and a rest- 
lessness of body and mind, as we see in delirium tremens. 
Delirium occurs under conditions which involve defective 
nutrition of the brain, either consequent on brain disease 
proper, or on morbid states of , the blood. It is very 
frequently seen in fevers, both symptomatic and idiopathic, 
and is typically present after abuse of alcohol. Some have 
supposed that each kind of fever has its characteristic form 
of delirium, but my observations do not confirm this view 
to any great extent. We may regard hypochondriasis as 
another form of perverted consciousness, patients often having 
delusions as to their bodily condition. 

Hallucinations, Illusions, and Delusions are varieties of 
perverted consciousness. The terms are often used loosely ; 
but strictly speaking, hallucinations are purely subjective. 
The patient imagines that he sees objects, or hears sounds, 
or is touched by things which have no real existence. 



176 



ILLUSIONS, DELUSIONS, ATTENTION. 



A delirious patient or an insane person imagines that he 
sees before him objects which are not really present. He 
sees people or animals perched on his bedstead or careering 
about his room, he hears noises or even articulate sounds 
or voices blaming him or threatening him with the most 
dreadful punishments. These are examples of hallucinations. 
Illusions, strictly speaking, are incorrect interpretations of 
objects within the sphere of the patient's observation. 
A patient, for example, sees his own clothes laid over the 
back of a chair, and imagines that they are some person 
keeping watch over him. I remember a patient in the 
delirium tremens ward of the Old Infirmary, drawing my 
attention to a fiend, who, he said, was sitting on the top 
of a pillar glaring at him and prepared to pounce upon 
him when the suitable moment shoiild arrive. "Look at 
his round staring eyes," said the patient ; and I saw that 
the capital of the pillar was ornamented with two prominent 
knobs, which he, in his illusion, imagined to be the eyes of 
a fiend. When you study insanity, you will find in the 
asylum wards many patients, especially those suffering from 
alcoholic insanity, who constantly misinterpret sounds, who 
have illusions of hearing. Delusions, again, are insane ideas 
of any kind — not mere sensory abnormalities, like hallucina- 
tions and illusions. A patient who imagines himself to be a 
king or an emperor, or one who imagines that he has 
swallowed and has in his stomach Christopher North, or 
believes that he is the Deity or an ancient prophet, or that 
he is the victim of some imaginary conspiracy, is labouring 
under delusion. 

Attention or the faculty by which we direct our minds to 
a subject is often interfered with in disease. You see this 
markedly in many acute maladies. It often persists during 
convalescence from these, and in chronic diseases is very 
liable to occur. While it is common in general maladies, it is 
of course more frequent in those of the brain, and you wiU 
in practice constantly have to observe it, as it occurs in 
connection with softening and other degenerative changes, 
as well as after apoplexies. 

Memory. It is probable that every perception and every 



MEMORY. 



177 



thouglit remains permanently recorded on tlie brain, and 
may be called up by an appropriate stimulus. You must 
have observed how some circumstance of which you had not 
thought for years is suddenly flashed upon the mind under 
some special condition. In that case it appears that the 
appropriate stimulus having been applied, the recorded 
circumstance was recalled. Very extraordinary instances of 
such storing of impressions are to be found in literature. 
I have read of a servant girl who during an illness began to 
recite long passages from ancient poets and orators, in 
languages with which she was quite unacquainted. The 
explanation was found in the fact that, while serving in the 
family of a gentleman of literary tastes, she had often heard 
him declaim his favourite passages from classical authors. 
If we reflect upon such facts, we are filled with astonishment 
at the marvellous capacity for storing impressions which the 
brain possesses. Recollection or the recalling of remembered 
impressions may be voluntary or automatic. You will some- 
times notice the one process interfere with the other. A 
person who is automatically repeating or singing the verses 
of a song, sometimes breaks down entirely when he turns 
his attention to making a voluntary effort to recall the words, 
while he could have gone on smoothly in an automatic way. 
Often no amount of effort may suffice to enable one to recall 
a name, an idea, a circumstance, a face ; and then suddenly, 
by mere association of idea and in a purely automatic way, it 
flashes upon you. Within the limits of health there is the 
greatest variety both of memory and of recollection. Many 
people have so little power of concentrating their attention 
that no impression is definitely made upon them; and you 
must have observed that some people in speaking present 
ideas with a point and force which make them memorable, 
while others telling you the same things do it in such a way 
as to make little or no impression. You will find that some 
people have good verbal memories, and can reproduce long 
series of words exactly as they have heard them ; while 
others can tell you nothing of the words, but can clearly 
reproduce the ideas. Some people never forget a face, 
although they may not be able to attach a name to it, and 

M 



178 



JUDGMENT AND WILL. 



some again may remember the name, voice, and other points 
in connection with the individual, but fail to remember the 
physiognomy. The memory, like other faculties, improves 
greatly by practice. You have found, as you have gone 
on in your studies, that your memories have improved. You 
will find that after some experience in professional work, you 
learn more easily to recall the points in your cases than was 
possible at first. 

In disease, all the processes connected with memory may 
be modified. You find often that the patient is incapable of 
attending closely. That may be a result of exhaustion of the 
system, or of definite brain disease. The automatic memory 
may be greatly exaggerated, recollections of all kinds spring- 
ing up in the mind in a way that to the onlooker betokens 
incoherency. This you see in febrile states, in certain 
alcoholic cases, sometimes in the early stages of cerebral inflam- 
mations, in hysterical and other functional nervous diseases. 
I am not aware that recollection by effort of will ever becomes 
exaggerated in disease. Diminution of automatic recollection 
is very common. People in exhausted states of the nervous 
system, and in chronic cerebral disease, in various forms of 
imbecility and dementia, fail to have anything suggested by 
impressions. They see or hear, they appear to understand, 
but no memory is awakened in consequence. The failure of 
voluntary memory is seen in many diseases. We shall have 
occasion to study some of its manifestations when we discuss 
aphasia ; but you will remember in the meantime that all con- 
ditions which interfere with the nutrition of the brain lead, 
more or less, to failure of the memory, judgment, will, emotion, 
and moral sense. 

The judgment and the vdll frequently become modified in 
disease in ways and under conditions essentially correspond- 
ing to what I have said about memory. The perversion of 
judgment and will is most marked in cases of insanity and 
hysteria. 

The emotions frequently become exaggerated in disease, 
sometimes become diminished or absent, sometimes perverted. 
Their exaggeration is due, for the most part, to loss of self- 
control — a diminution of the inhibitory influence. Nervous 



EMOTIONS. 



179 



irritability, culminating sometimes in violent passion, is often 
seen in cases of overstrain of the nervous system. A tendency 
to immoderate laughter, and to laughter under unsuitable con- 
ditions, you meet with in many people of unstable nervous 
system. An unnatural and unreasonable tearfulness is 
common after apoplexies, and in some cases of cerebral 
softening, such patients often bursting into tears in the 
midst of an ordinary conversation, or at a business meeting. 
Absence of emotion is seen in connection with degenerative 
changes, is often remarked as life advances, and in some 
forms of insanity emotion seems to be entirely absent. 

The moral sentiments — sense of right and wrong — are 
often blunted in brain disease, especially in the hysterical 
and the insane. 



LECTURE XI 1. 



Language. 

Diagrammatic Scheme of Speech Relationship. — Peripheral Structures 
— Seeing Centre. — Hearing Centre. — Word-Seeing Centre. — 
Word - Hearing Centre. — Hlustration. — A utomatic Language. — 
Its Levelo2}ment. — Organic and Functional Changes. — Loss of 
Voluntary Speech. — Varieties. — Loss of Sj)oken Language. — 
Aphasia. — Loss of Written Language. — AgrapJiia. — Delayed 
Conduction. — Scanning Utterance. — Motor Paralysis. — Aphonia. 
— Mirror W7-iting. — Interference with Co-ordinating Function. 
— Stammering. — Functional Aphasia. — Anatomical Changes in 
such Cases. — Definition of Terms. 

/GENTLEMEN, — Having thus far considered among the 
^ cerebral and mental functions the various modifications 
of consciousness, attention, memory, judgment, will, emotions 
and moral sense, we proceed to-day to investigate the 
interesting group of symptoms connected with alterations of 
the speech relationship. Men communicate with one another 
by signs, by writing, and by speech. It is probable that 
interesting observations might be made regarding communi- 
cation by means of signs, but I am not aware that much 
practical importance can be attached to an investigation of 
the subject. I shall, therefore, not discuss it here. With 
regard to communication by speech and writing, the case is 
far otherwise. Indeed, it may be said that not to the 
physician alone, but to the physiologist, the anatomist, and 
the student of mental philosophy, this subject ranks as a 
question of very high interest. ' Passing, therefore, over 
communication by signs, I shall try to explain carefully the 
other two. 

You will find it convenient to have a diagrammatic scheme 
180 



SCHEME OF SPEECH RELATIONSHIPS. 



181 



to serve as a guide in connection with these questions, and 
the one (fig. 88) which I have been in the habit of using for 
many years is the following :■ — 



Intelligence Centre. Will Centre. 




O O O O 

Sight. Hearing. Speech. Writing. 



Fig. 8S. 

You observe that I represent by two circles the peripheral 
organs of sight and hearing. Each of these communicates 
with a corresponding circle, which represents " sight centre " 
and "hearing centre." Beyond these again, there are circles 
marking " word-hearing " and " word-seeing " centres. These 
two converge in the larger circle, which we have named 
"intelligence centre." Connected with this is the highest 
circle in the other half of the diagram, which we have termed 
" will centre." From this there proceed lines to two lower 
circles, the "speech centre " and " writing centre." From 
each of these again we have diverging lines, leading to 
circles marked respectively "co-ordinating" and "motor." 
The lines from these again converge in " speech " and 
" writing." 

Alterations of the language relationships may occur at any 
of these circles, or in the course of any of the lines connecting 



182 



DEAFNESS. 



the circles. There is no necessity for my adverting specially 
to the alteration of the peripheral organs of sight and hear- 
ing. In them, changes occur with great frequency, and 
unless otherwise compensated for, the want of hearing deprives 
the patient of all language relationship ; while the want of 
sight of necessity precludes certain kinds of language 
impressions. The same remarks apply to the lines of con- 
duction from these circles to the next. With regard to 
seeing and hearing circles, there can be no doubt that 
central disease may be of such a kind as to desfroy sight or 
deprive the patient of hearing. I have at present under 
my care a patient whose case illustrates this point. He was 
a perfectly healthy man until August, 1881, when he was 
present at the great review of volunteers held by the 
Queen in Edinburgh. Many of you will remember that the 
day was extremely wet, and this patient, as he left the 
ground, sHpped and fell on the back of his head. He was 
somewhat stunned and uncomfortable, but soon seemed to 
get well, and about nine o'clock on the same evening went 
out to see a friend. In some way that he cannot explain, he 
fell and was found unconscious, was taken home and examined 
by my friend, Dr. Caird, who found that he had the symptoms 
of fracture at the base of the skull. He gradually recovered 
consciousness, but from that day to this has remained 
absolutely deaf, both to aerial and to skull vibrations. His 
intelligence is perfect, and he speaks quite correctly, though 
somewhat too loud ; and, excepting the deafness, there is no 
trace of nervous disease. In particular, the ears are normal, 
and we can find no evidence of interference with the functions 
of the semicircular canals. Now, as the patient is living, 
we cannot with certainty say what the lesion is from which 
he suffers ; but it seems to me more likely to be a central 
affection resulting from contre-coup than one destroying 
both auditory nerves. Whether this view is correct or not, 
he illustrates very perfectly a condition of persistent and 
absolute nerve-deafness. I need not illustrate the corre- 
sponding change in the nerve-centres affecting sight. 

It is necessary to put in a separate category the functions 
referred to in the next circles — the "word-seeing centre," 



WORD-DEAFNESS. 



183 



and the " word-hearing centre." I was lately called to the 
country to see a lady -who was suffering from various cerebral 
symptoms. I found her, on examination, to be a person of 
much intelHgence, and of unusual energy. She had been a 
great reader of newspapers and books, and I judged her to 
be rather a keen politician ; but she had quite suddenly, a 
feAv days before my visit, lost the power of reading. I showed 
her a book which was lying near her bed, and asked her to 
read me a short passage. She tried to do so, but could not 
succeed. She began to name the individual letters, and try 
to put them together, but could scarcely make out a single 
word. She could repeat the words when I said them ; she 
had no diflSculty in speaking, and expressed her astonishment 
at the fact that she could think perfectly well, that she could 
see everything quite clearly, that she could make out, as well 
as ever, the pattern of the wall-paper in her room, could name 
and describe any article shown to her, but could not read a line 
of a printed book. I wrote a few words on a slip of paper, 
and asked her to read them. She declared herself unable, 
because the writing was bad. Her family doctor then wrote 
the same words, but his writing proved equally unintelligible 
to her. She afforded a typical example of what has been 
called "word-blindness." Within a week or two, I heard of 
her gradual improvement. She was learning to put letters 
together, much as a child does in learning to read, and 
had got the length of reading three or four lines ; but, 
after such an effort, began to waver, and was unable to 
proceed further. You observe that here no speech relation- 
ship was interfered with excepting the one — that one of 
gathering up the letters and recognising the word which they 
formed. This power is one acquired by education, and 
different people vary very much in the degree of rapidity 
with which they can accomplish it. An imperfectly educated 
person laboriously puts the letters together, spelling the word 
out syllable by syllable, while one of better education takes 
it up at a glance. I have heard it said of Lord Macaulay 
that he was able to take up a sentence, a paragraph, or 
even a page of a book, as most people take up a word or 
a sentence. You must have seen some readers who went 



.184 



.WORD-BLINDNESS. 



through a page as a heavy Dutch lugger makes its way 
through the sea, while others rush forward like an ocean 
express. The loss of the faculty may be gradual or it may 
be sudden, and there are many degrees of impairment. In 
Professor Kussmaul's admirable treatise on disturbances of 
speech, in Von Ziemsscn's Encyclopaedia, he tells of a patient 
who could write quite well to dictation, but afterwards 
was unable to read the words ^he had written. By 
means of a stratagem, however, as he himself explained, 
he succeeded in reading the word he had written, and 
his method was to move his fingers over the letters, as 
in writing, and to see to what letters the movements 
corresponded. By this means he could read both the 
letters and the words. You perceive that this case was very 
different from the one which I have just described. My 
patient could read the letters quite well, but could not form 
them into words ; Kussmaul's patient could not make out 
the letters, but, given the letters, seemed to have little 
difficulty about the words. 

A beautiful illustration of word-deafness is recorded by Dr. 
Schmidt of Miinstermaifeld. I quote it from Dr. Kussmaul's 
paper : A woman, twenty-five years of age, became suddenly 
•unconscious during severe straining at stool ten days after 
confinement. After consciousness returned she was not 
paralysed, but suffered from aphasia and paraphasia. She 
found the words with difficulty, or not at all ; reversed or 
mutilated them, said ' butter ' instead of ' doctor,' threw out 
letters and syllables, inserted others, used the infinitive 
instead of the proper mood, and conjugated irregular verbs 
regularly. She was thought to be deaf, because at first she 
did not understand a single word. It was soon discovered, 
however, that she heard a knocking at the door, or the ticking 
of a watch as clearly as a well person, that she could dis- 
tinguish between two house clocks by the tone. Words, 
on the other hand, as she afterwards stated, were perceived 
only as a confused murmur. She heard the separate vowels, 
and repeated them. When a word of one syllable was 
repeated in the ordinary way she did not understand it, but 
when the different letters were separated distinctly from each 



APHASIA. 



185 



Other so that they stood forth in the pronunciation, she was 
able to repeat the word. With words of more than one 
syllabic it was necessary first to pronounce one syllable dis- 
tinctly, then another, then the two together, or she would not 
understand the word. It was the same with her reading. 
She studied the words very carefully, and tried to pronounce 
them at first separately, and then together. Recovery took 
place slowly. She did not understand short sentences until 
after the lapse of half a-year, and then only when they were 
pronounced slowly and distinctly. Even at the last there 
remained some little difficulty in speaking. In this case you 
observe that there was no real deafness. She heard sounds 
quite well, but words seemed only a confused murmur. She 
heard separate vowels, and could repeat them, but she could 
not frame them into a word, could not conceive the word 
which they formed. Her condition thus corresponded to 
that of my patient with the word-blindness. She differed 
from it, however, in respect that other nervous symptoms 
co-existed with this special one. 

It is more common for us to find the higher centre — the 
intelligence centre — affected. When it is involved, the 
patient fails to understand any kind of language. Words 
written or spoken are alike meaningless to him. Although 
I represent it by a separate circle, believing that it must be 
performed by some other portion of the brain than that 
which is trained to synthetise letters or sounds into words, it 
is manifestly difficult to bring forward evidence from clinical 
experience of affection of this function, which might not be 
explained on the hypothesis of a general affection of the lower 
circles. But there is no difficulty in producing evidence that 
the word centres may be sound and in active exercise, while 
the intelligence centre is affected and out of use. This 
brings me to draw your attention to reflex and automatic 
speech, which plays so important a part in the language 
relationships. 

If you refer to the diagram (fig. 89), you wiU see that I have 
traced lines across from the word-seeing and word-hearing 
centres to the speech centres and the writing centres. These 
lines mark the communication which comes to be opened up 



18G 



AUTOMATIC SPEECH. 



between the centres, apart from the intellectual apprehension 
or the voluntary utterance of words. When a child is 
learning to read, every effort at reading aloud involves an 
intellectual process and a voluntary effort, but after a time 



Intelligence Centre. Will Centra, 




o o o o 

Sight. Hearing. Speech. Writing. 

Fig. 89. 



it learns to read aloud without thinking of what is read, and 
often learns to write to dictation without mental effort. You 
have observed the difference between a sermon or a lecture 
read and one delivered without slavish dependence on the 
manuscript. You have noticed how often the former seems 
pointless and indistinct compared with the latter, and one 
reason is that the manuscript reader is apt not to receive so 
fully into his intelligence the words that he is uttering. His 
eyes see them, his word-seeing centres make them out, his 
word-utterance centres give them forth, but his intelligence 
centres have not been much moved ; while he who has 
spoken without his manuscript has of necessity uttered the 
thoughts which were at the moment living and real to his 
own consciousness. 

It is possible for patients to speak automatically Avhen 
they are unable to do so by voluntary effort. I was one day 



AUTOMATIC SPEECH. 



187 



demonstrating in the clinical class a case of aphasia. He 
had failed to name various objects held up before him and 
to repeat words which were said in his hearing. I said to 
him, "Say 'No.'" He made a great eflfort, bringing many- 
muscles into play in his attempt to do as I wished. Then he 
found it was hopeless, and giving up the attempt, shook his 
head and said " No." By an automatic process he uttered 
the very word that he could not produce by an effort of the will. 

Sometimes the automatic speech supplies in a curious 
way the defects of voluntary language. A Scottish clergy- 
man one day met a parishioner with whom he was familiar, 
and wished to address him by his name, but what the name 
was he could not remember. Thinking it best to be honest, 
he made up his mind to state his difficulty, and whenever 
the man came close to him, he said, " Thomas, is your name 
John ?" Automatically he applied the right name, while his 
voluntary effort had resulted only in an absurd question. 

It occasionall}'- happens that people somewhat advanced in 
life acquire a habit of automatically repeating words that are 
said in their hearing. I have heard a curious story of an 
Irish barrister who was affected in this way. One of his 
friends sitting beside him in the court listened to an appeal 
that he was making in behalf of some accused persons. 
Having shown good grounds for believing them innocent, the 
barrister finished his speech by appealing to the jury for an 
acquittal. " The men had done good rather than evil ; 
therefore, gentlemen, you will find them not guilty." His 
neighbour whispered, " and have them whipped at the cart- 
tail." Automatically these words were added to the intended 
speech. Occasionally, also, you will find that people acquire 
a habit of thinking aloud. A former Lord Dudley and Ward 
is said to have illustrated this habit, and was sometimes placed 
in awkward circumstances in consequence. On one occasion, 
leaving a friend's house, his carriage was not waiting for him, 
and a gentleman undertook to drive him home. Scarcely 
had they taken their seats in the carriage when his Lordship 
said in a dreamy way, " I hope this fellow won't expect me 
to ask him to dinner." His companion, well acquainted 
with the peculiarity, lent back in his corner and murmured 



188 



APHASIA. 



to himself, " I 'm sure I hope this old fellow won't suppose 
that I wish him to do me a favour." The old gentleman, 
hearing this, at once realised that he must have spoken 
aloud, of which up to that time he had had no suspicion. 

The will centre may be affected either with or without 
affection of the intelligence centre. Sometimes at one period 
of an attack with disease of the will centre, there is also 
word-blindness and word-deafness, and these may pass away, 
while the power of voluntary speech continues in abey- 
ance. The case of Professor Lordat of Montpellier illustrates 
this. He tells that he lost all power of expression in words. 
Words fell uncomprehended on his ear. Words, presented 
to his eye, could be spelt letter by letter, but conveyed no 
meaning. He says, " Syntax had disappeared along with the 
words — the alphabet alone remained to me ' " But in this 
condition he remained able to think and to reason of the 
nature of his illness. He tells that one happy day his eyes 
fell upon a book in his library, and, to his surprise and 
delight, he was able to make out the words " Hippocratis 
Opera." It may be questioned whether the intelhgence 
centre was ever impaired in Lordat's case, but certainly it is 
unimpaired in many cases of aphasia. A patient can read, 
can understand what is said to him, but is unable to utter 
any word. You hold up before him a knife or a pencd- 
case, and ask what it is ; he fails to name it. You suggest 
to him that the knife is a pencil-case. He signifies his 
dissent. You name it as a knife, and he at once acquiesces. 
In such cases, you perceive the patient has not lost the 
memory of words. He has lost the power of originating 
words by voluntary effort. 

Such a patient is totally unable to name any article shown 
him, and yet he knows at once whether a name which you 
apply is correct or not. If you hold up a watch before him, 
he strives to name it, but cannot. You say, "Is it an 
hour-glass ? " He shakes his head. You suggest that it is 
a clock. He again dissents. You tell him it is a watch- 
key. He won't admit it. You say it is a watch. He nods 
acquiescence. Some patients when they have heard the 
article named can repeat the name- Some repeat it more 



APHASIA. 



189 



or less imperfectly, wHle some of these again tend to go on 
applying the same name to different objects shown to them. 

Not unfrcquently mere functional alterations give rise to 
interference with language. I have known a Scottish 
student, familiar with German, walking into the country 
with a companion, and speaking German at the beginning of 
the walk with ease and accuracy, become unable to express 
himself at all in that language when exhausted towards the 
end of his excursion. In advanced age, the vocabulary often 
becomes less copious and the diction less easy than it had 
been in the prime of life. Names of persons, of places, of 
things are often forgotten, even when by a periphrasis an 
accurate enough description may be given. A story is told 
of a high official in Eussia, who, on making a formal call, 
was asked what name should be announced. After puzzling 
a little while, he turned to his aide-de-camp and said, " What 
is my name ?" 

It is curious to notice how some individuals have a diffi- 
culty in recalling certain proper names or names of articles. 
I know a medical man who, although he has often to pre- 
scribe it, has constantly a difficulty in recalling the name of 
santonin. Sometimes, after an injury, sets of words, proper 
names, and names of things are forgotten, while descriptive 
words and verbs are retained. Sometimes the patient forgets 
the initial letter of a word, or remembers only that, and has 
to hunt about for the rest. 

Sometimes the aphasic patient has no vocabulary ; at 
others, he retains a single syllable or a simple phrase, which 
he uses indiscriminately, whatever he may wish to say. It 
may be a meaningless syllable : it may be such words as 
"No, no," "Yes, yes"; it may be some oath or modified 
form of an oath. 

Cases are on record in which, from .disease or injury, an 
acquired language became lost, and the native tongue 
retained. I have read of a Welshman, resident in London, 
who, from the time of his receiving an injury to his head, 
forgot his English and resumed Welsh, which for years he 
had not been accustomed to speak. And a case is recorded 
of an Italian, resident in America, who during his illness 



190 



APHASIA. 



used at first to speak only English, then only French, and 
ultimately lost both of these and used only Italian. 

Sometimes the aphasic cannot indicate his thoughts either 
by speech or writing ; at others you find that speech is lost 
and not writtng, or writing is lost and not speech. I have 
heard of a gentleman who suffered from aphasia with loss of 
speech, but retained the power of writing, and so was able to 
retain an official position, and discharge with ability and suc- 
cess its somewhat complicated duties. More rarely do we 
find the power of writing lost, while that of speech is retained. 
It constantly happens that movements of the tongue or of 
the fingers may in these cases be made with the greatest 
exactitude, while the patient is unable to utter a word. I 
have heard a patient who was unable to utter any word, both 
whistle and hum the tunes of " Auld Lang Syne " and the 
" Old Hundred " quite correctly, and persons who have 
become absolutely agraphia have remained skilful needle- 
women. In these conditions you observe that the defect is 
situated in the will centre, the speech centre, or the writing 
centre, but does not affect the motor or the co-ordinating 
functions. 

I have seen the communication from the will centre down- 
wards greatly delayed. One patient whose case was often 
demonstrated in the clinical wards, and who suffered from 
locomotor ataxia, understood in a moment whatever was said to 
him, but frequently took a long time to get out his reply. 
Before I had found out this peculiarity it once or twice 
happened that I asked him a question, and, supposing him 
quite unable to answer, had passed on to other topics before 
the answer came. It seemed noteworthy that when once 
speech began it went on with little interruption. The diffi- 
culty was to make a start with a sentence. 

You are familiar in the wards with the " staccato " or scan- 
ning speech so characteristic of multiple cerebro-spinal 
sclerosis. You have heard the patients utter syllable by 
syllable the words that they were asked to repeat. Mani- 
festly, the conduction downwards of the voluntary impulse is 
in some degree interfered with. 

On the other hand, there are many alterations both of 



APHONIA. 



191 



speecli and writing dependent upon motor and co-ordinating 
changes. It sometimes happens that, when a patient 
attempts to speak, he is unable to do so in consequence of 
spasm of the muscle supplied by the hypoglossal nerve. 
Sometimes other muscles contract — e.g., the abdominal 
muscles and those of respiration. My friend, Mr. James 
Blaikie, tells me that in inspecting schools he often meets 
with defects more or less resembling this. Some children, 
when asked to read aloud, remain silent for a time, and then 
begin with a sudden burst. Sometimes they altogether fail 
to read, although they can answer questions on the lesson 
intelligently. And he has known a child spell the answer 
correctly, which he could not give in the word form, and 
write what he was unable to utter. You have all seen 
cases of patients who have partially recovered from hemi- 
plegia, in whom the movements of the tongue are so 
imperfect that the voice is altered and the articulation 
indefinite. The laryngeal movements may be accomplished 
well enough ; the movements of the lips and teeth also 
tolerably correctly ; but the tongue lies in the floor of 
the mouth, incapable of performing the appropriate 
movements. You may have seen also patients with bulbar 
paralysis, whose lips were so paralysed that they failed to 
form labial consonants, or whose tongue movements were 
imperfect; and possibly some of you may have seen an 
example of the more advanced disease, in which the laryngeal 
muscles also failed to perform their office. During and after 
diphtheritic attacks, paralysis of the soft palate often gives 
the voice a nasal tone. You have seen many instances of 
patients who, from paralysis, had become unable to write, 
this loss of power being associated with other impairments 
of motor function. There is no need of my dwelling upon 
these impairments, which are so obvious. 

Aphonia may result also from diphtheritic paralysis, the 
laryngeal muscles being paralysed in consequence of the 
process. And you will occasionally see cases of functional 
aphonia in hysterical women — a condition which usually 
yields rapidly to localised electrisation. 

You may meet with functional agraphia conditions — condi- 



192 



MIRROR-WRITINQ. 



tions in which for a time the patient fails to express himself 
in writing or displaces words. Kussmaul tells of a pro- 
fessor who wrote a ' certificate — " Mr. has attended my 

admirable Jectures with clinical regularity." From such 
slight transpositions of words, you may meet with every 
degree up to an utter failure of power of writing even a 
word of one syllable. 

A curious phenomenon related to agraphia is that which 
is known as mirror- writing. The patient writes with the left 
hand and in the reverse way, forming the letters quite well, 
so that they are 'easily read when reflected in a mirror. 
It occurs sometimes in imbeciles, sometimes in those who 
have suffered from apoplexy with paralysis of the right 
side and aphasia. On recovering from, the somnolence 
which often exists during the earlier days of the attack, the 
patient may be inclined to write with his left hand. When 
he does so he traces the letters from right to left in distinct 
mirror- writing, and such a tendency may persist for many 
months. It is interesting to know that Leonardo da Vinci 
wrote in this way a very distinct codex, which is now 
preserved in the Milan Library. It was for long supposed 
that he had adopted this method in order to avoid being 
read by superficial observers ; but Professor Erlenmeyer has 
shown that as he had an attack of paralysis of the right side, 
it is probable that he had become incapable of writing 
otherwise. 

Failure of co-ordination sometimes interferes with speech. 
You have seen this in various forms of stammering, where a 
patient, on attempting to speak, is sometimes hindered by 
the impossibility of making the appropriate co-ordination ; 
sometimes by an irresistible impulse to utter some inappro- 
priate syllable or phrase ; perhaps the expression, " Don't you 
know," or some other form of words. Some patients, after 
giving vent to this little preliminary, are able to go on with- 
out hesitation. I have already in these lectures described to 
you co-ordinating spasms and failure of co-ordination for 
writing. Let me recall to you the fact that this co-ordination 
frequently fails, while other movements continue to be 
accurately and easily performed. 



LESIONS IN APHASIA. 



193 



Aphasia sometimes occurs apart from organic change ; the 
patient suddenly, and perhaps only for a short time, loses the 
power of speech. Such conditions are seen in hysteria, but 
are also met with in connection with epilepsy. I was lately 
called to see a gentleman, whom I found well able to con- 
verse rationally about the peculiarities of his case. The 
day before I saw him he had been leaving his house in the 
country to transact business in town, when he was suddenly 
seized with aphasia, became unable to speak as he wished 
to do, and sought in travelling to avoid the observation of 
his friends ; but some of them noticed that he walked 
unsteadily, had a peculiar expression, and spoke differently 
from his usual. Finding himself unable to transact business, 
he made his way home, went to the telegraph office and 
telegraphed for his doctor. Instead of putting his own name, 
he put that of his firm, and he omitted to put the name of 
the town in which his doctor resided. In his message each 
individual word was correct, but the whole conveyed no 
meaning. The message, as he wrote it, was (I change 
names), "Dr. Johnson, come as Newhaven in Fairhaven." 
He then went home, and by the time the doctor arrived, was 
able to speak fairly. Such attacks came and went occasion- 
ally for several weeks. He was seized from time to time, as 
an epileptic is seized, with this aphasia. After some weeks 
he recovered, no important symptoms being superadded, 
excepting some giddiness. It appeared probable that the 
symptoms were due to some alteration of the vessels in 
certain areas of the brain. 

We have now to inquire what parts of the nervous system 
correspond to these different functions. 

It has long been known that the aphasic conditions are 
specially connected with lesions in the left hemisphere, and 
this is probably to be explained on the hypothesis that, just as 
most people are right-handed, and develop the finer powers 
of movement on that side of the body only, so most people 
develop their speech-faculty in connection with the left 
hemisphere. And just as individuals may laboriously acquire 
the power of using the left hand when the right is disabled, 
so people have learned to speak, using the right hemisphere 

* N 



194 



LESIONS IN APHASIA. 



"when the speech-regions of the left have been permanently 
destroyed. 

We have already traced what is known of the course 
of the nerves of sight and hearing on their way from the 
peripheral organs to the centres for these functions. The 
recent results of Ferrier's researches seem to show that the 
sight centre is situated in the occipital lobe and angular 
gyrus, while the hearing centre is situated in the superior tem- 
poro-sphenoidal convolution. According to Wernicke, those 
failures — which, following Kussmaul, I have called word- 
blindness and word-deafness — result from destruction of the 
left first temporal convolution, with some degree of affection 
of the second. It seems clear that word-deafness should 
result from lesions in this part. Word-blindness also seems 
to result from lesions in the same part. If this be so, it is 
very remarkable, inasmuch as the sight centre is at a distance 
from this point. We can say nothing with certainty as to 
the seat of the intelligence centre, which we have seen 
clinical grounds for separating from those just named ; but 
the motor centre or will centre is undoubtedly to be referred 
to Broca's convolution — the third left frontal convolution. 
With lesion there, the speech muscles may be used, but the 
patients are either speechless, or have only a few words, 
while the comprehension of language remains perfect. The 
fibres leading from the motor part, passing down by the 
region of the island of Keil to the internal capsule, may be 
diseased, and so results similar to those caused by lesions of 
Broca's convolutions may be produced, which are, however, 
often of a temporary character. There may be interference 
with the commissural fibres in the corpus callosum, connect- 
ing the two Broca's convolutions, and it would appear that 
this is capable of leading to the same result. We may 
suppose that lesions may exist in fibres connecting the sensory 
and motor speech centres, and in those connecting either of 
these with the intelligence centre, which also give rise to 
various aphasic conditions. The motor and co-ordinating 
changes are determined mainly by lesions in the nuclei of 
the medulla oblongata and neighbouring parts, and of the 
nerves proceeding from them. 



TERMS RELATING TO APHASIA. 



195 



While I have described the alterations of the functions of 
language in the way that seems to me the most satisfactory, 
it may be convenient if I indicate to you the precise mean- 
ings attached to certain words of common occurrence in 
treatises dealing with the subject. By amnesic aphasia, we 
understand a form of speechlessness in which neither spoken 
nor written words can be recalled. The idea is present, but 
does not suggest the proper speech symbol, so that either no 
word is uttered or an unsuitable one. The appro^Jriate word 
may be correctly pronounced if it is heard by the patient. 
Ataxic or atactic aphasia is that variety of speechlessness in 
which a patient, although he remembers words, cannot 
enunciate them. He has a want of power of making the 
necessary motor combination for articulate sound, and that 
even although the sounds themselves may be correctly 
produced when other words are used. Dysarthria is a term 
applied to disturbance of speech from defects of articulation. 
Dyslalia designates those which are dependent on gross 
mechanical defects in the external apparatus of speech. 
Dysphasia implies disturbance of diction, rather than loss of 
diction. 



LECTUKE XIII. 

The Structures which are the Seat of Lesion in Nervous Disease. — 
Histological Elements of the Nervous System. — Lesions occurring 
in the Nervoits System. — Vascular Distribution in Relation to 
Nervous Disease. — Observations of J^uret andHeubner. — Vascular 
Supply of Basal Ganglia and Neighbouring Parts. — Vascular 
Supply of Cortex. — Of Cerebellum. 

C\ ENTLEMEN, — In tliis lecture I purpose to describe or 
^ recall to your memories — (1) the different structures 
which are the seats of lesion in nervous disease ; (2) the 
histological elements of the nervous system ; (3) the lesions 
which occur in the nervous system ; and (4) certain points 
in regard to vascular distribution, which influence the produc- 
tion of various lesions. 

1. The Structures which are the Seats of Lesion in Nervous 
Disease. I need not do more than catalogue these. The 
bones of the cranium or of the vertebral column are 
frequently altered so as to interfere with the performance 
of the functions of the nervous system, and these altera- 
tions may be the result of injury or of morbid processes. 
The dura mater may have changes in its structure, with 
alterations on its external or internal surface. The arachnoid 
and the pia mater are frequently, especially the latter, the 
seats of important morbid processes. The ventricles of the 
brain and the central canal of the cord are frequently 
altered. The cerebro-spinal fluid, which may be increased 
or diminished in quantity, is probably a more important 
element in morbid conditions of the nervous system than is 
usually recognised. The arterial, capillary, venous, and 
l3nnphatic systems are more frequently the starting-point of 
196 



NERVE-CELLS. 



197 



lesions than any other structure in the nerve-centres. The 
nerve-cells in the grey matter, the nerve-fibres, and the 
neuroglia, are the remaining elements which we find altered 
in nervous diseases. 

2. The Histological Elements of the Nervous System. 

(a) The cells, which exist in the grey matter of the nerve- 
centres, vary much in shape. Some of them are spindle- 
shaped, some spheroidal, some angular and irregular, some 
pyramidal, and some flask-shaped. They vary also in size 
and in number in different parts. They contain a nucleus, 
a nucleolus, and sometimes an intra-nuclear network may be 
made out. The cell sub- 
stance is finely granular, 
often pigmented. From the 
cell processes extend, some- 
times one, sometimes two, 
often many. The processes, 
from a multipolar cell (fig. 
90), are not all the same ; 
usually one, which is known 
as the axis-cylinder pro- 
cess (a), contains the minute 
fibrils, which, at some little 
distance , from the cell, be- 
come clothed with a sheath. 
The others are more fibril- 
lary, and break up into many 
minute ramifications. Some- 
times two axis-cylinder pro- 
cesses proceed from a cell, 
especially from the bipolar. 

(6) Nerve -fibres. The 
essential element of the 
nerve - fibre is the axis- 

Cyimaer. it consists Ol a cess (a), a well-defined nucleus (6), and many 

number of minute fibrils ^'^^^'^y'^^ (-''^'^ ^^'^'-y 
bound together, the primitive fibrillte. They are con- 
tinuous from the nerve-centres outwards, and, at the termina- 
tion of nerves, may be seen breaking up into a number of 




Fig. 90. 



198 



NERVE-FIBKES. 




Fia. 91. 

Kerve fibre, showing 
axis-cylinder, surround- 
ed by its double sheath; 
the nodes of Kanvier(K), 
and the oval nucleus (c) 
(Quain). 



NEUROGLIA. 



199 



minute fibrils. The axis-cylinder appears to be surrounded 
by a very delicate structureless sheath (fig. 91, a). But far 
more distinct is the medullary sheath or white substance of 
Schwann, which surrounds many of the axis-cylinders. The 
medullary sheath is broken up into divisions, first described 
by Ranvier ; and the constrictions or nodes (ii), known by his 
name, separate different portions of the sheath. Each inter- 
val between the nodes contains an oval nucleus (c). Outside 
of the medullary sheath is the primitive sheath, on the inner 
side of which are the nuclei just referred to. This sheath 
turns in at the nodes, and closely surrounds the axis-cylinder 
as it passes from one segment to the other. Within the 
brain and the cord this outer sheath is not found, and the 
nodes of Ranvier are also absent. 

Besides these medullated fibres, there are pale or non- 
meduUated fibres, often spoken of as the fibres of Remak. 
They are chiefly seen in the sympathetic, but also occur in the 
cerebro-spinal nerves. They contain nuclei, and frequently 
branch and communicate with one another (fig. 9 2). 

(c) Neuroglia. This is the supporting substance, among 
which the cells and fibres of the nervous 
system are imbedded. It is a connective 
tissue substance, and contains minute cells 
or connective tissue corpuscles (fig. 93). 

3. The Lesions which occur in the 
Nervous System. It is only necessary to 
remind you of the changes which may 
occur in bone, — fractures and displace- fig. 93. 

ments, inflammations (with resultinsr caries, Microscopic prepara- 

^ O ' tion of neuroglia (after 

necrosis, suppuration), new formations, — Koiuker). 
these morbid processes originating sometimes in the bone 
itself, sometimes in the periosteum. The dura mater may 
be affected with congestion, inflammation, thickening, hemorr- 
hage, and new formations. The arachnoid is often inflamed. 
The pia mater, with its numerous vessels and lymphatic 
structures, is frequently the seat of congestion, inflamma- 
tion, and of tubercular and other new formations. The vessels 
are frequently over-distended, the arteries are liable to athero- 
matous changes, with endarteritis, and with thickening of 




200 



LESIONS IN NERVOUS SYSTEM. 



the tunica adventitia, as well as to aneurismal dilatation. 
The capillaries are liable to degenerative changes, often also 
to aneurismal dilatation. The veins are liable to inflamma- 
tion, while in any of the vessels, but especially the sinuses, 
thrombosis, and in the arteries and the capillaries embolism, 
frequently occurs. The vessels are also subject to rupture. 
The embolic processes are followed in many cases by softening 
of the brain substance. The htemorrhages necessarily tear up 
the brain substance and induce inflammatory changes and 
softening in the neighbourhood of the clot. Sometimes the 
clot becomes absorbed, and a reddish-brown cicatrix, studded 
with hsematoidin crystals, marks its seat. Sometimes a cyst 
is formed, containing a watery fluid, surrounded by fibrous 
tissue, lined often with a reddish layer of haematoidin. In 
connection with the vessels and their sheaths new formations 
of various kinds are common, especially tubercular and 
Syphilitic. The lymphatic spaces are sometimes found 
greatly dilated. The nerve structures proper are liable to 
inflammatory and degenerative changes, breaking down the 
elements by a process of fatty degeneration, sometimes 
incrusting them with calcareous matter. The neuroglia 
appears frequently to be increased in inflammation, especially 
in chronic forms. It is also frequently affected with new 
formations, gliomata, sarcomata, tubercular nodules, and 
syphilitic processes. The brain may also undergo atrophy, 
as a result of a considerable variety of processes. Hydatid 
cysts ' occasionally occur within the cranium. You must also 
bear in mind that there are numerous congenital malforma- 
tions which you may meet with in practice. 

The effects of these lesions are produced in different ways. 
Sometimes they are the result of direct irritation or destruc- 
tion of portions of the nervous system ; at others they result 
from compression. Rupture of a vessel, for example, result- 
ing in hsemorrhage, leads to destruction of a certain amount 
of tissue, irritation, and inflammation in an area surround- 
ing that, and usually compression of the brain substance 
generally, or of the neighbouring portions of grey or white 
matter. These mere compression-results usually subside 
by degrees as the circulation accommodates itself to the 



VASCULAE SUPPLY OF BKAIN. 



201 



altered conditions, or as the effusion becomes partially 
absorbed, while the torn tissue remains broken up, and 
that which is inflamed and irritated undergoes further 
changes. In the case of tumours, on the other hand, whil6 
a certain amount of destruction and displacement of tissue 
necessarily results, we generally find a steady and increasing 
amount of pressure, which may result in general changes or 
in local interferences with function. 

4. The Vascular Distribution in Relation to Nervous 
Disease. We are mainly indebted for our knowledge of the 




Fio. 94. 

Arterial distribution at base of brain. V, vertebral artery ; B, basilar 
artery ; C, internal carotid ; CA, anterior cerebral ; S, Sylvian or middle 
cerebral , CP, posterior cerebral ; 1, antero-median group of nutrient 
arteries ; 2, postero-median nutrient arteries ; 3, antero-lateral nutrient 
arteries ; 4, postero-lateral nutrient arteries (Charcot). 

importance of this subject, and for the elucidation of its 
details, to Dr. Buret, who worked in the Salpetri^re in Paris, 
and Professor Heubner of Leipsic. The first point which you 



202 



VASCULAR SUPPLY OF BRAIN. 



ought to grasp is, tliat the cerebral convolutions are supplied 
with blood by a different set of arteries from those supply- 
ing the basal ganglia and neighbouring parts in the interior 
of the brain. The second is, that the supply to these ganglia 
is much more direct, and consequently the supplying vessels 
must be exposed to a considerably greater pressure, than is 
the case with those supplying the cortex. The third is, that 
the cerebral vessels belong to the class called terminal ; that 
is, each ultimate branch supplies its own area, and has no 
connection with the neighbouring vessels. Thus, the vessels 
of the ganglia do not intercommunicate freely with one 
another, and have no communication with those of the 
cerebral cortex ; and, in like manner, Duret maintains that 
the vessels of the cortex do not communicate. 

Let me remind you of the points at which the vessels are 
given off for the supply of different parts. You remember 
the general vascular arrangement at the base of the brain — 
the internal carotids, the vertebral arteries uniting to form the 
basilar, and then again dividing, the circle of Willis, and the 
communicating arteries (fig. 94). From the anterior communi- 
cating artery, and from its immediate neighbourhood, vessels 
run straight up into the substance of the brain (1). This is 
known as the antero-median group of nutrient arteries. 
From the posterior part of the posterior communicating 
arteries, and from the posterior cerebrals close to their point 
of origin from the basilar, a group of vessels, the postero- 
median group, arises (2). From the middle cerebral artery 
on each side groups of vessels pass into the substance, the 
right and left antero -lateral groups (3). And from the 
posterior cerebrals on each side, after they have turned 
round the crura cerebri, a group of vessels proceeds. These 
groups are known as the right and left postero-lateral 
groups (4). Let me now indicate the precise points supplied 
by each of the groups. The antero-median group supplies 
the front part of the head of the caudate nucleus. The 
postero-median group supplies the internal surface of the 
optic thalami and the walls of the third ventricle. The 
right and left antero-lateral groups supply the lenticular 
nucleus and adjacent part of internal capsule and anterior 



YASCULAR SUPPLY OF BRAIN. 



203 



part of the optic thalami. Among its branches there is one 
which Charcot has called the artery of cerebral hcBmorrhage. 
It is of relatively larger size, and enters the substance of the 
caudate nucleus by crossing the upper part of the internal 
capsule. It spreads forwards to the most anterior part of 
this nucleus. The postero-lateral groups supply a larger 
part of the optic thalami. When you consider the mode of 
origin of these arteries, and their terminal distribution, you 




Fig. 95. 

Cortical arterial supply (after Duret). For explanation see text. 

will understand how liable they are to rupture, and what an 
important part they play in the production of hemorrhagic 
apoplexies. 



204 



YASCULAll SUPPLY OF BRAIN, 



The vascular supply to the cortex proceeds from the vessels 
•which form the angles and sides of the circle of Willis. The 
■anterior cerebral turns round the corpus callosum, and is 
distributed over part of the inferior surface of the frontal 
lobe, and a considerable portion of the internal surface of the 
hemisphere — the area marked by fine dotted line in the 
diagram. The middle cerebral or Sylvian artery is the largest 
and by far the most important of the vessels. Its area of 
distribution is marked by the interrupted line on left of 
figure. It supplies that part of the frontal lobe not connected 
with the anterior cerebral, and the whole of the parietal lobe. 
It is divided into four principal branches. The first is the 
external and inferior frontal artery of Duret (fig. 95 i.). It 
is the artery of the third frontal convolution. The second 
branch is the anterior parietal artery of Duret. Charcot calls 
it the artery of the ascending frontal (ii.). The third is the 
posterior parietal artery of Duret, named by Charcot the 
artery of the ascending parietal convolution (iii.). The fourth 
branch goes to the angular gyrus, and the superior and 
upper part of the middle temporo-sphenoidal convolution (iv.). 
You thus see that the branches of the middle cerebral artery 
supply the convolution which is specially associated with 
aphasia and the great motor centres of Ferrier. It is in this 
artery and its branches that one most frequently finds emboli 
impacted, and on the left side oftener than on the right. The 
posterior cerebral artery springs from the basilar, turns around 
the crus cerebri, and divides into three branches, which are 
distributed to the lower surface of the brain, supplying the 
lower portion of the temporo-sphenoidal lobe, and the occipital 
lobe — marked with interrupted line on the right of the figure. 
The mode of distribution of these vessels would lead one to 
expect less tendency to haemorrhage. They are certainly 
much more liable to embolic and thrombic processes. Thus, 
broadly expressed, the region of the ganglia is specially, 
though not exclusively, subject to haemorrhage from rupture 
of vessels ; whilst the cortical region is specially, though not 
exclusively, subject to local softenings from blocking of 
vessels. 

The pons is supplied by lateral branches of the basilar 



VASCULAR SUPPLY OF NERVE-CENTEES. 



205 



artery ; the medulla oblongata and spinal cord by branches 
from the spinal arteries ; but the distribution of these vessels 
has not the same clinical significance as that of the cerebral 
vessels. 



LECTURE XIV. 



The General Treatment of Nervous Diseases. — Prevention. — Treat- 
ment. — General Management and Diet. — Intervxil Medicines. — 
Nutrients and Tonics. — Stimulants. — Sedatives. — Specific Reme- 
dies. — Electricity. — Faradisation. — Galvanisation. — Other Ex- 
ternal Applications. — Massage. — Sedative Liniments. — Counter- 
irritants. — E load-Letting. — Regulated Muscular Exercise. — 
Ling and Zander's Methods. — Spinal Supports. — Elastic Con- 
trivances. — Surgical Methods. — Nerve-Section. — Nerve-Stretch- 
ing. — Removal of Tumour. — Tapping the Cranium. — Trephin- 
ing for Local Injuries. — To relieve Tension. 

r\ ENTLEMEN, — I intend to devote this lecture to a con- 
^ sideration of certain facts and general principles, which 
should guide you in the management of nervous cases, 
I shall speak first of prevention, and second of treatment — 
(a) by general management and diet ; (h) by internal medi- 
cines ; (c) by electricity ; {d) by other external applications ; 
(e) by regulated muscular exercise ; (/) by surgical methods. 

First, in regard to prevention. The physician must use 
his influence to prevent the inter-marriage of individuals of 
neurotic constitution, and particularly of different members of 
the same neurotic family. He need not be surprised if 
nervous disease occurs in individuals of such constitution who 
are disappointed in love ; but, for the well-being of the indi- 
viduals themselves, and still more of their possible progeny, 
such marriages are very undesirable. Most of you are 
familiar with one of Du Maurier's sketches, in which the 
feeble, pigmy, neurotic son of such a marriage appeals to his 
parents to know why they became united, the only fault of 
the picture being that one scarcely sees how the lad should 

206 



GENERAL MANAGEMENT OF NEKVOUS CASES. 



207 



have had intelligence enough to divine the cause of his 
disabilities. 

In the upbringing of children of neurotic families, special 
care should be taken. The nutrition should be good, an 
open-air life should be inculcated, and muscular exercise 
encouraged, while lessons should be kept moderate, and the 
attention concentrated for a short time each day on an 
amount of work that the child can really master without 
undue effort. In the choice of occupation, also, those 
demanding heavy strain should, as far as possible, be avoided 
by the neurotic. Vicious habits, particularly sexual, and 
alcoholic indulgence, should be most carefully avoided. 

Second, in regard to treatment, (a.) By general manage- 
ment and diet. The patient who is suffering from nervous 
disease should, as far as possible, be placed amid favourable 
surroundings. His life should be regular, laborious effort of 
body or mind should be avoided, and he should have long 
hours of rest. The diet in many cases should be liberal. 
Only in epilepsy, and in patients with a tendency to haemorr- 
hagic apoplexy, should it be scanty, and with little butcher's 
meat ; and, even in these, occasionally you may find it wise 
to allow a more liberal nourishment. In such diseases as 
acute alcoholism, supplying abundant nutrition in easily- 
digested form is of the utmost importance. And often in 
neuralgia this indication is of equal moment. In the latter 
of these diseases, also, alcoholic stimulation is not unfrequently 
required, but it must be used with great caution. 

Change of air and change of scene, visiting foreign 
countries, all have their place in the treatment of chronic 
nervous disease. In particular, in the case of overworked 
men whose nervous systems have broken down, so that they 
feel themselves unfit for business that had previously been 
easy, nothing proves so useful as a summer in the High- 
lands or in Switzerland, or a voyage to the Cape or to the 
Antipodes, 

Moral management is essential in many nervous diseases. 
In the hysterical, the hypochondriacal, and other conditions, 
it is more important than anything else. You must some- 
times remove your patient from home surroundings, and 



208 



MEDICINAL TREATMENT. 



put her under the care of considerate but determined nurses, 
before you can accomplish any good. So long as an over- 
indulgent mother or sister is hanging over the patient and 
gratifying every whim, you will find yourselves helpless. 
But when a good discipline is established, self-control will 
return. 

(&.) By internal medicines. Internal medicines of many 
kinds are required. 1. Nutrient and tonic substances. 
Among these, the most important are cod-liver oil, iron, 
arsenic, phosphorus, and zinc. They are demanded in low 
states of the nervous system, and in those attended by 
anaemia, but they are also of service in the more chronic 
stages of most nervous diseases. Phosphorus, in particular, 
has been praised by many writers, and I concur in thinking 
that it is of real service ; but you must pay attention to 
the form in which it is administered, for I have known a 
certain variety of phosphorus pills pass through the 
alimentary canal unchanged. In my opinion phosphorated 
oil and the hypophosphites are the most serviceable forms. 
It is difficult to say where quinia should be placed among 
the nervine remedies. It certainly ranks among the specifics, 
but it may be also placed with the present category, seeing 
that it proves so serviceable in cases of neuralgia which are 
not due to malarious influences, nor even periodic in character. 

2. Stimulants. These are often required for the purpose 
of increasing the activity of the nervous system, and among 
them ammonia, alcohol, nux vomica, strychnia, f»nd valerian 
are the most valuable. Ammonia and valerian are fre- 
quently of service in the paroxysms of hysteria and in other 
nerve-storms. Alcohol, although it must always be carefully 
handled, is often of service in diseases of the brain and 
nerves, while strychnia is of the utmost service as a stimulant 
to the motor structures. 

3. Sedatives. No remedies are more important than these 
in nervous cases. Opium is perhaps the most valuable of 
all. You may give it by the mouth, the rectum, or sub- 
cutaneously. And you will find it of the utmost service for 
soothing pain, diminishing spasm, obtaining sleep, and 
calming excitement. But you must avoid it or use it very 



MEDICINAL TREATMENT. 



209 



cautiously in cases where there is a tendency to coma, and 
always remember the great risk of patients becoming unable 
to do without it. I have known some who began to use it 
for relief of urgent pain, and continued for years secretly to 
indulge in it as a luxury, and others whose life has been 
embittered by a consciousness of the power it had acquired 
over them. Chloroform is of the utmost service for relieving 
pain and spasm, especially in convulsions due to alcohol, and 
to renal disease. But you must keep your patients from its 
habitual use, for, besides its direct dangers, it possesses the 
attraction to some that opium and alcohol have. Chloral 
hydrate is another very valuable sedative. It quiets the 
nervous system and often procures sleep where other remedies 
fail, but it seems, even more than those I have already 
named, to tend to be abused. Croton chloral is frequentlj^ 
helpful in cases of neuralgia of the fifth nerve. Belladonna 
and atropine are useful sedatives. They sometimes relieve 
pain, and certainly diminish certain forms of spasm. In 
whooping-cough and in epilepsy, I would particularly recom- 
mend them to your notice. Hyoscyamus and hyoscyamin 
are also sometimes serviceable in a similar way. Cannabis 
indica proves very useful as a sedative, particularly in 
chorea. Physostigma has also been found useful for diminish- 
ing spasm, as in tetanus. Conium diminishes the irritability 
of the cord, acting solely upon the motor structures. It is, 
therefore, particularly to be recommended where there is 
undue irritability of the spinal centres, as in tetanus and 
strychnia poisoning. The Bromides you will find extremely 
useful as sedatives in cases of epilepsy. They must some- 
times be given in large doses before their effect can be fully 
brought out. And they may be continued for long' periods. 
I have known some patients who used them as regularly as 
salt is taken with the food. They tend to bring out a rash 
on the skin, which may, however, in many cases be averted 
by combining arsenic with the bromide. 

4. Specific remedies. Quinia exerts a specific influence in 
cases of malarious disease, such as neuralgia and paraplegia. 
I have known it rapidly cure the most alarming cough. 
And whatever nervous symptoms you may meet with in a 

o 



210 



TREATMENT BY ELECTRICITY. 



person of malarious constitution, you will find it your best 
remedy. Sometimes small doses sulBQce ; at others, you 
have to go up to twenty or thirty grains several times 
a-day. Arsenic and Salicin sometimes avail where quinia 
is not well borne or does not succeed. Colchicum and 
the alkalies are of great service in gouty nervous disease, 
such as neuralgia and asthma. Salicylate of soda and Iodide 
of lootassium, along with alkalies, are often useful in neural- 
gias of rheumatic origin. Iodide of 'potassium is eminently 
serviceable, as is mercury, and especially the solution of 
perchloride, in many of the varieties of syphilitic nervous 
diseases, as well as sometimes in cases which you cannot 
distinctly class as syphilitic. Nitrate and other salts of 
silver are praised by some in the treatment of locomotor 
ataxia ; but I have not seen good results follow their use. 
In epilepsy, they appear to be sometimes of service. It is 
doubtful whether they should be ranked among the specifics. 

(c.) By electricity. The form of electricity more commonly 
employed is Faradisation. It may be applied generally in 
either of two ways — viz., by placing one pole at the coccyx, 
and moving the other over different parts of the body, 
particularly over the spine and the sides of the neck, the 
epigastrium, and along the lines of the large nerve-trunks 
in the extremities, or by placing the patient's feet and legs 
in a bath, with one pole applied to some point of the body 
which remains exposed, and the other in the water. Such 
applications appear to exert a general tonic influence, and 
may be recommended in cases of hypochondriasis or 
unexplained debility. It may also be applied locally. If 
we wish to act on the sldn, dry rheophores of different kinds, 
for example the brush, are employed. They are moved 
over the surface, and cause considerable smarting, or actual 
pain. This method may be recommended in cases similar 
to those requiring general electrisation, but it is also often 
serviceable in skin diseases. Obstinate cases of muscular 
rheumatism, lumbago, and chronic articular stiffening are 
often relieved by currents applied with moistened rheo- 
phores. In such conditions you will find it advantageous 
to use electrodes of considerable surface. Thus, in the case 



TREATMENT BY ELECTRICITY. 



211 



of an affected joint, the electrodes should cover a large part 
of two opposite aspects of the articulation. But by far the 
most important application is that localised to individual 
nerves and muscles. The rheophores, and the surface of the 
patient's body to which the application is made, must for 
this purpose be well moistened with salt and water. When 
applied to nerves, it may be passed from the spine to 
superficial portions of nerve, or to the periphery, or from 
one part of the nerve to another. You will find that it often 
gives instantaneous relief in cases of neuralgia, and that in 
many cases of paralysis of nerve, whether functional or 
organic, it contributes towards cure. Where your object is 
to influence the muscle, the application may be made 
directly over it, according to the method of Duchenne, or 
may be conducted into the muscular substance by needles ; 
but the method of Ziemssen, of indirect Faradisation — that 
is, the application of one rheophore over the points of nerve- 
supply to the muscles — is preferable. The one pole, well 
moistened, is placed over the sternum or other indifferent 
part, and a fine rheophore is applied to the individual points, 
which I indicated in Lecture IX., when speaking of the 
employment of electricity in diagnosis. 

Faradisation may also be applied directly to internal 
organs — for example, to the larynx — by means of a slender 
rheophore, introduced with the aid of the laryngoscope, or 
applied externally. Such treatment is of great use in cases 
of hysterical aphonia, and sometimes in the later stages of 
chronic laryngitis, where a degree of paralysis co-exists. 
Such an application may also be made to the bladder, an 
insulated bougie being passed in while the organ is full of 
water. It is sometimes applied to the male genital organs, 
the rectum, the uterus, and other points. 

Galvanisation may be applied generally or locally by the 
same methods as those used for Faradisation ; but it is of 
importance to bear in mind when you use it that different 
results will be obtained according to the relative position of 
the rheophores. It may be laid down as a general rule, 
although subject in many cases to modification, as you will 
see in practice, that where soothing action is demanded — 



212 



TKEATMENT BY ELECTRICITY. 



for example, in conditions of spasm or neuralgia — tlie 
positive pole is to be applied over the aft'ected part, while, if 
a nerve requires stimulation, the negative pole should occupy- 
that position. The rheophores may be kept fixed — stabile 
application ; or they may be moved about — labile. 

General Galvanisation may be obtained by the electric 
bath, one pole being connected with the water of the bath, the 
other in contact with the hand of the patient. Drs. Beard 
and Rockwell recommend what they call centralised Gal- 
vanisation, which is intended to affect the central nervous 
system. The anode is passed over the forehead and head, 
along the inner border of the sterno-mastoid and do\m the 
whole length of the spine, while the cathode is placed over 
the epigastrium. Localised Galvanisation may be applied to 
the skin, the nerves and muscles, or internal parts. When 
applied to the skin, it is often useful by improving its 
nutrition, as in cases of chronic inflammation, atrophy, and 
gangrene. Thickenings of joints may also be diminished by 
its use. It often reheves neuralgia, when applied over the 
painful point. Muscles may often be brought into play by 
Galvanism when Faradisation is unsuccessful. Anodal open- 
ing in such cases forms the most powerful stimulus to the 
muscle. The cathode should be applied over some indifferent 
point. Galvanism may be applied to the brain, one pole being 
placed over each mastoid process, each temple, or over the 
front and back. This must be done with great caution, and 
for a very short time. It may be applied to the cord, the 
current laeing passed from the nape of the neck to some 
important nerve, or both poles being placed over the spinal 
cord. It is said also to be applicable to the sympathetic, one 
electrode pressed deeply into the auriculo-maxillary fossa, the 
other over the sixth or seventh cervical vertebra. This also 
is to be used with great caution, and continued for but a 
short time. It is said to be specially useful in exophthalmic 
goitre. It is at the making and breaking of the current that 
muscular movements are produced. And you will find that 
by following the method of Remak — i.e., by reversing the 
current by the action of a commutator — you get more 
distinct contraction than by simply making and breaking. ■ 



]^LA.SSAGE. 



213 



It is often a matter of difficulty to determine which 
current should be used in any particular case, and this 
difficulty has led to considerable vagueness in electro- 
therapeutics. Making a broad, general rule, we may say that 
Faradisation is indicated — firstly, where excitation of motor 
nerves and muscles is desirable, provided that the reaction 
of degeneration is not present ; secondly, for the stimulation 
of sensory nerves, in ansesthetic conditions, or by way of 
counter-irritation in hysterical cases ; thirdly, where you 
wish to obtain a rapid succession of powerful muscular 
contractions, as in the troublesome rheumatic cases to 
which I have already referred. Galvanisation, on the other 
hand, is called for — firstly, as an excitant to motor nerve and 
muscle, when these have ceased to react to Faradism ; and, 
secondly, as a soothing agent in spasm and in neuralgia. 
Lastly, you must bear in mind that many cases are benefited 
by the combined or alternate use of the two methods. 

(d.) By other external aioplications. Simple rubbing of the 
surface with the hand, either dry or moistened, or with a 
brush, is often useful in nervous disease, both by quieting 
the nervous system and relieving pain in superficial parts. 
Rapidly-produced mechanical vibrations, as suggested by 
Dr. Mortimer Granville, seem to produce a similar effect. 
The a|)plication of stimulating oils, or of sedatives, adds to 
the value of the simple friction. For rehef of pain nothing- 
is better than the rubbing in of aconite, belladonna, and 
chloroform. Of late years, the combination of rubbing, 
kneading, and clapping the surface, included under the term 
massage, has been shown to be of very great service. It is 
well carried out in such places as Aix-les-Bains, by the 
shampooers connected with the baths. Dr. Weir Mitchell 
and Dr. Playfair have shown its great value in neurasthenia, 
both by reUeving symptoms and increasing the general 
nutrition of the body. In cases of paralysis, as well as of 
neuralgia, it materially aids the other plans of treatment. 

It is difficult to assign to blistering its proper place in the 
treatment of nervous diseases. It is, undoubtedly, of service 
in relieving neuralgia ; it is probably helpful in some cases 
of Bell's paralysis ; but is it of any use in cases of intracranial 



214 



COUNTER-IERITATION, BLEEDING. 



inflammation ? Practitioners, in former days, used to blister 
and rub in croton-oil, or an antimonial ointment, into the 
scalps of children suffering from tubercular or other forms of 
meningitis ; but I think you will do well to abstain from 
this method of treatment, for its disadvantages are obvious, 
and its benefits problematical. I think that many of the 
cases in which practitioners supposed that they had cured 
the disease by this means were really examples of typhoid 
fever with marked head symptoms. I must admit, however, 
that I once had a patient who suffered from a localised 
meningitis in the neighbourhood of an intracranial syphilitic 
tumour, and that formidable head symptoms yielded after 
counter-irritation. But I am uncertain whether the blistering 
effected the cure. The diagnosis was verified when the 
patient died some time afterwards. Some practitioners set 
much store by the use of Corrigan's button or Pacquelin's 
thermo-cautery, and of the seton in some nervous conditions. 
I have sometimes seen the last named prove beneficial, but 
it does not often succeed. 

Along with this question I shall refer to that of local 
blood-letting. Do we ever benefit our cases of cerebral 
congestion or inflammation by bleeding ? I have, in one 
case at least, of chronic spinal meningitis, seen marked relief 
follow local blood-letting — relief of the symptoms, and 
particularly the pain. And I have known a patient suffering 
from disease of the ear, who became drowsy and torpid, and 
exhibited other symptoms of intracranial disturbance, relieved 
by bleeding behind the ear. I am, on the whole, inclined 
to think that the treatment is beneficial in some cases, 
although, in a large proportion of cases in which it is tried, 
it proves absolutely useless. In some cases of haemorrhagic 
apoplexy, blood-letting is, in my opinion, sound practice. It 
rarely happens that we see cases in which we can positively 
diagnose hasmorrhage into the brain and be certain that 
haemorrhage is still going on ; but, if we do meet with such 
a case, bleeding may prevent or diminish further mischief. 

(e.) By regulated muscular exercise. While it is true that 
excessive muscular effort is apt to induce nervous disease, it 
is also certain that in the treatment of many of these 



KEGULATED MUSCULAR EXERCISE. 



215 



maladies, systematic use of the affected muscles is of value. 
In the case of paresis, or in patients recovering from paralysis, 
mechanical contrivances have long been in use ; but the 
Swedish movement cure, worked out by Ling and Zander, 
has inagurated a new era in this plan of treatment. Their 
principles may be said to be — first, to supply definite instru- 
ments, which shall exercise individual groups of muscles ; 




Fig. 00. 

Apparatus for regulated muscular moremeut of arms, shoulders, and chest. 

second, to exercise the muscles in such a way that they shall 
not be exerted beyond what is reasonable; and, that 
mechanical aids are supplied to facilitate the movement 
and lighten muscular effort. In figs. 96 and 97, you see 
illustrations of the kind of instruments employed, — the one 
is intended for the muscles of the arms, shoulders, and chest ; 



216 



EEGULATED MUSCULAR EXERCISE. 



the other, for those of the legs and back. In the Zander 
institutes, which are now estabhshed in Scandinavia, in 
London, Bath, Baden-Baden, and other places, you will find 
that facilities are given for the restoration of muscular power 
in every part of the body. In many cases, you cannot have 
the advantage of such methodical treatment, but you must 
encourage your patient to use the enfeebled muscles, and 
not to let them get further enfeebled by inactivity. 
Kemember that exercise, short of fatigue, is always good for 
muscles. 




Fia. 97. 

Apparatus for regiilated muscular movement of legs and back. 



Among external applications suitable in nervous cases, I 
must not omit to mention mechanical supports. The best 
results are obtained in cases of slow compression of the 
spinal cord in consequence of Pott's disease of the vertebrte. 
The form of support which I generally employ is that com- 
posed of a pelvic piece, with crutches for the shoulder rising 
on each side, and, if necessary, with a curved iron rod, 
supported at the sacrum and fitted with straps, so as to bear 
the weight of the head. I have seen the application of such 
an instrument relieve the patient at once both of j)ain and 
of paralysis. In that case, I suppose, the symptoms were 



MECHANICAL SUPPORTS. 



217 



due to the pressure on the spinal cord of a mere bag of debris, 
resulting from the disintegration of the bodies of the verte- 
br£e. You will rarely meet with this precise condition ; but 
even when the disease has led to meningitis, or to lesion of 
the cord itself, you may obtain recovery by the use of such 
instruments. I once had a patient who exhibited distinctly 
Brown-Sequard's unilateral spinal paralysis, having marked 
motor paralysis on the one side, and loss of sensibility on the 
other. In this case it was clear that serious lesion of the cord 
existed, but he ultimately made a 
perfect recovery, some deformity of 
the spine alone remaining to mark 
the old disease. He suffered a severe 
relapse after having been at sea for 
some time, and was dismissed as 
incurable from an hospital in another 
part of the country ; but by the 
patient use of mechanical supports 
and Faradisation of the muscles of 
the legs, he again made a good, and, 
I beheve, a permanent recovery. 
Sometimes, of course, the lesion in 
the cord is too advanced for recovery 
to take place, but I advise you in 
all cases to give a trial to the 
method, even although there seems 
little hope. The use of Sayre's 
jackets is also often serviceable. 
Your surgical teachers will tell you 
whether they are preferable to the 
older forms of support. I think 
that the employment of an appar- 

■■ • , 1. i 1 fvy 1 Distortion of vertebral column after 

atus WtnCn can be taken on and. recovei-y from caries of cervical verte- 

put on, and easily modified as occa- 

sion arises, has at least some advantage over the fixed case. 

Occasionally you will meet with cases in which the danger 
arises from secondary or compensatory curvature, the primary 
caries having been perhaps in some of the higher cervical 
viertebrse. This having been recovered from, an extraordinary 




Fig. 88. 



218 



SURGICAL TREATMENT. 



curving forwards of the lower cervical and upper dorsal regions 
was gradually developed. I have seen iu such a case many of 
the physical signs of aneurism result from the forward arching 
of the vertebral column, and under treatment with mechanical 
support of the kind described, the urgent symptom.s have 
entirely disappeared (fig. 98). 

In some cases of permanent paralysis, elastic mechanical 
contrivances are useful. For example, in advanced lead 
paralysis, if the extensors of the forearm have undergone 
atrophy, an india-rubber structure may keep the wrist and 
fin gers extended. And in cases of hemiplegia, the movements 
of the arm, and even of the leg, may sometimes be helped 
by similar contrivances. 

(J. ) Surgical methods. Operative interference will help you 
in many conditions. You are familiar with the advantages 
of tenotomy in cases of infantile paralysis. You have also 
seen the good result obtained from acupuncture in obstinate 
cases of sciatica, and from section of nerve, and from excision 
of portions of nerve in severe cases of neuralgia ; and you 
are also acquainted with the extraordinary benefits which in 
some cases result from nerve-stretching. It is true that the 
benefit is usually only temporary, but it is very complete 
while it lasts. Take a case of epileptiform neuralgia, for 
example. The patient has, for years, been tortured with 
frequently recurring paroxsyms of agonising pain. The 
sargeon cuts down upon the nerve, and stretches it. There 
may be pain for a day or two after the operation, but 
speedily there is relief, and perhaps for a year there is no 
return of what had previously recurred every day. Notice 
that in these cases sometimes more than one branch requires 
stretching. A patient who has got rid of infra-orbital pain 
by stretching that branch of the fifth, may still have 
paroxysms originating in the inferior maxillary, and gets 
complete relief only when that branch also has been subjected 
to operation. Do not expect too much from it, but remember 
that, with antiseptic precautions, the operation may be quite 
safely done, and that in a large proportion of cases it relieves 
pain. You must not expect it to do material good in 
locomotor ataxia ; but sometimes even in that disease it 



TREPHINING. 



219 



relieves pain. The plan of stretching without incision— 
that is to say, by forcible movements of the affected parts — 
does not seem to be of much service. 

Eemoval of tumours pressing upon nerves, whether of the 
nature of an exostosis or otherwise, may sometimes give 
rehef in obstinate cases. I have known a patient suffer from 
sciatica for a long period, and be at once cured by the removal 
of a node which pressed upon one of the branches of the 
sciatic nerve. 

Tapping of the cranium has been recommended in cases 
of chronic hydrocephalus. I have seen the operation per- 
foi-med without any injurious efifect, but with no perceptible 
benefit. 

Ligature of the vertebral arteries has been found very 
useful in some cases of epilepsy. Dr. Alexander, of Liver- 
pool, who suggested this operation, states that out of twenty- 
one cases operated on, three remained free from fits for nearly 
a year, nine were very greatly improved, and eight have in 
many respects improved. He considers that it should be 
done in every case so soon as it is apparent that drugs have 
no effect. It is believed that by cutting off the vascular 
supply the irritability of the medulla oblongata and upper 
part of the cord is greatly lessened. 

The last surgical plan of treatment to which I shall refer 
is trephining. No one doubts the advantage of removing in 
this way depressed portions of skull ; but I incline to think 
that two other conditions may warrant this method of opera- 
tion. In some cases in which the occurrence of Jacksonian 
epilepsy, or some other characteristic symptom, enables us to 
determine that there is pressure upon or injury of some 
individual portion of the brain, I believe that we are 
warranted in cutting down, with the antiseptic precautions, 
upon the part — at least in certain cases. An accumulation 
of pus may be evacuated with the effect of permanently 
relieving the patient. In other cases, again, where there is 
violent headache, either accompanied by convulsions or not, 
as in cases of cerebral tumour, trephining sometimes gives 
relief. I once had a patient in the Old Infirmary, who had 
received a severe blow on the head by the falling of a barrel 



220 



TREPHINING. 



on his head from the third or fourth tier of a brewery in 
which he worked. It struck the vertex, and led to a shght 
depression. From that time he began to have occasional fits and 
to suffer from severe headache. His sight also became dim, 
and distinct ophthalmoscopic changes manifested themselves. 
Sir Joseph Lister, who was then in Edinburgh, agreed to 
operate, as we thought it possible there might be a depressed 
fracture of the inner table. A portion was removed, and the 
patient from that time had no recurrence of headache, had 
no convulsive seizure, the fundus of his eye became natural, 
and his sight was completely restored. There was no depres- 
sion of the inner table, and we could not satisfy ourselves 
as to the explanation of this result, but thought that 
the relief might have been due to the diminution of intra- 
cranial tension, in the way that iridectomy relieves a glaucoma. 
Since that time, I have on two or three occasions thought it 
right to try this operation. In the case of a young man, 
who suffered most excruciating headache, with blindness, 
from great effusion into the ventricles, the consequence of 
pressure on the veins of Galen, the distress of the patient 
was so great, that I asked one of my surgical colleagues to 
operate in the hope of giving relief Whenever the piece of 
bone was removed, the dura mater bulged out with extra- 
ordinary prominence, and for some days the patient was freed 
from his distressing pain. Certainly, no bad result followed 
the operation. In other cases there was no relief; but I 
have not had occasion to regret such interference, for I have 
not seen it do harm. I should like you, then, to remember 
that I believe we may be now and again warranted in recom- 
mending such operative interference. 



I 



INDEX. 



INDEX. 



— ♦ — 

Abdominal reflex, 111 
Abducens ocnli, course of, 31. 
Acupuncture, treatment by, 218. 

Acuteness of general sensibility, methods of determining, 64. 
Acuteness of vision, 83 ; metliods of testing, 83. 
Addison's disease, 155. 
^sthesimeter, 64. 
Agraphia, 190. 
Ageusia, 106. 

Airey on eye-symptoms in megrim, 74. 
Allochiria, 69. 
Alternate paralysis, 118. 
Amblyopia, 83. 
Amnesic aphasia, 195. 

Anaemia, localised, from nervous changes, 148. 

AnsBsthesia, cerebral, 9 ; general, 67 ; of hearing, 163 ; of smell, 104 ; of 

taste, 104. 
Ansesthetic leprosy, 156. 

Anatomy, medical, of nervous system, explanation of term, 1. 
Antle-clomis, 114. 
Anosmia, 104. 

Anterior comua, disease through alteration of, 164. 
Anterior roots of spinal nerves, 28. 

Aphasia, 186 et seq. ; amnesic, 195 ; atactic, 195 ; from disease of intelligence 
centre, 187 ; functional, 193 ; localisation of, 193 ; relation of, to 
vascular supply, 204. 

Aphonia, 191. 

Apoplectiform attacks, 175. 

Area of vision, 75. 

Argyll Robertson symptom, 89. 

Artery of cerebral hsjemorrhage, 203. 

Arthropathies from nerve-lesions, 166. 

Articular changes from nerve-lesion, 166. 



224 



INDEX. 



Articitlation reflex centre, 111. 

Articuloruni hydrops intermittens, 167. 

Asphyxia, 174. 

Astigmatism, 90. 

Ataxic or atactic aphasia, 195. 

Athetosis, 125. 

Atrophy, optic, 99 ; progressive muscular, 165. 

Attention, 176. 

Auditory centre, 18. 

Auditory illusions, 103. 

Auditory nerve, 16. 

Auditory nerve-endings, 16. 

Automatic speech, 186 ; cases of, 186 et seq. 

Bamherger, Prof., on saltatory spasm, 125. 
Barnes, Dr., on eclampsia nutans, 125. 
Basal ganglia, 38. 

Bastian, Dr. Charlton, on temperature as modified by nerve-lesion, 149. 
Bed-sore, acute, cerebral, 161 ; spinal, 161. 

Bernard, Claude, on glycosuria, 152, 153 ; on polyuria, 152 ; on salivary 
secretion, 151. 

Betz on histological structure of grey matter of motor area, 25. 
Biesiadecki, drawing of touch corpuscle, 4. 
Bile, secretion of, 151. 

Blaikie, Mr. James, on defects of speech in school children, 190. 

Blindness, 75 ; to colour, 85 ; word, 183. 

Blistering, treatment by, 214. 

Blood-letting, treatment by, 214. 

Bones, alterations in, from nerve-lesions, 167. 

Bottrne\'ille on temperature as modified by nerve-lesion, 149. 

BrUI, Dr., on colour blindness, 85. 

Broadbent, Dr., on bilateral innervation of certain muscles, 119. 
Broca's convolution, 22, 194. 

Brown-Sequard, Dr., on loss of sensibility to impressions, 63. 
Caird, Dr. F., case of cerebral deafness, 182. 

Carj)enter, Dr., on suggestion of ideas through the muscular sense, 71. 
Cataleptic rigidity, 127. 

Caton, Dr., drawings of gangrene from nerve-disease, 160. 

Centres, auditory, 18 ; general sensory, 9 ; gustatory, 19 ; intelhgence, 185 ; 
motor, 21 ; temperature, 149 ; vaso-motor, 149 ; visual, 14 ; word- 
hearing, 183 ; word-seeing, 183. 



INDEX. 



225 



Central scotoma, 78. 

Cerebelliun, afiferent fibres to, 33 ; efferent fibres from, 35 ; ganglia in, 39 ; 

minute structure of, 35. 
Cerebral antestbesia, 9. 
Cerebral breathing, 110. 
Cerebral and mental functions, 170. 
Cerebral vascular supply, 202. 

Charcot on acute bed-sores, 161 ; on dysaesthesia, 68 ; on vascular supply of 

cerebrum, 202. 
Cheyne-Stokes breathing, 110. 
Chilblains, 155. 
Choked disc, 94. 
Choreic movements, 121. 
Choroid, changes in, 100. 

Clarke's column, relation of to sensory nerves, 6 ; relation of to cerebellar 

fibres, 34. 
Clonic spasms, 122. 

Cold, subjective feeling of, 60 ; sensibility to, 64. 
Colour-hearing, 74. 
Colour- vision, 84. 
Coma, 174. 

Commissural fibres, groups of, 39. 

Conduction of impressions, rate of, 66 ; retarded, 69. 

Conduction, lines of motor, 21 ; lines of sensory, 2. 

Congestion from neuro-paralytic changes, 146. 

Conjugate deviation, 131. 

Conjunctiva, end-organs in, 4. 

Consciousness, 170 ; diminution of, 171 ; exaltation of, 170 ; loss of, 174 - 

perversion of, 175. 
Contracture, 127. 
Convulsions, 122. 

Co-ordination, 128 ; failure of, 129. 
Cord, ganglia in spinal, 36. 
Corona radiata, motor fibres of, 26. 
Corrigan's button, treatment by, 214. 

Cortex, sensory centres in, 9 ; gustatory centre in, 19 ; visual centre 
in, 14. 

Coughing, 123, 131 ; reflex centre for. 111. 
Cramp, 126 ; writers', 130. 
Cranial nerves, ganglia on, 36. 
Cremasteric reflex, 111. 

P 



226 



INDEX. 



Crura cerebri, ganglia in, 38 ; motor fibres in, 26 ; sensory fibres in, 8. 
Cyon on glycosuria, 153. 

Davidson, Dr., on dancing mania, 126. 
Deafness, 103 ; cerebral, 182 ; word, 184 

Decussation of muscular sense fibres, 7 ; of optic nerve, 12, 13 ; of pain 
fibres, 7 ; of pyramids, 21 ; of sensory fibres, 7 ; of temperature fibres, 
7 ; of touch fibres, 7. 

Defecation reflex centre. 111. 

Degeneration, reaction of, 142. 

Delayed movement, 120. 

Delirium, 175 ; tremens, 175. 

Delusions, 176. 

Deviation, conjugate, 131. 

Diabetes, 153. 

Diaphoresis, 151 ; coloured, 151. 

Diet, treatment by, 207. 

Dimness of vision, 83. 

Diplopia, 83. 

Drowsiness, 172. 

Dubler on herpes zoster, 154. 

Duchenne's method of using electricity, 132, 211. 

Duret on vascular supply of cerebrum, 201. 

Dynamometer, 116. 

Dysesthesia, general, 68 ; of hearing, 103. 
Dysarthria, 195. 
Dyslalia, 195. 
Dysphasia, 195. 

Ear of insane, 154. 

Eclcer, median aspect of human brain, 10. 
Eckhard on glycosuria, 153. 
Eclampsia nutans, 125. 
Eczema, 155. 
Electric bath, 212. 
Electrical equations, 142. 

Electrical reactions, normal, 141 ; qualitative alterations in, 141 ; quantita- 
tive alterations in, 141. 

Electricity, cautions in using, 145 ; forms of, 132 ; in diagnosis, 132 ; in 
feigned disease, 144 ; in trance, 145 ; in treatment, 210. 

Electrisation, methods of testing amount of reaction to, 140. 



INDEX. 



227 



Electro-motor points, 133. 

Elements, histological, of nervous system, 197. 

Embolism of retinal vessels, 99. 

Emotions, 178. 

Epigastric reflex, 111. 

Erb, Professor, nuclei of cranial nerves, 15 ; on reaction of degeneration 

144 ; on tendon reflex, 113. 
Erectores spinal reflex. 111. 

Erlenmeyer on Leonardo da Vinci's mirror- writing, 192. 
Epilepsy, Jacksonian, 54. 
Erythema, 155. 

Eulenburg on methods of estimating sensibility to pressure, 65. 
Eye symptoms, in megrim, 74 ; in nervous disease generally, 73. 
Exophthalmic goitre, 147. 

Eacial hemiatrophia, 168. 
Eacial nerve, course of, 31. 
Facial spasm, 123. 

Earadism, in diagnosis, 132; methods of estimating amount of reaction, 

140 ; in treatment, 211. 
Eeelings of heat and cold, subjective, 60 ; of numbness, tingling, pins and 

needles, sleeping of a limb, 61 ; of pressure or weight of limbs, 62. 
Ferrier, Professor, on general sensory centre, 9 ; on visual centre, 14 ; on 

auditory centre, 18 ; on motor centres, 21 ; on case of ageusia and 

anosmia, 106 ; on reversed reflex, 112. 
Fibres, difl:erent groups of commissural, 39. 
Fibrillary twitching, 122. 
Fidgets, 70. 
Field of vision, 75. 

Fifth nerve, motor portion of, 29 ; sensory portion of, 15. 
Fillet, 8. 

Flashes of light, 73. 

Formatio reticularis, 8. 

Formication, 60 

Fourth nerve, course of, 29. 

Fritsch and Hitzig on motor centres, 21. 

Fundus, normal, 93. 

Funiculus cuneatus, 9. 

Funiculus gracilis, 8 

Galvanism, in diagnosis, 132 ; methods of use, 139 ; methods of estimating 
amount of reaction, 140 ; in treatment, 211. 



228 



INDEX. 



Gfilvanometer, 140. 

Ganglia, at base of brain, 38 ; in cerebellum, 39 ; in cord, 36 ; in crura 
cerebri, 38 ; in medulla, 37 ; on nerves, cranial and spinal, 36 ; in 
pons, 37. 

Gangrene from nerve-disease, 157. 

Gastric crisis in locomotor ataxia, 152. 

Gastric juice, secretion of, 151. 

General paralysis of the insane, pupil in, 88. 

General sensory centre, situation of, 9. 

Giddiness, 62. 

Girdle-pain, 59. 

Globus hystericus, 62. 

Glosso-pliaryngeal nerve, motor portion of, 31 ; nerve-endings of, 18 ; sensory 

portion of, 19. 
Glossy skin, 156. 
Gluteal reflex, 111. 
Glycosuria, 152. 

Golgi, on histological structure of motor area, 25. 
Goltz, on motor centres, 22 ; on methods of estimating sensibility, 65. 
Gowers, Dr., on saltatory spasm, 125 ; on skin reflexes, 112 ; on tendon 
reflexes, 114. 

Granville, Dr. Mortimer, on vibration in treatment of nervovis disease, 213. 
Gustatory nerve, 19. 

Hsematoma aurium, 154. 

Haemorrhage, artery of cerebral, 203 ; effects of, 200 ; of nervous origin, 154. 
Hair, alterations in colour of, 155 ; loss of, 156 ; alterations in structure of, 155. 
Hallucinations, 175. 

Hamilton, Professor, sections of brain, 43 et seq. 
Hammond, Dr., on athetosis, 125. 
Hay, Professor, case of reflected pain, 59. 
Headache, from eye defects, 89. 

Hearing, acuteness of, 103 ; modifications of, 103 ; subjective sensations, 

100 ; tests of, 103. 
Heat, subjective feeling of, 60 ; sensibility to, 64, 
Hemeralopia, 83. 

Hemianopsia, 80 ; homonymous, heteronymous, 81 ; due to cenli-il 

lesion, 82. 
Hemiatrophia, facial, 168. 
Herpes zoster, 154. 

Heubner, Professor, on vascular supply of cerebrum, 201. 



INDEX. 



229 



Hiccough, 123. 
Hippoccompal region, 9. 

Histological elements of nervous system, 197 ; structure of cortex of cere- 
bellum, 35 ; structure of grey cerebral matter, 24. 
Histrionic spasms, 124. 

Huguenin, sensory band radiating to cortex, 9. 
Hydrops articulorum intermittens, 167. 

Hyperaestliesia, general, 66 ; of bearing, 103 ; of smell, 104 ; of taste, 106. 

Hyperalgesia, 67. 

Hypergeusia, 106. 

Hypermetropia, 90. 

Hyperosmia, 104. 

Hypnotism, 173. 

Hypochondriasis, 175. 

Hypogeusia, 106. 

Hypoglossal nerve, course of, 32. 

Hyposmia, 104. 

Hysterical laughter, 179 ; weeping, 179. 
Hystero-epilepsy, 126. 

Ichthyosis, 155. 

Idiot, ansesthesia in, 68. 

Illusions, 176. 

Impressions, rate of conduction of, 66 ; retarded conduction of, 69 ; sensory, 

varieties of, 7, 63. 
Impulse, irradiation of, 121. 
Infantile paralysis, 164. 

Inflammation of skin through nerve-lesion, 154. 
Insane ear, 154. 
Insomnia, 171. 
Intelligence centre, 185. 

Internal capsule, motor fibres in, 26 ; sensory fibres in, 9. 

Intra-cranial tension, relief of, 220. 

Ireland, Dr., on auEBsthetic patches in idiots, 68. 

Irradiation of impulse, 121. 

Irritability of muscle, increased, 121. 

Jacksonian epilepsy, 54 ; treatment of by trephining, 219. 

Jaundice from nerve-lesion, 153. 

Joints, changes in, from nerve-lesion, 166. 

Judgment, 178. 



230 



INDEX. 



Key and Retzius, end-organs in conjunctiva, 4. 
Knee phenomenon, 113. 

Kocher, on changes induced by extirpation of thyroid gland, 157. 
Kolliker, Pacinian body, 3. 
Krause's end-organ, 4. 

Kussmaul, Professor, case of agraphia, 192 ; case of word-blindness, 
184. 

Landois, Professor, on loss of pigment of hair from nerve-disease, 155. 

Laughter, hysterical, 179. 

Laycock, Professor, on nervous oedema, 153. 

Leonardo da Vinci's mirror- writing, 192. 

Leprosy, anaesthetic, 156. 

Lesions in nervous disease, as dependent on vascular supplj-, 202 ; efl'ects 

of, 200 ; localisation of, 40 ; seats of, 196 ; varieties of, 199. 
Leucoderma, 155. 
Lichen, 155. 

Liebreich, drawing of normal fundus, 92 ; of optic neuritis, 95 ; of oi)tic 

atrophy, 95 ; of embolism of retinal vessels, 98. 
Ligature of vertebral artery, treatment by, 219. 
Ling, treatment by regulated muscular exercise, 215. 
Lister, Sir J., case of trephining, 220. 

Localisation of nervous lesions, 40 ; of lesion in aphasia, 193. 
Lordat, Professor, case of aphasia, 188. 
Ludwig, Professor, on secretory changes, 150. 

Macleod, Dr. M. D., on infantile paralysis from brain disease, 1 65. 
Malarial influence in nervous disease, 209. 
Marginal scotoma, 80. 
Massage, treatment hj, 313. 
Mechanical supports, treatment by, 216. 

Medulla oblongata, ganglia in, 37 ; motor fibres in, 26 ; sensory fibres 
in, 8. 

Megrim, 148 ; eye symptoms in, 74. 
Memory, 176. 
M'Hardy's perimeter, 76. 
Mictitrition, 107. 
Mimic spasm, 124. 
Mirror-writing, 192. 

Mitchell, Dr. Weir, on glossy skin, 156 ; on massage, 213. 
MoUe, on sensory centres, 9. 



INDEX. 



231 



Moos, Professor, case of deafness to liigli notes, 104. 
Moral sentiments, 1 79. 
Motion, voluntary, 116. 
Motor centres, 21. 

Motor fibres in corona radiata, 26 ; in internal capsule, 26 ; in crura 

cerebri, 26 ; in pons, 26 ; in medulla, 26 ; in spinal cord, 26. 
Motor functions, 107. 
Motor lines of conduction, 21. 
Motor nerve-endings, 29. 
Motor oculi nerve, 29. 
Motor points, electrical, 133. 
Motor roots of spinal nerves, 29. 
Munk, on sensory centres, 9 ; on visual centre, 14. 
Muscae volitantes, 73. 

Muscle, weakness from disease of, 120 ; increased irritability of, 12h 
Muscular atrophy, 163 ; progressive, 165. 
Muscular power, tests of, 116 ; modifications of, 117. 

Muscular sense, 70 ; modes of testing, 70 ; increase of, 71 ; diminution of, 71 ; 

fibres, decussation of, 9. 
Mydriasis, 89. 
Myoidema, 122. 
Myopia, 90. 
Myosis, 88. 

Myotatic contraction, 113. 
Myxoedema, 156. 

Nails, alterations of, 155. 

Nerve, abdiicens oculi, 31 ; auditory, 16 ; facial, 31 ; fifth, sensory portion 
of, 15 ; fifth, motor portion of, 29 ; fourth, 29 ; glosso-pharyngeal, 
sensory portion of, 18 ; glosso-pharyngeal, motor portion of, 31 ; hypo- 
glossal, 32 ; motor oculi, 29 ; olfactory, 10 ; optic, 12 ; pneumogastric 
19, 31 ; seventh, 31 ; sixth, 31 ; spinal accessory, 32 ; third, 29 ; 
trochlear, 29 ; vagus, motor portion of, 31 ; vagus, sensory portion of, 19. 

Nerve-ceUs, 197. 

Nerve-endings, auditory, 16 ; gustatory, 18 ; in muscle, 29 ; olfactory, 10 ; 

optic, 12 ; sensory, 2. 
Nerve-fibres, 199. 

Nerves, cranial, ganglia on, 36 ; spinal, ganglia on, 36. 
Nerve-stretching, treatment by, 218. 

Nettleship, pupillometer, 88 ; tests for acuteness of vision, 83 ; for colour 
vision, 84 ; for astigmatism, 90. 



232 



INDEX. 



Neuralgia from eye defects, 89. 
Neuritis, optic, 94. 
Neuroglia, 199. 
Neuro-paralytic changes, 146. 

Nieineyer, Professor, case of diminution of muscular sense, 71 ; case of 

loss of co-ordination, 129. 
Notlinagel, Professor, on tremor, 122. 

Nuclei, of auditory nerve, 17 ; of facial, 31 ; of fifth, 15, 30 ; of fourth, 29 ; 
of glosso-pharyngeal, 19, 31 ; of hypoglossal, 32 ; of pneumogastric or 
vagus, 19, 31 ; of sixth, 31 ; of spinal accessory, 32 ; of third, 29. 

Numbness, subjective feeling of, 61. 

Nutrients, treatment by, 208. 

Nyctalopia, 83. 

Nystagmus, 131. 

(Edema, nervous, 153. 

Ogle, Dr., on anosmia with aphasia, 105. 

Olfactory centre, 12. 

Olfactory nerve, 10. 

Olfactory nerve-endings, 10. 

Operative treatment in nervous disease, 218. 

Ophthalmoscope, use of, 93. 

Ophthalmoscopic appearances in health, 93 ; in optic neuritis, 94 ; in optic 
atrophy, 99 ; in embolism of retinal vessels, 99 ; in tubercle of choroid, 
100. 

Optic atrophy, 99. 
Optic commissiire, 12. 
Optic neuritis, 94. 

Optic nerve, course of, 12 ; decussation of, 12, 13. 
Optic nerve-endings, 12. 

Ord, Dr., on loss of muscular power in rheimiatism, 164. 
Organic reflexes, 107. 

Origin of spinal motor nerves, 28 ; of cranial nerves {vide separate headings). 
Pacinian bodies, 2. 

Pacquelin's cautery, treatment by, 214. 
Paget, Sir J., on glossy skin, 156. 
Pain fibres, decussation of, 7. 
Pain, girdle, 59. 

Pain, sensibility to, 66 ; subjective, 57 ; varieties and seats of subjective, 58. 
Papillitis, 94. 



INDEX. 



233 



Paradoxical contraction, 116. 

Pai-alysis, 117 ; alternate, 118 ; from disease of cerebrum, 119 ; from 
disease of cord, 118 ; from disease of crura cerebri, 119 ; from disease 
of internal capsule, 119 ; from disease of medulla, 118 ; from disease 
of nerve, 118; from disease of pons, 118; infantile, 164; pseudo- 
hypertrophic, 165. 

Paresis, 119 ; from disease of muscle, 120. 

Parturition reflex centre, 111. 

Patellar tendon reflex, 113. 

Pellagra, 156. 

Pemphigi^s, 155. 

Perforating ulcer of foot, 162. 

Perimeter, M'Hard/s, 76. 

Perspiration, alterations in, 151. 

Pigmentation, dependent on nerve influence, 155. 

Pins and needles, subjective feelings of, 61. 

Plantar r efl ex. 111. 

Play fair. Dr., on massage, 213. 

Pneumogastric nerve, course of, 19, 31. 

Poliomyelitis anterior acuta, 164. 

Polysesthesia, 169. 

Polyuria, 152. 

Pons, ganglia in, 37 ; motor fibres in, 26 ; sensory fibres in, 8 ; vascular- 

si;pply of, 205. 
Posterior roots of spinal nerves, 5. 
Pressure, feeling of, in limbs, 62 ; sensibility to, 65. 
Progressive muscular atrophy, 165. 
Pseudo-hypertro]Dhic paralysis, 166. 
Pseudo-phlegmon, 155. 

Pupil, contraction of, 88 ; dilatation of, 89 ; in general paralysis of insane, 

88 ; innervation of, 88 ; irregularity of, 88 ; measurement of, 88. 
Pupil dilatation centre. 111. 
Pupillometer, 88. 
Pyramidal tracts, 26. 
Pyramids, decussation of, 26. 

Ranvier, nodes of, 197. 

Raymond and Artaud on hypoglossal nerve, 32. 
Raynaud's disease, 162. 
Reaction of degeneration, 142. 
Recollection, 177. 



234 



INDEX. 



Eeflexes, 107 ; abdominal, 111 ; cremasteric, 111 ; epigastric, 111 ; of 
erectores spinre, 112 ; gluteal, 111 ; organic, 107 ; plantar, 111 ; respir- 
atory, 108 ; scapular, 112 ; skin, 111 ; tendon, 112. 

Keflex speech, 186. 

Eemak's commutator, 212. 

Eesistance of tissues, 140. 

Eespiratory reflex, 108. 

Eetardation of conduction of impressions, 69. 

Eetina, changes in, 100. 

Eigidity, cataleptic, 127. 

Eitchie, Dr. James, schema of lines of motor and sensory conduction, 8. 

Eolando, substantia gelatinosa of, 5, 

Eoots of spinal nerves, sensory, 5 ; motor, 28. 

Eiidinger, auditory nerve-ending in vestibule, 17. 

Saliva, alterations in secretion of, 150. 
Saltatory spasm, 125. 
Sayre's jacket, 217. 
Scanning utterances, 190. 
Scapular reflex. 111. 
Schiff on glycosuria, 153. 
Schmidt, case of word-deafness, 184. 

Schultze, Max, nerve-ending in cornea, 5 ; oKactory nerve-ending, 11. 
Schwalbe, on fifth nerve, 30. 

Scotoma, central, 78 ; marginal, 79 ; in patches, 80. 

Seats of lesion in nervous disease, 196. 

Secretory changes, 150. 

Sedatives, treatment by, 208. 

Seeligmiiller, on nervous dropsy of joints, 167. 

Sensations, subjective, 57 ; peculiar visceral, 62. 

Sense, muscular, 70 ; modes of testing muscular, 70 ; alterations of mus- 
cular, 71. 

Sensibility, methods of determining acuteness of, 64 ; to pain, 66. 

Sensory centre, 9. 

Sensory conduction, line of, 2. 

Sensory fibres, decussation of, 7 ; in cord, 6 ; in crura cerebri, 9 ; in 

internal capsule, 9 ; in medulla, 8 ; in pons, 8 ; in tegmentum, 9. 
Sensory impressions, varieties of, 63. 
Sensory nerve-endings, 2. 
Sensory roots of spinal nerves, 5. 
Sentiments, moral, 179. 



INDEX. 



235 



Seton, treatment by, 214. 
Seventh nerve, course of, 31. 
Sexual action, reilcx centre for, 111. 
Sickness, sleep, 172. 
Sixth nerve, course of, 31. 
Skin, glossy, 156. 

Skin reflexes. 111 ; increase of, 112 ; diminution of, 112. 
Sleep, 171. 

Sleeping of a limb, subjective feeling of, 61. 

Sleep-sickness, 172. 

Smell, 104 ; acuteness of, 104. 

Sneezing reflex centre. 111. 

Snellen, tests for acuteness of vision, 83. 

Somnambulism, 174. 

Somniloquy, 174. 

Spasms, 122 ; clonic, 122 ; mimic or histrionic, 123 ; tonic, 124 ; sal- 
tatory, 125. 
Specifics, treatment by, 209. 

Speech, automatic or reflex, 186 ; cases of, 186 et seq. 

Speech relationships, alteration of, 180 ; diagrammatic scheme of, 181. 

Spinal accessory nerve, coiu'se of, 32. 

Spinal cord, course of motor fibres in, 26 ; course of sensory fibres in, 6. 

Spinal nerves, anterior roots, 28 ; posterior roots, 5 . 

Staccato utterance, 190. 

Starr, Dr. Allen, on hemianopsia, 82. 

Stilling on course of sensory fibres in cord, 6. 

Stimulants, treatment by, 208. 

Stirling, A. B., preparation of taste-bulbs, 19. 

Stomach and intestines, centres connected with. 111. 

Stupor, 174. 

Subjective eye-symptoms, 73. 

Subjective feeling of heat and cold, 60 ; of numbness, 61 ; of pain, 57 ; of 
pins and needles, 61 ; of pressure or weight of a limb, 62 ; of sleeping 
of a limb, 61 ; of tingling, 61. 

Subjective sensations, 57. 

Substantia gelattnosa of Kolando, 5. 

Siirgical methods, treatment by, 216. 

Swedish method of treatment, 215. 

Symbols used in electrisation, 139. 

Sympathetic system , 54. 

Syncope, 174. 



236 



INDEX. 



Tache cerebrale, 148. 

Tapping cranium, treatment by, 219. 

Taste, 105 ; acuteness of, 105; alteratiuns of, 105. 

Taste-bulbs, 18. 

Teeth, changes in, 156. 

Temperature, 149 ; alterations of, from nerve-inlluence, 149 ; fibres, decus- 
sation of, 7 ; sense of, 65 ; methods of estimating sensibility to, 65. 
Tendon reflexes, 113 ; increase of, 113 ; loss of, 113 ; theory of, 114. 
Tetany, 125. 

Thii-d nerve, course of, 29. 
Thomsen's disease, 120. 

Thyroid gland, changes induced by extirpation of, 157. 

Tickling, sensibility to, 66. 

Tingling, subjective feeling of, 61. 

Tinnitus aurium, 100. 

Tonics, treatment by, 208. 

Torpor, 174. 

Touch corpuscles, 3. 

Touch fibres, decussation of, 7. 

Trade spasm, 130. 

Trance, 172. 

Treatment of nervous disease, 205 ; by blistering, 214 ; by blood-letting, 214 ; 
by counter irritation, 214 ; by diet and general management, 207 ; by 
electricity, 210 ; by external applications, 213 ; bj' internal medicines, 
208; by massage, 213; by mechanical supports, 217; by moral 
influence, 207 ; by nutrients, 208 ; by regulated muscidar exercise, 
214 ; by sedatives, 208 ; by specifics, 209 ; by stimulants, 208 ; by 
surgical methods, 218 ; by tapping craniimi, 219 ; by tonics, 208 ; by 
trephining, 219 ; general, 205 ; preventive, 205. 

Tremor, 121. 

Trephining, treatment by, 219. 
Tripier on sensory centres, 9. 
Trochlear nerve, course of, 29. 
Trousseau on tache cerebrale, 148. 
Tubercle of choroid, 100. 

Turner, Professor, on relation of skull to convolutions, 52 ; taste- 
bulbs, 19. 

Ulcer of foot, perforating, 162. 
Ulceration from nerve-lesion, 161. 
Underbill, Dr., case of excessive sleep, 172. 



INDEX. 



237 



Upbringing of neurotic cliildren, 206. 
Urine, alterations in secretion of, from nerve disease, 154. 
Urticaria, factitious, 148 ; of nervous origin, 155. 
Utterance, staccato, 190 ; scanning, 190. 

Vascular distribution in relation to nervous disease, 201. 
Vaso-motor centre, 149 ; reflex, 111. 
Vagus, motor portion of, 31 ; sensory portion of, 19. 
Vertigo, 62. 

Visceral sensations, peculiar, 62. 
Vision, colour, 84. 
Vision, field of normal, 75. 
Visual centre, 14. 
Voluntary motion, 116. 
Vomiting reflex centre, 111. 

Wagner and Meissner's touch corpuscles, 3. 

"Waldeyer, Professor, auditory nerve-endings, 16. 

Weber on sensibility to pressure, 64. 

Weeping, hysterical, 179. 

Weight in limbs, subjective feeling of, 62. 

Wernicke on word-hearing and word-seeing centre, 194. 

Westphal, Prof, on tendon reflex, 113 ; on paradoxical contraction, 115. 

WiU, 178. 

Will, Dr. Ogilvie, case of unilateral sweating, 151. 

Word-blindness, 183. 

Word-deafness, 184. 

Word-hearing centre, 183, 194. 

Word-seeing centre, 183, 194. 

Writers' spasm, 130. 

Writing, mirror, 192. 

Writing, modification of power of, 190. 

Zander institutes, 216. 

Zander, treatment by regulated muscular exercise, 215. 

Ziemssen, Prof., on method of using electricity, 133 ; motor points, 133. 



I.ORIMEK AND GILLIES, I'RINTERS, 31 ST. ANDREW SQUARE, EDINBURGH. 



Preparing for Publication, Third Edition. 
A PRACTICAL TREATISE 

ON 

BRIGHT'S DISEASES OF THE KIDNEYS. 

By THOMAS GRAINGER STEWART, 

M.D., F.RC.P.E., F.E.S.E., 

Physician in Ordinary to Her Majesty the Queen for Scotland ; Professoe . 
OP the Practice op Physio and of Clinical Medicine in the 
University op Edinburgh. 



"... An excellent contribiition to the subject of renal disease." — Edinburgh 
Medical Journal. 

" It is written from first-hand knowledge, and is indispensable to the student." 
— Westminster Review. 

" It is with pleasure we turn to this book, for it is a record of good work care- 
fully and well done, impressed throughout with the marks of original thought. 
But it is more, for it contains also, duly amalgamated, the conclusions of brother- 
workers on the subject." — Medical Times and Gazette. 



Preparing for Publication, in Demy 8vo, 

CLINICAL LECTURES 

ON 

IMPORTANT SYMPTOMS. 

By THOMAS GRAINGER STEWART, 

M.D., F.R.C.P.E., E.E.S.E., 

Physician in Ordinary to Her Majesty the Queen for Scotland ; Professor 
OF THE Practice of Physic and of Clinical Medicine in the 
University of Edinburgh. 



A few of the Lectures will be Published separately. 



No. L— GIDDINESS. Ready, Price Js. 6d. 

"These Lectures on Giddiness would be exceedingly useful reading for any 
student preparing for one of the higher examinations in medicine, as the subject 
is treated in a more complete way than in any text-book with which we are 
acquainted, and as, after reading of Giddiness as a symptom of so many and 
such diverse diseases, a review of the subject from a different point would greatly 
assist in fixing the facts in the memory." — The British Medical Journal. 



EDINBURGH : BELL & BRADFUTE, 12 BANK STREET. 
LONDON ; SIMPKIN, MAESHALL & CO. 



Jtost Published, Second Edition, in Crown 8vo, 10s. 6d. 

MEDICAL DIAGNOSIS: 

A MANUAL OF CLINICAL METHODS. 
By J. GRAHAM BROWN, M.D., 

FELLOW OF THE ROYAL COLLEGE OF PHYSICIANS OP EDINBURGH ; 
LATE SfiNIOK PRESIDENT OF THE ROYAL MEDICAL SOCIETY OF EDINBURGH. 



"A clearness and completeness which is not to be found in any book of the kind 
with which we are acquainted. Indeed, the amount of information which the 
author has succeeded in compressing into so small a space, and that without any 
appearance of overcrowding, is astonishing. It is difficult to choose out any 
part of this book for special notice, since it is distinguished throughout by the same 
clearness and completeness. ... A valuable addition to medical literature, and 
we heartily recommend it to the notice both of students and of physicians." — 
British Medical Journal. 

" The author of this manual deserves the thanks of all clinical students (and we 
may add of teachers also) for the excellent work he has produced. We have been 
extremely pleased with the accuracy of the statements it contains, no less with 
the careful and methodical way in which the whole book is planned ; and we may 
predict for it considerable popularity in a field which has been long occupied by 
works far inferior to it in thoroughness and exactitude." — The Lancet. 

" We can congratulate the author on the thorough and cotnplete manner in 
which he has performed his task. . . . The range of Medicine is now so vast, that 
to master all the various methods of physical examination in the short time allowed 
for the student's curriculum is becoming a matter of real difficulty : hence the 
publication of a work which, in the compass of a single, not large, volume, embraces 
almost every known method of investigation is a most timely occurrence." — 
Medical Times. 

" We should be glad to learn that this excellent guide to clinical work was 
accepted as the basis of every medical student's labours in the wards of hospitals. 
It is admirably adapted to assist the acquisition of ideas in regard to system and 
detail, which is often painfully conspicuous by the utter want of them displayed by 
clinical assistants and ' clerks.' " — The Medical News. 

" On voit que cet ouvrage, qui d'ailleurs est trfes au courant de la science, n'est 
pas une simple compilation, mais qu'il renferme des parties vraiment originales." 
— Revue de Midecine. 

EDINBURGH : BELL & BRADFUTE, 12 BANK STREET. 
LONDON : SIMPKIN, MARSHALL & CO.