1874 Wernicke The Symptom Complex of Aphasia

1874, Wernicke, The Symptom Complex of Aphasia
.J1IODRRX· CLI.NICAL ~IR])IC/~VE
DISEASES
OF THE
NERVOUS SYSTEM
EDITED BY
ARCHIBALD CHURCH, M.n.

PKOF.~'R OF lO:RVO!:K ANI> MENTAl. DISEASES AND MEDll.'AJ. JIlRIflPRtrllKNCE
.sOBTHWESTERN l'NIVEB8ITY MEDICAL DEPARTMENT
CHICAGO, ILLINOII!
A:oi AUTHORIZED TRANSI.ATIO~ FR031 .. DIE DEUTSCHE KLINIK"

UNDER THE GENERAL El>ITORIAL SUPERVISION OF
JULlt;S L, SALINGER, M.D,
lVITLI ONN lIFSbIlED AND NISETY-PlVE ILLfTSTRATIONS

IN TlJE TEXT AND "'IVE COLORED PLATES
NEW YORK' AND LONDON

D. APPI.ETON AND COl\1PA~Y
190R
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HARVARD MED,eA1. UIRARY
IN ThE
FRANCIS A. COUNtWAY
LIBRAAY OF MEDICINE
COPYRIGHT, 1907, BY
D. APPLETON AND <"'OMPANY
PRINTED A.T THE A.PPLETON PRESII

NEW YOBlt, U. 8. A.
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EDITOR'S PREFACE
EVERY practitioner must have been frequently impressed with thc inade-
quacy of the usual text book description of the various diseases with which
he is brought into contact. Even books of reference do not always give thc
scope to special topics that are requisite to place the physician in a satisfac-
tory position relative to any particular disease he may be called upon to treat.
The articles on nervous diseases embraced within this volume meet this actual
want in a manner so admirable that it is a satisfaction to have been associated
with their production in English. To the beginning practitioner to some
extent they supply the place of personal experience, and even to the specialist
they furnish a most admirable resume and guide.
The various subjects having been assigned to men of known experience,
with large opportunities for their study, insured a presentation that is essen-
tially practical and embraces the value of an authoritative personality. The
manner in which the subject matter is presented also appeals to the medical
reader, and while the statements are carefully made they are marshalled in
an interesting and instructive fashion.
One is struck throughout the book with the fact that while Germany is
supposed to be the land of therapeutic nihilism these various authors have
found therapeutics of real help and afford the reader the benefit of their
experience and judgment in this important branch of practice.
At first the editorial work was taken up with the expectation of· making
numerous addenda to the text, but when the proper scope of thc work was
realized it was deemed expedient to let eaeh author stand responsible for thc
t'ubject mattcr which he had personally presented and not to confusc thc
medical J"l'llder by discussions of disputed and unesscntial features.
AltClllBALD CHURCH.
PuLLIIAN BUILDING,
Chicago, nt.
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LIST OF CONTRIBUTIONS
TIle .\Iacroscopic Anatomy of the Central Nenw/ls System, with Special Ref-
erence to tlte Physiology of the Brain. By M. ROTHMANX. Berlin.
Surmal and Pathological Histology of the Central Ner'votls System, with
Special Reference to the Netlron Theory. By H. ROSIN, Berlin.
General Neurological Dia!lnosis, Including, the Examination of l'atienlswith
Diseases of the NervotlS System. By P. SCHUSTER, Berlin.
Modem Aids in tlte Diagnosis of Diseases of the Brain. By E. REDi.WH,
Vienna.
l.umbar Puncture. By H. QUINCKE, Kiel.
Cerebral II emorrlwge and Embolism. By R. GElOEL, Wiirzlmrg.
The Symptom-Complex of Aphasia. By C. WEUNICKE, Brcslau.
The Nature and the Treatment of Disturbances of Speech. By H. GUTZ-
MANN, Berlin.
Xeoplasms of the Spinal Cord and of its Membranes. By Fu. SCHULTZE,
Bonn.
jlyelitis. By E. v. LEYDEN and P. LAZARUS, Berlin.
Tabes Dorsalis (Gray Degeneration of the Posterior C'oltlmn.~ of the S[nnal
C()f'd: Ataxic Locomotrice Progressive; Locomotor Ataxia). By WIL-
HELM ERB, Heidclbt·rg.
Multiple Sclerosis. By E. REDLICH. Vienna.
Syringomyelia. By Fu. SCHULTZE, Bonn.
Hereditary Ataxia (Friedreich's Disease). By H. LO'l'IIJI;, ErlangcIl.
Spastic Spinal Paralysis, and Hereditary Spastic Spinal. Paraly.~is. By
E. REDLICH, Vienna.
Progressive J/tlScular Atrophy (Dystrophy), Progressive Spinal Muscular
Atrophy and Bulbar Paralysis. By FR. SCHULTZE, Bonn.
Paralyses of the Peripheral Nerves. By M. BERNHAUDT Berlin.
X euritis and Polyneuritis. By R. CASSIRER, Berlin .
...\" euralgia. By H. EICHHORST, ZUrich.
Heodache alld Migraine. By L. EDINGER, Frankfort-on-thc-lfain.
Paralysis Agitans (Parkinson's Disease). By W. ERB, Heidelberg.
Athetosis. By L. v. FRANKL-HoCHWART, Vienna.
Tetany of Adults. By L. v. FRA,NKL-HoCHWART, Vienna.
vii
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viii LIST OF CO~TRIBUTIONi:;
Thomsen's Disease (Myotonia Congenita). By L. v. FRANKL-HoCHWART,

Vienna.
Localized Spasm. By E. REMAK, Berlin.
The Present Status of Graves' Disease (Exophthalmic Goiter, Ba.sedouls
Disease). By A. EULBNBURO, Berlin.
Sexual Neurasthenia. By A. EULENBURO, Berlin.
Epilepsy. By W. VORKASTNER, Berlin.
Hysteria. By TH. ZIEHEN, Berlin.
Traumatic Neuroses. By P. SCHUSTER, Berlin.
Vasomotor Trophic Neuroses. By R. CASSIUER, Berlin.
Occupation Neuroses. By H. CASSIREU, Berlin.
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CONTENTS
PAGE
THE }'IACROSCOPIC ANATOMY OF THE CENTRAL NERVOUS SYSTEM WITH SPECIAL
REFERENCE TO THE PHYSIOLOGY OF THE BRAIN 1
NORMAL AND PATHOLOGICAL HISTOLOGY OF THE CENTRAL NERVOUS .sYSTEM, WITH
SPECIAL REFERENCE TO THE NEURON THEORY • 34
I. Preliminary Remarks: The Histologic Components of the Nervous System 35
....1. The Nerve Tissue 35
B. The Supporting Substance (The Gray or Vesicular Substance) 42
II. The Grouping of the Nervous Substance and the Neuron Theory 44
111. The Fibrillre Theory. (Neuro-Fibrils) 46
IV. Neuron Systems and Neuron Diseases 47
.4. The Motor Tract 48
1. The First Motor Neuron 48
2. The Second Motor Neurons 60
B. Di~ of the Motor Tract . 69
1. Diseases of the First Motor Neuron . 70
2. Diseases of Both Motor Neurons 72
C. The Sensory Tract . 73
1. The First Sensory Neuron . 73
2. The Second Sensory Neuron 86
3. The Third Sensory Neuron 97
D. Diseases of the Sensory Neurons. Tabes Dorsalis 100
E. Other Known Tracts in the Central Nervous System 103
1. In the Cerebrum and Peduncles of the Brain . 103
2. In the Cerebellum 107
F. Neuron Diseases of the Cerebellum. Friedreich'/l Ataxia 112
G. Combined System Diseases 113
V. Other Diseases of the Central Nervous System 113
A. Acute Myelitis, Encephalitis, and Acute Softening 114
B. Acute Poliomyelitis 117
C. Acute Bulbar Paralysis. 118
D. Chronic Myelitis and Encephalitis 118
E. Chronic Poliomyelitis 119
F. Multiple Sclerosis . 120
G. Secondary Degenerations 120
1. Secondary Descending Degeneration of the Spinal Cord 122
2. Ascending Degenm:ation in the Spinal Cord 124
3. Secondary Degeneration in the Brain 125
H. Syphilis of the Nervous System . 125
GENERAL NEl1ROLOGICAL DIAGNOSIS INCLUDING THE EXAMINATION OF PATIENTS WITH
DIsEAl'ES OF THE NERVOUS SYSTEM 129
Introduction . 129
History (Anamnesis) 130
ix
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x CONTENTS
PAlir.
The Present Condition (Status Prresens) 131i
. The Skull and the Vertebral Column 137
Vasomotor and Trophic Disturbances . 141
Motility 149
Examination of Coordination of Muscular Movements 16H
Involuntary Motor Symptoms 175
Epileptic and Hysteric Spasmodic Attacks 179
Examination of the Sensory Functions and of Sensation 183
Examination of the Optic Nerve . 184
Examination of the Sense of Smell 187
Examination of the Sense of Taste 188
Examination of the Sense of Hearing 159
Sensory Conditions of the Skin 190
Sensibility of the Deeper Tissues 194
Examination of the Reflexes 196
The Tendon Reflexes 196
Cutaneous Reflexes . 202
The Internal Reflexes 20t)
MODERN AIDB IN THE DIAGNOSIS OF DIIIEABEII OF THY. BUAIS 213
LUMBAR PuscruRE . 223
CEREBRAL HEMORRHAGE AND EMBOLISM 258
THE SYlIPl'OM-COMPLEX OF APHASIA . 26.')
I. Disturbances of Phonetic Speech 265
II. Disturbances of Written Language and General Pathology of Speech Dis-
turbances . 2114
Treatment. 323
THE NATURE AND THE TREATMENT OF DISTURBANCES OF SPEECH 321i
Peripheral Impressive Disturbances 325
Central Disturbances: Stammering 333
Peripheral Expressive Disturbances 343
NEOPLASMS OF THE SPINAL CORD AND OF ITS MEMBRANI!l8 347
Varieties of Neoplasms 347
SymptoInatology 348
The Seat, Extension and Composition 352
Treatment 369
MYELITIS 371
History 371
Pathological Anat.omy 372
The Clinical Picture . 382
The L'linical Picture of Dorsal Myelitis . 384
1. ProdroInaI Stage . 384
2. The Stage of Paralysis 386
3. Stage of Regeneration 403
4. Termination of Myelitis 403
The Segmentary Lol'Blization of the FIID!,tion of Motion 404
Spinal Localization of the Motor Functions 406
Spinal Localization of the Reflexes 409
Transverse Diagnosis 410
1. Cervical Myelitis 413
2. Lumbar Myelitis 417
3. Sarral Myelitis 418
4. Diseases of the Cauda Equina 423
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coNTENTS xi
"AU.,;
Etiology of Acute MyelitiH 424
Differential Diagn08is 428
Prognosis of Myelitis 432
Therapy of Myelitis 433
1. Prophylaxis 433
Treatment . 434
TABEIl DoRSALIS ·l51
1. Introduction and History 4.51
11. Etiology (The Causes of Tabes) 454
Ill. Symptomatology 471
IV. Pathological Anatomy 494
V. Pathologic Physiology of Tabes. Pathogenesis of the Different SymptomH 508
VI. Course, Termination, and Definite Forms of Tabes 521
VII. Diagnosis . 527
VIII. Prognosis 53:!
IX. Treatment . 534
MULTIPLE SCLEROSIS 557
Etiology 5.58
Symptomatology fm3
Course .570
Pathology . 570
Diflerential DiagllOtlis .57/;
Prognosis . .580
Treatment . 5RO
SYRINGOMYELIA 58:!
Symptomatology .592
Course and Prognosis 605
Occurrence and Etiology 606
DiagnOBis and Differential Diagnosis 607
Treatment . 611
HEREDITARY ATAXIA (FRIEDREICU'8 DI8KA8K) • 612
Clinical Course . 613
Pathological Anatomy and Histology 61.5
Pathogenesis 620
Etiology 623
Differential Diagnosis 623
Prognosis, Course and Treatment 625
SP.U!TIC SPINAL PARALYSIS, AND Ht:REIJITAIIY SPASTIC SI'lSAL PARALYSIS 627
Symptoms 628
Pathology 6214
Diagnosis 629
Treatment . 632
PaooR1!'.I!II1\·X ~IUSCULAR ATROPHY (DVSTltuPHY), l'RU(lREI!8IVP; /iPIN.\L MI1RGUI.AR
ATROPHY AND BULBAR PARALYSIS 633
1. Progressive Dystrophy (Myopathie Primitive, of the French) . 63:i
2. Progressive Neurotic Muscular Atrophy 646
3. Progre8lJive Spinal Muscular Atrophy with and without Bulhar ParalYHis 64!1
(0) Infantile Hereditary Form (Werdnig-Hoffmann) . 64!)
(b) Progre8lJive Spinal Amyotrophy, Aran-Dul"henne Type 6.52
(c) Chronic Anterior Poliomyelitis . . . . . 654
-l Amyotrophic l.ateral Sclerosis and Amyotrophic Progressive Bulbar Paralysis
(Charoot', Dieeaae) • . 6.56
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xii CONTENTS
rA..G~
P ARAL Y818 OF THE PERIPHEItAL N EItVES 662

1. Paralysis of the Facial Nerve . 662
Pathology 671
2. Paralysis of the Trigeminal Nerve 676
3. Glossopharyngeal Paralysis 681
4. Paralysis of the Pneumogastric Kerve 683
5. Paralysis of the Spinal Accessory Nerve 687
6. Paralysis of the Hypoglossal Nerve 690
7. Multiple Cerebral Nerve Paralysis . 693
8. Paralysis of the Diaphragm 695
9. Paralysis of the Suprascapular and Postscapular Xerves 698
10. Paralysis of the Anterior Thoracic and Subscapular Nerves 700
11. Paralysis of the Thoracicus Longus Nerve 701
12. Paralysis of the Axillary Nerve 70i>
13. Paralysis of the Musculocutaneous Nerve 707
14. Musculospiral Paralysis 70S
15. Paralysis of the Ulnar Nerve . 712
16. Paralysis of the Median Nerve 715
17. Combined Paralysill of the Nerves of the Arm and Shoulder 7UI
18. Paralysis of the Muscles of the Back, Neck, and Abdomen 724
19. Paralysis of the Crural Nerve 726
20. Paralysis of the Obturator Nerve . 728
21. Paralysis of the External Cutaneous Femoral Nervc 72U
22. Paralysis of the Superior and Inferior Gluteal Nervcs and of thc 1'1I"tt.·rillr
Cutaneous Femoral Nerves. no
23. Paralysis of the Sciatic Nerve. n1
(n) Paralysis of the Peroneal Nerve 7:32
(b) Paralysis of the Tibial Nerve 733
24. Paralysis in the Course of the Pudendic and Co('cygcal PlexutICs 736
NEURITllI ASD POLYNEURITIS 742
Neuritis 742
Symptoms 771
Diagnosis 774
Treatment 77·1
Pathology 777
Polyneuritis . 7X2
Symptomll 7xa
Pathology XVi
Treatment R26
NEUltAWIA S2X
Symptoms . 821-:
Disturbances of Taelile Senile S:i3
Diagnosis 835
Etiology 836
Treatment 84.'>
HEADACHE AND MIGItAI="1E 8M
Differentiation of True Headache 8.51
CauSl'>!, Course, and Treatment 8.'>6
Headache of Children &56
Headache of Adolescents . 8,5R •
Headache of the Anemic . 859
Headache, Vasoparalytic . 861
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CONTENTS XllI
PAUl!;
Headache due to Organic Cau:;c 863
Headache, Indurative 863
Headache, Syphilitic 869
MIGRAINE , 870
The Theory of Headache 87S
PARALY8I8 AGITANS 880
Definition 881
Etiology 881
Symptoms 884
Course 889
Pathology 889
Diagnosis 893
Prognosis 89S
Treatment 89S
ATHETOSIS, 899
Pathology 902
TETANY OF ADULTS 907
History 907
Etiology 911
Symptoms 914
Diagnosis 918
Prognosis 919
Pathology 920
Treatment 920
THOlfSEX'S DISEASE 922
Etiology 921)
Symptoms . 926
Pathology . 929
Diagnosis , 930
locALIZED SPASM 933
Differentiation of Forms , 934
Symptomatology 936
Etiology
Course
.' 938
9:i9
Treatment U39
Clinical Varieties !HO
TilE PRESENT STATUS OF GRAVE:;' DU';.:AS.; U60
Symptomatology !XH
Diagnosis , 962
Theories Concerning Graves' Disease 96a
Treatment. 970
SzxCAL ~EURA8THENIA , 976
Definition and History 976
General Symptomatology 980
Special Symptomatology 982
Pathologic Pollutions 982
Spennatorrhea and Prostratorrhea 985
Pathologic, Erections, .. Priapism" 986
Neurasthenic Impotence ' , 988
Hypospennia (Oligospermia) and Aspermia 993
Etiology 994
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XIV CO~TENTS
PAGF.
Prophylaxis 9W
1'reatment 1002
EPILEPSY. 1012
History 1012
General Symptoms . 1013
Individual Symptom::! 1023
Theoril's of Epilepsy 1024
Intervals between Attacks 1028
Prognosis. 1030
Etiology . lo.'U
Pathology 1037
Diagnosis. 1037
Treatment 1040
HYSTERIA. 1045
Etiology . 1047
Symptomatology 1050
Permanent Somatic Hymptolll<! 1051
Disorders of Motility 1051
Paralyses . 1051
Contractu res 1055
Clonic Muscular RpuslIU! 1059
Tremor 1061
Disturbances of Coordination 1062
Sensory Disturbancl'S 1063
Disturbancl's of Sight 1067
Disturbances in Hearing 1069
Disturbancl'S in Toste and :;mell . !069
Spontaneous Pains . 1070
Reflexes 1073
Sympathetic Nervous System 1075
Psychical Permanent SymptollL~ 1077
Paroxysmal Symptoms . 107R
The Phrure of Coordinatlod Movelllcntll 1079
Course and Prognosis 1081
Differential Diagnosis 1085
Treatment. 1091
TR.~UMATIC NEUROSES • I09R
History l09R
Etiology and Pathogene~i:J 1101
Symptomatology 1105
Diagnosis; Simulation . 1116
Prognosis and Course 1122
Prophylaxis and Treatment lJU
VASOMOTOR TROPHIC NEUROSEK . 1128
Acroparesthesia 1130
Raynaud's Disease 1132
Erythromelalgia 1139
Scleroderma 1141
Acute Circumscribed Edema. 1144
OCCUPATION NEUROSES II 49
Writer's Cramp 1149
Typist's Cramp 1154
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CUXTEN'f8 xv
PAGE
Cramps CauSN.I by Playing Other l\itillil'allru;tnllncnts 1156
l'rampt; of the Lowcr Extrcmit,icl:! 1157
Other Fonus of Occupation ~eul'OSClS , 1157.
Pat hogenesis ' 1159
Tn"dtlllt'Ut 1159
ISDEX 01" AUTHOIIS 1161
INDEX OF ~UB.JEC'TS 1173
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LIST OF COLORED PLATES
PLATE I • l<'acing JKIIJc 450

Fig. I.-Influenza myelitis.
Fig. 2.-Acute myelitis in the puerperium.
Fig. 3.-Hematomyelia in the puerperium.
PLA'fE II . l<'ulluwi"'!J page ~2(j

Fig. l.-8ciatic nerve of a rabbit, peripher.d portioll; 10 days
after severing the trunk.
Fig. 2.-:Serve-eicatrix from the brachial plexus aft.er all ineisL-d wuund.
PLATE III .
Fig. 3.-Ulnar nerve in parenchymatous neuritis.
Fig. 4.-Thc same WI Fig. 3.
PLATE IV .
Fig. 5.-."ciatic nerve in acute polyneuritis.
Fig. 6.-Ulnar nerve in polyneuritis leprosa.
PLATE V Following pagc 826

Fig. 7.-11Inar nerve in polyneuritis leprosa; different view than Fig. 6.
Fig. B.-Vlnar nerve in polyneuritis leprosa; the same field lIB Fig. 6.
xvi
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LIST OF ILLUSTRATIONS
no. I'AGE
l.-~ledian sagittal 8eCtion through the brain of a human embryo at the end of the
first month 2
2.-The development of the ventricular system 3
3.-Brain of a human fetus at the end of the fifth month 4
4.-Brain of a human fetus at seven months . 5
5.-Lateral view of the brain 7
6.-Longitudinal section through the middle of the human brain 10
i.-Cortex of the cerebrum of apes 12
S.-Left cerebral cortex of a female chimpanzee, showing the results o( c1cdric
irritation 13
D.-Horizontal section through the brain with the nucleus caUdatlls, thalamus
optiCUB, and nucleus lentiformis 14
lO.-Portion of a median section through the cerebrum . 15
n.-Arrangement of the motor fibers in the anterior capsule 18
12.-Horizontal section through the inter-brain, one-half centimeter below thc
lII11iace of the thalamus and the nucleus caudatus 19
13.-Diagram of the cerebrsl peduncles 20
H.-The cerebellum from the dorsal side 21
lS.-The cerebellum from the ventral side 22
16.---Combined sagittal section through the stern of the brain 23
17.-The base of the brain, showing the origin of the roots of the cranial nerves 2.5
18.-The distribution of the arteries at the base of the brain and the circle of Willis 27
19.-The lumbar cord, pars lumbalis medullro spinalis, with the conus medullaris,
the filum terminale, and the cauda equina, seen from behind 29
2O.-Transvefse section through the cervical enlargement, intumescentia cervicalis.
of the spinal cord at the point of exit of the roots of the sixth cervical
nerve 30
2l.-Topographic relations between the surface of the brain and the skull 31
22.-~erve-cell from the anterior hom of the spinal cord of a rabhit . a.';
23.-.-1, Sudan staining of the anterior hom of the spinal cord (man); H, Sudan
staining of cerebral cortex (man) . ;~7
24,-Motor anterior hom cell with its processes . an
2.').~nglion cell of the anterior hom. an
26.-senaory nerve-eell . • . ·10
27.-Xerve-cell of the sympathetic. . . 40
28·-Diagram of a motor neuron; first division 41
29·-Diagram of a sensory neuron; first division 41
~.-Yedullated nerve fiber . . . . . . . 42
3l.-Transverse section through the cervical enla~mcnt . . . . . . 42
32.-Transverse section through the upper lumbar (~ord. . . . . . 43
33.-Transverse section through the normal gray suhstance of the anterior horn of
the spinal cord . 43
xvii
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xviii LIST OF ILLUSTHATIONS
1'10. PAG>:
:H.-Tmnsycrsc sect.ion through thc norn131 white sub!!hmec of the spinul l·ord H
35.-Glia cells H
36.-Diagram of the structure, the rourse, and the branching of motor ncuronB of
the first and 8Ccond divisions . 4.i
37.-Diagram of the conduction tmcts of the white substance of the spinaleord 47
38.-Diagram of the various tmcts and neuron systems in the spinal rord 48
39.-The anterior roots and their relations to the membmnes 49
4O.-Transverse section through the intervertebral disc, between the third and fourth
cervical veretebrre 49
41.-From the anterior horn of the gray substance of the spinal cord 49
42.-Medulla oblongata, pons, pedundes, and adjacent parts seen from the husc 50
43.-Base of the bmin and cerebml nerves . .51
44.-Prolonged cord with the rhomboid fOBBa and corpora qU8.drigeminll frum
above 52
45.-Diagram of Fig. 44 .52
46.--8ection through the anterior corpom quadrigemin8. 52
47.-The nudear origin of the oculomotor and trochlear nervc!! in the middle "min .'>3
48.-Nudear origin of the cerebral nerves ii4
49.-Nuclear origin of the cerebml nerves 5;'
5O.-Facial origin and its surroundings . 56
51.--8ection in the region of the origin of the abducens . 57
52.--8ection through the medulla oblongata 58
53.--8ection through the medulla oblongata at the point of cxit of the pncllluo-
gastric 59
M.--8ection through the medulla oblongata at the height of the posterior hypo-
glOBSaI roots . 51)
ss'.-Convexity of the brnin from above 61
56.--Qmvexity of the brain seen from the side 62
57.-Motor region of the cerebml cortex in nmn 62
58.--8ection through the cortex of a frontal convolution. 63
59.-A partly diagramnmtic presentation of the cortex of the eerebrum 64
6O.--Section through the internal capsule 64
61.-The pymmidal tract . 6.')
62.-The pyramidal tmct beside the tract of the hypoglossal and facial nerves 66
63.-Frontal section through the hemispheres behind the optic chiasm 67
64.-Horizontal section through the hemispheres 68
65.~ourse of the serond motor neuron in the spinal cord 69
66.-Tmnsverse section through the spinal cord in atrophic spustic buloospinul
pamlysis 7a
67.-Diagram showing the bmnching of the dorsal roots . 74
68.-Diagram of a tmnsverse section of the spinal cord . 7.5
61).-Diagramnmtic course of the first 8Cnsory neuron 76
70.-Diagram showing the origin and termination of the ncrve root~ in the gmy
substance of the spinal cord and the distribution of thc Ill!rve ("cll", in thc
latter 7U
71.-Diagram of the course of the 8Cnso'Y tmcts from the postcrior roots to thc
prolonged cord 77
72.-The nuclear origin of the cmnial nerves 78
73.-The nuclear origin of the emnial nerves 79
74.--8eetion through the medulla oblongata RO
75.--Scetion through the medulla ohlongata at t.he point of l'xit of the pneulIJo-
gastric H()
76.--Scction through the medulla oblongata at the height of the posterior hypo-
glOBSaJ roots . HI
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LIST OF ILLUSTIL\'TIO~S XiX
PIG. PAGE
77.-Base of the brain and cranial nerves . 82
7S.-~ledulla oblongata with the fourth ventric'le and the corpora quadrigemina,
seen from above. 83
79.-Diagram of the course of the cochlear nerve 84
~.-Region of the corpora quadrigemina, thalamus, and medulla, from the right
side 85
81.~orpora quadrigemina, thalamus, and medulla, from allO\-C 8:)
82.-Tract of the optic nerve . 87
8.1.-The bulbus olfactorius of the mouse 88
8ol.-Diagram of the origin and termination of the nerve roots in the p;ray suhlltanre
of the spinal cord and the distribution of the nerve-rells of the latter 88
sa.-Diagram of the course of the sensory tracts from the posterior roots to the
medulla. 89
86.-Diagram of the motor and sensory condu('tion t.ract.s 90
87.-Diagram of the lemniscus tract 91
88.-0rigin of the facial nerve and ita surroundinp;s . 92
89.-..~('tion in the region of the abducens . 93
9().-Transverse section through the pyramidal de('uSSll.tion 93
91.-Transverse section through the medulla below the olivcs 94
92.-Transverse section through the lower portion of the olivcs and the fourth
ventride . . . . . . . . . . 94
93.-Transverse section through the middle of the olive and the lower portion of
the fourth ventricle 94
94.-Transverse section through the middle of the fourth ventricle 95
g,5.-Transverse section through the lower border of the pons immediatl'ly ahove
the olives and through the middle of the fourt,h ventride 9.5
96.-Transverse section through the middle of the pons and the anterior medullary
velum 96
9fJa.-Section through the pons 96
97.-Transverse section through the upper margin of the POllR and the posterior
corpora quadrigemina 97
98.-Transverse section through the upper ('orpora ql\lldri~elllinll, thc tl'/{IIICllt.UIll
and the crus cerebri . fl8
99.-Transverse section through the upper I'orpora IllIadrip;emina in it" mORt lLlltcrior
portion . 99
lOO.-Posterior roots and anterior roots in tabes . 102
IOl.-Tabetic degen'eration . 102
10:.?-Tahetie degeneration in the lumbar cord 102
10:l.-Tabetie disease of the cervical cord 102
104.-Tabetie disease of the lumbar cord 102
Io.'>.-Posterior columns in tabes 103
IOO.-Assoeiation bundle projected upon the median 8urf,u'c of the hClllisl'hcl'tl 104
l07.-Median sagittal section through the brain . 101)
108.-The most important commissure fibers, 10.5
109.-Diagram showing the arms of the rerebellur trUl'ts lOR
110.-Cerebellar tracts • 109
111.~rtex of the cerebellum 110
112.-Friedreich's disease III
113.-Friedreich's ataxia 112
114,~mbined system diseases . 113
115.-Lumbar cord after an attack of acute poliolllyl'iitis on the left side 117
1 16.~'klerotie foci in the spinal cord 120
117.-Multiple sclerosis. . . . . . . , . . . 120
111l.-TraIlll\'erse myelitis with aRCending and deRI'Clllling degeneration ] 21
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xx LIST OF ILLUSTRATIONS
FIG. .1.011:
119.-Descending degeneraiion of a pyramidal tract of the spinal roM 122
120.-Bilateral descending degeneration of the pyramidal traet 122
121.-Diagram of descending degeneration of a pyramidal tract 123
122.-8econdary degeneration af~r disease of the conus medullaris 124
122a.-Ascending degeneration (right-sided myelitic focus) 125
123.-8econdary ascending degeneration . 125
124.--8yphilitic endarteritis and gummatous infiltration of the surrounding area 126
125.-The normal and the syphilitically diseased anterior spinal artery. 126
126.--8yphilitic spinal paralysis. 127
127.-Brain and skull . 225
128.~rebel1um 233
129a.--8ite for lumbar puncture 236
129b.--8ite for lumbar puncture 236
130.-Instrument for lumbar puncture 237
131a.--()auda equina of the new-born 238
131b.--()auda equina of the adult 238
132.-Lumbar vertebral column of a I'hild one yoor old 239
133a.-Lumbar vertebral column 240
133b.-Lumbar vertebral column 240
134a.-Lumbar vertebral column 240
134b.-Lumbar vertebral column 240
135.-Transverse section through the lumbar vertehral rolumn, the punl'ture nl-'edle
in situ • 241
136.-Instrument for lumbar puncture 253
137.-Diagram of aphasia . 281
138.-Diagram of aphasia . 282
139.-Diagram of the brain 311
14l.-Diagram of the brain 314
143.-Diagram of the brain 3l!l
144.-Ancestral tree 3."J!i
145.-Diagram showing the nomllli prol'eSR of IIJl1'C(·h in man 3.'«1
146.--8tuttering in a girl 3:l7
147.--8tuttering in a girl 3.18
14R.--8tuttering during the emJnl'iat.ion of " I" and" p" ill t he word "lamp" :138
149.-Diagram of stuttering :139
150.-Diagram of stuttering 340
15l.-8egment innervation of the skin 355
152.-8egment innervation of the skin 3.')5
153.-Diagram 356
154.-Diagram 357
155.-Diagram 358
156.-Diagram 359
157.-Diagram 360
158.-Diagram 360
159.-Diagram 362
HIO.--8arcoma of the cauda equina 366
16l.-Inflammation of the dorsal cord 374
162.--8yphilitic myelitis of the lumbar enlargement 381
163.--8yphilitic myelitis 382
164.-Arrangement in Brown-:-;eql:'.... i".. pllralYllis 392
16.'l.-Pofolt.erior view of Fig. 1M 393
166.-TI"'.llImatic hematomyelia . 400
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LIST OF ILLUSTH.ATIONS xxi
nil. PAO.
16i.-Destruction of the cord from the eighth dorsal segment down 401
168.-8cheJDatic repre&entation of the sensory and motor spinal cord tracts 411
169.-Distribution of tactile and thermic anesthesia and analgesia 420
170.-Posterior view of Fig. 169 421
lil.-Apparatus 448
1i2.-Apparatus 449
li3.-DiagraUl of the course of the spinal roots and of the nerf radi("lilaire 503
li~.--SyringoUlyelia 583
liS.--SyringoUlyelia 584
Ii6.--8yringoUlyelia of the cervical enlargement 588
In.-Transverse section through the dorsal portion of the spinal cord. 589
178.-Transverse section through the dorsal part of the spinal cord 589
li9.-Transverse section of a dorsal part of the lumbar ("Ord 589
180.-Transverse section through the medulla oblongata 591
181.--8yringobulbia 591
Itt2.-The various limits of the zones of sensory disturbance upon the head 597
18.1.-Disturbance of the pain sense . 598
184.-Infantile muscular dystrophy . 634
1S.5.-Xeurotic muscular atrophy 647
186.-Infantile hereditary spinal muscular atrophy 650
187.-Diagram of the motor innervation tract for the facial nerve. 670
188.-Facial nerve from the base of the skull to its exit . 671
189.-Diagiam showing the distribution of the sensory cutaneous nerves of the
head 678
190.-The facial nerve and its communications . . 679
191.-Distribution of the sensory nerves in the head, the trunk, and the extremities 737
192.-Distribution of sensory nerves 739
193.-Diagram of spinal sensation 740
194.-The points upon which indurations are mostly found 865
195.-Uiagram 990
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THE SYMPTOM-COMPLEX OF APHASIA
By C. WERNICKE, BRJ:8LAU
1. DISTURBANCES OF PHONETIC SPEECH

A woman, aged 46, the wife of a tailor, presented on examination a remarkable
defl'C.'t. She had rect'ived the average education of people of her class; at least, it was
n-rtain that she had been able to read fluently and to write. All signs indicated a
focal diIWase of the left half of the cerebrum. There was right·sided hemiplegia
combined with severe sensory disturbance of the entire right half of the body. In the
course of nine months, at first slowly developing, an increasing weakness of the right
hand had appeared, followed by three acute exacerbations of the disease, the second
1x>ing followed by a pt>riodical loss of the power of speech. After the third and last
pxacerbation hpr condition remained unchanged. Only a slight disturbance of speech
was found, namt>ly, some difficulty in articulation, which did not affect the distinctness
of expression. This condition of moderate anarthria could not be left entirely out of
consideration, yet at the present time it can be disregarded in the investigJition of her
caMe. The woman was thoughtful, attentive, and apparently of normal mental grasp.
She answeTt'd all questions intelligently, a proof that she had. understood what was
spoken and had followed a definite train of thought. She read aloud fluently, and it
was evident that she understood what she read. Every letter, every figure, was read
corrl'C.'t1y without the least hesitation, and she recognized and immediately understood
all pictures, diagrams, and outlines. On the other hand she had completely lost the
ability to write. She was under prolonged observation which gave her abundant oppor·
tunity for practice of this kind; the only result was that once, under urgent persua-
sions and with visible subjective difficulty, she wrote upon a slate at dictation the
"mall lettf'r a and the figures 2,. 3 and 4. The art of writing spontaneously without
di("tation was wholly lost. This was, therefore, a case of quite isolated lol'ls of a
previously possessed power of writing, a classical case of so-called pure or isolated
agraphia. t
Here we mUMt natumlly consider that the right hand, although not wholly para-
lyzro. was A'l!nf'rally incapacitated. There was ("omplete ta("tile paralysis as far as all
the fint'r movt'mf'nts were ron("erned, so that only gross massive movements could be
performPd. Nothing furtht'r was nott>d. But the art of writing, as we know from
pXpt'rit'n('f'. i!l by no ml'anll I'ntiTt'ly ron fined to the right hand. Normally every person
who has IMrnl'd to write can also Il'arn to writl' with the Il'ft hand; less l'a"i1y of
course than with the right, much more slowly, and in a more painstaking way, as if
dmwing. In this writing, as we mUllt admit, there is a diffl'rent tt>chnic of individual
movl'ments. but it may he done without extreme difficulty, and each letter and word
may be leogiblp. Usually awkwardnl'ss is noted only upon the first attempt, and com-
paratiVf'ly good rt>8ults follow a little pmctice. In the case of this woman, however,
there was an almost absolute lack of power to write syllablt's, words, or evt'n letters
aloOf'. All the power of mallllive movl'ments of thl' right hand had b!'pn rl'tained she wall
p!'l'IIuadro to gra"p with tht' right hand a !!mall block of wood to whi~h chalk was
attachM. Standing before a bla~kboard with this block of wood in her hand the patient
could write nothing, although she was able to lift the right hand and guide it with
th,. l,.ft.
------- -----
1 Monatllllchr. f. Pll1Jch. u. Neurol., Aprilheft, 1903.
265
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266 THE SYMPTOM-COMPLEX OF APHASIA
The peculiar psychical condition of the patient on any attempt to write deserves
mention. Her expression and posture denoted' extreme embarrassment and helplessness.
She seemed lost in thought for a few minutes, was coaxed, made several efforts, and
finally exclaimed that she was tired and could try no more.
The apparently perfect analogy of this peculiarly circumscribed mental

defect with the more frequent and familiar pathological picture of aphasia is
so remarkable that the case is especially suitable as an introduction to the
questions concerning this realm of disease which are still 80 much discussed.
That in this case the faculty of writing .was lost in consequence of a local
disease of the brain is at least no more noteworthy than the familiar experi-
ence that the power of speech may .be similarly lost; if we adhere to the
definition given by Broca (the discoverer of a circumscribed center in the brain
for human speech) of the resulting speech disturbance, the analogy appears
complete, for in his patient the power of articulate speech, the faculty of
speaking, which we know must be acquired like the art of writing, had been
lost, and this isolated defect could no more be explained as a paralysis of a
group of muscles than in our case. Therefore, if we may assume that these
defeets are of kindred nature, we are also forced to assume a writing center
as well as a special speech center in Broca's convolution. As a matter of
fact many authors have drawn this conclusion from their clinical experience;
among them we find no less a one than Charcot--the man who, as long as
he lived, was regarded as the intelleetual leader in lIedicine in France.
Nevertheless, a closer study of the entire symptom-complex of aphasia as
well as of the symptoms of the case under discussion shows that if we admit an
actual writing center we have already passed beyond the most obvious as:mmp-
tion, and that this assumption is by no means borne out by autop~y finding,:.
We should be particularly cautious in the study of aphasia, for a too hasty and
erroneous generalization of facts in themselves strictly correct and comprehen-
sive is dangerous, and has caused every attempt at localization in aphasia to be
regarded as Utopian. I must call to remembrance the fact that the discovery
of Broca (1861) occurred at a time when the principles of cerebral pathology
taught by clinicians such as Bouillaud and Andral were directly opposed to
those of physiology as taught by Flourens. Where the first exponents pointed
to facts which apparently favored the varying importance of different parts
of the brain, the latter was inclined to ascribe these to the effect of Gall's
teachings of phrenology which have quite properly been diseredited, and ex-
periments in animals were referred to as proof of the resemblance of the animal
cerebrum in all of its parts to that of man. lienee a clinieian who disputed
the truth of Broca's discovery found a soil well prepared by skepticism. When
Trousseau expressed his doubts, he found scientific opinion easily swayed to
his side. The celebrated discussion of this subject which arose in 1864 in the
French Academy of Medicine is an instructive illustration of this. But it was
at the same time evident that in the defect which Broca called aphemia he
meant something very different from what his opponent, Trousseau, under-
stood. Pure cases of Broca's aphemia, as Rroea expressly maintained, are
characterized only by the" impossihilite de parler" without oth"er disturbance.
'fhis patient, according to Broca, lost" la faculte d'articuler les mots," "Ie
souvenir du procede, qu'il faut Ruivre pour articuler les mots." Broca ex-
pressed himself still more clearly when he characterized the process by which
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DISTURBANCES OF PHONETIC SPEECH 267
the child learns to speak, as follows: "Par Ie developpement d'une espece
particuliere de memoire, qui n'est pas la memoire des mots, mais celIe des
mouvements necessaires pour articuler les mots." Now there was no reason
why Trousseau should not develop a picture of aphasia differing entirely from
that characterized as aphemia, which is very rarely seen in a pure type; and
he pointed out the many remarkable and perfectly incomprehensible phenomena,
at that time observed in these patients. But these cases were of entirely unlike
character; it is true they seemed to belong to the same aphasic symptom-com-
plex, as we understand it to-day, but they were vastly different from the con-
dition described by Broca as aphemia. If the necropsy findings in many
of these cases showed Broca's convolution to be uninjured, we to-day are
inclined to regard this as favoring rather than opposing Broca's localization.
The presumable proof of the contrary, which Trousseau evolved from the vary-
ing necropsy findings, therefore related to an entirely different clinical picture.
In addition, numerous cases in which Broca's symptom-complex was observed
as an indirect focal symptom could not at that time be satisfactorily explained,
and these also appeared to contradict Broca's discovery. This led to the
inevitable and undesirable result that the symptomatology of aphasia was in-
creased by the addition of many individual points; but these, although a
fundamental gain, and although at first welcomed with great enthusiasm
as marking an epoch of advance in the knowledge of cerebral functions, were
finally considered to be unproven and were discredited. Not until an enor-
mous impetus was given to the study of the anatomy of the brain by Meynert,
and to the understanding of the experimental physiology of the brain by
Fritsch and Hitzig, was a more profound interest awakened in the clinical
picture of aphasia in Trousseau's sense, as well as a correct appreciation of
Broca's discovery. Even the name aphemia, employed by Broca in its re-
stricted sense for the previously described clinical picture, had been relegated
to oblivion.
If we recall that it was chiefly the hope of discovering a localization for
cerebral functions that introduced Broca's discovery, which was vitiated by
Trousseau's influence, we will be inclined to ascribe a paramount role to the
experimental proofs furnished by Fritsch and Hitzig that there are motor
points in definite areas of the animal brain which may be stimulated, and
that this led to the consideration of aphasia in the sense of cerebral localiza-
tion. But even Hitzig's experiments would have proven. incomprehensible,
and he would probably have found no adherents, if Meynert had not given
us such ingeuious and convincing descriptions of the anatomical structure of
the human and animal brain as to enable us clearly to understand the func-
tion of the cerebral cortex. We are indebted to Meynert for our conception
of "the projection systems" which in a physiologic sequence embrace, on
the one hand, all of the sensory and motor tracts leading from the organs
of special sense to the musculature, and, on the other hand, also to the cortex
of the cerebrum. While stimulations from the body can be conveyed to the
" sensory sphere" of the cerebrum only through this tract, the impulses which
arise in the latter are projected to the muscles. According to lJeynert, a trans-
verse section of the cerebral peduncles would include the entire organism,
which U would be devoid of the senses of smell and sight." The ganglion cells
of the cortex of the cerebrum have everywhere the same elementary function,
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268 THE SYMPTOM~MPLEX OF APHAsIA
and only from the variation of their combinations with the periphery of the
body by means of the projection systems are their specific qualities arising
from different localities of the cortex manifested. From anatomical investi-
gations, Meynert came to the conclusion that the cerebrum may be divided
into two large territories, an anterior one of motor, and a posterior of sensory,
importance. Memory pictures produced by this function, and which fill the
cerebral cortex, are motor in the anterior structures and sensory in the pos-
terior.
Viewed from this standpoint, the movements which Fritsch and Hitzig
produced by galvanic irri~tion of the anterior portion of the brain of a dog
appeared in a new light. They did not resemble those evoked by irritation of
special peripheral nerves, but involved several muscle groups, and produced
distinct movements simulating those which are voluntary. Both of Hitzig's
extirpation experiments, which were at once published, permitted the inter-
pretation that the resulting disturbance of movement depended upon loss of
motor memory pictures or conceptions of movements, and Broca's aphemia
also appeared to be a loss of motor memory pictures, particularly for the
movements of speech which had been acquired. The time at which a child
learns to speak is especially the time for this fUIK!tional acquirement of motor
memory pictures, or, more definitely stated, "du developpement d'une espeee
particuliere de memo ire, celle des mouvements necessaires pour articuler les
mots." It will be observed that Broca, with the remarkable acuity of great
discoverers, had taken into consideration only those functions of definite parts
of the brain which (in Meynert's opinion this was subsequently fully con-
firmed) more nearly corresponded to the motor area of the cerebral cortex.
Nevertheless, the remarkable variety of the clinical forms of aphasia con-
stituted a fact which demanded consideration and explanation. Here also the
ground was broken by Meynert, for this author believed he had found in this
peculiar structure (in his opinion the claustrum was entirely composed of
association cells, its area of distribution being in the island and its cortical
convolutions) the central termination of the auditory nerve, and at the same
time a sound area for speech. Although the auditory nerve could not be
traced up to the island of Reil, nevertheless, the significance of this nerve and
of the island for the function of speech called attention to their previously
ignored connection.
It is evident that, after Meynert's investigations, we had all the prerequi-
sites for the full and comprehensive understanding of aphasia. My work upon
"The Aphasic Symptom-Complex" which appeared in 1874, was merely a
minute explanation of Meynert's theories and their special application to
human speech. In the anterior region of the brain, Broca's convolution, we
possess a motor speech center which we regard as the region of motor memory
pictures of speech, or conceptions of speech movements, and the origin of
t.:peech impulses; in a posterior region we assume a sensory speech center,
the region for pictures of speech sounds, and at the same time the terminal
point of the auditory nerve. The child's brain receives and stores up memory
pictures of the sounds of speech which it has heard and gradually imitates
these; thus speech becomes the functional acquirement of every individual.
Combined fiber masses, "association tracts," between the sensory and motor
speech centers, transmit this act of imitation, and also the power of speech.
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From general anatomical considerations which permit us to regard the entire

island covered by the first embryological convolution arches as an anatomical
entity, I believe the sensory speech center to be situated in the first temporal
convolution, and the postulated association tract in the association organ de-
scribed by Meynert as located in the fiber system extending through the cortex
of the island, the deepest layer of which loses itself in the claustrum. Fortu-
nately the findings at two autopsies confirmed this presumption that the sensory
speech center was in the first convolution. In both cases the posterior half
of the longitudinal course of the first temporal convolution and a closely
adjacent area of the second temporal convolution were destroyed by a focus
of softening. This, of course, permitted the differentiation of three clinical
forms of aphasia, a motor, a sensory, and a third form which I designate
conduction aphasia. The motor form had already been clearly described by
Broca; it was the aphemia of this author. Sensory aphasia was chiefly char-
acterized by the fact that the sounds of speech were heard, and the power of
articulate speech was retained, but the speech liOunds were not understood.
This symptom, the confounding of words (the paraphasia of Kussmaul), was
explained by the hypothesis that the sound pictures of phonetic speech pre-
sumably regulated the speech. The clinical existence of conduction aphasia
appeared to be proven by cases of paraphasia in which both the power of
speech and its understanding were retained. The article published in 1874
explained the seeming contradiction, which, according to Kussmaul, still
existed. in a desCription regarded as classical, and which was opposed to any
localization of speech. After the opinion had been expressed that Broca's
convolution was the only speech center, and this was assigned its proper
position as being exclusively the center for motor speech, skepticism, which
had opposed furthcr efforts at localization, at once gave way. With the
appearance of Kussmaul's book, which in a clinico-symptomatologic sense
is still \"Sluable, skepticism was routed. And as Meynert's point of view in
regard to one realm of the pathology of the brain was accepted, that one
which had heretofore been regarded as especially difficult and impenetrable,
this opened the way to further revelations of the secrets of the brain, and to
expectations which have not failed of realization.
The clinical picture of sensory aphasia with its localization in the first
temporal convolution and the adjacent parts of the second temporal con-
volution was soon generally recognized. Kahler and Pick, subsequently
Lichtheim, also French, Italian and English authors, helped to bring about
this recognition, and we maintain to-day that the clinical picture of this
special form of aphasia and the necropsy findings are just as surely based
upon facts as is Broca's motor aphasia. It, therefore, becomcs my duty to
emphasize that the chief symptom of sensory aphasia, arrest of the under-
standing of speech with retention of the power of hearing, had already been
recognized by two authors, by Schmidt 1 upon the basis of his own observa-
tions, and by Bastian 2 after reports of strange cases. These authors did
not ascribe defective speech to a definite locality of the brain; hence we are
constrained to admire their acuity which enabled them to grasp the true
1 Allg. Zeitschr. f. P8ychiatr., 1871, XXVII, p. 304.
2 On the various forms of loss of speech in cerebral disease. British ana For~g,.
Jlf:d. Clir. Review, April 1869.
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270 THE SYMPl'OM-COMPLEX OF APHASIA
condition while ignorant of }ieynert's point of view and the process of its
development. .
As already stated, the most important point is proof (which I attempted
to demonstrate) of the fact that the aphasic symptom-complex embraces the
conflicting clinical pictures of motor and sensory aphasia, and the anatomical
localization of these contrasting conditions has been proven to be in two
entirely different areas of the brain. Historic retrospect here teaches us but
little, and is therefore unnecessary. But an essential and very important
advance was made in this direction when we arrived at a clear understanding
of the relation which must be ,assumed he tween the diametrically opposite
functions of these two centers, and upon this standpoint we base the follow-
ing description.
The sensory speech center is the region in which, corresponding to the
central termination of the auditory nerve, the memory pictures of speech
sounds that have been heard, sound pictures (Helmholtz), have their ana-
tomical substratum in the ganglion cells of the cerebral cortex, "cortical
units" ( H. Sachs) .
Hence this transmits the understanding of word sounds (Liepmann), the
recognition or the "identification" of the perception of sounds which form
the word, a function which must be strictly differentiated from the under-
standing of the "sense of the word." The mere thought of a foreign lan-
guage enables us to understand the necessity of this differentiation, for we
learn to comprehend our mother tongue in the same way in which we learn
a foreign language. Most children understand spoken words, and even their
meaning long, even years, before they acquire the power to articulate these
words. From this, as we shall soon see, a certain independence of the sen-
sory speech centers arises, in comparison with the much more dependent
motor center. But we must admit individual variations in this duplex rela-
tion, since undoubtedly there are children whose power of articulation keeps
pace with their understanding of word sounds. The words which the child
learns to speak have at first nothing to do with the artificial sound forma-
tion of written language. There are complicated words the sound picture
of which, as well as the speech movement conception thereof, must be slowly
acquired by practice. The possession of both of these memory pictures, inti-
mately combined for each word, is what the French authors have designated
as "internal speech," which suggests also a mental power, a kind of memory
-and this may be likened to Broca's definition given above. We will subse-
quently see that a firm combination of associated memory pictures consti-
tutes for us the nature of conception. For this reason I proposed the desig-
nation ulOrd conception, recognizing the acquirement of word conceptions to
be the most important process in learning to speak. Dejerine has accepted
this view and employs the phrase" notion du mot." The expression "speech
conception of words" (Caro) appears to me to be happily chosen, for the
correct articulation of words, the intactness of both components of word
conception, the sensory as well as the motor, is absolutely necessary. Hence.
if only the method of learning to speak is unquestionable, it is nevertheless
very doubtful whether subsequently the impulses for movements of speech
are not referable to the tract through which speech was originally learned
by imitation. A number of authors hold this to be so self-evident (1 shall
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mention only Kussmaul and Bastian) that they scarcely deign to discuss
the question. Yet clinical experience up to the present time is overwhelm-
ingly opposed to this view. As we shall soon see, these are chiefly experi-
ences of. sensory aphasia attributable to destruction of the sensory speech
centers. We must therefore assume that the main impulses of speech are
directly transmitted from the remaining cerebral cortex to the word concep-
tion, and when this is deranged by an absence of the sensory center th('
impulse is transmitted to the speech movement conceptions; hence the power
of articulate speech is retaincd, but is disturbed only because of the lack
of a regulating influence of the sensory speech center which determines the
choice of the correct conceptions of movement.
This description enables us clearly to understand the clinical picture of
sensory aphasia as well as its principal characteristics.
(1) The comprehension of the sound of words is defective, and as this
comprehension by way of the hearing is a prerequisite to the understanding
of the 8en8e of words the comprehension of spoken words is also defective.
In any case the defect is purely acoustic, and the investigator is very liable
to fall into error if he attempts to facilitate the understanding of the sense
of the word by signs, looks or gestures. If, however, by refraining from
this, it becomes evident that none of the speech sounds heard by the patient
have been understood, he may prove by means of these signs and gestures that
the hearing is still intact or, if defective, that the degree of deafness present
by no means explains the defective comprehension of the sense of words. As
is well known, even with extreme peripheral deafness the ability to under-
stand the sound of words is usually unimpaired. ,
(2) The power of articulate speech is retained, the patients' speech even
being remarkably voluble, perhaps in consequence of the frequent misunder-
standings to which they are exposed. For, although they speak rapidly, use
a comparatively rich vocabulary. and form their phrases properly, they fre-
quently make mistakes in the choice of an expression, or employ incorrect or
distorted words without ·observing it. Under excitement speech is sometimes
much better than at others, and entire sentences may be spoken perfectly.
Objects shown them may be incorrectly named, or distorted words are fre-
quently used in naming them. Their confusion of words in spontaneous
speech may so increase that it is impossible to understand them, and we
then designate their speech a8 jargon aphagia. On attempting to answer
questions these patients never use words in the same sense in which they
have heard them. Their inability to comprehend the sounds of words appar-
ently also makes them incapable of imitating the sounds they have heard.
(3) I shall not here discuss written language, since it is not yet the
common property of mankind. and consequently it often fails to throw light
upon the clinical picture. We shall see later that,. this ability to write is
combined with an intact power of internal speech, what we have called the
conception of words, and therefore is invariably and severely damaged in sen-
sory aphasia.
Sensory aphasia in the overwhelming majority of cases is due to the occlu-
sion of veRsels. therefore, usually has an acute beginning. As a rule the
symptomR of the attack are slight, sometimes entirely lackin~, and there may
be no sign of unilateral paralysis. As to the prognosis of the disease, views
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differ. Dejerine concluded from his observations that there is usually a

permanent defect; the majority of authors, with whom my experience leads
me to coincide, are of the opposite opinion, and believe that a comparatively
rapid compensation of the defect is the rule. In fact the difficulty appears
to remain at its acme only for a few weeks, when, provided no intercurrent
condition appears, it gradually disappears in the course of a few months.
Thus, by means of a returning sense of hearing, pictures of word sounds
are newly acquired, and those sound pictures are permanently lost which the
daily intercourse of the patient gives him no opportunity of using. I have
repeatedly succeeded in demonstrating traces of the preceding disease by prov-
ing the patient's absolute inability to understand words or phrases in rare
use, such as vertebral column, popliteal space, axilla, and the like. The
inability to name correctly any objects presented to view appears to persist
for a long time. The conditions in regard to the restitution of writtep lan-
guage have not been thoroughly studied.
No less easy is the description of motor aphasia, the aphemia of Broca.
In adhering to the preceding train of thought the following symptoms are
prominently revealed, so that the clinical picture is easy of recognition.
(1) The power of articulate speech is wanting. The patients have for-
gotten the proce:'1s, the mechanism, which they formerly called into action
to produce its s.ounds. They are therefore mut~at least, they have only
a minimal power of speech. In some typical cases even this is lacking, and
nothing remains but the power to make and repeat a few inarticulate sounds.
The defective speech most frequently observed consists of senseless syllables,
perhaps of a few words or phrases, or it may be some profane or emotional
expressions.
These few words, monotonously repeated, to which 'speech is limited are
not articulated voluntarily and exclusively to express what they mean, but
they appear as an invariable reaction to all the demands which are made
upon the patient's power of speech. It may happen after some exceptional
emotion that these patients, who are usually mute, will give utterance to a
natural expression, as a rule merely an interjection, yet subsequently they
are unable to do this voluntarily. It has also been observed that during
sleep words and phrases are uttered. which the patient at other times is in-
capable of enunciating. As a rule, the faculty of speech is entirely lost.
This loss of speech cannot be ascribed to any paralysis of the muscles, for
a test of their functions excludes all forms of bulbar paralysis.
Often we find as an accompanying phenomenon a hemiplegia or hemi-
paresthesia, a unilateral weakness in the right lower facial or lingual region,
sometimes only in the region of the right lower facial or right hypoglossal
branches. A clinical symptom of the latter is the deviation of the tongue
to the right whenever it is protruded. As these signs of paralysis also accom-
pany articulation which· is really unimpaired, they have merely the signifi-
cance of an accompanying symptom, as has been sufficiently demonstrated
by dinical experience.
A certain impairment of the mechanism of speech which we must assume
to be analogous to defective speech is so common as to demand attention.
This is manifested by the impossibility of producin~ complicated movements
in the region of speech muscles. Thus, some of these patients cannot put
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out their tongues, cannot inflate their cheeks, cannot gnash their teeth, or
they are unable to open their mouths upon being bidden to do so, without
simultaneously protruding the tongue, etc. '1'hese futile attempts at speech
movements, which could be previously performed with ease, permit us to
recognize most distinctly the patient's inability to perform the required
maneuvers. According to Broca's excellent definition they lack for this "Ie
souvenir du procede qu'il faut suivre." Sometimes these symptoms occur
only during the early and acute stages of the disease.
(2) In the main, the power of understanding speech is retained; at least
this appears to be the case on ordinary tests. The faulty reaction may in part
be referred to an impossibility of movement, analogous to that in the case
just described and of the same significance. Therefore all orders given may
be promptly carried out, objects asked for may be produced, questions, to
judge from the expression of the face, are clearly understood, and the like.
There is almost invariably a certain inability to understand complicated
. constructions and the finer differentiations of speech, as was first pointed out
by Dejerine, and illustrated by numerous convincing examples. Here the
contrast to sensory aphasia is so marked that a sharped differentiation is
justifiable, and the sensory defect is amply compensated for as soon as we
furnish the necessary mental stimulus and corresponding surroundings. I no
longer am of the opinion that in pure motor aphasia the apility to under-
stand speech always remains unimpaired, because I consider the acquirement
of word conceptions an important phase in the process of learning to speak.
Since, in this respect, we must admit a decided individual difference, proper
allowance must be made for this in examining the patient and in estimating
his case.
(3) What is true of sensory aphasia is also true of written language. If
the i.ndividual in question had previously possessed this faculty it is lost
simultaneously with articulate speech.
Motor aphasia like sensory is a pathologic picture which is most frequently

of acute development, usually with the symptoms of apoplexy and more or
less profound right-sided hemiplegia.
The prognosis quoad restitutwnem is generally unfavorable unless the
affection is transitory and functional, i. e., unless there is an embolism which
is compensated for by the immediate production of a collateral circulation
or is an indirect focal symptom in which motor aphasia is only the secondary
effect of a focus in the vicinity of Broca's convolution. This is a frequent
occurrence; we sometimes even observe that motor aphasia appears indirectly
as a focal symptom with left-sided hemiplegia if extremely severe symptoms
of apoplexy accompany it. If there is an improvement ill motor aphasia
without the previously mentioned exceptional conditions, and this is rare,
speech is permanently impaired. I had under observation a patient who,
by very painstaking efforts and by methods similar to those used with deaf-
mutes, was in the course of years taught to speak and, in the main, could
be understood. But the force and exaggeration of his speech processes, the
constrained movements like grimaces which involved the entire face, and his
slowness of speech, were remarkable. In my experience this helplessness,
this recognizable and, to the expert, extremely characteristic want of control
19
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of the "procede qu'il faut suivre pour articuler" is permanent even in the
most favorable cases.. On repetition the speech continues to be almost as
faulty as when spontaneous. But Dejerine and Thomas have recently re-
ported that under the systematic optical instruction usually practised. with
deaf-mutes we may often achieve remarkable results even in long-standing
cases (fifteen years!) in a surprisingly short time (six weeks I) . I shall
revert later to this theoretically important point. In comparatively rare
cases motor aphasia is not so complete, or after some time it becomes evident
that considerable power of speech remains. In such cases it is possible to
induce the patient to repeat easy, simple words, although always with evident
effort, but he never succeeds with longer or more difficult words or with com-
plicated sentences, and he becomes greatly confused so that, for example,
instead of saying "I" he says "you," instead of saying "good" he pro-
nounces his own name, no matter how dissimilar; therefore the most unlike
conceptions of movement, if retained in any appreciable degree, are con-
founded on attempting to speak. An unexpected interjection such as "0
God I ". may sometimes be ejaculated by these patients. I admit such occur-
rences, but the clinical resemblance to motor aphasia extends no further, and
the contrast between sensory and motor aphasia is evident even to the tyro
in medicine.
Of conduction aphasia, the third clinical form which I attempted to
differentiate from the many aspects of the aphasic symptom-complex, there
are as yet but few reports, and even these fail to coincide, hence it is impos-
sible to describe a uniform clinical picture on empiric foundation. I was
at first inclined to regard the majority of the cases which did not show the
Broca clinical picture but only the symptom of paraphasia or confusion of
words as sensory aphasia, because in these forms the power to comprehend
speech was retained. This opinion was shattered by finding that I had
much over-estimated the possibilities in these cases, and the view was shown
to be untenable. Of course certain positive characteristics are necessary, par-
ticularly the loss or impairment of word conceptions, the clinical signs of
which I shall subsequently minutely consider, as well as the impossibility of
repeating words; according to the views developed above, the tract which
serves for the repetition of acoustic word sounds is especially implicated.
In both directions positive reports are wholly lacking, and I therefore limit
myself to one important observation. If, under some circumstances, the mere
sound of a word is sufficient for its full understanding-and. as shown above,
this is true of the majority of words frequently used-and if, on the other
hand, words can be spontaneously spoken without the previous stimulation
of the sound picture, .after interruption of the association tracts between the
sensory and motor speech centers it should still be possible to repeat at com-
mand words whose meaning is understood. But this repetition will not be
so infallibly successful as in the tract developed in childhood while learn-
ing to speak; it will be partially correct and partiaUy paraphasic. When
paraphasic, the patient will notice his error and endeavor to correct it. It
is positive proof that this earlier tract is unimpaired if the patient can imme-
diately repeat on request, so-called echolalia, which is purely automatic and
often evoked without command at the moment of speaking, and also if he
is able to repeat incomprehensible, meaningless words or phrases, for exam-
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·
pIe, words from a foreign language. If this particular form of repetition
is lmpossible, yet on the other hand the power of speech and its understand-
ing be retained, also paraphasia and the ability to criticise errors that have
been. made, I consider the clinical requirements to have been sufficiently ful-
filled. I cannot, however, refrain from emphasizing that the autopsy findings
tfor example, exclusive or predominating destruction of the island) are not
calcuhlted to support the view of conduction aphasia postulated by me.
If, as I believe I have demonstrated, the assumption of a sensory and
motor speech center has been corroborated by anatomical findings, as well
as by clinical observations, it follows in logical sequence that still other
clinical pictures must be embraced in the rich aphasic symptom-complex.
Lichtheim was the first to recognize clearly this logical principle, and he
also deduced the necessary corollary. In rare cases, and the pure cases are
always rare, it seems possible that the 'medullary substance which contains
the projection fibers of both centers is alone interrupted by a focus, while
the centers themselves remain intact. If these centers still exist in com-
bination, a condition which of course can only rarely be possible, a new clin-
ical type must result bearing some resemblance to the previously described
ones inasmuch as it presents the fundamental symptoms, loss of power to
understand spoken words and the power of articulate speech; they have, how-
et'er, the differentiating factor of retained "internal speech," the intact
"word conception." As a matter of fact the corresponding clinical picture
in the motor region is not so infrequently met with, especially if there is
simultaneously hemiplegia. The counterpart, sensory aphasia, is much rarer
but has unquestionably been observed. In the light of anatomical researches
the designation of subcortical motor or 8ensory aphasia would be applica-
ble to these two types of disease. According to clinical criteria the desig-
nations" pure word mutism," and" pure word deafness," are more wisely
chosen. '
PuRE WORD MUTISM differs from cortical word mutism due to destruction·
of Broca's convolution in the fact that efforts to speak, although futile, per-
mit us to recognize the undamaged "internal speech" or "word conception"
even though merely from the sound or rhythm. This is most apparent when
the power to produce sounds is to some extent still present. Never do such
absolutely dissimilar reactions occur on trying to repeat words as in cortical
motor aphasia. What is spoken is perfectly understood, even when compli-
cated demands are made upon the faculties. }loreover, the ability to write
is unimpaired, the patient reading and writing without effort, the latter,
in spite of the almost invariable accompaniment of right-sided hemiplegia,
being somewhat clumsily done with the left hand. The mechanical power of
translating the intact word conception into sounds has simply been abol-
ished. Similar conditions prevail with PURE WORD DEAFNESS; here also the
entire internal apparatus of speech, both the cortical centers, and their simul-
taneous action, so that the word conception remains clear, and spontaneous
speech is absolutely free and coherent, the power of written expression does
not suffer, and that of reading is unaltered. The understanding of the word
sounds, of what has been spoken, is alone lacking, an adequate power of
hearing being evidently retained.
We must DOW investigate somewhat more minutely both of these clinical
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pictures with which we have become familiar, no~ only on account of their
theoretic interest but on account of the diversity of opinions concerning their
recognition and correct appreciation. Pure word mutism, or subcortical motor
aphasia, is undoubtedly of vast importance in both of these disturbances.
Long recognized as a clinical picture, just as Trousseau recognized the re-
markable fact that aphasic mutes could occasionally still read and write, these
rare cases were considered to be the purest examples of motor aphasia, since,
according to Charcot, there was a special center for reading and writing. We
are indebted particularly to Dejerine, who was the first to obtain autopsy •
findings which, contrary to the opinion of Charcot, absolutely proved the
true nature of these cases and the existence of a subcortical form of motor
aphasia, that they were brought into general recognition.
In regard to the anatomical location exclusively involved in the subcorti-
cal interruption of the corona radiata fibers coming from Broca's convolu-
tion, authors are quite unanimous. Only the medullary layers of Broca's
convolution itself or its point of entrance at the centrum ovale can be con-
sidered; if the projection fibers lower down and within the trunk of the
brain are affected, the picture of motor aphasia is no longer produced but
disturbances of articulation prevail, while there is still a distinctly recogniz-
able use of words; this is probably due to the position of the fibers, but of
this we have as yet no exact knowledge. The uncommonly frequent right-
sided hemiplegias from focal disease of the corpus striatum or the internal
capsule are usually unaccompanied by motor aphasia, or at most it is of
exceedingly brief duration and must be regarded as an indirect focal symp-
tom. The facts which led me to assume a special motor speech tract extend-
ing continuously from Broca's convolution to the nuclei of the nerves of speech
movement in the medulla oblongata and skipping the internal capsule, I shall
refer to subsequently. Here I limit myself to the mere mention of the ques-
tion of an exclusively unilateral innervation of the bulbar apparatus in speech;
. this question must later be discussed, but now it would lead us too far afield.
The intactness of word conception is a sign which permits us to recognize this
form also in those who cannot read or write. Lichtheim proposed a method
by which the patient infonns us of the number of syllables in a word which
he understands but cannot speak because of his infirmity; for instance, on
being shown an article to be named, the patients are told to squeeze the
hand of the physician as many times as there are syllables in the word. The
objection may be raised to this that those who do not know how to spell are
often ignorant of the number of syllables in a word. For this reason the
ability to count has been accepted as evidence of retained internal speech
(Frankel and Onuf). A far more reliable guide it appears to me is that the
sounds which are indistinctly articulated permit us at least by their rhythm
to guess the word intended. The same aids must be resorted to if, in advanced
cases of progressive bulbar paralysis, we desire to demonstrate the intactness
of "internal speech."
A somewhat more elaborate description must be given of pure word deaf-
ness, or subcortical sensory aphasia. That this in its perfect purity is not
rare in the clinical picture above described 'is acknowledged by all. The
objections to it which have been made refer, on the one hand, t~ the postulated
unilateral position and the subcortical seat of lesion, and, on the other hand,
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to the possibility which has been maintained of the peripheral development
of the pathologic picture from disease of the terminal distribution of the
cochlear nerve in the labyrinth of the organ of hearing. The question of this
unilateral position will be more minutely discussed later. But there can be
no doubt that the motor as well as the sensory speech center is generally
unilateral and situated in the left hemisphere. For the motor speech center
-and this has been universally done-acting on the principle of a saving
of labor, we may assume that a facility in learning to speak, being combined
with a symmetrically acting musculature, stimulated from etch hemisphere,
is also derived from only one hemisphere. We must also assume anatomically
similar conditions and relations in the projection system and the cortex for
both auditory nerves, in that each hemisphere contains a central projection
field for these. But it is difficult to believe that this should occur in the act of
sensory projection in only one and that the left hemisphere, and that only
in this are there memory pictures of speech soungs that have been heard,
as well as a center for the understanding of word sounds. The facts of corti-
cal sensory aphasia permit no other explangtion, and since we must be con-
tent with this plausible principle of a saving of labor, recent investigations
have shown that for the acoustic picture memory, and even the simplest per-
ceptions of tone, a motor component is admixed from the start so that the
labor saving principle, or, more accurately expressed, the conservation of
motor nerve activity, must also be operative in acquiring acoustic memory
pictures. At all events, if a center for the understanding of word sounds
is unilaterally located, it also seems possible that the projection fibers extend-
ing to it may be unilaterally interrupted, and the conduction path to the
center for the understanding of word sounds be blocked, while the intactness
of the same projection fields of the other hemisphere may permit other tones
and sounds to be perceived and correctly appreciated.
A few anatomical considerations are justifiable. The clinically indisputa-
ble connection of each auditory nerve with the hemispheres must have its ana-
tomical substratum in a semi-decussation of the auditory nerves. As such
area, only the posterior field of the medulla oblongata can be considered.
Later the posterior corpora quadrigemina and the internal geniculate body
form primary centers of hearing (analogous to the primary centers of sight
in the anterior corpora quadrigemina and the external geniculate body),
hence the posterior superior peduncle, that is, the pedi"cle of the internal
geniculate body from the first temporal convolution is certainly the portion
of the tract here under discussion. Besides this peduncle of the internal
geniculate body, it is possible that a special portion of the optic thalamus
from the temporal lobes also belongs to the central auditory tract. This can
be situated only in the immediate vicinity of that previou:;l)' mentioned. It
is certain that portions of both acoustic nerves are within these areas of the
corona radiata fibers of the temporal lobes. That a unilateral focus in this
region of the corona radiata fibers of the temporal lobe may produce pure
word deafness as a permanent symptom has been proven by Liepmann's
undoubted case.
S. Freund has maintained that pure word deafness must be assumed to
be the consequence of peripheral disease of the auditory nerve in the laby-
rinth. He bases this assumption upon his observation of a case in my Clinic,
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which he has, however, incorrectly reported 1 since he ignored the positive

symptoms of cerebral disease which are mentioned in the history. Even less
conclusive are his' two other cases. However, S. Freund has done us a great
service in having shown the necessity in such cases of minute examination
of the ear by a specialist. Bezold 2 has proven that the majority of the fibers
of the auditory nerve are not involved in the comprehension of sounds of
speech, and that" in the entire musical scale there remains only the short dis-
tance from b'-g" inclusive, therefore a large sixth, the perception of which is
absolutely neceJ!sary for the understanding of speech." Liepmann 8 showed
that a few tones besides these, either above or below and amounting to an
octave, are also involved in the understanding of human speech, so that from
the entire series of tones less than two octaves are necesio1ary. In the case
from my Clinic which Freund utilized it was deemed advisable to investigate
with a continuous series of tones. This was subsequently done, and it was
demonstrated that in th~s patient these two octaves in particular were well
retained. In H. Liepmann's case in my Clinic, on which a necropsy was
held, the .same examination was made and proof established.
The human faculty of hearing appreciates a series of tones ranging
through more than eight octaves.· Since merely two of these are absolutely
necessary for the understanding of speech, and all of the parts of the auditory
nerve in the cochlear are uniformly distributed, we come to thc conclusion that
only the fourth or the fifth part of the projection fibers of the auditory nerve
need find its central end in the sensory speech center. This circumstance may
possibly explain the relatively slight extension of the sensory speech center;
this, according to numerous autopsy findings, extends only to the posterior
third or the posterior half of the first temporal convolution and the adjacent
area of the second temporal convolution; hence from anatomical and
physiological considerations there can be no doubt that the remaining part
of the temporal lobe also serves in part as the termination of the auditory
nerve.
These newly determined facts force us to assume that the sensory speech
center coincides with the termination of those projection fibers which include
the series of tones from b'-g". From this results the postulate that in cases
of subcortical sensory aphasia the left temporal convolution would always
be actually deaf to the aforesaid tones-if its function could be separately
examined, which of course is impossible. In other words, that word deaf-
ness, and not an actual although partial deafness for certain tones, results
from unilateral lesions, and is explained by the fact that the affected portion
of the fibers of the auditory also reach the right temporal lobes, and thus
permit the perception of the same tones.
This view also explains the above mentioned possibility of acquiring new·
acoustic word pictures, and thus compensating for the defect. If the corre-
sponding cortical areas of the second right temporal lobe are subsequently
affected, permanent sensory aphasia supervenes, and can no longer be com-
1 Compare H. Liepmann, " Ein Fall von reiner Sprachtaubheit." Psychiatr. Abhand·
lungen. HeftI' 7-8, Bre!!lau. 1898.
2" DnR Hllrvermlljren der TnubRtummf'n und Nnchtr!\ge dazu." Wiesbaden, 1895-
lR1l6. 7.f'itschr. f. Ohrenheilkunde, XXXVI.
3 L. e.
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pensated for, as O. Berger has proven by one of the earliest observations

bearing on this affection.
If we extend our researches still further, we arrive at the postulate that
ca..~s of sensory aphasia from bilateral disease of the temporal lobes run their
course with actual tone deafness in the area of the previously mentioned tone
heights. The future will reveal whether this supposition is actually correct.
But, up to the present time, such investigations in cortical sensory aphasia,
the difficulty of which we do not deny, have not been systematically at-
tempted.
On the other hand it becomes quite clear that with distributed bilateral
disease of the temporal lobes the picture of word deafness is less prominent
than that of general deafness. In the majority of cases the nearest point
of termination of the auditory fibers is then destroyed, and this makes possi-
ble the development of central cortical deafness. A. Pick has described two
such cases in which the patients were so deaf that the almost total inability
to understand words was only explained by the fact that extreme deafness
from peripheral causes leads to absolute inability to comprehend words. At
all events thesc cases do not show the clinical factors of subcortical sensory
aphasia, or pure word deafne8s, and do not justify Pick's conclusion that pure
word deafness is due to cortical destruction extending throughout both tem-
poral lobes. A third case of Pick's 1 which presented besides extreme deaf-
ness the essential characteristics of pure word deafness may be readily ex-
plained as a combination of both these defects, which opinion was borne out
by the autopsy findings.
While we have so far especially considered those forms of aphasia which

are generally recognized, either anatomically or clinically, such as cortical
sensory and motor aphasia, or those which, as a rule, are regarded as special
clinical types, such as the subcortical forms of aphasia, we now come to debata-
ble forms which still rcquire the support of additional observations and. ana-
tomical findings. From a purely logical standpoint we cannot reject the con-
clusion that a transcortical motor and a transcortical sensory aphasia are
possible; i. e., an aphasia caused by an interruption of the tracts which bring
about the combination of the two previously assumed speech centers with
the so-called region of conception, therefore the greater part of the general
surface of the cerebrum. The discussion of these clinical varieties is justi-
fied by the fact that there are abundant clinical examples corresponding to
the theorctically constructed picture. And although I attach great weight
to the opinion of Dejerine, who declares these to be erected on a purely theo-
retical foundation, I cannot recognize as conclusive the proofs he advances.
r shall soon revert to this point.' We shall first attempt to develop theoreti-
cally the principal criteria of ~he clinical picture as has been done with the
other forms.
We must clearly understand what is meant by the conception of an object
or "the concrete conception" (Ziehen), for, as already emphasized, the con-
ception of an object must be awakened by a 8en80ry speech or word sound
CE.'nter so that the word sense may be understood. Therefore a conception
1 Arch. f. Psych., XXIII, p. 909.
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280 THE SYMPTOM-<XJMPLEX OF APHASIA
center has been spoken of; this would be identical with our center for the
understanding of the word sense. Naturally it is pure fiction, and merely an
artifice which diagrammatically simplifies the subject, to speak of such a
center. In fact, in these processes which are extensively distributed through-
out the regions of the ccrebral cortex, we are dealing with conditions such
as appear in the following considerations: If we take Meynert's point of view
described at the beginning of this article in regard to the regions of spccial
sense, we assume the conception of concrete objects to be the function of
different projection fields at the cortex; for example, the conception of a rose
is composed of "a tactile memory picture" or "a tactile picture" of the
rose in the centra1 projection field of the palpating surface of the hand, of
an optical memory picture in the optical projection field, and a smell mem-
ory picture in the olfactory projection field of the cerebral cortcx. By the
constant rcpetition of the same impressions of special sense so firm an asso-
ciation of these memory pictures is formed that even the stimulation of one
sense by the object is sufficient to remind us of the sum of its essential prop-
erties; in other words, to awaken the conception of the object. Sometimes
there are more, occasionally less, memory pictures of various regions of special'
Aense which correspond to a conception, but it is always a definite and firm
grouping due to the nature of the objcct which forms the anatomical sub-
stratum of every conception .. 'l'his definite sum (which must always be dc-
termined) consisting of associated memory pictures, must" enter into con-
sciousness," provided not only the sound of the corresponding word is
appreciated but also that its sense is understood. In accordance with ana-
tomical views we postulate also for this act an anatomical tract of fiber
communication or an association tract between the sensory speech center,
or center for the understanding of word sounds, and the projection fields
in which the conception is produced. These tracts we may call transcortical,
inasmuch as they extend beyond the nearest cortical termination of the audi-
tory nerve in contrast with the generally recognized subcortical tract areas.
As is obvious they can be considered only as a radiating bundle that fu"e;;
into one termina.l point. the sensory speech centers, and only in this vicinity
can it be, focally f!eparated.
The condition must be quite similar if, spontaneously, i. e., in consequence
of internal cerebral processes, the word "rose" is spoken. First the con-
ception must appear, then the impulse of the movement conception corre-
sponding to the word "rose" must reach the cortex of Broca's convolution.
For this purpo~c the analogous "transcortical" tracts are neceR8ary which
can only be conceivcd in the form of a convergiJ!g radiating bundle. The
following diagram represents the relations of a " concrete conception" to both
speech centers/ and also possesses acoustic factors as, for instance, a bell and
a dog.
1 The definition of a. concrete conception here given as the definite grouping of

a!<sociated memory pictures with each other necessitates only the most necessary assump-
tions. In my opinion it would he superfluous to allllume anything more than this:
That for association between the memory picture~ of various projection fields special
fJ88ociation center8 are necessary which thereforc might anatomically be considered as
collective points of association tracts from. the various projection fields of the organs
of special sense. Flechsig claims that he has proven the existence of such association
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According to the preceding we have a perfectly clear definition of the
clinical picture of transcortical sensory aphasia: An abolition of th.. under-
iitanding of the word sense with a retained understanding of the word sound.
The iipeech sounds as such are perfectly understood. This is shown by the
retention of the ability to repeat them, but the accompanying conception is not
awakened. The power of speech is actually retained but is slightly impaired
in that spoken language is not understood and consequently its correct appre-
ciation cannot be tested. A paraphasia extending beyond this with an admix-
ture of incorrect or distorted words or syllables is usually only suggested.
The repetition may consist of entire sentences or may be limited to the last
few words according to the degree of the retention of memory, and sometimes
discloses no error; at other times there are paraphasic distortions. The
repetition may be in obedience to command, sometimes it is involuntary. It
may be combined with what has been heard in the form of a question, some-
times it is spasmodic, sometimes almost reflex. In the last case we have
• echolalia, a symptom which usually indicates a weakening of the sensorium
or general intellectual decay. The unintelligible repetition of a question is
characteristic of this.
The contrast in the motor realm is transcortical motor aphasia, consisting
in the arrest or very decided impairment of spontaneous speech, while on repe-
tition it is fluent, perfect,
and there is no lack of
understanding of lan-
guage. The speech still
at command is not made
up of a few words or syl-
lables constantly repeat-
ed. as is the case in cor-
tical motor aphasia, but
there are occasional ex-
pres..;;ions of discontent,
of anger, of helplessness,
therefore emotional ex-
pr~sions; the command
of langua~e, a.~ may be
prol"en by repetition, is
unlimited, au tomatic.
Serjes of sen tences
Flo. 137.
learned by rote, such as
the Lord's Prayer, the mUltiplication table, and the like, may be smoothly
recited by the patient, either at command or after being repeated to him.l
ct'ntt>rs or "coagilotion ClMter-II" as be calls thl'm. Thl'Y are said to be eharsett>rized

anatomically by the fact that no projection fibers or corona radiata fibers entt>r them.
Since then it has been proven that corona radiata fibers extend to all coagitation cen·
tl'rs. I t'aJl onlv lUlBumt> that the anatomical Aubstratum for centers of thil! kind is in
one cortical tt>n=itory-that is, in the insula with its claustrum which Meynert regarded
. . aD JUIIIO(!iated organ.
J Compare Hell bronner, "Ueber die tran~ortieRIl' motorj,.ehe Aphasie und die als
, Amnesie' bezeiehnete SpraehsWrung." Arch. f. 1'.~ych . , XXXIV, p. 341.
SO
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But the simplest communication, conversation, or difference of oplDlOn, is

impossible through speech; only in the rarest cases can questions be answered
except by gestures ; once in a while it is possible to obtain a single short
answer. Articulation is absolutely faultless.
These are the clinical types. 'rhey are complemented in some cases, i. e.,
in those with a fair degree of education, by the no less characteristic impair-
ment of the power to write. Here also there is a striking contrast between
the perception of speech and its expression: In sensory transcortical aphasia
there is no comprehension of what is read, but, owing to the integrity of
word conception, reading may be fluent and without visible effort; in other
cases it is more or less paraphasic. In motor transcortical aphasia spontaneous
writing is impossible, while, in contrast to this, at dictation it is sometimes
correct, at other times it is accompanied by many paraphasic distortions.
These patients read silently with full understanding, but on reading aloud
we perceive the influence of paraphasic admixtures.
In the first case the reading may be compared to the reading of a lan- •
guage which is not understood but is composed of the same sounds, and the
same comparison can be made with the difficulty on writing at dictation,
for, while not faultless, it is relatively good. On the other hand, spon-
taneous writing shows to an increased extent the disturbance (paraphasic)
of active speech, therefore paraphasic distortions may render the speech utterly
incomprehensible. It will have been observed that in proceeding from the
consideration of simple and associated facts to more complicated pictures, the
significance of which may still be considered as disputed, we have left far
behind us what Trousseau and Kussmaul in- their time had considered to
be strange and entirely incomprehensible observations. A more minute study
of the impairment of the power to write may even throw light upon other
related points, which as yet have been merely
touched upon, and enable us to complete our
clinical sketches. Before proceeding it is advis-
able as an aid to the diagnosis briefly to recapit-
ulate the essential factors in the various forms
of aphasia which have been described. Hcre I
follow Lichtheim who, in connecting a supposed
conception center with the two speech center,;.
the motor and sensory, which I separated, was
the first to rear a framework for the diagram-
matic presentation of all aphasic symptoms. In
the subjoined diagram (Fig. 138) B indicates
the conception center, i. e., the localization of
important memory pictures of a concrete object
FIG. 138. which, in fact; occupy very different cortical
regions; but, a8 has been shown by their firm
functional connection with a psychological unit, they produce harmony in the
concrete conception. The sensory speech center is indicated by a, the motor
~peech center by b.
The tract from a to b represents the association tract which serves for
the repetition of speech sounds. The tracts a Band b B are those association
tracts which serve to connect the concrete conception with both speech centers.
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DISTURBANCES OF PHONEl'IC SPEECH 283
In the center, a, b, is a centripetal and centrifugal tract; in other words,

here the sensory and motor tracts enter parts of the p~jection system. The
sen80ry speech tract contains at least a certain number of fibers of the audi-
tory nerve of the same tone heights which were previously mentioned, and
the motor speech tract contains the fibers running to the internal capsules
(intended for the nuclei of the bulbar nerve) which function in speech. The
diagram enables us to understand why the transcortical forms of aphasia are
very rarely observed in their pure form; for a Band b B are, in fact, radiat-
ing bundles only the terminal parts of which, a, b, are identical. The sepa-
ration of these two tracts by a focus can therefore only occur in the most
favorable cases in the immediate vicinity of both centers, a, b. If the numer-
als in the diagram are chosen for illustration, 1-3 are the sensory forms, 4-6
the motor forms of aphasia. According to the position of the cortical centers,
a and b, we find upon each side a cortical, subcortical and transcortical form.
If, for reasons previously mentioned, we disregard the form of conduction
aphasia designated as 7, we must with Lichtheim admit that the mere occur-
rence of the various forms of aphasia indicated by the diagram is a certain
proof that these conditions actually occur in nature. But I can accept this
proof only as positive in the case of the cortical and subcortical forms, 1 and 2
and 4 and 5; in the case of the transcortical forms, 3 and 6, there is only
some degree of probability. In fact the mere coincidence of such peculiar
symptoms as mark the transcortical forms is difficult to explain.
Objection has been made to the name chosen by me, especially for the
transcortical forms, and, I must admit, with some degree of justice, for I
find that its anatomical foundation is insufficient. But, in support of this
nomenclature, I may state that I am aware of no other name which expresses
the peculiarity of these cases. For the subcortical forms we possess very apt
designations in the names pure word deafness and pure word mutism. But
I see no particular reason for dropping an anatomical designation when, in
my opinion, it has been deemed fitting. As to the designation transcortical,
there are theoretic reasons for its retention to which I shall refer at the con-
clusion of this article.
The question of localization, that is, of the pathologico-anatomica1 find-
ings, will later be considered in detail, but here I wish to call attention to
certain decisive points of view. One of these has already been emphasized,
for I have repeatedly referred to the general experience that pure cases are
exceedingly rare. We cannot, therefore, expect that every case of aphasia will
show that grouping of symptoms which is typical of the pure form which has
been described. The second point, the possibility of grouping the correspond-
ing anatomical findings of different clinical pictures, is no less important.
Two such combinations must be mentioned, both of which appear as total
aphasia, the one with inability to understand language, the other with loss
of the power of speech. therefore as sensory plus motor aphasia; but they
are unlike in their different response to the word conception, or so-called
internal speech. The more common condition is associated with loss of inter-
nal speech, therefore is the sum of the above described cortical forms. It
is always associated with hemiplegia. The other form in which the power
of internal speech is more or less perfectly retained is rare, but, nevertheless,
has been observed; it is the combination of both transcortical forms of
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284 THE S:YMPTOM-{''OMPLEX OF APHASIA
aphasia, and occurs without hemiplegia. Furthermore, a glance at the dia-

gram shows that combinations of subcortical and transcortical forms of both
motor and sensory aphasia are favored by anatomical conditions, and are more
readily produced by foci in Broca's convolution or the first temporal convolu-
tion than by individual forms. Other combinations which must be regarded
as natural groupings, and therefore somewhat more common, are met with
under the explicit discussion of written language.
The clinical facts enumerated, and the consequent guiding points of view,
enable us more minutely to criticise our case of pure agraphia. In demon-
strating the existence of a motor writing center, analogous to Broca's motor
speech center, there must be a defect just as circumscribed as in Broca's
aphasia, a loss of this faculty: "Ie souvenir du procede qu'll faut suivre pour
ecrire les mots." But internal speech, word conception, the" notion du mot"
must be intact. }~or we do not write words but definite groups of letters,
and this act, particularly the definite sequence of letters which form a word,
presupposes an intact word conception.
But in our case even the first requirement was not fulfilled. The patient
could neither tell us how many syllables a word contained, nor could she select
letters from tables of letters handed to her and form a word, not even when
only three letters, a, n, d, were given her to form the word" and." And this
is the almost invariable condition. Experience shows that agraphia, as under-
stood at present, i. e., when not limited to one hand, is always accompanied
by and is due to a disturbance of internal speech. More explicitly stated,
it is a disturbance of the influence which the "word conception" has upon
the choice of letters to form a word, and is a purely transcortical function.
II. DISTtJR.BANCES OF WRITTEN LANGUAGE AND GEl'fERAL

PATHOLOGY OF SPEECH DISTURBANCES
That the disturbances of written language to which we now turn are of
individual importance, and that they take place not only in connection with but
independently of aphasic disturbances, proves their occurrence although they
are rare, as is apparently isolated agraphia, with which we began our con-
sideration. The contrast to this, isolated alex,ia, has also been observed with-
out any other disturbance of speech, and so much more frequently that it
obviously tempts us to assume a special center independent of the other func-
tions of speech, or a cortical center for written language quite analogous in
a motor and sensory respect to the true speech centers, of which the first is
to be regarded as the seat of conceptions of writing movements, the second
as the optical field for the memory of words. Charcot has been recognized
as the most prominent exponent of this conception, which simply transfers
the diagram of sound language to written language. However, the unten-
ability of this gross diagrammatic consideration has gradually become obvious,
and it has now but few adherents, existing and being widely distributed only
in the consideration of a special and unilateral visual speech center in the
angular convolution of the lower parietal lobe (Dejerine) ; even this v. Mona-
kow denies.
Correctly to appreciate the importance of written language as compared
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DISTURBANCES OF WRrITEN LANGUAGE 285
with spoken language, we must remember first of all that the former is a
comparatively late acquirement, and that it is not the common property of
all persons as is spoken language. Because the possession of this faculty by
different people is not invariable, it cannot be uniformly included in the
mechanism of the brain, as is j;poken language. Hieroglyphics, for example,
presuppose a mechanical process in the brain different from that in the usual
writing of individual letters among people more highly cultivated. The
importance of the alphabet in written language is shown by the fact that
reading is generally achieved by spelling. No matter how self-evident a sen-
tence appears to us now, Grashey's investigations have shown that we learned
to recognize it only by the previously described process. Grashey's successors,
particularly Goldscheider, have found that this is not invariably the case,
for combinations of even four letters are understood "at a glance," familiar
words as a whole, and independently of the letters which compose them, so
that we must admit a faculty for optical word memory pictures commensurate
with the individual vocabulary, either printed or written; usually the written
picture of the name will be considered. In the course of our description
we find another limitation. As a rule which applies to the majority of readers,
we must regard spelling, reading and, consequently, optical memory pictures,
as being only for letters and not for words, and comparatively few excep-
tions to this can be admitted. When, in writing, we bring to remembrance
the written picture of a word and for this purpose place letter after letter,
it is evident from the process itself that we proceed by spelling. What we
here produce is a manifold combination of letters similar to that we analyze
by spelling when we read. Hence it follows that, aside from the previously
mentioned exceptions, a direct relation of the conception of an object to writ-
ten language must be denied. This point is so important that we shall sub-
sequently discuss it more minutely.
By what process internal thought is communicated by means of speech
and written language is almost unknown to us. In many persons it is prob-
ably and chiefly by means of sound pictures. That it may be by written
pictures and not sound pictures appears absurd after our previous reason-
ing; for we possess optical memory pictures merely of letters, not of words;
certainly all the phenomena of reading and writing are explained by this sim-
ple view; should we proceed beyond the most obvious and most simple assump-
tions, no one can tell to what extremes the pathology of the brain might lead
us. The twenty-six letters of the alphabet are certainly not material for
thought. Nevertheless, such an assumption is accepted in the differentiation
hy many psychologists and some pathologists, particularly Bastian, of three
different formulas ot thought, according to which human beings are classi-
fied as "moteurs, auditifs and visuels." The promulgator of this opinion
was Charcot. He reported a case in which, during the act of speaking, there
was a certain reading of the internal picture of the written word; far be it
from me to attack his observation, although I have never seen anything simi-
lar. But I regard such an occurrence as the rarest exception, and such a gen-
eralization as not permissible. The possibility of its occurrence in deaf mutes
does not disprove my theory, at least only in so far that by special training
the brain may be enabled to perform such feats. But with most persons in
possession of their faculties, there can be no question of such a training.
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286 THE SYMPTOM-boMPLEX OF APHASIA
There is no doubt that intelligent deaf mutes may learn written language
independently of speech. The combination of letters which form a word is
for them an entirety, the separation of the word into letters is a later and
artificial acquirement, analogous to the phonetic spelling of a word. If we
admit that some persons usually think in word (of course not in letter)
sounds, therefore, in deaf mutes this will appear in a corresponding optical
combination of letters each of which in like manner is associated with a cor-
responding concrete conception, or is united by transcortical tracts with the
corresponding pictures of word memory, as was previously explained (Fig.
137). In deaf mutes, therefore, we may distinguish between optical word im-
ages and images of letters. This particular class of unfortunates must here be
omitted from consideration, since they require special and precise investiga-
tion. In all other persons the brain would be over-burdened if it retained
all combinations of letters as special optical memory pictures of words, the
corresponding word sound pictures being already present, and we must there-
fore assume that this is not the case. It is positively disproven by the fact
that in rare cases (Rieger and Sommer) a permanent loss of power to use
certain letters of the alphabet in writing has been observed, the patients hav-
ing no conception of the form of certain letters, yet there was no correspond-
ing speech disturbance affecting the sounds represented by these same letters.
In Rieger'S 1 celebrated case this was true of three letters of German text.
also of seven small and fourteen capital Roman letters, the identical letters
in both the German and Roman alphabets. These cases are further remark-
able from the fact that aphasic symptoms were merely indicated; they are
the purest cases of disturbance of the function of written language alone
which have yet been reported.
It is quite remarkable that Sommer,2 who published one such case,
having invel'tigated it by Rieger's method, comes to the conclusion of an
immediate connection between object conceptions and writing movement con-
ceptions. In Grashey's case he believes this explanation to be absolutely neces-
sary. Here he goes a step further than the adherents of a substantive optical
word center, some of whom (Dejerine, for instance) deny a motor writing
center. His hypercritical tendency and his apparently unprejudicial stand-
point here become apparent; for in reality there could scarcely be more
positive proof of the connection of an optical word picture with its com-
ponents, the pictures of letters, than the way in which Grashey's case found
his words, and the explanations which we owe to the subsequent investiga-
tion of this case by Sommer a and Wolff.'
Grashey's patient showed the peculiarity that he could only find words for objects
shown him, and, as was observed later, only for objects and their properties brought.
within his psychical conception, by writing. Without this artifice it was impoesible
for him to express himself in words, but after he hRd finished writing the word he wa.'I
able to speak it; if he was disturbed while doing this. eRl'h part of it remained discon-
1" Besl'hreibung der Intel1i~nzstllrun/l'Cn infolge einer Himyerleizung." S. A. aus

Verhandl. der Phys. med. Gesellllchaft reu Wiirzburg. N. F. 22. u. 23. Bd.
2 Sommer, "Zur Theorie der l'erebralen Sehreib- und Lesestllrungen." Zeitscllr. f.
Psych. fl. Phys. d. Sinnesorgane. V, p. 305.
3 C'entralbl. f. Nert·Nlheilk. fl. PII1,ch. l'tfllrzheft. 1894.
• Gustav Wolff, "Ueber krankhafte Di~sociation .der Vorstellungpn." Habilitalioft·
IIchri". INipzig, 1897.
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DISTURBANCES OF WRITTEN LANGUAGE 'lS7
nl'Cted from the objl'Ct and useless. But OJIly the complete word bore any resemblance
to the word conception of spoken language which corresponds with the concrete object;
parts of it, letters, a combination of letters, or even an unfinished word, have no con-
nection with the object that is seen, or felt, etc.
Grashey's case is an example of the possibility mentioned above of special training
of the brain. Here the choice of the word independent of the object is imp088ible, a
defect which we will consider later. To compensate for this defect he resorts to the
artifice of utilizing written language, as, for instance, a deaf mute would, but, unlike
the deaf mute, he must proceed by spelling. His writing is only a result of the intensely
stimulated optical memory pictures of letters in which the motor components of II con-
ception of direction" are the main thing, as we shall see later.
In one respect I agree with Sommer: The defect in Grashey's case cannot be
explained by ll88uming a loss or diminution of memory for recent impressions. Its vast
importance for the conception of written language and its relation to spoken language
have not been shattered by subsequent investigations, but have rather been strengthened.
After these preliminary remarks I consider myself justified in assuming
the same cause for disturbances of written speech as those contained in my
report of 1886, to which I refer the reader for details. 1
Ziehen's "concrete conception," as well as all abstract conceptions and,
as we shall see, the entire material of thought, has no immediate connection
with written language, being essentially a language of letters communicated
only through the center~ for speech. Therefore, reading and writing are
transcortical subordinated activities from the centers of spoken language,
and nothing more positively proves the necessity of separating focal symp-
toms with a transcortical seat than the fact that there are isolated disturbances
of written language due to a focal disease of a definite area.
Hence the faculty of writing depends upon spoken language, and is lost
as soon as the word conception or internal speech is damaged; it is retained,
and furnishes a valuable criterion, when word conception and internal speech
remain uninjured.
Integrity of the power of articulation is an important sign in subcortical
motor aphasia or pure word mutism, as well as in subcortical sensory aphasia
or pure word deafness. In the transcortical disturbances of speech, the intact-
ness of the word conception is also evident from the fact that purely mechan-
ical reading and writing reveal no disturbance. The patient may read aloud
either at dictation or from copy. Some individual points in the symptom-
complex of written language are not yet sufficiently proven. As a rule, we
may maintain that a defective power to write is analogous to defective speech,
for with the loss of the power of speech the comprehension of what is read
is also lost, with the loss of the spontaneous power of speech, the faculty of
spontaneous writing also disappears; in reading aloud and in writing at dic-
tation paraphasic admixtures and distortions are as numerous as on repeti-
tion. This is particularly true of transcortical sensory aphasia, provided that
the paraphasic symptoms are involuntarily increased by the act of writing
so that writing becomes even more difficult. In the discussion of such cases,
the terms paralexia and paragraphia are objectionable, and the expression
paraphasic disturbances in reading and writing is preferable. In transcortical
motor aphasia, it is evident that spoken language is characterized by an
absence of spontaneity, and this becomes more marked on trying to write.
It also appears in writing at dictation, for this form of writing. although
1 Fort.c1t.r. d. Mea., IV, pp. 371 u. 463.
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288 THE SYMPTOM~OMPLEX OF APHASIA
possibly to a less extent, presupposes the spontaneous coaction of the Wl"iter.

"Word finding" for the act of spontaneous speech, the actual function of
the tract B b, necessitates for writing the further exercise of finding the
letters, as the sounds of the letters, in our sense, belong to the word conception.
Tht! power of writing, as previously stated, is most severely aamaged in
the cortical forms of aphasia, for here the word conception itself sustains
a lesion. Cortical motor aphasia, as a direct focal disease, usually results
in just as persistent an alexia and agraphia. But the letters continue to be
optical structures, and may be written individually, as is proven by the reten-
tion of the ability to copy. For reasons to be subsequently more minutely con-
sidered, in an intact brain which still responds, there is a greater probability
of the restoration of the receptive faculty of reading than of the expressive
faculty of writing. The sequence in which reading returns after cortical
motor aphasia has been studied by Thomas and Roux under Dejerine's direc-
tion; the inverse relation of learning to read was revealed by the circumstanC'e
that at first entire words, then syllables, finally the individual letters which
compose a word, were read with confidence. Besides mutism, isolated or
very marked agraphia may persist for years; an agraphia, however, which
is characterized by the retention of the power to copy as well as to change
letters from one form into another form, and this power prevents confusion
with the substantive agraphia of our case detailed at the beginning of this
article. Generally the ability to write improves just as does articulate speech;
it is slower at dictation than on spontaneous writing (Dejerine). In writing,
the integrity of the word conception is absolutely necessary; on this point
I agree with Dejerine and differ with v. Monakow. My experience does not
permit me to coincide with the observation of v. lIonakow that motor aphasics
often find written expression easier than speech. This probably refers to cases
of predominant subcortical motor aphasia, for I believe that v. Monakow's
clinical picture of cortical motor aphasia has been based on too broad a con-
ception; he recognizes a partial motor aphasia of much wider extent than
I do. At all events there are exceptional cases--a case of Banti's is a proof
of this--in which cortical motor aphasia leaves intact the faculty of written
expression as well as the understanding of Wl"itten expression. Monakow
assumes that this can be due only to a partial disease of :proca's convolution,
a condition to which we shall refer when describing the pathology.
Sensory aphasia of cortical origin is generally admitted to occur without
severely damaging the power to write. On the restoration of the power of
speech the art of reading is sooner learned than that of Wl"iting; in a word,
according to universal experience, agraphia usually persists as a severe per-
manent disturbance. This corresponds with the fact that we attach the
highest value to the acoustic components of the word conception during the
time of its attainment. Perhaps, however, purely anatomical conditions are
not unimportant, since the posterior and upper end of the first temporal
convolution almost forms an important association tract for the motor act
of Wl"iting.
Moreover, there is a lack of casuistic material consisting of wen observed
cases of inability to write to show that in disturbances of speech the symp-
toms disappear during the stage of improvement.
The relation of written to spoken language enables us to appreciate in
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DISTURBANCES OF WRITTEN LANGUAGE 289
a double sense the clinical symptoms of alexia, agraphia, paralexia and para-
graphia whether they are the sequels of a damaged word conception or whether
they appear independently. The former may be designated verbal, the second
literal. The substantive disturbances of written language, which are observed
with intact word conception or internal speech, relate also to the form of
letters so that, for example, literal agraphia consists mainly in the fact that
the reproduction of this form is impossible for the patient, and the case whose
history was given in the beginning of the article is a marked example. In
literal. alexia the actual defect consists in a non-recognition of letters, and
in consequence of this of words also. A special form of alexia and agraphia
is produced, as we shall soon see, by a damage of the tracts which connect
the word conception with the psychical elements represented by letters.
It would lead us too far from our theme and would not be in consonance
with its importance here to trace diagrammatically all the true disturbances
of written language, as was done for those of speech. But in regard to the
form which such a diagram must take, if it is to correspond with the major-
ity of the facts, the most important points may be indicated. It generally
corresponds to that developed for speech (Fig. 138) if, in place of the con-
ception center, B, we use the word conception, c, in place of the motor speech
center, we use the conception of writing movements; fl, and in place of the
·sound pictures we substitute the optical memory pictures of letters, a. While,
however, in the diagram of speech processes we must adhere to the fact that
a direct tract, B, b, exists, it is very unlikely that a corresponding tract, c fl.
comes into question in written language. The diagram thus becomes more
simple than for speech. It appears that in writing a path over the optical
field of memory, a, is absolutely necessary, probably because of the method
most often used. in learning to write. I do not doubt that a change in this
method might influence the clinical importance of this tract. 'rhus, the
older among us, without exception, first learned to read letters and then
to write them. Now these arts appear to go hand in hand, so that children
are first taught not only to read and then to write, but are taught to read
while learning to write. Under this method the motor components in the
production of a letter gain an increase in dignity.
On the other hand the difference between printed and written letters
teaches us that the motor components of the conception of writing move-
ments, at least in recognizing a letter, are indispensable, so that the concep-
tion of writing movements of the letters cannot be regarded as an essential
factor of this.
In employing the expression, " conceptions of writing movement8," I desire
not to be misunderstood. The term signifies only that conceptions of move-
ments, in Meynert's sense, produce writing movements just as, in quite a
different muscular area, they produce speech movements. A certain recol-
lection of the process to be followed in writing is therefore admissible and
cannot be denied; neither can we deny a certain localization of this special
function of memory in the left arm region, provided we write with the right
hand. But it will. be the same locality in which originate all the finer move-
ments of the right hand which are not specially localized, but serve this pur-
pose, as in conceptions of speech movement. "L'ecriture n'est qu'une des
formes de motilite de 10. main" (Dejerine). W'hen writing is done with the
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290 THE SYMPTOM~MPLEX OF APHASIA
left hand, the same, although less common conception of movements, is local-
ized in the right arm region, and we localize these in the right leg region
when we write in the sand with the left foot. These are the conceptions of
movement described by Storch, which in writing, as in every motor act, dic-
tate the movements of a. certain portion of the body, because we have in the
optical fields for memory of letters a special depot and a complete diagram
of the conception of those movements of direction involved in writing. There
are persons who can produce writing movements with their tongues. Exner's
theory of a special motor center for writing at the base of the second frontal
convolution therefore seems scarcely plausible, to say nothing of the fact that
it was based on an uncritical utilization of doubtful casuistic material, and
has not since been supported by pathologico-anatomical findings. An absence
of these conceptions of movement, analogous to Broca's aphasia, must there-
fore be assumed in all cases of paralysis of the right hand from a left-sided
cortical focus. The general incapacity of the right hand includes actual
inability to write, while thc retained motility of the left hand permits writ-
ing, and proves the continuance of its necessary conceptions of direction.
Such a unilateral agraphia can under no circumstances be synonymous with
Broca's aphasia. .This was probably present in Pitres' case in which there
was a cortical lesion, and, in spite of recovery of the finer motility of the
right hand, an exclusively right-sided agraphia was permanent. I shall later
discuss the explanation of this extraordinary and instructive case.
There is no unanimity of opinion among authorities as to the existence of
a so-called optical word center, actually an optical letter center. This mooted
question from a purely practical and clinical standpoint, might well be left
out of consideration, and we might be content with recognizing the insig-
nificance of a circumscribed unilateral lesion in the posterior lower area of
the lower parietal lobes in the sense of localization, an area which is important
as the seat of origin of what N aunyn, upon the basis of statistics, called indefi-
nite aphasia. Here the decisive point which belongs among the most positive
facts of cerebral localization, is that a unilateral focus deeply situated in
the medullary strucfure of the parietal lobe produces a combination of right-
sided hemianopsia and isolated writing blindness or alexia as persistent symp-
toms. If the affection is diRseminated and reaches the cortex of this portion
of the brain, agraphia is added to alexia (Dejerine).
If these facts are grouped and explained like those of spoken language
in our diagram, the cortex of this portion of the brain would be considered
the point of optical "alphabet memory pictures," and pure writing blindness
as subcortical alexia analogous to subcortical sensory aphasia. It is self-
evident that experience alone can determine whether or not we will accept
this conclusion. and theoretic considerations must be held in abeyance. It
may even be admitted that there are theoretic grounds for the assumption
of such a center. The principle of conservation of energy appears to favor
the unilateral condition, the especial peculiarity, which characterizes the mem-
ory pictures of letters of the alphabet above all other optical memory pictures
as a corresponding special localization; I shall revert to this later. Finally,
it must be observed that this is the standpoint of such competent authorities
as Bastian, Dejerine and A. Pick. Nevertheless, I cannot agree with them
without sacrificing the theory of the internal connection and the fundamental
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principles for the understanding of the structure of the brain which were
taught with such conspicuous success by Meynert. This is alsO v. Monakow's
view; he doubts the existence of a true optical word center, and maintains
that optical memory pictures of letters of the alphabet are double. I had
previously expressed this opinion and had declared myself opposed to the
localization of the so-called optical pictures of word memory. Since a posi-
tive theory of localization, if erroneously taught, may imperil the advance
of the law of localization, as we have seen in the case of Broca's aphemia, I
feel forced to explain somewhat more minutely the untenability of the assump-
tion of an optical word center in the cortex of the gyrus angularis.
Theoretically all that we know of the nature of optical memory pictures
is opposed to such a narrowly limited localization of alphabet memory pictures,
particularly to a unilateral one. :More recent investigations have clearly
shown that the memory pictures of the special senses have motor components
which from their nature are inseparable. Storch has designated optical mem-
ory pictures by the appropriate term, direction conceptions. Such concep-
tions of direction also apply to all motor projection fields, but nowhere so
clearly as in the optico-oculomotor projection field which, in contrast to the
true field of light ( H. Sachs), includes the convex surface of the occipital
lobe and the gyrus angularis of the lower parietal lobe. For example, such
conceptions of direction, in so far as they relate to the arm and hand, are
localized in the so-called middle third of the central convolution. As shown
above, they coincide with conceptions of writing movements. Now the optical
memory pictures of letters, like those of figures or any other objects which
have but two dimensions, differ from concrete things by the fact that to
the sense of sight they each have but one form (Storch 1) while all other
concrete objects possess innumerable ones. Their limited number, and the
exceedingly frequent use which we make of them, will cause them (accord-
ing to the principle of well grounded tracts) to appear as a particularly firm,
and consequently easily utilized, possession in pictures of memory. Finally,
optical memory pictures of letters are characterized, as I previously attempted
to explain, by the fact that they bear no direct relation to concrete concep-
tions. Except a single tract which is the most marked, hence the most easily
understood tract, they have no communication with a unilateral speech region
nor, we may presume, primarily with the acoustic sound center. These three
properties which they possess in a greater degree than any other optical mem-
ory pictures, give us no reason to assume a specially circumscribed localization,
except that the point of most distinct sight and of the finest differential oculo-
motor conceptions of direction has a special localization in the cortex which
has not yet been proven. Only one of these properties, namely, exclusive
association with the left temporal lobe, is a factor important for the unilateral
nature of the alphabet memory pictures. But to this I shall refer later. If
we consider the functional acquirement of memory pictures of letters of the
alphabet, it does not favor the predominance of the left hemisphere. In
typical hemianop8ia the form of the field of vision permits us to conclude that
the immediate surroundings of the point of fixation are almost always bilat-
J Details in an article by Storrh: II Versuch einer psycho.physiologiBchen Dar!'tel·

tung des BewusswiDB." Berlin, 1902.
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292 THE SYMPI'OM-COMPLEX OF A}'HASIA
eral, and supplied by each optic tract. Usually the picture of a letter is
formed exclusively within this central area of sight so that its memory
picture is formed in each hemisphere. If the letter is large, the glance will
wander as with every large object, but central sight will always be exclusively
implicated.
\V e might believe that the possible unilateral nature of optical memory
pictures of letters might be directly determined by ascertaining whether there
is a difference in the peripheral portion of the field of vision, and whether
the patient reads with the right or the left half of the visual field. This
theory, however, is shattered by the fact that even the largest letters can be
read only in the immediate vicinity of the point of fixation, while beyond
this it is impossible to say with certainty whether or not there are any letters.
It is usually maintained that central acuity of vision rapidly declines out-
wardly from the point of fixation. How rapidly this becomes apparent on
an attempt to recognize letters, and there is no difference between the right
and left halves of the field of vision. But certain facts in the pathology of
the brain are much more important than these academic considerations. Above
all, we can form no conception of the combination of isolated word blindness
with right-sided hemianopsia in the sense that hemianopsia, i. e., the functional
interruption of the subcortical tracts which substitute for the left cortical
tract, is to be regarded as the cause of word blindness, as the acoustic tract
which terminates in the left temporal lobe is the cause of subcortical sensory
aphasia. On the contrary, the majority of cases of typical right-sided hemi-
plegia show no trace of word blindness or alexia; at most, reading is made
difficult by the hemiopic defect itself, from the fact that the patient cannot
see the letters or words immediately following, but every letter or syllable
is recognized unless there is an impairment of memory as in a case of Red-
lich's. It is noteworthy that with the sudden appearance of hemianopsia
this defect is soon recognized, therefore reading need not be even temporarily
prevented by the hemiopic defect. In all of these cases we must assume that
the patients depend exclusively upon the right hemisphere in reading. In
occlusion of the tractus opticus the left hemisphere must to a certain extent
be regarded as blind. If, in spite of this, the patient recognizes letters and
their sequence it must be because of the termination of the optic tract in the
cortex of the right hemisphere. This conclusion is so obvious, and so con-
vincingly disproves the theory of the unilateral nature of the so-called optical
word center in the left hemisphere, that its exponents, particularly Dcjerine
and Bastian, were forced. to consider it. They attempted to nullify its im-
portance by assuming that fibers of the corpus callosum, which pass from
the optical projection field of the cortex of the right hemisphere to the sym-
metrical cortical fields of the left hemisphere, were still able to reach the
optical word center upon the left side. For this purpose they differentiated
between a general visual center and a special optical word center: The for-
mer is bilateral, the latter unilateral, and present only upon the left side. In
the same way they differentiat,ed a general center of hearing in both tem-
poral lobes, and only a left unilateral and special center for the understand-
ing of word sounds. I believe this entire reasoning to be erroneous, as it
controverts the views of the pioneer Meynert, and ascribes functions to the
fibers of the corpus callosum, which are merely a continuation of the fibers
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of the tract of the optic nerve, or of the auditory nerve, beyond. the cortical
projection field into the opposite hemisphere. Were these the true conditions,
the hemiopic defect in a unilateral lesion of the optic tract would eventually
be compensated for by the other hemisphere, and no longer be noticeable.
}'inally, I must refer to the clinical condition known as soul blindness, which
frequently accompanies word blindness or literal alexia.
H pathology thus disPFoves the unilateral and narrowly circumscribed
localization of an optical word center, all the more necessary is it specially
to review the circumstances which produce this unilateral and circumscribed
condition. Apparently it is the relation brought about by association fibers
between the unilateral speech region and the optical memory pictures o.f let-
ters, and chiefly of their acoustic components which are calculated to simulate
t.his unilateral condition. Here two possibilities become obvious, but further
investigation by necropsies will alone clear the situation. One view, accepted
by }fonakow, is that foci in the gyrus angularis, besides interrupting the optic
radiation of Gratiolet, have also implicated the crossed optic-acoustic com-
missure (Bastian), i. e., the association fibers between the left temporal lobe
and the right optical oculomotor projection field. The optical memory pictures
of the left hemisphere are then obliterated by the interruption of the optic
radiation of Gratiolet (hemianopsia). The optic memory pictures in the
right hemisphere might yet. be stimulated by means of the right optic tract,
but could not be utilized in reading because they could no longer evoke by
means of the previously mentioned commissures the absolutely necessary acous-
tic or word sound constituents of the letters. In other words, the power to
form words from the individual letters would be lacking, and reading by
spelling the words would be quite impossible. As an exception to the rule
of reading by spelling, reading would be limited to the few words which the
patient had previously learned to recognize. The majority of patients expe-
rience great difficulty in naming objects shown them, and this is usually
observed in cases of word blindness; it is ascribed to a lesion of the communi-
cating tract which leads to the left temporal lobe, but incorrectly so, as we
shall soon see. Moreover, this does not explain the fact that letters, especially,
are seen Dut not identified, all other objects being clearly recognized. We
have seen that other relations than those of letters to the acoustic projection
fields do not exist. It is a question, too, how in word blindness thus pro-
duced the form of the letters themselves can be recognized, copying being
done correctly, and also how it is that the same letters in different arrange-
ment appear identical, being transferred from one arrangement to the other,
the purely optical components remaining undamaged. For some of the cases
so far observed this expectation has not been realized; on the contrary, a most
conspicuous feature of these cases is that the patients do not actually write
the letter of the alphabet while anxiously following the copy provided, but
are only able to draw it. If we have ever noted how these patients laboriously
draw each letter, and how they find this equally difficult whether the copy
be written or printed, we will scarcely search for the cause of this defect in
the interruption of the decussated optico-auditory commissure.
Of course we must bear in mind that the optical memory pictures of letters
represent complexities of form conceptions, and these attain definite impor-
tance only from the fact that they are associated with the word conceptions
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294 THE SYMPl'OM~MPLEX OF APHASIA
of the letters belonging thereto. Articula~ speech is composed of word con-

ceptions, i. e., it represents the combination of a sound picture and a definite
conception of speech movement, and these bear to the optical memory pictures
the relation above described, and when this relation ceases the latter at once
deteriorate into meaningless signs. 'This may explain why the identity of
a printed and a written letter, or of a Latin and a German word, is no longer
recognized if the sound which produces the relati.on can no longer be inter-
nally produced. It is even questionable whether the pure optical components
of letters, detached from their sounds, will permit us to recognize that we
are dealing with the letters of the alphabet.
If we transfer this first possibility to the diagram it would correspond to
a combination of subcortical and transcortical symptoms. The unilateral
affection of the tract would be subcortical, and the interrupted continuity of
the crosscd optico-acoustic commissure, transcortical. Alexia would arise be-
cause only one of the tracts, ,c and a, the crossed and the uncrossed, would
be interrupted, but the othcr, in conscquence of the interruption of its sub-
cortical. tract, would be useless. On the other hand the unimpaired, uncrossed
tract c a would bc amply sufficient for the power to write as before.
The second possibility is that which simultaneously assigns to the left
optico-oculomotor projection field a predominant and indispensable role by
permitting an ability to read; this is quite in contrast to the first theory,
according to which the left-sided projection field appears to be especially
excluded. According to the principle of the conservation of energy it permits
the view that only the optical memory pictures of letters in the left side are
united to the acoustic projection field by a well beaten tract; that, therefore,
there exists only one uncrossed acoustico-optico commissure or tract c a. This
would lead to the further assumption that the connecting link, c and a, neces-
sary for reading, must always follow a circuitous route over the left optico-
oculomotor projection field even when, in consequence of right-sided hemi-
anopsia, reading is accomplished solely by means of the right hemisphere.
The interruption of communication which alexia causes must be sought in
the commissure between the two optico-oculomotor projection fields, particu-
larly between the oculomotor projection fields, a view which in the main
coincides with that of Bastian and Dejerine. The only difference would be
that the memory pictures, not the point of perception, are united by fibers
of the corpus callosum. I have elsewhere expressed myself concerning this
possibility.1 Transferred to the diagram this interruption would not affect
the tract, c a; therefore in regard to a, it would be of double subcortical
. importance; first, on account of the tract fibers of the same side, and sec-
ond, on account of its dctachment from the optical memory pictures of
,the right side which are still susceptible to light. From this point of view
the power to write which emanates chiefly from the left center, a, would,
because of thc integrity of the tract, c a /J, show no disturbance.
The question of the unilateral origin of an optical word or letter center
is evidently of great importance for the entire law of localization. If we
deny it, as in my opinion we must, there is still some hope of a pathology
of the fibers of the corpus callosum; for it would be comparatively easy to
_ 1 L. c.
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decide which part of the corpus callosum must be implicated in order to pro-
duce the symptoms of subcortical alexia or pure word blindness.
I must admit also that our case of apparently isolated and literal agraphia
described at the beginning of this article cannot be better explained than by
adopting the view of the unilateral location of the center, a. The tract, II fl.
would then be interrupted at a point transcortically beyond II; the assumption
of two tracts, namely, one upon the same side and one upon the crossed arm
region, makes this the more plausible because they have the same point of
origin in II. Nevertheless, as we shall soon see, the apparently natural and
obvious explanation is in absolute opposition to other experiences. In con-
trast to the view of a special position for the letter center among the optical
pictures of memory, this case exhibits a singular feature since the patient,
besides having lost the faculty of writing, had also lost the power of drawing
the simplest figure.
The clinical picture of pure word blindness, more correctly letter blind-
ness, or, in accordance with my suggestion, subcortical alexia, is based upon
quite a number of cases; Redlich 1 has collected from literature no less than
twenty-seven pure cases and, as has already been stated, there is no lack of
anatomical foundation for this view. The chief symptom of the clinical pic-
ture may be delineated by a case which is quite typical. .
L., a plasterer, aged 66, understood questions I addressed to him, and answered
them all correetly. He was intelligent and showed no defect in speech. When asked
to \\Tite something at dictation he did it correctly and uninterruptedly, and also wrote
down any figure required of him. At my request he wrote a letter to his married daugh·
ter; although there were errors in spelling and the alignment of the writing was poor,
and although there were breaks and repetitions as from uncertainty of motive, the
letter was upon the whole correct and comprehensive; had he been a man of education
it would probably have been perfectly correct. The man was then asked to read what
he had written, and the surprising fact was reveaied that he could not read a word,
not even a letter or a figure.
The same condition is found in all analogous cases, provided they are as
well marked as that of my patient. The cases differ only in that figures are
often clearly recognized. We learn from this case that the difficulty is not
due to visual disturbance, for the patient said his sight was good, which was
also proven by the fact that he could copy letters and words which he did
not know, of course in a mechanical way, copying character for character like
entirely unfamiliar figures. Hence he did not understand what he had writ-
ten, and it has been repeatedly observed in analogous cases that by this cir-
cuitous method the patients are able to decipher what has been written,
although slowly and with great difficulty. The investigation of the acuteness
of vision proves that this is quite sufficient for the recognition of letters.
Neverthelefts, this patient:s sight was defective; this was evident from the
peculiar position of his head while writing, from the running together of the
words, and the defective alignment. That is, he had a typical right-sided
hemianopsia, with vertical separation of the halves of the field of vision into
the familiar fonn in which a narrow portion, passing over to the right, still
1 Redlich, .. Ueber die sag. Bubcorlicale Alexie. Jahrb. f. Psych.,Bd. XIII, 2 und
3 Heft.
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retains the faculty of sight. Bilaterally the acuity of vision was at least
one-half of the normal; the eye-ground was absolutely normal. This defect
manifested itself by making fluent reading impossible, because there was no
view of the following letters, and in our case the only letter seen in totality
was not recognized. By showing objects we convinced ourselves that the
patient's sight was sufficient; he was able to recognize any object. But a
phenomenon is frequently observed in analogous cases, and is sometimes more
highly developed than in this case: Difficulty in properly naming an object.
In our patient this occurred only now and then. Expressions of embarrass-
ment or descriptive terms were first uttered; finally, on being prompted, the
correct word was eagerly accepted. In other cases not a single object shown
can be correctly designated, and this was the case with a patient that I saw
about 25 years ago in the Charite. It was the only symptom which indicated
aphasia. In spontaneous speech, words are not lacking, not even those for
visible objects. When, on the other hand, this symptom is more conspicuous,
as, for example, in my earlier case, there is more or less difficulty in finding
words for concrete objects, even in spontaneous speech, but, as a rule, this is not
so difficult as naming objects which are shown.
During the first period of observation another phenomenon appeared which
is apparently of much more serious import than the mere difficulty of finding
words. The patient for a time was absolutely unable to recognize objects that
he saw, although he perceived them distinctly; he therefore presented the
well known symptom of mind blindness. This condition is not the result of
accident, but is frequently observed in cases of so-called pure word blindness.
Deducting conclusions from the course of our case, we recognize an increase
of this defect in alexia, and in our case an apparently secondary effect depend-
ing upon an indirect focal symptom of the lesion producing alexia. In regard
to the simultaneous occurrence of these two phenomena, experience teaches
that mind blindness usually leads also to word blindness, but isolated writing
or word blindness frequently occurs without mind blindness. In the first
case I observed there was no indication of mind blindness. In the case just
considered it was remarkable that during the time of soul blindness the patient
was unable to recognize objects even by touch. Mind blindness, therefore.
existed even to the extent of asymbolia, the most severe sensory defect which
can be referred to focal disease. Concerning the history of our case, its course
so far and experience in similar cases permit the conclusion that ~e are deal-
ing with a stationary condition in which a possible improvement may be hoped
for. While there is no present sign of hemiplegia there were symptoms of
this six months ago, but these completely disappeared within two to three
weeks, a faef which indicates that embolic processes were present. The
symptom-complex now existing attracted attention because the patient was
no longer able to read his newspaper as usual. Weare justified in attribut-
ing this to embolism and to resulting softening. 1 The probable locality of
the pathologic focus will be subsequently pointed out.
Besides the typical pathologic picture which our case presents, no doubt
there are other isolated disturbances of the faculty of reading which are of
1 E. Storch, "Zwei FlUe von reiner A]pxip." JlonatscAr. f. Psych. fl. l>'eurol.,
X I II, Ergilnzungsheft.
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D~BANCES OF WRITTEN LANGUAGE 297'
different nature; for example, the dyslexia first described by Berlin, l a partial
inability to read which manifested itself subjectively, and soon increased to
complete inability to read; after a little rest the patient was able to go on
reading but it was with recurring signs of exhaustion which rapidly increased.
Here the feeling of disinclination was remarkable (" fear of reading,"
Bruns). We cannot refrain from assuming that this is a functional affection
of the same or similar origin as is pure word deafness, and the suspicion of
an organic foundation, no matter of what nature, must be borne in mind all
the more as Berlin's experience led him to emphasize the unfavorable prog-
nostic significance of this symptom which usually appears suddenly. Hemi-
opia may be present but it is not a requisite as in alexia. Most of the cases
succumbed in a few years from serious affections of the brain. Atheromatous
and syphilitic disease of the cerebral arteries were repeatedly found.
As we have seen, isolated word blindness is a combination of various con-
ditions, usually of the interruption of a subcortical tract and the integrity
of a transcortical tract. From the well known location of the pathologic focus
,,·hich corresponds to these requirements, deep in the medulla of the gyrus
angularis, we may conclude that the tract of thc cortical surface of the gyrus
angularis, which has remained intact; must lie nearer than the destroyed one.
Therefore, the fact mentioned above (which was utilized by Dejerine in the
eonsideration of a center of optic word memory pictureR), that widespread
destruction in this region produces literal agraphia as well as literal alexia,
entirely destroys the perception of written language, also the fact that if a
disease at the cortex be added to a disease of the decp medullary substance,
agraphia is added to the previously isolated word blindness. According to
our diagram, agraphia and alexia are produced by the interruption of the
tract, c a. that tract which forms the necessary power for all perception of
written language. As I have reiterated, this power most likely exists in nature
in two entirely different tracts whose anatomieal relations we have yet to dis-
cuss. This may explain why their common division causcs an exclusive arrest
of the function of written language without any implication of speech, a
condition I!O far very rarely observed; we shall see that the two cases of
Rieger and Sommer are the only examples which approach this. It would,
however, be a somewhat common occurrence if the cortcx of the gyrus angularis
,,'ere actually an optic word center, ~s Dejerine maintains. It is evident from
the diagram, which illustrates Dejerine's views of the extension of the speech
region, that this author ascribes an influence to spoken language, to the so-
called optical word center, similar to that of the acou~tic word center. This
opinion we cannot accept; it is opposcd to our theory dcveloped above that
in persons mentally sound letters, not words, form optical memory pictures.
As already indicated. the coincidence of literal alexia and agraphia with-
out essential affection of speech has been observed only in the two cases of
Rieger and Sommer. They are of such great importance that I mu~t relate
some of their details. Rieger's report. which is a remarkable example of
impartial ,description in a difficult realm, shows that the patient had 10flt
all conception of three of the small letters of the German alphabet, p, x, and y,
1 Arch. f. P8Ych., 15. Bd., p. 276. "Wanderversammlung slldwestdeutsch. Irrenllrzte

u. Neurologen," 1883.
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and of the small Roman letters these three as well as d, h, k, and v. Of the
capital letters he had lost the conception for fourteen of the Roman as well
as the German alphabet; namely, all those previously mentioned with the
exception of D, as well as B, E, F, M, N, R, T, and W, so that he retained
the power to use only eleven letters. This defect included both written and
printed' letters. When the patient was shown these letters he behaved as
though they were absolutely foreign things, and when he was told "This is
a B" or "This is an E" he shook his head and said "I do not know."
But he at once recognized the letters he knew, being able both to name and
to write them. He responded in the same manner to words composed of
letters with which he was familiar. He was absolutely unable to write spon-
taneously the missing letters; he could laboriously draw them from a copy
as if they were unfamiliar arabesques. So far as his perception of letters
extended, the patient could write from dictation or from copy, but at first
without understanding what he wrote. Spontaneous expression by writing
was absolutely impossible, and in general he read without any comprehension
of the subject. In his spontaneous speech there was nothing conspicuous.
Now and then he was disturbed by being at a loss for a word, usually a sub-
stantive. Of figures he knew only 0, 1; 2, and 3, all others and all combina-
tions of those he knew being absolutely incomprehensible to him. Besides
this more or less localized defect the patient exhibited another which usually
belongs to the realm of speech; that is, an inability to name objects shown
him. He handled these, and in a general way had some perception of them,
as well as of iheir properties. There was also an impairment of memory
and of all the realms of special sense; this was no less marked than in
Grashey's celebrated case which was subsequently investigated by Sommer
and Wolff. As showing other defects, we must also mention the loss of the
art of drawing in thi~ man who was previously a skilful sculptor. All appre-
ciation of curves was gone. In a restricted, practical sense there was no
diminution of intelligence. For our purposes it is interesting to report that
this patient could always find words for objects shown him, even though after
an abnormally long time, and that among the objects presented to him he
secmed to prefer letters inasmuch as he could name these in one-half the
time consumed in naming other objects. According to Rieger's explicit report,
this condition remained unchanged for two and a half years. The patient
was a sculptor and teacher of drawing, aged 32, who had sustained a seve'te
fracture of the skull in a railway accident. The defect did not appear at
once, at least not to its full extent, but developed. six months after the acci-
dent and finally reached the degree which has been described. In Sommer's
case 1 there was a similar and persistent lack of perception of certain letteTll,
and a partial literal alexia and consequent agraphia, the result of an attack
of apoplexy. In this case the recognition of a number of other letters varied
and was uncertain. Moreover, the patient was unable to combine the lett{!rs
he knew into words, and thus to read. so that the condition was practically
a complete alexia. Still more complicated was the perception of written
language whieh was somewhat better retained; hence the case reminds us of
1 Sommer, "Zur Theorie der cerebral en Rcbreib- u. Lesest6rungen." Zt8chr. f.

Psych. U. PhY8. der Sinnc8organe, 5. Bd., p. 305.
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subcortical alexia. For all practical purposes there was also agraphia.. It is
interesting to know that immediately after the apoplexy, and for about a year
and a half, the patient was unable to read or write. At first he had little
command of words. After fourteen days the right-sided hemiplegia improved,
and while under observation right-sided hemianopsia was demonstrated.
Aside from this disturbance of the power to read and write and his inability
to find words with which to express himself, the patient was intelligent and
sensible, hence we must assume that this disturbance of speech was not so
marked as in Rieger's case. No autopsy was held in either of these cases.
In explanation of the peculiar partiality of this isolated impairment of the
perception of written language it has been pointed out that in all disturbances
of reading the more infrequently used letters, such as x and y, are more apt
to be implicated than those in frequent use. However, in these patients it
was not the letters most seldom used which were lacking but the quite com-
mon ones, and the persistency of the defect appeared to exclude a purely func-
tional nature. In all our experience in speech disturbances in focal diseases
of the brain we know of nothing analogous except one case of mental disease
after recovery from which a partial motor sensory aphasia and a defective
Use of words persisted. 1 In fact, as in mental diseases which show a prefer-
ence for certain association tracts and functions, we must assume in the first
case a similar degenerative process as a consequence of shock to the brain,
and in the second case an apoplectic attack. Obviously the affected tract is
the tract c a.
As an illustration of pure isolated agraphia the case might answer which
I mentioned at the beginning of this article (unusual and rare as this case is)
because it presents the postulated defect in a comparatively pure form, and
careful investigation demonstrates that the patient also suffered from a dis-
turbance of internal speech and word conception. Besides we would neces-
sarily assume that there was formerly a decided disturbance of speech which .
had greatly improved. The reduction in the power of spontaneous speech
which was conspicuous during the time of observation and even two years
later, was in contrast to the otherwise active intelligence of the patient, and
this justifies the differentiation of the disturbance as one of transcortical motor
aphasia, although not of high grade. In this connection I may refer to the
published report of my own case/l Therefore, it will be seen that the same
complication was present in the few comparatively pure cases of agraphia
which I compiled from literature, and I reached the same conclusion as
Dejerine that there is no pure literal agraphia, or motor agraphia, as Pit res
called it. Notwithstanding this it is certain that the peculiar symptoms of
the case cannot be explained solely by the disturbance in word conception, but
that aside from this, the exquisitely literal or, better, the motor, character
of the agraphia forms the predominant feature in the pathologic picture.
This is also true of the few analogous cases which I was able to find. My
patient, as is proven by the comparatively well retained faculty of reading,
undoubtedly received optical memory impressions of letters. but, unlike a
1 Hl'i1bronnl'r, "Aphallie und Gf'iRteRkrnnkhl'it." Psychiatrillche Abhandlun/!l'n.
herausgl'geben von Wernicke und ZeitBchr. t. Paych. u. Phyllial. d. 8inneBorgane. XXIV,
p.83.
I L. c.
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normal person, these could not be transmitted to the motility at his command.
Comparing this with our diagram of written language there appears to be
an interruption of the tract a fl. From my previous presentation it is evi-
dent that this tract is bilateral, and the especial peculiarity of my case, as
well as of the few analogous ones, is the bilateral absence of function.
In this case symmetrically situated foci in both hemispheres, but less
marked in the right, might possibly be thought of; the periodic appearance
of left-sided symptoms might be regarded as favoring this view, and such a
possibility must be borne in mind. But the analogous cases presented signs
of left-sided focal disease exclusively, and cannot be explained by the assump-
tion of symmetrical foci. Weare therefore forced to the conclusion that the
disturbance of word conception and also a general damage to the functions
of the brain might under some circumstances have such an effect that besides
directly damaging the unilateral tract it might render the other also incapable
of function. In our case the transcortical disturbance of speech, still evident,
is probably insufficient to permit the utilization of a tract on one side for a
function which is too difficult and, therefore, impossible to perform. As a
rule, when these conditions exist we must consider the unilateral interruption
of the supposed tract. We actually find an excellent example of this in the
case which Pitres, in spite of the unilateral nature of the disease, designated
as "agraphic Olotrice pure." In this case it appears that some time pre-
viously an agraphia similar to that of my case had existed. This, however,
improved, persisting only in the right hand, although the motility of the hand
was otherwise restored. Right-sided hemiopia with good vision was perma-
nent. There was originally a right-sided hemiplegia with severe general
symptoms. In these cases of unilateral disturbance of the power to write, the
use of the term agraphia might very properly be questioned. But no doubt
this is such, and scarcely any other explanation is permissible than that it
is a unilateral interruption of the tract a fl of our diagram. Liepmann's case
of unilateral apraxia showed on minute investigation the same phenomenal
motor agraphia limited to the right hand, only this formed a part of the
total picture of unilateral apraxia. . The patient was able to write with the
left hand, but he performed mirror writing. This example, it appears to
me, throws light upon the function of the right-sided tract, a fl.
According to Liepmann mirror writing or, more appropriately, abduc-
tion writing, is a striking proof of the purely mechanical way in which mem-
ory pictures of letters are transferred to motility. While learning to write
most persons practise this process by chiefly using the left-sided tract, a fl;
which, we may at once explain, is in accordance with the principle of the
conservation of energy. But we must also take into account the general
experience that in such practice symmetrical movements of the other half of
the body are unconsciously practised, movements which we attribute not only
to the functions of the motor anterior horn cells of the spinal cord but also
to complicated cerebral functions. The so-called conclusion by analogy de-
pends upon this. If, however, the same innervation of the right arm center
takes place by means of right-sided memory pictures of letters in the right-
sided tract, a fl. a~ in ordinary writing, and the left arm center by means
of the left-sided tract a fl. mirror writing or ahduction writing must result.
Now it is also the function of this tract voluntarily to conduct writing move-
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ments of the left hand in such a way that they correspond to the identical
direction conception instead of to the symmetrically opposed ones, as in writ-
ing with the right hand. But this is primarily drawing, which is done with-
out practice, and even in opposition to the involuntary innervation passing
in an opposite direction. It therefore represents a much more difficult cere-
bral activity than mirror writing, which is produced by a tract which is some-
what well marked. Subjectively this necessitates a special exercise of the
will. Thus we comprehend that a transcortical motor aphasia, even though
only feebly indicated, renders correct writing by means of this tract impossi-
ble; the necessary stream of innervation is too weak at its source. What,
however, is not so easily understood is the fact that our patient with agraphia
never showed the slightest inclination to mirror writing; our suspicion of a
very circumscribed, symmetrical focal affection of the right hemisphere must
be thereby increased. Moreover, the conditions which produce mirror writ-
ing are still imperfectly understood. Accompanying right-sided hemiplegia,
either with or without disturbance of speech, it- is apparently sometimes ob-
served under the same conditions, and sometimes not. It is chiefly noted in
persons whose minds are somewhat impaired, with or without signs of uni-
lateral atrophy of the brain, and especially in idiotic children (Soltmann).
If normal children who have had the same elementary instruction are forced
to write with their left hands, some produce mirror writing, others do not.
When min:or writing is noted it is usually quite cdrrect, and proves that there
is no literal agraphia.
I shall return to the presumable position of the tract a 13. We see that
a certain point in this tract may be determined with some degree of likelihood,
and thus isolated agraphia as a focal symptom becomes as important in local
diagnosis as is isolated alexia as a focal symptom of the gyrus angularis.
One of Rieger's cases which was reported by Wolff 1 appears to be an
example of pure cortical agraphia. Here total central blindness due to bilat-
eral destruction of the optical projection fields of course also resulted in cor-
tical alexia. -
For the rare cases of isolated literal agraphia which are analogous to our
first case, it is practically unnecessary to search our diagram for a designation.
Nevertheless it is instructive to consider this analogy and the corresponding
disturbances of speech; it then appears to be the much- disputed conduction
aphasia which forms the prototype for the assured possession of this form,
so that a lesion of the tract a 13 would justify the conception of conduction
agraphia. As I have repeatedly emphasized, its nature is evident from the
fact that in writing there is no conception of the form of the letters, while
the power to produce them is still intact; hence those cases of agraphia in
which the conception of the form of the letters is well retained, no matter
how incorrect the writing, do not belong to the pure disturbances of written
language, but to the sequels of disordered speech or disturbed communication
of word conceptions. Such cases are therefore differentiated from the previ-
ously described literal agraphia as verbal agraphia. That this verbal agraphia
may possibly result from a lesion of the traet c a is shown by a case which
t G. Wolff, "Ueber krankbafte DiBsoc.iati~n der Voratellungen." Habilitation-

lelwif', Leipzig, 1897, pp. 43 eI Hq.
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I mentioned in my previous report; certainly it is an extremely rare occur-

rence, for I have never seen anything similar. It is quite conceivable that
cases of sensory aphasia which have recovered, and these are not infrequent,
may leave such a circumscribed defect because restitution if not perfect may
perhaps be incomplete in only one respect; namely, that the most difficult
function is impaired. Without doubt the transmission of the internal word
conception to its written expression is the most difficult function which is here
called into exercise. 'l'his view bears out the general experience that among
all the symptoms of aphasia the disturbance of writtcn expression is the most
intense and tenacious. This explains why paraphasic symptoms which are
not noticeable in speaking are observed in writing. It often happens that
paraphasia which is only slightly evident in speaking becomes most obvious
on spontaneous writing, or the existing paraphasia may be greatly aggravated.
Thill condition is frequently noted in paralytics with aphasia of varying
degree.
Paragraphia in a restricted sense, or literal paragraphia, in which the form
of letters is distorted, is of practical importance, being the disturbance of the
power to write noted in paralytics. A tentative diagnosis of progressive paral-
ysis may not infrequently be made by observing a few words whiCh contain
distorted letters. A general impairment of the memory in senile or other
organic atrophy of the brain, in presbyophrenia and polyneuritic psychosis,
produces a similar paragraphia, apparently because the patient forgets the
exact formation of the letters.
A review of the disturbances of written language shows that I was justi-
fied in claiming that we are dealing with essentially transcortical symptoms,
and it is especially interesting to note that these transcortical symptoms may
follow lesions of quite definite areas of the brain, just like cases of pure word
blindness and so-called pure literal agraphia.
It is not a mere accident, therefore, that the study of written language
has up to the present time enabled us to arrive at most valuable conclusions
concerning the purely transcortical process which, according to prominent
authors, we may most aptly designate as "word finding." Word finding, par-
ticularly for individual letters, is a prerequisite for ordinary reading by means
of spelling and, for practical purposes, the letters which must be found are
like all other word conceptions. Therefore, reading is a part of the expressive
portion of the speech process, in which the finding of words for different con-
ceptions is the first and most necessary object. According to Rieger and G.
\\' olff, word finding for letters that are seen occurs normally and unisensually
by optical conceptions, like those of color. Word finding for letters is, how-
ever, the most necessary and most common part of expressive language;
therefore, in comparison with all other visible objects, it may be preferable
or easiest. In Rieger's case word finding for visible objects was about twice
as rapid as for others; in Wolff's case (identical with Grashey's) it occurred
instantly, and apparently even without the otherwise necessary writing move-
ments, for reading was immediately possible. For word finding the optical
memory pictures of the letters equals the different memory pictures of con-
crete substances which form the conception, B. If we cast a glance at Fig.
137 it at once becomes apparent that the direct communication, B b, which
we must maintain for clinical purposes, is probably unnecessary for letters,
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hence we postulate merely the association tract, B a. This tract which, like
B, here equals the optical memory picture, is contained in the optico-acous-
tic commissure (Bastian) of the same and of the crossed side. I ts ana-
tomical foundation for the same side is perhaps the lower longitudinal
bundle; for the crossed side, the forceps tapetum tract, as it was called by
H. Sachs.
C. S. Freund and H. Sachs also assume that the same association tract
produces word finding for objects shown, and its injury is held responsible if,
under some circumstances, an object which when first seen cannot be correctly
named, although it is clearly recognized, is correctly designated after exam-
ining it by the sense of touch.
:For this symptom, if restricted as above, the name optical aphasia
(S. Freund) is not inappropriate. It occasionally appears in the form just
described, and then belongs to the interesting group of conditions known as
"dissociation of conceptions." It cannot, however, be referred to the previ-
ously mentioned tract, since all experience shows that for visible objects a
recognition of their meaning is indispensable to word finding, and no case
hIlS yet been observed (for instance, of mind blindness) in which objects not
recognizable by the sense of sight were nevertheless correctly named. For the
recognition of visible concrete things their secondary identification (in this
case the association of their optical .fields of memory) is absolutely necessary
for the tactile conceptions belonging thereto. As we have seen, the conditions
are different with letters.
Although most conspicuously lacking for visible objects, the symptom of
impaired or entirely arrested power of word findings may usually be deter-
mined more quickly than any other impression of the general senses. In
Rieger's case all of the special senses responded to the same stimulus which
proved so successful in word finding, but they invariably required a certain
time which was about uniform.
The preponderating power of the sight in comparison with the other senses
was noticeable in the Wolff-Grashey case; the object seen, not merely the one
felt or heard, enabled the patient to find the word (in writing). In the
unisensual conceptions of the tactile realm some exceptions were noted, such
as wind, heat, cold, and in the auditory thunder, polka, waltz. That word
finding for such paramount tactile conceptions as smooth, rough, pointed,
sharp, and the like, requires the conjoint action of optical perception, also
proves the special influence in this case of optical memory pictures.
From the valuable work of Wolff it appears that various conceptions,
according to their meaning, cannot be composed of partial conceptions or
memory pictures of equal value, but that a main determining area of special
sense, and secondarily of memory pictures, may be differentiated. He pre-
sumes by analogy that the sense of sight is the chief and determining one
for word finding, as in his case; but this is quite unlikely, and is disproven
by Rieger's case. If, however, in Wolff's case, we ascribe to the optical tract
a comparatively better retained function than to the other projection fields.
we can readily understand its exceptional action, otherwise never observed,
which shows that the patient found his words by the roundabout method of
writing pictures.
When, as in the cases of Rieger and Sommer, the power to find words
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for letters is so disturbed that only the perception of certain letters is miss-
ing, others being perfectly unimpaired, we may quite properly maintain that
the patient had. lost all conception of the letters in question. Much more
common is a condition in which there exists merely an uncertainty in word
finding, especially for certain letters, without this symptom being constant.
In spite of this, patients can occasionally read without effort words contain-
ing letters of which previously there had been no conception. An example
of this was furnished while our case of agraphia was under observation.
Inability to read because of the loss of individual letters was much more
marked in a case of Bastian's in which, in consequence of extreme paraphasia,
not a single letter could be correctly named nor could words be read. aloud;
nevertheless the patient understood what he read. I mention these cases
because, more than any others, they expose to probable criticism our view
ihat reading is the result of spelling. They are explained, however, by two
generally recognized experiences. The one is this, that every virtuosity in
the sequence of individual acts, which is acquired by practice, suffers as soon
as close attention is directed to this individual act.. The simplest exam pic
of this is running down stairs, with or without observing the individual steps.
Attention drawn to the individual act, in this case manifested for the indi-
vidual letters, is therefore a deleterious factor for the complete performance
of an act, and we therefore understand that the complete act would much more
readily follow than the individual performance. A similar experience is found
in the more frequently observed cases of pure word blindness, in which ordi-
narily there is no impediment of speech nor paraphasia, but in which thc
name for objects shown cannot be recalled or only with the greatest difficulty.
Here also the attention bestowed upon the object may prevent the word find-
ing. It appears to me that Bleuler maintains the same in differentiating the
more automatic and fully conscious association processes. A second general
fact, in which spelling appears to compensate for some defects in reading.
is the familiar one that all impression processes are facilitated by secondary
identification. The most marked example of this is the recognition (in spite
of demonstrable and severe sensory disturbances) of objects that are only felt.
'fhat this process, closely akin to guesswork~ normally plays a great role, is
known to us all (as in the reading of handwriting).
The celebrated case of Grashey was first explained by the supposition that
the aphasic disturbance and inability to find words were due to a purely func-
tional disturbance, namely. the loss of memory for recent impressions or, morc
accurately, a decrease in the power of memory. I formerly agreed with the
opinion that in Grashey's case it was necessary to recognize a special form of
amnesic aphaf:lia. In the meantime, Sommer showed the untenability of this
view, and G. Wolff's subsequent careful investigation of the case lid to the
same result. The peculiarity of Grashey's case must not be sought in the
nature of the aphasic disturbance, but in the artifice dependent upon the indi-
vidual activity which the patient resorted to in order to conceal the actual
aphasic defect of word finding for visible objects. We have noted how this
artifice favors the fact that our written language is essentially a language of
letters. The difficulty of word finding has. however, always been regarded as
an important aphasic factor; very early Trousl'Cau. for example. contrasted
it with Broca's aphasia, and it actually corresponds to the practical require-
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menta according to which Pitres 1 lately included under the definite term of
amnesic aphasia all cases in which this symptom is either observed alone or
is prominent in the clinical picture.
We cannot go beyond the recognition of this practical requirement, for,
on the contrary, we must emphasize the other variations in the cases which
in this one point agree. The majority of cases of isolated word blindness
belong in this group, also Rieger's case, and the very peculiar case of Grashey.
Both of these have the common symptom of an almost complete loss of mem-
ory, but this phenomenon alone could not have been the cause of the inability
to find words, for this is absent in some cases of pure word blindness marked
by difficulty in word finding. Besides, the majority of cases are of different
origin, for they are usually cases of aphasia in which there is a certain com-
pensation as regards speech.
Pitres collected 10 cases in 8 of which he found that the lower parietal
lobe was implicated; this is not mere coincidence, but agrees with Naunyn's
statistical report that in the cases which he called" indefinite aphasia" there
was the predominance of a lesion at the boundary of the lower parietal and
occipital lobes. Of all the disturbances of speech, motor aphasia appears to
be the one in which, when recovery follows, a real disturbance of word finding
is most rarely found; we are therefore forced to agree with Pitres, inasmuch
as he alllO fails to include the implication of Broca's convolution. For the
rest, however, the great dissimilarity of the cases proves either that very dif-
ferent localities are implicated, or that functional disturbances of different
localization must act together. Pitres, who recognized the majority or the gen-
erally acknowledged disturbances of speech and written language, emphasizes
the great rarity of pure cases which would fulfil all of his requirements. He
considers it essential that they show absolutely no disturbance of the under-
standing, "either in reading or in writing, but only a difficulty in word finding.
The meaning in such cases of a severe impairment of the memory has not
escaped him. He points to the universal experience that a patient with diffi-
culty in word finding, notwithstanding repeated instruction, has the same
difficulty in finding definite words (which he gladly accepts if prompted)
as when only the beginning of the word is given him. Moreover, Pitres
attempts to explain th~ want of understanding in reading by the theory of
a disturbance of the memory, but this is opposed by Grashey's case of mark-
edly impaired memory with intact ability to read. It is very interesting,
however, to know that Pitres does not absolutely accept the view that the
lower parietal lobe is the seat of disturbance; on the contrary. he recognizes
that in word finding the stimulus of the true speech center is !1istributed
by neurons over the entire cerebral cortex, and these are to be regarded as
the carriers of psychical operations; the lesions therefore have no fixed topog-
raphy, but act by the interruption of the commissure between the different
centers of the word pictures and the cortical areas in which the higher psy-
chical acts are carried out. "Amnesic aphasia consists solely and alone in a
lack of connection between the conception and the word which serves to express
it." In a note we even find the statement that amnesic aphasia should prop-
erly be designated "transcortical aphasia."
----------------------------------------------------
1 A. Pitres, "L'Aphasie amn~ique et Res varij!tEs cliniques." Paris, la9S.
21
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306 THE SYMPI'OM-COMPLEX OF APHASIA
For the practical recognition of amnesic aphasia it might be advantageous

to differentiate between those cases which show only a difficulty in word finding
and those which disclose, in addition, the symptoms of paraphasia. The latter,
by far the most common, are almost always the residua of past disturbances
in speech, and therefore need not be considered. Aside from these, difficulty
in word finding shows itself almost exclusively or most markedly when objects
are presented to view (and also probably when listening, touching, etc.), and
sometimes by the absence of definite expressions, especially substantives, in
the otherwise fluent and correct spontaneous speech. A defect scarcely notice-
able at first becomes more prominent when we ask the patients to name objects
that have been shown. To cover their confusion the patients frequently use
roundabout expressions which denote embarrassment, such as "thingumbob."
The choice of incorrect or unsuitable expressions, however, belongs to the realm
of paraphasic symptoms.
The difficulty in finding words may, as is well known, be met with under
normal circumstances. Rieger very aptly remarks that this occurs in normal
persons only when using words of limited importance; for example, the word
" magnolia" cannot be recalled. "When, however, a person can no longer
say , This is a tree,' he must unquestionably be regarded as having a disease
of the brain." It is also true that the extent of these terms of limited impor-
tance may vary greatly according to the occasion, therefore according to the
mental condition in which the person happens to be. Rieger, so far as I know,
was also the first to call attention to the fact that all persons whose command
of a foreign language is imperfect show a very marked inability to eXpress
themselves in words, many 0.1 which they may understand perfectly. Were
this equally true of their mother tongue, it would correspond to our concep-
tion of amnesic aphasia. Under the same conditions an increase of this defect
may be apparent when they attempt to name objects shown them. This is
generally more difficult in the course of conversation than at other times, and
probably is due to the closer attention devoted to the object.
Pitres shows that the "systematic aphasia" of polyglots presents a stage
in which word finding in the foreign tongue is impossible, while the power
to understand has been retained; therefore a stage of amnesic aphasia.
After this description it is obvious that difficulty in word finding is noth-
ing more than a special form of transcortical motor aphasia; in other words,
a disturbance of the function of the tract B b of our diagram. In Rieger's
case, as well as in that of Wolff-Grashey, this disturbance consisted of a slow-
ing in the function which, however, was finally performed correctly. In
other cases, word finding is either impossible or to a certain degree is acci-
dental, and this is prone to be the case in the individual whose brain is not
actually diseased.
Nothing is more obvious than the assumption that 8. disturbance "within
the complicated tract B is the cause of the difficulty in word finding. Aside
from the already mentioned defect in the conception of letters, the fact that
in Rieger's case there was also a decided and demonstrable impairment of
conception favors this view; all conception of playing cards, coins, paper
money, stamps and similar things had been completely obliterated, and it
was impossible to awaken any conception of these objects, as well as of any
figures higher than figure 3, of algebraic signs, of musical notes, of the mean-
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ing of piano keys, or of punctuation marks. Something analogous, a decrease
in the number of conceptions, appears only in consequence of mental disease,
and the condition Rieger reported reminds us most forcibly of a case of
aphasia following mental disease which I described, as did also Heilbronner
in its later stages; 1 in this instance partial motor and sensory aphasia were
manifested by the fact that there was only a number of words for which
conception was lacking. For the retained power of conception we assumed
a damage of slighter extent, namely, a decreased stimulation of the con-
ceptions themselves as well as of the partial conceptions of which they were
composed (for instance, memory pictures), which change we were forced to
assume by the clinical findings, since the slowing of the process for the
recognition of objects could be physiologically explained only as a slowing
of the stimulation of some special sense. The same slowing could be demon-
strated in regard to the understanding of words which express the concep-
tions. The contrast between word understanding and word finding, which
might be urged in opposition to the theory of an affection of the conceptions,
is therefore not absolute; both processes were slowed, but one much more so
than the other. When objects were shown or handled, etc., the period of
time required for the recognition of the conception could be determined, and
it was at the same time evident that the chief delay was caused by the act
of word finding.
At the same time it was demonstrated that the conception itself, not its
partial memory pictures, always led to the knowledge of the name. In Wolff-
Grashey's case the conception in toto, not a partial conception, produced the
word. To the above emphasized unisensual conceptions there were naturally
some exceptions. The contrast between sensory and motor functions, between
the apparently retained understanding of a word and the difficulty in word find-
ing, is also evident here, but the intactness of the conception itself is far from
proven. If, for example, in answer to the question "Is the leaf blue?"
Wolff's patient had answered" It may be" or "I do not know," this would
indicate that his understanding of the sense of the words "leaf" and "blue"
was also affected; therefore, for the receptive portion of the process of speech,
a defective conception 1t"88 demonstrated. If the condition is such as to neces-
sitate a certain stimulation of the entire association complex which we term
conception in order to innervate upon the tract B b the correct word concep-
tion, or the correct movements of word conception, we may understand the
inftuence which perception by the senses may under some circumstances have
upon word finding: The corresponding conception thereby gains in intensity.
This influence is greater the closer the relation of distinct individual ideas
'Which together form the conception. In referring again to the diagram; Fig.
137, the importance of the foregoing conclusion is obvious. No less than
four equally important innervation streams must unite in b in order to pro-
duce the correct word conception.
We now understand why disturbance in word finding is so common after
focal diseases of the brain which run their course with sensory defects. Of
the many tracts which unite in b, only one or the other will be damaged,
only the innervation of a partial conception need be decreased, to render
lL. o.
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308 THE SYMPTOM~MPLEX OF APHASIA
word finding difficult. That conceptions are also less intense under relaxa-
tion is readily understood.
It may perhaps not be deemed superfluous when I remark that neither
in Grashey-Wolff's case nor in Rieger's case had the understanding of speech
suffered, for both patients were able to repeat words without any slowing
of the speech.
Usually we refer to transcortical motor aphasia only when the impairment
of the power to find words has increased to an entire absence of spontaneous
speech or to a state which almost equals this defect. If. however, the disturb-
ance is confined within the limits of amnesic aphasia (Pitres), the phenome-
non of a focal disease is apparently no longer present, but we suspect a dis-
turbancc of conception or intellect which, as we have seen, finds its analogy
chiefly in mental diseases. Since Rieger has given his excellent directions
for the investigation of such cases I do not doubt that in most instances some
such intellectual defect will be found. Any focal symptoms which are also
found will be only of secondary importance as indicating the area which is
the seat of general decrease of cerebral activity; as, for instance, in cases of
post-apoplectic dementia. That the symptoms of transcortical motor and
sensory aphasia due to senile atrophy of the brain may frequently be recog-
nized even without traces of a focal disease has been shown by Heilbronner.
In such cases there are usually signs of mental blindness, or asymbolia, which.
when there is mental disease, depends upon a disturbance of the power of
secondary identification. To enter more minutely into the study of -thesc
phenomena is impossible, since the richness of their number and their impor-
tance demand special treatment. But I must point out one of the most recent
developments in this borderland between mental disease and focal affection
of the brain, because it is most intimately connected with the explicitly treated
theme of word finding. This is the pathologic picture of unilateral apraxia,
constructed and masterfully described by Liepmann. As an unusually favor-
able coincidence is necessary in order to produce the t~'Pical pathologic picture
of transcortical motor aphasia, we also owe it to such a coincidence that in
Liepmann's case a focal disease of the brain was so situated, and of such
nature, that it severed the innervation of the transcortical tracts for the motil-
ity of one-half of the body. Moreover. as the patient in consequence of sub-
cortical motor aphasia was deprived of the power of speech, the intelligence
could be tested only by means of his motor reactions. The reaction of the
members on thc right side of the body indicated that the most extreme psy-
chical defect, absolute dementia, existed. However, when the left members
of the body were exclusively used in carrying out the reactions, a compara-
tively high degree of intelligence could be demonstrated. The autopsy of this
case, which has not yet been published, confirmed the diagnosis of focal dis-
ease of the brain. .
I shall not give explicit instructions for the examination of aphasics; it
seems unnecessary, for this article embodies the main points. But two phe-
nomena require special mention and careful consideration. One of these is
the extreme exhaustion which these patients often manifest and which soon
compels the physician to interrupt the examination, which can be only resumed
after the patient recovers from the fatigue. If no attention is paid to this
point, the different examinations will lead to absolutely contradictory results.
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DISTURBANCES OF WRI1TEN LANGUAGE 309
The second source of error is perseveration (Neisser); it consists in the in-
clination of the patients to repeat a reaction they have once found, even though
they know or observe that they are doing wrong qr are speaking incorrectly.
The patients often express their annoyance at this, and show plainly that the
second reaction was not intended. They are therefore subjected to a certain
constraint. In the case of aphasics this very common symptom is extremely
annoying, for the physician is often forced to pause, or to divert the attention
of the patient into another channel, in order to obtain a new and correct
reaction. As A. Pick has demonstrated, this disturbance may be so increased
as to form a variety of pseudo-apraxia.
I cannot conclude these essential, clinical, symptomatologic considerations
without discussing more explicitly the question of the unilateral position of
the centers of speech, as set forth in the preceding. My entire description is
ba..o;;ed upon the fact, learned by experience, of the unilateral position of the
so-called centers, and this fact must have been particularly impressive, for
one of the earliest investigators in attempting to localize these centers main-
tained that the left hemisphere of the brain was exclusively the seat of the
function of speech (Marc DU).l In my presentation of the subject I have
referred only to the left hemisphere, my purpose being to speak of the excep-
tions subsequently. Here two series of facts, abstractly connected, must be
chiefly considered. One series of exceptions relates to speech disturbances in
left-handed persons: These are almost exclusively due to disease of the right
hemisphere, the seat of the focus and the symptomatology bearing the same
relation to each other as the corresponding focal diseases of the left hemi-
sphere in the right-handed. We do not know how to explain the fact that the
conspicuous right-handedness observed in most persons, i. e., the choice of
the right hand for all movements which require great strength or dexterity,
causes the functional development of the speech center situated in the left
half of the cerebrum, and only this one principle is absolutely plain, that the
unilateral location in itself appears justified because it indicates a conserva-
tion of energy. A step forward is noted in Oppenheim's report of a case in
which. marked sensory aphasia due to a tumor appeared simultaneously with
left-sided hemiplegia; the history revealed the fact that the patient was not
left-handed from birth, but that in her seventeenth year, after sustaining an
injury to her right hand, she was compelled to use the left, and had since
become left-handed. Autopsy revealed the suspected tumor in the right hemi-
~phere. This observation leads to two conclusions: first. that the right hemi-
!lphere may assume thl,! function of speech even in adult life in place of the
left hemisphere who!'e function it is normally; seeond, that the left hemi-
sphere may completely lose the previously acquired function of speech if the
per;:on becomes left-handed. I know of no other observation which so strongly
confirms our view that the localization of speech centers is the functional
acquirement of each individual.
The other exceptions are pathological experiences in childhood. In focal
diseases of the left hemisphere in childhood, disturbances of speech are ob-
served which vary in degree according to the development of the child; these
1 The 11m invl'lltigator was BouillRud, who taught that the anterior lobes of the
brain were the _ t of the faculty of speeeh.
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are proportionally and rapidly compensated for, even when subsequent find-
ings reveal the complete destruction of the well known left-sided speech cen-
ters. Apparently, especiaijy in childhood, the preexisting left-sided cerebral
function is readily transferred to the right hemisphere. Under these circum-
stances left-handedness is not necessarily at the same time produced; if the
case comes to autopsy at a more advanced age there may be no symptom
referable to the left hemisphere, and the lesions may simulate those in right-
handed persons; or, fresh lesions of the right-sided centers may cause aphasia
in persons who are not really left-handed. As is evident, the faculty of purely
individual acquirements belonging to the centers in question leads to a num-
ber of possibilities which, under some circumstances, especially when the
history is obscure, may form an incomprehensible exception to the otherwise
regular localization of the speech centers. In fact we cannot deny a greater
individual latitude than heretofore to the presumption, according to which
at one time the left hemisphere, at another time the right is exposed, or
perhaps both in the same case, with or without the predominant assumption
of the function of speech by one hemisphere.
This point of view becomes especially important when we consider the
greatly discussed question whether in the fully developed brain, and in how
far, a substitution for destroyed speech centers takes plice by means of tracts
in the same localities of the other hemisphere. The explanation of the symp-
toms during convalescence from aphasic disturbance, in the widest sense of
the term, depends chiefly upon this prior question, but, concerning it, we are
still in ignorance. It is generally conceded that slowly growing pathologic
foci which act exclusively by displacement, at, least to the same extent as is
otherwise the case, produce no symptoms, not even of speech disturbance,
although the autopsy findings may indicate that the center or the tracts under
consideration have been severely affected. But this experience is by no means
general. There are cases which appear to prove the contrary, as for exam-
ple, Oppenheim's case, in which during the growth of the tumor the trans-
mission of the sensory speech function to the left hemisphere would have
been much more likely, as this merely involved the resumption of a function
previously exercised. The explanation of this contradiction need not be based
entirely on individual differences. It may readily happen that the number
of general symptoms accompanying the focal symptoms will guide us to a
decision. The two focal diseases which here come chiefly into consideration
are brain tumor and brain. abscess. These diseases may sometimes present
but few accompanying general phenomena, at other times the general symp-
toms are most pronounced. The activity of the other hemisphere is to the
same extent preserved or damaged; and it is obvious that its injury does
not favor the re-establishment of function. According to general experience,
the sensory speech function shows a greater resistance to injury than the
motor. In this connection it is more strictly correct to differentiate between
the impressive and the expressive parts of any speech process.· The conditions
are clearer when we consider the substitution by the other hemisphere in pure
diseases of the brain, or in those in which there is a predominant destructive
action, such as cerebral hemorrhage or cerebral softening. Here the possi-
bility of restitution by a new acquirement may be markedly influenced by the
general symptoms of the apoplectic insult, for we have often noted that a
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. DISTURBANCES OF WRITTEN LANGUAGE 311
severe attack, besides leaving unilateral focal symptoms, produces general in-
jury to the brain as shown by the ready exhaustion, the impaired memory,
and the emotional weakness which become chronic. Since experience teaches
that the accompanying insult in motor aphasia is usually decided, and in
sensory aphasia and pure word blindness is usually only slight or absent,
we also conclude that this favors restitution of the sensory speech function,
which is the rule, and heightens the importance of pure alexia as a focal
symptom.
Concerning the unilateral position of the speech centers there is another
condition which, in my opiniol' can only be explained by the theory that the
F,
•
Flo. 139.
motor or, more correctly, the expressive, portion of the speech process is not
always, and is not exclusively, unilateral. As is well known, the indirect
focal symptoms of acute focal disease of the brain after well marked apoplectic
attacks in general are limited to the affected hemisphere. To this, however,
there are often exceptions; for instance there may be a more or .less well
developed motor aphasia and a resulting left-sided hemiplegia after severe
apoplectic attacks. This condition usually lasts for only a few days, a proof
that we are not dealing with left-handed persons in whom aphasia, even as
an indirect focal symptom, must persist for a longer time. It can be explained
only by the assumption that in the affected individual, prior to the attack,
the right hemisphere with a certain portion of the process of innervation
was implicated in active speech; when, therefore, the apoplectic insult origi-
nating from the right hemisphere causes any injury whatever to the left
hemisphere, obviously that function which was previously exercised by the
conjoint action of the right hemisphere is most easily affected by the disease.
Whether we are here dealing with a permanent damage to the left-sided
Broca's convolution by the trauma of apoplexy, or only with a temporary func-
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tiona I disturbance, will be evident in the further course. There is a symp-

tom which is positive proof that the apoplectic insult has damaged Broca's
convolution. This is the condition designated as syllable stumbling, usually
regarded as a reliable indication of progressive paralysis, and therefore a
so-called paralytic speech disturbance. Exactly the same speech disturbance,
syllable stumbling, is observed in the majority of patients who have recovered
from motor aphasia, even though it has been merely an indirect or transitory
focal symptom of the affection of the left hemisphere. Little as this fact
is appreciated, it is nevertheless proven by many experiences, and I call special
FIG. 140.
attention to it because of its importance in differentiating this affection from

progressive paralysis.
We must now discuss the anatomical region of speech in the brain, or, as
Dejerinc briefly called it, on the basis of the preceding description, the" zone
du langage." I believe this cannot be better done than by presenting the
illustrations (Figs. 139 and 140) taken from the works respectively of Mona-
kow and Dejerine; the darkly shaded portions in both illustrations are the
centers which have been positively recognized, and the shaded areas represent
the speech rcgions. On comparison these two illustrations show a very satis-
factory agreement, especially when we consider that the two investigators
worked independently. It is evident that, with the exception of the anterior
processes and the lower connection of the central convolutions, the entire
first embryonic convolution, 1. e., the convolution limited by the Sylvian fis-
sure, may be included within the speech region. The portion situated in the
frontal lobe corresponds tc Broca's convolution, therefore to the motor speech
center; that situated in the temporal lobe, therefore below the Sylvian fissure,
is the sensory speech center; that above the termination of the posterior Syl-
vian fissure, the so-caned marginal convolution which is also known as the
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supra-marginal convolution, both authors ha\le included within the regions of
speech, without having assigned to it a definite and specific function. These
authors are also unanimous in no longer considering that the part above Broca's
convolution, the so-called foot of the second frontal convolution, belongs to
the speech region, although Exner, Charcot and Pitres, and recently Ziehen,
locate the motor writing center in this region. Moreover, these authors con-
cur in believing that the part of the convolution situated in the lower parietal
lobe and adjoining the first embryonic convolution·is still included with the
speech region, inasmuch as it is prolonged posteriorly hy means of an anas-
tomosing and communicating bridge to the second embryonal convolution.
This area extending horizontally and posteriorly is the angular convolution,
the" pH courbe" of French authors. Dejerine also includes in his speech
zone a neighboring part of the second temporal convolution, but tuis is not
depicted in Monakows illustration; in my opinion it corresponds with the
majority of the findings.
Within the shaded speech region of Monakows illustration there are
two, and in Dejerine's three, darker areas which, in the latter, are sharply
demarcated j two of these almost absolutely agree, and they correspond to
the more sharply defined sensory and motor speech centers. Dejerine alone
indicates in a restricted sense a third center, which occupies the region of the
angular convolution, and is designated by him as the center for optical mem-
ory pictures of words. I have explain~d above in what sense we are to under-
stand this; v. Monakow does not recognize such a special center. The two
illustrations show distinctly that the speech region not only consists of the
centers previously differentiated but also embraces the neighboring parts of
the convolutions of the convexity. Nevertheless, .they represent only a part
of the speech region, for, according to the two previously mentioned authors
and almost all other authorities, the entire island covered by the first embry-
onic convolution and situated in the depths of the Sylvian fossa should also
be included. In order to understand this, the Sylvian fossa must be deeply
penetrated and the adjoining convolutions-those belonging to the embry-
onic convolution-should be separated. The island is then exposed to view
as a deeply situated, triangular, cortical area covered with compartment-like
convolutions which ar~ separated from the cortical substance, according to
Burdach, by three deep spaces, an anterior, an upper, and a lower space.
Where the lower and' upper spaces meet and form an acute angle, a deep
furrow covered by the marginal and first temporal convolutions passes to some
extent in the direction of the upper space and backward, so that in the brain
it almost reaches the transverse plane of the angular convolution. The adjoin-
ing illustration (Fig. 141), which is taken from Henle's" Anatomy," gives us
an idea of these relations.
The importance of the island for the function of speech, everywhere rec-
ognized, permits us to conclude that it is the objective point for the association
~s. and the area where the two centers of speech, and presumably also
the different areas of the speech region, unite with each other. In fact the
finer anatomy of the region of the island permits no other explanation than
that we are dealing with an actual association center. This is obvious, not
merely because the three deep spaces which bound the island show everywhere
at their bases the well known U -shaped, so-called, fibrim proprie or lamine
22
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arcuatre Arnoldi to be richly developed, but also because of the typical struc-
ture of the cortex of the island. As is well known, the extension of the cortex
of the island reaches the external border of the largest ganglion of the brain,
the lenticular nucleus. Between the lenticular nucleus and the cortex of the
island are found two layers of white substance, of which that adjoining the
lenticular nucleus shows a very delicate internal structure known as the cap-
sula externa, that belonging to the cortex of the island a much coarser one
following its outline, and designated as capsula extrema. Between the capsula
externa and capsula extrema we note a structure of gray substance, the claus-
trum, which is found nowhere else in the brain. This compartment-shaped
ganglion, formed like the cortex of the island, is broader from above down-
Upper apa.ce
FIo. 141.
ward, while it narrows longitudinally ; as Meynert has said, with its processes
pointing toward the periphery it wholly disappears in the first embryonic
convolution; he tells us, too, that it consists exclusively of spindle or associ-
ation cells, and is nothing more than a cortical layer of unusual development
and deeply penetrating the medullary substance which everywhere consists of
spindle or association cells. In fact it disappears at the so-called foot of the
island, i. e., at the lower point of the junction of the radially situated convo-
lution of the island with some of the cortex of the island as well as with the
substance of the amygdalate nucleus. Besides the cortex of the island and its
('\austrum, there are still two important association bundles which must be
considered in the anatomy of the speech regions. One of these is the fa.':lcicu-
Ius uncinatus, penetrated by the widened base of the claustrum which divides
it into several layers, and this suggests the thought of a connection between
the cells and fibers. If the cortex is detached, the chief mass of the associa-
tion bundle is found at the foot of the island and further toward the interior.
and here is best seen its hook-shape which reminds us of the composition of
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the lamirue arcuatre. From this mixed piece the bundle splits and bifurcates
into the two cerebral lobes (whose shortest combination it represents), the
frontal and the temporal lobes. Some portions of it certainly extend to the
third frontal convolution, including Broca's convolution and the speech region
of the first temporal convolution.
While the fasciculus uncinatus appears to unite by the shortest connec-
tion with parts of the frontal and temporal lobes, the second bundle, or
fasciculus areuatus, is not actually a special bundle, but a general system of
association fibers of the convex surface of the brain having a sagittal direction.
Nowhere are the ganglion cells included in this. The anatomical conditions
of the brain are such that a special bundle of association fibers is most read-
ily produced where the foot of the corona radiata passes from the internal cap-
sule, therefore above and outwardly from the lateral edge of the lateral ven-
tricle to the upper border of the lenticular nucleus. As it is also contained
in the substance which bounds the Sylvian fossa, it is perceptible in the hard-
ened brain if the cortex of the upper space with its fibrire proprire is detached.
This will then convince us that a special bundle pen~trates the deep medullary
substance of the marginal convolution as far as the first temporal convolu-
tion, encircling the posterior process of the Sylvian fissure in an arch. The
portion of the arch extending sagittally in the former direction lies medially
from the just described path, and the interparietal furrow penetrating deeply
into the convexity as well as the posterior processes of Burdach's upper space
narrowly constricts this portion. In this area fibers which originate from the
marginal convolution and the posterior third of the temporal convolutions
no doubt join the arch bundle. The medullary substance of the lower parietal
lobe consists largely of these fibers, which are closely pressed together in all
extremely narrow space. When we consider that a part of the anterior por-
tion of the fasciculus arcuatus extends to the top of the lateral ventricles above
the lenticular nucleus, and that its sagittal continuation for the parietal and
occipital lobes is first narrowed by the previously described furrows, the usu-
ally very deep posterior end of the parietal or first temporal furrow at once
makes it obvious that the medullary substance of the lower parietal lobe in a
comparatively small space interrupts a large part of the association fibers con-
tained in the fasciculus arcuatus.
I will limit myself to these anatomical remarks which mainly show the
peculiarity of the lower parietal lobe (that is, the angular convolution) which
must contain a very important passage for the region of speech. Besides this
passage to the interior, i. e., toward the ventricle, we find anatomically three
sharply demarcated layers, namely, the most external one, that of the lower
longitudinal bundle, then the so-called optic radiation of G.ratiolet, and, finally,
the tapetum of the. corpus callosum, which together form the sagittal, medul-
lary layer of the occipital lobe ; in this restricted space lie tracts of such varying
importance that the appearance of a center may readily be simulated, and
in my opinion this is the origin of Dejerine's erroneous conception. To those
more deeply interested in these anatomical relations I recommend Dejerine's
" Anatomy of the Central Nervous System" and my " Atlas of Sections of
the Brain." Fig. 142 is taken from the work of v. Monakow, and shows a
horizontal section through the left hemisphere of the brain at the height
of the first temporal convolution, the third frontal convolution, and the
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316 THE SYMP1't>M-COMPLEX OF APHASIA
splenium of the corpus callosum. The three obliquely shaded areas upon the
convexity show the seat of lesion in motor and sensory aphasia and in pure
FIo. 142.
alexia. In contrast to the oblique shading, we observe in the illustration a

long-stranded fiber mass composed of three bundles; it shows diagrammat-
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ically the above mentioned sagittal medullary portion of the occipital lobes
which in the hardened preparation is. likewise sharply demarcated from the
medullary layers of the temporal and lower parietal lobes, as in the illustra-
tion. 'I'he circular shaded area which is noted in the lower parietal lobe,
v. Monakow considers to be the interruption of these three fiber layers which
is 8 prerequisite for the occurrence of pure alexia, and which, according to
his conception, arises from the destruction of the connecting link between the
sensory speech center and the two occipital lobes.
As already indicated, I concur in v. Monakow's opinion that Dejerine's
assumption that the cortex of the angular convolution is the seat of 8 uni-
lateral writing picture center is not at all proven. Dejerine's observations
do not permit this conclusion, but only prove that the destruction of this
region invariably and severely impairs the power to write, and the degree
of this action varies according to whether the deeper layers alone or simul-
taneously the superficial layers of the angular convolution are implicated. In
the first case pure alexia results, in the second, alexia and agraphia. But in
either case the cortex of the angular convolution may not be at all involved.
The anatomical relations which have been outlined merely permit us to
conclude. that the medullary substance of the lower parietal lobe; to a com-
paratively slight extent, severs all of the connections between the centers
of speech and the two occipital lobes. In the near future autopsy findings
must be utilized for the study of these points, and the following anatomical
tracts, which I shall briefly enumerate, then come under consideration: First,
the sagittal medullary substance of the occipital lobe with its three individual
layers. The middle layer is the so-called "optic radiation of Gratiolet," the
one which presents the most marked clinical symptoms, namely, the accom-
pan~ing hemianopsia. The internal layer, the so-called tapetum, originates
in the splenium of the corpus callosum, and contains at least two known
tracts, namely, that which connects the two temporal lobes with each other,
and that which unites the temporal lobe of one side with the occipital lobe
of the opposite side, the forceps tapetum tract of H. Sachs. It also appears
certain that the latter tract, which corresponds to the crossed optico-acoustic
commissure of Bastian, passes the splenium of the corpus callosum. The
external layer, as the fasciculus longitudinalis inferior, permits a free com-
munication between each of the temporal lobes and the occipital lobe of the
same side; it may, therefore, perhaps contain Bastian's optico-acoustic com-
mis.'>ure of the same side. According to Probst's recent investigations it con-
sists exclusively of corona radiata fibers which pass to the optic thalamus;
this, however, I cannot confirm. It may be admitted for the upper half of Hs
extension, but for the rest we acknowledge only its importance as an asso-
ciation tract between the temporal and occipital lobes. The sagittal medullary
layer with· its three component parts is situated not only within the lower
parietal lobe but also within the sensory speech center in the posterior third
of the first temporal convolution. Secondly, the true medullary substance
of the angular convolution lies not only external to, but also above, the sagittal
medullary laycr. In a diffuse medullary mass, which cannot be further ana-
lyzed, it contains at least two principal constituents, namely, the fibers of
the corpus callosum originating in the splenium of the corpus callosum which
comes from the forceps major, bundles of which permeate the sagittal medul-
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lary layer, and the above described component parts of the fasciculus arcuatus.
This is composed of all the tracts which unite the motor cerebral regions
with the occipital or lower parietal lobes of the same side, and is the shortest
means of communication between the sensory speech center and the lower
parietal or occipital lobes. The above considerations make it seem to a high
degree probable that, besides destruction of the sagittal medullary layer, the
intactness of the latter tracts contained in the medullary substance of the
angular convolution is a prerequisite for the production of pure alexia.
Autopsy findings in pure word blindness combined with hemianopsia do
not always reveal merely one focus localized as in v. Monakow's illustration, but
often several foci interrupt the optic radiation, that is, their point of origin
in the occipital lobe, as well as portions of the fibers of the corpus callosum.
The splenium of the corpus callosum is especially involved, and it is pointed
out that the same artery-the posterior cerebral-supplies the occipital lobe
and the splenium of the corpus callosum, the regions belonging to the area
of softening. Which portion of the corpus callosum is interrupted, whether
the forceps major which unites symmetrical areas of the convexity or the
forceps tapetum tract of H. Sachs, is still doubtful.
The tapetum of the temporal lobes can no 10llger be supposed to exist in
the area designated by v. Monakow (identical with that of Dejerine), for it
lies too near the occipital region; hence my thorough description, previously
given. This, however, does not preclude the consideration in the clinical
picture of both tracts with their variations; for example, the ability to copy
may be due to this.
In the relatively rare form of pure, isolated, literal agraphia, the approxi-
mately definite seat of the focal lesion may be determined by the comparison
of a few positive cases. This corresponds to the point where the sensory
corona radiata of the extremities decussate certain deeply situated portions
of the fasciculus arcuatus, its frontal plane lying anterior to the angular con-
volution in the region of the marginal convolution, its horizontal plane being
higher than the lesion of the medulla of the angular convolution found in pure
word blindness. Explicit details will be found in the report of my case.
The complexity of the anatomical relations of the regions of speech ren-
ders it obvious that objections may often be made to the meager description
of the pathologic findings in those infrequent cases which have been thor-
oughly investigated clinically and reported by reliable observers. A purely
casuistic standpoint does not affect the utilization of autopsy findings, for,
on the contrary, we then find that almost all such experiences as I considered
of general application are opposed by other observations. The unbiased study
of C. H. Bastian's valuable report. noted for its rich material, and the most
exhaustive compilation on the subject since the time of Kussmaul, forms the
best proof of this statement. In spite of this, it is a great satisfaction to
me to maintain the operation of a fixed law in this realm. which is also the
standpoint of A. Pick, v. :Monakow, and Dejerine, investigators who, in addi-
tion to their undoubted clinical ability, have at the same time shown them-
selves to be masters of the structure of the brain. The following remarks are
based partly upon the observations of these authors, partly upon my own expe-
riences and conclusions.
As to the exact limits of the motor and sensory speech center, I shall
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confine myself to the description given above. The anterior obliquely shaded
area in Fig. 142 shows the usual extent of the destruction in cases of pure
motor aphasia; this, according to our nomenclat~re, at the same time includes
verbal agraphia. Most cases of motor aphasia without agraphia have proven
to be subcortical motor aphasia. According to the findings at hand, we must
also reckon with a partial destruction of Broca's convolution, a damage to
the lower part of which toward the Sylvian fossa causes word mutism; the
integrity of the remaining parts, according to v. Monakow, permit& the power
.. ·l1Iat. opt.
FlO. 143.-CI, C1awrtrum; Ci, internal C&plUle; Li, lenticular nucleU8; y, fasciculU8 arcuatU8;
a, aeeondary degeneration after cortical motor aph88ia. (After v. Monakow.)
to write. Fig. 143 shows the seat of the lesion in cases of cortical motor
aphasia which, exceptionally, are not combined with agraphia.
The secondary degeneration which persists after cortical motor aphasia
has its definite seat in the internal capsule, indicated by a 1 in the accompany-
ing figure. The accurate seat of the slightest destruction which causes sub-
cortical sensory aphasia or pure word deafness can unfortunately be proven
in only a single case, but in this, in my opinion, absolutely beyond doubt. It
is the case of Liepmann, previously mentioned, the autopsy report of which
was recently published. On account of accompanying conditions this proof
was merely by exclusion; the destruction of the corona radiata of the tem-
poral lobes at the point where it unites with the island of Rei! was evident,
but this proof was convincing hecal1!~e at the sa~e time a secondary degenera-
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tion of the tapetum of the temporal lobe of the opposite side, the right hemi-
sphere, was found which could be looked upon only as an old lesion in the
medulla of the temporal lobe of the left side, since the cortex of the temporal
lobe and the entire occipital lobe upon the left side were well preserved, the
right hemisphere alone showing recent destruction. In explaining his case
Liepmann quite properly refers to H. Sachs who, on account of the narrow
compressed course of the corona radiata of the temporal lobe between the poste-
rior and lower processes of the third link of the lenticular nucleus and the
tail-piece situated upon the roof of the lower horn of the caudate nucleus,
stated that subcortical sensory aphasia is most readily produced by an injury
of this area.
Many years ago I quoted experiences 1 which show that within the poste-
rior processes of Burdach's· upper space must lie fibers whose injury produces
motor aphasia. I believed at that time that these fibers extended to the inter-
nal capsule and formed a special motor speech tract, that they therefore con-
tained the fibers of Broca's convolution which projected to the nuclei of the
bulbar nerves. After much experience had taught me that sensory' aphasia,
if combined with motor aphasia, is usually overlooked, and that lesions of
the internal capsule do not produce subcortical motor aphasia, I finally came
to the conclusion that thcRe experiences refer to cases of transcortical motor
sensory aphasia. v. lIonakow, who still adheres to the opinion that the im-
pulse for spontaneous speech must be transmitted over the sensory speech
center, positively declares that except the cortex of the island the fasciculus
arcuatus is the only association tract between the motor and sensory speech
centers. Aside from this view, Heilbronner has recently and quite properly
emphasized that the richness of the fiber communications between the tem-
poral lobes and the third frontal convolution forces us to consider the tem-
poral lobe as the chief point of origin of the transcortical fibers for Broca's
center. In deciding this question I attach great weight to a case reported
by Heubner which admits of no other explanation than that the principal
constituents of the fasciculus arcuatus were separated; certainly the layer in-
tended for the medullary substance of the first temporal convolution must
have ruptured. Clinically, however, this case unquestionably presents the
characteristics of sensory as well as of motor transcortical aphasia. In this
case there was an area of so-called cortical softening which took the form of a
furrow, and the marginal convolution and the posterior third of the first tem-
poral convolution almost appear to be sequestered from the surrounding cortical
substance; this proves that foci of softening may be of remarkable form and
extent, and that the .conditions produced by nature in pathologic cases may
present the most manifold combinations, and admit of the most instructive
applications.
In regard to diagnosis, I refer to the leading facts in the general pathol-
ogy of the brain, according to which, when focal symptoms are present (and
to these the phenomena of aphasia in the widest sense belong) we must deter-
mine whether we are dealing with direct. indirect, or transitory focal symp-
toms. I shall not here descrihe these, as I take it for granted that they are
known. But it appcarR to me that the transitory focal symptoms are not
1" Lehrbuch der Gehimkrankheiten," 2. Bel., 173, 176, 179.
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always sufficiently appreciated. I ~ust therefore state that these phenomena
are caused by the occlusion of an artery with succeeding compensation. The
affected cortical area is then periodically in a state of ischemia, but does not
soften because the circula.tion is re-established. Substantive and acute focal
symptoms which disappear in the course of one to three weeks must always
awaken a suspicion of this sort of development. . In an individual case, pre-
ceding transitory focal symptoms may enable us to make a positive differ-
entiation between embolism and cerebral hemorrhage, which in the majority
of cases is otherwise impossible. The diagnosis of subacute and chronic focal
diseases and also of aphasia is I based upon the same common principle, i. e.,
the utilization of the accompanying general symptoms. The sa.me is true of
the diagnosis of aphasic disturbances occurring in meningitis 8Qd progressive
paralysis; here I must emphasize that motor as well as sensory aphasia is fre-
quently observed after paralytic attacks, and these usually share the favorable
prognosis of the focal symptoms. In all cases, the preliminary question of the
right-handedness or left-handedness of aphasic disturbances in childhood from
which the patient recovered, the full possession, the absence, or an impair-
ment of the ability to write prior to the attack, must be decided. Thanks to
the researches of A. Pick, the processes of a chronic and progressive disease
of the brain, namely, of simple cerebral atrophy usually of senile or alcoholic
etiology, have recently been made susceptible to diagnosis. A. Pick has shown
that, when general cerebral atrophy occurs, localized atrophies of more decided
character may betray themselves as focal symptoms; one or both temporal
lobes, and combined with this or even by itself the first temporal convolution,
may be the seat of extreme focal atrophy. This shows itself· by a diminution
in the size of all the constituents of the convolution, of the cortex as well
as of the medullary substance. The resulting pathologic picture is that of
trallBCOrtical sensory aphasia, the occurrence of which is unilateral focal atro-
phy, although indicative of a slowly increasing process, is comprehensible
because the generalized atrophy, although only slight, makes compensation
by the other hemisphere difficult. A. Pick and Dejerine have given reliable
descriptions of cases which, on account of accompanying extreme deafness,
were considered to be subcortical sensory aphasia or pure word deafness.
Liepmann, however, bas proven that tbe clinical picture was that of trans-
cortical sensory aphasia, but the conspicuous bilateral deafness rendered the
diagnosis of the cases difficult. A more extreme bilateral deafness, especially
if the atrophy is chiefly seated in the comparatively small sensory speech cen-
ter at either side, may really lead to absolute pure word deafness, which of
course prevents us from recognizing a simultaneously existing transcortical
sensory aphasia. We must therefore reckon with the occurrence of such tran-
sitional cases. That the cortical function from the periphery can still be
determined when a process almost uniformly implicates all parts of the con-
volution which suffers damage, although one and the same medullary layer
of the convolution contains 'subcortical as weH as transcortical fibers, is read-
ily explained by the well known persistence of sensory memory pictures once
, acquired, and their faculty of complete reproduction even when very deficient
impulses are transmitted in a distorted way from the periphery. The most
familiar example of this is the fact that the tactile property of one hand
may be retained even when there are serious sensory disturbances of both
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nerve tracts, the median and ulnar, so that only very imperfect tactile impres-
sions are transmitted from the periphery to the cortex of the brain. Monakow
takes the opposite standpoint, and believes that this specific function of the
cortex of the sensory centers may suffer damage by a slight disturbance in
function; upon the basis of much experience I must deny this. The preced-
ing explanation embodies the important diagnostic law that slowly develop-
ing sensory aphasia of a transcortical nature (the recognition of which may
be rendered difficult by extreme deafness), always permits the assumption
of a localized atrophic process in the first temporal convolution upon the left
side, and we here have a rare example of a definite focal symptom permitting
the recognition not only of the area but also of the nature of the pathologic
process. ~ory aphasia due to embolism or thrombosis always occurs sud-
denly, and often with more or less conspicuous symptoms of apoplexy.
• In the later stages of motor aphasia it will be noted that syllable stumbling,
and in sensory aphasia a difficulty in finding words for objects shown, usu-
ally persist, and if there are deeper lesions of the affected centers further com-
pensation is not to be expected. As a rule w!! cannot utilize the symptom of
difficulty in word finding for a focal diagnosis; on the contrary, it is often
merely the expression of a general impairment of function, which may at
different times develop to a different degree. A. Pick has shown that im-
provement of sensory aphasia occasionally occurs by a stage of agrammatism,
i. e., by a disturbance of speech in which merely the essential parts of a sen-
tence are used, without connectives or conjunctions, and without any regard
to the tense of verbs, as is common in sending a telegram, or with a very
rudimentary knowledge of a foreign language. This fact also may be of
value in the diagnosis.
In by far the great majority of well developed cases we must remember
that of the two opposite types of arrested or still fluent speech, only the for-
mer can be designated as motor aphasia. With a well retained power of
speech, paraphasia of varying grades is the most conspicuous symptom, ina-
bility to understand what has been said is usually not appreciated, even by the
most expert observers, and in every case is a symptom that must be sought
for and determined with the utmost care. Apparently the prevalent opinion
in regard to the present situation, and its power to readjust itself, is the
reason why such a gross defect is so frequently overlooked. This may very
readily Occur if partial compensation has taken place for ordinary questions
or commands. If motor aphasia at the same time exists, naturally an opinion
as to whether spoken sounds are understood is even more difficult, therefore
we must be the more cautious in examining for this symptom. In regard
to disturbances in writing. I refer to my above descriptions. Anyone desir-
ing additional instruction for the diagnosis of finer speech disturbances and
their importance as focal symptoms will find these in A. Pick's book 1 which
indicates a decided advance in this branch of disease.
1" Beitrllge zur Pathologie und pathologischen Anatomie des Centralne"ensystems."

Berlin, 1898.
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TREATMENT 323
TREATMENT
In the therapy of aphasia I may be brief, as this can only come into ques-
tion when the focal symptom exists in an otherwise healthy brain.
The best treatment is exercise, which in sensory aphasia will of itself
produce a gradual compensation of the defect. This spontaneous improve-
ment is lacking when there are special circumsi;aJl.ces, for ex~mple, an accom-
panying general ~trophy of the brain or a bilateral disease of the temporal
lobe. In motor aphasia, as has already been observed, even systematically con-
ducted exercises are usually of little use. But the successes in the treatment
of motor aphasia which Dejerine and Thomas report indicate that, under
some circumstances, and after systematic practice, speech movements may be
understood by the sense of sight, therefore all persons who understand this
method should be advised to employ it. The few physicians who have de-
voted themselves to this specialty and teachers in deaf-mute institutions will
be the most suitable instructors. In pure word blindness we usually succeed
in teaching the patients to trace writing with their fingers, and by this method
they learn to write themselves, and also learn to read. The patient whose
history I related at the beginning of this article has in this way learned to
recognize most letters and to read some words. But the method presupposes
such attention, energy and endurance that compensation of the def~t is only
attainable in very exceptional cases.
My description will have given the impression that the aphasic symptom-
complex, while to-day incomplete, forms a full, exceedingly rich, and inter-
esting chapter in cerebral pathology; not in the remotest degree do I claim
that it is complete, but I limit myself in the present state of our knowledge
to presenting its principal characteristics, so that to some extent we may learn
to recogni?.e the outlines of this large and complicated structure. A few his-
toric notes I have used for the purpose of elucidating certain points of view,
which have so far aided in rearing this structure.
As in every investigation not yet concluded, we have here found that our
field of activity appears to widen more and more, that even now the mind
can hardly grasp all the facts that have come to light, and new questions
constantly arise and demand an answer. If we penetrate beyond the true
aphasic symptom-complex, we meet with ever expanding fields which are
actually the offspring of aphasia; I need only mention mental blindness,
asymbolia and aprturia. I am not claiming too much when I maintain that
the pathologic picture presented by these affections would not have been \!or-
rectly observed, described, nor understood if the points of view which I have
delineated as the true kernel of the teaching of aphasia had not facilitated
their understanding. Everywhere we meet with complicated psychical phe-
nomena which are not infrequently also observed as partial symptoms of true
mental disease. These form, in fact, a borderland between focal diseases of
the brain and mental diseases. But even the restricted realm of aphasia fur-
nishes in itself such transitional cases, which lead us to the conclusion that
so-cal1ed mutacism, the strange muteness of patients with mental disease, is
often only a peculiar form of trauscortical motor aphasia. A minuteness of
clinical observation and analysis, of which we. may be justly proud, is begin-
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324 THE SYMPTOM-illMPLEX OF APHASIA
ning to form a special pathology for localized psychical disturbances. . I need

mention only the researches of Lissauer into mental blindness, and of Liep-
mann into the pathologic picture of unilateral apraxia, both of which may
be termed classic. A purely descriptive presentation of mental diseases which
would include all of this recently acquired knowledge might be attempted.
If the value of a scientific hypothesis depends upon the question in how far
it renders research possible and leads to new questions, we must admit that
the much disputed and actually the most disputable question, the transcor-
tical form of aphasia, owes its origin to a valuable and at present indispensable
hypothesis, which justifies and maintains its position. Moreover it gives me
satisfaction to state that the best text-books, such as Oppenheim's, v. Mona-
kow's and Goldscheider's, practically recognize the transcortical forms of
aphasia, i. e., as indispensable for the symptomatologic differentiation of cer-
tain pathologic pictures.
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1874 Wernicke The Symptom Complex of Aphasia

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1874, Wernicke, The Symptom Complex of Aphasia

.J1IODRRX· CLI.NICAL ~IR])IC/~VE

ARCHIBALD CHURCH, M.n.

A:oi AUTHORIZED TRANSI.ATIO~ FR031 .. DIE DEUTSCHE KLINIK"

JULlt;S L, SALINGER, M.D,

lVITLI ONN lIFSbIlED AND NISETY-PlVE ILLfTSTRATIONS

NEW YORK' AND LONDON

D. APPLETON AND <"'OMPANY

PRINTED A.T THE A.PPLETON PRESII

Thomsen's Disease (Myotonia Congenita). By L. v. FRANKL-HoCHWART,

P ARAL Y818 OF THE PERIPHEItAL N EItVES 662

ISDEX 01" AUTHOIIS 1161

INDEX OF ~UB.JEC'TS 1173

PLATE I • l<'acing JKIIJc 450

PLA'fE II . l<'ulluwi"'!J page ~2(j

PLATE V Following pagc 826

1. DISTURBANCES OF PHONETIC SPEECH

The apparently perfect analogy of this peculiarly circumscribed mental

From general anatomical considerations which permit us to regard the entire

differ. Dejerine concluded from his observations that there is usually a

Motor aphasia like sensory is a pathologic picture which is most frequently

which he has, however, incorrectly reported 1 since he ignored the positive

pensated for, as O. Berger has proven by one of the earliest observations

While we have so far especially considered those forms of aphasia which

1 Arch. f. Psych., XXIII, p. 909.

1 The definition of a. concrete conception here given as the definite grouping of

ct'ntt>rs or "coagilotion ClMter-II" as be calls thl'm. Thl'Y are said to be eharsett>rized

But the simplest communication, conversation, or difference of oplDlOn, is

In the center, a, b, is a centripetal and centrifugal tract; in other words,

aphasia, and occurs without hemiplegia. Furthermore, a glance at the dia-

II. DISTtJR.BANCES OF WRITTEN LANGUAGE AND GEl'fERAL

1" Besl'hreibung der Intel1i~nzstllrun/l'Cn infolge einer Himyerleizung." S. A. aus

possibly to a less extent, presupposes the spontaneous coaction of the Wl"iter.

J Details in an article by Storrh: II Versuch einer psycho.physiologiBchen Dar!'tel·

of the letters belonging thereto. Articula~ speech is composed of word con-

1 Arch. f. P8Ych., 15. Bd., p. 276. "Wanderversammlung slldwestdeutsch. Irrenllrzte

1 Sommer, "Zur Theorie der cerebral en Rcbreib- u. Lesest6rungen." Zt8chr. f.

t G. Wolff, "Ueber krankbafte DiBsoc.iati~n der Voratellungen." Habilitation-

I mentioned in my previous report; certainly it is an extremely rare occur-

For the practical recognition of amnesic aphasia it might be advantageous

tiona I disturbance, will be evident in the further course. There is a symp-

attention to it because of its importance in differentiating this affection from

alexia. In contrast to the oblique shading, we observe in the illustration a

1" Lehrbuch der Gehimkrankheiten," 2. Bel., 173, 176, 179.

1" Beitrllge zur Pathologie und pathologischen Anatomie des Centralne"ensystems."

ning to form a special pathology for localized psychical disturbances. . I need

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