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CONCEPTS OF APHAS|A;
HiSTORICAL AND CONTEMPORARY

Thesis {or the Degree of M. A.

MICHIGAN STATE COLLEGE

_. Ralph R. Leutenegger
1949

 

This is to certilg that the

thesis entitled

" Concepts of Aphasia: *1
Historical and Contemporary" ‘

presented In]

Ralph R. Leutenegger

has been accepted towards fulfillment

of the requirements {or

M.A. degree in SPEGCh

”/1

K A; 7: / ‘KZI‘; {4;{4/

Majnr prufessur }

 

llate JUIY 19. 1949

0-169

 

 

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‘

 

 

 

CONCEPTS OF APHASIA: HISTORICAL AND CONTEKPORARY

By

RALPH R. LEUTENEGGER

A Thesis

Submitted to the School of draduate Studies of Michigan
State College of Agriculture and Applied Science
in partial fulfillment of the requirements
for the degree of

MASTER OF ARTS

Department of Speech, Dramatics, and Radio fiducation

1949

‘f {.i V.“

TABLE OF CONTENTS

‘9 RJL‘F'ACE . o 0 o o O o o o o o O O

AC1HJOVJLEDGLHL111FES Q o o g Q o O 0 O O O

BIOGRAPHY . o . . . . . . . . . .

PART I: INTRODUCTION

HAPTER
I. APHASIA: DEFINITION AND ETIOLOGY OF . . . .
II. EARLY HISTORY . . . . - . . . . .
PART II: HISTORICAL VIEWPOINTS
III. THE PSYCHOLOGICAL VIEWPOINTS OF HUGHLINGS JACKSON
IV. THE CONTROVERSIAL LOCALIZATION IDEAS OF MARIE AND
OPINIONS OF HIS CONTELPORARIES . . . . .
V. HENRY HEAD AND REVIVAL OF THE PSYCHOLOGICAL
APPROACH . . . . . . . . . .
V1. S. E. HENSCHEN AND THE ANATOMICO-CLINICAL
INTERPRETATION . . . . . . . . .
VII. S. A. KINNIER NILSON'S ECLECTIC ANALYSIS AND
OTHER RECENT WRITINGS . . . . . . .
PART III: CONTENPORARY VIENPOINTS
VIII. THE NEUROLOGIST DISCUSSES APHASIA--J. N. Nielsen
IX. THE PSYCHOLOGIST'S CONCEPT OF APHASIA--Kurt
Goldstein . . . . . . . . . .
X. THE SPEECH PATHOLOGIST'S VIEWPOINT OF APHASIA--

Jeanette 0. Anderson . . . . . . .

2.18351.

II
III

PAGE

26
42
56
63

67
72
92

116

CHAPTER PAGE

XI. DIAGNOSTIC AND THERAPEUTIC APPROACHES OF BACKUS,

SHEEHAN, AND OTHERS . . . . . . . . 126
XII. A LAST ‘VVJORD O o o o o o o o o o 159

BIBLIOGRAPHY . . . . . . . . . . . 153

PREFACE

Early in his studies of aphasia the student discovers
controversy among the published authorities, as well as dis-
agreement over terminology. The possibility of approaching
the problem from anatomical, physiolOfiical and psychOIOgical
vieWpoints partly accounts for the existing Confusion. The
loose transference of terminology-~as well as of conceptions
themselves-~from one frame of reference to another, does
much to discourage the conscientious student.

Share is no one existing source in which a resume of
the conflicting theories, much less their consequent therapies,
has been compiled and discussed. The student of this speech
defect has to ferret out the divergent schools of thought in
the few available books, in inaccesible medical journals,
and psychological and speech publications.

It is the purpose of this particular study to gather
and adequately describe the leading theories or ccncepts of

aphasia.

II
ACKNOWLEDGMENTS

The author wishes to express his gratitude to Dr.
Charles Pedrey, Director of the Nichigan State College
Speech Clinic, for his understanding, encouragement and
guidance during the writing of this thesis, as well as for
his superb example in the role of speech.therapist with
aphasics as well as with other types of speech defectives.

Appreciation is extended to Dr. Wilson B. Paul for
insights into the problems encountered in graduate work.
For her OXpert help in the final stages of the writing,
the author wishes particularly to extend his gratitude to
Miss Lucia Noraan. For his valuable assistance in editing
the finished study, the author wishes to thank Dr. A. T.
Cordray. Fbr encouragement in the initial stages of writing,
the author is indebted to kiss Elsie Edwards.

The author is additionally indebted to Dr. J. N.
Nielsen and Dr. Kurt Goldstein for their considerable
donation of time towards the editing of the chapters at-

tributed to them.

PART I

INTRODUCTION

CHAPTER I
APHASIA: DEFINITION AND ETIOLOGY OF

The earliest description of aphasia, as far as neuro-
logist Henry R. Viets of Boston can ascertain, can be found
in the medical works of C. Linnaeus1 dated 1745. He set
forth the classical symptom of knowing what one wishes to
say, but being unable to say it. Linnaeus called this con-
dition "forgetfulness."2

Immediately priOr to Broca3 there was only one type of
aphasia recognized--the "alalia" of Lordat.4 In 1861 Broca
proposed the term "aphamia" to designate what we now under-
stand by Broca's aphasia, or disorders of articulated
language. jThe term “aphasia" was first applied in.1861 by

Trousseau5 to loss of Speech due to a cerebral lesion exclu-

sive of that due to paralysis of the muscles concerned with

 

l. (Carolus Linnaeus, or Karl von Linne:--Swedish
physician and naturalist, 1707-1778)

2. Henry R. Viets, “Aphasia as Described by Linnaeus
and as Painted by Ribera," Bulletin 22 the History 9; Medicine,
15:5:328, March, 1945.

3. (Paul Broca:--Parisian anthropologist and surgeon,
1824-1880) ,

4. \Lordat:--A Frenchman who published a book on speech
in 1825 and who later (1845) described his own condition of
aphasia beginning in 1828)

5. (Armand Trousseau:--One of Broca's associates and
fellow students of aphasia, 1801-1867)

a
speech.and exclusive of dementia. This replaced the "aphemia"
of Broca and was accepted as the preferable term. Later, '
suggestions were made to render the terminology more definite
and suitable. McLane Hamilton (cited by Jackson, 1878)
suggested the term ”asemasia" (meaning the inability to com-
municate by signs or language), and Headsgrecommended
"dysphasia" (disturbance of language). However, as Jackson7z~
observed in 1878, it was already too late to displace the
term "aphasia".

Kussmaulg noted, in a BOO-page monograph on aphasia
printed in 1885, that the word "aphasia" was then used to
signify the entire symptom.complex of disturbances of all
types of man's communication-~not merely speech disturbances
alone. Déjerineg, in 1914, defined "aphasia" as the loss of
the memory of the signs by means of which civilized man
exchanges his ideas with his peers. Here can be observed the
flexible use of the word to include what we now term

"agnosias" (loss of the function of recognition resulting from

 

. 6. (Henry Head:--English Physician, 1861-1940. See
Chapter V)

7. (Hughlings JackSon:--The founder of English neuro-
logy. See Chapter III)

8. (Adolf Kussmaul:--German physician, 1822-1902)

9. (Joseph Jules DeJerine:--Parisian Neurologist,
1849-1917)

5

an organic cerebral lesion and through one sense organ onlylo),

and "apraxias" (loss of ability to perform as desired or as
requested, through loss of memory of how to performll) in

addition to the "aphasiast. However, Bastianl2 attempted to
indicate motor speechlessness or pure word mutism.in 1898.
In this sense its application was greatly advanced by
Henschen15 in.his monograph of 1922.

A good working definition of "aphasia” for contempor-
ary use might be that of Michael Osnato14 who defined it as

loss of or encroachment upon the ability to change
concepts into words, in spite of the integrity of the
speech musculature, and a loss of the ability to under-
stand thingi spoken despite the integrity of the sense
of hearing. 5 ’

Another adequate explanation of the aphasic's condi-
tion is Russell Meyers':

The term.aphasia should be reserved for disturbances
of speech which are manifested only as a disability of

 

10. J. M. Nielsen, A nosia, A raxia, Aphasia. (New
Yerk: Paul B. Hoeber, Inc., 48 , p. 2 .

11. Ibid., p. 268.

12. (H. Charlton Bastian:--British M.D. and Censor of
the Royal College of Physicians of London at the end of the
nineteenth century)

15. (Salamon Eberhard Henschen:--Swedish neurologist,
See Chapter VI)

14. (Michael Osnato:--American neurologist)

15. Michael Osnato, "Aphasia and Associated Speech
Problems," Neurological Bulletin, 1:414, Nov.-Dec., 1918.

formulating and communicating the arbitrary social
symbols of perceptual patterns. Aphasia implies that

the speech dysfunction now in evidence does not rest
upon a paralysis of the receptor, effector, or co-
ordinating mechanisms involved in the language function.
By simple clinical devices it should be readily possible
to demonstrate that the patient can both see and hear and
that he is able to produce non-language sounds co-
ordinately ang execute refined movements with his hands
and fingers.

Robert West defines ”aphasias" as “failures of the
faculty of forming, retaining, and reproducing mental con-
cepts in association with purely arbitrary combinations of

speech sounds."17
J. M. Nielsen;8 writes of aphasia as
the term in common use for all disturbances of language,
motor or sensory, due to a lesion of the brain but not
due to faulty innervation of the musculature necessary

for speech or to involvement of the Sense organs them-
selves or to general mental defect.l

More briefly Nielsen suggests that "aphasia consists in

organic disease of the cerebral memory engrams for

 

16. Russell Meyers, "Aphasia: A Problem in Dif-
ferential Diagnosis and Re-education," The Quarterly
Journal g£_s eech, 25:364, October, 1937.

 

17. Robert West, "Aphasias and Related Alexias,
Agraphias and.Amentias," Brennemann's Practice 2; Pediatrics,
p. 15.

18. (Johannes Maagaard Nielsen:--Los Angeles neuro-
lOgist and psychiatrist, 1890- )

19. Jeanette 0. Anderson, "Aphasia From the Viewpoint
of a Speech Pathologist,“ (unpublished Ph.D. Thesis, The
University of Wisconsin,-Madison, 1942), p. 180.

language.“20 Nielsen warns his readers to distinguish care-
fully between the object and its symbol, for "loss of

recognition of the object or its symbol is agnosia for the

 

object or the symbol. Loss of significance of the symbol is
aphasia."21

We must realize that aphasia is simply a convenient
name for a rather large group of disorders, the various types
and classifications of which are described in Chapter XII.

The two main etiologic categories of aphasia are
disease of and trauma to the brain. Disease can be thought
of in general terms as infection, lack of nourishment (oxygen),
and tumors.- Trauma, a bodily injury produced by violence, or
any thermal, chemical, etc., extrinsic agent, embraces cutting
and tearing, as well as "strokes" and the formation of blood
clots.

In cases of damage to the sensory nerve fibres, aware-
ness of sensation is lost; damage to motor fibres results in
loss of the power to move muscles; and damage to the associa-
tion nerve fibres causes the loss, to some degree, of the
power to correlate certain sensory and motor functions. When

the association fibres having to do with the language function

7
are damaged, the patient exhibits aphasia.22

 

200 Nielsen, 920 Cito, p. 2540
21. Ibido, p. 2550

22. 01116 Backus, 33, E&!' Aphasia‘in Adults (Ann
Arbor, Michigan: University of Michigan Press, 1947)

Russell Meyers affords us a comprehensive listing of

some of the most common etiologic factors underlying aphasia:

1.
2.

5.

4.

5.

6.

7.

Brain trauma, at birth or subsequently duringthe life

of the patient

Pathological process of the cerebral blood vessels

a. Embolism, the sudden plugging of a vessel by a
foreign body borne by the blood stream.

b. Thrombosis, the slow occlusion of a vessel by a
process of thickening of its wall or lining

c. Hemorrhage, the rupture of a vessel leading to
the extra-vasation of blood into surrounding
tissues

d. Mechanical occlusion by pressure from without the
vessel

6. Vasospasm, the transient narrowing of the vessel
lumen under the influence of hormones and vaso-
constrictor nerves

Brain tumors

a. Primary neOplasms of the brain tissues

b. Secondary neOplasma, representing metastaces or
extensions

Infections of the brain

a. Meningitides (epidemic and non-specific forms)

b. Encephalitides (epidemic and non-specific forms)

c. Abscesses

d. Gromelomata (syphilis and tuberculosis)

e. Parasitic cysts

f. Araohnoiditis

Degenerative brain diseases

Gower's "abiotrophic" processes, lipoid histiocytosis,
tuberous sclerosis, etc.

Allergic cerebral edema, as in some migrainous mani-
festations

Pre- and post-convulsive seizure states25

.—
‘—

23. Meyers, op. cit., p. 365.

CHAPTER II
EARLY HISTORY

The beginning of any history of the function of speech
and the theories built up around cerebral localization is
apt to be clouded in.mystery, doubt and confusion. During
the Middle Ages the common belief was that the brain contained
three ventricles, each of which.was the dwelling place of one
or more aspects of the psyche. The seat of the "sensus
communis" was the anterior chamber which received the nerves
(of taste, smell, sight and hearing. The faculties of cogita-
tion and reasoning resided in the middle ventricle. The
posterior ventricle was the seat of memory.

At the beginning of the nineteenth century, the
activities of the mind and theories of speech.remained mixed
with vague theological and metaphysical conceptions. Cerebral
localization had not yet been discovered. The teaching
current at that time was that all parts of the brain served
the same function. In the event of injury or disease of one
portion, any portion.might take over. Physiologic-~not
anatomic--uniformity was being taught. Foremost of the men
who emphasized the unified functioning of the cerebral lobes
was Marie Jean Flourens.1

A ~- -—.-—

1. (Jean Pierre Marie Flourens:--Parisian physiologist,

1794-1867)

The first real attempt to localize the faculty of
articulate speech was made in 1808 by Franz Joseph Gall, an
Austrian physician (1758-1828). He advanced the idea that
the brain was a group of organs with individual functions,
not a single organ. Correspondingly, each.mental condition
was attributed to the activity of one brain element.

Advancing such radical views, Gall encountered strong
Opposition. In a personal letter from the Kaiser, he was
forbidden to antinue his Vienna lectures (1796-1801) on the
new theory of functions of the brain because "his views were
considered so subversive of religion and morals."2

In 1808 Gall presented his memoir entitled "Introduc-i
tion au'Cours de Physiologie du Cerveau" to the Institute of
France. The following year all his views appeared in a
publication called "Recherches sur 16 systems nerveux en
general et sur celui du cerveau en particulier", written with
Spurzheim.as co-author. The faculty of speech Gall attributed
to the anterior parts of the frontal lobes of the brain,
"mainly on phrenological grounds."5

Today Gall's name is frequently associated with phren-
ology, the study of bumps on the head. However, "it is to

this man that we are really indebted for the beginning of the

 

2. Henry Head, "Aphasia: An Historical Review",-
Brain, 433391, 1920.

3- Donald Core, "Some Modern Conceptions of Aphasia",
The Medical-Chronicle, 27(4th Series):309, April-August, 1914.

conceptions we now hold of the relations of the various por-

tions of the nervous system to one another."4

Many of Gall's ideas have been accepted into the body

of general knowledge.

He was the first to insist that the brain should be
examined anatomically from the spinal cord upwards; for
he laid down that the functions of the brain could only
be explained by considering their relations to those of
the Spinal cord. All nerve fibres ended in grey matter,
and the white matter of the nervous system served for
conduction only. He pointed out the analogy between the
grey matter which covers the hemispheres of the brain
and of the cerebellum, with that which forms the corpora
quadrigemina and Optic thalamus. A11 nerves, whether
they belonged to the brain or to the spinal cord, took
their origin in grey matter, and the substance of the
cerebrum and cerebellum.could not be considergd to be in
direct connection with the peripheral nerves.

However, ideas such.as these appeared interspersed with fan-
tastic theories of the "moral" qualities.

Gall's greatest supporter and disciple, appointed
Professor of Clinical Medicine at the "Charite" in 1831, was
Jean Baptiste Bouillaud.6 In.1825 he published a memoir
called "Clinical Researches to Demonstrate That Loss of
Speech Corresponds With Lesions of the Anterior Lobules of

the Brain, and to Confirm Gall's Opinion on the Seat of the

 

4. Head, .920 Cite, p. 591.
5. Ibido’ p. 391-2.

6. (Jean Baptiste Bouillaud:--French physician,
1796-1881)

10
Organ of Articulate Language.'_'7 Apparently this was the same
paper presented before the Royal Academy of Medicine under the
name "Some Clinical Researches to Establish the Theory That
Aphasia is Due to a Lesion of the Brain and to Confirm the
Opinion of M. Gall as to the Site of the Lesion."8 Bouillaud,
the first man to point out that aphasia is correlated with a
lesion in the anterior lobes of the brain, came to the
following conclusions as a result of post mortems on a great
many Specimens:

l. Movements of the organs of speech are controlled by
a cerebral centre, special, distinct and independent.

2. This centre is situated in the frontal lobes.

5. Loss of speech is due sometimes to loss of word
memory and sometimes to a loss of power over the
muscular apparatus that is responsible for articula
tion. ‘

4. Loss of speech.does not involve loss of movements of
the tongue as far as mastication and deglutition are
concerned.

5. Nerves that innervate the tongue associated with the
production of speech either have their origin in the

anterior lobes of the brain or are closely connected
to that region by means of communicating branches.

It is to be noted that Bouillaud did not specify laterality.
Working quietly at this same time was a Frenchman

named Marc Dax (cited by Nielsen, 1947). He noticed that

persons afflicted with hemiplegia, along with a loss of

ability to eXpress themselves, were nearly always afflicted

 

7. Everett M. Ellison, "Sensory Aphasia”, New York
Medical Journal, 1133153797, June 1, 1921.

8. Core, SE. (3113., p0 5090
9. Ibido, p. 609‘100

11
with a right and not a left hemiplegia. Presenting his views
of cases gathered for thirty-six years, Dax published an
article in 1856 in support of his conviction that "the anatomic
structure on which speech.was based was located in the left
side of the brain."10 This is the first time that one of the
hemispheres was considered to be dominant. Hitherto, the two
cerebral hemispheres were considered identical, not only ana-
tomically but physiologically.11

Perhaps the greatest single influence on the entire
history of aphasia was that of the French surgeon and brain
specialist, Pierre Paul Broca (1824-1880). In 1861 he pre-
sented his report of 2 cases to the Anthropological Society
of Paris. He contended that the faculty of language was at
the base of the third frontal convolution of the left hemi-
sphere (the so-called pars cpercularis, or Broca's convolution).
The clinical cases supporting his statement were three brains.
(Inaccuracies exist in the literature as to whether it was 2
or 5 brains). It is difficult to ascertain why his conclusions
were so violently supported since the lesions were large, and
"it was only by deduction that Broca determined the lesion to
have started in that area."12 Making the acceptance of

10. Nielsen, gp.‘g$§., p. 2.

11. J. M. Nielsen, "Function of the Minor (Usually
Right) Cerebral Hemisphere in Language", Bulletin'gf EEEHEEE
éggeles Neurological Societ , 3:67, 1958.

12. J. M. Nielsen, Arnosia, A raxia, Aphasia. (New
York: Paul B. Hoeber, Inc., 1947), p. 2.

12

Broca's views appear even more implausible are the 1914 Ob-
servations of Dr. Eugene Dupuy of Paris. He wrote:

This localisation was founded on pathological Observations,

and the three brains which Broca showed are at present--

where they have been preserved from the beginning--in the

Museum of Pathological Anatomy in Paris: they are to be

seen every day. They show that they never have been

Opened--i.e., cut into sections--so that it is impossible

to say what other lesions exist, if any, beside those

seen on the surface of those brains. 9

Broca called the loss of function in his cases aphemie,

or aphemia (absence of ability to speak). The lacking faculty
which he thus designated was that of word articulation.
Broca's foremost champion was Trousseau who added the
‘weight of his authority and invented the word "aphasia" to
replace Broca's "aphemia".14 By 1864 the French Academy
recognized the term "aphasia" for all disturbances of phonetic
speech.15 The reason for this change in terminology is well
explained by J. M. Nielsen. He relates how
Trousseau learned from a well-educated Greek named
Chrysaphis living in Paris that while a meant without and
hemia meant speech, the term aphemia'did not mean speechr
Eessness but infamy. On the other hand, aphasia (which,
according to Skwortzoff, had been used in 200 B.C.) meant

speechlessness. Broca accepted Trousseau's correction,
and since that time aphasia has withstood all attempts to

 

15. Eugene Dupuy, "Localisation of Motor and Speech
Centers in Definite Areas of the Cortex of the Brain", The
Lancet, Vol II for 1914: 207, July 25, 1914.

140 Head, 2E0 Cite, p0 3900

15. Arthur Ernest Davies, "Speech Reactions and the
Phenomena of Aphasia", Psychological Review, 55:6:425, Nov.,
1926.

15
change it in spite of the obvious impropriety of the term
since the enormous expansion of its meaning has been
accepted.16

Trousseau, although at first accepting Broca's
doctrine, soon voiced disagreement, with the discovery of
several cases in which aphasic patients were found at autopsy
to have lesions in the temporal and parietal lobes of the
left side.

In all fairness to Broca, the little-known fact must
be admitted that he too departed from his original stand of
extreme localization. Several years later he insisted that
"the insula and the lenticular nucleus are almost always in-
volved together with the third frontal convolution.“l'7

However, Broca's followers were so carried away in their
enthusiasm with.his first publication that they overlooked
his later cautions and instead accepted the third frontal
convolution as the exclusive seat of motor aphasia.

This exclusivism.continued to exist in its entirety up

to 1906, when Marie [See Chapter Ii] first dared challenge
the scientific accuracy of the generally adOpted doctrine,
which up to his time had Been considered incontrovertible

and therefore classical.1

Among the neurologists who agreed with Broca were

Gustav Fritsch (1858-1897) and the man who in 1870 established

 

l6. Nielsen, 22. cit., p. 2.

17. Alfred Gordon, "A Contribution to the Study of
Aphasia", New York Medical Journal, 97:10, Jan-June, 1913.

18. Loc. cit.

14
the electric excitability of the brain, Edouard Hitzig (1858-
1907).

As early as two or three years after Broca's publica-
tions, Charcot19 published observations which would prohibit
absolute acceptance of Broca's principle that speech depends
upon Broca's convolution in the left hemisphere only for
right-handed persons, and in the right hemisphere for left-
handed persons. He stressed the difference among individuals
in the importance to them.of auditory, visual, and motor
centers. He noted that "symptoms of lesions in certain cases
differed from symptoms of identical lesions in others."20
This he attributed to the relative development of the various
centers during the acquisition of language. Accepting the
dominance of one center over another in speech, he postulated
visualdminded, auditory-minded, and motor types of individuals.
Lesions in the guiding center would therefore cause greater
aphasic damage than lesions in the minor center.

The foundation for the anatomico-physiologic concept
of senSOry aphasia was laid in 1866, according to J. M.
Nielsen, by Wyllie's observation that "word ideas of associated

motions which form the faculties of speech are suprarmotory,

while the situation of associated sensations which form the

“h -.—— w- - —-‘ —-,

19. (Jean Martin Charcot:--French physician, 1825-
1893)

20. Nielsen, g3. cit., p. 5.

15
faculty of word comprehension is supra-sensory."21 In other
words, the loss of expressive ability was motor in character
and the loss of receptive ability was sensory. Eight years
later this theory received scientific confirmation by the
cases of Wernicke of Breslau. Carl Wernicke (1848-1905), the
26 year old who established sensory aphasia on an anatomic
basiszz, designated the auditory center to be the transverse
gyri of the superior temporal convolution, and Broca's region
as the conceptual center for articulated speech. He also
"outlined the syndrome of what soon became known as Wernicke's
aphaSia; this was a fourfold syndrome including auditory and

visual agnosias for symbols, alexia and agraphia."25

Wernicke described the subcortical fibers radiating
from various sensory centers, converging into one point, a
sensory speech center, and giving rise to a definite group of
memory images. The classic explanation of sensory aphasia is
"loss of memory images from a lesion in this center of the
fibers radiating to it."24 The area we now speak of as

21. Ibid., p. 2-3.

22. Nielsen, gp. 933., p. 4.

23. Anderson, gp.‘git., p. 11-12.

24. Lauretta Bender, "Disturbances in Visuomotor Ges-
talt Function in Organic Brain Disease Associated With

Sensory Aphasia", Archives 2; Neurology and Psychiatgy,
30:3:518, Sept., 1935. '

l6
Wernicke's area is the posterior half of the first temporal
and closely adjacent second temporal convolution of the left
hemisphere. The type of aphasia resulting from degeneration
of the third frontal convolution of the left hemisphere
(Broca's area) is designated motor aphasia. Wernicke's
aphasia represented loss of comprehension Of spoken language
and of written or printed matter, inability to write, and
paraphasia.

Contemporary with these deveIOpments, the little-known
efforts of an Englishman named Moxon (cited by Nielsen, 1947)
resulted in the recognition that the right hemisphere had a
governing influence over the left in the performance of
voluntary acts. It remained until 1900 for H. Liepmann to
uncover this "foundation for the most important principle of
modern apraxia."25

In the period immediately ensuing, a great many public-
ations appeared. This period has been aptly termed the age of
the "Diagram Makers". These men tried to map out the various
language centers and their interconnections.

Soon after the publication of Wernicke's article,
Kussmaul recommended that his term sensory aphasia be changed

to word deafness. The term "agraphia" was introduced in 1867

by William Ogle (cited by Nielsen, 1947) to characterize

 

*- -—- .I-n— “r--

25. Nielsen, 22. cit., p. 3-4.

l7
inability to write. Exner26 in 1881 described a writing center
at the foot of the second frontal convolution on the left aid 6.
Dejerine, in 1881, postulated a visual speech center in the
left angular gyrus. Deterioration of this center would result
in word-meaning blindness.

While these research.workers were discovering "centers"
and studying cases, synthetic thinkers were correlating these
discoveries. "The first actual diagram was published by
Baginsky in 1871 . . . From.this time onwards the rage for

diagrams became a veritable mania."‘¢'7

Shortly after the appearance of Wernicke's work,
Lichtheimg8 began to make diagrams of Wernicke's centers.
Lichtheimfis, of all the various diagrams, attained the

greatest popularity.

It was definite and precise; every form of aphasia was
accounted for by a lesion of some hypothetical centre or
purely imaginary path. Teachers of medicine could

assume an easy dogmatism at the bedside and candidates
for examination rejoiced in so perfect a clue to all
their difficulties. But serious students could not fit
these conceptions Of aphasia with.the clinical manifesta-
tions; incredulous of such scholastic interpretations,
they lost ingerest in a problem of so little practical
importance.d

 

26. (Siegmund Exner:--Viennese physiologist, 1846-
1926)

270 Head, 220 Cite, p. 5960
28. (Ludwig Lichtheim:--German physician, 1845-1915)

29. Head, Opgit., p. 397.

18

In his diagramming of Wernicke's theory, Lichtheim
added a new link with his concept center connected to the
motor and acoustic centers. Apparently he intended this cen-
ter to bridge the gap between the anatomical and psychological
views of aphasia. But "these schematic structures were built
of flimsy, theoretical material, on scanty clinico-anatomical
foundation, and it is not surprising that a radical departure
from the existing views on aphasia was soon to follow.“;50

It was H. Charlton Bastian31 that Henry Head accuses of
Opening "the catastrOphic road to schemes and diagrams."°2
Bastian's papers, first appearing in 1869 and undergoing sub-
sequent revisions as time passed, included a scheme involving
four centers: glossokinesthetic (tongue), cheirokinesthetic
(hand), visual word, and auditory word centers. He called
these the organic seats of physiological types of memory, and
designated Broca's region--"the posterior part or foot of the
third frontal and the inferior part of the ascending frontal
convolutions“33--as the part of the brain which.he called the

"glosso-kinaesthetic" centre.

 

_—‘—V

30. William J. German, "Aphasia", Yale Journal.2§
Biology and Medicine, 1:365- 1928-29.

31. (Henry CharltOn Bastian:--English neurologist,
1837-1915)

520 Head, 220 Cite, p. 2960

33. H. Charlton Bastian, "Some Problems in Connexion
With Aphasia and Other Speech.Defects“, The Lancet, Vol I for
1897:935, April 3, 1897. _

19

In further clarification of his concept of a center
Bastian states

Although I am not a believer in the complete topographical
distinctness of the several sensory centres in the
cerebral hemisphere, I consider it clear that there must
be certain sets of structurally related cell and fibre
mechanisms in the cortex, whose activity is associated
with one or with another of the several kinds of sensory
endowment. Such diffuse but functionally unified nervous
networks may differ altogether from the common conception
of a neatly defined "center", and yet for the sake of
brevity it is convenient to retain £213 word and refer to
such networks as so many "centers".

Bastian contended that we think in words, and words are
remembered sounds revived in one or more of the word-centres.
Association fibres would be involved in addition to the
afferent fibres of the organic seats of the different kinds
of word memory.

Bastian utilized Charcot's division of "auditives",
"visuals", "motors", and "indifferents" for speech. (“There
may be a revival of sounds of words as we hear them in
ordinary speech; there may be a revival of visual impressions
of words as we have seen them in written or printed

characters; and, lastly, there may be a revival of the feel-

ings of muscular contractions concerned in the pronunciation

35

of words.") He upheld Jackson's theory that the auditory

centre was the primary reviver of words in the majority of

 

54. Ibid., p. 954.
55. Ibid., p. 955.

20
persons. After revival of words in the auditory centre, he
contended that through commisural fibres the corresponding
glosso-kinaesthetic elements were aroused to effect pronuncia-
tion. He also allowed for a degree of concurrent activity
during speech in related portions of the visual word centre.

To explain more completely why he does not limit
cerebral activity to narrowly localised centres, but rather
widespread activity in varied regions, Bastian rationalizes
on our acquisition of speech:

Words that are heard are first of all associated in

the mind of the child with external objects, so that such

auditory impressions become linked, by means of associa-
tional fibres, with the organic seats of the several sen-
sor impressions. . .

The sight of the mother recalls the name "mamma", just
as the sound of this word would revive the corresponding
visual, tactile, and other images. After a time the
auditory representative of the name becomes reinforced
by glosso-kinaesthetic impressions as soon as the child
learns to utter the word; later by visual impressions,
when it learns to read, and by cheiro-kégaesthetic im-
pressions when it has learned to write.

Thus Bastian denied the existence of a "naming" or
“concept" centre as proposed by Broadbent57, Kussmaul, Charcot,
and Lichtheim. Instead he sought to explain speech defects
arising, not from a lesion in a localised centre for concepts,
but from lesions situated in or near the sensory inlets:

A destructive lesion of the portions of the cortex which
are most remotely connected with the sensory inlets would

 

:56. Ibid., p. 938.

37. (Sir William.Henry Broadbent:--London physician,
1835-1907)

21
destroy the capacity of the patient for highly abstract
reasoning, and would no doubt inflict considerable damage
on the language in which abstract thought is embodied,
but this condition would not be recognized as an aphasia;
and even the intermediate portions of the cortex in which
conceptive thought is carried on might be seriously
damaged without giving use to a special speech disorder,
inasmuch as any impairment of speech which might be pre-
sent would only be regarded as a part of a general decay
of the reasoning faculties. When, however, the lesion is
situated in or near to the sensory inlets a disorder of
language results which is out of all proportion to the
general impairment of the reasoning faculties.

He believed that the "annexes“ of the sensory centers
are thrown into functional activity more or less simultaneously
with the combined sensory area. This inseparability makes
distinct localization impossible; the anatomical substrata
for perception, conception, and revival of linguistic symbols
occupies "a very considerable extent of the cortex of both
hemispheres."39

Up to about the year 1889, with the exception of the
little-heeded Jackson, the trend of thought remained in the
direction of localization. However, M. Allen Starr40, one of
the first Americans to become interested in aphasia,

announced in 1889 that he had found no case to substantiate

 

—m

38. Bastian, Op. cit., D. 942.
39. Ibid., p. 9410

40. (Moses Allen Starr:--American neurologist, 1854-
1952)

22
Broca's pronouncement.41 Then Freud42, two years later,
suggested that there was no such thing as a center.45 Dejerine
also declared against the autonomy of the so-called centers.44
In 1897, Lautzenberg (cited by Ellison, 1921) sum-
marized the situation regarding the disorders of speech as
follows: "The Outstanding characteristic of aphasia is that
every observer thinks it necessary to formulate a theory of
his own before recording the facts that he has noticed."45
To sum up the situation,
Up to 1906 four centres of speech were considered; one
centre of motor aphasia located in the third frontal
convolution and three centres called centres of sensory
aphasia: first, temporal convolution for word hearing;
second, angular gyrus for word seeing, and third,
second frontal convolution for the faculty of writing.46
The stage was now set for Marie's47 dramatic entrance.

The history from.this turning point to the present has been

treated in Part II of this study through detailed analyses of

 

4le “derson, QBe Cite, pe lle

42. (Sigmund Freud:--Viennese neurologist, 1856-
1939)

43. Nielsen, 22. cit., p. 7.

44. Ibid.

45. Ellison, 22o Cite, pe 797e

46. Alfred Gordon, "Diagnostic Consideration of the
Older and Later Views on Aphasia Based on the Anatomical
Findings of a Case of Typical Motor Aphasia“, Medical Journal
and Record, l28:ll:564, Dec. 5, 1928. c

47. (Pierre Marie:--Parisian neurologist, 1853-1929)

23
the viewpoints of certain outstanding thinkers on the subject.
However, to complete the historical picture, a cursory sketch
of this period is herewith set forth.

Marie's 1906 pronouncements which so startled the
neurological world were that (1) Broca's convolution takes no
part in the producing of aphasia, and (2) aphasia is dependent
upon intellectual loss or deficit.

The aftermath of the keen controversy caused by these
statements revealed that Marie had simply redefined aphasia,
recognizing only one type--sensory, or Wernicke's aphasia.
Other types he dismissed as anarthria. Another service
rendered the study of aphasia by Marie was the interest he
restimulated in this speech defect.

The next major trend of thought was given impetus by
the publication of Henry Head's psychological views. He
argued that aphasia was not so much a defect in general
intelligence, but rather, difficulty in abstract symbolize-
tion. It is not the intelligence which is primarily affected,
Head argued, but behavior which suffered.

In.his recognition of aphasia as the disturbance of a
highly organized act, he anticipated today's organismic

approach advocated by Kurt Goldstein.48

 

48. See Chapter IX

24

However, the psychologists were not to take over the
field unchallenged upon the appearance of Head's study. S. E.
Henschen, a Swedish.physician, published views almost the
exact antithesis of Head's. His strict localization views,
based on analysis of almost 1500 autopsy findings, greatly
influenced the present-day neurologist J. M. Nielsen.

There evolved in the next few years, a realization
that to successfully study aphasia one needs to use all three
frames of reference--anatomical, physiological and psycho-
logical. This synthesis of methods of approach appears to
be gaining wide support by the authorities of the present.

For a more complete comprehension of the changes in
aphasic concepts since the turnlof the century, various of
the outstanding authorities have been treated in greater

detail in Part II of this study.

PART II

HISTORICAL VIEWPOINTS

' CHAPTER III
THE PSYCHOLOGICAL VIEWPOINTS OF HUGHLINGS JACKSON

Persuing his solitary way during the age of the
diagram.makers was the founder of English neurology,
Hughlings Jackson. His minute clinical studies extended
over an interval of thirty years and included the first
recorded studies in speech psychology.

Although Jackson began publishing as early as 1864,
his papers were quite generally neglected until Arnold
Pick,1 realizing their value, dedicated his "Die Agrammatis-
Chen Storungen" to Jackson in 1913. In view Of Jackson's
importance in the history of the study of aphasia, at first
it is difficult to understand why his writings, which spanned
a period from.1864 to 1893, were so long neglected. One of
the reasons given is that "Jackson derived all his psycho-
logical knowledge from Herbert Spencer,2 and adopted his
phraseology almost completely. This has tended to alienate

psychologists, blinding them.to the truths underlying this

somewhat uncouth nomenclature.“5 Another maior reason for the

 

1. (Arnold Pick:--neurologist and Professor Of the
German University of Prague)

2. (Herbert Spencer:--English philosopher, 1820-
1903)

3. Henry Head, Aphasia and Kindred Disorders 2; Speech,
(Cambridge: The University Press, 1926), p. 3 .

27
comparative neglect of Jackson's writings might be his form-
idably difficult style of writing which is apt to discourage
even the most enthusiastic student of language, speech,
psychology and/or neurology. In addition, Jackson presented
his dynamic approach in the face of an all-out functional
interpretation at that time.

Speech to Hughlings Jackson is a function of mental
activity. It is primarily a psychological problem, regardless
of how closely it may be linked with the integrity of some
portion of the brain-substance. Henry Head, in 1915, says in
comment that "no one except Jackson has recognized that all
the phenomenaare primarily psychical and only in the second

place susceptible of physiological or anatomical explanation.“4

Because of this belief he insisted upon an absolute distinottn
between psychological terms and anatomical or physiological
terms.

Jackson recognizes that this mental process can be
divided into two distinct forms: “(1) Intellectual, i.e.,
the power to convey prOpositions. (2) Emotional, i.e., the
ability to exhibit stress of feeling."5 But before we can
elaborate on this dual aspect it is necessary first to under-

stand Jackson's concept of propositionizing.

 

4. Ibid., p. 32.

5e Ibide, pe 55e

28

Jackson's views of the problems of speaking and think-
ing deviate most strikingly from those of the neurologists,
and anticipate by many years a viewpoint pOpular with students
of language. He points out that it is not in words or signs
only that we speak, but "in words or signs referring to one
another in a particular manner."6 Thus we visualize a sen-
tence not as a pile of words but as a unit. Actually, Jackson
considers single words as meaningless; they are propositions
only if other words in relation are implied. This viewpoint
was voiced in 1866 when scientists believed that we thought
in words. 'Clarifying his conception of the proposition being
the expression of a relation between two things, Jackson
states: "It is not enough to say that speech consists of /
words. It consists of words referring to one another in a
particular manner; and, without a prOper interrelation Of its
parts, a verbal utterance would be a mere succession of names
embodying no proposition."7 Speaking is not simply the
utterance of words; speaking is "propositionizing."

After stating that speech is essentially the formation
of propositions, Jackson further points out that there is no
difference in this respect between external and internal

speech. The only difference lies in that uttered, or external,

 

6. Ibid., p. 40.
7e Ibide, pe 40'1e

29

speech has not passed over the vocal organs. Or in Jackson's

own words

Or,

Anatomically and physiologically regarded, we say that
the same nervous processes are concerned in internal as
in external speech. The difference is that the excitation
of these nervous processes in speaking to oneself is so
slight that the nerve currents developed do not spread to
the articulatory and vocal muscles; in speaking aloud the
excitation is strong, and currents do reach.those muscles.
This fundamental similarity and superficial difference
betwegn internal and external speech must be kept well in
mind.

in other words, we can say with Jackson that

the anatomical substratum of a word is a nervous process
of a highly special movement of the articulatory series.
That we may have an "idea" of the word, it suffices that
the nervous process for it energizes; it is not necessary
that it energizes so strongly that currents reach the
articulatory muscles.

What then do we mean when we speak ofifihe loss of the

power to speak? Jackson would say we have lost the power to

propositionize, implying either internally or externally.

When Jackson speaks of the loss of the power to speak he does

not mean that

the speechless man has lost any "faculty" of speech or
prepositionizing; he has lost those words which serve in
speech, the nervous arrangements for them.being destroyed.
There is no "faculty" or "power" of speech apart from
words revived or revivable in prOpositions, any more than
there is a "faculty" of co-ordination of movements apart

 

8. Hughlings Jackson, "On the Nature of the Duality

of the Brain," Medical rress and Circular, 1:19, Jan. 14, 1874.
(Reprinted in.Brain, 58:82, 19l5)

9. Ibid., p. 85.

50
from.movements represented in particular ways.10
Because of the tendency to attribute the involvement
of some mental property, through their use, Jackson seldom
used Greek terms such as agnosia, alexia, apraxia, et cetera.
If, then, the person who has lost speech cannot pro-
positionize in any fashion--either internally or externally--
we must not say that speech is external thought, for there
is no essential difference betwixt internal and external
speech. We speak not only to tell other people what we
think, but to tell ourselves what we think. Speech is a
part of thought--a part which we may or may not exterior-
ze. Again it is not well to say that thought is internal

speech, for the man who is speechless (the man who has no
internal speech) can think.

Jackson explains the speechless man's ability to think
in terms of his still possessing in automatic forms all the
words he ever had. However he does recognize that the patient
"will be lame in his thinking because not being able to revive
words he will not be able to register new and complex
experiences of things."13

"There are two ways in which words serve in thought;

speech is but one way, and this, whether it be internal or

external, is speaking physiologically, a function of the left

 

10. Hughlings Jackson, "0n Affection of Speech From
Disease of the Brain," Brain, 1:304, 1879. (Reprinted in
Brain, 38:114, 1915)

11. Henry Head, "Hughlings Jackson on Aphasia and
Kindred Affections of Speech," Brain, 58:16, July, 1915.

12. Ibid., p. 17.

51
cerebral hemisphere."15 In what other way do words serve
thought? Jackson differentiates between propositionizing
and receiving propositions. When receiving a prOposition,
the process is entirely automatic. To illustrate:

When anyone says to me "Gold is yellow", I am, so to
speak, his victim, and the words he utters rouse similiar
ones in me; there is no effort on my part; the revival
occurs in spite of me if my ears be healthy. Moreover,
the speaker makes me a double gift; he not only revives
words in.my brain, but he revives them in a particular
order--he revives a preposition. But if I have to say,
"Gold is yellow," I have to revive the words, and I have
to put them in propositional order. The speechless man
can refzive propositions, but he cannot form theme-cannot
speak.

Tb understand this difference we must understand
Jackson's dual concept of the brain's function and how the
functions of the two hemispheres differ. Here Jackson voiced
one of his major breaks with the doctrine of cerebral
localization and its attendant ignoring of the recessive
hemisphere. He believes that the brain acts as a whole in
the language function and that a speech "function" could not
be localized in the left hemiSphere. Jackson observes that
patients who had lost the power of Speech still retained some

forms of utterance. If a person whose left language area

was destroyed could still utter words, the assumption of an

 

l5. Hughlings Jackson, "On the Nature of the Duality
of the Brain", Medical rress and Circular, 1:19, Jan. 14,
1874. (Reprintedin Brain, 58:85, 1915)

14. Ibid., p. 84.

52

anatomical basis for them on the other side was mandatory.
In 1874, Jackson set forth his belief that the right hemi-
sphere of the brain--emotionally motivated--facilitated the
automatic use of words, and the left hemisphere facilitated
both automatic and voluntary use. These views were published
in the same year as Wernicke's major contribution. Hence they
were presented prior to the establishment of the anatomical
basis for sensory aphasia. While he considers them both alike
in that they both contain processes for the automatic use of
words, the left hemisphere has additional processes for the
voluntary use of words for speech. Specifically, "The left
half of the brain is that by which.we speak, for damage of it
makes us speechless; the right is the half by which we
receive preposition-"15 "The right is the automatic side for
words and the left the side where automatic use of words
merges into voluntary use 23 Egggg (speech). In healthy
persons, I suppose there is automatic revival of words prior
to their voluntary revival(speech)."16

What then precedes the preposition? The prior process
of the mind is an arousing in propositional form. This
initial process Jackson called the "subject-prOposition".

This is a sort of "pre-conception" occurring in all voluntary

 

15. Ibid.
16. Ibid., p. 86.

53

operations.

The Operation is nascently done before it is actually
‘done; there is a "dream” of an operation as formerly
doing before the operation; there is dual action. Before
I put out my arm voluntarily I must have a "dreamfl of the
hand as already put out. So, too, before I can think of
now putting it out I must have a like “dream”, for the
difference betwixt thinking of now doing and actually
doing, is, like the difference between internal and
external speech, only one of degree.

What proof, if any, have we that words must be auto-
matically revived before voluntarily used or uttered in a
proposition? Jackson states:

That automatic action must precede voluntary action is,

I submit, certain. In gross physical operations we see
that it is so. We cannot use the hand before we fix the
wrist, nor the arm before the shoulder is fixed, and in
heavy strains with this limb, the chest is first fixed
and the glottis is closed, after a full inspiration. The

more automatic muscles must be in action before the more
voluntary, or there would be no point d'a ui. Taking a

psychologgcal illustration, we note a we esire before
we will.

Returning now to the theory of Jackson's with which
this chapter opened, let us examine further his dual aspect
of intellectual and emotional expression. Jackson designates
those dual aspects as superior and inferior speech. The
inferior speech, or automatic service of words Jackson

believes to be associated with activity of the right hemi-
sphere. The left hemisphere (in right-handed people) not

 

17. Head, 22. cit., p. 18.

18. Hughlings Jackson, "On the Nature of the Duality
of the Brain (Continuation)“, Medical Press and Circular,
1:41, Jan. 21, 1874. (Reprintea In Brain, 5§:93, I§IS)0

54
only subserves the use of words in propositional forms, but
also had a lower use in the automatic service of words. Al-
though these more automatic activities are centered in both
hemispheres, the power of exciting words in propositional
forms is in the left only.

This line of thought can be easily traced to Herbert
Spencer who said in his essay, "The Origin and Function of
Music“: 1

All speech is compounded of two elements, the words
and the tones in which they are uttered-~the signs of
ideas and the signs of feelings. While certain arti-
culations express the thought, certain vocal sounds

express the mafe or less of pain or pleasure which the
thought gives. 9

Through the means of voice we give outlet to our

emotions. Voice "expresses various states of feeling common
- 20
to man, rather than ideas special to the individual."

Jackson likens swearing to a strong expression of the
emotions. In fact, he does not consider it a part of lang-
uage, strictly speaking. Rather,

It is a habit which has-grown up from the impulse to

19. Hughlings Jackson, "Clinical Remarks on.Emo-
tional and Intellectual Language in Some Cases of Disease of
the Nervous System," The Lancet, 1:174, Feb. 17, 1866. (Re-
printed in Brain, 58:437’1915.

zO. Hughlings Jackson, "Loss of Speech: Its Asso-
ciation with Valvular Disease of the Heart and with Hemi-
plegia on the Right Side--Defects of Smell--Defects of Speech
in Chorea--Arterial Lesions in Epilepsy,“ Clinical Lectures
229 Reports, London Hospital, 1:588, 1864. (Reprintedfin
Brain, 58:03, 19:55.

35

add the force of passing emotions to the expression of
ideas. It belongs to the same general category as loud-
ness of tone and violence of gesticulation. 1 '

While it is true that oaths consist of articulate words, they ,
nevertheless are generally used ,
not to eXpress ideas, but to make up by vigour in de-
livery what is wanting in precision of expression.
They may, indeed, be considered as phrases which emotion
has filched from the intellect, to express itself in

more definite terms than it could do by mere violence
of tone or manner.22

Similarly Jackson explains the stereotyped swear-
phrase so frequently the only vestige remaining of language
in an aphasic. Expressions such as "Damn.it", "Bless my
'lifeJ", and "Ch Dearl", when.used in anger or vexation, are
used to clothe feelings rather than to convey intellectual
propositions. Jackson feels that these ejaculatory expres-
sions are prompted by the emotions and not by the will. As
a possible explanation of the production of these phrases
Jackson suggests that they may be reflexes:

It is quite obvious that they are not voluntary, as the
patients cannot repeat the phrases. The will cannot
act, but, somehow, an emotion, e.g., anger, gets the
words passed through the convolution of language. Just

as a paralysed foot will jump up when the sole is
tickled, so these words start out when the mind is ex-

 

21. Ibid., p. 40.
22. Ibid.

36

cited. Such ejaculations as I have mentioned would.have
become easy of elaboration by long habit, and would re-
quire but slight stimulus for perfect execution.25

It is quite obvious from.the foregoing that Jackson
believes that both sides of the brain are probably educated.
However, it is the left that begins to act. Those phrases
which are in a sense involuntary have become so by habit and
may be the result of the action of the right hemisphere only.
In comment Jackson states: "How from the right side they
are set a-going I do not know any more than I know how a per-
son laughs, not only without effort, but even when he tries
to keep quiet."24

If the function of the two hemispheres now seems to be
confused, let us review Jackson's analysis.

The division we made was not that the left half of
the brain serves in speech, and the right in receiving
speech and in other ways, but that "nervous arrange-
ments for words used in speech lie chiefly in the left
half of the brain", and "that the nervous arrangements
for words used in understanding speech (and in other
ways) lie in the right also." It is believed that the
process of verbalizing and every other process is dual,
but that the more automatic a process is, or becomes by
repetition, the more equally and fully is it represented
double in each half of the brain. But the utterances
show too, for the most part, that the speech possible
by the right side of the brain is inferior speech. In

 

25o Ibid., p. 410

24. Hughlings Jackson, "Notes on the Physiology and
Pathology of'Language", Medical Times and Gazette, 1:659,
R

June 25, 1866. eprinte ed inB Br mi 58 8:55, 1915).

57

nearly all cases it was well organized, automatic or
"old", and nearly every utterance required a special oc-
casion; was, to speak pOpularly, surprised out of the
patient by a sudden accustomed stimulus. And it is to
be borne in mind that the patient cannot repeat, say
voluntarily, what he thus utters.25

In cases of brain damage, it is intellectual language
that suffers most; emotional language is conserved. Not only
do vocal inflections go undisturbed, but so do smiles and
gestures. Jackson expounds his general law underlying these
speech disturbances that "voluntary power is diminished with
retention of the power to carry out the same movement in a

26
more automatic manner." J. M. Nielsen in 1947 makes essen-
tially the same explanation:
There is no doubt that the anatomic and physiologic pat-
terns for the utterance of any word are still present
in the brain after destruction of Broca's convolution
of the major (left) side...The patterns are located
anatomically in the right Broca's convolution as Jack-
son thought and need only the proper stimulus to bring
them into action. They can be stimulated ghrough the
emotions, though the mediation is unknown. 7
Far too frequently we hear that disease or injury has

caused the utterances peculiar to various aphasics. To these

erroneous observations of speech disturbances Jackson, as far

 

25. Hughlings Jackson, "On Affections of Speech.From
Disease of the Brain--II", Brain, 2:208, 1880. (Reprinted in
gain, 58:146, 1915).. ......._... g

26. Head, 22. cit., p. 9.

27.1 Nielsen, 22. cit., p. 21.

58
back in 1868, applied the general law of nervous activity
that "a destructive lesion can never be responsible for posi-
tive symptoms; pure destruction produces negative effects,

and any positive symptoms are the consequence of the released
28
activity of lower centres."

In explaining the speech phenomena he notes that

the disease is destruction of nervous arrangements, and
that could not cause a man to do something; it has

enough to answer for in leaving him.unable to speak.

The utterances are effected during activity of nervous
arrangements which have escaped injury. This remark may
seem a truism here, but in.more complicated cases it is
very common to hear of positive symptoms being ascribed
to negative lesions--to loss of function of nervous ele-
ments. It is common at any rate for disease to be
thought of vaguely as something "disorderigg the func-
tions of the brain". . . It is an error to ascribe such
positive symptoms as the recurring utterances in speech-
less men, the erroneous words uttered by those who have
defect of speech. . . etc., to loss or to defect of func-
tion. These positive mental symptoms arise during activ-
ity of lower centres or lower nervous arrangements which
have escaped injuring9

With this analysis, then, we must recognize the exist-
ence of a negative and a positive side to every speech affec-
tion due to neurological pathology. The negative aspect is
the patient's inability to speak, to write, to read, or to

express by signs. The positive symptoms such as swearing or

 

28. Head, 22, cit., p. 5.

29. Hughlings Jackson, "0n Affections of Speech.From
Disease of the Brain--III", Brain, 2:525, 1880. (Reprinted
in Brain, 58:154-5, 1915).

59
uttering other emotional expressions are the expression of
lower mental activities. Whatever function exists in a given
case does not depend directly on the lesion, but on the func-
tion of the cerebral structures remaining. Thus, "the dis-
ease causes loss of speech; it ermits the increased dis-

5U
chargeability of the right half."

Destruction of function of a higher centre is a re-
moval of inhibition over a lower centre. The lower
centre becomes more easily dischargeable, or popularly
speaking, "more excitable", and especially those parts
of that centre which are in activity when control is
removed.31

That parts suffer more as they serve in voluntary,
and less as they serve in automatic Operation, is, I be-
lieve, the law of destroying lesions of the cerebral
nervous centres.52

In analyzing the recurring utterances of one whose
left half of the brain is so extensively damaged that he can-
not speak, Jackson offers the hypothesis that "the words
were being revived at the time when the patient was taken

50. Ibid., p. 158.

31. Ibid., p. 157‘80

52. Hughlings Jackson, "0n the Anatomical and Physio-

logical LOcalization of Movements in the Brain", The Lancet,
1:84, Jan. 18, 1875. (Reprinted in Brain, 58. 76, 1915).

40
55
ill." He notes that these words are the result Of certain
nervous arrangements which remain permanently in a state of
dischargeability far above normal.

It would seem, from this discussion Of Jackson's notes,
that we have begun stressing the psychological aspect Of
speech only to end up emphasizing the anatomical basis of
speech. To clarify his double emphasis Jackson states:

We have, as anatomists and physiologists, to study
not ideas, but the material substrata Of ideas (anatomy)
and the modes and conditions of energizing of these sub-
strata (physiology). Where most would say that the
speechless patient has lost the memory of words, I
would say that he has lost the anatomical substrata Of
words.54

In the light of this explanation we can more readily
understand the "altering" Of a person's disposition in cases
Of deterioration of the brain--how our more animal instincts
and desires are no longer subordinated. "There is reduction
to a more automatic condition; there is dissolution, using

this word as the corresponding Opposite Of evolution. The

weaker the mind the more do the more automatic desires have

 

55. Hughling Jackson, ”0n Affections of Speech From
Disease Of the Brain--III", Brain, 2:525, 1880. (Reprinted
in Brain, 583157, 1915).

54. Hughlings Jackson, "0n the Nature Of the Duality
Of the Brain", Medicgl Presg and Circular, 1:19, Jan. 14,
1874. (Reprinted in.Brain, 58:84, 1915).

41
55

their own way."

56
In retrospect, Weisenburg and McBride list the follow-

ing ideas of Hughlings Jackson as having become foundation

stones in modern theories:

his emphasis on aphasia as a psychological problem, his
attack through the clinical findings rather than the
pathological destruction, his concept Of higher and Of
lower, more automatic forms Of response, his apprecia-
tion of the complex relations Of language and thinking,
his discovery Of related disorders later called apraxia

and agnosia, and some Of his important views on local-
ization.57

The same authorities list as no longer significant

his differentiation Of types Of disorder, much Of his
theory of pre-verbal formulation, his Opinions on the
role of the right hemisphere in speech, and his Obser-

vational methods as Opposed to the test methods now
in use.58 '

 

55. Hughlings Jackson, "0n the Anatomical and Physio-
logical Localization of Movements in the Brain", The Lancet,

1:84, Jan. 18, 1875. (Reprinted in Brain, 58:79, 1915).

56. (Theodore Weisenburg:-American neurologist,
1876-1954)

57. Theodore Weisenburg and Katherine E. McBride,
Aphasia: 5 Clinical and Psychological Study. (New YOrk:
The Commonwealth Fund, 1955), p. 19.

58. Loc. cit.

' ’/
'f _/
I.

CHAPTER IV

THE CONTROVERSIAL LOCALIZATION IDEAS OF MARIE
AND OPINIONS OF HIS CONTEMPORARIES

In 1906 a series of papers appeared which caused a
considerable controversy in neurological circles. Pierre
Marie published three papers in the Semain Medicale on
"Revision Of the Question Of Aphasia". These, and the sub-
sequent series Of papers culminating in moutier's1 monograph
of 1908, demanded a revision Of the Whole subject Of aphasia.
Marie boldly struck out with the unqualified declaration that
the inferior left frontal convolution (Broca's region)
played no particular part in language functions; it could not
be considered a speech center. Since Marie‘s theory explicit-
ly denied one of the hitherto incontrovertible facts Of the
literature, Opponents arose in storms Of abuse and hotly con-
tested his localization views.

Besides denying that lesions in Broca's convolution
take no part in the production of aphasia, Marie denied the
existence Of auditory, visual and motor speech centers wherein
speech.memories are registered in the cortex. Marie recog-
nized no distinction between motor and sensory aphasia and,

in place of the classical doctrines on localization, postulated

 

1. (F. Moutier:--Marie's co-worker)

45
only one speech center diffusely localized in the left temporo-
parietal lobe. Hence, he insisted that there existed only one
type of aphasia from a lesion of the cortex-~sensory, or
Wernicke's aphasia, which he called "true" aphasia. This type,
he stated, always resulted from a destruction Of the region
which he called Wernicke's zone (an area around the end of
the Sylvan fissure). Since he interpreted this center as a
region of intelligence specialized for language, and not
solely a center of sensory images, he also challenged Broca's
classic description that the aphasias were a disturbance of
speech with preservation Of intelligence. "He further com-
plicated the picture by introducing a psychological factor,
in the form of a disturbance Of comprehension and a reduction
of the intellectual capacity."2

Thus we have Marie's "true" aphasia defined as
not the inability to utter words, but the inability to
understand what is said, what is written or what is heard,
and the disability to represent mental concepts by their
accepted vocal or written equivalents. It is not, there-
fore, the result of the destruction of a "centre" in the
Old sense Of the word, but a disorder of the integrating
mechanism Of the nervous system (Sherrington) a condition
Of"diasc sis" (v. Monakow) or "apraxia" according to
Liepmann.

Wernicke's zone he defines as

composed Of the supramarginal (inferior parietal) and
inframarginal gyres and the posterior extremities Of the

 

2. German, 22. cit., p. 565.

5. Core, 22, cit., p. 514.

44
first two temporal convolutions,--in other words that
cortical region composed Of the gyral masses which curve
around thz extremities of the Sylvian and the parallel
fissures.

A lesion to this zone gives rise to a disturbance Of intelli-
gence, Marie contended.

Pure motor aphasia (or subcortical motor aphasia) he
called anarthria. This defect came with subcortical lesions
Of what he called the "lenticular zone" in either hemisphere.
The lenticular zone, or "quadrilateral field" of Marie, is

bounded anteriorly by the white substance of the third
frontal convolution, posteriorly by Wernicke‘s area,
externally by the insula, and internally by the wall Of
the third ventricle. It, therefore, comprises the
external capsule, the caudate and lenticular nuclei, the
anterior and posterior portions Of the internal capsule,
and the Optic thalamus.
“Above, this quadrilateral area was prolonged to include the
Outlying gyri of the convexity Of the cortex, while below it
included the subthalamic region.”6 Any lesion within this
zone causes anarthria; lesions behind it cause aphasia. (J.
M. Nielsen calls our attention to the fact that Marie ”over-

looked the fact that an anarthric cannot properly use his'

muscles for any purpose. An aphasic may use them for any

 

4. Charles K. hills, "Discussion on Aphasia, Especially
With Reference to the Views of Narie", The Journal gf'hervous
and Mental Disease, 54:459, 1907.

5. German, 22. cit., p. 565.

 

6. Osnato, 22. cit., p. 420.

 

45
purpose but speech").7

Broca's aphasia he declared a combination Of the true
aphasia and anarthria due to a double lesion: one in the
quadrilateral area, and one in the general speech intelligence
area (Wernicke's area) or the tracts to or from it.

In evaluating Marie's contribution.we must not overlook
the value Of his "calling attention to a chapter Of patho-
logical physiology which.no longer could remainunchallenged.“8
He is praised by J. M. Nielsen for "reOpening the whole sub- ‘
ject, which really needed reconsideration"9, and by Henry Head
for his fight for simplification. Both of these outstanding
men, however, label much Of his work as being merely a matter
Of changing definitions--"the greater part Of the discussion
of the clinical manifestations was purely a verbal battle."10
He simply redefined aphasia and this made his statements
sound startling.

While Marie's theory Of intellectual defect has en-
listed many adherents, outstanding being Michael Osnato,

Albert G. Odellll noted in 1950 that "by far the greater

 

7e Nielsen, 9E0 Cite, p. 90

8. Alfred Gordon, "A Contribution to the Study of
Aphasia", New York Medical Journal, 97:14, Jan-June, 1915.

9. Nielsen, .920 Cite, p. 90

10. Henry Head, "Aphasia: An Historical Review",
Brain, 453599, 1920.

11. (Albert Grove Odell:--Clifton Springs, N. Y.,
neurologist and psychiatrist, 1878- )

46
number accept the idea Of organic disturbance and locate
speech centers in the cortex.“12

In 1942 J. M. Nielsen anthrnOld P. Freidman published
the results Of a study to determine what semblance Of truth
there may have been in Marie's teaching. In a clinical study
Of 12 cases they found that

within the quadrilateral space Of Marie the external cap-
sule has much to do with language by virtue of its convey-
ing Of impulses from.the language formulation area forward
to Broca's convolution. Destruction Of it causes eithig
paraphasia and agraphia or motor aphasia and agraphia.

They go on to say that

after estructive lesion of the external capsule the
patient will either have to use the speech.mechanism Of
the minor hemisphere as a unit or he will perform one Of
the two functions (formulation or emission) on the minor
side and the other by means of the major side. If the
minor area Of Broca is utilized, motor aphasia results
until time is available for training. If the minor area
Of formulation is used andkhe impulses are conveyed across
the corpus callosum to the major Broca's convolution
paraphasia results. A lesion Of the anterior limb of the
major internal capsule will produce dysarthria or
anarthria by virtue Of interrupting the projection fiber
tracts from.the precentral gyrus to the pons apd medulla.
Such a disturbance has no relation to aphasia. 4

They conclude that his Observations have some use if properly
appraised. However, he exerted a definitely harmful influence

by assuming his predecessors completely in error. He could

 

12. Albert G. Odell, "Aphasia, A Case Report“, The
Clifton Medical Bulletin, 16:4:165, October 1950.

15. J. M. Nielsen and Arnold P. Friedman, "The Quadri-
lateral Space of Marie", Bulletin 2; the Los Angeles Neuro-
logical Societ , 7:5:155, I942.

14. Ibid., p. 155-6.

47
have helped to clarify the subject instead of retarding
progress if he had given due credit for scientific observation.

One Of Marie's most articulate followers was Michael
Osnato Of New York City. In attempting to OOpe with the
problem.of aphasia Osnato refers to the failure Of anatomy
and pathology in elucidating the problem. He therefore sought
to enlist the aid Of clinical medicine.

Prior to the time Of Marie and moutier's publications,
Osnato felt that classifications of "centers" were based more
on theory than upon trustworthy pathOlogical evidence. These
two men, however, examined all the autopsied cases of aphasia
which.were reported in the literature from the time Of Broca
in 1861 up to 1905. They called attention to the sparcity Of
material for Broca's original statement. Osnato gives a good
account of the clinical statistics underlying Marie and
Moutier's contentions:

Between the years Of 1861 and 1906, 504 cases with
autopsy have been published upon the subject Of the third
left frontal convolution, or Broca's motor speech area.

Of these, 201 cases were not Of value for statistical
purposes because in 26 of these cases the clinical or
pathological records were incomplete and in the remaining
175 cases the lesions were too vast for accurate localiza-
tion. There remained, therefore, 108 cases in which the
lesions were localized, the records and clinical histories
being Of sufficient detail for use in the study Of the
subject. Of these 108 cases only 19 showed facts which
appear to support Broca's theory, and in 11 of these, the
lesion was not cortical at all, but was found in the sub-
cortex. 0f the 108 cases Which were considered of suffi-
cient value, only 8 showed the cortex of the left third
frontal convolution to be affected. All the other cases
were almost entirely against the classical theory that

it“.

48

Broca's area was an area for the motor mechanism Of speech.
Including the 11 subcortical cases, only 19 were apparently
favorable to this theory and even in a number Of these
cases there were ample lesions. In one there were exten-
sive lesions of the right temporal lobe with no mention

as to whether this patient was left-handed or not.

Both Marie and Moutier agree that there does not exist
in medical literature one observation of Broca's aphasia
in which a single lesion strictly localized to the foot

Of the left t rd frontal gyrus has been proved to exist
upon autopsy.

Citing other investigations, Osnato Observes that only
four of the 104 cases studied by Frankel and Onuf (cited by
Osnato, 1921) seemed to confirm Broca's theory of the local-
ization of motor speech. However,

they found at the same time 5 cases of motor aphasia in
which the left third frontal convolution was absolutely
intact and the subcortical association fibers going from
and to this pagt Of the cortex showed no trace Of
degeneration.1

In view Of these clinical statistics Osnato concurs

with Marie's warning that "to use the symptom of aphasia as

a localizing diagnostic aid is impossible and a dangerous
procedure."17
In attempting to disprove the existence Of any sharply

defined, diagrammatic localization of speech functions in any

 

15. Osnato, 22. cit., p. 420.

16. Michael Osnato, "Speech, Its DevelOpment and
Integration With the Intelligence", Neurological Bulletin,
5:2:58, Feb., 1921.

17. Ibid., p. 56.

49
group Of "centers", Osnato quotes Piersol18 on the development
of the cerebral cortex. (Except for the immediate vicinity of

the upper end of the Rolandic fissure)--

the cerebral cortex at birth is unprovided with associa-
tion fibers which.have acquired their medullary coat and
are therefore capable Of functioning. Within the early
months after birth, however, the myelination Of these, as
well as of other tracts, progresses rapidly, although this
process is not even moderately completed until after the
lapse Of several years. Indeed there is sufficient
evidence to believe that myelination Of additional fibers
continues so long as intellectual effort is progressive,
the demands made by education and special mental exercise
being met by a corriaponding completion Of additional
association fibers.

In addition to this argument based on anatomical
evidence, Osnato describes the develOpment Of speech in the

individual child and notes how the method of education of one

child differs from another.

since the variations occurring with the individual child
in the use Of the various special senses (including the
proprioceptive as one of these) are so great for the
production Of simple associations, and later of conception
and thought which find their expression in speech, the
nature Of the develOpment in the brain Of this function

will also vary greatly.20

Insofar as one child may learn speech by purely auditory

means, while another has the concurrent visual representation,

and still another may grasp the art of talking by tactile and

 

18. (George A. Piersol:--American physician, 1856-1924)

19. Osnato, 92, ci ., p. 55.
20. Ibid., p. 54.

50
kinesthetic training, each.has developed, to some extent,
different parts of the brain and different association fibers.
This extreme possibility of variation--when we consider that
each receptor is in potential synaptic reference to every
effector--undoubtedly is the reason why no diagrammatic scheme
Of definite speech intelligence centers can be applied to
everyone alike.

Further militating against the theory Of one particular
Speech center is the clinical Observation that aphasics
improve with re-education. Undoubtedly for any improvement
to occur it would be necessary for new association pathways
to replace those previously used which.are now destroyed by
injury or disease. Therefore, "This Observation alone would
be enough to cast serious doubt on any notion that only cer-
tain parts of the cortex are capable Of developing the power
to control speech."21

Osnato, in attempting to prove his contention that the
whole cortex is indivisibly associated with the development
Of the function Of speech and its expression, quotes at great
length various of the neurologists of his day. He voices his
agreement with such men as the neurologist C. J. Herrick in
the belief that

no cortical area can properly be described as the exclu-
sive center of a particular function. Such "centers" 5’

 

21. Ibid., p. 59.

51

are merely nodal points in an exceedingly complex system
of neurons which.must act as a whole in order to perform
any function whatsoever.22

The only sense in which there is a specific localization of
function in the cerebral cortex is

in the sense that particular systems of sensory projection
fibers terminate in special regions (the sensory pro-
jection centers), that from other special regions (the
motor projection centers), particular systems Of efferent
fibers arise for connection with the lower motor centers
related to groups Of muscles concerned with the bodily
movements, and that between these projection centers there
are association centers, each of which has fibrous
connections Of a more or less definite pattern with all
other parts Of the cortex. The destruction of any part Of
the cortex or Of the fiber tracts connected therewith,
involves, first, a permanent loss of the particular
functions served by the neurons affected, and, in the
second place, a transitory disturbance Of the cortical
equilibrium as a whole (diaschisis effect Of von Monakow).
Specific mental acts or faculties are not resident in
particular cortical areas, but all conscious processes
probably require the discharge Of nervous energy through-
out extensive regions Of the cortex, and the character Of
the consciousness will depend in each case upon the
dynamic pattern Of this discharge and the sequence of
function of its component systems. This pattern is in-
conceivably complex and only the grosser features are at
present Open to gbservation by experiment and patho-
logical studies. 5 .

The two leading contestants Of Marie's doctrine were
M. and Mme. Dejerine. They maintained that aphasia was not
dependent upon intellectual loss or deficit. Rather, "the
diminution Of intelligence sometimes exhibited by aphasics

is dependent upon disruption or disturbance of the cerebral

 

22. Michael Osnato, "Aphasia and Associated Speech
Problems (Continued)”, Neurological Bulletin, 2:1:51, Jan. 1919.

23. Ibid., p. 50’1.

52
mechanism of speech."24
The Dejerines insisted upon the localization of speech
and attributed true motor aphasia to a lesion of the "anterior
speech zone"--"a region that is very variable in its extent,
but which.may be said to comprise the area Of Broca at the
foot or the third left frontal convolution, the anterior
segment Of the island of Rail and a variable area Of the
adjacent regions.“5 Sensory aphasia they attributed to a
lesion in the zone Of Wernicke. Anarthria was believed to be
due "either to a bulbar lesion, or if of central origin, to a
degeneration Of the internal capsules.“6
‘ Also aligned against Marie was the American investiga-
tor, Charles K. Millsz7. Although he was a firm believer in
cerebral localization, "he was also aware Of the philosophical
and the psychological aspects of the prOblem, but seemed to
slight them in favor Of more tangible and, as he saw them,
more practical facets of the question.”8 He wrote of

functional areas, sub-areas and centers.

 

24. Mills, 22. cit., p. 460.
25. Core, 920 Cite, p. 3170
26. Ibid.

27. (Charles K. Mills:--Philadelphia neurologist,
1845-1951)

28. Anderson, Oé’Cite, p. 180

55
His interpretation of "centers" is indeed interesting:
Much objection has been.made at times to the use or
such expressions as centres and memorial images, because
of their supposed lack Of definiteness; but it matters
little how these centres of function are designated or
explained, if the fact is recognized that they are in some
sense foci Of activity resulting in special phenomena.
In.limiting the region, lesion Of which produces motor
aphasia, Mills includes the anterior portion of the insula in
addition to the hinder part Of the left third frontal con-
volution. He also believed "it is not impossible that it may
also in some individuals take in a part Of the first temporal
convolution where this merges with the insula."30
Although Mills accepted Marie's idea that an intellec-
tual deficit underlay disturbance and impairment in the
comprehension Of language, he demanded the necessity Of
adhering to Dejerine's explanation that "this deficit in its
turn is dependent upon destruction or disruption Of a
mechanism which is made up of associated centres."51 If we
did not accept this maxim, Mills felt we would be thrown back
upon some ancient metaphysical theory Of the existence Of

mind outside Of the body.
Another protagonist in the theoretical battle at this

 

29. Charles K. Mills, "The Different Theories Of
Aphasia", New York Medical Journal, 99:861, May 2, 1914.

50. Ibid., p. 864.
51. Ibid., p. 865.

54
time was von Monakow.52 He considered Speech a function of the
entire cortex. He insisted on the difference between locating
speech itself and localization Of aphasic symptoms. In his

Die Lokalisation.im Grosshirn he described the anatOmical

 

 

region attacked by aphasia, extending the motor speech area
to include Broca's area, the Operculum, the pars triangularis,
and the anterior part Of the insula.35
Von Monakow is of interest chiefly for his "diaschisis"
theory. This is a doctrine based upon recognition of integra-
ting mechanisms. When one suffers a cerebral lesion, von
Monakow ascribes its importance, not as damage to this one
particular area, but as a disturbance of a widespread function
due to damage of one of the vital parts. He suggests that the
concept Of both centers and associating mechanisms be accepted.
The very existence Of associations indicates something to
be associated. Associating structures are not simply
paths which come from nowhere and go nowhere. They are
lines Of conneztion between important structural and
dynamic foci.°
In 1910 the voice of Adolf Meyer35 made itself heard

on the subject Of aphasia through the Harvey Lecture. Drawing

upon his wide clinical eXperience, he warned against strict

 

52. (Constantin von Monakow:--Swiss histologist,
1855-1950).

550 German», 5320 Cite, p0 365’60
34. 1.11113, 92. Cite, p0 8650

55. (Adolf Meyer:--American psychiatrist, 1866- )

55
adherence to the popular diagrammatic conception of aphasia.
He pointed out the keen desire for condensation and simpli-
fication, but at the same time noted that the disorders were
compound and could not be thus easily simplified. He did
not want mixed terminology, but insisted that "the only real
and lasting solution comes from the utilization of adequately
defined anatomical and functional mechanisms."36

Jeanette Anderson notes that it was Meyer who bridged
the gap between the anatomical and the psychological f
approaches to the problem of aphasia.37 In the clinical
handling of aphasics Eeyer "emphasized the importance of a
knowledge of the patient's educational level, a complete

neurological examination, and accurate tests of hearing,

vision, and other senses."38

 

36. Anderson, pp. cit., p. 18.
37. Ibid., p. 19.

58.. Weisenburg and McBride, pp. cit., p. 26.

CHAPTER v
HENRY HEAD AND REVIVAL OF THE. PSYCHOLOGICAL APPROACH

Just as the Marie-created tempest was dying down, the
medical world was given another interpretation and system of
aphasic classifications with which to contend. Henry Head's
theories, appearing in the early 1920's, were in many ways a
modernized form of one of the earliest theories, that of
Hughlings Jackson. Jackson's theory that aphasia is a dis-
turbance of the power to form propositions was couched in
different terminology. Head and his followers looked upon
all aphasic manifestations as "defects of symbolic formulation
and expression" rather than a disturbance of the memory of
1 words or the faculty of language. By symbolic formulation
and expression Head.meant "a mode of behaviour, in.which some
verbal or other symbol plays a part between the initiation
and execution of the act."1

Thus he considered aphasia "a defect in the special
mental activity of symbolic expression such that the greatest
difficulty will occur in higher propositional speech or more
abstract symbolization; it is not a defect in general intel-

"2

ligence. Jeanette Anderson explains Head's basis for the

 

1. Henry Head, gphasia and Kindred Disorders 9; Speech,
(Cambridge: The University Press, 1926), p. 211.

2. Bender, 22' cit., p. 518.

57
latter statement:
Head tended to emphasize the formulative and expressive
side of speech rather than the integrative, and the sym-
bol as a unit of expression rather than as a part of the
symbolic significance of the whole. For this reason
perhaps, he did not consider speech as a part of the
higher integrative function, which is after all general
intelligence and which would tend to rise and fall
together with speech in lesions of the cerebral centers.
He did, however, recognize that in aphasia the symbol is

affected so far as it expresses relational processes in
constructive thinking.

Aphasics appear more stupid than others because they
cannot satisfactorily participate in verbal intercourse.
Because of this isolation from the sources of mental life,
many aphasics gradually deteriorate. However, "general
intelligence," according to Head, is not primarily affected.
Behavior suffers specifically.

In Head's classification cerebral localization relin-
quished its predominant importance. He insisted on a psycho-
logical interpretation of speech defects. He stressed the
need for studying aphasia as a disorder of function. It is
the disturbance of a highly organized act which results in a
defect of cerebral activity, not a destruction Of a strictly
definable anatomical center.

Gross organic injury does not remove the structural basis
of a "faculty" or the repository of "images", but disturbs

the march of events necessary for the perfect accomplish-
ment of some acquired act; this can be relearnt, even after

 

5. Anderson, 22, cit., p. 518-9.

58
the ablation of the whole of its "cortical centre".4

Head definitely denied the existence of "centres” for
speaking, reading, writing, or any other form of behavior
comprised in the normal use of language. Instead of local-
izing certain cortical areas which actuate speech, Head noted
that

the processes which underlie an act of speech run through
the nervous system like a prairie fire from bush to bush;
remove all inflammable material at any one point and the
fire stops. 'Clearly, it is as reasonable to call the site
at which there is discontinuity of the nervous mechanism
a "speech centre" as it would be to call the place where
the fire ceased a "fire centre".

He maintained that the normal production of any psychic
act has no exact correspondence with the independent activity
of any particular group of cells. These "centers" are solely
integrating foci where central neural activities undergo
integration and other changes in relation to one another.

When they are physiologically disturbed by a lesion, Head
postulated the resulting disturbance as a loss of "vigilance,"

::6

or of the "high-grade physiological efficiency underlying

all types of activity from.muscle tonus to the complex

 

4. Sr. Mary Jean Schwalback, “Motor Aphasia: A Case
Study" (Unpublished Master's Thesis, Marquette University,
Milwaukee, Wis., 1940)

5. Tudor Jones, "Brain and Speech", Nature, 115:499-
500, April 5, 1924.

6. Henry Head, 22. cit., p. 486.

59

processes of speech.

When this vigilance is lowered by any organic or func-
tional condition, the most complex forms of behavior are the
first to suffer.

Vigilance seems in some way to express the tone of the
nervous activity which functions by way of integration
and eXpresses itself in intelligence on the psychic side.
Focal brain lesions prevent the normal fulfillment of
some specific form of behavior, but nevertheless the
reaction that follows any given situation still expresses
the response of the organismras-aewhole under the new
conditions, or, one may say, the new-organismras-a-whole,
which is, perhaps, reacting at a lower organized level or
like a more primitive organism

The aphasic clinical manifestations, he contended,
could not be classified as "motor" and "sensory" (or as motor,
visual, and auditory): since speech is an integrative function
standing higher in the neural hierarchy than.motion and sen-
sation. It is "built up on a level of integration superior to
that of motion."8 To analyze in temns of motion and sensation
would be unsuitable since they imply interference with a
definite physiological function.

Head's classification was entirely new, discarding all
of the previous ones. He used none of the old terms, and
based his study on exhaustive examinations with living

material. His classification uses grammatical terminology and

is based on language concepts. The defects are divided into

 

7. Bender, 22, cit., p. 518-19.

8. Jones, 92. Cite, p. 500.

60
verbal, nominal, syntactical, and semantic aphasia, according
to the most prominent clinical symptoms In setting forth this
arbitrary classification, he acknowledges that they are not
fixed and that there is overlapping and indefiniteness.

Verbal aphasia manifests itself in disturbances in
external speech, or articulate eXpression. A difficulty is
experienced in evoking words. The vocabulary is greatly re-
stricted. Errors are recognized, however. Drawing and the
understanding of pictures remain unimpaired. The British
physician J. M. Gill attributes this type to a lesion
"situated in the lower part of the precentral gyrus."9

In gyntactical aphasia the patient tends to talk jargon.

 

He is apt to omit or slur prepositions, conjunctions, and
articles. In addition to the articulation of the words, the
rhythm of the phrase is also defective. There is also a want
of grammatical coherence. Writing, too, is impaired. How-
ever, that which is read may be understood. The lesion,
according to Gill, is "in the temporal lobe."10

Nominal gphasia is the defective use of or understand-

 

ing words as names or indicators of letters, words, or objects.
The patient may recognize objects, but he cannot name them on

written or verbal command. Names may be correctly repeated

 

9. J. M. Gill, "0n Aphasia", The Medical Journal 9;
Australia, 1:4:125, Jan. 27, 1954.

 

10. Loc. cit.

61
when heard, but they are not understood. In addition, both
writing and reading are affected. "The lesion is in the

occipital lobe."11

In Semantic gphasia the patient cannot recognize the

 

full significance of words and phrases. He cannot comprehend
"the general significance of a word as part of a complete act
Of language."12 The ability to draw or play games is also
lost. The lesion is "in the supramarginal gyrus."13

The related defect of "apraxia" consists of inability
to execute purposive movements or complex acts in the absence
of paralysis and with perfect comprehension of the meaning
and ultimate intention of the commands. "Agnosia" Head de-
fined as a perceptual defect--the failure to recognize objects,
pictures or sounds in the absence of sensory defects.

In comparison.with the classifications generally
accepted at the time of Head's publications, his classification
seems superior to them in theory. "It is based on the right
principle; that is, the differentiation of forms of language
deterioration in terms descriptive of the predominant psycho-
logical changes."14 Although excellent in theory, it is

inferior in practice in that "it fails to cover too many cases

 

11. Ibid.
12. German, pp. cit., p. 576.
15. Gill, pp, cit., p. 125.

14. Weisenburg and McBride, pp, cit., p. 51.

62

of so-called motor and amnesic aphasia."15

Later attempts to correlate these types of defects with
localized cerebral lesions led to the conclusion that "neither
the areas of localization nor the resulting loss of function
determines the 'elements out of which language is composed',
but rather the manner in which 'the use of language can be
broken up'".16

Head's greatest contributions to the study of aphasia
have been cited by Anderson as his "exposition of heirarchies,

his study of functionizing at higher levels and his discussion

of semantic aphasia."l7

 

15. Anderson, 92. C to, p. 5O.
16. German, pp. cit., p. 566.
17. Anderson, pp. cit., p. 25.

CHAPTER VI
S. E. HENSCHEN AND THE ANATOMICO-CLINICAL INTERPRETATION

Almost diametrically Opposed to the psychological
analysis of Head was the work of the Swedish professor
emeritus of medicine at Stockholm, Salomon Eberhard Henschen.
Henschen began his major research on aphasia in 1917 at the
age of 70. He insisted that the question of aphasia could be
placed on a sound basis only through a thorough study of the
clinical aspects of aphasic cases, correlated with the patho-
logical findings in the brain. As a result of his insistence
on a sound anatomico-clinical basis, he gathered together 60
of his own autopsies and personally collected autopsy material
in Germany, Austria, France, England and *taly. In addition,
he wrote to Russia and America for further cases. His efforts
resulted in the accumulation of detailed records on nearly
1500 aphasic patients.

Henschen's synthesis of all this data resulted in a
monograph of three large volumes of abstracts and analysis
published in 1920 and l922. He carried anatomic localization
in the brain so far as to assert that every psychological
activity could be localized--even logical thought.

The question of the function of the minor cerebral
hemisphere in speech was discussed by nenschen in great

detail. He agrees with Jackson in the contention that the

64
minor hemisphere takes over the function of speech in cases of
injury to the major hemiSphere. Specifically, he states that
"the localization of a motor speech center, or any other
specialized speech center, could not be upheld were it not for
the initiation of a vicarious action of the right hemisphere."1
He belieVes that the theory of vicarious activity of the cortex
in the immediate vicinity of the damaged third frontal gyrus
(or the so-called Monakow's extended region of Broca) is far
less plausible than the theory that the third right frontal
convolution acts as a substitute in case of destruction of the
third left frontal. To further support his contention, he
goes on to say that "if both the left and the right frontal
gyri are destroyed speech disappears completely and forever."2

Fifty years prior to Henschen's research Jackson
postulated that the right side of the brain functioned in
emotional speech. In 1920 Henschen asserted that the entire
structure of aphasia would disintegrate if we could not
utilize the right side of the brain in our explanation of
facts in aphasia. ‘

For comprehension of spoken language he concludes that
"the right side fails entirely in about 50 per cent of cases;

it performs to some extent but imperfectly in about 60 per

 

l. Schwalback, pp, 0 t.

-

2. Loc. cit.

65

cent."5 In the few cases which show a remarkable degree of
recovery, the right temporal lobe takes over the function very
well. He admits his inability to explain satisfactorily the
variability of recovery.

The disturbance of the faculty of speech as shown in
echolalia, paraphasia, senseless reading, etc., Henschen
attributes to the performance of the right cerebral hemisphere.
His cases showed the inferiority of the right half in being
unable to carry on the highest function of reading.

Some of Henschen's conclusions of interest in this

study follow:

1. A lesion in the left third frontal convolution
results in motor aphasia, or, in the term Henschen
prefers, "aphemia".

2. When in addition to the left third frontal convolution,
the neighboring parts of the precentral gyrus are
affected, the patient will show dysarthria as well as
aphemia.

5. The transverse gyrus is the hearing center; the first
temporal convolution the center for the hearing and
understanding of speech. With bilateral destruction
of the first temporal, there is permanent word-
deafness; with destruction only on the left in the
right handed there may be partial recovery through
the activity of the right.

4.- Lesion of the angular gyrus produces a second form of
sensory aphasia, word—blindness. The right angular
gyrus, Which.may take over some of the function of the
left, is a very imperfect substitute.

5. The left third frontal convolution in front of Broca's
area is the important region for s;nging, but the
right third frontal may suffice if the left is injured.
The left temporal pole is probably the important area

 

5. J. M. Nielsen, "Function of the Minor (Usually
Right) Cerebral Hemisphere in Language", Bulletin 9; the Los
Angeles Neurological Society, 5:67, 1958.

66

for the hearing and comprehension of music, but activity
on thz right can often compensate for destruction on the
left.

0n the basis of the extent of J. M. Henschen's collec-

tion and analysis of the available postmortem literature,
Nielsen states that "his views must have more weight than
those of any other one man."5 Harry A. Teitelbaume, on the
other hand, suggests that in analyzing Henschen's data the
student take cognizance of

the many discrepancies that prevent precise correlation

between clinical symptomatology and post-mortem findings,

and, the existence of the various disturbances in higher

cortical functions in all sorts of combinations, thus

permitting the interpretation that these disturbances are

interdependent to a great degree, rather than each being

the direct effect of focal impairment of cortical tissue.7

 

4. Weisenburg and McBride, pp, cit., p. 50-1.
5. J. M. Nielsen, pp. cit., p. 68.

6. (Harry Allen Teitelbaum:--Baltimore neurologist
and psychiatrist, 1907- )

7. Harry A. Teitelbaum, "The Principle of Primary
and Associated Disturbances of the Higher Cortical Functions
as Applied to Temporal Lobe Lesions," The Journal pg Nervous
ppp Mental Disease, 96:265, July-Dec.,-l942.

CHAPTER VII

S. A. KINNIER WILSON'S ECLECTIC ANALYSIS

AND OTHER RECENT WRITINGS

In 1926 a monograph on aphasia appeared under the
authorship of S. A. Kinnier Wilson1 of England. He advocated
striving for an anatomico-physiologic nomenclature. He found
himself unable to accept a psychologic terminology. Yet he
also warned against divorcing the psychological component from
its anatomico-physiological counterpart. He insisted on a
separation of anatomic, physiologic and psychologic classifi-
cations of terms. His contention was that all three types of
approach are necessary, but that the terms should not be used
interchangeably. To clarify,

it is the confusion of the spheres of thought and avenues
of approach in the past which has led to the drawing of a
psychologic concept center, an anatomic foot of the third
frontal convolution, and a physiologic writing center all
on the same diagram of a cerebral cortex, and the drawing
of lines from one to the other as though association

fibers‘connected them and impulses passed along these
lines.

Wilson believes Speech to be an intellectual process
behind the expression of which lies thought. Hence, he con-L”:

siders it unwise to attempt to distinguish Speech disorders

 

1. (Samuel Alex. Kinnier Wilson:--English neurologist,
1877-1957)

2. J. M. Nielsen, A osia, A raxia, Aphasia. (New
Ybrk: Paul B. Hoeber, Inc., 947), p. 15.

68
from intellectual disorders. He warns against the psycho-
logist's tendency to ignore "the patiently acquired facts of
cerebral localization of function."5 Attention is called to
the evidence from the work of the Swiss School (von Honakow,
Berze, Frankhauser, etc.) that "certain layers of the cortex,
considered in their whole extent, constitute the anatomico-
physiological basis for certain forms of paychical activity."4

Physiologically, many aphasics experience an inability
to use certain motor cells of the cortex--those innervating
mouth, lips, tongue and palate--for speech, while still
capable of other functions such as chewing, swallowing, etc.
It would appear foolhardy to localize the physiological defect
in the cell groups concerned. Theoretically, therefore,

apart from clinical and pathological considerations,
disorders of speech must be disorders, physiologically,
of higher mechanisms which play on those of a lower
physiological level.

Wilson's chief contribution to the subject is his
insistence that an aphasic symptomrcomplex be looked at in
three ways:

What is the anatomical site of the lesion producing the
defect? What are the physiological mechanisms involved?

What is the nature of the psychological disorder? No
study of the subject can make any pretense at completeness

 

5. S. A. Kinnier Wilson, "An Introduction to the Study
of Aphasia”, The Lancet, 201:2 for 1921:1145, Dec. 5, 1921.

4. Loc. cit.

5. Ibid., p. 1144.

69
if any of these three aspects is ignored, nor, on the
other hand, can it be harmonized with clinical data, if
anyone is elaborated at the expense of the others.

In recent years another outstanding study of aphasia
has been completed by Theodore Weisenburg and Katharine
McBride. Their study, presented in the publication "Aphasia:
A Clinical and Psychological Study", was more concerned with
mental functioning from the psychologist's viewpoint than
with therapeutic measures to be used for specific speech
problems.

The authors contributed another system of classifica-
tion--a four part grouping of aphasic manifestations including
the following types: predominantly expressive, predominantly
receptive, expressive-receptive, and amnesic.

While the study contributed little to the theoretical
consideration of localization or retraining, it does have
merit--according to Jeanette Anderson--in being a "careful
study and presentation of the functioning of neural tissue
and the nature of the loss and return of function without,
in most cases, specific re-training."7

Another recent publication is Louis Granich's "Aphasia:
A Guide to Retraining". As its title implies it is essentially

an aid to therapy, rather than an inquiry into the nature of

aphasic disturbances.

 

6. Ibid., p. 1143.

7. Anderson, pp. cit., p. 55.

PART III

CONTEIHEPORARY VIENPOII-ITS

71

NOTE

Chapters VIII, IX and X are condensations of the
respective authorities' writings which seemed most applicable
to this study. They are digests, in the authors' own words,
of their published thoughts pertinent to concepts of aphasia.
The articles drawn upon are listed in the Bibliography under
the author's name. With the exception of one article, the
contents of which were first published in 1950, all the
source material for these three chapters dates from 1958 on.

The chapter contents were sent to the individual
authors for editing and approval. The revised chapters,

. herewith presented, are the endorsed statements of Nielsen,
Goldstein and Anderson. They have, therefore, the added
merit of being current and of being endorsed by the authori-

ties to whom they are attributed.

** The author regrets to note that as of the date of the
binding of this thesis, Miss Jeanette Anderson's edited

copy of her viewpoints had not been received.

CHAPTER VIII
THE NHUROLOGIST DISCUSSBS APHASIA
by J. M. Nielsen as

All efforts to base the study of aphasia purely on
anatomic structures have failed because of insufficient know-
ledge. Physiology without anatomy to support it will always
fail to provide localizing data as will a purely psychologic
study. We must grant that in the present state of our know-
ledge of aphasia all three methods of approach must be simul-
taneously considered: psychological, physiological and
anatomical. It is impossible for any single approach to be
successful.

Until 1947, except for the few results of electrical
stimulation of speech centers by Foerster the science of
aphasia rested on clinico-pathologic materiaL Penfield has
now outlined some of the speech areas by electrical stimula-
tion. The defects in clinico-pathologic material are partly
due to incomplete studies of the clinical manifestations,
partly to the poor general condition of patients with cerebral
vascular lesions, and partly to incomplete study of autopsy

specimens. But, the greatest difficulty encountered by

 

as See Note on p. 71.

73
students of the subject is the fact that nature does not often
produce discrete lesions so placed as to make the case a good
experiment.

For the sake of a coherent discourse, let us begin with
the premise that language is symbolization which is used to (“
exchange thoughts with one's peers.

The human brain has develOped in its cortex (probably
wi£h_its cortex) a highly complex system.of language symboli-p
zation, the anatomical structures of which are neurons with
cell bodies situated in the cerebral cortex, the complex
function of which when comprehended by the student is called
physiology, and when conceived functionally but not anatomic- '
ally is called psychology. Various portions of the cerebral
cortex are variously constructed and have different functions.
The different areas have been elaborately studied and mapped
by Brodmann, Campbell, Elliot Smith, the Vogts, Economo and
Koskinas, and by Bailey, and physiologically by Foerster and
Bailey and his co-workers. Certain of these areas of the
cortex.may be rendered functionless by natural experiment, and
the resultant disturbance of function may be recognized as the
direct result of such localized destruction. By correlation
of certain functional defects with certain specific anatomic
defects, signs of agnosia, apraxia, and aphasia may be valuable
in cerebral localization. Thus it comes about that a patient

who has been able to read and is rendered incapable of reading

74
while still relatively unimpaired in other functions of symbol-
ization is known to have a lesion in the major (usually left)
angular gyrus.

One must be careful to say "relatively" unimpaired,
because there is always some degree of impairment of general
cerebral symbolic and other functions when the defects make
possible a diagnosis of agnosia or aphasia. This is obvious,
as the deleted portion of the brain is part of the area used
in general symbolic mentation, and the structure as a whole
does not function so well after the deletion of a part as it
did before that deletion.

Language is a highly complex cerebral function requir-
ing for its use one side of the brain behind area 6 of
Brodmann. The fact that the portion of the brain anterior to
area 6 is not essential to language is shown by cases of
bilateral prefrontal lobectomy.

Areas of cortex having apparently certain specific
functions have been called centers. There is frequent
reference to centers in the literature in the anatomic sense,
the physiolOgic sense, and in the psychologic sense. What we
are concerned with here is the definition of a center in the
Clinico-pathologic (anatomico-physiologic) sense. From this
viewpoint, a center is a cortical area the functional removal F
of which causes a definite deficiency syndrome which can be

recognized clinically. Such a center is not a functionally

75
independent area devoted to one certain function exclusively
as it is often conceived of. It is an area essential to nor-
mal performance of a certain function. It may be an area

where a certain group of impulses pass or where synapses occur

in the ordinary process of certain functions. This leaves the” ,

inevitable conclusion that although an aphasic disturbance
may seem to be either more sensory or more motor in character,
it can be neither of these fundamentally. Rather, it is
associational.

In ordinary speech one hears what one has already
said, "checks up" on it, analyzes it, and corrects it; and
this often causes one to change one‘s diction or even one's
phrases in the course of a sentence. The portion of the
brain which thus holds the thought and checks up on the speech
to determine whether the speech.mechanism prOperly expresses
the concept is the attention or the concept center. It would
seem that the reasons for the impossibility of placing the
concept center in the diagram.are that the center is con-
stituted of much of the cortex and that we know practically
nothing of the multitudinous paths traversed in the elabora-
tion of a thought.

Speech is a mental process. Differences of opinion
center about the degree of divisibility of the psyche for
various elements of speech. Certain writers have taken the

stand that there is a disturbance of the entire psyche in

76
every case of aphasia. They have correctly pointed out, for
example, that in every case of motor aphasia the patient does
not comprehend.spoken language as well as the normal person
does and that in every case of acoustic verbal agnosia the
patient fails to speak spontaneously as well as the normal
individual. These statements are true. How, indeed, can
the brain function as well after the functional deletion of a
portion as it could before? On the other hand, there are
innumerable cases on record to show that except for the
specific loss in the various types of aphasia, as the great
diminution of spontaneous speech in motor aphasia, forgetting
of names in amnesic aphasia, loss of comprehension of spoken
words in acoustic verbal agnosia, or loss of recognition of
written words in visual verbal agnosia, the remainder of the
psyche is often comparatively little affected. The general
loss which is seen in every case seems to correspond to the
form well named by Head-~semantic aphasia. We grant, then,'i
that there is an element of semantic aphasia.in nearly every L
case.

What physiologic and anatomic data do we have with
which to work? The first transverse gyri of Heschl, one on
each side, are the sites for perception of sounds. An area
immediately adjacent to these (para-transversal area), in the
superior temporal convolution (Wernicke's area) is the site

essential for recognizing memory pictures of the sounds of

77
words.

To consider the comprehension of sounds of words,
associations must be taken into account-~not merely the sound
itself. The associations are composed of other auditory
memories, of visual memories, kinesthetic memories, and usually
many other types. This means, then, that before the signi-
ficance of the word can be determined, the greater portion of
the cortex must be consulted, i.e., impulses must travel over
it. In other words, there cannot be such a center as a word-
meaning center.

In Broca's convolution are engrams laid down by efforts
to make the movements necessary for production of vocal sounds.
When these engrams or the neurons which constitute them.are
destroyed, the patient still knows what he wishes to say,
i.e., he still has clear thoughts; he can still hear the
sounds silently in his head, but he has forgotten how to make
the movements necessary to produce the sounds. But as the
area of.Broca with its association neurons to and from the
center of Wernicke are part of the mechanism of speech, there
is imperfect comprehension. He can still move all the muscles
for chewing, clearing his throat, expectorating, etc.; it is
only movements to make sounds constituting symbols of speech
that he has forgotten. This is apraxia, a very specific
apraxia. Motor aphasia is then a type of apraxia. But since

it pertains to language and symbols, it is by definition a

78
type of aphasia.
A review will convince any unbiased observer that
Broca's convolution contains patterns of motor speech, i.e.,

engrams (neurograms), which constitute the anatomic basis of.

memory of how to articulate words. Penfield has now shown

.iq._.._‘_~‘

that electrical stimulation of that small gyrus, while the_1:f

 

patient i5 speaking, prevents him.from uttering words.

Just how Broca's area of the major side receives its
impulse to speak is not entirely clear. It certainly cannot
alone initiate impulses. Even when Broca's area on the left
side is destroyed the patient can still say something. Jackson
noted that emotional language was not curbed in aphasia. His
idea (1878) that expletives and similar emotional expressions
are produced by the right side of the brain has gained great
support from the ideas of Moxon and the corroboration by
Liepmann (1906) that the left side of the brain takes the lead
and hence that the right may not be entirely passive in
speech. Since subsequent evidence has borne out Jackson's
contention, he can be credited with reaching an anatomic fact
through a psychologic approach. Zollinger's patient with the
entire left cerebral hemisphere (pallium) removed had ability
to say a few words. The impulses must have originated on the
minor side. I have had numerous cases proving that the right
Broca's convolution performs after the left is destroyed.

Nomenclature is the chief hindrance to one's trying to

79
bring order to the vast accretion of chaos found in the
literature of agnosia, apraxia, and aphasia. Wilson (1926)
points out the desirability of having an anatomic basis but
at the same time the impossibility of this at the time of
writing. A physiologic basis is also impractical. A psycho-
logic basis is easy to obtain, especially as Head (1925) has
already presented one, but a nomenclature based on psychology
dissolves all connection between cerebral anatomy and patho-
logy and the subjects to be classified. I believe the
acceptance of such a nosology would be too destructive to
justify itself. I have adopted a terminology which is so
far as possible based upon usage, which avoids the coinage
of new elemental terms but attempts a systematization on the];
basis of physiologic (functional) hierarchies, or levels offg_‘
integration. H

To clarify this last eXpression somewhat, attention is
directed to the obvious facts that, physiologically Speaking,
the first cerebral activity in the reception of an impulse is<3>
the function oqprimary perception. For vision the anatomic
site of perception is on the borders of the calcarine fissure,
for audition, in the first transverse gyri of Heschl. So far
as language is concerned, the first element of cerebral func-
tion takes place mainly at these two sites. This, then, is
the first functional hierarchy.

If we continue to follow the paths physiologically, the

80
next step is, for visual impressions of langua:e, the formation
of engrams of symbols seen in the region of the left angular
gyrus (cortex), for hearing, the formation of engrams of sounds
heard in the region of the posterior superior left temporal
convolution. This is the second functional hierarchy. So
far, we have localization of cerebral function. Still speak-
ing physiologically, above this, though there are higher
hierarchies of function, there is very little, if any,
localization known as yet. There are at least three hier-
archies in the sensory sphere: perception, formation of
engrams for recognition, and higher elaboration. This
higher elaboration is not all on the same level, at least two
levels being definitely discernible, significance and recall.

While this division of aphasias into those on a lower
level and those on a higher level has not to my knowledge been ‘
done before it seems to me particularly appropriate. Reflec-
tion will show that, while agnosias are disturbances of recog-
nition, all of the aphasias--above the level of agnosia--so
far described are disturbances of recall, or to use a better
term, of reminiscence. The fundamental difference between
recognition and reminiscence is that whenever one recognizes
an object or a symbol one has the object or symbol before one;
one receives a visual, auditory, tactile, gustatory, or ol-
factory impression of it and this impression is compared with

engrams previously formed by similar impressions. If the two

81
are essentially identical the object or symbol is recognized.
The crux of the matter is that one starts with the object or
the symbol and looks for its meaning. But in reminiscence’
one starts with the idea or concept and searches one's cortical
engrams of memory for the corresponding object engram or the
symbol engram. The two processes are reversed.

The same process (of starting with the concept) applies
to motor speech; one starts with an idea and looks for the
motor pattern with which to express the concept?” The motor
pattern is found through the medium.of the language formula-
tion area in which the synthesis of concept into speech
symbols is carried out and from which the motor patterns are
stimulated.

There is a still higher hierarchy of language, however,
higher than that of reminiscence. This is the hierarchy of
semantics and calculation. Head's most valuable contribution
to the subject of aphasia was the introduction of the term
semantic aphasia: By it he meant one's inability to determine
the full significance of speech though able to comprehend
spoken or written language to some extent.“ In the study of
cerebral localization in aphasia it is useful to draw a rather
sharp line between recognition and comprehension because
there‘are all degrees of comprehension. A physician compre-
hends much more of a medical article than does an attorney,

but the reverse is true of a legal document. It is question-

82
able whether anyone ever gathers the full significance of what
an author writes and we must thus all have semantic aphasia
if we use the old terminology. If, however, we draw the line
between recognition of a word and its significance we have a
valuable distinction. Loss of the first is agnosia; of the
second, aphasia. Significance is still not reminiscence; it
is a higher function because one can recall a word of which
the significance is unknown.

It is customary to speak of the two cerebral hemispheres
as being dominant and recessive, respectively. The terms are
based on the conception that the one ordinarily takes the lead
and leaves little or nothing for the other to do in the
associative sphere of activity. The basal ganglia, the motor
and sensory projection fiber systems, and the primary percep-
tion areas for the special senses are commonly exempt from
inclusion in the concept of unilateral cerebral dominance.

While there is a hereditary determinant to make a
certain hemisphere the major one, there is no essential
difference between the functional capacity of major and minor
hemispheres at birth. This has been shown repeatedly by in-
stances of severe trauma to the major hemisphere early in life.
In such cases the minor hemisphere invariably takes over the
function of the major with such precision and dexterity that
observers do not notice any disturbance of language. landed-

ness does not develop until the age of about 9 months to a

pa"

83
year. Even when it begins to manifest itself the superiority
of the major does not appear great. This is proved by the fact
that injury to the major hemisphere at the age of 4 or 5 years
causes only transient aphasia. Whenever a minor hemisphere
is called upon to take over a function it at first fatigues
with astonishing rapidity. As it becomes trained it develOps
endurance rather than specific capacity.

The question of unilateral dominance in the sphere of
language is intimately related to handedness but the question
of handedness is extremely complex. Handedness and brained-
ness are not necessarily contra-lateral. Instances have been
reported in which persons who considered themselves right-
handed have become aphasic as a result of right cerebral lesion.
These occurrences have been ascribed to conversion of the
patients from left- to right-handedness so early in life that
they themselves were unaware of it. This explanation does not
hold in the cases equally well established in which strongly
left-handed persons have developed aphasia from a lesion of
the left hemisphere. When one in addition considers that,
regardless of handedness, children who suffer a severe (ii
cerebral lesion early in life never develop aphasia at all, \ '
or recover in a remarkably short time, it becomes clear that
both sides are almost equally capable of assuming any function
of language if compelled to do so. There is apparently no

way to determine absolutely whether a given person is left-

84

or right-brained for a given function except to study the
case after a unilateral cerebral lesion and determine the
laterality of it by some sign not pertaining to language.

While there is undoubtedly an hereditary tendency to
unilateral dominance in general and some of the cases of
right cerebral dominance in language in right handed persons
can certainly be explained on the basis of stockhandedness
as outlined by Foster Kennedy, there are certain important
elements relative to ontogenetic development of dominance
which must be considered. A child learns during the first
year to recognize objects and geometric relations in its en-
vironment long before visual-language associations are
established. In these matters the child may develop dominance
of one occipital lobe but there seems to be no reason for
develOping this on the left any more than on the right side.
If by chance the right occipital lobe becomes dominant for
non-language functions before the right or left temporal lobes
does so in comprehension of auditory language, the occipital
patterns may not shift laterality of dominance; it may be
easier to have the right occipital lobe dominant over the
left and send all necessary impulses across the corpus cal-
losum to the left temporal lobe (indirectly) than to suppress
the right occipital patterns and develOp similar ones on the
left side. This is the explanation here offered for the

occurrence of crossed occipital-temporal dominance. If by

85
chance the laterality of dominance is the same for the
occipital and temporal lobes there is no problem or question
or retrainir; an occipital lobe.

It is suggested that crossed temporo-occipital dominance
(major temporal lobe on the left and major occipital lobe on
the right) may be due to establishment of occipital dominance
on the right before temporal dominance (dependent on language)
becomes established, i.e., during the first year of life. In
some cases the occipital dominance is formed on the left at
first; in others it shifts to the left with establishment of
language dominance; in some nature finds it more economical to
leave the right occipital lobe dominant and shunt impulses
across the corpus callosum.rather than to establish engrams
in the left occipital lobe to replace those already well-
established in the right.

Right hemispheres travel through life with the left
until an accident occurs to the leader. Some learn to under-
stand; fewer learn to speak, still fewer learn to read, and
only an occasional one learns to write.

In the evaluation of a given case of aphasia all this
must be taken into account. The ability of a patient to speak
does not prove the integrity of the left frontal lobe, nor to
comprehend, the preservation of the left temporal lobe. But

the loss of a specific function proves destruction of the

areas concerned. What a patient can do with language after a

86
lesion of the major side depends on the inherent ability of
the right hemiSphere. Hughlings Jackson was entirely correct
in his views; proof has come after sixty years.

An analysis of cases places the clinical manifestations
following lobectomy (i.e., the performance of the minor (right)
temporal lobe) beyond the realm of chance and proves that a
person without any left temporal lobe is in general far
superior to one with a slightly damaged lobe still in situ.

Necessary surgical Operations in the last few decades,
more particularly in the last decade, have also given us cases
which prove crucial points. One of the best is the removal
of the entire pallium of the major side. This operation
showed that the minor side can, to some degree, perform the
function of language.

Inasmuch as both cerebral hemispheres have a function
in language but that one is far more capable than the other
the two may be designated as major and minorJ/ If cases of
destruction of the entire major language area are gathered for
study we can readily tell what capacity the minor hemisphere
possesses. Destruction of the area supplied by the sylvian
artery is equivalent to hemispherectomy so far as language is
concerned because the occipital and frontal extremities have
no function in language.

"How complete must the defect be to constitute agnosia

or aphasia?" If, following a lesion of the convolution of

87
Broca, a person is able to speak but with stammering and
hesitancy, some students might say that he does not have
Broca's aphasia. But we know that from the standpoint of
cerebral localization he does have a lesion and that the
reason for his being able to talk at all is either that the
crippled area is performing or the imperfectly trained minor
convolution of Broca is doing the work which we observe. We
should therefore say that the patient does have aphasia
(apraxia of speech). If the patient, after such a lesion,
speaks as well as he did before he either had two equally
capable convolutions of Broca or it was the minor one which
was destroyed, the minor one merely having been located on
the side where we expected the major one to be. Our misinter-
pretation is due to the erroneous assumption that handedness
is an infallible guide to brainedness.

A word of caution is offered regarding the diagnosis \\
of aphasia after acute cerebral injury. One cannot study
aphasia resulting from cerebral trauma until general cerebra-
tion has been recovered and only specific defects remain. It
is necessary, therefore, to await recovery from the acute
effects of trauma before attempting the study of aphasia.

In testing the elements of speech, the functions which
should be tested separately and specifically are:

l.‘ Motor speech (spontaneous speech and repetition).

2. Comprehension of spoken language (questions such:

\.

7”,. yfiw Ln.

88
as "Hold up two fingers; Put your finger on top of your head;
Put your hand on your right ear; Touch your index fingers
together."

5. Ability of the patient to find the words he wishes
and to make orderly sentence.‘

4. Reading. Note is made of ability to recognize and

 

ability to comprehend significance 2: written and printed

 

matter.-

5. Writing. Spontaneous writing of something other
than the patient's own name, the ability to copy from print
to handwriting should be tested.

If these five tests are carefully interpreted the site of the
lesion is usually determined.

1. If the patient is unable to speak spontaneously
except for a few simple words or phrases and if that defect
is his only aphasic manifestation, it may safely be concluded
that the trauma has involved the convolution of Broca or the
external capsule between the insula and the putamen (major
side). A subcortical hemorrhage is just as potent as a
cortical contusion in causing motor aphasia.V The reason that
a lesion of the external capsule can cause motor aphasia is
that the convolution of Broca functions merely in coordination
of the muscles of speech for enunciation of words. It does
not contain the engrams of ideas to express or engrams of

the organization of words into grammar. Such functions are

89
performed in the (posteriorly located) language formulation
area, chiefly area 57 of Brodmann, and Broca's convolution
cannot perform its function unless supplied with organized
language for it to emit. The pathway from the area 57 to
Broca's convolution is via the external capsule.

2. Comprehension of Spoken language is mediated throug
Wernickefs area (the para-transversal portion of the superior
temporal convolution of the major side): The function of

recoggition is performed by a relatively small cortical area

 

but comprehension necessitates coordinated function of a

 

larger portion of the temporal lobe in the direction of area
57. Hence rapid fatigue of comprehension of spoken language
indicates that the trauma has affected the major temporal lobe.”’

3. “Word-finding", i.e., the ability of a person to
find in his mental index any apprOpriate word corresponding
to an object or to an abstract idea, requires coordinated
function of the language formulation area and Wernicke's area.
Hence a lesion of the posterior portion of the temporal lobe
will lead to "amnesic aphasia". That symptom.means, there-
fore, a lesion of the temporal lobe. The patient says, ”I
know it but I can't say it."

4. Reading may be disturbed in several ways. If the
patient is unable to recognize written or printed words which
formerly were familiar to him the angular gyrus is destroyed
or its connections with the occipital or the temporal lobe

are severed. If he is merely unable to determine the signi-

90
ficance of what he can read the lesion may be anywhere in the
general parieto-temporal region. If he is able to write but
is unable to read what he has written there is a subcortical
lesion of the major angular gyrus. This fact is based on the
necessity of the angular gyrus cortex for the function of
writing and the capacity for a sub-cortical angular gyrus
lesion to prevent occipital (visual) impulses from reaching
the cortex of the angular gyrus.

5. Writing is so complex a function that a localizing
value must not be ascribed to agraphia unless the agraphia is
isolated. When agraphia is the only defect of language
presentpn a given case there are still two possible sites
which the lesion may occupy. One is at the writing center
in the frontal lobe, the other is at the border between the
angular gyrus and the occipital lobe of the major side.

The examiner must never lose sight of his general know-
ledge of cerebral physiology. For example, a lesion of the
temporal isthmus (area between the posterior extremity of the!
insula and the posterior horn of the lateral ventricle)
completely disrupts all language function by separating the
entire temporal love from the other language centers. The
patient in such a case cannot speak, cannot comprehend spoken
language, cannot read or write. This is the "global aphasia"
of the older writers.

If an anatomical area subserving a functional unit of

81
language is destroyed it never recovers. Recovery of the
function depends on training of the homologous area of the
other hemisphere. When a language center is irrecoverably
destroyed the prognosis depends entirely on the ability of
the patient to train the corresponding area on the minor side.
Prognostic factors of importance are then: the age of the
patient (young persons may train the opposite side in a week),
the general health, the intellectual capacity and the
incentive.

It is an aphorism that one can operate practically with
impunity in the language areas of a child below six years,
with little damage to the function of speech between the ages
of 6 and 15, with recovery in a few months between 15 and 20
but with a progressively higher incidence of prolonged troubl e
later in life. Of course, there are surprising exceptions,
cases late in life in which recovery is rapid due either to
ambidexterity or to unusual natural resourcefulness and

dynamism.

CHAPTER IX
THE PSYCHOLOGIST'S CONCEPT OF ArHASIA
by Kurt Goldstein **

My concept of the function of the organism was based
on analysis of a great number of physiologic and psychologic
phenomena--normal and pathologic--in man. I came to the
conclusion that the basic motive of organismic life is the
trend of the organism to actualize itself, its "nature," its
capacities, as well as possible. I have tried to formulate
the rules which govern behavior of the normal organism and
guarantee self-actualization.

Applying my point of view to the study of the nature
of language and its disturbances, I came to the following
conclusion: Language is a means of the individual to come (_
to terms with the outer world and to realize himself. Hence, '
the aphasic patient tries to achieve a condition which allows
him to react as well as possible to the tasks arising from
the environment. If he is successful in this endeavor, at
least to such a degree that he can fulfill those performances
which are "essential" to his nature, he will be in a new
order, will avoid catastrOphic occurrences, and be able to
use his remaining capacities. From this point of view, it

follows that every individual speech-performance is under-

%* See Page 71.

95
standable only from the aspect of its relation to the function
of the total organism in its endeavor to realize itself as
much as possible in the given situation.

How does a definite lesion modify the function of the
brain so that a definite symptom comes to the fore? We are
by no means justified in inferring directly from a correlation
between a localized defect and a defect in performance a
relationship between the concerned area and a definite per-
formance corresponding to the defect. The facts allow only
localization of defects, but not a localization of performan-
ces.

We are confronted with two realms of facts which we
try to bring into relation: anatomic findings and observa-
tion of disturbed performances. If we survey the findings of
microscopic studies of the cerebral cortex we are confronted
with differences of structure which surely hold a Special
significance for different functions. We can assume with a
fair degree of certainty that there are areas which are de-
signed to receive stimuli from the outer world, and others to
mediate motor performances. It remains unsettled how these
cortical areas, which I called the periphery of the cortex,
do function. Analysis of the defects in lesions of this part
does not at all allow us to bring a circumscribed defect into
relation to a circumscribed lesion, still less to localize a

definite performance in a definite group of cells, etc.

94

The so-called classic theory of localization is based
mainly on the material gained from postmortems. It should be
observed that the objections against the theory stem first
from a more careful consideration of the pathologic-anatomic
data. There are the so-called negative cases: on the one
hand, absence of symptoms in a lesion affecting an area which
was considered characteristic of this locality; on the other
hand, appearance of symptoms without the presence of a corres-
pondingly localized lesion. A critical consideration of
these numerous cases shows that they are inexplicable if one
considers the symptoms as simply depending upon locality and
extension of the lesion.

A lesion of a special locality in different cases may
differ very much regarding the degree to which the substratum
in general is affected, and particularly its different strata.
Such a selective character of the process may be of paramount
significance for the develOpment of symptoms. It is very
difficult, indeed, to evaluate the degree of damage; it is
not only dependent on the direct destruction of the nerve
cells but also on the condition of the glia, blood vessels,
etc. Further, we have no idea of the relationship between a
definite anatomic condition and a Specific performance. We
are far from being able to decide whether the preserved tissue
is still functioning sufficiently to allow for a certain H
performance or not. We have no definite criteria for this '/

.fiféé*”“'
’ K v [C‘,'L,/
d l-Jpvl/ v

95
decision. We are facing here a methodologic difficulty which
seems scarcely surmountable.

Whether certain symptoms will appear or not on account
of a local injury certainly depends on many factors other
than locality: i.e., on the nature of the disease process,
on the damage of all or only some structures of the cortex,
on the condition of the rest of the brain, on individual
differences in cooperation of both hemispheres, on the state
of circulation in general, on the functional reactions of the
organism to the defect, on the psycho-physical constitution
of the personality, etc. .

The symptoms which are related to a localized lesion
cannot be understood from the destruction of so-called
residuals of previous performances; they cannot be under-
stood simply as due to memory defects. Each performance is
due to the function of the total organism in which the brain
plays a particular role. In each performance, the whole
cortex is in activity, but the excitation in the cortex is
not the same throughout. There is a definite configuration
in which one part of the cortex is in that particular excita-
tion which corresponds to the "figure," while the rest is in

that excitation which corresponds to the "background". Dis-

tribution in this configuration varies depending on whether

motor activity or perception or a mental attitude is requested.

A particular locality in the brain matter is characterized

96
by the influence which the structure of this locality
exercises on the total process, by the contribution of the
excitation of this locality to this process--as effect of
its particular structure. Thus, for instance, the area
striata contributes to this process something which is ne-
cessary for the experience of vision, the frontal lobes,
something which is the presupposition for the mental pheno-
menon we call abstract attitude, etc., but, to reiterate,
we may not localize corresponding functions in these parts of
the brain.

To each performance corresponds an excitation of
definite structure in the cortex, indeed, not in a circum-
scribed area but widespread over the whole cortex, differently
in each performance. This is what we should term localiza-
tion. To restate, localization may be defined as a definite
distribution of excitation within a structurally differentia-
ted nervous system, with a particular structuration of the
excitation in a definite area.

Even if the entire cortex participates, certain well
known Speech areas stand forth as special performers on the
ever-present background. The play of figure (or the activity
of a special center) and background (or the general cortex)
is variable and always changing, hence it is that a patient
will show a certain constellation of aphasic symptoms under

one set of circumstances, whereas a few hours later some

97
differences in the reaponses will be noted.

The various symptoms of aphasia are the manifestations
of a single functional disorder, loss of the ability to grasp
the essential nature of a process. This is equivalent to the
Gestaltstorung or the inability to differentiate the "figure"
and the "ground".

I think it is correct to assume that to each mental
performance there corresponds a particularly constructed sub-
stratum in thdFrain, that functions in a definite way. The
nervous mechanisms are, so to speak, predisposed. They
develOp during the growth of the individual and gain a par-
ticular organization by experience. They extend from the
peripheral sense organs to the substrata of the most come
plicated mental performances. If such a substratum is damaged
in its functioning, the organization as a whole may be main-
tained, the mechanism losing only some of these functions
acquired by training. In such cases it may be possible and
apprOpriate to retrain the functional mechanism by the same
means by which it was built up in childhood. Hence it may be
possible to acquire again the lost performances. This
happens also in spontaneous recovery, where the apparatus is
retrained by the demands of the environment.

If after thorough analysis of the symptoms, one is
convinced that the brain matter is damaged to such a degree

that some former functions are irreversibly lost, it will be

necessary to proceed in another way. We shall have to help

98
the patient to build up compensatory procedures in the same
performance field.

In order to better understand the various symptoms, I
have devised a classification of four general types of symp-
toms. The first general type of symptom represents direct
sequelae of impairment of the substratum and consists of
defects of performance. (These are the negative symptoms of
Hughlings Jackson). All direct damage causes a rise of the
threshold and retardation of excitation. The receptivity of
the patient is reduced. It takes him much longer to react.
Excitation of a damaged field requires an abnormal amount of
energy. If excitation takes place despite the obstacles, it
spreads abnormally and lasts an abnormally long time. The
effects of the lesion are generalized because the increased
energy output for the reeducated performance of the destroyed
function diverts the added energy from channels normally sub-
serving other modes of behavior. A word graSped by an aphasic
with great difficulty sticks and influences subsequent per-
formances, perseverates. A further characteristic effect of
the damage is that performances of the organism are determined
to a much greater extent than normally by external factors.

As a result of loss of structure, patients are deprived of
former experiences; thus external stimuli acquire an abnormal
importance.

A second category of symptoms is of those due to

99
separation of an undamaged area from a damaged one. (Here
we are dealing with the positive symptoms of Jackson). It is
reasonable to assume that in the normal nervous system all
parts function in interrelation with the whole, or at least
with.more extensive fields. Performances in a given field
are therefore also determined by the functioning in other
fields. Loss of certain performances, through.damage of their
substrata, brings about the modification of other depending
performances.

A third group of symptoms is due to the effect which
the pathological process in the damaged area exerts on other
parts of the nervous system, for instance by irritation of
the immediate neighborhood.

The fourth group of symptoms are expressions of the
tendency of the organism to avoid catastrophic conditions.

In situations of success, the total behavior is typified by

an ordered condition. The person is steady, interested,
c00perative, more at ease. In situations of failure, however,
the person looks definitely dazed, changes color, becomes
agitated, starts to fumble, his pulse becomes irregular, he

is sullen, evasive, exhibits temper, or even becomes aggresive.
This catastrophic condition prevents the patient not only

from doing the required task which exceeds his impaired
capacity, but also from doing performances which he is able

to carry out in the ordered state. The sick organism has a

-

100
strong urge to meet all demands as well as possible; its
existence is bound up with such an endeavor even to a greater
degree than in the case of the healthy organism. In order to
avoid catastrophes the patient resorts to: self-exclusion
from the world, i.e., loss of consciousness; he seeks
tranquility, avoids company; he tries to avoid anything
unexpected; he seeks to surround himself with a protective
fence that will prevent impinging stimuli from entering. He
may build such a fence by everlastingly doing something.
Concentration upon a particular activity makes him relatively
impervious to the undesired and dreaded stimulation from
outside. When he is confronted with a task he cannot cape
with he will stick to the performances he is able to fulfill.
Thus he appears abnormally fixated and rigid. A particularly ‘
interesting and important phenomenon resulting from this
tendency to avoid catastrophies is excessive orderliness.
Everything in the patient's environment must have a definite
place. Behind this formal geometry there is quite a
utilitarian motive, namely bringing each object within the
patient's reach.with a minimum of effort in his part. He
gets excited if somebody changes the arrangement.

Through this description of aphasic symptoms one can
see more clearly how a definite abnormality is an expression
of the struggle of the particular individual with his defect
and his attempt to perform as well as possible the tasks

arising from the environment.

101

There is one group of patients where the difficulty in
finding words is mainly an expression of a personality change,
an expression of impairment of "abstract attitude". To
clarify this, it is necessary to understand my theory of the
types of language--concrete and abstract--and their corres-
ponding aphasic symptom complexes.

Concrete language, which belongs to concrete behavior,
consists of speech automatisms, of the "instrumentalities of
Speech": of sounds, words, series of words, sentences, one
form of naming and of understanding of language in familiar
situations for which it has been conditioned, and finally of
emotional utterances.

Abstract language belongs to abstract attitude:
volutional, prOpositional, rational language. It is disturbed
somewhat isolatedly if abstract attitude is impaired; further,
in slight damage of instrumentalities which.may leave intact
other speech functions but disturbs the highly complex per-
formance of voluntary actions.

It would seem more correct to speak of disturbance of
language belonging to the abstract attitude and of language
belonging to concrete behavior, than of rational and emotional
language, and to consider emotional language a particular form
of concrete language. ”

Not allpatiants with brain injury have impairment of
abstraction. Whether it is present or not depends on the

localization and severity of the injury. It is particularly

102
prominent in frontal lobe lesions, even when the lesion is
relatively small and circumscribed, but it can occur also in
other localizations.

Nomenclature in the field of aphasia is somewhat con-
fused as a result of the use of different points of view from
which the symptoms are considered. Disturbances of speech
are biologic phenomena. As such they can be considered from
two different aSpects: as modifications of performances of
the patient, or as modification of the anatomic structures,
and their modified functioning (the anatomico-physiologic
aSpect). The anatomico-physiologic approach usually appeared
in the form of localization of separate performances and
their disturbances in circumscribed areas of the brain cortex.
As I have eXplained, the results of this approach are very
ambiguous in general.

A nomenclature based on an analysis of the characteris-
tic picture of performance disturbances promises more success;
this means analysis by psychologic means. Opposition to this
approach was raised long ago. Men like Wilson and Nielsen
are not much in favor of it. But this Opposition overlooks
the fact that all clinical distinctions of aphasic symptom
complexes are finally based on psychologic analysis.

In this state of affairs, our nomenclature cannot be
very homogeneous. Sometimes we may base it on anatomic

findings, sometimes on psychologic analysis, sometimes on

lOb
clinical experience. The main point is that the nomenclature
should allow for such a clear characterization of symptom
complexes that the names can be used for comparison and
correlation. Thus, the following list of terms is considered

only as a means of orientation.

Disturbances of the expressive side of language due to cor-
l. Dysarthria. tical lesions:
2. Peripheral motor aphasia (cortical and subcortical
aphasia of the old nomenclature, Broca's aphasia, pure
aphasia)
3. Central motor aphasia: Disintegration of motor Speech
due to impairment of abstract attitude and the function
of motor instrumentalities
Disturbances of the receptive Side of language due to cortical
lesions:
1. Cortical deafness: disturbance of acoustic perception
due to cortical lesion
2. Noise and music cortical deafness: Disturbance of per-
ception of the characteristic sounds of noises and music
with maintenance of hearing
3. Sensory aphasia
a. Peripheral sensory aphasia (pure sensory aphasia,
. "reine Worttaubheit")

b. Central sensory aphasia (cortical sensory aphasia,
combination of pure sensory aphasia and central
aphasia, and more or less amnesic aphasia)

Central aphasia

Amnesic aphasia

Transcortical aphasias, characterized through better preserva-
tion of repetition than understanding and spontaneous Speaking
1. Transcortical motor symptom complexes
2. Transcortical Sensory symptom complexes
3. Mixed transcortical aphasia

(PLUS: the various agraphias and alexias with.which this

study is not concerned)

Due to various interpretations in the past of some of
these identical terms, certain of them need clarification.

Motor aphasia, as I interpret it, is that difficulty in

104
uttering sounds and words which is due to a defect of the
learned specialized motor speech performances, i.e., due to a
defect of definite motor "Gestalten," or of the function by
which these motor complexes are built. By this we distinguish
motor aphasia from apraxia of the speech muscles.

We distinguish now, primarily on the basis of Broca's
observations: the foot (pars Oparcularis frontalis), the
pars triangularis (designated as "cap" by Broca) and the pars
orbitalis. Later investigators have sometimes used synony-
mously the expressions foot and posterior third of the third
frontal convolution.

For a long time, the foot of the third frontal con-
volution was assumed to be the place lesioned in cases of
motor aphasia. Ferrier added the neighboring parts of the
Insula and the pars opercularis centralis, other investigators
also the pars triangularis and orbitalis. Later, particularly
after the critical discussion of von Monakow, the crucial
area was extended in anterior and caudal direction. fionakow's
delineation of Broca's area includes: the third frontal
convolution, the anterior part of the Island of Neil, the
small gyrus connecting the third frontal with the operculum
of the precentral convolution, and the operculum itself.

In order to understand the variety of syndromes observed
in lesions ofkhe extended area of Broca we have to consider

the relationship of the third frontal convolution to the

105
Operculum Rolandi and to other parts of the brain. From such
a survey, we come to the following conclusion:

Without any doubt there are in the Operculum Rolandi the
foci for the musculature of mouth, tongue and larynx. The
injury to this substratum produces impairment of the use of
these muscles with regard to non-linguistic as well as
linguistic activities, e.g., sound formation. We assume that
the more complicated a given motor activity, the larger the
area of its representation: in the case of language activity
it includes the third frontal convolution. Indeed, this is
probably a very essential part, since in cases of lesions
exclusively in the third frontal convolution, with intact
operculum Rolandi, severe motor aphasia has been observed,
occasionally even of permanent nature. This can hardly be
explained by assuming that the focus in the third frontal
convolution causes the aphasic symptoms be affecting secondar-
ily the neighboring cperculum Rolandi, which is free of
primary defect.

There are numerous anatomic components involved in the
structure of motor speech and, in any given case, we have the
greatest difficulty in attempting to determine the signifi-
cance of the various defects for the impairment of motor
speech, for restitution or absence of restitution; similar
lesions can produce very different symptoms and we can only

speculate about the reasons therefor.

106

Central motor gphasia is a combination of motor speech

 

disturbances similar to peripheral motor aphasia plus an ex-
pression of impairment of abstract attitude. In central

motor aphasia, the lesion is located in the anterior part of
the brain, damaging the frontal lobe and the motor speech area,
and thus producing a picture in which, besides impairment of
abstraction, motor speech phenomena are prominent.

On the receptive side, understanding of heard language
is based on perception of sounds and sound complexes. Sensory
aphasia exists if sound and sound complexes are perceived in
a normal way but are not recognized as language, or, if this
is the case, are not comprehended in their meaning. Three
forms of sensory aphasia have been distinguished: p332
sensopy aphasia, where sounds are not recognized as language.
The patient is not able to understand or repeat them. There
are no other speech disturbances; particularly speaking,
reading and wording are intact (also called pure word deafness,
subcortical sensory aphasia, peripheral sensory aphasia). A
second type, sensory aphasia proper (Cortical sensory aphasia,
Wernicke's sensory aphasia, central sensory aphasia), is a
complex picture where perception of sounds as language is
somewhat preserved, but not so well that the patient would be
able adequately to recognize the heard 1anguage--he cannot
perceive the heard words in order to recognize what they mean.

This sensory defect is accompanied by other speech defects,l

107
particularly paraphasia. In a third form, the so-called
transcortical sensory a hasia, perception of language is
perfect, but the words do not evoke the right meaning. The
patient is able to repeat heard language, but does not under-
stand the heard word. Repetition is more or less echolalic.

My concept of the organization of the temporal lobe
in respect to speech is not so much in contrast to that of
Henschen as it may appear at first. He assumes that we have
to distinguish three parts: one center for word hearing, one
for perception of word sounds, and a word sense center. This
corresponds to my dedifferentiation of a smaller part of the
area sufficient to guarantee hearing in general, a larger
area to guarantee hearing of word sounds and another part
which belongs to the area for "inner speech". Indeed, I do
not assume separate areas but more or less complicated func-
tions of a great region.

Apart from the significance of this result for under-
standing this special form of aphasia, it is of general im-
portance for the theory of brain function:

1. In so far as it brings an aphasic picture which.was
often considered as effect of interruption of pathways into
relation with a damage of cortical function, and thereby
considerably undermines the theory that destruction of

pathways can produce aphasia--a theory which I have always

rejected.

108

2. In so far as it makes the assumption of acoustic
perceptions unnecessary and considers the perceptive speech
phenomena only as complicated phenomena of these. This
brings us to a standpoint similar to the interpretation of
motor aphasia which is, for our interpretation, also the
effect of impairment of more complicated motor activifles
which do not differ essentially from the other voluntary
movements.

In central aphasia we find damage of inner speech.

 

Inner speech is the totality of processes and eXperiences
which occur when we are going to express our thoughts, etc.,
in external speech and when we perceive heard sounds as
language.

In addition to these functions, inner speech consists
also of material fixed more or less by previous functioning
of the "apparatus," by experience. The concepts of letters,
words, phrases, are more or less fixed wholes, patterns which
we are aware of in the framework of an inner speech attitude
and used as wholes to start the speaking activity. These
patterns are developed to a different degree in different
individuals. They can be impaired to a greater or less
degree in dedifferentiation of inner speech. In this field,
dedifferentiation follows also the laws of impairment of

figure and ground configuration valid for pathology in

general.

109

To summarize our ideas of central aphasia, it is a
symptom.complex which consists mainly of: (l) impairment
of spontaneous speech and understanding, the latter less than
the first; (2) literal and verbal paraphasia; (3) paralexia
and particularly paragraphia; (4) disturbance of repetition;
(5) disturbance of spelling and of the capacity to combine
letters into words. To be noted as not infrequent complica-
tions are amnesic aphasia and signs of pure acousticaphasia.

The outstanding symptom of amnesic gphasia is the lack
of nouns, adjectives, verbs and especially names for concrete
objects in speech. The defect shows most strikingly in the
task to name objects; the patient is unable to find the names
for the most ordinary objects of everyday life. He need not
present any additional disturbance of speech; at least others
need not become manifest immediately. He repeats words with-
out hesitating, he accepts among a number of words presented
orally or written, only the one which belongs to the object;
he shows no paraphasia, no disturbances in writing and
reading.

We have explained before that difficulty in finding
words can be due to different causes. Only those cases with
word finding difficulties where this defect is related to
impairment of abstract attitude should be called amnesic
aphasia. Thus, symptoms due to impairment of abstract attitude

belong intrinsically to this form of aphasia.

llO

Anatomically, if amnesic aphasia occurs in a localized
affection, the latter usually concerns the temporo-parietal
,region; but it must be of a particular kind, it must not
damage this region too much, otherwise disturbances of in-
strumentalities of speech and of the mental phenomena are so
predominant that amnesic aphasia does not come clearly to the
fore. A fine damage in this region which is suited to produce
a fine diffuse damage of the cortical function, can take place
particularly in tumOr or abscess in this region-~the two
conditions in which particularly amnesic aphasia appears. I
stressed such an origin of thissymptom.complex years ago.
Impairment of abstraction appears in lesion of various parts
of the brain, in lesions of the frontal and parietal lobe,
and in both cases we observe the defect in naming. However,
it seems that the clearest development of symptom complex
occurs if the lesion is located in the temporo-parietal
region; this would mean if the speech area were affected to
a certain degree too. One may argue that with this statement
I give up my theory of the origin of amnesic aphasia as due
to impairment of abstract attitude. Not at all. Impairment
of abstract attitude remains, to my experience, the prerequi-
site without which the defect in "naming" never occurs. A
lesion of the "speech area" alone is never followed by the
amnesic-aphasic defect in word-finding.

The main characteristic of transcortical aphasia is

damaged understanding, much more than spontaneous speech.

Ill
The patients speak much, they usually show some reduction of
words, particularly lack of nouns, probably due to a concomi-
tantly existing amnesic aphasia. If one subtracts this
latter defect, the language appears correct, meaningful,
the syntactical and grammatical structure quite well organized.
Some paraphasia may be present, probably as effect of a
slight damage of the central speech area.

Special difficulties and uncertainties regarding
restitution are based on a lack of knowledge regarding the
relation of the "other" hemisphere to the functions of the
active hemisphere. This problem demands special consideration,
since the assumption of restitution by means of the corres-
ponding area of the other hemisphere is extensively recog-
nized. The main difficulty with this conception is that in a
given case it is impossible to know how much the "inactive"
hemisphere had not always been cofunctioning, especially in a
restored function. In a patient in.whom this was the case,
one should not Speak of restitution, but rather of the taking
over of the entire function by a part of the appropriate
apparatus, since it is not a question of the taking over of
a function by a substrate that formerly was not engaged with
this function.

It must also be denied that one part of the brain can
substitute for another part, that latent material can take

over the function of destroyed tissue and that the corres-

112

ponding opposite hemisphere can replace the damaged one. A
true return of function takes place only by the reestablish-
ment of the substrate or, under definite, rare and limited
circumstances, through painstaking reeducation with the
assistance of the remaining part of the substrate which had
already been of service in the function. The acquired
functions are usually incomplete, especially in adults.

We could assume a real taking over of a speech function,
a new learning by the other hemisphere only under the follow-
ing conditions: (I) If the patient had a definite premorbid
prevalence of one hemisphere (that allows us, within definite
limits, to assume that the other hemiSphere did not act
together with the "leading" one); (2) If we can assume a total
destruction of the leading hemisphere, or at least of that
part which.we bring into relation to a certain performance;
(5) If the symptomatologic defect was of a longer duration
and recurrence of the performance took place slowly, possibly
under the influence of definite training.

In general, one can say that adaptation to an irrepar-
able defect can occur in two ways. The organism can yield to
the defect; it restricts its performances to the preserved
reduced ones, but the normal functioning of the organism is
in principle unchanged. It is the more natural procedure,
seems more automatic, demands less voluntary activity on the

part of the individual, and hence secures more security than

115

the second way in which the organism.may react to a defect.
Here the organism gives up the old procedure; because its
maintenance would give too little effect, it tries to com-
pensate by other performances. This represents a more
volitional kind of behavior, leads more readily to fluctua-
tion, involves less constancy and less security and admits
a greater possibility for catastrOphic situations.

Restitution or real return of former function takes
place only when complete anatomic restitution takes place.
If complete anatomic restitution does not take place, there
is no return of function, but repair. Repair is recognized
by a number of characteristics. The following are always
present: (a) A greater breaking up occurs, corresponding to
the damage in the function; (b) the functions are changed in
a qualitative way; the reactions in a definite milieu are
more constant and the stimuli more bound; in changeable
stimuli there is a greater inconstancy of the reaction than
in the normal; (c) rest and orderliness of control are easier
than in the normal, and more readily disturbed. An order-
liness in qualitative normal relation in this sense is ob-
served only by a narrowing of the milieu, in finding an
adequate milieu for the disturbance. There the orderliness
and rest are even greater than in the normal.

The restitution picture depends on: (1) the total

capacity of the organism.before the disease set in (the

114
amount of former ability and especially of the functional
quantity); (2) the greater or lesser degree of inviolability
that the entire organism can withstand (circulation of the
blood, general condition of strength, etc.), especially in
regard to the brain; (3) the energy present for the use of a
function, which as a result of the relative constancy of the
total energy is dependent also on the use of energy in other
places; this results in the retraining of certain functions
at the cost of others. The selection is determined by the
tendency of the organism to maintain those functions which,
from the standpoint of the total task of the organism (its
nature), are the most important, and, among the most im-
portant ones, those best capable of accomplishing the given
objectives of the surrounding world. The favorable result of
restoration is therefore dependent on the milieu in which the
particular organism is living, as well as on the demands being
made. A defect is the more restored the more the organism is
capable of reaching its surrounding world with the restitu-
tion.

From the foregoing considerations one learns a definite
therapeutic procedure, which must be considered as a general
rule: Never attempt to improve a definite disturbance in
itself; its importance must always be considered as a task
for the entire organism, for the corresponding nature of the

organism, the more so as the nature is altered by the illness,

115
and the therapeutic measures are to be determined from such
considerations. An attempt is to be made to bring the patient
into a situation in which an adequate milieu may develop for
the changed organism; in which the organism, regardless of
the defect when compared with its former being, may perform
its most useful functions, and in which it can work as regular-
ly as possible without the intercurrence of too severely
catastrophic reactions. When this is accomplished, the
organism, although not normal, is none the less not sick.
Subjectively it feels well, and objectively it shows little
disturbance. This condition appears as the goal in the
process of restitution; it must also form the object of any
therapeutic attempt. From this it follows as the most impor~
tant negative problem that one should not proceed therapeuti-
cally with certain symptoms, because an organism, thus
functionally more able, will "recover better" than when
attempts are made to control all symptoms. The task is
therefore to determine which defect is to be controlled and
whfl3h is not. The scientific considerations of the manifest-
ations, however, are not sufficient for such a decision; a
comprehension of personality in its essence and a willingness
to enter into the personality of the patient are essential

here.

CHAPTER X
THE SPEECH PAThOLOdIST'S VIEWPOINT OF APHASIA
by Jeanette 0. Anderson as

In formulating a basic concept of aphasia, the speech
pathologist is compelled to consider in parallel the psycho-
logical, physiological and anatomical aspects of the problem.
A study of aphasia made from any one Specific point of view
is incomplete. This perhaps eXplains why there seems to be
no universally satisfactory classification of aphasias.

The Speech pathologist can follow the psychologist in
his concept of aphasia as a disorder of propositionizing or
of symbolic formulation, but he cannot agree with.him that
there is little or no localization of function. He can say
with the anatomist that certain cerebral areas tend to sub-
serve specific language function, but he cannot subscribe to
exact anatomical localization. In general, he can follow the
lead of the physiOlogist in admitting that certain areas sub-
serve certain linguistic functions more than others and that
the entire brain is needed for normal linguistic activity.

The Speech pathologist's concept of aphasia should be
not only as precise as that used in localization by the
surgeon; it must also be as general as that of the psycho-

logist who insists that the linguistic mechanism is a Gestalt

as See Note on p. 71.

p 117
and functions wholly. More than any other investigator in
this field, the speech pathologist must see both the parts
and the whole clearly and simultaneously in their mutual
relationships.

In order to discover aphasic manifestations and to
prescribe techniques of special re-education in speech, the
speech pathologist needs to consider not only three aspects
of the problem, but a fourth as well: the possibility of
retraining in terms of all three. Although concerned with
the receptive and eXpressive formulation of linguistic
symbols, he is even more interested in the restitution of
function than in gross or specific losses or even remnants
of linguistic ability. It is not enough for him to realize
the extent of the damage, to have an idea of functioning in
both physiological and psychological terms; he must plan to
use the uninjured neural tissue and to reroute language
activities over, to and through this sound brain-stuff.

A basic concept of aphasia for the Speech pathologist
evolves: aphasia is a linguistic impairment; there tend not
to be "pure" aphasias; each aphasic patient exhibits a dis-
turbance made up of certain aphasic manifestations peculiar
to the given case; any classification is of aphasic mani-
festations and not of aphasias. Examination reveals the
manifestations; they form the specific aphasic picture seen

in each case. Once he has this concept of the inconstancy,

118

unpredictability and irresolution of the aphasic problem,
the trained speech pathologist is ready to examine and to
attempt re-education of aphasic patients.

The speech pathologist is confronted with two tasks
in work with aphasics: (l) to examine patients carefully
and diagnose speech impairments accurately, and (2) to pre-
scribe and administer suitable therapeutic measures for each
case. The examination and diagnosis is fundamentally im-
portant in that localization of brain lesions is often.made
on the basis of detailed language observation in conjunction
with other neurological and clinical findings; and therapeutic
measures prove more efficient if we know at once the exact
abilities and disabilities of the patient.

The following classification of aphasic manifestations
is suggested as a first step toward a practical solution of
the problem confronting the Speech pathologist:

I. EXpressive manifestations
A. Implicit (probably caused by a parietal lesion)
1. Ideational aphasia
2. Ideo-kinetic aphasia
B. Overt (probably caused by a frontal lobe lesion)
1. Spoken language
a. Broca's aphasia (third left frontal convo-
lution, cortex)
b. Subcortical aphasia (subcortical Broca's
region)
0. Transcortical aphasia (questionable)
2. Written language
a. Agraphia (Exner's writing center, second
left frontal convolution
II. Receptive manifestations
A. Auditory (superior temporal convolution)
l. Agnosia (Heschl's convolution)
2. Aphasia (Posterior part of superior temporal
convolution)

119

B. Visual (temporo-parieto-occipital area)
1. Agnosia
a. For linguistic symbols
b. For objects and colors
0. Geometric-optic
2. Aphasia

8.0 Alexia
b. Agraphia
c. Anemia
C. Other sensory media
10 TaCtile

2. Cutaneous
5. Kinesthetic
III. Associative manifestations
A. Aphasia on lower levels
B. Aphasia on higher levels
IV. Combinations of manifestations
A. Wernicke's aphasia
B. Total aphasia
C. Uther combinations of aphasic manifestations
V. Manifestations indicating special abilities useful in
planning speech therapy
A. Expressive
1. Oral facility for building new motor synergies
2. Manual facility for building new motor synergies
3. Kinesthetic imagery
B. Receptive
1. Visual imagery
2. Auditory
a. Imagery
b. Memory span
5. Other sensory imagery
C. Assotional
D. Constitutional predisposition of patient

Although its fundamental purpose is to guide the speech
pathologist in diagnostic, prognostic and therapeutic pro-
cedures, this classification may prove of some use in the
consideration of aphasic patients by other specialists. It
is realized that any classifications used are merely arbitrary;
repeated examination seems to reveal few cases that can be
grouped under any system of classification without further

eXplanation.

120

Neither the aphasic child nor the aphasic adult profits
from speech correction until he wants so much to express his
inner verbalizations that he spontaneously attempts some form
of overt communication with other organisms, human or not, in
his environment. This effort to speak may be made orally,
manually, grimacingly, graphically, or chirographically. Once
the aphasic tries to communicate, he will respond to speech
training or retraining.

There can be no one testing procedure set up for
determining the presence of aphasia; procedure must be adapted
to each patient. On the basis of language findings combined
with clinical findings, surprisingly accurate localizations
of intra-cranial pathology may be made; however, we need to
take into consideration the fact that pressure and edema
affect language centers quicxly and that the causative lesion
or neoplasm may be some distance from the centers affected.
This means, of course, that language findings alone are not
sufficient basis for diagnosis. They do help, however, and
in the study of aphasic patients we have found an excellent
Opportunity for the speech pathologist to work in close co-
Operation with the neurologist. This pre-therapeutic work is
invaluable to the speech scientist in planning his reeduca-
tional procedures and techniques. In our experience, neuro-
logists welcome the testing of language functions that we may

do in conjunction with their work and the post-operative or

121
post-traumatic retraining that we may help to effect.

Diagnostic techniques include testing receptive
abilities (obeying oral commands, following written instruc-
tions, etc), checking writing and copying abilities, and
testing expressive abilities (producing spontaneous Speech and
repetitive ability). In addition, tests for aphasias on
higher levels than those of simple recognition, comprehension
and expression are necessary in many cases. These would in-
clude mathematical calculations, following complex instructions,
giving opposites in word lists, etc. In testing, the examiner
should always record relative Speech of response, emotional
stability or lability, perseverations, following of instruc- ;
tions, use of objects, alertness, spontaneous speech, as well
as how the patient reacts to the testing.

With no identical cases and therefore no comparable
test results, we cannot treat our findings statistically and
say that a given correlation indicates the presence of aphasia
sand that anything less does not; the pattern that constituted
aphasia for one individual need not point in that direction
for another person of lesser intelligence and/or training.

We are compelled to treat each case separately; the thorough
case-study methods recommended by Adolph Meyer in psychiatric
practice are adaptable to aphasic patients.

Perhaps the most important factor to keep in mind is

Backus' restatement of Yacorzynski's tenet: "the process of

122
rehabilitation must itself be part of the reality of living
for the patient. He will not wait to live while those powers
of implicit and explicit verbalisation are growing again in
the months of re-education."

The adult aphasic patient suffers an emotional abor-
ration that interferes with.what language abilities he has.
This breakdown of morale tends to inhibit language in an
individual who is adult in all except linguistic functions
and who is able, moreover, to compare his present linguistic
failures with his past achievements.

After the first few lesson periods, retraining in
speech seems to contribute to increased emotional stability
in these aphasic patients. Morale-building is a fundamental
part of speech therapy with aphasic patients. It is one of
the jobs of the therapist to make the patient willing to start
his linguistic rehabilitation where a child starts and to see
his linguistic successes and failures in their proper per-
spective.

In the initial stages of training, the aphasic child
learns well when objects, toys, pictures, and situations are
associated with speech sounds. The adult, on the other hand,
usually responds better to written or printed symbols than to
the realities for which they stand. Only when situations,
objects, persons, colors, or pictures are fraught with

emotional significance do they provoke an attempt at speech

125
as rapidly as do printed or written symbols.

Although it may be necessary at first to employ strongly
emotional stimuli to secure overt response from a patient,
this practice is to be avoided and discouraged because it
leads in the aphasic, even more than in the so-called normal,
to noncortical language, to uncontrolled speech, to excesses
of emotion that eventually inhibit rather than stimulate
volutional speech, to hysteria, to behavior on a thalamic
level. It is important to guard an aphasic from emotional
excesses. He is no longer able to guard himself very
effectively. He has to relearn cortical control not only of
Speech but of all his overt behavior.

Concomitant sensory stimuli and corollary motor
activities are helpful in the retraining process. The simul-
taneous strengthening of many pathways seems to reinforce
each of them and to contribute to those of speech. The
aphasic will speak and/hr write a word more quickly if he hears
it 329 sees it while he tries to write it 229 say it than if
only one stimulus were presented and only one reSponse re-
quested. There are at least two reasons for this: first,
each stimulus and response tends to reinforce others made
simultaneously; second, if one avenue of reception or expres-
sion is blocked, anatomically or psychologically, concomitant
stimuli and responses provide alternate routes by which

necessary neurological associations may be effected.

124

To effect these associations, neural impulses must be
rerouted to their usual association areas through healthy
tissue; remaining tissue of the dominant hemisphere must
associate impulses previously synapsing elsewhere; or the
intact, usually nondominant, cerebral hemiSphere must take
over the function of damaged brain areas. This is the theory
upon which neurologists and psychOIOgists eXplain restitution
of linguistic function.

Ontogenetic develOpment of speech seemed to recur in
restitution of linguistic activities and can be utilized by
the speech therapist. The last four stages, babbling,
lallation, echolalia and verbal utterance, in the child's
normal speech develOpment can be used effectively as a
therapeutic device in teaching aphasic children and in re-
training aphasic adults.

In the teaching of aghasic children, speech ought to
be an outgrowth of daily experience. For adults, speech
should never be taught as an entity, an end in itself, but
always as an integral part of the business of living, a means
to an end. It cannot be separated from emotional, social,
and vocational retraining. Only as a patient achieves personal,
social, and economic stability will his speech stabilize. He
cannot be taught speech while he waits to live. He has to go
on living and his speech training will be useful to him only

as it keeps pace with his needs.

125

The success of re-training in speech seems proportional
to: (1) active cooperation of the patient; (2) former
training of the patient; (5) success in re-building morale in
connection with linguistic problems; and (4) resolution of
economic, personal and social problems attributable to the
patient's illness and residual disabilities.

Formal re-education in speech for mature aphasic
patients seems valuable for at least five or six years;
however, plateaus are reached in relearning long before the
regaining of former levels of excellence. Further training
seems not to aid the patient in going beyond such plateaus
but does appear to aid materially in the maintenance of re-

learned linguistic skills.

CHAPTER XI

DIAGNOSTIC AND THERAPEUTIC APPROACHfiS

OF BACKUS, SHBEHAN, AHD OTHERS

With what sort of person are we dealing when an
aphasic appears in the speech clinic for diagnosis and
therapy? Usually, in addition to the obvious speech de-
ficiency, three major complications will be present:
paralysis, personality change, and emotional instability.
With every attempt to speak, the patient has experienced
mental confusion and, ultimately, fatigue. The frustrations
experienced through continually futile speech attempts bring
about deSpondency, resignation, apathy. Mentally he is
capable of comparing his speech failures with past accomplish-
ments. The resultant breakdown of morale tends to cause the
patient to retreat more and more within himself.

Add to these things the actual personality changes, the
tension, the need for rest and sleep, the anxieties, (the
contrary euphoric state), the concern about and yet lack
of understanding of his condition, the almost complete
lack of a sense of humor, and the hundred and one
additional almost freakish neurological defects which may
be involved in individual cases, and you have a picture
of the state of confusion which is typical of the aphasic.
This brief picture of the patient should be sufficient

to point out the great needs beyond formal speech training.

 

l. Vivian Mowat Sheehan, "Rehabilitation of Aphasics
in an Army Hospital", The Journal 23 Speech Disorders, 11:2:

150, 1946 O

127

Along with the regaining of verbal adequacy, the patient is
in dire need of personality adjustment. "Speech is an integral
part of the whole individual. It cannot be taught as a
mechanical process apart from the complex behavior pattern to
which it belongs."2 As Kurt Goldstein points out, its resti-
tution must be considered as a task for the entire organism.
It is the speech clinic that must meet the socio-psychological
needs of the patient. Yet, zealous therapists must realize-
that "speech re-training can be instituted successfully only
after there is some spontaneous attempt at communication
through overt expression, or otherwise."3

Preparatory to the speech examination, the therapist
need s to know the patient's general medical condition and the
neurologist's diagnosis of whether the cerebral condition is
static or progressive. Entering into the prognosis of recovery
are many factors: the general health of the patient, the site.
and severity of the cerebral injury, the condition of the brain
as a whole, the patient's age, his previous type of mental and
linguistic habits, his intelligence, educational and cultural
status, the type and.amount of impairment of motor skills, as
well as the patient's motivation--his emotional drives,

determination, and stability.

 

2. Joseph Jastak, "The Treatment of Expressive Aphasia
in a War Veteran", Delaware Dtate Medical Journal, 17:5:104,

lay, 19450

5. Anderson, pp. 01 ., p. 168.

128
The techniques of examination have had almost as wide
a variance as the number of examiners. The methods of inquiry
have ranged from
(a) the brief, informal clinical approach of the con-
ventional neurological examination, and (b) the relatively
systematic, though unstandardized, clinical enquiry
recommended by Nielsen, to (0) use of formal tests with
prepared materials as emplgyed, for example, by Head and
by Weisenburg and McBride.
Because of the many different conceptions of the nature of
aphasic disturbances, there is little uniformity in the tests
employed. The therapist is faced with the dilemma that "tests
are bound to differ as long as theoretical differences exist,
and on the other hand, theoretical differences must exist and
must even appear greater as long as the tests lack uniformity."5
Regardless of the method of testing to be used, we must
determine what the patient can do, what he cannot do, and what
things he needs most to meet his immediate social and economic
demands. The actual diagnosis should result in the establish-
ment of immediate and reasonable sub-goals which the patient
can understand, accept, attain, and appreciate. Goals of

this type will permit the successes necessary for further

motivation.

 

4. Ward C. Halstead and Joseph M. Wepman, "The Halstead-
' Wepman Aphasia Screening Test," The Journal 2; §peech and
Hearing Disorders, 14:1:11, March, 1949.

 

5. Weisenburg and McBride, 2p, cit., p. 92.

129
To ascertain the abilities and disabilities of the

individual case it is necessary to make an analysis of the
following spheres: speech, reading, calculation, time sense,
drawing, comprehension of pictures, vision, visual imagery,
auditory performance, auditory imagination, tactile sense,
tactile imagery, the imagination of movements of his own
body, and measurements of reaction times.6

In order to “determine the functional mental capacity,
to estimate loss of capacity by comparison with previously
recorded test scores, and to measure improvement as training
progresses,"7 the following tests are recommended by the
U.S. War Department for the use of clinical psychologists in
the testing of aphasics: the A.G.C.T. (retest) or Basic
Battery for permitting comparisons, the Wechsler-Bellevue
Intelligence Score for the determination of amount of mental
deterioration and loss of mental efficiency, and the
Goldstein-Scheerer Cube Test of Abstract and Concrete Behavior
to ascertain the impairment of abstract thinking or ability
to generalize.

The modified Head serial test #1 used by many therapists
includes the following activities: naming objects seen,

repeating single words, understanding the spoken word, reading

 

6. Konrad Zucker, "An Analysis of Disturbed Function
in Aphasia", Brain, 57:109-27, 1954.

7. War Department Technical Bulletin (TB MED 155),
"Aphasic Language Disorders", War Department, Washington 25,

D.C., April, 1945, p. 2.

150
the printed word aloud, understanding the printed word,

writing spontaneously, writing from dictation, copying,
spelling aloud. Daily testing in these activities permits a
graphic recording which allows comparisons in self improve-
ment as well as comparison in improvement with others.

There are three types of training facilities available
for aphasic adults: individual treatment supervised by a
Speech therapist and carried out by a tutor, nurse, or member
of the patient's family, the out-patient clinic where the
patient reports for short training periods several times a
week, and the in-patient training center. This is usually a
hospital where the patient's training extends over many hours
‘a day. For the training of the aphasic child, Alice G. Rooney
recommends the school for the deaf. Here, as in no other
service of an educational system, "endless associated repeti-
tions arecbligatory in order to strengthen the weakened
faculty of association between the cortical senses that should
function integrally."8 In the school for the deaf the child
patient can have a thorough sense training program in the
develOpment of muscular tone and in the cultivation of sight,
touch, and hearing, in addition to training in reading and
Speech.

Since the brain-injured represent problems in every

 

8. Alice G. Rooney, "An Aphasic Child in a School for'
the Deaf", The Volta Review, 47:559, October 1945.

 

131
phase of living, every agency available should be utilized--
the doctor, neuro-surgeon, psychologist, psychiatrist, social
worker, physio-therapist, speech therapist, educational
agencies, vocational counselors, and members of the patient's

family.

. ' "’ ““2... ,_

Of the techniques basic to speech re-education Dr.
Backus lists voluntary inhibition (to stop trying so hard and
eliminate random facial movements and sound), voluntary
relaxation, sense training (lip reading, hearing, kinesthesia),
rhythmic training, and shifting of handedness, in addition to
formalized speech re-training. Shift of handedness is advised
except when a shift was made earlier in life, or in cases of
confused dominance, or paralysis of both sides. The shift
will help develop function in the association areas of the
undamaged hemisphere and can be aided through such activities
as throwing a ball, playing ping pong, writing on blackboards,
and eating with the Opposite hand.

In most of the pedagogic methods the utilization of
the five senses is stressed in aiding the retention of speech
symbols. Thus, the patient is more apt to recall a word if
while re-learning it he is exposed to the auditory symbol
simultaneously with being able to see the object named, feel
it, and in some cases, smell and taste it. This technique
plus constant repetition of material aids greatly the

regaining of speech. Gestures and pantomime will also enable

132
faster learning since "speech is a total bodily response and
accompanies motor activity."9

In aphasic re-education Backus stresses the fact that
"the impulse for speech grows out of group activity in real
life situations."10 Because of this she advocates an in-
tensive program of from five to seven hours daily utilizing
a great deal of group rehabilitation. Vivian Mowat Sheehan,
another enthusiastic advocate of the benefits of group
therapy, finds that "the contact with others has a therapeutic
value in itself. It lessens self-pity and shame."11 In
actual therapy she conducts work on greetings and farewells,
identification (names, home towns, age, names and values of
coins and currency, names of days, months, etc.), special
holidays, directions, parts of the body, numbers, the
alphabet, weather, members of the patient's family, furniture,
food, shaving, smoking, maps, automobiles, meeting peOple,
telling time, naming colors, playing cards, sports and
games, animals, etc.

Among the specific techniques utilized by Mrs. Sheehan
is that of training in conversing. She trains patients in

asking questions by using such common question.words as how,

 

9. Ollie Backus,‘g£..gl., pp, cit.,
10. BaCImS, 220 Cite

11. Sheehan, 22. cit., p. 151,

153

when, what, etc. Telling little incidents, describing people,

 

indicating locations, and keeping chronological order
(speaking on topics involving time sequence) are among other
conversational devices. Additional help is given in varying
responses, listening to others converse, telling something in
a crowded room, interrupting politely, maintaining eye con-
tact, and using contractions.

Her "small talk" helps give the aphasic a degree of
certainty in the use of a practiced pattern or recurrent
phrase. This can be used in giving introductions, paying
compliments, thanking the hostess, asking a girl for a date,
commenting on the weather, greeting friends and strangers,
begging pardon, and telephoning. The use of these phrases
will automatically help put the patient at ease, enable him
to save face, and make further and more difficult learning
easier.

Work under Mrs. Sheehan's guidance is also done in
attempting to eliminate verbal crutches such as pet phrases,
over-used gestures, and substitutions. Avoidances are
detected and the patient is then prepared forthe difficult
situations which he is avoiding and sent deliberately into

them. Nor is the patient allowed to let others say something
for him. In this event, the therapist insists on the patient's

repeating any word said for him.

Special attention is given to using the "little words"

134

such as 23, lg, but, 23, was, 23, lg, from, out, etc.

 

Assignments are made to use these words three times a day.
Use of the above devices has indicated that aphasic
training can be accomplished without the use of fatiguing
drills and other monotonous activities. Mrs. Sheehan further
advises therapists to
keep assignments exact and specific, limited to a simple
task which can be completed. The clinician must be wary
of the assignment which sets such high standards of
performance that the aphasic is doomed to failure. . . He
must work toward specific and well-defined sub-goals of
achievement which he can reach.within a reasonably short
period of time. Let general impfovement be a by-product
instead of an ever-elusive goal. 2

The therapist must be continually on guard to encourage and

maintain realistic levels of aspiration.

Summarizing her methods for the re-training of aphasics,
Mrs. Sheehan lists "stating the goals specifically in terms of
immediate needs, Specialized techniques, using questions and
answers, class discussion, the assignment method, and indivi-
dualized group therapy."13

Since many aphasic patients have greatest difficulty in
regaining those parts of speech concerned with qualifying and

correlating (adjectives, adverbs, prepositions, articles and

conjunctions), Charles K. Mills advocated the use of primers

 

12. Vivian Mowat Sheehan, "Techniques in the Management
of Aphasics," The Journal 23 Speech and Hearing Disorders,
15:246, Sept., 1§48.

15. Loc. cit.

135
and grammars in retraining-~especially with patients who have
had a good educational background. He recommended that

patients should be taught the grammar as a child is
instructed, in other words, by teaching him the meaning

of the different parts of speech.and the exact methods
of using them in phrases and sentences. 4

Also
the patient with the book before him.should be taught to
conjugate verbs, decline nouns and pronouns, compare
adjectives, and in other ways to go through the routine
methods of studying language employed in the schools,
these beifg modified by the particular requirements of
the case.

Above all, he warns against a method of simple memorization.

He contends that the patients must relearn all the parts of

speech and how they are used in the construction of a sentence

to express thought.

Augmenting the speech therapist's techniques, attempts
have been made to aid treatment medically through narco-
synthesis. Although this technique has not undergone any
long-term rehabilitation programs to the writer's knowledge,
it can be noted that in the cases exposed to this treatment,
the patient relaxed and found themselves able to speak more

easily and confidently after injection with a solution of

sodium amytal. The elationhver their success carried over

 

14. Charles K. Mills, "Treatment of Aphasia by Train-
ing”, The Journal 2; the American Medical Association, 45:26:
1945, December 24, 1904.

 

15. Loc. cit.

156
and they continued to improve after the drug were off. The
experimenters attributed the immediate improvement displayed

by postulating the removal of the inhibiting effect of

anxiety.

The individual with organic brain disease is aware that
he no longer possesses his original mastery of the en-
vironment. He responds to this awareness with anxiety
and feelings of personal inadequacy. He reacts to new
situations 3% withdrawal, to avoid the anxiety engendered

by failure.

Regardless of the techniques utilized in aphasic
training, one general principle stands out as mandatory: the
aphasic patient must be surrounded by an atmosphere of cheer-
fullness and confidence. The therapist must at all times
exhibit a calm, interested, and understanding attitude. All
indications of hurry, irritation, or disappointment in pro-
gress must be absent. The therapist must continually help
the patient to understand his difficulty. Sheehan uses

drawings of the brain, simple eXplanations, stories of
others' eventual success despite their losses. We are
busy offering encouragement, getting rid of false notions,
and overcoming disillusionment. We build a cheerful
working atmosphere with plenty of informality and

freedom from tension. We try to develop a sense of

humor through teasing, telling jokes, pulling:little
pranks, etc. We try to help the men look forward to the

future with % feeling of pleasant anticipation rather
than dread.l

 

16. Louis Linn and Martin H. Stein, "Sodium Amytal in

Treatment of Aphasia; Preliminary Report", The bulletin pf the
U.S. Army Medical Department, 5:6:707, June, 1946.

17. Vivian Mowathheehan, “Rehabilitation of Aphasics
in an Army Hospital," The Journal pf Speech Disorders, 11:2:

155-6, 1946 o

157
The very hope of success does much to combat the depression
to which these patients are so susceptible. Being kept busy
with occupational therapy helps to occupy time which might
otherwise be Spent brooding.

Keeping the patient cheerful is of prime importance.
This can be aided by group work and group singing. Develop-
ing a sense of security will be helped by keeping the patient
productively busy. He has a need for consistent routine
with all needless confusion avoided. Being stimulated to
take an interest in other things and people is another factor
of great importance in the patient's rehabilitation.

To be most successful, rehabilitation must be adapted
to the patient's special interests and abilities. In this
respect the patient's family can be helpful in supplying in-
formation relative to the patient's early preference for
handedness in writing, educational background and achievement,
previous employment, interests and hobbies, friends and
associates, family, temperament and disposition, likes and
dislikes, attitudes, personal habits and peculiarities, etc.18

The patient's family must be fully instructed in the
nature of the disorder so they do not hide the patient from

others who might think him insane or mentally deficient.

They should be redirected in any false displays of affection

 

18. Backus, pp. cit.

158
manifesting themselves in keeping the patient home and idle
and administering to his every wish. They must have impressed
upon them the importance of treating the patient as a normal
person and not as a handicapped dependent. They must conceal
any feelings of worry or repulsion they may entertain. They
should help him to realize his maximum potentialities socially
and vocationally by enabling him to have the best of Specialized
training--not only surgical and medical, but rehabilitation in
speech as well.

Of supreme importance in therapy through family co-
operation is the need to convince members of the patient's
family that "they will be a greater source of inspiration to
him and will be happier themselves about him if they turn from
past thoughts of what he used to be to the reality of the

present with its hopes for what he can become."19

 

19. Ibid., p. 470

CHAPTER XII
A LAST WORD

A retrospection of this study must necessarily include
an explanation of its omissions. The authorities primarily
treated have been those which seemed, to the writer, at the
time of his writing, to epitomize the thoughts of the re-
searchers in his particular field of approach--be it
anatomical, physiological, psychological, neurological, etc. «\
Availability of material also accounts for various omissions
and minimized treatment of certain authorities. Of necessity,
there has been omission of reference to hundreds of men who
have directed, influenced, and inspired the thoughts of their
more articulate disciples.‘

In one circumscribed reSpect, the completed work
represents a compilation of what Henry Head felt was deleter-
ious to further progress in understanding aphasia--namely, the
evolved hypotheses of the various authorities, while their
clinical investigations have been neglected. Head noted that

the world clings to theories, for they are easier to
remember, can be reproduced with effect and lead to a
clarity of exposition foreign to a description of the
crude eXperimental facts. There is in consequence a

tendency to carry over the conceptions of one age on to
the observations of the next.

 

1. Henry Head, gphasia and Kindred Disorderg of
Speech, (Cambridge: The University Press, 1926), p. 154-5.

140

However, despite this viewpoint in which there is a
good deal of truth, a compilation of clinical facts would be
of little value without some sort of synthesis. Since much
of the world autopsy literature has been collected and synthe-
sized'by far more qualified authorities than this writer, it
was the purpose of this study to present the main trends in
thought as evolved from the observed facts. It is this task
which the compiler hopes has been in some measure accomplished.

Reviewing, then, the material in hand, we find at the
beginning of the nineteenth century, the idea of physiologic
uniformity of the entire brain. All parts were thought to
serve the same function; injury to any portion would cause
another portion to take over its function.

Into a field of medicine imbued with this belief,

Franz Joseph Gall introduced the concept of localization.
Certain faculties (moral and intellectual qualities) were
described as localized in definite areas. Control of move-
ments of speech was attributed to a cerebral center located
in the frontal lobes. These were our first ideas of anatomic
localization.

With Pierre Paul Broca's localization of the speech
center in the third frontal convolution of the left hemisphere,
the anatomic vieWpoint gained great impetus and was accepted
by nearly everyone exposed to it.

This type of localization was shortly supplanted by

141
localization in terms of motor and sensory areas of the brain
and their inter-connections. Sensations, images and percep-
tions were thought to lie dormant in definite areas awaiting
excitation. Using the hypothesis that we think in words,
Bastian noted that "words were revived as sound impressions
in the auditory perceptive centres, whence they were trans-
mitted to the more immediate motor centers for speech."2

Over a period of time Bastian's views began to deflect
from their original adherence to strict anatomical localiza-
tion of function. However, he apparently pointed out the
path which led to the period of the "diagram makers."

The increasing amount of attention given to individual
differences during this period demanded some deviation from
the strict concept of rigidly marked cortical areas. The
explanation was supplied by Charcot and his "auditives",
”visuals” and "motors" for speech. Thus the use, in varying
degree, of the different centers during the learning process
offered an explanation of differences which did not conflict
with the localization.

From.this stand it was but a minor step to emphasizing
the importance of the association pathways in explaining
individual differences. Slowly the use of the word "localiza-

tion" was changing from an anatomical to a physiological

 

2. Ibid., p. 157‘8.

connotation.

142

No longer could speech be considered a combination of

independent elements. Disease could not be thought of as

resolving language into the various elements of articulatory,

visual and auditory activities.
demand a dynamic interpretation
longer could they see conscious
or motor presentations and laws

Foremost in causing this

The psychologists began to
of mental activities. No
processes reduced to sensory
of association.

rupture with the old ideas

was Henry Head. Many of his ideas stemmed from.Hughlings

Jackson whose works had been so

Head denied the idea of centers

long ignored or slighted.

for the use of language and

granted only "certain areas within which destruction of

tissue produces a disorder of some particular mode of

behaviour."3

Head's final views seem.but the prologue to those of

Goldstein, just as Jackson's views anticipated Head's. The

following quotation climaxing Head's great work anticipates

the foundation for Goldstein's organismic approach:

When some act or process
of an organic or functional

is disturbed in consequence
lesion, the abnormal mani-

festations are the result of a fresh integration carried
out by all available portions of the central nervous
system. It is a total reaction of the organism.to the
new situation, in which conscious processes play their

part as a.mode of response.

 

Certain aspects are

3. Head, pp. cit., p. 137.

145
psychical, others are somatic, but there is no separation
of mind and body so long as we are examining the con-
sequences of disintegration.

Thus the three milestones in the psychological approach
are Jackson, Head, and Goldstein. The latter argues against
the study of postmortem findings and advocates instead the
study of living tissue. This insistence--in our present
state of knowledge--would seem to minimize much of the neuro-
logist's findings since we are not yet able to clearly inter-
pret the relationship between a definite anatomic condition
and a specific performance. Indeed, even the psychologist
can say little more than that speech disturbances due to
brain lesions are symptoms of the disturbance of certain
functions or mechanisms.

In disagreement with-~if not in Opposition to--the
psychologist's view are those of Henschen and Nielsen. These
men have insisted on an anatomico-clinbal basis. Indeed,
Henschen went so far as to state that every psychological
activity could be localized, even logical thought.

Although primarily a neurologist, Nielsen is more
cautious.and asks instead for a three-way approach (psycho-
logical, physiological, and anatomical). His work, however,

favors the anatomico-physiologic side. The psychological

side, although slighted, is not denied.

 

4. Ibid., p. 5490

144

At the present time there is no one generally accepted
system.of classifying aphasic disorders. Aphasia can be
classified according to anatomical, physiological, or psycho-
logical schemes. Much of the confusion over terminology has
arisen by the carelessness of various writers in transfering
terms from one frame of reference to another.

Anatomically we could designate aphasia in terms of the
site of the lesions calculated to produce it. Then we could
Speak of frontal, parietal, temporal aphasia, etc. Physio-
logically the aphasias could be classed as motor, sensory,
mixed, or transcortical. The aphasias are also capable of
psychological classifications such as that of Head.

Classifications in each of these frames of reference
have proven unsatisfactory by themselves. Wilson sums up the
dilemma in that "a psychological arrangement has the disadvan-
tage of losing touch with cerebral function, while an anatomico-
physiological arrangement is calculated to introduce an
artificial simplicity into a particularly complex subject and
‘to ignore what must always be its fundamentally significant
side.”5

Perhaps, the words of Henry Head most fittingly describe

and explain the many systems of classification. He remarks

that

 

5. S. A. Kinnier Wilson, "An Introduction to the Study
of Aphasia", The Lancet, 41:2 for 1921:1145, Dec. 5, 1921.

 

145

The tendency to appear exact by disregarding the come
plexity of the factors is an old failing in medical
history. Each patient with a speech defect of cerebral
origin is stretched on the procrustean bed of some
theoretical scheme: something is 10pped away at one part,
Something added at another, until the phenomena are said
to correspond to some diagrammatic conception, which.never
has and never could have existed. And yet neurologists
continue to cling to these schemes, modifying them to
suit each case, conscious that they do not correSp nd in
any way to the facts they are supposed to explain. ”7

However, in the systems of classification that do
exist, there is a quite prevalent agreement on the division of

aphasias into two general categories—-motor or expressive, and

 

sensory or receptive. These both, in turn, have been divided

 

into so-called pure and complex types. There is a third
general division not properly included in these main two
categories. It is the disorder known as amnesic_gphasia or
anomia. In this disturbance the patient has difficulty in
using nouns.

In another sense there also are aphasias on the lower
levels and aphasias on the higher levels. Those on the lower
level are so severe that they are easily recognized. Those
on the higher levels are quantitative rather than qualitative
limits.

The Broca's aphasia (or motor or expressive) is the

 

loss of the power to speak, write, and/or draw, although the

comprehension of writing and speech is relatively retained.

 

6. Henry Head, "Hughlings Jackson on Aphasia and
Kindred Affections of Speech”, Brain, 58:1-2.

146

The motor aphasic is not mentally dull; he is unable to
express himaif by spoken words. He is speechless but not
wordless. (It is assumed that the few words he can utter he
does so by means of the uninjured speech centers in the
Opposite cerebral hemisphere). The defect is believed
attributable to a lesion in the cortex of the left third
frontal convolution, "but it may extend into neighboring
parts of the frontal lobe and even into the insula."7fl$

Various writers have described two varieties of motor
aphasia: the p2£§_(Dejerine) or subcortical (Wernicke), and
the cortical (Wernicke) or true cortical (Dejerine). In the

pure or subcortical variety speech alone is involved. The

 

patient can speak neither spontaneously or by repeating what
he hears, though he understands all that he hears or reads.
"In this form the pathway from the center in the cortex is
blocked although the center itself is intact."8f7This sub-
cortical motor aphasia is frequently found in hysterical
states. "It is likely that it is the mental state and not
the location of the lesion that is important."9hiThis type
is recognized by Goldstein and Kleist, while Marie described

it as anarthria.

7. Andersen, 22. cit., p. 186.
8. Odell, 22, cit., p. 164.

9. Leland B. Alford, "The Mental State Associated
With Cerebral Lesions", Psychosomatic Inedicine, 5:1:16, 1945.

147

The cortical variety--synonymous with Broca's aphasia,

 

Head's verbal aphasia, and Goldstein's central form of mgtgr
aphasia-~13 like the pure type plus a certain loss of co-
ordination of memories of words either spoken or written by
himself. The patient has difficulty in articulation and
retarded, scanty speech. The lesion underlying the sub-
cortical type is "thought to involve not only the third fron-
tal convolution, but a larger area including the neighboring

part of the frontal lobe and the anterior part of the Island."10 '

In transcortical motor aphasia (Wernicke) the patient

 

is usually able to repeat speech and to write from dictation
and to copy, although he cannot speak or write spontaneously.
Although the cortex in the region of the posterior part of the
third frontal convolution may be responsible for this type,
this localization is in great diSpute.

Wernicke's (or sensory or receptive) aphasia is

 

characterized by an inability to understand the spoken or

written word. There are two main divisions of the pure or

 

subcortical forms: auditory aphasia or word-deafness, and

visual aphasia or word-blindness. In auditory aphasia, or

 

 

word-deafness, the patient hears sounds but does not under-
stand Spoken words. -In visual aphasia, or word—blindness (or -

alexia), the patient can see but not understand printed or

10. Weisenburg and McBride, op. cit., p. 60.

148
written characters.

The cortical sensory aphasia (Wernicke's aphasia, or

 

 

Marie's true aphasia) involves defects in speaking and writing

 

in addition to difficulties in the understanding of speech and
reading. He continues to talk even though he may recognize
many errors in his speech. "His volubility seems to be due

more to an inability to cease rather than a press of activity."11 I

The localization of cortical sensory aphasia
is considered to be, roughly, the Wernicke area, the
posterior part of the first temporal convolution together

with the neighboring part of neschl's convolution, the J,
parietal lobe, and the posterior section of the Island."12

Transcortical sensory aphasia is similar to Wernicke's
aphasia except that the power of repetition is retained. In
other words the patient manifests a loss of understanding
although still able to repeat and write to dictation. He
also reads aloud without comprehension.

Total_aphasia is a combination of the symptoms of

 

Broca's aphasia and Wernicke's aphasia. Hence the patient

is speechless apg'wordless, usually with loss of ideation.
Amnesic aphasia (Goldstein, Pick, Heilbronner) is

"difficulty in finding words as names when words and phrases

in certain uses could be evoked more easily and when other

 

ll. Nielsen, pp. cit., p. 69.

12. Weisenburg and McBride, gp. cit., p. 71.

149
language processes remain relatively undisturbed."15J The
patient knows the word he wishes to use but cannot recall it.
He accepts it (but no substitute) as soon as he sees it written
or hears it Spoken. The statement "I know but I can't say it”
expresses the essence of amnesic aphasia. Although there is
a good deal of argument over localizing the lesion underlying
amnesic aphasia, it would seem to be

a lesion of the major posterior temporo-occipital region

or its superior connection.with the rest of the brain

through the temporal isthmus. In terms of the areas of

Brodmann those potent in production of amnesic aphasia

when a lesion occurs in them are the 812%)37 and the

posterior portions of areas 21 and 22. J

In addition to the traditional two-fold classification

of aphasias, with its various subdivisions, there is the four-
way classification of Weisenburg and McBride. These authors
listed expressive, receptive, expressive-receptive, and amnesic
categories. Those which they listed as predominantly
eXpressive showed the most serious disturbancesin expression
in speech or writing. Those predominantly receptive showed
greater deficiency in the receptive processes than in the
eXpressive, and changes in speaking and writing most of which

differ in nature from those in the expressive disorder. The

eXpressive-receptive type showed extreme limitation in speaking

 

13. Ibid., p. 78.

14. J. M. Nielsen, "The Unsolved Problems in Aphasia
III. Amnesic Aphasia", Bulletin 2f the Los Anaeles Neuro-
lqgical Society, 5:84, I940.

 

150
because of defective articulation and word formation. Errors
in spelling and gross changes in word form tion would also
reveal themselves in writing. The amnesics show qualitative
defects by being unable to evoke words as names of objects.

K. Kleist (cited by Weisenburg and Hceride, 1955) has

given us a system of classification which embraces word-sound-

 

Ideafnoss, word-deafness, name-deafness, and sentence-deafness

 

as sensory or receptive disorders. His motor disorders are

divided into sneech-sound-muteness, word-muteness, name-

 

 

muteness, and sentence-muteness.

 

Another set of four major categories is postulated by

Head. These are verbal, nominal, syntactical, and semantic.

 

(See Chapter entitled "Henry Head and Revival of the Psycho-
logical Approach"). His nominal aphasia is evidently the same
as the previously described amnesic aphasia. It is a tendency
to forget names. His verbal aphasia definition quite
accurately fits Broca's aphasia.

Sir James Purves Stewart's comment on Head's new
classification in 1920 would seem to apply equally to several
of the other systems of classification. Commenting on the
fact that each was describing the same thing in different
terminology, Stewart noted that

Dr. Read by a series of ingenious and elaborate tests has
arrived at a new, useful and philos0phical basis of
classifying aphasias. But this does not necessarily mean
that other classifications may not also be correct. Just
as one observer may classify a crowd of people into men,
women and children; whereas another may classify them

them.into Englishmen, Scotsmen, *rishmen, welshmen and
foreigners: or another again into soldiers and civilians.

151
It all depends on the angle from which the facts are
viewed. Dr. Head has Opened a new window into the chamber
of aphasia. But this does not compel us to close up all
the other windows, especially the anatomical and patho-
logical windows, throurh which so much light has been
admitted in the past.

At the present time research on aphasia is dominated
by neurologists who, in general, neglect its psychological
implications. Perhaps symposiums attended by the leading
neurologists and psychologists might aid our understanding
of aphasia as a result of their concerted efforts in
intelligent argumentation and the exchange of ideas.

In closing this study, I cannot help but speculate, as
did the Philadelphia neurologist James Hendrie Lloyed nearly
half a century ago, whether we are attempting to try to make
an anatomical dissection of a complicated psychological
process.16 Since attempts at viewpoints blending psychology,
anatomy and physiology have proven unsuccessful, perhaps we
need to think more along the line delineated by Samuel
Brock17--thet it is a matter of the art, rather than the

science, of knowing when to leave off the one approach and

take up the other.18

 

15. Sir James Purves Stewart, (Discussion on Aphasia),
Brain, 43:455, 1920.

16. James Hendrie Lloyd, "Sensorimotor Aphasia", New
York Medical Journal, 99:916, 1914.

 

 

17. (Samuel Brock:--New York neurologist and psychia-
trist, 1893- - ) '

18. Samuel Brock, "Apraxia and Aphasia”, Bulletin of
the Neurological institute 2; “ew York, 7:3:321, Dec., I938?

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