Aphasia With Nonhemorrhagic Lesions
in the Basal Ganglia and Internal Capsule
Antonio R. Damasio, MD; Hanna Damasio, MD; Matthew Rizzo, MD; Nils Varney, PhD; Frank Gersh, PhD

\s=b\ Atypical

aphasia syndromes

were

associated with circumscribed nonhemorrhagic infarctions of the anterior limb of
the internal capsule and of the striatum, in
the dominant hemisphere. None of the
several cases could be classified in terms
of the classic cortical aphasia syndromes,
nor did they correspond to the description
of aphasia produced by hemorrhage in the
thalamus or putamen. Control subjects
without aphasia had lesions in the same
structures of the nondominant hemisphere, or they had comparably circumscribed damage, which was located lateral or caudal to the previously indicated
locus. The findings raise the question of
participation of the dominant striatum,
and of the connectional systems that
course in the anterior limb of the internal
capsule, in language processing.
(Arch Neurol 1982;39:15-20)

rphe mostof frequentlyhaveencountered
been de¬
types

aphasia

scribed in association with pathologic
loci in the cerebral cortex. Despite
some variability in the cortical and
subcortical extension of the lesions,
the association has been verified
repeatedly, and the resulting anatomicoclinical correlation has been well
established.1- Yet, many cases of
aphasia deviate significantly from
those classic types, and the manner in
which the several language and motor
defects combine render them virtually
unclassifiable. Many such cases have
See also

2.

been traced to hemorrhagic lesions in
the thalamus or in the putamen, but
the lack of autopsy studies and the
nature of hemorrhagic lesions have
not permitted the thorough investiga¬
tion of the anatomic loci that are
possibly correlated with those atypical
aphasias. But now, computed tomog¬
raphy (CT) is permitting a more
extensive, albeit preliminary, apAccepted for publication April 20, 1981.
From the Department of Neurology (Division
of Behavioral Neurology), University of Iowa
College of Medicine, Iowa City.
Reprint requests to Department of Neurology,
University of Iowa Hospitals and Clinics, Iowa
City, IA 52242 (Dr A. R. Damasio).

proach to the problem. We report sev¬
eral cases of atypical aphasia that
appeared in relation to nonhemorrhagic lesions in the left basal ganglia
(neostriatum) and in the left internal

capsule (anterior limb), and contrast
these cases with appropriate control
cases.

PATIENTS AND METHODS
Six cases of atypical aphasia and five
cases of speech disturbance without apha¬
sia attracted our attention by virtue of the
unusually located lesion observed in their
CT scans: the lesion was located in the
basal ganglia and internal capsule. The
purpose of this study is to compare both the
clinical characteristics and the CT scan
correlates of the cases of atypical aphasia
with control cases without aphasia. The six
cases of atypical aphasia could not be clas¬
sified according to the Boston Diagnostic
Classification. Computed tomography
showed lesions in the left basal ganglia and
the left internal capsule in all cases. The
five patients who did not have aphasia had
dysarthria or dysprosody. Their CT scans
showed lesions in approximately the same
sites in the right hemisphere or in nearby
but different sites of the left hemisphere.
The cases were studied in the Depart¬
ment of Neurology, University of Iowa
College of Medicine, Iowa City, between
1976 and 1980. (Since the conclusion of this
study, four additional cases have come to
our attention with clinical characteristics
and CT scan findings comparable with
the ones reported here.) All patients had
nonhemorrhagic infarctions. All patients
received a comprehensive neuropsychologic
examination, which included the Multilin¬
gual Aphasia Examination.' Localization
of lesions was obtained by plotting the
pertinent CT scan cuts in templates of the
appropriate cerebral sections.

REPORT OF CASES
Case 1.—Aphasia and right hemiparesis
developed suddenly in a 55-year-old righthanded man in June 1979. Speech was

dysarthric, dysprosodic, effortful, and nonfluent with frequent semantic paraphasias.
Articulation improved steadily and was
almost normal by early 1980. Fluency
improved too, and the patient became able
to use four- to six-word sentences. Nev¬

ertheless, he was still nonfluent, and there
were still occasional semantic paraphasias.
Aural and reading comprehension were
severely impaired at first but improved

within a month and have been normal since
September 1979. Writing with the left
hand was intact. Visual naming of line

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drawings was severely impaired, but per¬

formance was slightly better with threedimensional objects. Verbal repetition was
severely impaired initially but became
normal within a month. Gestural praxis on
verbal command was defective, while
affect and nonverbal cognitive abilities
were intact. Strength improved but at a
slower pace than language. By April 1980,
there was only moderate weakness of the

right arm.

The presence of nonfluent speech, defec¬
tive repetition, and a right hemiparesis
suggested Broca's aphasia. Yet, the degree
of defective aural comprehension and of
semantic paraphasias brought to mind
Wernicke's or transcortical sensory apha¬
sia (but defective repetition would be com¬
patible with the former and not the latter).
The case did not fit any of the classic

syndromes.

In the CT scan (Fig 1), there was an area
of decreased density in the depth of the
left hemisphere. It involved the white mat¬
ter lateral to the body of the caudate
nucleus (and in all likelihood part of the
body itself) and extended, anteriorly and
inferiorly, into the area lateral to the tip of
the frontal horn of the lateral ventricle.
Case 2.-Acute aphasia and right hemi¬
paresis developed in a 53-year-old righthanded man in September 1979. Initially,
there was fluent speech with normal artic¬
ulation and semantic, phonemic, and neologistic paraphasias. Phonemic and neolo-

gistic paraphasias gradually disappeared.
By April 1980, speech remained fluent with
occasional semantic paraphasias and some
word-finding difficulty. Aural and reading
comprehension were severely defective at
first but were almost normal eight months
after onset. Verbal repetition was also
severely impaired but improved within
eight months. Writing was disturbed at the
first examination, with profuse neologistic
paragraphias. By April 1980, writing had
improved, but spelling was poor (this had
not been present before the disease). Prax¬

is, attention, and memory were always
intact. Weakness, which had been particu¬
larly severe in the upper extremity,
improved but reduced swinging of the
right arm remained. The patient's condi¬
tion resembled Wernicke's aphasia and, for
a while, as comprehension improved at a

speedier rate than repetition, it suggested
conduction aphasia. Yet, the presence of a
severe hemiparesis is unusual in Wer¬
nicke's aphasia.
In the CT scan (Fig 2), there was an area
of decreased density in the depth of the
left hemisphere. It involved part of the

anterior limb of the internal capsule and
extended into the white matter lateral to

Fig 1.—Computed tomographic scan (case 1) shows area of
decreased density in depth of left hemisphere.

the body of the caudate nucleus. There was
involvement of the putamen and, to some
extent, of the head of the caudate nucleus.
In comparison with case 1, the lesion
appeared to involve a lesser portion of the
caudate nucleus and to extend more anteri¬
orly in the capsule and frontal white mat¬
ter. Conceivably, small anatomic differ¬
ences might account for the major clinical
feature that distinguishes these two cases;
nonfluent speech in case 1 and fluent
speech in case 2.
Case 3.—Acute aphasia and paralysis of
the right upper extremity and right side of
the face developed in a 63-year-old righthanded man in March 1980. He became
severely hoarse and spoke in a whisper.
Speech was dysarthric and nonfluent with
frequent pauses for word finding with
circumlocutions. There were occasional
semantic paraphasias, but the speech did
not seem agrammatic. Aural and reading
comprehension were normal and so was
repetition. Writing was impaired with
semantic paraphasias. Visual naming of
drawings and objects was normal. Gestural
and buccofacial praxes to verbal command
were normal. Affect and nonverbal cogni¬
tive function were intact. Three months
later, there was some improvement in word
finding with less semantic paraphasias,
but there was persistent dysarthria and
hoarseness.
Nonfluent speech accompanied by right
hemiparesis suggests Broca's aphasia.
However, this patient's ability to repeat
words was intact. Hoarseness, hypophonia,
and severe dysarthria would be unusual in
Broca's or transcortical motor aphasia. No
classic syndrome fitted this patient's con¬
dition.

Fig 2.—Computed tomographic scan (case 2) shows area of

decreased density in depth of left hemisphere.

The CT scan (Fig 3) showed an area of
decreased density in the depth of the left
hemisphere. It involved most of the anteri¬
or limb of the internal capsule and the
white matter lateral to the body of the
caudate nucleus and of the head and body
of the caudate nucleus. There was some
involvement of the anterior and superior
aspects of the putamen. The area of
increased density in the anterior and
superior aspects of the putamen corre¬
sponded to gray matter enhancement
caused by injection of contrast material. In
comparison with case 2, it seems that the
involvement of the capsule was more
extensive, while that of the striatum was
possibly less.
Case 4.—Acute aphasia and right hemi¬
paresis developed in a 63-year-old righthanded woman in October 1979. The arm
was completely paralyzed and flaccid. Ar¬
ticulation was defective, but prosody
appeared normal. Speech was nonfluent
with profuse phonemic paraphasias; yet,
the patient spoke spontaneously and was
obviously intent on communicating. Aural
and reading comprehension were defec¬
tive. Repetition was severely defective.
The patient was unable to write. There
seemed to be neglect of the right hemispace. Yet, gestural praxis with the left
hand was preserved. She was able to hum
melodies in tune by following the examin¬
er. No improvement was noted in a nursing
home where the patient died six months
later. An autopsy was not performed.
The patient's speech resembled that of
early Broca's aphasia. Yet, the defect of
comprehension and the profusion of para¬
phasias recalled a severe fluent aphasia.
The degree of right-sided paralysis was

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typical of neither and was of the kind most
frequently seen in severe global aphasia,
but the characteristics of speech in such
cases

do not resemble

patient.

those of this

The CT scan (Fig 4) showed a large area
of decreased density in the depth of the
left hemisphere. It involved the head and
the anterior portion of the body of the
caudate nucleus, all of the anterior limb of
the internal capsule and its genu, white
matter lateral to the body of the caudate
nucleus, and a large amount of the anterior
and superior aspects of the putamen.
Case 5.—A 34-year-old right-handed man
experienced the sudden onset of right hem¬
iplegia and aphasia in 1976. Four years
later, severe paralysis of the right upper
extremity persisted, and there was mild
weakness of the right lower extremity and
right side of the face. Initially, there was
nonfluent speech with dysarthria and both
phonemic and semantic paraphasias. Grad¬
ually, fluency improved, but there was still
some word-finding difficulty, both subjec¬
tively and objectively. Aural comprehen¬
sion initially had been impaired and cur¬
rently was normal. Yet, the patient
reported serious difficulties in compre¬
hending multiple conversations or conver¬
sations on the telephone. Background noise
and accents, eg, foreign and Southern, to
which he was unaccustomed, impaired his
comprehension (the patient was a native
English speaker and had no such difficulty
before his illness). Repetition of sentences
had been severely impaired but was now
normal. Writing had been severely im¬
paired with both phonemic and semantic
paraphasias. Currently, there were occa¬
sional spelling mistakes that the patient

Fig 3.—Computed tomographic scan (case 3) shows area of

decreased density in depth of left hemisphere.

Fig 4.—Computed tomographic scan (case 4) shows large area of
decreased density in depth of left hemisphere.

Fig 5.—Computed tomographic scan (case
5) shows area of decreased density in
depth of left hemisphere.

did not make before his disease. Praxis,
attention, and general memory function
were always intact. The problems of clas¬

sification of this syndrome were similar to
those described for patient 1.
The CT scan (Fig 5) demonstrated an
area of decreased density in the depth of
the left hemisphere. It involved the head
and the body of the caudate nucleus, most
of the anterior limb of the internal capsule,
as well as the white matter lateral to the
body of the caudate nucleus, and the puta¬
men. Both the left frontal horn and the left
insular region were retracted toward the
lesion, producing a small degree of hydrocephalus ex vacuo and enlargement of the
Sylvian fissure.
Case 6.-A 19-year-old right-handed man
suffered an acute right hemiparesis and
aphasia in December 1978, after trauma to
the left carotid artery while he was wres¬
tling. Speech was dysarthric and nonfluent
with semantic and phonemic paraphasias.
There was impaired aural and reading
comprehension. Repetition was normal.
Visual naming was defective with frequent
paraphasic responses. There was remark¬
able improvement of all aspects of lan¬
guage, but speech remained dysarthric and

nonfluent, with word-finding difficulties.

Hemiparesis improved rapidly. One year
later, only mild facial weakness re¬

mained.
The presence of nonfluent speech, defec¬
tive aural comprehension, and normal repe¬
tition suggested a complex transcortieal
aphasia of the type described as isolation
of the speech area. However, the high level
of nonlinguistic cognitive behavior was not
compatible with that diagnosis, and the
dysarthria and the extensive right hemi¬
paresis are not common with border-zone
infarcts. One year after onset, the residual
disability in the patient's speech best
resembled a recovered Broca's aphasia.
The CT scan showed an area of
decreased density in the depth of the left
hemisphere. It involved the most anterior
portion of both the head of the caudate
nucleus and the anterior limb of the inter¬
nal capsule, as well as the anterior and
superior aspects of the putamen.
Case 7.-A 46-year-old right-handed man
experienced right hemiparesis and dysar¬
thria that started abruptly in December
1978. The upper extremity was severely
involved and remained paralyzed three
months after onset, while weakness of the

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face and lower extremity had improved.
Dysarthria persisted. Extensive testing
disclosed all verbal and nonverbal perform¬
ances to be normal.
The CT scan (Fig 6) showed a small area
of increased density (caused by contrast
enhancement) in the midportion of the
body of the caudate nucleus, adjacent
white matter in the corona radiata, and
medial aspect of the putamen.
Case 8.—A 55-year-old left-handed man
suffered acute onset of speech disturbance
and right hemiparesis in October 1979.
Articulation was normal, but prosody was
severely disturbed. There was abnormal
prolongation of vowel sounds that, in
effect, produced musical tones and con¬
ferred to speech an unusual melodic con¬
tour. This could be heard even on singleword utterances, and it was equally intense
in all forms of speech production, including
reading aloud and actual singing. Other¬
wise, speech was fluent and without para¬
phasias. Aural comprehension reading,
repetition, and writing were entirely
normal.
The CT scan (Fig 7) demonstrated a
round area of decreased density that
involved the anterior and lateral aspects of

Fig 6.—Computed tomographic scan (case
7) shows small area of increased density.

Fig 7.—Computed tomographic scan (case
8) shows round area of decreased density
involving anterior and lateral aspects of
left putamen.

Fig 8.—Computed tomographic scan (case
10) shows area of decreased density in

depth of right hemisphere.

the left putamen.
Case 9.-Left hemiparesis and a mild
confusional syndrome developed suddenly
in a 24-year-old right-handed woman in
July 1976. Confusion cleared, and speech,
though fluent, was poorly articulated. Lan¬
guage was otherwise normal, and exten¬
sive testing produced no evidence of apha¬
sia. The paresis improved rapidly, and in
October 1976, only mild flatness of the left
side of the face remained. Articulation had
improved as well, although it had not
returned to normal.
The CT scan (Fig 8) showed a large area
of decreased density in the depth of the
right hemisphere. It involved the head of
the caudate nucleus, most of the anterior
limb of the internal capsule, and the ante¬
rior and superior aspects of the putamen.
Case 10.—Mild confusion, speech disturb¬
ance, and left hemiparesis developed sud¬
denly in a 60-year-old right-handed woman
in September 1978. Confusion cleared, but
speech remained dysarthric and dysprosodic. Left hemiparesis persisted. Language
was otherwise normal, and extensive test¬
ing showed no evidence of aphasia. There
was neglect of the left hemispace that
cleared in two weeks.

The CT scan (Fig 9) disclosed an ovalshaped area of decreased density in the
depth of the right hemisphere that
involved a small portion of the head and
body of the caudate nucleus, the putamen,
the anterior limb of the internal capsule,
and a fraction of the posterior limb, spar¬
ing the genu.
Case 11.—An 82-year-old right-handed
man suddenly became mute with left hem¬
iparesis in July 1980. As the patient
regained the ability to speak, on the second
day, dysarthria was noted. Language was
entirely normal. There was neglect of the
left hemispace.
The CT scan showed a large area of
decreased density in the depth of the right
hemisphere that involved the head and
body of the caudate nucleus, the anterior
limb of the internal capsule, the white
matter lateral to the body of the caudate
nucleus, and the putamen.
RESULTS
Nature of Lesions

On the basis of clinical characteris¬
tics and CT scan appearance, all
lesions were produced by nonhemor-

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rhagic deep infarction. Considering

the maximal vertical and horizontal
diameters of each lesion, it seems
that, in all but two cases (cases 7 and
8), the lesions were too large to be
classified as lacunar. Interestingly,
patients 7 and 8 did not have aphasia.
Also of interest is the fact that only
two patients had a history of systemic
hypertension (patients 1 and 7.)
Localization of Lesions

In all but two cases, the lesion con¬

sistently involved three structures: (1)

the anterior limb of the internal cap¬
sule, (2) the head of the caudate
nucleus, and (3) the putamen (Fig 10).
In some of the cases, most of the
anterior limb of the internal capsule
and the superior aspect of the head of
the caudate were involved (cases 4 and
5), while in other cases, the compro¬
mise was more limited (cases 1
through 3 and 6). The involvement of
the putamen was almost always lim¬
ited to its anterior and superior

nearly resembled those described in
thalamic and putaminal hemorrhage,
in itself, a rather heterogenous group;
however, there were substantial dif¬

ferences since these patients did not
exhibit significant disturbances of
attention or memory.

Prefrontal
Cortex
Premotor
Cortex

Conclusion

Our results can be summarized as
follows.
1. Right-handed patients with leftsided lesions that involve the anterior
limb of the capsule, the head of the
caudate, and the putamen had apha¬

sia, right hemiparesis, and, often,

>
MO

Auditory
Association
Cortex

V

Pontine Nuclei

dysarthria and dysprosody.
2. A right-handed patient with a

lesion that failed to involve the pre¬
viously mentioned areas but did com¬
promise more posterior aspects of the
internal capsule, corona radiata, cau¬
date nucleus, and putamen had dysar¬
thria and right hemiparesis but no

aphasia.
3. Right-handed
patients with
right-hemisphere lesions, involving
the anterior limb of the capsule, head

of the caudate, and putamen had
dysarthria and left hemiparesis but no

aphasia.

COMMENT

Fig 9.—Major pathways traveling in anterior limb of internal capsule. CA indicates
caudate nucleus; PU, putamen; GP, globus pallidus; MD, medialis dorsalis; and VA,
ventralis anterior.

aspects. The pallidum did not seem to

be involved. The posterior limb of the
capsule was involved in only one of the
right-hemisphere cases without apha¬
sia. Judging from the affected area,
these lesions fall in the territory of the
lateral lenticulostriate branches of the
middle cerebral artery, thereby spar¬
ing the usual territory of the medial
lenticulostriate artery, eg, the palli¬
dum, as well as the territory of
Heubner's artery, eg, the lower aspect
of the head of the caudate nucleus and
its junction with the putamen.
Cases 7 and 8 were exceptional in
relation to the size of the lesions. The
lesion in case 7 failed to involve both
the anterior limb of the capsule and
the head of the caudate nucleus. How¬
ever, fibers in the corona radiata, en
route to the genu and posterior limb of
the capsule, were most certainlyinvolved along with a small portion of
the body of the caudate nucleus and of
the putamen. As noted previously, this
was in all likelihood a lacunar infarc¬
tion that produced hemiparesis and
dysarthria. The lesion in case 8 was
predominantly in the putamen. The
fact that the patient was left handed
limits the significance of the interest-

ing syndrome of dysprosody without
aphasia, which resulted from this
lesion.

Aphasias
Given the small number of cases, it
does not seem prudent to constitute
different syndromes on the basis of
the clinical variation exhibited in this
sample. This is not to deny that there
may be indeed different syndromes or
that a small anatomic deviation could
not be responsible for such differ¬
ences. But our data do not allow those
correlations.
On the other hand, the cases did
share some of the following distin¬
guishing features: (1) Dysarthria oc¬
curred in most cases, independently of
the degree of fluency and often
accompanied by dysprosody. (2) Hemi¬
paresis occurred in all cases. (3) Gestu¬
ral praxis on verbal command was
intact in most cases. (4) Recovery of
aphasie symptoms tended to occur
rapidly and preceded recovery of
motor disturbances.
The unusual clustering of symptoms
and the pattern of recovery precluded
categorization into the classic aphasia
syndromes. In general, the cases more

It is well accepted that subcortical
lesions can produce aphasia. Thus, at
least some cases of conduction and
transcortical aphasia are associated
with purely white-matter lesions/"
while atypical aphasie disturbances
have been noted after hemorrhage in
the thalamus7-* or in the putamen.""1
The pathologic nature of the latter
(substantial size of most hemorrhages,
mass effect, overriding of nuclear
gray masses, and surrounding white
matter) renders the interpretation of
the anatomicoclinical correlations
problematic. Most such patients have
important disturbances of attention
and memory in addition to aphasia,
which raises the question whether the
linguistic disorder is primary or sec¬
ondary to a nonverbal cognitive
defect.
The cases that we have reported in
this article help answer some of those
questions, given the limited size and
the nonhemorrhagic nature of the
lesions. These cases suggest that there
is a powerful association between
aphasia and a well-circumscribed ana¬
tomic region: the anterior limb of the
internal capsule and both the head of
the caudate nucleus and the anterior
aspect of the putamen. Lesions anteri¬
or to that locus, located in the depth of
frontal white matter, outside the
striatum, and rostral to the anterior

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limb of the capsule, produce transcor¬
tical motor aphasia (A. Galaburda,
MD, oral and written communications,
October 1980 and April 1981)."
Lesions that are located caudally to
that crucial locus, eg, in the genu and
posterior limb of the capsule, and in
the corona radiata immediately above
those structures, produce motor dis¬
turbances (affecting speech and con¬
tralateral movement) but not aphasia.
Lesions in a symmetric locus of the
right hemisphere produce motor dis¬
turbances (dysarthria and left hemi¬
paresis) but not aphasia. Some sup¬
port for these preliminary findings
comes from a study by Naeser and
associates (see 2) who have reported
cases of atypical aphasia in relation to
infarcts of the basal ganglia and cap¬
sule. Although several clinical and
anatomic features may be compara¬
ble, the lesions described by Naeser et
al appear to be much larger than the
lesions found in our study. In some
cases, the lesions extend into the tem¬
poral isthmus, well outside the deep
cerebral region that we are consider¬
ing here, and closer to the subcortical
white matter, which has been impli¬
cated classically in aphasia.
In all of the cases in our study, the
lesion was astride a major white-mat¬
ter funnel (anterior limb of the cap¬
sule) and major gray-matter nuclei
(caudate nucleus and putamen). In all
cases, then, the interpretation of the
several manifestations can be pro¬
posed by reference to (1) disconnec¬
tion of important fiber pathways, (2)
damage to gray-matter neuronal
operators, or (3) both. The interpreta¬
tion should take into account modern
concepts of structure and function of
both the anterior limb of the capsule
and the striatum.
The striatum is no longer regarded
as
a
pure motor structure that
mediates a collateral aspect of the
generation of movement. Rather, the
striatum receives input from all the
major sensory, suprasensory (multimodal), and limbic areas of the cere¬
bral cortex and is a high-level integra¬
tive organ. Input to the striatum is
highly patterned. For instance, areas
of the cerebral cortex that are recipro¬
cally connected by corticocortical
pathways project, in part, to the same
region of the caudate nucleus'-'; how¬
ever, projections from sensory areas
approach the caudate along its entire
length, and most enter the nucleus at
its head.1- The caudate nucleus and
putamen receive different preponder¬
ant projections, visual and auditory
mainly to the former, sensorimotor to
the latter.11-1· Practically all of the

striatal output is aimed at the palli¬
dum in which output is to the "motor
thalamus," which in turn projects

preferentially to the premotor, Rolandic, and somatosensory cortices, there¬
by closing one of the two reentrant

motor circuits.1"17 The striatum is
clearly a principal programmer of
movement in relation to ongoing mul¬

timodal perception and imagery and,
in all likelihood, also plays a role in the
organization of perception.,y~-" Dam¬
age to the striatum produces dyspros¬
ody and conceivably could produce
dysarthria. But it could also disrupt
language decoding and encoding, dis¬
turbing aural comprehension and giv¬
ing rise to paraphasias.
On the other hand, the anterior limb
of the capsule carries, among others,
the following major fiber systems: (1)
projections from the frontal cortex to
the pons,-1 (2) projections from the
auditory cortex to the head of the
caudate nucleus,--' (3) projections from
the motor thalamus to the frontal
premotor cortex,-1' (4) projections from
the head of the caudate nucleus
toward the pallidum, and (5) projec¬
tions from the mediodorsal thalamus
to the prefrontal cortex-' (Fig 10).
Damage to the first four systems
could contribute to the disturbances
that were seen in the patients in our
study, in different ways: by producing
dysarthria (systems 1, 3, and 4), and
by producing paraphasias and aural
comprehension defects (system 2).
The final clarification of which com¬
ponent results from white-matter dis¬
connection or gray-matter damage
depends on the ultimate but unlikely
discovery of a lesion exclusive to the
anterior limb of the capsule, to the
head of the caudate nucleus, or to the

putamen.

The interpretation of our findings
rests on the assumption that the
lesions were confined to the abnormal
areas that were seen in CT scans and
that there were no concomitant
lesions in cortical areas. In the
absence of pathologic verification,
such an assumption depended on criti¬
cal judgment of the images and con¬
sideration of the nature of lesions.
The quality of the images was satis¬
factory. The lesions were all located
deeply, far away from cortex, and
there were no suspect cortical areas.
The possibility of cortical lesions
smaller than the resolution of the CT
scanner is undeniable. Yet, it is
unlikely that such a small lesion could
produce the type and severity of
aphasie symptoms described in the
present study. Be that as it may, we
offer our preliminary findings in the

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hope that, by calling attention to the
problem, the necessary pathologic con¬
firmation will soon take place.
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