Aphasia Resulting From Occlusion
of the Left Anterior Cerebral Artery
Report of a Case With an Old Infarct in the Left Rolandic Region
Anis Racy, MD; Frank S. Jannotta, MD; Leslie H. Lehner, MS

\s=b\ A

62-year-old right-handed woman

was admitted to the

hospital with a cere-

brovascular accident in the left hemi-

sphere. She was aphasic as well as hemiplegic on the right. She had had a left

cerebrovascular accident 18 years earlier
that caused weakness in the right hand,
but no grossly detectable speech problems. Autopsy disclosed an old infarct
along the left Rolandic area, and a recent
infarct in the territory of the left anterior
cerebral artery. The clinical picture and
pathologic changes are discussed in an
attempt to relate the findings at autopsy to
the recently developed aphasia.
(Arch Neurol 36:221-224, 1979)

phasia as the result of injury to the
portion of the left frontal
lobe is a recognized syndrome.12 Char¬
acteristically, patients suffering from
"^ mesial

such a lesion show very poor sponta¬
neous speech output with preservation
of comprehension and repetition,
namely a transcortical motor aphasia.
On the other hand, a lesion involving
the left peri-Rolandic operculum
leads to a conduction aphasia,3 also
referred to as central aphasia, charac¬
terized by poor repetition in the face
of preserved comprehension and spon¬
taneous speech. The basis for the find¬
ings in conduction aphasia is pre¬
sumed to be interruption of the
arcuate fasciculus linking receptive to
motor speech areas. Recovery is
conceivable if connection between the
sensory and motor areas for speech is
reestablished via transcallosal path¬

had an old infarct in the left Rolandic
area showed no apparent communica¬
tion deficit when reexamined years
later, but became suddenly aphasie
from a recent infarct within the
distribution of the left anterior cere¬
bral artery.
REPORT OF A CASE
A 62-year-old right-handed woman was

admitted to George Washington Universi¬
ty Hospital, Washington, DC, on Oct 10,
1975, with right hemiplegia and aphasia.
She had been followed up at the hospital's
outpatient clinic for diabetes mellitus,
hypertension, and chronic heart failure. In
1957, she had suffered a stroke with right
hemiparesis followed by a relatively good
recovery. Details of that event are not
available, but she resumed an independent
life. A neurological examination in 1971
disclosed right-sided hyperreflexia with
weakness, especially in the arm, and rightsided hemisensory impairment to touch,
position, and vibration. She could walk
unassisted and had no apparent communi¬
cation deficit. Three days prior to admis¬
sion, she was seen in the clinic because of
increasing shortness of breath. Again, no

language deficit was observed. On the eve
of her admission, she complained of
nausea. The next morning, awakening, she
was unable to converse or to move her right

extremities.
Blood pressure was 130/60 mm Hg, with
a pulse rate of 60 beats per minute, and a
respiratory rate of 20/min. The lungs were
clear, and cardiac examination showed
increase in heart size, with a systolic
murmur. Results of the remainder of the
examination, except for the neurological
findings, were unremarkable.
Neurological examination disclosed an
alert woman with a profound speech
defect, who perseverated in her speech and
could not utter meaningful sentences. She
was unable to follow simple commands. She
had a right-sided hemiplegia, with hyper¬
reflexia of 3 + /4 compared to 2 + /4 on the
left side. A questionable right Babinski's
sign was described. The visual fields were
grossly intact. She was incontinent of
urine.
A complete blood cell count showed
normal hematocrit and hemoglobin levels,
a normal platelet count, and a WBC count
of 11.3 x lOVcu mm, with 80% neutrophils.
Prothrombin time and partial thromboplastin time were normal. Urinalysis

Fig 1 .—Reconstructed external view of left cerebrum, showing collapse of postcentral
gyrus and preservation of frontal and temporal areas.

ways.

In this case report, a patient who

Accepted for publication May 17, 1978.
From the Departments of Neurology (Dr Racy)
and Pathology (Dr Jannotta) and the Division of
Rehabilitation, Department of Medicine (Ms
Lehner), George Washington University Medical
Center, Washington, DC.
Reprint requests to Department of Neurology,

George Washington University Medical School
and Health Center, 2150 Pennsylvania Ave NW,
Washington, DC 20037 (Dr Racy).

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Fig 2.—Horizontal section of cerebrum,
showing recent infarct involving· corpus
callosum in region of genu and rostrum, as
well as adjacent mesial frontal lobe, with
preservations of Broca's and temporal
areas (top view).
showed 3+ sugar. Serum glucose level
varied between 268 and 516 mg/dl. The
electrolyte values were normal, the BUN
level was 15 mg/dl, and creatine level 1.0
mg/dl. Serum cholesterol level was 377
mg/dl. Chest roentgenograms were nor¬
mal. The ECG showed sinus bradycardia
(55 beats per minute). Thyroid function
studies gave normal findings.
One week following admission, the
patient underwent a formal language eval¬
uation. Her blood pressure was well
controlled and there was no evidence of
increasing cardiac failure. Her diabetes
was difficult to control. She died suddenly
on Oct 27, 1975. A complete autopsy was

performed.

Fig 3.—Photograph (top) and diagram (bottom) of complete set of horizontal slices of

Aphasia Testing
The Boston Diagnostic Aphasia Exami¬
nation was administered one week after
her most recent stroke. She was alert and
responsive throughout the evaluation, but
made few attempts to initiate conversa¬
tion. Her verbal output was nonfluent even
when she was asked to repeat words or
phrases. Considerable perseveration was
noted. Groping was evident before she
spoke, but all speech was clearly articu¬
lated, without any paraphasic errors. She
had difficulty executing voluntary oral
movements, particularly lateral and up¬
ward movement of the tongue.
She was able to correctly identify most
pictures of objects and geometric figures
and to point to body parts when named, but
she had great difficulty in recalling the
names herself. She had difficulty associat¬
ing actions depicted in pictures, such as
"running" and "smoking," when the word
for that action was furnished by the exam¬
iner. She did carry out simple commands
such as "make a fist" and "point to the
ceiling," but could not go beyond the first
part of multiple-step commands. She also

cerebrum, showing location and extent of both recent (hatched) and healed (stippled)
infarcts in left hemisphere.

showed left-right disorientation. When
given a series of questions requiring a
yes-no answer, she perseverated in saying
"yes" to all questions such as "Is a hammer
good for cutting wood?" or "Will a board

sink in water?"
She managed to complete the nursery
rhymes given to her, such as "Jack and
Jill..." and "There was an old woman who
lived in a shoe ...." She could correctly
repeat short phrases such as "you know
how," "down to earth," and "go ahead and
do it if possible," but failed on longer
sentences such as "They heard him speak
on the radio last night." When asked to
complete a series such as the days of the
week, the alphabet, or numbers from 1 to
20, she perseverated on one day, one letter,
or one number. She could correctly asso¬
ciate most letters or words written in
different scripts. When shown a series of
words to associate with verbal counter¬
parts, she made the correct choice in 60% of
them. Despite her ability to pick out words,

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she could not understand written words or
sentences. She could not read aloud. When
asked to write, she managed to correctly
scribble her first name, using the left hand,
but further testing had to be abandoned
because of fatigue and frustration.

Autopsy Findings
The fresh brain weighed 1,150 g. The
dura and sinuses were unremarkable.
External examination of the fixed brain
disclosed symmetrical cerebellar hemi¬
spheres; thin and translucent leptomeninges; normal cerebral veins; scattered
atheromata of the large arteries with
moderate narrowing of the lumina; and an
almost complete occlusion of the left
middle cerebral artery near its origin. An
occlusion in the anterior cerebral arteries
could not be found. A slightly swollen and
softened cortex was found in the mesial
and parasagittal area of the left frontal
lobe, extending from near the frontal pole
back to the level of the central sulcus. The

LEFT

Notwithstanding the fact that a
detailed description of the aphasia is
lacking in the majority of these

RIGHT

reports, it is difficult to estimate the

Fig 4.—Schematic diagram advanced to explain disconnection of receptive from
expressive speech areas. X indicates lesions interrupting arcuate fasciculus and corpus
callosum (modified from Geschwind").
left postcentral gyrus showed collapse and
softening extending from the Sylvian
fissure up over the convexity to within 2
cm of the midline. The left inferior frontal
gyrus (Broca's area), the left angular and
supramarginal gyri, and the left temporal
lobe including the planum temporale were
normal (Fig 1).
Multiple horizontal sections of the fixed
brain showed recent necrosis with coagula¬
tive softening, slight swelling, and punc¬
tate hemorrhages, involving parasagittal

and mesial portions of the left frontal lobe
within the distribution of the left anterior
cerebral artery; the area of necrosis
extended from near the frontal pole back
to the central sulcus, and included cortex as
well as subjacent white matter to a maxi¬
mal depth of approximately 2.5 cm, not
quite reaching the mediolateral midpoint
of the left hemisphere itself. Broca's area
with its subjacent white matter was not
involved (Fig 2). This recent necrosis
extended to include adjacent portions of
the left side of the rostrum, genu, and
anterior parts of the body of the corpus
callosum (Fig 2). Microscopic sections from
this region showed recent coagulative
necrosis of all tissue elements with punc¬
tate perivascular hemorrhages, scattered
gitter cells, rarefaction of neuropile, and a
narrow rim of slight astrogliosis, consis¬
tent with a stage of evolution of approxi¬
mately two to three weeks. The horizontal
sections also displayed cystic rarefaction
and collapse of the left postcentral gyrus,
resulting in virtual disappearance of this
gyrus through most of its extent; this
cystic destruction extended into subjacent
parietal white matter, involving extensive¬
ly the region of the arcuate fasciculus as
well as undercutting portions of the left
precentrai gyrus. The angular and supramarginal gyri with their subjacent white
matter were intact, as was the temporal

lobe (Fig 2). Microscopic sections from this
region showed the healed endstage of an
old infarct, with disappearance, collapse,
and cystic formation of neural parenchy¬
ma, a few remaining gitter cells, and
surrounding astrogliosis, consistent with a

stage of evolution of many years.

The location and extent of both infarcts
is shown in the diagram and photograph of
the complete set of horizontal brain slices

(Fig 3).

Other neuropathologic features included
almost complete stenosis of the left middle
cerebral artery by atheroma, and atrophy
of the left corticospinal tracts in the brain
stem.

Other autopsy findings included marked
coronary and aortic atherosclerosis; recent
and healed subendocardial myocardial in¬

farcts; multiple, bilateral pulmonary em¬
boli; and a hemorrhagic cyst of the right

thyroid.

In summary, the final neuropathologic
diagnoses were as follows: recent infarct of

the left cerebrum, in the distribution of the
anterior cerebral artery, involving mesial
and parasagittal frontal lobe and anterior
corpus callosum; healed infarct within the
territory of the middle cerebral artery,
involving postcentral gyrus and subjacent
white matter including arcuate fasciculus
and white matter subjacent to the precentral gyrus; and marked atherosclerosis of
intracranial arteries. Noteworthy is the
preservation in the left hemisphere of
Broca's area, Wernicke's area, and other
parts of the temporal lobe.
COMMENT

Most reported cases of aphasia
resulting from damage to the mesial

part of the left frontal lobe have been
caused by tumors,'-2'4"8 with improve¬
ment in many following excision.

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effects of edema and displacement of
brain tissue by a neoplasm. Thus,
some of Cushing's patients, reported
by Chusid et al,4 showed dysnomia,
dyslexia, dyscalculia, and even recep¬
tive aphasia (case R-B), while others
had difficulty only in initiation of
spontaneous speech. Reports of pa¬
tients with dysphasia due to occlusion
of the left anterior cerebral artery are
relatively few.1,2·9"12 Most cases in the
older literature also lack details of the
aphasie syndrome. Most recently,
Kyòrney1 described three patients
with pathologic confirmation of occlu¬
sion of the anterior cerebral artery.
The first was a 71-year-old woman
who survived for 12 days after her
stroke. Her speech output was re¬
duced, but she demonstrated pro¬
nounced echolalia even without com¬
prehending the content of what she
said and could repeat long sentences
with verbal and prosodie fidelity. At
autopsy, in addition to the above
mentioned infarct, there were three
small areas of softening deep in the
white matter of the left hemisphere.
The second patient was a 64-year-old
woman who had a left hemianopsia,
then developed a right hemiplegia
with global aphasia. At autopsy, her
brain showed occlusion of the left
anterior cerebral artery as well as old
infarcts in both occipital lobes. Pa¬
tient 3 was a 61-year-old man who
developed a right hemiplegia of sud¬
den onset with bilateral long tract
signs and an expressive dysphasia
with preservation of repetition and
comprehension. He could name objects
put in his left hand but not the right.
He showed a strong tendency to
repeat whatever was said to him.
Eighteen months later, a right homonymous hemianopsia developed. At
autopsy, in addition to softening in
the territory of the left anterior cere¬
bral artery, there were numerous
small infarcts in the territory of the
right anterior cerebral artery as well
as in the insular portion of the left
temporoparietal area. The parasagit¬
tal infarcts were pathologically older
than the others and the author
concluded that these were at the basis
of the speech defect, prior to the onset
of the right hemianopsia.
Rubens2 described in detail two
patients with sudden onset of right
crural hemiplegia, aphasia, and incon¬
tinence and whose radionuclide brain
scans, three weeks after onset, showed
uptake in the distribution of the left

anterior cerebral artery territory.
Both patients had an acute stage of
aphonia lasting several days, followed
by a prolonged period lasting several
weeks during which there was marked
diminution of spontaneous speech,
with a remarkably intact ability to
repeat even long and complex sen¬
tences. The first patient even showed
an interesting inability to refrain
from completing open-ended sen¬
tences and series of days or numbers.
Both patients showed good compre¬
hension and lack of paraphasic errors,
and the second had persistent leftsided apraxia and tactile anomia.
It is clear from these cases that the
cardinal features of the dysphasia
associated with infarction in the terri¬
tory of the left anterior cerebral
artery are the following: a marked
reduction in spontaneous speech, pres¬
ervation of comprehension and repeti¬
tion, and absence of paraphasia. Echo¬
lalia may be present. These findings
are consistent with those described
following ablation of parasagittal
epileptic foci12 and penetrating mis¬
sile injuries in the same area,11 where
the major deficit is initiation of
speech. Stimulation of the parasagit¬
tal prefrontal cortex on either side
induces vocalization and repetitive
utterances or words.14
It is well known that injury of the
posterior portion of the left inferior
frontal gyrus (Broca's area) also
results in paucity of spontaneous
speech, with groping and monitoring
behaviors. The difference with the
mesial, parasagittal lesion is the
preservation of repetition and ab¬
sence of paraphasic errors. Goldstein15
used the term "transcortical motor
aphasia" to describe this type of
communication deficit while Luria
and Tsvetkova16 called it "dynamic
aphasia." It is important to mention

that occlusion of the main trunk of the
left anterior cerebral artery may,
indeed, produce a motor aphasia that
is indistinguishable from Broca's
aphasia. This is probably due to under¬
mining of Broca's area by an infarct
deep in the territory of Heubner's
artery.117 This type of aphasia is
usually transient, with recovery of
spontaneous speech18 or persistence of
a transcortical motor aphasia (TMA).
Although one cannot put too much
weight on findings only one week
after the onset of illness as they may
be quite different from the outcome in
a chronic stable patient, the case
described in this report is nonetheless
interesting in that some features of
TMA were present whereas other
findings did not fit with only one form
of aphasia, probably because of the
combined effects of the old and the
more recent infarct. Those elements
that fit a TMA syndrome are the
reduction of spontaneous speech out¬
put, groping and monitoring behav¬
iors, and lack of paraphasic errors.
These findings can be explained by
the fresh infarct in the territory of the
left anterior cerebral artery. In con¬
trast to the other features of TMA,
this patient demonstrated impair¬
ment of repetition, although repeti¬
tion was better than spontaneous
speech. There was no echolalia, which
is commonly found in TMA. It is
thought that the discrepancy can be
accounted for by the presence, in addi¬
tion to the recent parasagittal lesion,
of an old infarct undermining the
parietal opercular area that inter¬
rupted the arcuate fasciculus connect¬
ing the sensory association cortex
with the motor association area. It is
unfortunate that no data are available
on any language difficulties that may
have accompanied the first stroke. It
is tempting to speculate that a tran-

sient dysphasia may have developed
and that recovery took place via transcallosal pathways, as shown in the
diagram (Fig 4). Instead of being
conveyed intrahemispherically from
Wernicke's area to Broca's area, audi¬
tory information could be relayed
through posterior callosal fibers to the
right auditory association cortex,
from there to the right premotor
cortex, and finally to Broca's area via
the anterior portion of the corpus
callosum. The recently infarcted area,
as can be seen in the brain sections,
does in fact involve the anterior part
of the corpus callosum. One would
expect, then, to find difficulty in repe¬
tition of auditory material as well as
dysnomia. This was indeed the case,
for the patient could not name objects
or figures, but could point to them
(using the left hand) when the names
were supplied. Her spoken language
did not by any means match her
comprehension. Thus she persever¬
ated in answering "yes" to questions
such as·"Is a hammer good for cutting
wood?" or "Does a board sink in
water?" while, on the other hand, she
did carry out at least simple com¬
mands, identify objects in pictures,
and use tools such as a knife or fork to
feed herself. The problem, then, was
not primarily one of comprehension or
of association of auditory stimuli with
visual ones, but rather of transferring
auditory and visual information to the
motor speech area. It is obvious that
her language deficits did not fit into
any well-defined category. The com¬
bined effects of the two lesions
resulted in a mixed pattern that is
clearly different from what one would
predict in a left anterior cerebral
artery syndrome alone.
Craig Linebaugh and
viewed the manuscript.

Penelope Myers re¬

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