The Aphasia Syndrome of Stroke in the
Left Anterior Cerebral Artery Territory
Michael P. Alexander, MD, Mary Anne Schmitt, MA, CCC

\s=b\ Two patients with transcortical motor
aphasia are described. Both had infarcts

in the distribution of the left anterior cerebral artery confirmed by computerized
tomography (CT). The distinctive language abnormality, unusual EEG pattern,
and nuclide and CT scan abnormalities all
allow ready diagnosis of the syndrome of
infarction in this distribution. The mechanism of the language disturbance is
reviewed and implications for treatment
and prognosis are discussed.
(Arch Neurol 37:97-100, 1980)

under the general heading
Captured
^ of nonfluent
are several

aphasia
syndromes. These include
global aphasia and three additional
syndromes in which auditory compre¬
hension is relatively or totally pre¬
served: aphemia (known also by other
names, including pure word dumb¬
ness, but implying a limited disorder
of speech secondary to a cortical
lesion), Broca's aphasia, and transcor¬
tical motor aphasia. The first two have
been well reviewed recently and their
pathoanatomic bases made clearer.1-2
Transcortical motor aphasia is a clinidistinct

Accepted for publication Feb 16, 1979.
From the Department of Neurology, Boston
University School of Medicine, Boston (Dr Alexander), the Departments of Neurology (Dr Alexander) and Speech Pathology (Ms Schmitt),
Braintree Rehabilitation Hospital, Braintree,
Mass, and the Department of Neurology, Boston
Veterans Administration Hospital, Boston (Dr
Alexander).
Reprint requests to Neurobehavioral Unit,

Boston Veterans Administration Medical Center,
150 S Huntington Ave, Boston, MA 02130 (Dr

Alexander).

cal

entity less well recognized by
neurologists and, we suspect, often
placed under the general and inaccu¬
rate rubric of motor aphasia or
expressive aphasia. It is characterized
by nonfluent conversational speech,
preserved auditory comprehension,
and near normal repetition.1 A few
reports document the nature of this

disturbance4 and outline its clinical
setting.57 We believe that the descrip¬
tion of transcortical motor aphasia in
one specific clinical setting, left ante¬
rior cerebral artery distribution in¬
farction, is useful for several reasons:
(1) this setting, while not common,
offers a unique and easily recognized
clinical picture; (2) computerized to¬
mography (CT) may clearly reveal the
lesion and either the EEG or the
nuclide brain scan may present dis¬
tinctive abnormalities; (3) the method
of speech therapy used for other
nonfluent aphasies may have to be
altered; and (4) the prognosis for
language recovery appears relatively

good.

REPORT OF CASES
Case

l.-A

56-year-old, fully right-

handed man was admitted to a local hospi¬
tal with a history of dizzy spells for several
days and syncope that day. He had a
history of alcohol abuse, diabetes mellitus,
and hypertension. On examination, the
patient was alert, with impaired speech
and right-sided weakness. The results of a
nuclide brain scan performed on the tenth
hospital day were negative. The patient
was transferred to Braintree Hospital for
evaluation of speech and rehabilitation.
Neurological evaluation performed 25 days
after onset of illness revealed an alert,

cooperative, and oriented man. Carotid
pulses were equal without bruits. Lan¬

guage examination results (see below)
showed very limited speech output, marked
difficulty in initiating speech, and perseveration of words; the auditory comprehen¬
sion was normal. Repetition and series
speech were dramatically preserved. There

buccofacial apraxia. Rightleft orientation and finger recognition
were normal. There was a flaccid right
hemiparesis of unusual distribution, maxi¬
mal throughout the leg, moderate in the
shoulder, and very mild in the hand, but
facial movements were normal. There was
mild bilateral and equal decrease in vibra¬
tory sense over both feet, and ankle jerks
were absent. Otherwise reflexes were
slightly brisker on the right; the toe
response was flexor bilaterally. There was
marked groping and a grasp reflex on the
right side. An EEG obtained on day 30
revealed a left frontal and frontopolar
semirhythmic slow wave focus. Computer¬
ized tomography scan revealed an infarct
in the distribution of the left anterior
cerebral artery (Fig 1). On follow-up evalu¬
ation at day 60, speech was improved, and
buccofacial apraxia was minimal. Careful
testing revealed a tendency to use a body
part as an object in tasks of limb praxis,
but only with the left hand. The pattern of
hemiparesis was unchanged, but rigidity
(paratonia) had developed in the right
was moderate

arm.

Formal Language Evaluation.—The Boston

Diagnostic Aphasia

Examination7 was
days after onset.
Spontaneous output consisted of short,
effortful, telegraphic speech with persev¬
eraron and difficulty in initiating all
phases. Occasional verbal paraphasias, of¬
first administered 25

ten

representing perseveration,

were

heard. Auditory comprehension was fully
functional, with minimal breakdown for
complex material. Naming was mildly
impaired. A marked inability to generate

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word lists was in direct contrast to func¬
tional responsive naming. Repetition was
well articulated and done well to long
phrase lengths. Automatic speech required
initial cues but was then completed with
intact articulation. Reading aloud was
minimally impaired, while reading compre¬
hension of sentences was moderately
impaired. With the nondominant left hand,
writing was almost unintelligible and func¬
tional only for name and address. Buccofa¬
cial apraxia was prominent; nonverbal agil¬
ity tasks were performed slowly and with
effort. Réévaluation at 75 days, following
two months of speech therapy, showed
continuing marked difficulty in initiating
speech, but frequent attempts were now
made to produce spontaneous responses in
a group setting. Most spontaneous produc¬
tions were grammatically complete sen¬
tences, and speech was virtually fluent
except for persistent hesitations, increased
latencies, and word-finding pauses. Per¬
severaron had decreased. Auditory com¬
prehension was normal except for very
complex material where failure may have
represented concreteness rather than lan¬
guage failure. Responsive naming had
improved and remained greatly superior to
generation of word lists (eight items in Vá
minutes). Repetition was flawless and well
articulated. Reading aloud was excellent.
Reading comprehension was within normal
limits. Writing was intact for short phrases
with verbal cueing. Buccofacial apraxia
was much decreased. Speech therapy had
focused on compensation for anomia
through use of appropriate circumlocu¬
tions, and alleviation of speech hesitancy
through a strategy in which the patient
was encouraged to continue and complete
any self-initiated production. Group thera¬
py served as a forum for arousing this
patient's interest and motivation to com¬
municate. It provided a structural setting
for learning facilitating techniques that
the patient later used in other settings.
Case 2.—A 62-year-old woman was
admitted to a local hospital with the abrupt
onset of right-sided weakness and difficul¬
ty speaking. She had a long history of
treated hypertension, a myocardial infarc¬
tion in 1965, treated hypothyroidism, and
mild diabetes mellitis. An EEG and nuclide
flow study revealed a nonlocalized disorder
of the left hemisphere. The patient was
transferred on day 15 for rehabilitation.
On examination, she was alert and cooper¬
ative. The left carotid pulse was dimin¬
ished, but without bruit. Spontaneous
speech was nonfluent with some echoing.
Comprehension was normal. Confrontation

naming was very good. Repetition, reading
aloud, and serial speech were perfect with
normal articulation (results of formal
language testing are described below).
There was mild buccofacial apraxia and a
tendency to substitute body part as object
bilaterally on praxis testing. There was a
flaccid right hemiparesis of unusual distri¬
bution, dense in the leg, moderate in the
proximal arm, and minimal in the distal
arm and lower face. Stretch reflexes were

brisker on the right; both toe responses
were flexor. There was a strong right-sided

Fig 1.—Noncontiguous sections from nonenhanced computerized tomographic scan
reveal large area of decreased density in medial left frontal region (case 1).

Fig 2.—Similar lesion in the medial left frontal region (case 2).
grasp reflex. Sensory examination results,

visual fields, and optokinetic nystagmus
were normal. An EEG obtained on day 22
revealed a striking frontopolar slow wave
focus with spread in the left hemisphere.
Computerized tomography scan revealed
an infarct in the distribution of the left
anterior cerebral artery (Fig 2). On rééva¬
luation at day 90, speech and buccofacial
praxis had improved. Right-sided limb
praxis was normal, but clumsiness and
posturing of the left hand in transitive
praxis tests (eg, pretend to comb your hair)
persisted. An attempt to use external
sequential stimuli to improve speech initia¬
tion (eg, pointing to successive papers,
rhythmically patting her hand, etc) was

right hemiparesis re¬
mained, affecting primarily the leg and the

unsuccessful. The

shoulder. Tone and sensation were normal
and the right grasp reflex persisted.
Formal Language Evaluation.—The Boston
Diagnostic Aphasia Examination7 was
first administered 19 days after onset.
Conversational speech was telegraphic,
consisting of fragmented sentences and
incomplete phrases (ie, "think, sink's over¬
flowing") with severely impaired speech
initiation. Auditory comprehension was
intact, although with increased latencies of
response and echoing on directional tasks.
Responsive and confrontation naming
were

intact, in contrast to formulating

word lists in which the patient produced

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only four items in V/i minutes. Repetition
was excellent and was normally articu¬
lated, in contrast to the severely limited
spontaneous output. Automatic speech was
normal, although an initiating cue was
required. Oral sentence reading was
normal. Reading comprehension was with¬
in normal limits. Writing with the domi¬
nant right hand was limited to production

of name and address. Buccofacial apraxia
was present. Réévaluation 90 days after
onset revealed persisting difficulty initiat¬
ing conversational speech but with im¬
proved performance when cued. Speech
was hesitant and effortful, often tele¬
graphic, but well articulated. There was
less perseveration and much less echoing.
Occasional fluent, grammatically normal
utterances were produced (eg, "She has an
18-year-old daughter who is in college").
The striking discrepancy persisted be¬
tween the labored spontaneous speech and
the normal, well-articulated repetition,
reading aloud, serial speech, and confron¬
tation naming. Ability to generate word
lists had improved but was significantly
poorer (12 items in IV2 minutes) than intact
responsive naming skills. She could write
short, grammatically correct sentences.
During narrative writing, the patient
spontaneously verbalized the words she
was writing and had great difficulty
producing words when asked to remain
silent during the task. Speech therapy
focused on extending the patient's use of
complete sentences, and at discharge, the
patient was capable of producing sentences
in response to direct questions and in
approximately 60% to 70% of spontaneous
utterances.

COMMENT

The clinical syndrome of anterior
cerebral artery occlusion has long
been known9 and is described in
modern textbooks on neurology.1" The
deficits include hemiparesis with cru¬
ral predominance, often flaccid, vari¬
able sensory loss in the lower extrem¬
ity, left sided ideomotor apraxia and
involuntary motor activity in the
paretic arm, such as grasping and
paratonia. Critchley's review of the
necropsy-confirmed cases up to 1930"
establishes that a speech disturbance
occurs with left anterior cerebral
artery occlusion, but he describes the
nature of this deficit only as "speech
disturbances of various types." Mod¬
ern texts expand little on this defini¬
tion, and language disturbances seen
in this setting generally remain un¬

recognized. Since Critchley's review,
the pertinent literature on language
disturbances following left frontal

lesions that spare Broca's area
has followed several independent
threads.
Numerous reports characterize the
alterations in verbal output secondary
to manipulation of the supplementary
motor area, that medial frontal pre-

motor region which lies entirely with¬
in the distribution of the anterior
cerebral artery. Either spontaneous
seizures arising from or electrical
stimulation of either supplementary
motor area produce repetitive vocali¬
zations, speech arrest, and bilateral
mouth movements."'" Surgical abla¬
tion or manipulation of the supple¬

mentary motor area produces tran¬

sient speech disturbances described as
failure of initiation, "motor aphasia,"
or mutism.111717 Permanent speech
disorders include difficulty in initiat¬
ing speech and anomia but are rare
residuals of damage to this area.1418
Reports of aphasia following dam¬
age in the distribution of the left
anterior cerebral artery have been
infrequent. Poppen reported the re¬
sults of anterior cerebral artery liga¬
tion during surgery for frontal tu¬
mors; in two patients, aphasia devel¬
oped that was "practically complete"
initially but apparently cleared rap¬
idly.1" Guidetti described a patient
whose left anterior cerebral artery
was ligated to control bleeding from a
ruptured aneurysm; postoperatively
there was "severe motor aphasia" that
resolved over several months.1" Ac¬
cording to Goodglass and Kaplan,8
transcortical motor aphasia (TCMA) is
marked by an absence of spontaneous
speech, with difficulty in initiating
speech and limited ability to name or
to make brief responses. Auditory

comprehension, reading comprehen¬
sion, and reading aloud are relatively
intact. "Repetition is remarkable in
that it is prompt, well articulated,
grammatically intact and free of
difficulty of initiation which marks all
other speech."

There are a few cases, labelled
TCMA and caused by a single vascular
episode, with which our cases may be
compared. Atkinson" briefly described
one patient with TCMA following a
large left frontal infarct but with
scattered left parietal infarction as
well and an atypical clinical syndrome.
Rubens7' described two patients with
TCMA and infarcts in the left anteri¬
or cerebral artery territory seen on
brain scan. The clinical syndromes
were typical except for the absence of
left body apraxia in one patient. In
another report, Rubens mentions nine
patients with TCMA, three with ante¬
rior cerebral artery distribution in¬
farcts and all but one of the others
with large lesions in the left frontal
lobe.' Von Stockert described a wom¬
an with a brain scan-proven infarc¬
tion of the left medial frontal lobe.2"
She could not initiate speech although
she could repeat. By three weeks after

onset, all language skills were within

normal limits. In a larger study of
localization in aphasia, Kertesz and
McCabe briefly mention three pa¬
tients with TCMA, one of whom had a
left anterior cerebral artery distribu¬
tion infarct.21 A recent report on
TCMA includes one case with left
medial frontal infarction.7 Only two of
the reports include detailed language
studies,"'-2" and neither was published
in a neurological journal.
Only a few well-described cases of
TCMA with clinical findings typical of
left medial frontal infarction have
been previously reported. The neuro¬
logic findings include right crural
paresis, involuntary motor activity of
the right arm, and variable sensory
loss in the right leg. Variable left
ideomotor apraxia is seen. If infarc¬
tion of the anterior 80% of the corpus
callosum is complete, callosal signs
should be seen.22 Our patients did not
have these signs when examined by
us. The language findings are poverty
of spontaneous speech, slow initiation
of speech, some capacity for brief
responses and naming, relatively to
completely intact comprehension and
reading, and excellent, well-articu¬
lated repetition. A similar language
syndrome may be seen in patients
with large lesions elsewhere on the
dorsolateral surface of the left frontal
lobe anterior to Broca's area4 or, rare¬
ly, even with lesions including Broca's
area,4-2' but the accompanying neuro¬
logical signs are different. The combi¬
nation of characteristic language and
speech changes with other specific
neurological findings is a powerful
indicator of infarction in left anterior
cerebral distribution. The EEG locali¬
zation is atypical of carotid or middle
cerebral artery occlusive disease and,
while not well described in standard
EEG texts,2' appears strongly indica¬
tive of infarction in anterior cerebral
artery distribution. Findings on brain
scan may also be diagnostic.
Since first described by Lichtheim,24
a rich literature has developed on the
features of TCMA suggesting mecha¬
nisms for its production in left frontal
lesions, some completely outside of the
perisylvian speech area. Lichtheim
postulated an interruption of fibers to
the motor speech area from a concepts
center. This center was not specifical¬
ly localized but rather represented the
combined action of much of the brain
converging on Broca's area. Bastian27'
theorized that partial damage to the
motor speech area caused the syn¬
drome by increasing the threshold for
motor speech performance.

Goldstein2" considered the problem

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aphasias in great
depth, suggesting two separate mech¬
anisms for producing the syndrome.
In one, partial damage to the motor
speech area altered the speech thresh¬
old, but in this case, repetition and
automatic speech, while better than
spontaneous, would not be so clearly
of transcortical

normal. A second form of TCMA did
not represent a language deficit so

as an "impairment of the
impulse to speak at all." Not a global
impairment of all verbal movements,
as intact repetition, oral reading, etc
proved, but an inhibition in initiation
of motor activity maximal in speech
functions produced by focal left fron¬
tal lesion, which may also partially
involve the motor speech areas. These
possibilities may account for some

much

of TCMA in which the lesion
affects the frontal convexity in or
near Broca's area, but our patients
had lesions far removed from the pericases

sylvian region.

Left frontal lesions in nonaphasic
patients produce another important

related effect. Milner27 demonstrated
in "verbal fluency" in
a deficit
patients following partial frontal lo¬
bectomy for control of epilepsy. In
addition to diminished spontaneous
speech, these patients have markedly
diminished ability to form a word list,
when compared with patients with

lesions elsewhere in the brain outside
the language region. Botez and Barbeau28 in a review of clinical and
experimental work concluded that the
medial frontal supplementary motor
area was part of the more primitive
system involved in a "starting mecha¬
nism" of speech but also in the main¬
tenance of speech fluency apropos
Milner's observations. This deficit was
seen in our patients.
Finally, studying cases of trauma
or cases not completely described or
localized, often with tumors, Luria2"
has extracted three apparently inde¬
pendent deficits from the perfor¬
mance of patients with TCMA. In
short, there is a combined failure to
form propositional units, to maintain
fluency and to initiate speech. The
deficits stem from large left frontal
lesions similar to those seen in our
patients. In addition, a lesion in the
left anterior cerebral artery distribu¬
tion may specifically damage a primi¬

tive system of speech organization,

magnifying the impairment in spon¬
taneous speech production. The surgi¬

cal literature described earlier indi¬
cates that this latter speech distur¬
bance is reversible.
While the implications for speech
therapy remain uncertain, traditional
therapeutic techniques based on ver¬
bal cueing and repetition and newer

therapies based on intoned repeti¬
tion™ are of limited value.11 They
address a function that is preserved
and performed almost automatically
in these patients. Luria has suggested
providing an external sequence to
speech by relating speech to some
other sequential movement, such as
pointing to squares or patting one's
leg.29 This helped his patients in initia¬
tion and maintenance of speech. We
attempted this and were unsuccessful,
but external rhythmic stimulation
remains a plausible approach for these
patients.
Regardless of therapy, there are
data suggesting that the prognosis of
TCMA may be relatively good,5·-'-· ''although some patients have persis¬
tent difficulty in initiating and main¬
taining narrative speech, even if
responsive speech is normal. In sum¬
mary, the deficits produced by infarc¬
tion in the distribution of the left
anterior cerebral artery produce a
distinct clinical syndrome. The find¬
ings on EEG and nuclide and CT scans
may confirm clinical localization.
Therapy for the speech disorder may
require individualized alterations; the
overall prognosis is favorable.
We wish to thank D. Frank Benson, MD, for
assistance in organizing our material.

References
1. Mohr JP: Broca's area and Broca's aphasia.
Neurology 28:311-324, 1978.
2. Hayward RW, Naeser MA, Zatz LM: Cranial
computed tomography in aphasia. Radiology
123:653-660, 1977.
3. Benson DF, Geschwind N: The aphasias and
related disturbances, in Baker AB, Baker LH
(eds): Clinical Neurology. Hagerstown, Md,
Harper & Row, 1976, chap 8, p 11.
4. Rubens AB: Transcortical motor aphasia, in
Whitaker H, Whitaker H (eds): Studies in
Neurolinguistics. New York, Academic Press
Inc, 1976, vol 1, pp 293-303.
5. Rubens AB: Aphasia with infarction in the
territory of the anterior cerebral artery. Cortex
11:239-250, 1975.
6. Atkinson MS: Transcortical motor aphasia

associated with left frontal lobe infarction.
Trans Am Neurol Assoc 96:136-140, 1971.
7. Damasio AR, Kassel NF: Transcortical
motor aphasia in relation to lesions of the supple-

mentary motor area. Neurology 28:396, 1978.
8. Goodglass H, Kaplan E: The Assessment of

Aphasia and Related Disorders. Philadelphia,
Lea & Febiger, 1972, p 73.
9. Critchley M: The anterior cerebral artery
and its syndromes. Brain 53:120-165, 1930.
10. Adams RD, Victor M: Principles of Neurology. New York, McGraw-Hill, 1977, p 506.
11. Elsberg CA: The parasagital meningeal

fibroblastomas. Bull Neurol Inst NY 1:389-418,
1931.
12. Penfield W, Welch K: The supplementary

motor area of the cerebral cortex. Arch Neurol

Psychiatr 66:289-317, 1951.
13. Erickson TC, Wodsey CN: Observations on
the supplementary motor area of man. Trans Am
Neurol Assoc 76:50-56, 1951.
14. Arseni C, Botez MI: Speech disturbances
caused by tumors of the supplementary motor
area. Acta Psychiatr Neurol Scand 36:279-299,

1961.
15. Guidetti B: D\l=e'\sordresde la parole associ\l=e'\s
de la surface interhemisph\l=e'\rique.Rev Neurol
97:123-131, 1957.
16. Alajouanine T, Castaigne P, Sabouraud O,
et al: Palilalie paroxystique et vocalisations it\l=e'\ratives au cours de crises \l=e'\pileptiquespar l\l=e'\sion
int\l=e'\ressantl'aire motrice suppl\l=e'\mentaire.Rev
Neurol 685-697, 1959.
17. Botez MI: Clinical contributions to the
study of the tumoral frontal syndrome. Psychiatr
Neurol 140:351-368, 1960.
18. Petit-Dutaillis D, Guiot G, Messing R, et al:
Apropos d'une aph\l=e'\miepar atteinte de la zone
matrice suppl\l=e'\mentairede Penfield. Rev Neurol
90:95-106, 1954.
19. Poppen VL: Ligation of the left anterior
cerebral artery. Arch Neurol Psychiatr 41:495\x=req-\
503, 1939.
20. Von Stockert TR: Aphasia sine aphasia.
Brain Language1:277-282, 1974.
21. Kertesz A, Lesk D, McCabe P: Isotope
localization of infarcts in aphasia. Arch Neurol
34:590-601, 1977.
22. Geschwind N, Kaplan E: A human cerebral

deconnection syndrome. Arch Neurol 12:675-85,
1962.
23. Kiloh LG, McComas AJ, Osselton JW: Clinical Electroencephalography. London, Butter\x=req-\
worth & Co, 1972, pp 130-137.
24. Lichtheim L: On aphasia. Brain 7:433-484,
1885.
25. Bastian HC: Some problems in connection
with aphasia and other speech defects. Lancet
1:1005-1017, 1132-1137, 1187-1194, 1897.
26. Goldstein K: Language and Language
Disorders. New York, Grune & Stratton, 1948, pp
292-324.
27. Milner B: Some effects of frontal lobectomy in man, In Warner JM, Ackert K (eds): The
Frontal Granular Cortex and Behavior. New
York, McGraw-Hill, 1964, pp 313-331.
28. Botez MI, Barbeau A: Role of subcortical
structures and particularly the thalamus in the
mechanisms of speech and language. Int J
Neurol 8:300-320, 1971.
29. Luria AR, Tsvetisova LS: Towards the
mechanisms of dynamic aphasia. Acta Neurol
Psychiatr Belg 67:1045-57, 1967.
30. Sparks R, Helm N, Albert M: Aphasia
rehabilitation resulting from melodic intonation
therapy. Cortex 10:303-16, 1974.
31. Helm N: What is the theoretical rationale
for using melodic intonation therapy? Tex J
Audiol Speech Pathol 3:11, 1978.
32. Kertesz A, McCabe P: Recovery patterns
and prognosis in stroke. Brain 100:1-18, 1977.

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