0148-396X/86/1803-0353$02.00/0
NEUROSURGERY
Copyright © 1986 by the Congress of Neurological Surgeons

Vol. 18, No. 3, 1986
Printed in U.S.A.

Transient Neurological Deficit after Therapeutic Embolization
of the Arteries Supplying the Medial Wall of the Hemisphere,
Including the Supplementary Motor Area

Gerald Schell, M.D., Charles J. Hodge, Jr., M.D., and Edwin Cacayorin, M.D.
Departments of Neurosurgery (GS, CJH) and Radiology (EC), State University of New York Upstate Medical Center, Syracuse, New York

A 27-year-old, right-handed woman underwent intraoperative embolization for a left parasagittal arteriovenous malfor-
mation as part of a two stage plan that included subsequent surgical resection of the arteriovenous malformation. This
report describes the neurological syndrome that developed after the first procedure. The relation of these deficits to
localization of function within the supplementary motor area are correlated with recent advances in our understanding

of this region. (Neurosurgery 18:353-356, 1986)

Key words: Anterior cerebral artery syndrome, Basal ganglia, Embolization, Primary motor cortex, Supplementary

motor area

INTRODUCTION

Many recent experimental studies of the supplementary
motor area (SMA) have suggested that it has a major role in
the cerebral control of motor planning (4, 27, 28, 33, 36).
Cerebral blood flow studies in humans have demonstrated
selective increase in regional cerebral blood flow in the SMA
when complex motor acts are performed or when they are
planned without movement (27, 28). Physiological studies in
nonhuman primates have demonstrated that SMA neurons
become active during the preparation for movement and
during the execution of some movements (4, 5, 33, 36).
Recent anatomical studies have shown that the SMA has
dense somatotopic connections with motor cortex (14, 18,
19, 22, 23). In addition, recent studies have demonstrated
that the SMA is the cortical motor area most directly influ-
enced by the basal ganglia (31).

This case report describes the clinical manifestations result-
ing from an insult to the medial wall of the hemisphere,
including the supplementary motor area. These deficits fol-
lowed a discrete intraoperative embolization of an arteriove-
nous malformation (AVM) of the medial frontal lobe. The
relation of these deficits to localization of function within the
SMA will be discussed and correlated with recent advances in
our understanding of this region. Pre- and post-embolization
arteriograms and CT studies provided accurate topographic
localization of the region being described.

CASE REPORT

AJ is a 27-year-old right-handed woman with a 4-year
history of seizures and severe headaches. Complete work-up
had previously included a cerebral angiogram that revealed a
large left midline hemispheric AVM. The patient had a pro-
gressive course of increasing difficulty with seizure control,
intermittent weakness of her right arm and leg, and occasional
difficulties with speech. The patient’s most bothersome com-
plaint, however, was the severe bitemporal throbbing head-
aches that were associated with these episodes of weakness
and speech difficulty.

Results of cerebral angiography demonstrated that the
AYM was supplied predominantly by distal branches of the
left callosal marginal and the left anterior pericallosal arteries.

353

Operation was considered because of the worsening of her
neurological condition, presumably secondary to steal phe-
nomenon (21). The patient underwent a right parasaggital
craniotomy to embolize the anterior vessels of the left hemi-
spheric arteriovenous malformation. The operative exposure
included a lateral retraction of the right medial frontal lobe
so that the falx cerebri was exposed inferiorly to the superior
sagittal sinus. A 2 X 5 cm opening was made in the inferior
aspect of the falx to allow access to the medial side of the left
frontal lobe. The most distal branch of the left callosal margin
artery as well as the main branch of the left pericallosal artery
were identified. A cannula was inserted into each of these
vessels which supplied the AVM and they were successfully
embolized with isobutyl-2-cyanoacrylate (Bucrylate; Ethicon,
Inc., Somerville, New Jersey). The embolic material was
deposited into the nidus of the malformation under fluoro-
scopic control. There were no intraoperative complications,
and there was no attempt at excision of this arteriovenous
malformation. The postoperative plain films, computed tom-
ographic (CT) scans, and angiograms illustrate the results of
the procedure (Figs. | and 2).

Postoperatively the patient was found to have akinetic
mutism that lasted appoximately 4 days. Physical examina-
tion on the day after operation showed the patient to be alert
and awake, but incapable of spontaneous speech and move-
ment. In addition, she had spasticity of the right lower extrem-
ity and a left gaze preference.

The patient’s speech and motor patterns began to improve
4 days after operation. She began speaking in response to
questions, but her speech was restricted to single words and
showed no spontaneity. During this recovery period, the
patient had no difficulty with repetition, speech comprehen-
sion, articulation, or naming. However on repeated exami-
nation, spontaneous speech remained sparse, and she became
very frustrated even though her speech disturbance was ap-
parently minimal. Purposeful movement of the upper extrem-
ities also first was noted on the 4th postoperative day. At this
time, weakness of her right arm was noticed. Neurological
examination demonstrated hypereflexia of the right leg, bilat-
eral Babinski reflex, resolution of the gaze preference, and a
normal sensory examination.

Speech and movement patterns gradually improved over
the next 3 weeks. Speech, nonfluent, slow, and deliberate on

Fic. 1. 4 and B. left common carotid, lateral view. (A) and right
common carotid. frontal view, (B). injections demonstrate a left
parasagittal frontal and frontoparietal AVM predominantly supplied
by the middle and posterior internal frontal and paracentral arteries.
C and D. cerebral arteriograms performed after intraoperative em-
bolization with tantalum-impregnated Bucrylate show significant ob-
literation of the AVM. A deeply situated residual AVM is still evident.
E and F, plain films illustrate the actual distribution of the tantalum-
impregnated Bucrylate occluding the arterial feeders and nidus of the
AVM.

day four, rapidly improved to its preoperative state. The
weakness of her right arm, the spasticity of her right leg, and
her gaze preference completely resolved. Weakness persisted
in her right leg. Although the patient could function well
when the right or left hand was used independently, she was
not able to coordinate motor functions when using both hands
simultaneously. Simple tasks involving bilateral manual co-
ordination, such as buttoning her shirt or transferring a cup
from one hand to another were performed very poorly. Si-
multaneous pronation and supination of her forearms was
very difficult, whereas this alternating movement pattern was
executed normally when each arm was tested independently.
This bimanual disturbance of alternating movements did not
improve during subsequent examinations.

DISCUSSION

Intraoperative embolization has become an integral part of
the management of AVMs. A major complication of this

Neurosurgery, Vol. 18, No. 3

procedure is infarction of potentially normal neural tissue in
and around the AVM (21, 35). Because embolization occludes
the major feeding arteries of the AVM and the smaller distal
branches that supply more distal neural tissue, there may be
neurological deficit from infarction of neural elements. This
case report emphasizes the transient neurological deficits.
particularly difficulties with speech and the lasting difficulty
with bimanual movements, that resulted from embolization
of an AVM that involved the left supplementary motor area.

The neurological findings resulting from tumors and in-
farcts affecting the medial aspect of the frontal lobe, including
the SMA, have been previously reported (1, 6, 10, 11, 13, 17,
25, 26, 30, 32, 39), but often go unrecognized in common
neurological practice (12). This cortical region is commonly
involved with lesions, such as parasagittal meningiomas, an-
terior cerebral artery vasospasm, and infarctions. Most lesions
in this area produce what has been termed the anterior
cerebral artery syndrome. This syndrome consists of contra-
lateral paralysis of the lower extremity, forced grasping of the
ipsilateral hand, a transient, but profound, expressive aphasia,
and an ideomotor apraxia of the left arm regardless of the
side of the lesion (30). However, the correlation of these
neurological signs with anatomical structures has been diffi-
cult because branches of the anterior cerebral artery supply
major anatomic structures, including the anterior “/s of the
corpus callosum, the anterior limb of the internal capsule, the
SMA, and the medial aspect of the sensorimotor cortex. Many
manifestations of this motor syndrome have frequently been
attributed to lateral hemispheric and callosal structures. How-
ever, this report, together with other recent reports (1, 11, 15,
29), indicates that the anterior cerebral artery syndrome may
be largely the result of damage to the SMA.

This patient displayed a striking profile of the anterior
cerebral artery syndrome after selective embolization of
branches of the left callosal marginal and pericallosal arteries
(Fig. 1C, D). The lesion included most of the SMA and some

Fic. 2. 4 and B, intravenously enhanced computed tomographic
scans demonstrate the cortical and subcortical location of the left
parasagittal AVM. C and D, plain computed tomographic study
defines the extent of the embolized AVM.

March 1986

of the “leg representation” of primary motor cortex. Lateral
hemispheric structures and regions supplied by Heubner’s
artery were not involved. Neurological deficit from retraction
of the right medial hemisphere cannot be excluded; however,
this was not thought to have played a major role in this
patient.

Preoperatively, the language disturbance in this patient
consisted of multiple episodes of speech arrest attributed to
either focal seizures (24) or local steal phenomena (21). These
language disturbances consisted of mutism lasting for 4 days,
initial severe impairment of spontaneous speech, rapid recov-
ery over 2 to 4 weeks from well-articulated but slow speech
to nearly normal speech, and a tendency to become very
frustrated when using complex language. Throughout this
period, comprehension of simple verbal and written material
was normal.

Rubens states that the aphasia associated with the anterior
cerebral syndromes can be distinguished from classic Broca’s
aphasia and attributes the speech disturbance to damage of
the SMA (30). The disorder of speech observed in SMA lesions
and in the anterior cerebral artery syndrome is transient
mutism with rapid improvement of the expressive aphasia.
The speech disturbance associated with the anterior cerebral
syndrome has been attributed to the undercutting of Broca’s
area by a white matter lesion in the distribution of Heubner’s
artery (30). However, even though there are similarities be-
tween the speech deficits associated with anterior cerebral
artery syndromes and Broca’s aphasia, patients with Broca’s
aphasia frequently have difficulty with articulation and are
seldom mute. The present case supports the concept that a
type of expressive aphasia does occur as a result of lesions
distant from Heubner’s artery and the perisylvian speech
areas.

Immediately postoperatively the patient had a transient
period of marked increase in tone of the right lower extremity
while tone remained normal in the right upper extremity.
This phenomenon of spasticity in this context has been the
subject of many experimental studies and is beyond the scope
of the present discussion (7-9, 34, 37, 38). The spasticity of
the right leg may have resulted from involvement of the “leg
representation” of both the primary motor area and SMA
(Fig. 1C, D). The residual right leg weakness can be explained
by infarction of the leg representation of primary motor
cortex. The absence of right arm spasticity may be related to
the sparing of the “arm representation” of primary motor
cortex, which is supplied by the middle cerebral artery (Fig.
IC. D).

This patient also demonstrated global akinesia for 4 days,
transient weakness of the right upper extremity for 2 weeks,
permanent weakness of the right lower extremity, and a
residual difficulty with complex simultaneous movements of
both hands. The transient motor disturbances have been
frequently reported after SMA lesions and anterior cerebral
artery syndromes (5, 10, 11, 15, 25, 29). The bimanual deficit
persisted even though there was no weakness demonstrated
in the upper extremities. A similar movement disorder was
demonstrated experimentally in monkeys after SMA abla-
tions (3) and in humans (15). The bimanual difficulty with
coordination is a feature unique to SMA lesions and may be
related to extensive bilateral connections of the SMA with the
motor cortex (18, 19. 22, 23) and the spinal cord (2, 20)
(Schell G, Strick PL: Unpublished observations).

The concept that the SMA is the cortical area most influ-
enced by the basal ganglia has significant functional implica-
tions relating to the study of motor control in humans (31).
Marsden has suggested that the major function of the basal

SUPPLEMENTARY MOTOR AREA 355

ganglia is to run a sequence of motor programs to achieve a
motor plan (16). Similarly, cerebral blood flow studies in man
have demonstrated selected increase in regional blood flow in
the SMA in man during movement sequence tasks (27, 28).
The anatomical relationship between the basal ganglia and
the SMA (31) suggests that certain aspects of movement
disorders associated with basal ganglia disease may be me-
diated by the SMA. The marked akinesia and associated
mutism observed in this patient after a lesion involving the
SMA might be compared with the akinesia of Parkinson’s
disease. Further observations on how lesions of the SMA
might affect the movement disorders related to basal ganglion
disease could add further understanding of the pathophysiol-
ogy of these motor systems.

ACKNOWLEDGMENTS

The authors thank Dr. Robert B. King and Dr. Peter L.
Strick for the critical review of this manuscript. This work
has been supported in part through funds from the Veterans
Administration Medical Research Service, United States Pub-
lic Health Service Grant 02957, and the Department of Neu-
rosurgery, State University of New York. Dr. Schell was
supported as the George W. Perkins Scholar.

Received for publication, February 21, 1985; accepted, November
2, 1985.

Reprint requests: Gerald Schell, M.D., Department of Neurosur-
gery, 750 East Adams Street, Syracuse, New York 13210.

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