O148-396 N/84/1505-0727802.00/0
NEUROSURGERY
Copyright 1984 by the Congress of Neurological Surgeons

Vol. 15, No. 5. 1984
Printed in U.S.A.

Ipsilateral Hemiparesis Caused by Subarachnoid Hemorrhage
in a Patient with a Ruptured Middle Cerebral Artery
Aneurysm: A Case Report

Tadashi Kudo, M.D., D.M.Sc., and Toshiro Uno, M.D.

Neurosurgery Service, Yokohama Chiuh-oh General Hospital (T.K.), and Section of Neurosurgery, Second Department of Surgery (T.U.),
St. Marianna University, Kawasaki, Japan

The authors report a patient with a ruptured middle cerebral artery (MCA) aneurysm who presented with ipsilateral
hemiparesis. A computed tomographic (CT) scan and cerebral angiograms suggested that the ipsilateral hemiparesis was
most likely due to compression by hematoma of the secondary motor area in the island of Reil. Two other cases that
demonstrated ipsilateral motor weakness after rupture of MCA aneurysms have been reported. We emphasize not only
the importance of considering dysfunction of the secondary motor area in patients with hemiparesis, but also the
difficulty in differentiating ipsilateral secondary motor area dysfunction from contralateral primary motor area
dysfunction in certain cases without CT scanning and angiography. (Neurosurgery 15:727-729, 1984)

Key words: Cerebral aneurysm, Hemiparesis, Island of Reil, Motor cortex, Secondary motor area, Stroke, Subarachnoid

hemorrhage

INTRODUCTION

The representation of secondary motor and sensory areas
in the island of Reil has been known for years, but reports on
the clinical significance of these areas are few (4, 7, 8, 10, 11).
Recently. Schneider and Crosby reported a patient with ipsi-
lateral sensory symptoms who had a ruptured arteriovenous
malformation in the secondary sensory area of the island of
Reil (10). In this article, we document a patient with ipsilateral
hemiparesis due to compression of the secondary motor area
by a hematoma in the sylvian fissure.

CASE REPORT

A 62-year-old woman complained of the sudden onset of
severe headache and became unconscious during the evening
of July 26, 1983. She was immediately brought to our hospital
by ambulance. On examination, she was comatose and re-
quired a nasal airway, She responded only to deep painful
stimuli with purposeful movements of the extremities. Her
neck was supple. The pupils were equal in size (3 mm in
diameter) and reacted to light promptly. No impairment of
the external ocular muscle was noted. The patient had a
moderate right hemiparesis with the upper extremity weaker
than the lower. but with no facial weakness. Her muscle tone
was decreased on the right. The deep tendon reflexes were
absent on the right. The plantar response was flexor bilaterally.

A computed tomographic (CT) scan showed subarachnoid
hemorrhage (SAH) in the basal cisterns bilaterally, the am-
bient cistern, and the cistern of the sylvian fissure; the SAH
was most severe in the right cistern of the sylvian fissure (Fig.
). There was no shift of midline structures, but the right
temporal horn was compressed and displaced posteriorly. The
chiasmatic portion of the basal cistern was compressed and
was visualized less well on the right side. No deformity or
deviation of the midbrain was noted. The right insular surface
was compressed and flattened compared to the left. These
findings were thought to be consistent with compression of
the right side of the insula by a hematoma in the cistern of
the sylvian fissure.

By the next afternoon, the patient’s level of consciousness
had improved. She could follow verbal commands and was
able to talk using simple words. Her right hemiparesis had
improved, and she moved her right extremities spontaneously.
Left carotid angiography demonstrated no abnormality, in-
cluding the cervical carotid artery. Right retrograde brachial
angiography showed an aneurysm at the bifurcation of the
middle cerebral artery (MCA) (Fig. 2).

The patient continued to improve. By the 3rd day after the
SAH, she had no neurological deficit. She complained only
of mild headache. Subtle nuchal rigidity was now noted. The
aneurysm was clipped on July 29, 1983, the 4th day after
SAH. Her postoperative course was uneventful. She was dis-
charged to her home 3 weeks after the operation without any
neurological deficit.

DISCUSSION

In evaluating the CT scan of this patient, we were unsure
about the side of the lesion because the most severe SAH was
demonstrated in the right cistern of the sylvian fissure, ipsi-
lateral to the patient’s hemiparesis. The left carotid angiogram
demonstrated no vascular lesion that could possibly affect the
cerebral blood flow of the left hemisphere, such as intracranial
vasospasm, stenosis, occlusion, aneurysm, arteriovenous mal-
formation, or atheromatous plaque of the cervical carotid
artery. Reversible ischemic neurological deficit (RIND) af-
fecting the left hemisphere without angiographic evidence of
a vascular lesion is certainly a possibility, but such an occur-
rence coincident with the rupture of a contralateral MCA
aneurysm would be too rare to consider. The patient’s clinical
condition, with normal oculomotor nerve function, argued
against Kernohan’s notch phenomenon. The CT findings
also spoke against this phenomenon. There was nothing to
suggest a cervical spinal cord lesion. Therefore, we came to
the conclusion that her left-sided hemiparesis was due to the
ipsilateral cerebral hemispheric lesion.

Four functionally distinguishable motor areas are known
in animals and humans: the precentral motor area (primary
motor cortex), the supplementary motor area, the first somatic

728 KUDO AND UNO

Fic. 1. CT scan of the patient. who had moderate right-sided
hemiparesis. SAH is shown in the bilateral basal cistern, the ambient
cistern, and the cistern of the sylvian fissure and is most severe in the
right cistern of the sylvian fissure. Black arrowheads indicate compres-
sion of the right chiasmatic portion of the basal cistern. White
arrowheads indicate compression and posterior displacement of the
right temporal horn. The right insular surface (white arrows) was
more vertical and flattened than the left insular surface (b/ack arrows).

sensory area, and the second somatic sensory area (secondary
motor area) (7). The primary motor cortex represents the
contralateral half of the body and the bilateral face, lips, and
tongue (5, 7). Ipsilateral representation in motor and in pre-
motor cortex in both animals and humans has also been
known for years (2, 3, 5. 6, 8). The supplementary motor area
and the first somatic sensory area represent movement of the
contralateral half of the body (7). The secondary motor area
represents both ipsilateral and contralateral movement (4, 8.
10, 11). Therefore, there are two possible causes for the
ipsilateral hemiparesis in our patient: impairment of the ip-
silateral premotor and motor cortex or impairment of the
ipsilateral secondary motor area. The ruptured left MCA
aneurysm could influence either site, but the presence of the
large hematoma in the right sylvian fissure shown by CT scan
suggested that the left hemiparesis was most likely due to
compression of the ipsilateral secondary motor area in the
insula.

Two patients with ipsilateral motor weakness among 148
operated patients with ruptured MCA aneurysms were docu-
mented by Sakurai et al. (9). One of their patients showed
temporary ipsilateral paralysis of the lower extremity, and the
other had a persistent ipsilateral hemiparesis. CT scans were
not available for either patient. However, marked SAH was
found on the same side as the aneurysm at the time of
operation. This description of operative findings suggests pos-
sible compression of the ipsilateral island of Reil by hema-
toma.

Neurosurgery, Vol. 15, No. 5

Fic. 2. Right retrograde brachial angiogram, oblique projection.
The arrow indicates an aneurysm at the bifurcation of the right MCA.

Schneider and Crosby reported a patient with ipsilateral
sensory symptoms after the rupture of an arteriovenous
anomaly in the area of the island of Reil. Their patient also
demonstrated some motor impairment described as a “com-
plaint of a slight loss of strength and coordination of her left
hand” (10).

According to Schneider and Crosby, the secondary motor
area is located in the precentral insular cortex and it represents
both homolateral and contralateral face, upper extremity, and
lower extremity, alternately from an anteroventral to a pos-
terodorsal direction (10). Discharges from this secondary mo-
tor area occur only through the extrapyramidal system via
the ansa lenticularis (4, 10). Thus, it is understandable that
our patient did not demonstrate an extensor plantar response
at the time of admission. In patients with primary motor area
dysfunction, an extensor plantar response was observed as
early as | hour after the onset of symptoms (1). In patients
with lesions of the cerebral hemisphere, if an extensor plantar
response is present, it is clear that the lesion involves primary
motor cortex. But the absence of this response does not
necessarily imply that the motor cortex is intact or that the
secondary motor area is involved because a flexor plantar
response has been observed even with primary motor cortex
lesions (1). It is not possible to differentiate between dysfunc-
tion of the contralateral primary motor cortex and that of the
ipsilateral secondary motor area by the presence or absence
of an extensor plantar response. A CT scan and angiograms
are mandatory to rule out a contralateral primary motor
cortex abnormality before hemiparesis due to dysfunction of
the ipsilateral secondary motor area is considered seriously.

Questions about our patient still remain. (@) Why did right-
sided facial weakness not occur? Is it because of bilateral
representation of the face in the left primary motor cortex or

November 1984

is it because the hematoma in the right side sylvian fissure
did not compress the facial part of the ipsilateral secondary
motor area as severely as the upper and lower extremity parts?
(b) If the secondary motor area represents both the ipsilateral
and the contralateral body, why did left-sided upper extremity
weakness not occur? According to Schneider and Crosby the
secondary motor area of the contralateral upper extremity
located between the ipsilateral upper and lower extremities in
the precentral cortex of the insula (10). It is unreasonable to
assume that compression of the insular cortex by the hema-
toma skipped just the area of the contralateral upper extrem-
ity. Instead, we postulate that ipsilateral representation is
dominant over contralateral representation in the secondary
motor area. Data from cortical stimulation testing show that
electrical thresholds in the secondary motor area are higher
than those in the primary motor area (7, 8, 11), However,
whether such a difference in threshold exists between ipsilat-
eral and contralateral representation of the secondary motor
area in the insular cortex is unknown (4, 10).

Finally, these concepts of dysfunction of secondary motor
or sensory areas seem more important to us when we consider
indications for carotid endarterectomy in patients with is-
chemic cerebrovascular disease. We occasionally see patients
with symptoms of carotid transient ischemic attack or RIND
whose CT scans and angiograms do not show significant
intracranial abnormality, but only ipsilateral lesions at the
cervical carotid bifurcation. The symptoms could be related
to cerebral embolus in the secondary motor or sensory area,
and some of these patients could be treated with ipsilateral
carotid endarterectomy to prevent further ischemic episodes
or major cerebral infarction. Without considering the second-
ary motor or sensory areas, patients with ipsilateral hemipa-
resis or hemisensory disturbance have been misinterpreted as
being hysterical or the phenomena have remained unex-
plained (9, 10).

ACKNOWLEDGMENT

The authors are grateful to Dr. Peter J. Jannetta, Depart-
ment of Neurological Surgery, University of Pittsburgh, for
his critical review of this manuscript.

Received for publication. April 24, 1984: accepted, July 8. 1984.
Reprint requests: Tadashi Kudo, M.D., D.M.Sc.. Kita-Karasuyama
7-26-6, Setagaya-ku, Tokyo, 157 Japan.

REFERENCES

1. Babinski M: On the phenomenon of the toes and its semeiotic
value. in Wilkins RH. Brody IA (eds): Neurological Classics.
New York. Johnson Reprint Corp. 1973. pp 7-10.

2. Bucy PC: Representation of ipsilateral extremities in the cerebral
cortex. Science 78:418. 1933.

3. Bucy PC. Fulton JF: Ipsilateral representation in the motor and
premotor cortex of monkeys. Brain 56:318-342. 1933.

4. Crosby EC. Augustine JR: The functional significance of certain
duplicate motor patterns on the cerebral cortex in primates
including man. Clin Neurol Neurosurg 79:1-14. 1976.

5. Foerster O: The cerebral cortex in man, Lancet 2:309-312. 1931.

6. Gardner WJ: Removal of the right cerebral hemisphere for
infiltrating glioma. Arch Neurol Psychiatry 28:470. 1932.

7. Henneman E: Motor function of the cerebral cortex. in Mount-
castle VB (ed): Medical Physiology. St Louis. CV Mosby, 1974.
pp 747-779.

8. Lauer EW: Ipsilateral facial representation in motor cortex of
macaque. J Neurophysiol 15:1-4. 1952.

9. Sakurai Y. Sato T, Oka N. Okada H. Enokida M. Suzuki J:
Symptomatology of ruptured intracranial aneurysm: I. Symp-
toms immediately after the occurrence of subarachnoid hemor-
thage. in Suzuki J (ed): Cerebral Aneurysms: Experiences with

IPSILATERAL HEMIPARESIS AFTER SAH 729

1000 Directly Operated Cases, Tokyo, Neuron, 1979, pp 51-60.
10. Schneider RC. Crosby E: Ipsilateral symptoms caused by an
arteriovenous malformation of the second or supplementary
sensory area of the island of Reil. Neurosurgery 12:557-560.
1983.
11. Sugar O. Chusid JG. French JD: A second motor cortex in the
monkey, J Neuropathol Exp Neurol 7:182-189, 1948.

COMMENT

This article is very important because it focuses on an
almost completely overlooked area, namely, the insular cortex
and the important clinical finding of ipsilateral symptoms
from a ruptured aneurysm and hematoma in that region. The
authors are to be congratulated on their clear presentation
and discussion.

1 was first alerted to the presence of secondary or association
areas and pathways by Dr. Elizabeth C. Crosby, the world-
famous neuroanatomist, when she identified ipsilateral symp-
toms from facial stimulation of the second or association
motor area in the macaque temporal lobe (3). Crosby and
Schneider wished to reproduce these findings in the human.
It was thought that this could be done ethically during a
trigeminal rhizotomy performed with a temporal approach.
However, most of the patients were too old or too ill to permit
stimulation of the temporal lobe to obtain such ipsilateral
movements from these second motor areas. Baldwin et al.
successfully achieved ipsilateral facial movements in humans
about this time (1).

Kudo and Uno have carefully examined other articles
dealing with this problem. Dr. Crosby and I have continued
to seek out such cases. In the case reported in the authors’
Reference 10, five program directors reviewed the case before
CT scanning and angiography were performed and judged
the patient to be hysterical.

The arteriogram in the currently recorded case shows the
aneurysm responsible for the hematoma and the associated
cerebral edema in the insular region, as seen in the CT scan
and the angiogram. The authors emphasized that a neurosur-
geon who does not have the access to these studies should
consider dysfunction due to stimulation of the second motor
areas in patients with ipsilateral hemiparesis and differentiate
such dysfunction from contralateral primary motor area neu-
rological deficit from the opposite motor area. The authors
stressed a new point of considerable significance, namely, the
recognition of this dysfunction of second motor or sensory
areas when considering the patient for carotid endarterec-
tomy. I am unable to supply an answer to the contributors’
question of why the compression of the insula by the hema-
toma skipped just the area of the contralateral extremity. This
could have been an uneven compression of the brain with
only partial occlusion of vascular flow to the area or possibly
the symptoms were influenced by dominance, as suggested by
the authors.

There are many other important clinical aspects related to
the significance of second or association areas that have been
dealt with by Elizabeth C. Crosby (2).

Richard C. Schneider. M.D.
Ann Arbor, Michigan

|, Baldwin M. Frost LL. Wood CD; Investigation of the primate
amygdala: Movement of the face and jaws. Neurology (NY)

598. 1954.

Crosby “in Schneider RC, Kahn EA. Crosby EC. Taren JT
(eds); Correlative Neurosurgery. Springfield IL. Charles C
Thomas. 1982. ed 3.

3. Schneider RC. Crosby EC: Stimulation of “second” motor areas

in the macque temporal lobe. Neurology (NY) 4:612-632. 1954.

to