1362

Case Reports

Ipsilateral Leg Weakness Associated
With Carotid Stenosis
Marc I. Chimowitz, MD, E. Frank Lafranchise, MD,
Anthony J. Furlan, MD, and Issam A. Awad, MD
Ipsilateral motor or sensory symptoms associated with carotid occlusive disease are rare. We
report a 52-year-old man who presented with aphasia, right hemiparesis, mild left leg
weakness, and bilateral Babinski's signs. During the previous 10 days, he had experienced three
episodes of left leg numbness and incoordination that occurred either alone or in association
with right arm and leg weakness. Computed tomography showed infarcts in the right
frontoparietal (parasagittal), left frontal, and left parietal lobes. Cerebral angiography revealed
60% stenosis of the right internal carotid artery, 80% stenosis of the left internal carotid artery,
absence of the Al segment of the right anterior cerebral artery, filling of the right anterior
cerebral artery from the left carotid circulation only, and a normal vertebrobasilar system. This
report illustrates that leg weakness may occur ipsilateral to carotid disease if the contralateral
anterior cerebral artery is supplied by the ipsilateral carotid artery. (Stroke 1990;21:1362-1364)

I

t is generally considered that weakness or sensory
dysfunction associated with carotid disease
occurs contralateral to the involved carotid
artery. However, a study by Yanagihara et al,1 which
focused on the mechanism of lower extremity weakness in carotid occlusive disease, described two
patients with lower extremity weakness ipsilateral to a
highly stenotic carotid artery. We report another
patient with leg weakness ipsilateral to carotid stenosis and attempt to clarify the clinical, radiologic, and
pathophysiological features of this unusual entity.
Case Report

A 52-year-old hypertensive man was transferred
from another hospital on September 15,1989, because
of aphasia, right hemiparesis, and left leg weakness.
Six months previously, over 2 weeks he had experienced three episodes of transient monocular blindness
in the left eye, each of which resolved after a few
minutes. The visual symptoms did not recur. On
August 30, he had an episode of right arm weakness
and tingling lasting <5 minutes. A similar spell on
September 5 prompted admission to an outside hospital, where the neurologic examination, a cranial
computed tomogram (CT scan), and an electroencephalogram were reported as normal. Carotid ultraFrom the Departments of Neurology (M.I.C., E.F.L., A.J.F) and
Neurosurgery (I.A.A.), The Cleveland Clinic Foundation, Cleveland, Ohio.
Address for correspondence: Marc I. Chimowitz, MD, Neurology Service, Veterans Administration Medical Center, Ann Arbor,
MI 48105.
Received January 17, 1990; accepted May 24, 1990.

sonography suggested >90% stenosis of the left internal carotid artery and 50-70% stenosis of the right
internal carotid artery. Dipyridamole was prescribed.
Over the next 10 days, the patient experienced two
brief (<5 minutes) episodes of right arm weakness
and tingling and three episodes of left leg numbness
that involved almost the entire leg from the foot to
the buttock and was associated with incoordination
of the leg. The left leg symptoms lasted from 30
minutes to a few hours and usually occurred independently of the right arm symptoms, although on
one occasion they occurred together. On September
15, the patient awoke confused and agitated with a
right hemiparesis. He was transferred to the Cleveland Clinic, where examination revealed a blood
pressure of 160/90 mm Hg, a regular pulse of 85/min,
bilateral carotid bruits, expressive aphasia, right
hemiparesis (arm 2/5, leg 4-/5), mild left leg weakness (proximal 4-/5, distal 4+/5), bilateral hyperreflexia and Babinski's signs, and mild sensory loss
(pinprick, touch, proprioception) of the right arm.
Heparin was prescribed.
A cranial CT scan on September 15 was normal,
but another scan on September 20 showed infarcts
involving the right frontoparietal (parasagittal), left
frontal, and left parietal lobes (Figure 1). Cerebral
angiography on September 20 revealed 60% stenosis
of the right internal carotid artery with a large ulcer,
80% stenosis of the left internal carotid artery with
an apparent filling defect in the proximal portion of
the vessel, filling of the proximal right anterior cerebral artery from the left carotid circulation only,
delayed filling of the distal right anterior cerebral

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Chimowitz et al Ipsilateral Weakness and Carotid Disease

1363

FIGURE 1. Cranial computed tomography
showing right parasagittal (large bold arrow),
left parietal (small bold arrow), and left frontal (large fine arrow) infarcts in 52-year-old
hypertensive man with 80% stenosis of left
internal carotid artery.

artery territory compared with the left, no evidence
of a filling defect in the right anterior cerebral artery
territory, and a normal vertebrobasilar system that
did not contribute flow to the right middle cerebral
artery (Figure 2). An echocardiogram and an electrocardiogram were normal.
The patient underwent left carotid endarterectomy
on September 21, 1989. At surgery a large ulcerative
plaque was found that severely compromised the
vessel lumen (residual diameter <2 mm). There was
no intraluminal clot. All motor deficits resolved within
1 week after surgery, and his expressive aphasia recovered during the subsequent 6 weeks. The patient has
not experienced recurrent cerebral ischemic symptoms in 4 months of postoperative follow-up.

Discussion
Although this patient had stenosis of both internal
carotid arteries, it is highly likely that the right frontoparietal (parasagittal) infarct was caused by the left
carotid stenosis since the right anterior cerebral artery
was supplied exclusively by the left carotid circulation.
This occurred despite a higher grade stenosis on the
left side, which suggests that the Al segment of the
right anterior cerebral artery was atretic.
It is difficult to determine whether embolism or
hypoperfusion was the underlying mechanism of our
patient's right hemisphere transient ischemic attacks
(TIAs) and infarct. The long duration of the right
hemisphere TIAs argues against a hemodynamic
mechanism,2 but the simultaneous occurrence of

F I G U R E 2. Cerebral angiograms showing 60% stenosis of
right internal carotid artery
(small bold arrow), 80% stenosis of left internal carotid artery
(large bold arrow), filling of right
anterior cerebral artery from left
carotid circulation only (arrow),
and delayed filling of distal right
anterior cerebral artery territory
(fine arrow) compared with left
anterior cerebral artery territory.

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1364

Stroke Vol 21, No 9, September 1990

right and left hemisphere TIAs on one occasion, the
location of the right frontoparietal infarct on CT
scan,3-4 and the angiographic finding of delayed filling
of the distal right anterior cerebral artery territory
suggest that hypoperfusion was the major factor.
Further evidence that hypoperfusion is the likely
mechanism of leg weakness ipsilateral to carotid
stenosis is provided by the two patients of Yanagihara et al1 who reported stereotypical episodes of leg
weakness prompted by walking, and by cerebral
blood flow studies in patients with carotid disease
and weakness of the lower extremity that show
hypoperfusion in the border zone between the anterior and middle cerebral arteries.1-5
A necessary condition for leg weakness ipsilateral
to carotid disease is that the contralateral anterior
cerebral artery be supplied by the ipsilateral carotid
artery. In the two patients of Yanagihara et al,1 this
occurred in the setting of prior occlusion of the
contralateral internal carotid artery; however, in our
patient the contralateral internal carotid artery was
patent but the Al segment of the contralateral
anterior cerebral artery was atretic. This finding
stresses the importance of evaluating the intracranial
circulation bilaterally in patients with extracranial
carotid occlusive disease since without this data our

patient's left leg symptomatology may have been
attributed to the moderate stenosis of the right
internal carotid artery.
Although our patient presented with bilateral
symptoms, signs, and CT-documented infarcts, the
two previously reported patients presented with leg
weakness only on the side of the stenotic carotid
artery. Therefore, ipsilateral carotid disease should
be considered in the differential diagnosis of episodic
or persistent weakness of one lower extremity.
References
1. Yanagihara T, Sundt TM Jr, Piepgras DG: Weakness of the
lower extremity in carotid occlusive disease. Arch Neurol 1988;
45:297-301
2. Pessin MS, Duncan GW, Mohr JP, Poskanzer DC: Clinical and
angiographic features of carotid transient ischemic attacks. N
EnglJMed 1977;296:358-362
3. Bogousslavsky J, Regli F: Unilateral watershed cerebral infarcts. Neurology 1986;36:373-377
4. Wodarz R: Watershed infarctions and computed tomography.
A topographical study in cases with stenosis or occlusion of the
carotid artery. Neuroradiology 1980;19:245-248
5. Powers WJ, Grubb RL Jr, Raichle ME: Physiological responses
to focal cerebral ischemia in humans. Ann Neurol 1984;
16:546-552
KEY WORDS • carotid artery diseases • cerebral infarction

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Ipsilateral leg weakness associated with carotid stenosis.
M I Chimowitz, E F Lafranchise, A J Furlan and I A Awad
Stroke. 1990;21:1362-1364
doi: 10.1161/01.STR.21.9.1362
Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1990 American Heart Association, Inc. All rights reserved.
Print ISSN: 0039-2499. Online ISSN: 1524-4628

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