Recurrent Right Hemiplegia Associated With Progressive Ipsilateral Carotid Artery Stenosis
Background Ipsilateral sensory motor symptoms associated with carotid artery stenosis are rare, and few reports are available in the literature.
Case Description We report the case of a 50-year-old man who presented with right hemiplegia that recurred 14 months later. A left hemisphere watershed infarction was detected. Repeated angiograms showed a left internal carotid occlusion and a right internal carotid stenosis that initially measured 50% and worsened to 80% after the second stroke.
Conclusions Repeated quantitative measurements of cerebrovascular reserve demonstrated the hemodynamic mechanism of the strokes and the role of a right internal carotid lesion in causing the recurrence of right hemiplegia.
It is usually thought that hemiplegia associated with carotid disease occurs contralateral to the involved carotid artery. However, Yanagihara et al1 and Chimowitz et al2 described two patients and one patient, respectively, who presented with deficits ipsilateral to a highly stenotic carotid artery. A hemodynamic mechanism was suspected in all cases. We report another patient with recurrent right hemiplegia and severe carotid lesions in whom the recurrence of right hemiplegia can be associated with a progressive stenosis of the right carotid artery. The hemodynamic mechanism of the strokes was investigated by repeated measurements of intracerebral vascular reserve with single-photon emission CT (Tomomatic 64, Medimatic) using 133Xe before and after acetazolamide injection.3 We conclude that a hemodynamic mechanism was responsible.
A 50-year-old man, an engineer, was admitted to the neurology department on April 15, 1993, for right hemiplegia. Neurological examination at admission showed a right motor deficit involving his right arm and hand and predominantly his right leg and foot. His face was spared. A mild global sensory loss was also detected. No aphasia or hemianopsia was noticed. The deficit occurred abruptly a few hours before admission and was preceded the week before by at least three similar transient episodes. Results of an early CT scan were normal. The scan was repeated a few days later and showed a left frontal cortico-subcortical hypodensity related to a watershed infarction. Cerebral angiography showed occlusion of the left carotid artery and mild (50%) stenosis of the right carotid artery. No major stenosis was detected on vertebral arteries. Cerebral blood flow (CBF) measurements before and after acetazolamide injection showed a large impairment of cerebrovascular reserve in the left sylvian territory (Fig 1⇓ and Table⇓). The patient was treated with aspirin (250 mg once a day). He recovered almost completely from his deficit and was discharged on day 20 after the stroke.
The patient was referred again to the neurology department 14 months later (June 1994) for a right hemiparesis of abrupt onset. Neurological examination at admission again showed a right motor deficit involving his right arm and leg and sparing his face. Mild sensory loss was also associated, but no aphasia was detected. The visual field was normal. CT scan showed the sequelae of the previous infarction, which extended from the front to the back of the border between the anterior and middle cerebral artery territories (Fig 2⇓). No hypotensive episode was noticed at the onset. CBF measurements before and after acetazolamide were lower, showing a steal phenomenon in the left sylvian territory after injection of acetazolamide. CBF decreased from 44 to 37 mL·100 g−1·min−1 (−15.9%) in the left sylvian territory after injection of acetazolamide (Fig 1⇑ and Table⇑). No clinical deficit was observed during or after the procedure. Cerebral angiography again showed the occlusion of the left carotid artery and indicated a worsening of right carotid artery stenosis, measured at 80% (Fig 4⇓). No dramatic changes were observed in the vertebrobasilar system.
It was decided that the patient’s progressive stenosis of the right internal carotid artery was causing the recurrent stroke mechanism, and a right carotid endarterectomy was proposed. Right carotid endarterectomy was performed on July 24, 1994, without complications.
A third measurement of CBF before and after acetazolamide injection was performed on October 28, 1994 (ie, more than 3 months after surgery). It showed a clear-cut improvement of cerebrovascular reserve in both left and right hemispheres. Reactivity of CBF after acetazolamide was positive (Fig 1⇑ and Table⇑).
The first right hemiplegia was related to the occlusion of the left internal carotid artery. A hemodynamic mechanism of the stroke was suspected because the first CBF measurement showed a massive reduction of intracranial vascular reserve of the superficial left sylvian territory (Fig 1⇑ and Table⇑); also, the topography of the infarct on the CT scan suggested a watershed infarct. The predominance of weakness in the leg has been described as one of the clinical characteristics of border-zone infarcts.1 4
The second right hemiplegia was clinically very similar and occurred more than 1 year after the first. The mechanism can be debated, but an embolic mechanism from the left carotid artery stump is unlikely, and there are several arguments in favor of a hemodynamic mechanism from the right internal carotid artery. First, the CT scan aspect of the stroke strongly suggests a watershed infarction located at the border between the left anterior and left middle cerebral artery territories (Fig 2⇑). Second, the angiogram confirmed that the left anterior cerebral artery was supplied by the patient’s right internal carotid artery (Fig 3⇑). This point is underlined in previous descriptions as essential in establishing the possible responsibility of ipsilateral carotid lesion in the genesis of the stroke.1 2 Finally, the repeated measurement of CBF before and after acetazolamide injection showed a worsening of the cerebrovascular reserve with a steal phenomenon in the left superficial sylvian territory (Fig 1⇑ and Table⇑). Because left internal carotid occlusion was already present after the patient’s first hemiplegia, the worsening of the left sylvian cerebrovascular reserve could be associated with right internal carotid stenosis, which was measured at 50% after the first hemiplegia in April 1993 and 80% after the second stroke in June 1994. These data suggest that the recurrence of right hemiplegia was of hemodynamic origin caused by an increase of right internal carotid artery stenosis.
The performance of the right carotid endarterectomy confirmed the influence of right internal carotid stenosis on the impairment of left sylvian cerebrovascular reserve. The effect of carotid endarterectomy was hemodynamically observable in both hemispheres (Fig 1⇑ and Table⇑).
To our knowledge, this is the first time that the role of a carotid stenosis ipsilateral to a stroke has been proved hemodynamically. Repeated quantified measurements of intracranial cerebrovascular reserve3 5 6 7 were extremely useful. Chimowitz et al2 reported one patient with severe bilateral lesions of carotid arteries and bilateral clinical deficit. The angiogram showed that the left carotid artery was supplying not only the left sylvian territory but also left and right anterior cerebral artery territories. No hemodynamic measurements were performed. Yanagihara et al1 also described two patients in their series with ipsilateral symptoms related to a severe hypoperfused border-zone area. CBF measurement with xenon was performed but with stationary detectors and without evaluation of intracerebral vascular reserve. No information on the follow-up was given.
Furthermore, our findings are in agreement with the results of a computer simulation of intracranial hemodynamics that was developed in our group.8 This study demonstrated quantitatively that the pressure reserve at entry of both anterior and middle cerebral arteries distal to an internal carotid occlusion depends greatly on the presence of patency of the anterior communicating artery, on mean arterial blood pressure, and on a contralateral carotid stenosis with two critical degrees of stenosis very close to those observed in our patient.
We want to thank sincerely G. Viallard, T. Pujol, and C. Blanchard for their technical assistance.
- Received September 25, 1995.
- Revision received November 16, 1995.
- Accepted November 23, 1995.
- Copyright © 1996 by American Heart Association
Chimowitz M, Lafranchise F, Furlan A, Awad I. Ipsilateral leg weakness associated with carotid stenosis. Stroke. 1990;21:1362-1364.
Chollet F, Celsis P, Clanet M, Guiraud-Chaumeil B, Rascol A, Marc-Vergnes JP. SPECT study of CBF reactivity after acetazolamide in patients with transient ischemic attacks. Stroke. 1989;20:458-464.
Bogousslavsky J, Regli F. Unilateral watershed cerebral infarcts. Neurology. 1986;36:373-377.
Vorstrup S, Brun B, Lassen NA. Evaluation of the cerebral vasodilatory capacity by the acetazolamide test before EC-IC bypass surgery in patients with occlusion of the internal carotid artery. Stroke. 1986;17:1291-1298.
Derlon JM, Bouvard G, Hubert P. Etude hémodynamique des lésions obstructives de l’artère carotide interne: intéret de la mesure couplée du débit et du volume sanguin cérébral. Rev Neurol. 1987;143;32-39.
Sabatini U, Chollet F, Celsis P, Viallard G, Rascol A, Marc-Vergnes JP. Intracerebral reserve assessment with SPECT: reactivity to acetazolamide and cerebral blood volume measurement. In: Hartmann A, Kuschinsky V, Hoyer S, eds. Cerebral Ischemia and Dementia. Berlin/Heidelberg: Springer-Verlag; 1991:322-326.
Cassot F, Vergeur V, Bossuet P, Hillen B, Zagzoule M, Marc-Vergnes JP. Effects of anterior communicating artery diameter on cerebral hemodynamics in internal carotid artery disease: a model study. Circulation. 1995;92:3122-3131.