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(Stroke. 1996;27:753-755.)
© 1996 American Heart Association, Inc.


Articles

Recurrent Right Hemiplegia Associated With Progressive Ipsilateral Carotid Artery Stenosis

F. Chollet, MD; Y. Rolland; J.F. Albucher; C. Manelfe, MD; J.P. Marc-Vergnes, MD, PhD B. Guiraud-Chaumeil, MD

From the Departments of Neurology and Neuroradiology (C.M.) and INSERM U 230, Hôpital Purpan, Toulouse, France.

Correspondence to Pr F. Chollet, Department of Neurology and INSERM U 230, Hôpital Purpan, Place Baylac, 31059 Toulouse, France.


*    Abstract
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*Abstract
down arrowIntroduction
down arrowCase Report
down arrowDiscussion
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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.


Key Words: carotid artery diseases • cerebral infarction • cerebrovascular reserve • hemiplegia


*    Introduction
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up arrowAbstract
*Introduction
down arrowCase Report
down arrowDiscussion
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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.


*    Case Report
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up arrowAbstract
up arrowIntroduction
*Case Report
down arrowDiscussion
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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 1Down and TableDown). 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.



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Figure 1. Single-photon emission CT images of intracerebral vascular reserve (cerebral blood flow [CBF] before and after acetazolamide injection) after the first stroke (A), after the second stroke (B), and after carotid surgery (C). The color scale indicates CBF values: dark blue corresponds to the lowest CBF values and red and white correspond to the highest CBF values.


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Table 1. Repeated Measurements of Intracerebral Vascular Reserve After First and Second Strokes and After Carotid Surgery

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 2Down). 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 1Up and TableUp). 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 4Down). No dramatic changes were observed in the vertebrobasilar system.



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Figure 2. CT scan of the patient showing the left hemisphere watershed infarction.



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Figure 4. Angiogram of the patient showing right internal carotid stenosis measured at 50% after the first stroke (left) and 80% after the second stroke (right).

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 1Up and TableUp).


*    Discussion
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowCase Report
*Discussion
down arrowReferences
 
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 1Up and TableUp); 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 2Up). Second, the angiogram confirmed that the left anterior cerebral artery was supplied by the patient's right internal carotid artery (Fig 3Down). 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 1Up and TableUp). 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.



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Figure 3. Angiogram of the patient showing that left anterior and middle cerebral arteries were supplied by the right internal carotid artery.

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 1Up and TableUp).

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.


*    Acknowledgments
 
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.


*    References
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowCase Report
up arrowDiscussion
*References
 

  1. 1. Yanagihara T, Sundt T, Piepgras D. Weakness of the lower extremity in carotid occlusive disease. Arch Neurol. 1988;45:297-301. [Abstract]
  2. Chimowitz M, Lafranchise F, Furlan A, Awad I. Ipsilateral leg weakness associated with carotid stenosis. Stroke. 1990;21:1362-1364. [Abstract/Free Full Text]
  3. 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. [Abstract/Free Full Text]
  4. Bogousslavsky J, Regli F. Unilateral watershed cerebral infarcts. Neurology. 1986;36:373-377. [Abstract/Free Full Text]
  5. 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. [Abstract/Free Full Text]
  6. 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.
  7. 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.
  8. 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. [Abstract/Free Full Text]
  9. Celsis P, Goldman T, Henriksen L, Lassen NA. A method for calculating cerebral blood flow from emission computed tomography of inert gas concentrations. J Comput Assist Tomogr. 1981;5:641-645.[Medline] [Order article via Infotrieve]



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