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(Stroke. 1995;26:422-425.)
© 1995 American Heart Association, Inc.

Articles

Stroke Patterns in Unilateral Atherothrombotic Occlusion of the Internal Carotid Artery

F. Mounier-Vehier, MD; D. Leys, MD J. P. Pruvo, MD

From the Departments of Neurology (F.M.-V., D.L.) and Neuroradiology (J.P.P.), University Hospital, Lille, France.

Correspondence to F. Mounier-Vehier, MD, Service de Neurologie B, Hôpital B, F-59037 Lille, France.

	Abstract

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Background and Purpose Stroke patterns in patients with occlusion of the internal carotid artery (ICA) and no potential cardiac cause of stroke remain unknown. The aim of our study was to determine the pattern of stroke in patients with an occlusion of the ICA of presumed atherosclerotic origin.

Methods Of 873 consecutive patients admitted for an acute ischemic event during a 49-month period, 40 (29 men and 11 women; mean age, 63 years) had a unilateral occlusion of the ICA of presumed atherosclerotic origin and no other potential cause of stroke. They underwent two computed tomographic scans, Doppler ultrasonography, and B-mode echotomography of the cervical arteries or angiography and echocardiography. We compared stroke patterns between both hemispheres.

Results We found ipsilateral infarcts in 32 patients (80%; 99% confidence interval [CI], 64% to 96%) and contralateral infarcts in 12 patients (30%; 99% CI, 11% to 49%). Infarcts ipsilateral to the ICA occlusion were more likely to be cortical (odds ratio, 9.33; 99% CI, 2.4 to 36.35) or subcortical infarcts 15 mm or greater (odds ratio, 16.71; 99% CI, 1.05 to 267.3). The prevalence of subcortical infarcts less than 15 mm did not differ between hemispheres.

Conclusions Symptomatic infarcts related to an ICA occlusion are more likely to be cortical or large subcortical infarcts. Small subcortical infarcts have the same prevalence in both hemispheres and therefore may be coincidental.

Key Words: carotid arteries • cerebral infarction • cerebrovascular disorders • stroke assessment

	Introduction

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The pattern of stroke in patients with an occlusion of the internal carotid artery (ICA) varies from an extensive hemispheric infarct to no visible infarct.¹ The first retrospective studies were based on postmortem findings, leading to an overrepresentation of large infarcts.^{2 3 4} The first studies with computed tomographic (CT) scan^{5 6 7 8 9 10} were done before the modern templates of Damasio¹¹ and Bogousslavsky and Regli¹² ; they did not provide information about echocardiographic data and did not take into account associated potential cardiac sources of emboli. Other studies were done exclusively in specific stroke subtypes, such as border-zone infarcts.^{13 14} The most recent studies included patients with various types of stenosis of the ICA, such as atherothrombotic occlusions, dissections, embolic occlusions, and even iatrogenic occlusions of the ICA.^{15 16} However, stroke patterns may be influenced by the mechanism of the occlusion of the ICA. The heterogeneity of the methodologies used in these studies explains why it is difficult to compare them and why their conclusions cannot be generalized. Moreover, no information on the hemisphere opposite to the vascular lesion has been reported.

The aim of our study was to determine the pattern of stroke in 40 selected patients with an occlusion of the ICA presumably due to atherosclerosis and no other potential cardiac cause of stroke.

	Subjects and Methods

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We conducted this study during a 49-month period (October 1, 1989 to October 31, 1993) in 873 consecutive patients admitted as emergency cases for an ischemic stroke or transient ischemic attack (TIA), after exclusion of those with previous neurosurgery, severe head trauma, and cerebral arterial or arteriovenous malformation. All patients were examined at admission by a resident in neurology and within 24 hours by a senior neurologist. One hundred seventy-eight patients (20.4%) had a TIA, defined as episodes of focal cerebral dysfunction, presumably ischemic in origin, lasting less than 24 hours and followed by return to normality. Six hundred ninety-five had an ischemic stroke, defined as clinical signs of focal disturbance of cerebral function lasting more than 24 hours, with no apparent cause other than of ischemic origin. All patients had standard blood and urine tests, electrocardiography, chest radiography, and noncontrast CT scan within 24 hours after onset. Those who survived underwent a second CT scan between day 8 and day 15, Doppler ultrasonography, B-mode echotomography, echocardiography, and 24-hour electrocardiography. Cerebral angiography was performed in selected cases only. CT scans were performed without contrast on a Siemens Somatom II machine with 5-mm contiguous slice thickness in a plane 15° negative to the canthomeatal plane. Scan time was 9.6 seconds per slice.

Stroke patterns were determined in the 873 subjects without knowledge of the presumed cause of stroke. In a conference, one neuroradiologist (J.P.P.) and one neurologist (D.L.), blinded to the clinical data, determined the types of focal lesions on the second CT scan of the first 322 patients. The interobserver and intraobserver reliability of this method of assessment of CT data has been previously evaluated as excellent.¹⁷ Therefore, the 551 subsequent scans were assessed by only one observer (F.M.-V.). The observers determined whether the following lesions were present: cortical infarcts (any infarct involving the cortical surface and cerebellar infarcts); small subcortical infarcts (any infarct <15 mm involving the basal ganglia, thalamus, and internal capsule and sparing the cortical surface) according to Damasio's templates¹¹ ; border-zone infarcts¹² (any infarct located between two arterial territories) and centrum ovale infarcts¹⁸ by the criteria of Bogousslavsky and Regli^{12 18} ; and hyperdense middle cerebral artery sign according to previously reported criteria.¹⁹ Patients with hemorrhagic changes within an infarct were classified in the infarct group. We defined silent infarcts according to the criteria used in the study of Mounier-Vehier et al.²⁰

We described stroke patterns ipsilateral to the ICA occlusion and then compared them between both hemispheres by means of the odds ratio method with 99% confidence intervals (CIs).²¹

	Results

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Of the 873 patients, 59 (6.8%) had an occlusion of the ICA diagnosed by Doppler ultrasonography and B-mode echotomography or cerebral angiography. We excluded 6 patients because of associated atrial fibrillation and 3 patients who died before the second CT scan. No patient had a cardiac source of stroke on echocardiography. Ten patients were excluded from the study because the presumed cause of the occlusion of the ICA was a dissection. The study was thus performed in the 40 remaining patients. They consisted of 29 men and 11 women with a median age of 63 years. Twenty-five of them (62.5%) underwent cerebral angiography.

Raw data are detailed in Table 1. No patient had a bilateral occlusion of the ICA. The three patients who had a contralateral stenosis of the ICA of 50% or more (patients 4, 18, and 33) had no infarct on the hemisphere opposite to the ICA occlusion.

View this table: [in this window] [in a new window]   Table 1. Stroke Patterns in Patients With Internal Carotid Artery Occlusion

Thirty-two patients had an ipsilateral infarct (80%; 99% CI, 64% to 96%), and 12 had a contralateral infarct (30%; 99% CI, 11% to 49%). Ipsilateral infarcts were more likely to be cortical infarcts or subcortical infarcts 15 mm or greater, but the prevalence of subcortical infarcts smaller than 15 mm did not differ between hemispheres (Table 2).

View this table: [in this window] [in a new window]   Table 2. Location of Infarcts in the Hemispheres Ipsilateral and Contralateral to the Occluded Internal Carotid Artery

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
This study suggests that infarcts ipsilateral to an ICA occlusion are more likely to be cortical infarcts or large subcortical infarcts and that small deep infarcts may be coincidental.

To our knowledge, this is the first study of stroke patterns in consecutive patients admitted for an acute ischemic event presumably due to an atherothrombotic occlusion of the ICA and no potential cardiac source of stroke. The prevalence of carotid occlusion was smaller in our study (6.75%) than in the Lausanne Stroke Registry (18%),²² probably because of the inclusion of patients with TIA. Although Castaigne et al⁴ found 12% of patients with bilateral occlusion of the ICA in their pathological study, no patient in our study had a bilateral ICA occlusion. However, we performed our study in patients who survived at least a few days, and this method may have excluded the most severe patients, such as those with bilateral occlusion of the ICA.

Although atherosclerosis of the ICA is a potential source of silent infarcts,²³ all silent infarcts were contralateral to the occluded ICA. Presence of silent infarct due to atherosclerotic stenosis of the ICA before the index stroke and occlusion of the ICA cannot be excluded. However, we could not determine the prevalence of silent infarcts ipsilateral to the occluded ICA because all our patients were clinically symptomatic.

An anterograde extension of the thrombus⁴ and variations in the anatomy of the polygon of Willis¹⁶ are the two main factors explaining the high variability of stroke patterns in patients with occlusion of the ICA. Isolated middle cerebral artery territory infarcts may also be due to distal embolic occlusion.¹⁵ A very small or absent ipsilateral posterior communicating artery could increase the risk of a watershed infarct due to an ipsilateral ICA occlusion.²⁴ Such a result obtained with magnetic resonance angiography has been a matter of controversy.²⁵ Further studies on ICA occlusion should be performed with systematic angiography, magnetic resonance angiography, and transcranial Doppler to understand the mechanism of stroke in these patients.

The prevalence of border-zone infarcts was surprisingly low. Bogousslavsky and Regli¹⁴ found a prevalence of 17%, but their patients frequently had severe contralateral carotid artery disease, and 54% of them had symptomatic heart disease. In our study only three patients had a contralateral ICA stenosis. Patients with a cardiac source of embolism were excluded from the study, and no patients had conditions that might cause acute lowering of cardiac output. These inclusion criteria might explain the difference in the prevalence of border-zone infarcts. Rodda and Path¹⁵ found only two patients with border-zone infarcts in 20 cases of internal carotid disease. The high frequency of anterior choroidal artery infarcts and the absence of isolated anterior cerebral artery infarct were previously noted by Castaigne et al.⁴ Since we analyzed the second CT scan during the period of possible fogging effect, we cannot exclude the possibility that some ischemic lesions may have been underestimated.

The prevalence of small subcortical infarcts did not differ between both hemispheres. This finding suggests that small subcortical infarcts ipsilateral to an occlusion of the ICA may be coincidental infarcts caused by associated small-vessel occlusion. Infarcts found in the opposite hemisphere might be due either to a transhemispheric passage of microemboli from the ICA²⁶ or to an associated source of stroke, such as small-vessel occlusion or even vertebrobasilar atherosclerosis.

	Acknowledgments

 
This study was supported in part by a grant from the Direction de la Recherche et des Etudes Doctorales.

Received August 3, 1994; revision received November 8, 1994; accepted December 1, 1994.

	References

Top Abstract Introduction Subjects and Methods Results Discussion References

 

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