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Lesion Patterns and Mechanism of Ischemia in Internal Carotid Artery Disease: a Diffusion-weighted Imaging Study

Overview
Journal Arch Neurol
Specialty Neurology
Date 2002 Oct 11
PMID 12374495
Citations 14
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Abstract

Context: Although embolism and low-flow phenomenon are the 2 main mechanisms of stroke in internal carotid artery (ICA) occlusive disease, the mechanism of border-zone infarction remains controversial. Diffusion-weighted imaging (DWI) can more easily detect small or multiple ischemic lesions than conventional imaging.

Objectives: To investigate the ischemic lesion patterns on DWI and to discuss the mechanisms of stroke in ICA disease.

Design: Case series.

Setting: A tertiary referral center.

Patients: We enrolled 35 consecutive patients who had an acute ischemic stroke and (> or = 70%) stenosis or an occlusion of the extracranial ICA confirmed by cerebral angiography and an acute relevant stroke lesion on DWI within 1 week of onset, but without cardiac sources of embolism and tandem intracranial arterial disease.

Main Outcome Measures: The lesion pattern on DWI was categorized as territorial or border zone. Multiple ischemic lesions were defined as noncontiguous lesions on DWI in more than 1 vascular territory.

Results: There were 3 distinctive stroke lesion patterns. (1) A territorial lesion without a border-zone lesion was found in 21 patients: superficial and superficial territorial in 9, superficial and deep territorial in 7, and single in 5. (2) A border-zone lesion with or without a territorial lesion was found in 10 patients: border zone and territorial in 9 and border zone alone in 1. (3) Bilateral hemispheric lesions were found in 4 patients. Multiple ischemic lesions were found in 29 (82.9%) of the 35 patients. No patient had episodes of hemodynamic compromise.

Conclusions: An acute ischemic lesion in ICA occlusive disease is mainly multiple. Border-zone infarction was mostly associated with territorial infarction. These results support the fact that embolism is the predominant stroke mechanism in ICA occlusive disease.

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