Dissemin is shutting down on January 1st, 2025

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Karger Publishers, Cerebrovascular Diseases, 1(24), p. 11-19, 2007

DOI: 10.1159/000103111

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Patterns of Infarction in Hemodynamic Failure

This paper was not found in any repository, but could be made available legally by the author.
This paper was not found in any repository, but could be made available legally by the author.

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Abstract

<i>Background and Purpose:</i> The mechanism of stroke in patients with atherosclerotic occlusive disease and hemodynamic failure may be primarily hemodynamic or a combination of hemodynamic and embolic factors. The purpose of this study was to investigate the clinical and imaging features of stroke in these patients. <i>Methods:</i> Eleven patients with complete atherosclerotic carotid artery occlusion and increased oxygen extraction fraction measured in the hemisphere distal to the occlusion developed an ischemic stroke during the observation phase of a prospective study of cerebral hemodynamics and stroke risk. The medical and study records related to the endpoint event for these 11 patients were reviewed. Records were reviewed for evidence of associated hypotension and for specific details of the neurological deficit. Infarct location was characterized, based on review of imaging and clinical features, as: (1) middle cerebral artery (MCA) core; (2) possible cortical border zone, or (3) internal border zone. <i>Results:</i> One patient had a retinal infarction; the remaining 10 had MCA territory strokes. Six of the 10 infarctions occurred in the MCA core territory. Two of these 6 were fatal hemispheric events. One of the 10 infarctions occurred in the cortical border zone region. Two of the remaining 3 infarctions were localized to the internal border zone. One was indeterminate. <i>Conclusions:</i> The clinical features and radiological patterns of stroke in many patients with hemodynamic impairment failure and carotid occlusion are most consistent with large artery thromboembolic stroke. These data suggest a synergistic effect between embolic and hemodynamic mechanisms for large artery thromboembolic stroke.