C F Bladin1, B R Chambers. 1. Department of Neurology, University of Melbourne, Heidelberg Repatriation Hospital, Australia.
Abstract
BACKGROUND AND PURPOSE: Infarction in the internal border-zone region has been described radiologically and pathologically. The aim of this study was to define the clinical and pathophysiological correlates of internal watershed infarction. METHODS: Eighteen consecutive stroke patients with evidence of internal watershed infarction on computed tomography (CT) were studied. RESULTS: Two CT patterns were identified: 6 patients had confluent internal watershed infarction (CIWI), and 12 patients had partial internal watershed infarction (PIWI). Syncopal symptoms and/or documented hypotension were prominent in both groups. Patients with CIWI usually presented with stepwise onset of contralateral hemiplegia and recovered poorly; patients with PIWI usually had discrete episodes of brachiofacial sensorimotor deficit and good recovery. Both groups had evidence of cortical involvement as part of their clinical deficit. Severe carotid occlusive disease was seen in 10 patients, and 12 patients had evidence of transiently impaired cardiac output. Carotid disease (P < .001), cardiac disease (P < .01), and diabetes mellitus (P < .01) were more prevalent in patients with internal watershed infarction compared with our stroke population as a whole. CONCLUSIONS: Distinguishing internal watershed infarction from lacunar and other subcortical infarctions is important because the different pathological mechanisms demand different therapeutic strategies.
BACKGROUND AND PURPOSE:Infarction in the internal border-zone region has been described radiologically and pathologically. The aim of this study was to define the clinical and pathophysiological correlates of internal watershed infarction. METHODS: Eighteen consecutive strokepatients with evidence of internal watershed infarction on computed tomography (CT) were studied. RESULTS: Two CT patterns were identified: 6 patients had confluent internal watershed infarction (CIWI), and 12 patients had partial internal watershed infarction (PIWI). Syncopal symptoms and/or documented hypotension were prominent in both groups. Patients with CIWI usually presented with stepwise onset of contralateral hemiplegia and recovered poorly; patients with PIWI usually had discrete episodes of brachiofacial sensorimotor deficit and good recovery. Both groups had evidence of cortical involvement as part of their clinical deficit. Severe carotid occlusive disease was seen in 10 patients, and 12 patients had evidence of transiently impaired cardiac output. Carotid disease (P < .001), cardiac disease (P < .01), and diabetes mellitus (P < .01) were more prevalent in patients with internal watershed infarction compared with our stroke population as a whole. CONCLUSIONS: Distinguishing internal watershed infarction from lacunar and other subcortical infarctions is important because the different pathological mechanisms demand different therapeutic strategies.
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