Affiliation:
1. Department of Neurosurgery, Helsinki University Central Hospital, Helsinki, Finland
Abstract
Abstract
Platelet aggregation induced by adenosine diphosphate and the release of thromboxane B2 were studied in 68 patients with subarachnoid hemorrhage during the second week after the hemorrhage, when delayed ischemic deterioration most often occurs. Follow-up computed tomographic scans were performed later than 1 month after subarachnoid hemorrhage to reveal permanent hypodense areas consistent with cerebral infarction. Occurrence of hypodense lesions on the follow-up computed tomographic scan was significantly associated with the presence of delayed ischemic deterioration (DID) (P<0.01). Patients with subcortical or cortical cerebral infarctions due to DID released more platelet thromboxane B2 than those with no evidence of a hypodense lesion on the computed tomographic scan (P<0.05). Hypodense areas caused by an intracerebral hematoma or small, deep-seated infarcts due to DID were not associated with significantly elevated release of thromboxane B2, but the lacunar type infarcts were associated with increased aggregation of platelets. The results suggest that augmented platelet function may be involved in the pathogenesis of cerebral infarction due to DID.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Neurology (clinical),Surgery
Cited by
14 articles.
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