(Stroke. 1999;30:2495-2501.)
© 1999 American Heart Association, Inc.
Abstracts of Literature |
Abstracts of Literature
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Cerebral Aneurysms |
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AB-14505-99
Human Arachnoid Villi Response to Subarachnoid Hemorrhage: Possible Relationship to Chronic Hydrocephalus—Massicotte EM, Del Bigio MR (Dept of Pathology, Univ of Manitoba, D212-770 Bannatyne Ave, Winnipeg, Manitoba, MB R3E 0W3, Canada)—J Neurosurg. 1999;91:80–84.
Object. The origin of chronic communicating hydrocephalus following subarachnoid hemorrhage (SAH) is not well understood. Fibrosis of the arachnoid villi has been suggested as the cause for obstruction of cerebrospinal fluid (CSF) flow, but this is not well supported in the literature. The goal of this study was to determine the relationship between blood, inflammation, and cellular proliferation in arachnoid villi after SAH.
Methods. Arachnoid villi from 50 adult patients were sampled at autopsy. All specimens were subjected to a variety of histochemical and immunohistochemical stains. The 23 cases of SAH consisted of patients in whom an autopsy was performed 12 hours to 34 years post-SAH. Fifteen cases were identified as moderate-to-severe SAH, with varying degrees of hydrocephalus. In comparison with 27 age-matched non-SAH controls, the authors observed blood and inflammation within the arachnoid villi during the 1st week after SAH. Greater mitotic activity was also noted among arachnoid cap cells. The patient with chronic SAH presented with ventriculomegaly 2 months post-SAH and exhibited remarkable arachnoid cap cell accumulation.
Conclusions. The authors postulate that proliferation of arachnoidal cells, triggered by the inflammatory reaction or blood clotting products, could result in obstruction of CSF flow through arachnoid villi into the venous sinuses. This does not exclude the possibility that SAH causes generalized fibrosis in the subarachnoid space.