{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T07:30:30Z","timestamp":1773041430443,"version":"3.50.1"},"reference-count":30,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2004,10,8]],"date-time":"2004-10-08T00:00:00Z","timestamp":1097193600000},"content-version":"vor","delay-in-days":2929,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[1996,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The central nervous system (CNS) is virtually isolated from circulating immunological factors such as complment (C), an important mediator of humoral immunity and inflammation. In circulation, C i constantly inhibited to prevent attack on host cells. Since a host of diseases produce an abnormal blood\u2013brain\/cerebrospinal fluid (blood\u2013brain\/CSF) permeability allowing C protein extravasation, we investigated if C activation occurs in CSF in vitro and in CNS in vivo during subarachnoid hermorrhage (SAH) or brain infrarction. After SAH (n = 15), the terminal complement complex (TCC) concentration on days 0 to 2 was higher in the CSF, 210 \u00b1 61 ng\/ml, than in the plasma 63 \u00b1 17 ng\/ml, but null in the CSF of controls (n = 8) or patients with an ischemic stroke (n = 7). TCC was eliminated from the CSF after SAH (24 \u00b1 10 ng\/ml on days 7 to 10) Incubation of normal human CSF with serum in vitro also activated the terminal C pathway. In 10 fatal ischmemic brain infrarctions, immunohistochemical techniques demonstrated neuronal fragment\u2010associated deposition of C9 accompanied by neutrophil infiltration. We conclude that the C system becomes activated intrathecally in SAH and focally in the brain parenchyma in ischemic stroke. By promoting chemotaxis and vascular perturbation, C activation may instigate nonimmune inflammation and aggravate CNS damage in diseases associated with plasma extravasation.<\/jats:p>","DOI":"10.1002\/ana.410400408","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T14:51:59Z","timestamp":1104591119000},"page":"587-596","source":"Crossref","is-referenced-by-count":116,"title":["Complement activation in the central nervous system following blood\u2013brain barrier damage in man"],"prefix":"10.1002","volume":"40","author":[{"given":"Perttu 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