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Methysergide (Sansert) Treatment in Acute Stroke Community Pilot StudyDepartment of Neurology, Phelps Memorial Hospital, North Tarrytown, New York Since its first discovery in 1948,1 serotonin (5-HT) has been the subject of considerable interest. Its potent vasoactivity led to the hypothesis that altered serotonin metabolism was responsible for the pathophysiology of cerebrovascu lar disease (infarction & hemorrhage) with documentation of elevated levels of serotonin in CSF.2 If (5-HT) serotonin-mediated release is ultimately responsible for cerebral edema, vasospasm and infarction in experimental and human stroke, then an opportunity exists to pharmacologically block these effects with serotonin-antagonizing agents. This hypothesis has been tested in the laboratory with several agents that inhibit biogenic amines3-6 resulting in promising data suggesting a reduction in damage and disability. Since the "natural history of human stroke" results in a 30-40% mortality within the first three weeks,7,8 an aggresive new attempt should be directed to increasing the number of survivors in this initial period of high risk. In this regard Sansert (methysergide) was considered worthy of clinical trials.
Angiology, Vol. 36, No. 3,
137-142 (1985) This article has been cited by other articles:
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