Methysergide (Sansert) treatment in acute stroke. Community pilot study.
Since its first discovery in 1948, 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 cerebrovascular disease (infarction & hemorrhage) with documentation of elevated levels of serotonin in CSF. 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 amines 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, an aggressive 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.
D000208:Acute Disease; D000368:Aged; D001921:Brain / Q000000981:diagnostic imaging; D002561:Cerebrovascular Disorders / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy*; D002986:Clinical Trials as Topic; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D008297:Male; D008784:Methysergide / Q000627:therapeutic use*; D008875:Middle Aged; D011859:Radiography; D011897:Random Allocation; D012701:Serotonin / Q000097:blood
D012701:Serotonin; D008784:Methysergide