Methysergide (Sansert) Treatment in Acute Stroke Community Pilot Study

Abstract

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 amines^3-6 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.