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Effect Of Serotonin In Migraine Patients

R. W. Kimball, A. Friedman, E. Vallejo
Published 2011 · Medicine

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LITTLE is known of the factors that predispose to migraine or the biochemical events that initiate the disturbances characteristic of this condition. Earlier studies by Marcussen and Wolffl have shown that an initial phase of vasoconstriction is responsible for the prodroma1 symptoms, while the pain follows a marked distention of cranial vessels that are temporarily hypotonic. They also have presented certain evidence which presumably indicates that a pain threshold-lowering substance renders the distention of the large arteries painfu1.2 However, alteration in tone, lumen, and pain threshold of the arteries alone cannot explain the complex symptomatology of the migraine attack. Jimenez Diaz and associates3 have indicated that, during the migraine attack, there is a release of a substance more stable than acetylcholine, which they term S.A.C. acetylcholinelike substance. They also conclude that the normal choline acetylate system is different in these patients. Kunkle4 also relates this multisystem disturbance to a preponderance of parasympathetic nervous activity as manifested by a release of acetylcholine. An acetylcholine-like substance has been detected in cerebrospinal fluid during some intracranial vascular headaches of migraine type. These and other studies cast light on the nature of the pathophysiology of migraine, yet the primary event in the migraine attack remains undetermined. The effects of serotonin (5hydroxytryptamine-HT) suggest themselves as a means of gaining further understanding of migraine. The present study undertakes to determine the effects-clinically, physiologically, and biochemically-of serotonin and its precursor, 5-hydroxytryptophane (HTP), on patients with migraine. The physiologic significance of HT is implied by its potency in the central nervous system, gastrointestinal tract, cardiovascular system, and blood. The cardiovascular phenomena associated with HT excess are particularly interesting, in that its ability to produce vasoconstriction in some instances, and in some instances vasodilation, raises the possibility that this or a similar substance is the trigger, or part of the trigger mechanism, in patients with vascular headaches, that is, migraine. The nervous, cardiovascular, gastrointestinal, and renal effects of HT all have their counterparts in the migraine syndrome. It has been stated by other observers that exogenous HT can elicit an attack of migraine,5 and observations with a monoamine oxidase inhibitor have been interpreted to indicate that HT aggravates the symptoms of migraine.s WOW and associates7 have reported that, in 3 cases, temporal perivascular-injected HT induced effects similar to clinical migraine. This and other clinical studies suggest that a biochemical lesion of fundamental importance exists in migraine.
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