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IN 1961, Sicuteri, Testi, and Anselmi¹demonstrated that the excretion in the urine of 5-hydroxyindoleacetic acid (5HIAA), the principal catabolite of serotonin (5-hydroxytryptamine, 5HT), was increased during some attacks of migraine headache. This was confirmed by Curran, Hinterberger, and Lance²in the majority of patients studied whereas Curzon, Theaker, and Phillips³were able to find such a correlation in only two out of nine migrainous subjects. Interest in the possible relationship of serotonin to the migraine syndrome had quickened following Sicuteri's preliminary trial of methysergide, a serotonin "antagonist," in the treatment of migraine.⁴The value of methysergide maleate has since been established, although the mechanism of its action is still unexplained.⁵Kimball, Friedman, and Vallejo⁶were unable to produce headache in migrainous subjects by the injection of serotonin or its precursor 5-hydroxytryptophan. Indeed they found that injection of these substances relieved spontaneous migraine headaches. These
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Anthony et al. (1967) studied this question.
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