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Michael Anthony, MB, MRACP; Herta Hinterberger, BSc, PhD; James W. Lance, MD, FRACP

Arch Neurol. 1967;16(5):544-552.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

IN 1961, Sicuteri, Testi, and Anselmi¹ demonstrated 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 Lance² in the majority of patients studied whereas Curzon, Theaker, and Phillips³ were 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.⁴ The value of methysergide maleate has since been established, although the mechanism of its action is still unexplained.⁵ Kimball, Friedman, and Vallejo⁶ were 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 . . . [Full Text PDF of this Article]

Author Affiliations
Sydney, New South Wales, Australia

From the divisions of neurology and clinical chemistry, Prince Henry Hospital, Sydney, and the School of Medicine, University of New South Wales, Australia. Dr. Anthony is a Sandoz Research Fellow in Neurology.

Footnotes
Submitted for publication Sept 13, 1966; accepted Dec 5.

Reprint requests to Division of Neurology, Prince Henry Hospital, Little Bay, New South Wales, Australia (Dr. Lance).

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