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Michael Anthony, MD; James W. Lance, MD

Arch Neurol. 1969;21(3):263-268.

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

THE WIDESPREAD use of monoamine oxidase (MAO) inhibitors followed the simultaneous discovery that iproniazid phosphate caused euphoria in tuberculous patients¹ and inhibited monoamine oxidase.² Since then, they have formed an important group of antidepressant drugs. The clinically important monoamine oxidases are present in the granular fraction of most parenchymatous tissues of vertebrates where they deaminate several aliphatic and aromatic amines, including serotonin (5-hydroxytryptamine [5HT] ), dopamine, tryptamine, tyramine, and, to a lesser extent, epinephrine and norepinephrine. Administration of MAO inhibitors increases the concentration of these amines in many organs, including blood platelets, which contain about 99% of blood 5HT.³

Spontaneous migraine is associated with a fall in plasma 5HT and increased urinary excretion of both 5-hydroxyindole acetic acid (5HIAA)^4,5 and 5 HT (unpublished observations). Depletion of platelet 5HT by the intramuscular administration of reserpine induces migraine in susceptible individuals, and intravenous 5HT relieves-both spontaneous and reserpine-induced . . . [Full Text PDF of this Article]

Author Affiliations
Sidney, New South Wales, Australia

From the Division of Neurology, Prince Henry Hospital, and the School of Medicine, University of New South Wales, Sydney, Australia.

Footnotes
Submitted for publication Jan 29, 1969; accepted May 19.

Reprint requests to Division of Neurology, Prince Henry Hospital, Little Bay, New South Wales 2036, Australia (Dr. Anthony).

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