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September 1969

Monoamine Oxidase Inhibition in the Treatment of Migraine

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.

Arch Neurol. 1969;21(3):263-268. doi:10.1001/archneur.1969.00480150053007

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with a fall in plasma 5HT and increased urinary excretion of both 5-hydroxyindole acetic acid (5HIAA)4,5 and 5 HT (unpublished observations).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

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