Abstract
It is proposed that the migraine attack is explicable by an interaction between the brain and the cranial circulation in subjects with unstable vascular and pain-control mechanisms. While peptides are undoubtedly involved in vasodilatation, there is strong evidence that 5-HT plays an important part in the genesis of migraine. Whether the place of 5-HT lies in central pain-control pathways, in the serotonergic project to the cerebral cortex, in a direct action on the cranial blood vessels or in its action at all three sites remains uncertain. It seems probable that the primary action of sumatriptan or ergotamine in terminating migraine headache is exerted on the cerebral and extracranial circulation whereas medications employed in prophylaxis may act centrally.
MeSH terms
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Brain Stem / physiology
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Calcitonin Gene-Related Peptide / blood
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Cerebrovascular Circulation / drug effects
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Cerebrovascular Circulation / physiology
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Cerebrovascular Disorders / complications*
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Cerebrovascular Disorders / metabolism
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Ergotamine / pharmacology
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Humans
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Hydroxyindoleacetic Acid / blood
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Hydroxyindoleacetic Acid / urine
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Hypothalamic Diseases / complications
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Hypothalamic Diseases / physiopathology
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Indoles / pharmacology
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Migraine Disorders / etiology
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Migraine Disorders / metabolism
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Migraine Disorders / physiopathology*
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Receptors, Cell Surface / drug effects
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Sulfonamides / pharmacology
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Sumatriptan
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Vasoconstrictor Agents / pharmacology
Substances
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Indoles
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Receptors, Cell Surface
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Sulfonamides
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Vasoconstrictor Agents
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Hydroxyindoleacetic Acid
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Sumatriptan
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Calcitonin Gene-Related Peptide
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Ergotamine