Migraine and the blood-brain barrier.
The prodromal (cerebral) symptoms of migraine are associated with a fall in cerebral blood-flow (C.B.F.). The suggestion that various circulating vasoactive agents might be the cause of this fall in C.B.F. ignores the contradictory findings that the cerebral vascular bed is normally unresponsive to such agents; but if the blood-barrier is disrupted, systemically administered monoamines and prostaglandins elicit pronounced changes in cerebral-tissue perfusion and metabolism. A defect in the blood-brain barrier of migraine patients (particularly those in whom an item of diet may trigger an attack) would make the cerebral circulation vulnerable to variations in circulating levels of vasoactive substances. Alternatively, the barrier could be intact in non-dietary patients, but release of monoamines or prostaglandins from the brain itself could account for the observed changes in the cerebral circulation.
D001812:Blood-Brain Barrier; D002560:Cerebrovascular Circulation / Q000187:drug effects; D005021:Ethylamines / Q000009:adverse effects / Q000494:pharmacology; D006801:Humans; D002546:Ischemic Attack, Transient / Q000139:chemically induced / Q000150:complications; D008881:Migraine Disorders / Q000209:etiology*; D011458:Prostaglandins E / Q000009:adverse effects / Q000494:pharmacology; D012701:Serotonin / Q000009:adverse effects / Q000494:pharmacology; D014439:Tyramine / Q000009:adverse effects / Q000494:pharmacology; D014662:Vasoconstrictor Agents / Q000009:adverse effects / Q000494:pharmacology
D005021:Ethylamines; D011458:Prostaglandins E; D014662:Vasoconstrictor Agents; D012701:Serotonin; D014439:Tyramine