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SYNOPSIS

Stimulation of the locus ceruleus produces vasoconstriction in the intracerebral circulation and vasodilatation in the extracerebral circulation. The latter is mediated by the seventh cranial nerve, involving a non-cholinergic transmitter. These vascular changes are reminiscent of those occurring in migraine. Stimulation of the trigeminal ganglion or of the trigeminal divisions produces a reflex dilatation in the external carotid territory also mediated by non-cholinergic fibers in the seventh nerve.

It is postulated that, in migraine, activation of the locus ceruleus would produce vasoconstriction in the cerebral circulation and dilatation extracerebrally. Such an effect would account for both the neurological symptoms of migraine and the observed changes in blood flow and vascular reactivity. Dilatation in the external carotid territory could lead to further reflex changes by activation of the central pathways described. Changes in locus ceruleus activity could be responsible for the pain of the headache phase of migraine, by disrupting a descending pain control system.