Vasoneuronal signalling plays a causal role in migraine pathogenesis: the ‘Con’ argument

Abstract

Migraine is a common and disabling brain condition, encompassing a broad range of symptoms, including many that can only be attributed to central neuronal dysfunction. The vascular hypothesis is that vasoneuronal signalling is responsible for the initiation of a migraine attack. Whilst we do not necessarily dispute that the cerebral vasculature is involved in mediating headache, and headache is a prominent part of the disorder for many, it is clear phenotypically, neurophysiologically and on functional neuroimaging that the migraine attack starts hours to days before headache onset in the brain. Attack genesis must therefore be before the onset of any vascular dilatation that may be involved in the headache phase. Many imaging studies have largely only supported vascular dilatation as being involved during headache rather than at other times during the attack. In addition, vasoconstriction has historically been thought to be important for attack abortion, but recent and emerging evidence from therapeutics research is inconsistent with this. In this article, we discuss these arguments for a neural pathogenesis of migraine.