Diencephalic and brainstem mechanisms in migraine

TLDR: Dysfunction of diencephalic and brainstem nuclei that can modulate the perception of activation of the trigeminovascular system may contribute to the cascade of events that results in other symptoms of migraine — such as light and sound sensitivity — thus providing a comprehensive explanation of the neurobiology of the disorder.

Abstract: Migraine is a complex and disabling brain disorder that is currently difficult to prevent or treat. Goadsby and colleagues review the evidence that regions of the brainstem and forebrain are involved in modulating migraine pain and that dysfunction in these areas may contribute to the pathophysiology of the disorder. Migraine is a common and complex brain disorder. Although it is clear that head pain is a key manifestation of the disorder for most patients, what drives the activation of neuronal pain pathways in susceptible patients is less obvious. There is growing evidence that migraine pathophysiology may, in part, include dysfunction of subcortical structures. These include diencephalic and brainstem nuclei that can modulate the perception of activation of the trigeminovascular system, which carries sensory information from the cranial vasculature to the brain. Dysfunction of these nuclei, and their connections to other key brain centres, may contribute to the cascade of events that results in other symptoms of migraine — such as light and sound sensitivity — thus providing a comprehensive explanation of the neurobiology of the disorder.