The pathophysiology of migraine

Area of Science:

• Neuroscience
• Neurology
• Human Physiology

Background:

• Migraine is linked to episodic central nervous system dysfunction in a hyperexcitable brain.
• Abnormalities include energy metabolism, phosphene generation threshold, and contingent negative variation.
• Cortical spreading depression is strongly suggested as the cause of migraine aura.

Purpose of the Study:

• To explore the underlying mechanisms of migraine pathophysiology.
• To investigate potential causes of brain hyperexcitability in migraine.

Main Methods:

• Review of functional magnetic resonance imaging and magnetoencephalography data.
• Analysis of biochemical and genetic factors associated with migraine.
• Clinical observations on nitroglycerine administration and nitric oxide synthase inhibitors.

Main Results:

• Brain hyperexcitability may stem from low magnesium, mitochondrial dysfunction, nitric oxide issues, or calcium channelopathy.
• Low magnesium can trigger cortical spreading depression via ion channel and neurotransmitter release.
• Evidence suggests mitochondrial dysfunction and nitric oxide pathway involvement in migraine.

Conclusions:

• Migraine generation is central, originating in the brain stem, sometimes preceded by cortical spreading depression and aura.
• Activation of the trigeminovascular system releases neuropeptides, causing vasodilation and pain signal transduction.
• Pain impulses are relayed to higher brain centers, activating autonomic nuclei and inducing associated symptoms.