Jun. 26, 2023
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Migraine is prevalent and is one of the leading causes of disability worldwide. The International Classification of Headache Disorders defines “migraine with aura” as recurrent attacks, lasting minutes, of unilateral fully reversible central nervous system symptoms usually followed by headache and associated migraine symptoms. “Migraine without aura” is defined as recurrent headache attacks lasting 4 to 72 hours with typical characteristics (eg, unilateral, pulsating, etc.). To tackle this condition and help the millions suffering worldwide, we must first understand the pathophysiology of migraine and how it is associated with the hypothalamus, cortical spreading depression, and the trigeminocervical complex. In recent years our understanding of the pathophysiology behind migraines has advanced (especially through functional imaging), leading us to put away old theories like the vascular theory and further evaluate involvement of the hypothalamus, cortical spreading depression, and the trigeminocervical complex in various migraine phases (premonitory, aura, headache, and postdrome). In this article, we review the pathogenesis and pathophysiology of migraines.
• The hypothalamus is a key contributor to multiple migraine phases, including the premonitory phase, headache phase, postdrome phase, and chronic migraine.
• Cortical spreading depression is an approximately 3 mm/min neural depolarization that spreads across the cortex leading to a release of neurotransmitters and regional changes in blood flow, likely corresponding to the conscious experience of “aura”.
• Cortical spreading depression involves changes in ion concentrations from various triggers that leads to a loss of membrane potential (associated with the buildup of glutamate) resulting in a current that releases vasoactive substances like nitric oxide, therefore increasing regional blood flow to meet the increased metabolic demand.
• A key process in understanding migraine headache is the trigeminal network; input from the meningeal vessels (via adenylate cyclase-activating polypeptide and calcitonin gene-related peptide) pass through the trigeminal ganglion and eventually synapse onto thalamic neurons, contributing to migraine pain and impairment.
• Increased pain states lead to increased activation of the trigeminal pain network resulting in peripheral sensitization, central sensitization, decreased threshold, and alterations in connectivity, together creating chronic migraine.
• Migraine is no longer thought of as primarily a vascular abnormality (eg, “vascular theory”) but instead as a disorder of neuronal excitability associated with head pain, sensory symptoms, and secondary vascular changes.
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