Migraine is a complex neurovascular disorder characterized by recurrent episodes of moderate-to-severe, typically unilateral, pulsating headache lasting 4–72 hours, associated with nausea, vomiting, photophobia, and phonophobia. The pathophysiology has evolved from the 'vascular theory' (vasoconstriction → vasodilation) to the current 'trigeminovascular theory.' The cascade begins with cortical spreading depression (CSD) — a wave of neuronal depolarization followed by suppression that propagates across the cerebral cortex at 3–5 mm/min. CSD is responsible for the migraine aura (visual scintillations, scotoma, sensory disturbances) and activates trigeminal nerve afferents in the meninges. Activated trigeminal neurons release vasoactive neuropeptides — calcitonin gene-related peptide (CGRP), substance P, and neurokinin A — from perivascular nerve terminals. CGRP is the key mediator: it causes potent meningeal vasodilation, mast cell degranulation, plasma protein extravasation (neurogenic inflammation), and sensitization of trigeminal nociceptors. This peripheral sensitization lowers the activation threshold of trigeminal afferents, making normal pulsatile arterial distension painful (explaining the throbbing quality). Signals travel via the trigeminal ganglion to the trigeminal nucleus caudalis (TNC) in the brainstem, then to the thalamus and cortex for pain perception. Central sensitization develops as...