Migraine is a neurovascular disorder involving activation of the trigeminovascular system. Cortical spreading depression (CSD) - a wave of neuronal depolarization followed by suppression spreading across the cortex at 3-5 mm/min - underlies migraine aura and activates meningeal trigeminal afferents. Activated trigeminal neurons release calcitonin gene-related peptide (CGRP), substance P, and neurokinin A at meningeal blood vessels, causing neurogenic inflammation: vasodilation, plasma protein extravasation, mast cell degranulation, and sensitization of perivascular nociceptors. CGRP is the primary mediator: it is a potent vasodilator, promotes neurogenic inflammation, and facilitates pain transmission in the trigeminal nucleus caudalis. Ascending pain signals travel via the trigeminothalamic tract to the thalamus and cortex. The trigeminocervical complex explains the referred pain pattern to the face, temple, and upper neck. Serotonin (5-HT) plays a dual role: low serotonin levels between attacks predispose to migraine, while triptans (5-HT1B/1D agonists) abort attacks by constricting meningeal vessels (5-HT1B), inhibiting CGRP release from trigeminal terminals (5-HT1D), and blocking nociceptive transmission in the trigeminal nucleus. Tension-type headache involves peripheral myofascial nociception with pericranial muscle tenderness; chronic forms may develop central sensitization similar to...