The trigeminal nerve system, the largest cranial nerve responsible for facial sensation, plays a central role in migraine pathophysiology. During an attack, the trigeminal nerve releases neuropeptides including calcitonin gene-related peptide (CGRP), which triggers inflammation of the meningeal blood vessels and amplifies pain signaling. Research shows that approximately 12% of the U.S. population suffers from migraines, with women affected three times more often than men.
This neurogenic inflammation creates a cascade of events: blood vessels dilate, surrounding tissue swells, and pain signals flood the brainstem. The result is the characteristic pulsating pain that intensifies with physical activity and can persist for 4 to 72 hours without effective intervention.
The sphenopalatine ganglion (SPG), a cluster of nerve cells located behind the nose, acts as a critical relay station in this pain pathway. When the SPG becomes overactive, it amplifies migraine signals and contributes to the autonomic symptoms many patients experience, including nasal congestion, tearing, and facial flushing.
