Role of TNF-α in the Pathogenesis of Migraine

Figure 5

Flow diagram depicts how migrainous brain is triggered by slow propagating wave (2–5 mm·min⁻¹) of all cortical neuronal and astrocyte depolarization leads to release of vasoactive product such as CGRP and neurotransmitter (glutamate). Microglial activation is caused by both CGRP and glutamate and stimulates the release of TNF-α which is the prime focus of inflammation. TNF-α also autostimulates and causes positive loop activation and is responsible for the sensitization of nociceptors, and this continuous stimulation will become a risk factor for the transition of episodic to chronic headache.