During a migraine attack, CGRP release contributes to which two processes?

During a migraine attack, CGRP release contributes to which two processes?

• A. Cardiac arrhythmias and decreased nociception.
• B. Vasoconstriction and reduced nociception.
• C. Meningeal vasodilation and neurogenic inflammation.
• D. Inhibition of CGRP release.

Answer: (C)

CGRP release during a migraine primarily drives two linked processes in the meninges: vasodilation of meningeal vessels and neurogenic inflammation. When trigeminal sensory neurons release CGRP, it binds to receptors on blood vessel smooth muscle, causing strong vasodilation. This widening of the vessels contributes to the throbbing head pain associated with migraines and increases blood flow in the meninges. At the same time, CGRP promotes neurogenic inflammation by enhancing inflammatory signaling in the meninges—stimulating plasma protein leakage, mast cell activation, and the recruitment of inflammatory mediators that sensitize nociceptors and amplify pain signaling. These vascular and inflammatory changes together underpin migraine pathophysiology. In contrast, vasoconstriction or reduced nociception would not describe CGRP’s actions, and inhibition of CGRP release or signaling is a therapeutic approach rather than what CGRP itself does during a migraine.

CGRP release during a migraine primarily drives two linked processes in the meninges: vasodilation of meningeal vessels and neurogenic inflammation. When trigeminal sensory neurons release CGRP, it binds to receptors on blood vessel smooth muscle, causing strong vasodilation. This widening of the vessels contributes to the throbbing head pain associated with migraines and increases blood flow in the meninges. At the same time, CGRP promotes neurogenic inflammation by enhancing inflammatory signaling in the meninges—stimulating plasma protein leakage, mast cell activation, and the recruitment of inflammatory mediators that sensitize nociceptors and amplify pain signaling. These vascular and inflammatory changes together underpin migraine pathophysiology. In contrast, vasoconstriction or reduced nociception would not describe CGRP’s actions, and inhibition of CGRP release or signaling is a therapeutic approach rather than what CGRP itself does during a migraine.