Which sequence describes the pathophysiology of migraine?

Which sequence describes the pathophysiology of migraine?

• A. Activation of the trigeminal system triggers trigeminovascular activation in the meninges, releasing neuropeptides that promote vasodilation and neurogenic inflammation, with increased sensory traffic through brainstem and cortex.
• B. Activation of the parasympathetic system causing vasoconstriction
• C. Decrease in trigeminal activity with reduced pain
• D. Peripheral nerve entrapment in scalp

Answer: (A)

The main idea is that migraine pain starts with activation of the trigeminovascular system. When the trigeminal nerves innervating the meningeal vessels are activated, they release neuropeptides such as CGRP and other mediators. These substances cause dilation of meningeal blood vessels and promote neurogenic inflammation, increasing vascular permeability and triggering a cascade that sensitizes pain pathways. This peripheral activation leads to enhanced signaling through brainstem and cortex, i.e., central sensitization, which contributes to the throbbing pain and associated symptoms of migraine. This sequence—trigeminal activation → trigeminovascular activation with neuropeptide release → vasodilation and inflammation → increased sensory traffic to brainstem and cortex—best fits what we know about migraine pathophysiology. The other options don’t fit: vasoconstriction from parasympathetic activity would worsen the mismatch with the typical inflammatory, vasodilatory phase; a decrease in trigeminal activity would not produce migraine pain; and peripheral nerve entrapment in the scalp isn’t how migraine originates.

The main idea is that migraine pain starts with activation of the trigeminovascular system. When the trigeminal nerves innervating the meningeal vessels are activated, they release neuropeptides such as CGRP and other mediators. These substances cause dilation of meningeal blood vessels and promote neurogenic inflammation, increasing vascular permeability and triggering a cascade that sensitizes pain pathways. This peripheral activation leads to enhanced signaling through brainstem and cortex, i.e., central sensitization, which contributes to the throbbing pain and associated symptoms of migraine. This sequence—trigeminal activation → trigeminovascular activation with neuropeptide release → vasodilation and inflammation → increased sensory traffic to brainstem and cortex—best fits what we know about migraine pathophysiology. The other options don’t fit: vasoconstriction from parasympathetic activity would worsen the mismatch with the typical inflammatory, vasodilatory phase; a decrease in trigeminal activity would not produce migraine pain; and peripheral nerve entrapment in the scalp isn’t how migraine originates.