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Brainstem pathways that modulate sensory input. The key pathway for pain in migraine is the trigeminovascular input from the meningeal vessels, which passes through the trigeminal ganglion and synapses on second-order neurons in the trigeminocervical complex. These neurons in turn project in the quintothalamic tract and, after decussating in the brainstem, synapse on neurons in the thalamus. Important modulation of the trigeminovascular nociceptive input comes from the dorsal raphe nucleus, locus coeruleus, and nucleus raphe magnus. Activation of cells in the trigeminal nucleus results in the release of vasoactive neuropeptides, particularly calcitonin gene-related peptide (CGRP), at vascular terminations of the trigeminal. | Chapter 015. Headache Part 5 Brainstem pathways that modulate sensory input. The key pathway for pain in migraine is the trigeminovascular input from the meningeal vessels which passes through the trigeminal ganglion and synapses on second-order neurons in the trigeminocervical complex. These neurons in turn project in the quintothalamic tract and after decussating in the brainstem synapse on neurons in the thalamus. Important modulation of the trigeminovascular nociceptive input comes from the dorsal raphe nucleus locus coeruleus and nucleus raphe magnus. Activation of cells in the trigeminal nucleus results in the release of vasoactive neuropeptides particularly calcitonin gene-related peptide CGRP at vascular terminations of the trigeminal nerve. Recently antagonists of CGRP have shown some early promise in the therapy of migraine. Centrally the second-order trigeminal neurons cross the midline and project to ventrobasal and posterior nuclei of the thalamus for further processing. Additionally there are projections to the periaqueductal gray and hypothalamus from which reciprocal descending systems have established anti-nociceptive effects. Other brainstem regions likely to be involved in descending modulation of trigeminal pain include the nucleus locus coeruleus in the pons and the rostroventromedial medulla. Pharmacologic and other data point to the involvement of the neurotransmitter 5-hydroxytryptamine 5-HT also known as serotonin in migraine. Approximately 50 years ago methysergide was found to antagonize certain peripheral actions of 5-HT and was introduced as the first drug capable of preventing migraine attacks. The triptans are designed to selectively stimulate subpopulations of 5-HT receptors at least 14 different 5-HT receptors exist in humans. The triptans are potent agonists of 5-HT1B 5-HT1D and 5-HT1F receptors and are less potent at the 5-HT1A receptor. A growing body of data indicates that the antimigraine efficacy of the triptans relates to .
