This theory suggests that migraine headaches occur as a result of an abnormal firing of meningeal nociceptors at the TGVS. Activation of trigeminal neurons releases vasoac-tive peptides including calcitonin gene-related peptide (CGRP, a vasodilator peptide), substance P, and neurokinin A (both play an important role in pain transmission as well as activation of immune responses and neurogenic inflammation) onto dural tissue where these peptides produce a local response known as neurogenic inflammation.259 These peptides induce cranial vasodilatation, especially at the dural membranes surrounding the brain (mainly a result of CGRP), thus producing the pain associated with migraine attacks. Further evidence supporting this theory as the underlying cause of migraines can be found from a recent study linking the dural mast cell degranulation to the prolonged activation of the trigeminal pain pathway and neurogenic inflammation.268
The discovery of these vasoactive peptides provides new targets for the future design of nonvasoconstrictors, nontriptan drugs such as CGRP antagonists for the acute and preventive treatment of migraine and cluster headaches.259,269
All clinically available triptans possess comparable phar-macodynamic properties. They all bind and stimulate serotonin 5-HT1B/1D with affinity in the low nanomolar ranges, thus they are equally effective for the acute treatment of migraine.262,270 However, they all have different pharma-cokinetic properties and side effect profiles that vary in type and severity.261 Thus, they are not equally efficacious in preventing migraine recurrence because of the differences in their elimination half-lives.262 They also differ in their potential to induce drug-related CNS side effects, especially somnolence and paresthesia that may lead to a patient's noncompliance of an otherwise effective migraine
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