title: Managing migraine associated with sensitization.
abstract: The majority of migraineurs seeking secondary or tertiary medical care experience throbbing pain and cutaneous allodynia during the course of migraine. Underlying the origin of these symptoms are peripheral and central trigeminovascular neurons, whose cell bodies are located in the trigeminal ganglion and the spinal dorsal horn, respectively. The development of throbbing in the initial phase of migraine is mediated by sensitization of peripheral trigeminovascular neurons, whereas the development of cutaneous allodynia later in the attack is propelled by sensitization of central trigeminovascular neurons which, unfortunately, are not equipped to respond to triptans directly. Triptans appear to act presynaptically in the dorsal horn, such as to inhibit signal transmission from peripheral to central trigeminovascular neurons. Reining in the central neurons using triptan treatment is possible as long as their excitability remains driven by incoming signals from the meninges, but not after they develop autonomous activity. Accordingly, attacks with allodynia can be effectively terminated, provided that the patient vigilantly resorts to triptan therapy before or soon after the onset of allodynia, but not after allodynia has become firmly established. On the other hand, allodynic patients who missed the critical window for effective triptan therapy can still be rendered pain-free using an intravenous infusion of non-steroidal anti-inflammatory drugs.
authors.affiliation: Departments of Anesthesia and Program in Neuroscience, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA. rburstei@bidmc.harvard.edu
authors.forename: Rami
authors.initials: R
authors.lastname: Burstein
authors.forename: Moshe
authors.initials: M
authors.lastname: Jakubowski
mesh_terms: D000894:Anti-Inflammatory Agents, Non-Steroidal; D006801:Humans; D008881:Migraine Disorders; D009474:Neurons; D010146:Pain; D010147:Pain Measurement
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal