Vida Demarin

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Acta Clin Croat,  Vol. 49,  (Suppl) No. 2,  2010 73V. Demarin Migraine JOINT MEETING OF THE PULA CONGRESS WITHALPSADRIA NEUROSCIENCE SECTION:DIAGNOSIS AND MANAGEMENT OF PAINMIGRAINEVida DemarinDepartment of Neurology, University Hospital Sestre milosrdnice, Zagreb, CroatiaMigraine is a primary recurrent headache mani-festing in attacks lasting 4-72 hours and aff ects 2-20% of world population. Women are more often aff ected, mostly during reproductive years. Th e migraine ef-fects quality of life and has negative impact on work-ing capability. Studies have showen that migraine is a common primary headache, but is not adequately diagnosed. Migraine is diagnosed in only 41% of women and 29% of men. Over 50% of patients with headacaches do not consult their medical doctors and among those who do, most of them do not go on check-ups. Also, migraine is an expensiv disease. A num-ber of studies so far have evaluated the costs due to migraine. Th e costs can be divided into direct costs which include visits to the general practitioner and the emergency departments, costs of hospitalization and farmacotherapy. Indirect costs comprise 2/3 of total costs and include absence from work and costs due to reduced productivity. Th e exact mechanism of  patophysiology of mi-graine hasn’t been established yet. Th e current state of knowledge in this fi eld suggests that a primary neuronal dysfunction leads to a sequence of changes intracranially and extracranially that account for mi-graine, including the three phases of premonitory symptoms, aura, and headache. Central and peripheral sensitization are thought to play a role within individual migraine attacks and in the transformation of episodic migraine to chronic migraine. Sensitization refers to the process in which neurons become increasingly responsive to nociceptive and non-nociceptive stimulation: response thresholds decrease, response magnitude increases, receptive fi elds expand, and spontaneous neuronal activity de-velops.Th e once popular vascular theory of migraine is no longer considered viable in its original form. While the exact mechanism of serotonin action re-mains obscure, there is evidence that a low serotonin state results in a defi cit in the serotonin descending pain inhibitory system, facilitating activation of the trigeminovascular nociceptive pathways in conjunc-tion with cortical spreading depression.Th e calcitonin gene-related peptide (CGRP) may also play a central role in migraine pathophysiology. CGRP may mediate trigeminovascular pain trans-mission from intracranial vessels to the central ner-vous system as well as neurogenic infl ammation. Elevated CGRP levels are normalized in patients with migraine following administration of the sero-tonin 1b/1d receptor agonist sumatriptan [34], sug-gesting that triptans may act to control migraine at least in part by reducing CGRP levels.Pharmacologic modulation of CGRP activity of-fers the promise of future treatment options for acute migraine attacks. Th e abortive (symptomatic) therapy of migraine ranges from the use of simple analgesics such as non-steroidal antiinfl ammatory drugs (NSAIDs) or ac-V. Demarin Migraine 74 Acta Clin Croat,  Vol. 49,  (Suppl) No. 2,  2010etaminophen to triptans or the less commonly used dihydroergotamine. Th e serotonin 1b/1d agonists (triptans) are consid-ered to be “specifi c” therapies for acute migraine since, in contrast to analgesics, they act at the pathophysi-ologic mechanism of the headache. All of the triptans inhibit the release of vasoactive peptides, promote va-soconstriction, and block pain pathways in the brain-stem. Triptans inhibit transmission in the trigeminal nucleus caudalis, thereby blocking aff erent input to second order neurons; this eff ect is probably mediated by reducing the levels of calcitonin gene related pep-tide (CGRP). Triptans may also activate 5-HT 1b/1d receptors in descending brainstem pain modulating pathways and thereby inhibit dural nociception.Th e available triptans include sumatriptan, zol-mitriptan, naratriptan, rizatriptan, almotriptan, elet-riptan, and frovatriptan. In Croatia are available only three triptans (sumariptan, zolmitriptan and riza-triptan). Sumatriptan can be given as a subcutaneous injection (usually admi-nistered by autoinjector in the thigh), as a nasal spray, or orally. Zolmitriptan is also available for both nasal and oral use. Th e others are available for oral use only. Prophylactic therapy is recommended when mi-graine attacks are frequent, are long-lasting, acute therapy is not effi  cient or the side-eff ectc are serious. Several groups of prophylactic medications can be rec-ommended. Beta blockers are the fi rst line for prophy-laxis in patients who are normo- or hypertensive. Among antidepressants, the most effi  cient seems to be the tricyclic antidepressant amitriptyline, while selective inhibitors of serotonine reuptake (SSRI) seem to be less effi  cient. In the antiepileptic group, the most effi  cient is the valproat acid, gabapentine and topiramate.Many studies pointed out the acupuncture to be eff ective in prophylaxis of migraine headache.

Joint Meeting of the Pula Congress with Alps-Adria Neuroscience Section: Diagnosis and Management of Pain - Migraine

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