Migraine headache

Abstract

A lthough there is a significant amount of data derived from multiple epidemiologic studies, it is difficult to establish the epidemiology of migraine headache with accuracy. The lack of a universally accepted definition, the absence of objective signs and diagnostic testing, the heterogeneity of the study population, and variability in the methodology accruing the data, make it difficult to study [1]. However, analysis of available epidemiologic data suggests that the prevalence of migraine is 3% to 5.7% in men and 7.4% to 17.6% in women. In a study of 10,169 individuals 12 to 19 years of age whom suffered with headache including migraine, the latter occurred more frequently in adolescents and young adults with a prevalence of 3% in men and 7.4% in women [2]. Genetics of MigraineThe familial inheritance of migraine has long been recognized. The recent literature supports this clinical impression [3]. However, as twin studies reveal a higher concordance rate among monozygotic than dizygotic twin pairs, the exact mode of inheritance is not clear [4,5]. Although several have been proposed, it is possible that the mechanism of migraine inheritance may differ from traditional patterns [6]. The discovery of a genetic locus on chromosome 19 for familial hemiplegic migraine has led to further interest in the genetic basis of more common forms of migraine [7]. Several genetic markers and their possible pathophysiologic relation to migraine are currently being studied [8].Family history of migraine predicts a decrease in the average age of onset of migraine headache [9]. The approximate risk of the offspring of parents affected with migraine is 70% if both parents are affected. The risk falls to 45% if one parent is affected and 30% in case of a close relative [10].Pathophysiology Sicuteri et al. [11] first considered migraine to be a systemic, metabolic derangement; he observed elevated levels of 5-hydroxyindoleacetic acid (5-HIAA) in the urine of patients following migraine attacks. Later, the discovery of platelet serotonin release during the attack resulted in exhaustive study of platelet function on migraineur. In this respect, review of the literature suggests that platelet membrane disturbance may be attributed to systemic and metabolic effects. Serotonin release appears to be the consequence and not the cause of the migraine attack [12]. Migraine MechanismA complete migraine attack has five phases: prodrome, aura, headache phase, termination of headache, and the postdrome. ProdromeAltered mood, libido, cognitive state, motor activity, response to sensory stimuli, thirst, and appetite characterize the prodromal phase. AuraMigraine with aura is characterized by increased neuronal central excitability and susceptibility to spontaneous neuronal depolarization. A wave of intense excitation followed by a spreading inhibition that originates in the occipital cortex and progresses anteriorly throughout the cerebral cortex at a rate of approximately 3 mm/min following the pattern of gyri and sulci and not vascular territo...