These changes greatly advance our understanding of multiple pathophysiologic underpinnings of migraine, from central “migraine generating” loci, to cortical spreading depression, intimate mechanisms underlying activation of neuronal pain pathways in vulnerable patients, central sensitization, and chronification. Structural imaging begins to explain the complex connections between migraine

and cerebral vascular events, white matter lesions, grey matter density alterations, iron deposition, AUY-922 purchase and microstructural brain damage. Selected structural and functional alterations of brain structures, as identified with imaging methods, may represent the foundation of new diagnostic strategies and serve as markers of therapeutic efficacy. Migraine is an episodic pain disorder that has the potential to develop into a chronic form, and is one of the most common neurological diseases in clinical practice, with important individual and societal implications. Migraine

affects approximately 12% of the population and ranks number 12 among women and 19 in the general population for the degree of disability it generates.1 In the US, of all migraine sufferers, 31.3% have an attack frequency of 3 or more per month and 53.7% report severe impairment or the need for bedrest. More than 1 in 4 migraineurs are candidates for preventive therapy, and a substantial proportion SB431542 order of those who might benefit from prevention do not receive it.2,3 Migraine episodes are characterized classically by unilateral, throbbing, pulsating headache. They frequently associate with nausea, vomiting,

photophobia, phonophobia, or allodynia (pain selleck compound after application of a non-noxious stimulus, such as light touch). Recent decades saw significant progress in understanding of this disorder through clinical observation and experimental studies. A plethora of reports have highlighted the neural circuitry responsible for generating migraine aura and pain; however, the precise pathogenesis underlying the disorder remains elusive. While the need for improved behavioral and pharmacological therapeutic interventions is acute, the ability to develop efficient abortive and prophylactic therapies hinges on uncovering disease mechanisms. Two initial theories were advanced that attempted to explain migraine pathogenesis. The vascular theory attributed migraine primarily to cerebral artery diameter change, with constriction resulting in local hypoxia and transient focal symptoms, followed by neurogenic extracranial or intracranial vasodilation causing pain. Another viewpoint regarded migraine mainly as a paroxysmal, transient depolarization of cortical neurons, resulting in focal symptoms and headache.4 At the time of this writing, data from numerous experimental and clinical studies paint an intriguing and much more complex picture of migraine underpinnings.