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Migraine Headache


Author: Jasvinder Chawla, MBBS, MD, MBA; Chief Editor: Helmi L Lutsep, MD
Updated: May 25, 2011

Background
Migraine headache is a complex, recurrent headache disorder that is one of the most common complaints in medicine. In the United States, more than 30 million people have 1 or more migraine headaches per year. Approximately 75% of all persons who experience migraines are women (see Epidemiology). The term migraine is derived from the Greek word hemikrania. This term was corrupted into low Latin as hemigranea, which eventually was accepted by the French translation as migraine. Migraine was previously considered a vascular phenomenon that resulted from intracranial vasoconstriction followed by rebound vasodilation. Currently, however, the neurovascular theory describes migraine as primarily a neurogenic process with secondary changes in cerebral perfusion (see Pathophysiology). Approximately 70% of patients have a first-degree relative with a history of migraine. In addition, a variety of environmental and behavioral factors may precipitate migraine attacks in persons with a predisposition to migraine (see Etiology). The classic migraine episode is characterized by unilateral head pain preceded by various visual, sensory, motor symptoms, collectively known as an aura. Most commonly, the aura consists of visual manifestations such as scotomas, photophobia, or visual scintillations (eg, bright zigzag lines) (see Clinical Presentation). In practice, however, migraine headaches may be unilateral or bilateral and may occur with or without an aura. In the current International Headache Society (IHS) categorization, the headache previously described as classic migraine is now known as migraine with aura, and that described as common migraine is now termed migraine without aura. Migraines without aura are the most common, accounting for more than 80% of all migraines. The diagnosis of migraine is clinical in nature, based on criteria established by the International Headache Society. A full neurologic examination should be performed during the first visit; the findings are usually normal. Neuroimaging is not necessary in a typical case (see Workup). Migraine treatment involves acute (abortive) and preventive (prophylactic) therapy. Patients with frequent attacks usually require both. Measures directed toward reducing migraine triggers are also generally advisable. Acute treatment aims to stop or prevent the progression of a headache or reverse a headache that has started. Preventive treatment, which is given even in the absence of a headache, aims to reduce the frequency and severity of the migraine attack, make acute attacks more responsive to abortive therapy, and perhaps also improve the patient's quality of life (see Treatment and Management). See Migraine in Children for a pediatric perspective on migraine. Also seeMigraine Variants.

Migraine classification
The second edition of the International Classification of Headache Disorders [1]lists the following types of migraine:

         

Migraine without aura (formerly common migraine) Probable migraine without aura Migraine with aura (formerly classic migraine) Probable migraine with aura Chronic migraine Chronic migraine associated with analgesic overuse Childhood periodic syndromes that may not be precursors to or associated with migraine Complications of migraine Migrainous disorder not fulfilling above criteria Hemicrania continua

Etiology

CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) is a genetic disorder of the notch 3 gene on chromosome 19 that causes migraine with aura. and meats with nitrites. it generally demonstrates a maternal inheritance pattern. as follows:              Stress Excessive or insufficient sleep Medications (eg. and leukoencephalopathy). artificial sweeteners (eg. such as menstruation (common). saccharin).[24] Although no genetic basis has been identified for common migraine. Familial hemiplegic migraine Familial hemiplegic migraine (FHM) is a type of migraine with aura that is preceded or followed by hemiplegia. chocolates. caffeine.[29] pregnancy. which is also linked to the 19p locus. lactic acidosis. Such foods include the following:             Aged cheese Yogurt Sour cream Chicken livers Sausages Bananas Avocados Canned figs Raisins Peanuts Soy sauce Pickled fish . which typically resolves. SCNA1.Approximately 70% of patients have a first-degree relative with a history of migraine. monosodium glutamate (MSG). including RVCL (retinal vasculopathy with cerebral leukodystrophy) and HIHRATL (hereditary infantile hemiparesis. which occurs in approximately 50% of affected families. Three loci have been identified in FHM. such as MELAS (mitochondrial myopathy. The risk of migraine is increased 4-fold in relatives of people who have migraine with aura. Evidence suggests that the 19p locus for FHM may also be involved in patients with nonhemiplegic migraine. encephalopathy. colognes. perfumes. Foods containing tyramine may provoke migraine. ice cream headaches) Certain foods and food additives can precipitate migraine.[27] Migraine precipitants Various precipitants of migraine events have been identified. FHM type 2 is due to mutation in the sodium channel gene ATP1A2 on chromosome 1. petroleum distillates) Hormonal changes. FHM may be associated with cerebellar ataxia. is linked to band 19p13 or a mutation in the calcium channel gene (CACNA1A4) at the 1q locus. aspartame. FHM type 1. The mechanisms by which these genetic vasculopathies give rise to migraine is still unclear. These include alcohol. and ovulation Head trauma Weather changes Metabolic or infectious diseases Physical exertion or fatigue Motion sickness Cold stimulus (eg. retinal arteriolar tortuosity.[25] FHM3 is a rare subtype of FHM and is caused by mutations in a sodium channel α-subunit coding gene. citrus fruits. vasodilators. oral contraceptives[28] ) Smoking Exposure to bright or fluorescent lighting Strong odors (eg. and strokelike episodes).[26] Migraine in other inherited disorders Migraine occurs with increased frequency in patients with mitochondrial disorders. Migraine is also a common symptom in other genetic vasculopathies.

Reliable evidence comes from the Women's Health Study. 20. and red nucleus.8% of Asian Americans were considered to have migraine. more than 30 million people have 1 or more migraine headaches per year. This association is not seen in migraine without aura.2% of Asian Americans met International Classification of Headache Disorders (ICHD) criteria for migraine. 16. both the prevalence and incidence of migraine are higher in boys than in girls.[37] Before puberty. migraineurs had increased local iron deposits in the putamen. .[31] Migraines during pregnancy are also linked to stroke and vascular diseases.5:1 at age 40 years. stroke and heart attacks).4% of whites. 1 in 6 American women has migraine headaches. This roughly corresponds to approximately 18% of females and 6% of males.    Fresh-baked breads Pork Vinegars Beans Migraine and other vascular disease People who suffer from migraine headaches are more likely to also have cardiovascular or cerebrovascular disease (ie. the prevalence increases in both males and females. In individuals older than 12 years. possibly the cause of chronification of the disease. Attacks usually decrease in severity and frequency in individuals older than 40 years. One study showed that among women. globus pallidus. Onset of migraine after age 50 years is rare.5:1 at puberty to 3.[38] Onset of migraine after age 50 years is rare. and only 9. Approximately 75% of all persons who experience migraines are women. [32] Migraine with aura for women in midlife has a statistical significant association with late-life vascular disease (infarcts) in the cerebellum. This increase probably reflects greater awareness of the condition. [36] Migraine accounts for 64% of severe headaches in females and 43% of severe headaches in males.2% of African Americans. The incidence of migraine with aura peaks in boys at around age 5 years and in girls at around age 12-13 years. [35] Epidemiology In the United States. except for women in perimenopause. 7. The female-to-male ratio increases from 2. which found that migraine with aura raised the risk of myocardial infarction by 91% and ischemic stroke by 108% and that migraine without aura raised both risks by approximately 25%. A study by Hsu et al suggests that women in aged 40-50 years are also more susceptible to migrainous vertigo. reaching a peak at age 30-40 years.2% of African Americans. and 4. in males.6% of whites.[34] This increase in iron deposits may be explained as a physiological response induced by repeated activation of nuclei involved in central pain processing or by the damage of these structures secondary to formation of free radicals in oxidative stress. The prevalence of migraine appears to be lower among African Americans and Asian Americans than among whites. Currently. Similarly. 8. [33] Other related factors In a population-based magnetic resonance imaging study by Kruit et al. compared with controls. The incidence of migraine without aura peaks in boys at age 10-11 years and in girls at age 14-17 years. The reported incidence of migraine in females of reproductive age has increased over the last 20 years.[30]The physiopathology of the mechanism is still unknown.