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Migraine
From Wikipedia(View original Wikipedia Article)Last modified on 29 May 2011, at 06:10

This article is about the disorder. For other uses, see Migraine (disambiguation). Migraine Classification and external resources

The pain of a migraine headache can be debilitating. ICD-10 G43. ICD-9 OMIM 346 157300

DiseasesDB 8207 (Migraine) 31876 (Basilar) 4693 (FHM) MedlinePlus 000709 eMedicine MeSH neuro/218 neuro/517emerg/230 neuro/52 9 D008881

Migraine (from the Greek words hemi, meaning half, and kranion, meaning skull ) is a debilitating condition characterized by moderate to severe headaches, and nausea. It is about three times more common in women than in men. The typical migraine headache is unilateral (affecting one half of the head) and pulsating in nature and lasting from 4 to 72 hours; symptoms include nausea, vomiting, photophobia (increased sensitivity to light), phonophobia (increased sensitivity to sound); the symptoms are generally aggravated by routine activity. Approximately one-third of people who suffer from migraine headaches perceive an aura—unusual visual, olfactory, or other sensory experiences that are a sign that the migraine will soon occur. Initial treatment is with analgesics for the headache, an antiemetic for the nausea, and the avoidance of triggering conditions. The cause of migraine headache is unknown; the most common theory is a disorder of the serotonergic control system.[citation needed] Studies of twins indicate a 60- to 65-percent genetic influence upon their propensity to develop migraine headaches. Moreover, fluctuating hormone levels indicate a migraine relation: 75 percent of adult patients are women, although migraine affects approximately equal numbers of prepubescent boys and girls; propensity to migraine headache is known to disappear during pregnancy, although in some women migraines may become more frequent during pregnancy.
[1] [2] [3][4] [5] [6][7] [8]

Table of Contents 1 Classification 2 Signs and symptoms 2.1 2.2 2.3 2.4 3 3.1 3.2 3.3 3.4 3.5 3.6 3.7 4 4.1 4.2 5 6 Prodrome Aura Pain Postdrome Triggers Depolarization Vascular Serotonin Melanopsin receptor Neural Unifying theory Initiation Pain

Cause

Pathophysiology

Diagnosis Prevention 6.1 6.2 6.3 6.4 Medication Surgery Other therapies Migraine diary Analgesics Triptans Ergotamines Corticosteroids Other

7

Management 7.1 7.2 7.3 7.4 7.5

8 9 1 0

Prognosis Epidemiology History

These guidelines constitute arbitrary definitions. If a close relative has had the same condition. an aura can occur without a headache. 2nd edition" (ICHD-2). where a headache and aura are accompanied by difficulty speaking.1 1 Society and culture 11. Another variety is basilar-type migraine. or a number of other brainstem-related symptoms. see below). According to ICHD-2. in which a patient has migraines with aura and with accompanying motor weakness. Less commonly. and benign paroxysmal vertigo of childhood (occasional attacks of vertigo). otherwise it is called "sporadic". but not motor weakness. 1 Economic impact 1 2 1 3 1 4 Research References External links Classification Main article: ICHD classification and diagnosis of migraine The International Headache Society (IHS) offers guidelines for the classification and diagnosis of migraine headaches. involves migraine headaches that are not accompanied by an aura (visual disturbance. usually accompanied by nausea).  Migraine with aura usually involves migraine headaches accompanied by an aura. and are not supported by scientific data. there are seven subclasses of migraines (some of which include further subdivisions):  Migraine without aura. or common migraine.  Childhood periodic syndromes that are commonly precursors of migraine include cyclical vomiting (occasional intense periods of vomiting). abdominal migraine (abdominal pain. vertigo. it is called "familial". [3] [3] . Two other varieties are Familial hemiplegic migraine and Sporadic hemiplegic migraine. in a document called "The International Classification of Headache Disorders. or with a non-migraine headache. ringing in ears.

2. The pain phase. greater or equal to 15 days/month for greater than 3 months. increased urination. The severity of the pain. stiff muscles (especially in the neck). Additionally.Retinal migraine involves migraine headaches accompanied by visual disturbances or even temporary blindness in one eye. also known as headache phase. dizziness.yawning. The prodrome. An aura only occurs in a small percentage of people.  Probable migraine describes conditions that have some characteristics of migraines but where there is not enough evidence to diagnose it as a migraine with certainty (in the presence of concurrent medication overuse). This phase may consist of altered mood.  [9] [10] Signs and symptoms Migraines typically present with recurrent severe headache associated with autonomic symptoms. and other visceral symptoms.not all the phases are necessarily experienced. The aura. Prodrome The postdrome. 3. chocolate). or associated with a seizure or brain lesion. the phases experienced and the symptoms experienced during them can vary from one migraine attack to another in the same person: 1. A migraine lasting 72 hours is termed status migrainosus and can be treated with intravenous prochlorperazine.g. hot ears. which immediately precedes the headache. excessive sleepiness. Prodromal symptoms occur in 40–60% of those with migraines. is a "complication of migraine"s and is a headache fulfilling the diagnostic criteria for "migraine headache". according to the American Headache Society and the international headache society. which occurs for a greater time interval. depression or euphoria. Specifically. constipation or diarrhea. which occurs hours or days before the headache. These symptoms usually precede the headache phase of the [12] . duration of the headache. There are four possible phases to a migraine attack. and frequency of attacks is variable. fatigue.  Complications of migraine describe migraine headaches and/or auras that are unusually long or unusually frequent. [11] [11] [11] [3] 4. craving for certain food (e. They are listed below .  Chronic migraine. irritability.

[13] For the 20–30% [14][15] of migraine sufferers who experience migraine with aura. but it is sometimes delayed up to several hours. vertigo. and hypersensitivity to touch. tingling or numbness of the face and extremities. this aura comprises focal neurological phenomena that precede or accompany the attack. Oliver Sacks's book Migraine describes "migrainous deliria" as a result of such intense migraine aura that it is indistinguishable from "free-wheeling states of hallucinosis. illusion. Aura Screenshot of a YouTube video showing a computer simulation of visual field defects during migraine with aura based on a neural network. or. in some cases. Visual aura is the most common of the neurological events and can occur without any headache. temporary dysphasia. The pain may also begin before the aura has completely subsided. lips and tongue. They appear gradually over 5 to 20 minutes and generally last fewer than 60 minutes. hence the alternative terms "fortification spectra" or "teichopsia" ). Other symptoms of the aura phase can include auditory. and it can be missing entirely (see silent migraine). The headache phase of the migraine attack usually begins within 60 minutes of the end of the aura phase. or dreaming.migraine attack by several hours or days. The paresthesia may migrate up the arm and then extend to involve the face. Some patients complain of blurred or shimmering or cloudy vision. The somatosensory aura of migraine may consist of digitolingual or cheirooral paresthesias. There is a disturbance of vision consisting often of unformed flashes of white and/or black or rarely of multicolored lights (photopsia) or formations of dazzling zigzag lines (scintillating scotoma. gustatory or olfactory hallucinations. tunnel vision and hemianopsia. Symptoms of migraine aura can be sensory or motor in nature. a feeling of pins-and-needles experienced in the hand and arm as well as in the nose-mouth area on the same side. and experience teaches the patient or observant family how to detect that a migraine attack is near. often arranged like the battlements of a castle." [16] [17] Visual symptoms of migraine aura . as though they were looking through thick or smoked glass.

and moderate to severe and can be aggravated by physical activity. and may occur [3] primarily on one side or alternate sides from one attack to the next. or sweating may be noted during the headache phase. a variation of the typical migraine. from a few in a lifetime to several a week. gastrointestinal symptoms. Many sufferers report a sore feeling in the area where the migraine was. The patient may feel tired or "hungover" and have head pain. prominence of a vein or artery in the temple. The pain of migraine is invariably accompanied by other features. and weakness. Not all these features are necessary. or stiffness and tenderness of the neck.[citation needed] and a feeling of faintness may occur. delirium. Postdrome The effects of migraine may persist for some days after the main headache has ended. has also been described. The onset is usually gradual. mood changes. According to one summary. nasal stuffiness. Nausea occurs in almost 90 percent of patients. Vertigo may be experienced.Enhancements reminiscent of a Negative scotoma. The pain peaks and then subsides and usually lasts 4 to 72 hours in adults and 1 to 48 hours in children. scalp tenderness. diarrhea. and osmophobia and seek a dark and quiet room. Blurred vision. The head pain varies greatly in intensity. called vestibular migraine. The extremities tend to feel cold and moist. phonophobia. Lightheadedness. and the average sufferer experiences one to three headaches a month. loss of zigzag fort structure awareness of local structures Positive scotoma. The frequency of attacks is extremely variable. Many patients experience sensory hyperexcitability manifested by photophobia. There may be localized edema of the scalp or face. throbbing. "Some people [18] . The pain may be bilateral at the onset or start on one side and become generalized. Impairment of concentration and mood are common. local perception of additional structures Mostly one-sided loss of perception Pain The typical migraine headache is unilateral. cognitive difficulties. polyuria. pallor. tinnitus. and some report impaired thinking for a few days after the headache has passed. rather than true vertigo. and vomiting occurs in about one third of patients.

feel unusually refreshed or euphoric after an attack. This is in line with other reviews. A prospective diary study showed that menstruation had the most prominent effect. The most common triggers quoted are stress. however. Furthermore. a divorced marriage and consumption of beer decreased the risk. Nutrition played no role at all. if any effect on headaches and migraines. [11] [21] [22] [21] [23] [24] [25] [26] [27] [28] [29] Depolarization Animation of cortical spreading depression . the strength and significance of these relationships are uncertain. A 2005 literature review found that the available information about dietary trigger relies mostly on subjective assessments. and fatigue. relaxation after stress. While monosodium glutamate (MSG) is frequently reported as a dietary trigger evidence does not consistently support this. Days off. whereas others note depression and malaise. data from the same diary study suggested that weather change has little. Triggers [20] A minority of migraines may be induced by triggers. psychic tension. . While many things have been labeled as triggers. hunger. noise and odours increased the risk by less than 35 %. A 2003 review concluded that there was no scientific evidence for an effect of tyramine on migraine. A 2009 review found little evidence to corroborate the environmental triggers reported. Other factors such as muscle tension in the neck. increasing the risk of headache and migraine in migraineurs by up to 96%. tiredness." [19] Cause The cause of migraines is unknown. these equally contribute to tension headaches.

Serotonergic agonists like triptans. only about one third of migraineurs experience an aura. blood vessel diameters return to normal more than an hour before the migraine headaches occur. The reduced flow of blood from the occipital lobe triggers the aura that some individuals who have migraines experience because the visual cortex is in the occipital area. pain sensation. as arteries spasm. First. can cause migraines. [unreliable [31] source?] When the constriction of blood vessels in the brain stops and the aura subsides. In cortical spreading depression. This may start in theoccipital lobe. This leakage is recognized by pain receptors in the blood vessels of surrounding tissue. the body supplies the area with chemicals which cause inflammation. [32] [31] [33] Serotonin Serotonin is a type of neurotransmitter. as well as dilation and constriction of the blood vessels among other things. which conveys the sensory information for the face and much of the head. blood passes through this sensitive area causing a throb of pain. In response. It has been suggested that situation results in the release ofinflammatory mediators leading to irritation of cranial nerve roots. then depressed over an area of the cortex of the brain. or "communication chemical" which passes messages between nerve cells. neurological activity is initially activated. [31] [31] Melanopsin receptor . It helps to control mood. and there are indeed cogent arguments against it. most particularly the trigeminal nerve.[citation needed]Second. many migraineurs have a prodrome (see above). sexual behaviour. The walls of these blood vessels become permeable and some fluid leaks out. Low serotonin levels in the brain may lead to a process of constriction and dilation of the blood vessels which trigger a migraine. in the back of the brain. LSD or psilocinactivate serotonin receptors to stop a migraine attack. With each heart beat. and those who do not experience aura do not have cortical spreading depression. without any supporting evidence. [30] [12] Vascular Studies have shown that the aura coincides with constriction of blood vessels in the brain.It has been theorized that the phenomenon known as cortical spreading depression. sleep. which occurs up to three days before the aura. This theory is however speculative. which is associated with the aura of migraine. [unreliable source?] Although cerebral vasodilation can trigger migraine attacks. the blood vessels of the scalp dilate.

but the vascular changes of migraines are now considered by some to be secondary to brain dysfunction. chemicals including substance P irritate nerves and blood vessels causing neurogenic inflammation and pain Pathophysiology Migraine is a neurovascular disorder. although this concept has not been supported by the evidence. a migraine begins.The emerging evidence would suggest that just as alterations in neuronal activity can lead to downstream effects on the cerebral blood vessel. These chemicals cause further irritation of the nerves and blood vessels and results in pain. there are likely patients. these changes cause serotonin to be released 3. but this is currently speculation. In response to the irritation.' Some have even attempted to show that vascular changes are of no importance in migraine. This was eloquently summed up by Dodick who wrote ‘There is no disputing the role of the central nervous system in the susceptibility. and/or at least attacks in certain patients. so too can changes within endothelial cells or vascular smooth muscle lead to downstream alterations in neuronal activity. 1. where primarily vascular mechanisms predominate. [34] Neural When certain nerves or an area in the brain stem become irritated. [31] [35] . Therefore. modulation and expression of migraine headache and the associated affective. stress triggers changes in the brain 2. Although migraine is thought by some to be a neurological disease. in the absence of scientific evidence. this remains a hypothesis. based on the available evidence. [11] [31] Initiation Migraines were once thought to be initiated exclusively by problems with blood vessels. Pain then increases because substance P aids in sending pain signals to the brain. sensory. cognitive.A melanopsin-based receptor has been linked to the association between light sensitivity and migraine pain. is naïve at best and unscientific at worst. and neurological symptoms and signs. the body releases chemicals which cause inflammation of the blood vessels. However to presume that migraine is always generated from within the central nervous system. blood vessels constrict and dilate 4. [31] Unifying theory Both vascular and neural influences cause migraines. Substance P is one of the substances released with first irritation.

Tender muscle trigger points can be at least part of the cause. Pericranial (jaw and neck) muscle tenderness is a common finding in migraine It has actually been shown that muscle tenderness is present in 100% of migraine attacks. [unreliable source?] [3] [32][39][40][41][42][43] [44][45] [46] [47][48][49] [50] [51] Diagnosis Migraines are underdiagnosed and often misdiagnosed. there is a great deal of irrefutable evidence to show that the pain of migraine (the third phase) is in some patients related to painful dilatation of the terminal branches of the external carotid artery. 2. Because these arteries are relatively superficial.  4 hours to 3 days in duration. It was previously thought that dilatation of the arteries in the brain and dura mater was the origin of the vascular pain. it is probably because both vascular and neurogenic mechanisms for migraine exist and are important'. 4. according to the International Headache Society.J Edmeads [36] [37] [38] Pain Although the initiating factor of migraine remains unknown.but this claim is unsubstantiated and has not been supported by scientific evidence. The diagnosis of migraine without aura.  Pulsating. and perpetuate most kinds of headaches.  2 or more of the following:  Unilateral (affecting half the head). then they are also accessible to a form of migraine surgery that is being promoted. 3.  "Moderate or severe pain intensity". but it has now been shown that these vessels do not dilate during migraine.  "Aggravation by or causing avoidance of routine physical activity". two attacks are sufficient for diagnosis. 1 criteria":  5 or more attacks.  1 or more of the following: [52] [53] [54] . 'If we swing between vascular and neurogenic views of migraine. the "5. If they are. For migraine with aura. so muscle tenderness is the single most common finding in migraine. largely to the efforts of Dr Elliot Shevel. a South African surgeon. can be made according to the following criteria. who has reported excellent success using the procedure. it is easy to diagnose whether they are the source of the pain. and in particular its superficial temporal and occipital branches.

otherwise known as rebound headache. The duration of the common attack is 15 minutes to three hours. is that unpleasant side effects are [61] . Onset of an attack is rapid. one-quarter of patients find that their migraine frequency is reduced by half or more. can diagnose migraine with:  sensitivity of 81%  specificity of 75% Migraine should be differentiated from other causes of headaches such as cluster headaches."Nausea and/or vomiting". This is a common problem among migraneurs. The goals of preventive therapy are to reduce the frequency. The major problem with migraine preventive drugs. If 4 of the 5 criteria are met. migraine surgery. The mnemonic POUNDing (Pulsating. [11] Prevention Main article: Prevention of migraines Preventive (also called prophylactic) treatment of migraines can be an important component of migraine management. nausea or sensitivity.  Sensitivity to both light (photophobia) and sound (phonophobia). and actual treatments often far exceed this figure. and avoidance of migraine triggers. including taking preventive drugs. Disabling) can help diagnose migraine. Even with a placebo. . The presence of either disability. and/or duration of migraines. lifestyle alterations such as increased exercise. Unilateral. painfulness. Such treatments can take many forms. [57] [58][59] [60] Medication Preventive migraine drugs are considered effective if they reduce the frequency or severity of migraine attacks by at least 50%. unilateral headaches of a piercing quality.[citation  [55] [56] needed] Medical imaging of the head and neck may be used to rule out secondary causes of headaches. duration of 4–72 hOurs. These are extremely painful. then the positive likelihood ratio for diagnosing migraine is 24. and most often without the preliminary signs that are characteristic of a migraine. and can result in chronic daily headache. and to increase the effectiveness of abortive therapy. Another reason to pursue these goals is to avoid medication overuse headache (MOH). apart from their relative inefficacy. Many of the preventive treatments are quite effective. Nausea. taking nutritional supplements.

There are many medicines available to prevent or reduce frequency. Tricyclic antidepressants have been long established as efficacious prophylactic treatments. Anti-depressants offer advantages for treating migraine patients with comorbid depression. Selective serotonin reuptake inhibitors (SSRIs) are not approved by the U. the results of surgery are outstanding and provide permanent pain relief. and in those who have not had an adequate response to prophylactic medications. There is no consistent evidence that SSRI antidepressants are effective for migraine prophylaxis. They may also prevent complications of migraine. Patients often still experience a poor quality of life despite an aggressive regimen of pharmacotherapy. but have been found to be effective by some practitioners. light sensitivity.common. Tricyclics have been found to be more effective than SSRIs. the anti-depressant nefazodone may also be beneficial in the prophylaxis of migraines due to its antagonistic effects on the 5-HT2A and 5-HT2C receptors It has a more favorable side effect profile than amitriptyline. surgical solutions to migraines have been developed. [62] [63] [61] [61] [64] [65][66] [61] [61] [67][68][69][70] Surgery Migraine surgery is a field that shows a great deal of promise. Once a positive diagnosis has been made. and metoprolol. These drugs. however. often to find one with a profile of side-effects that is acceptable to the patient. a definite diagnosis can be made before the surgery is undertaken. other tricyclic antidepressants are believed to act similarly and are widely prescribed. For this reason. vomiting. In addition to tricyclics a. For these reasons. Food and Drug Administration (FDA) for treatment of migraines. atenolol. such as insomnia. There is some evidence that low-dose asprin has benefit for reducing the occurrence of migraines in susceptible individuals. as well as relief from the associated symptoms such as nausea. While amitryptiline (Elavil) is the only tricyclic to have received FDA approval for migraine treatment. Beta blockers such as Propranolol. with the correct diagnostic techniques. particularly in those who suffer more frequent attacks. sedation or sexual dysfunction. A major advantage of migraine surgery is that. theanticonvulsants sodium valproate. flunarizine and verapamil. duration and severity of migraine attacks. may give rise to undesirable side effects.S. a tricyclic antidepressant commonly used for migraine prophylaxis. divalproex gabapentin and topiramate and tricyclic antidepressants are some of the commonly used drugs. [71] [72][73][74][75][76][77][78][79][80][81][82][83][84] . preventive medication is limited to patients with frequent or severe headaches. calcium channel blockers such as amlodipine. which have excellent results.

however the research had some problems with methodology. and analgesics. Finally. acute symptomatic control. especially narcotics analgesics. and pharmacological prevention. as insufficient evidence exists to justify this dangerous procedure. ergotamines. There is also evidence that the correction of a congenital heart defect. in which the headaches become more severe and more frequent. Medications are more effective if used earlier in an attack. The value of arterial sugery for migraine treatment is gaining recognition as a result of the efforts of a South African surgeon. It is a safe and relatively atraumatic procedure which can be performed in a day facility. Dr Elliot Shevel. [85] [73] [86] [87][88] Other therapies A systematic review stated that chiropractic manipulation. [89] Migraine diary A migraine diary allows the assessment of headache characteristics. but only in patients who respond well to Botox injections in specific areas. [11] [11] [3] Analgesics A number of analgesics are effective for treating migraines including: . The frequent use of medications may however result in medication overuse headache (MOH). Recent studies have advised caution. though. reduces migraine frequency and severity. These may occur with triptans. who has produced a number of papers on the subject. A diary also helps to analyse the relation between migraine and menstruation. to differentiate between migraine and tension-type headache and to record the use and efficacy of acute medication. patent foramen ovale (PFO). The removal of muscles or nerves in areas known as "trigger sites" provides good results. A trigger may occur up to 24 hours prior to the onset of symptoms. Surgical cauterization of the superficial blood vessels of the scalp (the terminal branches of the external carotid artery) is only carried out if the clinical examination has shown these vessels are indeed a source of pain. [90] [11] [11] Management There are three main aspects of treatment: trigger avoidance. massage and relaxation might be as effective as propranolol or topiramate in the prevention of migraine headaches. physiotherapy. in relation to PFO closure for migraines. however the majority of migraines are not caused by identifiable triggers.and sound sensitivity. the diary can help to identify trigger factors.

[101] . In addition some antiemetics such as metoclopramide are prokinetics and help gastric emptying which is often impaired during episodes of migraine.  [91] [92] [93] [94] [95] [96][97] [97] Triptans Triptans such as sumatriptan are effective for both pain and nausea in up to 75% of people. Even by itself. but may cause medication overuse headaches if used more than 10 days per month. Most side effects are mild such as flushing however rare cases of myocardial ischemia have occurred.  Paracetamol/acetaminophen either alone or in combination with metaclopramide is effective for migraines. with buclizine as the antiemetic) and paracetamol/metoclopramide (Paramax in UK). which was 5% less than the benefit of sumatriptan. [11][98] [11] [11] [99] Ergotamines Dihydroergotamine is an older medication that some find useful. there are three combination antiemetic and analgesic preparations available: MigraMax (aspirin with metoclopramide).Non-steroidal anti-inflammatory drugs (NSAIDs): Ibuprofen provides pain effective pain relief in about half of people. injection. In the UK. They come in a number of different forms including oral. is associated with a 26% decrease in headache recurrence in the following 72 hours. [100] Other Antiemetics by mouth may help relieve symptoms of nausea and help prevent vomiting. A 1000 mg dose of Aspirin (also called ASA) could relieve moderate to severe migraine pain. The earlier these drugs are taken in the attack. the better their effect. which can diminish the effectiveness of orally taken analgesia. Naproxen can abort about one third of migraine attacks. with similar effectiveness to sumatriptan. They were the primary oral drugs available to abort a migraine prior to the triptans. [11] Corticosteroids A single dose of intravenous dexamethasone. despite the fact that in general migraine-sufferers are advised to limit their caffeine intake. They are much less expensive than triptans and continues to be prescribed for migraines. They are non addictive.  Simple analgesics combined with caffeine may help. when added to standard treatment of a migraine attack. caffeine can be useful during an attack. (paracetamol/codeine for analgesia. and oral dissolving tablets. nasal spray.

Death from cardiovascular causes was higher in people with migraine with aura in a Women's Health Initiative study. but chronic abnormalities of cerebral blood vessel tone may be involved. Young adult sufferers and women using hormonal contraception appear to be at particular risk.to threefold in migraine sufferers. but more research is needed to confirm this. [102] [102][103] [104] [105] [103][106] Epidemiology Disability-adjusted life year for migraines per 100. no data less than 45 45-65 65-85 85-105 105-125 125-145 145-165 165-185 185-205 205-225 225-245 more than 245 . (Note: Women who experience auras and also take oral contraceptives have an even higher risk of stroke).000 inhabitants in 2002. Women who experience auras have been found to have twice the risk of strokes and heart attacks over non-aura migraine sufferers and women who do not have migraines. The mechanism of any association is unclear. Migraine sufferers seem to be at risk for both thrombotic and hemorrhagic stroke as well as transient ischemic attacks.Prognosis The risk of stroke may be increased two.

There is a strong relationship between age.5:1 and 2:1. By early middle age. The incidence of migraine is related to the incidence of epilepsy in families. migraine with aura is somewhat more common than amongst 15–50 year olds. At all ages. These figures vary substantially with age: approximately 4–5% of children aged under 12 suffer from migraine. so that in the over 70s there are approximately equal numbers of male and female sufferers. one year prevalence of migraine ranges from 6–15% in adult men and from 14–35% in adult women. compared with fewer than 10% of men. In Europe migraines affect 12–28% of people at some point in their lives.Incidence of migraine by age and sex Worldwide migraines affect more than 10% of people. Incidence figures show that the excess of migraine seen in women of reproductive age is mainly due to migraine without aura. After menopause. [20] [11] [2] [2] [107] [108] [109][110] [111] [2][112] [2][112] [113][114] [113] [111][115] [116] [117][118] [2][112] [119] History . with prevalence returning to around 5%. sex and type of migraine. attacks in women tend to decline dramatically. but they do not fall outside the range of values seen in European and North American studies. and more common in epilepsy sufferers themselves. with little apparent difference between boys and girls. Thus in prepubertal and post-menopausal populations. In the United States approximately 6% of men and 18% of women get a migraine in a given year with a lifetime risk of about 18% and 43% respectively. with a ratio of between 1. There is then a rapid growth in incidence amongst girls occurring after puberty. with migraine twice as prevalent in family members of epilepsy sufferers. Based on the results of a number of studies. which continues throughout early adult life. around 25% of women experience a migraine at least once a year. Studies in Asia and South America suggest that the rates there are relatively low. migraine without aura is more common than migraine with aura.

the patient cannot tolerate the sound of speaking and light. In the Middle Ages migraine was recognized as a discrete medical disorder with treatment ranging from hot irons tobloodletting and even witchcraft[citation needed].. the deliberate and (usually) non-fatal drilling of holes into a skull.. He would like to rest in darkness alone.000 years ago and earlier. He thought there was a connection between the stomach and the brain because of the nausea and vomiting that often accompany an attack." [121] [120][122] [120] . Galenus of Pergamon used the term "hemicrania" (half-head).. was practiced 9. Followers of Galenus explained migraine as caused by aggressiveyellow bile. from which the word "migraine" was derived. George Cruikshank (1819) Trepanation. Some scholars have (controversially) speculated that this drastic procedure might have been a migraine treatment. and sounds provoke the pain. small movements. also known as Abu El Qasim. with headache-free intervals in between attacks. drinking and eating. based on [120] cave paintings and on the fact that trepanation was a historical migraine treatment in 17th-century Europe... Ebn Sina (Avicenna) described migraine in his textbook "El Qanoon fel teb" as ".The Head Ache." Abu Bakr Mohamed Ibn Zakariya Râzi noted the association of headache with different events in the lives of women. Aretaeus of Cappadocia is credited as the "discoverer" of migraines because of his second century description of the symptoms of a unilateral headache associated with vomiting. For relief of migraine. Andalusian-born physician Abulcasis.And such a headache may be observed after delivery and abortion or duringmenopause and dysmenorrhea. suggested application of a hot iron to the head or insertion of garlic into an incision made in the temple. ".. written around 1200 BC in ancient Egypt. An early written description consistent with migraines is contained in the Ebers papyrus. In 400 BC Hippocrates described the visual aura that can precede the migraine headache and the relief which can occur through vomiting.

Recently however. including the "Megrim". a South African headache specialist. who has published a number of articles providing compelling evidence that Wolff was in fact correct.309 per sufferer. and has been replaced by the term "Migraine with aura" Graham andWolff (1938) published their paper advocating ergotamine tartrate for relieving migraine. [3] [46][123][124][40] Society and culture Economic impact Chronic migraine attacks are a significant source of both medical costs and lost productivity. recognizable as classic migraine. Recently it has been found that calcitonin gene related peptides (CGRPs) play a role in the pathogenesis of the pain associated with migraine as triptans also decrease its [126] . which has come under attack as the pendulum again swings to the neurogenic theory. The term "Classic migraine" is no longer used. With education and understanding an employer could compromise with an employee to create a workable solution for both. It has been estimated to be the most costly neurological disorder in the European Community. The workplace model of 9–5. published in London in 1712.[citation needed] [125] Research Merck Corp is developing a new drug called Telcagepant which is intended to relieve pain without causing vasoconstriction (narrowing of blood vessels) as current medications such as triptans do. 5 days a week may not be viable for a migraine sufferer. Employers may benefit from educating themselves on the effects of migraines in order to facilitate a better understanding in the workplace. Annual employer cost of lost productivity due to migraines was estimated at $3. in addition to lost productivity estimated at thirteen to seventeen billion dollars per year. Medical costs per migraine sufferer (mostly physician and emergency room visits) averaged $107 USD over six months in one 1988 study. Telcagepant would be a safe therapy for migraine suffers with risk factors for cardiovascular disease. Medic. Later in the 20th century. five major types of headaches are described.[citation needed] with total costs including lost productivity averaging $313. Chirurgica. there has been renewed interest in Wolff's vascular theory of migraine led by Elliot Shevel.In Bibliotheca Anatomica. Harold Wolff (1950) developed the experimental approach to the study of headache and elaborated the vascular theory of migraine. costing more than €27 billion per year. Total medical costs associated with migraines in the United States amounted to one billion dollars in 1994.

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More Related Questions » Related Images . ↑ "Migraine cause 'identified' as genetic defect". allergies. primarily CNS (G04–G47.128. it is necessary to understand the migraine process.21 MB)  World Headache Alliance  [show]v · d ·Pathology of the nervous system... What is not often talked abou. External links Migraine at the Open Directory Project  Migraine Information from the US National Institute of Neurological Disorders and Stroke  Diagnostic criteriaPDF (1. Wines. What is Migraine To understand how triptans relieve migraines. certain foods.. hormone fluctu. the many causes. aged cheeses. We hear about this all the time. 2010-09-27. Migraines begin when a trigger event . 323–349) [show]v · d ·CNS disease: Headache (G43–G44. 339.... 346) [show]v · d ·Antimigraine preparations (N02C) Categories: All pages needing cleanup | Wikipedia articles needing page number citations from September 2010 | Articles with invalid date parameter in template | Pages with DOIs inactive since 2010 | All articles with unsourced statements | Articles with unsourced statements from February 2011 |Articles with unsourced statements from September 2009 | All articles lacking reliable references | Articles lacking reliable references from March 2009 | Articles lacking reliable references from March 2011 | Articles with unsourced statements from September 2007 | Articles with unsourced statements from February 2007 | Articles with unsourced statements from July 2010 | Episodic and paroxysmal disorders | Headaches | Migraine The content on this page originates from Wikipedia and is licensed under the GNU Free Document License or the Creative Commons CC-BY-SA license. Have a gr.. What causes migraine headaches Oh. and beneficial to some. BBC News.such as lack of sleep. and chocolate being the most popular culprits. Related Web Searches Home Remedies for Migraines Migraine Symptoms Migraine Relief Types of Migraines Atypical Migraine Symptoms Related Questions Does chocolate milk stop migraines Chocolate is harmful to some people's headaches. Diet/Allergy: Many foods can trigger migraines.

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