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Migraine From Wikipedia, the free encyclopedia Migraine (from the Greek words hemi, meaning half, and kranion, meaning skull[1]) is a debilitating condition characterized by moderate to severe headaches, and nausea, about 3 times more common in women than in men.[2] The typical migraine headache is unilateral pain (affecting one half of the head) and pulsating in nature, 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.[3][4] 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.[5] 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 headache.[6][7] 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.[8] Migraine Classification and external resources The pain of a migraine headache can be debilitating. ICD-10 G43. ICD-9 346 OMIM 157300 DiseasesDB 8207 (Migraine) 31876 (Basilar) 4693 (FHM) MedlinePlus 000709 eMedicine neuro/218 neuro/517 emerg/230 neuro/529 MeSH D008881 Contents n 1 Classification n 2 Signs and symptoms n 2.1 Prodrome n 2.2 Aura n 2.3 Pain n 2.4 Postdrome n 3 Cause n 3.1 Triggers n 3.2 Depolarization n 3.3 Vascular relationship to the aura n 3.4 Serotonin n 3.5 Melanopsin receptor n 3.6 Neural 页码，1/18Migraine - Wikipedia, the free encyclopedia 2011/3/23http://en.wikipedia.org/wiki/Migraine Un Re gis te re d Classification Main article: ICHD classification and diagnosis of migraine The International Headache Society (IHS) offers guidelines for the classification and diagnosis of migraine headaches, in a document called "The International Classification of Headache Disorders, 2nd edition" (ICHD-2).[3] These guidelines constitute arbitrary definitions, and are not supported by scientific data.[3] According to ICHD-2, there are seven subclasses of migraines (some of which include further subdivisions): n Migraine without aura, or common migraine, involves migraine headaches that are not accompanied by an aura (visual disturbance, see below). n Migraine with aura usually involves migraine headaches accompanied by an aura. Less commonly, an aura can occur without a headache, or with a non-migraine headache. Two other varieties are Familial hemiplegic migraine and Sporadic hemiplegic migraine, in which a patient has migraines with aura and with accompanying motor weakness. If a close relative has had the same condition, it is called "familial", otherwise it is called "sporadic". Another variety is basilar-type migraine, where a headache and aura are accompanied by difficulty speaking, vertigo, ringing in ears, or a number of other brainstem-related symptoms, but not motor weakness. n Childhood periodic syndromes that are commonly precursors of migraine include cyclical vomiting (occasional intense periods of vomiting), abdominal migraine (abdominal pain, usually accompanied by nausea), and benign paroxysmal vertigo of childhood (occasional attacks of vertigo). n Retinal migraine involves migraine headaches accompanied by visual disturbances or even n 3.7 Unifying theory n 4 Pathophysiology n 4.1 Initiation n 4.2 Pain n 5 Diagnosis n 6 Prevention n 6.1 Medication n 6.2 Surgery n 6.3 Other therapies n 6.4 Migraine diary n 7 Management n 7.1 Analgesics n 7.2 Triptans n 7.3 Ergotamines n 7.4 Corticosteroids n 7.5 Other n 8 Prognosis n 9 Epidemiology n 10 History n 11 Society and culture n 11.1 Economic impact n 12 Research n 13 References n 14 External links 页码，2/18Migraine - Wikipedia, the free encyclopedia 2011/3/23http://en.wikipedia.org/wiki/Migraine Un Re gis te re d Administrator 高亮 Administrator 高亮 Administrator 下划线 Administrator 下划线 Administrator 下划线 Administrator 下划线 temporary blindness in one eye. n Complications of migraine describe migraine headaches and/or auras that are unusually long or unusually frequent, or associated with a seizure or brain lesion. n 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. Signs and symptoms Migraines typically present with recurrent severe headache associated with autonomic symptoms.[9] An aura only occurs in a small percentage of people.[9] The severity of the pain, duration of the headache, and frequency of attacks is variable.[9] There are four possible phases to a migraine attack.[3] They are listed below - not all the phases are necessarily experienced. Additionally, the phases experienced and the symptoms experienced during them can vary from one migraine attack to another in the same person: 1. The prodrome, which occurs hours or days before the headache. 2. The aura, which immediately precedes the headache. 3. The pain phase, also known as headache phase. 4. The postdrome. Prodrome Prodromal symptoms occur in 40–60% of those with migraines. This phase may consist of altered mood, irritability, depression or euphoria, fatigue, yawning, excessive sleepiness, craving for certain food (e.g. chocolate), stiff muscles (especially in the neck), hot ears, constipation or diarrhea, increased urination, and other visceral symptoms.[10] These symptoms usually precede the headache phase of the migraine attack by several hours or days, and experience teaches the patient or observant family how to detect that a migraine attack is near. Aura For the 20–30%[12][13] of migraine sufferers who experience migraine with aura, this aura comprises focal neurological phenomena that precede or accompany the attack. They appear gradually over 5 to 20 minutes and generally last fewer than 60 minutes. The headache phase of the migraine attack usually begins within 60 minutes of the end of the aura phase, but it is sometimes delayed up to several hours, and it can be missing entirely (see silent migraine). The pain may also begin before the aura has completely subsided. Symptoms of migraine aura can be sensory or motor in nature.[14] Visual aura is the most common of the neurological events and can occur without any headache. 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; often arranged like the battlements of a castle, hence the alternative terms "fortification spectra" or "teichopsia"[15]). Some patients complain of blurred or shimmering or cloudy vision, as though they were looking through thick or smoked glass, or, in some cases, tunnel vision and hemianopsia. For those suffering from this the prodrome is a small blurred spot that we cannot focus on. This is followed by a growing into a larger object such as a three sided square with the zig-zag line interfering with vision. This grows to a maximum size Screenshot of a YouTube video showing a computer simulation of visual field defects during migraine with aura based on a neural network. [11] 页码，3/18Migraine - Wikipedia, the free encyclopedia 2011/3/23http://en.wikipedia.org/wiki/Migraine Un Re gis te re d Administrator 高亮 Administrator 高亮 Administrator 高亮 Administrator 高亮 Administrator 高亮 Administrator 高亮 Administrator 高亮 Administrator 下划线 Administrator 下划线 Administrator 下划线 Administrator 下划线 and then starts moving slowly through the field of vision until it exits the field of view. For all practical purposes the aura phase has then ended even if brain activity could be detected that would indicate an active aura. The somatosensory aura of migraine may consist of digitolingual or cheiro-oral paresthesias, a feeling of pins-and-needles experienced in the hand and arm as well as in the nose-mouth area on the same side. The paresthesia may migrate up the arm and then extend to involve the face, lips and tongue. Other symptoms of the aura phase can include auditory, gustatory or olfactory hallucinations, temporary dysphasia, vertigo, tingling or numbness of the face and extremities, and hypersensitivity to touch. 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, or dreaming." n Visual symptoms of migraine aura n n n Enhancements reminiscent of a zigzag fort structure Negative scotoma, loss of awareness of local structures Positive scotoma, local perception of additional 页码，4/18Migraine - Wikipedia, the free encyclopedia 2011/3/23http://en.wikipedia.org/wiki/Migraine Un Re gis te re d n n Pain The typical migraine headache is unilateral, throbbing, and moderate to severe and can be aggravated by physical activity.[3] Not all these features are necessary. The pain may be bilateral at the onset or start on one side and become generalized, and may occur primarily on one side or alternate sides from one attack to the next. The onset is usually gradual. The pain peaks and then subsides and usually lasts 4 to 72 hours in adults and 1 to 48 hours in children. The frequency of attacks is extremely variable, from a few in a lifetime to several a week, and the average sufferer experiences one to three headaches a month. The head pain varies greatly in intensity. The pain of migraine is invariably accompanied by other features. Nausea occurs in almost 90 percent of patients, and vomiting occurs in about one third of patients. Many patients experience sensory hyperexcitability manifested by photophobia, phonophobia, and osmophobia and seek a dark and quiet room. Blurred vision, delirium, nasal stuffiness, diarrhea, tinnitus, polyuria, pallor, or sweating may be noted during the headache phase. There may be localized edema of the scalp or face, scalp tenderness, prominence of a vein or artery in the temple, or stiffness and tenderness of the neck. Impairment of concentration and mood are common. The extremities tend to feel cold and moist. Vertigo may be experienced; a variation of the typical migraine, called vestibular migraine, has also been described. Lightheadedness, rather than true vertigo,[citation needed] and a feeling of faintness may occur. Postdrome The effects of migraine may persist for some days after the main headache has ended. Many sufferers report a sore feeling in the area where the migraine was, and some report impaired thinking for a few days after the headache has passed. The patient may feel tired or "hungover" and have head pain, cognitive difficulties, gastrointestinal symptoms, mood changes, and weakness.[16] According to one summary, "Some people feel unusually refreshed or euphoric after an attack, whereas others note depression and malaise."[17] Cause The cause of migraines is unknown.[18] Triggers A minority of migraines may be induced by triggers.[9] While many things have been labeled as triggers, the strength and significance of these relationships are uncertain.[19][20] The most common structures Mostly one-sided loss of perception 页码，5/18Migraine - Wikipedia, the free encyclopedia 2011/3/23http://en.wikipedia.org/wiki/Migraine Un Re gis te re d triggers quoted are stress, hunger, and fatigue; however, these equally contribute to tension headaches.[19] A 2003 review concluded that there was no scientific evidence for an effect of tyramine on migraine.[21] A 2005 literature review found that the available information about dietary trigger relies mostly on subjective assessments.[22] This is in line with other reviews. A 2009 review found little evidence to corroborate the environmental triggers reported.[23] While monosodium glutamate (MSG) is frequently reported as a dietary trigger[24] evidence does not consistently support this.[25] Depolariation It has been theorized that the phenomenon known as cortical spreading depression, which is associated with the aura of migraine,[26] can cause migraines. In cortical spreading depression, neurological activity is initially activated, then depressed over an area of the cortex of the brain. It has been suggested that situation results in the release of inflammatory mediators leading to irritation of cranial nerve roots, most particularly the trigeminal nerve, which conveys the sensory information for the face and much of the head. This theory is however speculative, without any supporting evidence, and there are indeed cogent arguments against it. First, only about one third of migraineurs experience an aura, and those who do not experience aura do not have cortical spreading depression. [citation needed] Second, many migraineurs have a prodrome (see above), which occurs up to three days before the aura.[10] oascular relationsiip to tce aura Studies have shown that the aura coincides with constriction of blood vessels in the brain. This may start in the occipital lobe, in the back of the brain, as arteries spasm. 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.[27] When the constriction of blood vessels in the brain stops and the aura subsides, the blood vessels of the scalp dilate.[28] The walls of these blood vessels become permeable and some fluid leaks out. This leakage is recognized by pain receptors in the blood vessels of surrounding tissue. In response, the body supplies the area with chemicals which cause inflammation. With each heart beat, blood passes through this sensitive area causing a throb of pain.[27] Serotonin Serotonin is a type of neurotransmitter, or "communication chemical" which passes messages between nerve cells. It helps to control mood, pain sensation, sexual behaviour, sleep, as well as dilation and constriction of the blood vessels among other things. Low serotonin levels in the brain may lead to a process of constriction and dilation of the blood vessels which trigger a migraine.[27] Serotonergic agonists like triptans,[27] LSD or psilocin activate serotonin receptors to stop a migraine attack. Melanopsin receptor A melanopsin-based receptor has been linked to the association between light sensitivity and migraine Animation of cortical spreading depression 页码，6/18Migraine - Wikipedia, the free encyclopedia 2011/3/23http://en.wikipedia.org/wiki/Migraine Un Re gis te re d pain,[29] but this is at this stage speculation. Ieural When certain nerves or an area in the brain stem become irritated, a migraine begins. In response to the irritation, the body releases chemicals which cause inflammation of the blood vessels. These chemicals cause further irritation of the nerves and blood vessels and results in pain. Substance P is one of the substances released with first irritation. Pain then increases because substance P aids in sending pain signals to the brain.[27] ínifying teeory Both vascular and neural influences cause migraines. 1. stress triggers changes in the brain 2. these changes cause serotonin to be released 3. blood vessels constrict and dilate 4. chemicals including substance P irritate nerves and blood vessels causing neurogenic inflammation and pain[27] Patfopnysiology Migraine is a neurovascular disorder.[9] Although migraine is thought by some to be a neurological disease, in the absence of scientific evidence, this remains a hypothesis. Initiation Migraines were once thought to be initiated exclusively by problems with blood vessels, but the vascular changes of migraines are now considered by some to be secondary to brain dysfunction,[27] although this concept has not been supported by the evidence. This was eloquently summed up by Dodick who wrote ¦There is no disputing the role of the central nervous system in the susceptibility, modulation and expression of migraine headache and the associated affective, cognitive, sensory, and neurological symptoms and signs. However to presume that migraine is always generated from within the central nervous system, based on the available evidence, is na ve at best and unscientific at worst.The emerging evidence would suggest that just as alterations in neuronal activity can lead to downstream effects on the cerebral blood vessel, so too can changes within endothelial cells or vascular smooth muscle lead to downstream alterations in neuronal activity. Therefore, there are likely patients, and/or at least attacks in certain patients, where primarily vascular mechanisms predominate.'[30] Some have even attempted to show that vascular changes are of no importance in migraine,[31] [32] but this claim is unsubstantiated and has not been supported by scientific evidence. 'If we swing between vascular and neurogenic views of migraine, it is probably because both vascular and neurogenic mechanisms for migraine exist and are important'- m Edmeads[33] Pain Although the initiating factor of migraine remains unknown, there is a great deal of irrefutable evidence to show that the pain of migraine (the third phase)[3] is in some patients related to painful dilatation of the terminal branches of the external carotid artery, and in particular its superficial temporal and occipital branches.[34][35][36][37][38][39] It was previously thought that dilatation of the arteries in the brain and dura mater was the origin of the vascular pain, but it has now been shown that these vessels do not dilate during migraine.[40][41] Because these arteries are relatively superficial, it 页码，7/18Migraine - Wikipedia, the free encyclopedia 2011/3/23http://en.wikipedia.org/wiki/Migraine Un Re gis te re d is easy to diagnose whether they are the source of the pain. If they are, then they are also accessible to a form of migraine surgery that is being promoted, largely to the efforts of Dr Elliot Shevel, a South African surgeon, who has reported excellent success using the procedure.[42] Pericranial (jaw and neck) muscle tenderness is a common finding in migraine[43][44][45] It has actually been shown that muscle tenderness is present in100% of migraine attacks, so muscle tenderness is the single most common finding in migraine.[46] Tender muscle trigger points can be at least part of the cause, and perpetuate most kinds of headaches.[47] Diagnosis Migraines are underdiagnosed[48] and often misdiagnosed.[49] The diagnosis of migraine without aura, according to the International Headache Society, can be made according to the following criteria, the "5, 4, 3, 2, 1 criteria":[50] n š or more attacks. For migraine with aura, only two attacks are sufficient for diagnosis. n š hours to ¦ days in duration. n ¦ or more of the following: n Unilateral (affecting half the head); n Pulsating; n "Moderate or severe pain intensity"; n "Aggravation by or causing avoidance of routine physical activity". n 1 or more of the following: n "Nausea and/or vomiting"; n Sensitivity to both light (photophobia) and sound (phonophobia). The mnemonic POUNDing (Pulsating, duration of 4–72 hOurs, š nilateral, ¦ ausea, Disabling) can help diagnose migraine. If 4 of the 5 criteria are met, then the positive likelihood rati