migraine: Definition from Answers.com

Migraine comes from the Greek ‘hemicrania’, or half-sided headache, and is in essence a form of ‘primary headache’, which is to say that the headache is itself the disorder and is not secondary to some other process, such as infection or injury. Migraine has been recognized throughout recorded history and there are reasonably clear descriptions that date back to Sumarian times. Migraine is as real as high blood pressure or a broken bone. It is an important, biologically-based disorder that should never be thought of as psychosomatic. Migraine is characterized by episodes of often severe, usually one-sided, frequently throbbing or pounding pain, associated with other features, such as nausea or vomiting, sensitivity to body movement, sensitivity to light (photophobia), or sensitivity to sound (phonophobia).

Migraine is probably best viewed as an inherited tendency to have headache, or perhaps headacheyness, rather than just the limited view of episodes of severe headache. Certainly many migraine patients suffer very severe, disabling headache that does not shorten life but can make it virtually a living hell. However, a broader view is necessary to explain everything that the physician encounters, and other aspects of the problem may dominate in the individual.

The frequency of migraine varies greatly between individuals — occurring almost every day, once or twice a year over many years, or just a few times in a whole lifetime. The biology of migraine does not always obey the rather strict rules that have been evolved to describe it: although these are very useful for research, one should not be a slave to rules for a problem with such a complex biology.

The cause and incidence of migraine

Migraine is probably for the most part inherited. It is thought to be autosomal dominant (see genetics, human), which means that about half the children of an affected parent will carry the genes irrespective of sex. Its expression in any one patient varies and so while most migraine sufferers will have an affected relative this is not always the case. Migraine can start at almost any time in life but the peak incidence is in the 20s and 30s. About 4-6% of children are affected, slightly more boys than girls, and about 10% of most adult Caucasian populations that have been studied. Probably fewer people are affected in African populations, and fewer still in oriental Asian populations. At puberty, with the onset of menstrual periods, the prevalence (number of people with the problem) of migraine increases in females and remains greater than in males right up to the 80s. The peak prevalence is about the age of 40; in this age-group about 1 in 5, or 20%, of adult Caucasian women have migraine. This is an enormous public health issue that has barely been addressed, yet has been with humans for several millennia.

Migraine aura — the flashing lights and zigzags

Migraine aura is a very special part of the problem that affects only about 20% of sufferers. It consists of zigzag flashing lights, loss of vision, bright sparkles, pins and needles over the face or arms, or even weakness, speech problems, or balance problems. Aura usually comes at the beginning of an attack and lasts about 30 min; less commonly it can occur during or even after the headache; it very rarely lasts more than an hour. It has two very important features: firstly, it moves slowly across the field of vision, or up or down the limb, almost never moving suddenly; and secondly, it is completely reversible — it always gets better. Changes to such symptoms should result in prompt medical review. Recently, the nature of a very special, rare form of aura, called hemiplegic aura, involving complete loss of use of the limbs on one side, has been elucidated. It is often due to a mutation, a change in the gene for a particular protein that allows electrically charged chemicals into body cells and controls the release of messenger molecules in the brain. These mutations on chromosomes 1 and 19 are pointing to ways in which we might understand how ordinary migraine starts: this is an active area of research.

The pain of migraine

This does not have a single explanation, which is perhaps why it has been difficult to characterize precisely. The pain in migraine involves abnormal signals in nerve fibres from the large blood vessels in the head — both from those within the skull (brain blood vessels) and also some from outside the skull, as well as from the protective covering of the brain, the meninges, particularly the tough fibrous part, the dura mater. The brain does not feel pain itself but because of an episodic defect in the nerve systems that control pain and other signals coming into the brain, normal or somewhat abnormal signals are amplified. So a normal or slightly dilated blood vessel gives a pounding or throbbing pain, often in time with the pulse. The pain is felt on the forehead, behind the eyes, over the top, around the sides, or over the back of the head, because the nerves that take pain signals from all over the inside of the skull go to the same place in the brain stem, to the trigeminal nucleus. Just as it can be impossible to locate the source of pain arising from organs in the body cavities — the abdomen or the chest — so migraine pain can be all over the head, or just on one side, or just in one place, wherever the source of the signals. Pain location in migraine, particularly over the back of the head, does not therefore necessarily implicate that area as diseased. This applies, for example, to the neck, which is often blamed for migraine but is seldom the true cause. The poor location of pain from within body cavities, referencing it elsewhere, is called referral of pain, and is a well-established, important concept that also applies to migraine. Referral of pain takes place because pain fibres from a deep structure, (such as, in this case, a brain blood vessel), and a superficial structure (such as the skin), both project to the same nerve cell in the trigeminal nucleus. The body cannot thus distinguish where the signal comes from, and wrongly attributes, or ‘refers’, the pain to the skin or other superficial structure.

The other symptoms of migraine can be thought of broadly as sensitivities to various things: movement, noise, light, smells, even something in the stomach to cause nausea (although we currently think that nausea has an important component from connections of the pain nerves with nausea cells in the brain). The areas in the human brain that have been shown to be active in migraine have two very interesting roles in normal physiology. One area in the brain stem controls, ‘gates’, or modulates incoming sensory information. It allows us to concentrate on something and to ignore irrelevant noise or even tactile (feeling) information. It is likely that this area, called the nucleus locus coeruleus, dysfunctions in migraine so that normal light or sound are perceived by the brain as too bright or loud, or normal smells as unpleasant. Many migraine sufferers report that their brain seems clouded, they cannot concentrate, and their thought processes are just not right. It seems likely that it is abnormalities in the locus coeruleus and associated areas that form the basis of the biology of these very real symptoms. One of the areas shown by imaging techniques to be active in migraine is also active during sleep induction, so it is no surprise that migraine sufferers for thousands of years have appreciated the benefit of sleep.

Much has changed in our understanding of migraine in the last decade, such that sufferers can now be given a reasonable explanation of most of their symptoms and thus be optimistic that soon their disease will be even better understood.

Meanwhile, the main thing that sufferers can do is to understand their limits. Many triggers for migraine can be identified, such as stress. (However, stress can trigger just about any type of headache, and there can therefore be no distinct thing called stress headache.) Environmental situations, some chemicals and foods, and a host of other situations are patient-specific triggers. These triggers have one general theme. The migraine sufferer is less tolerant of altering circumstances — such as skipping meals or eating late (and this is particularly true of children). They may not tolerate stress but, in an apparent paradox, may also get headache when they relax, or when they over-sleep or under-sleep, or when they exercise too much or not enough. In short, the migraine sufferer must be a little more careful with their life and think out what situations they can avoid; this may apply particularly to women during the menstrual cycle.

The remedy then is to exercise, eat, and sleep regularly and perhaps, oddly enough, always have a little stress! If one has headaches on Saturday mornings, is it just because of ‘sleeping in’, or because of the sudden relaxation at the end of a hard week, or even a change in caffeine consumption? Often a simple solution is to get up at a similar time to the weekdays and organize something to do. A trap for people to watch out for if they suffer headache regularly — and perhaps particularly migraine — is that of analgesic over-use. Over time, many patients increase their use of over-the-counter or even prescribed medications to a point where they get a ‘rebound headache’: as the dose of the headache medication wears off the headache comes back and more medication is taken. A vicious cycle commences that may require medical intervention.

A doctor who is consulted about migraine will want to take a medical history to be sure of the diagnosis, compared with other forms of headache, and to make a full clinical examination. The approximate rule for headache action is that new or changing headache, especially of sudden onset, requires urgent attention, while persistent long-standing headache requires time, patience, and thought when planning management. Among the many other questions that might be asked, one of the most important pieces of information can be what medication has been used in the past, in what amounts, and for how long.

With detailed information from the patient about the nature and pattern of the pain, and with knowledge gleaned from experimental work from the last ten to fifteen years, migraine is now relatively well understood and can be better managed than at any time in the last 4000 years. Treatments include preventative medicines and those for use in acute attacks. The preventative medicines are drawn from a number of other areas of medical practice; migraine is not caused by high blood pressure, depression, or epilepsy, but the drugs used in treating these conditions work also in migraine and should be viewed as anti-migraine drugs. (Thus they include b blockers, serotonin blockers, antidepressants, or anticonvulsants.) For acute attacks, there are the common pain-killers such as aspirin or paracetamol, together with an anti-sickness tablet, such as domperidone, or so-called Non-Steroidal Anti-Inflammatory Drugs (NSAIDs), again with an anti-sickness medicine. There are also drugs specific for migraine, and for a rare form of headache called cluster headache, but not generally useful for other headaches, there are the ergot derivatives, and the family of triptans. The triptans were developed specifically for migraine and are certainly the most effective and best studied medicines for the condition.

There is currently considerable research into the condition. It is better understood than it has ever been, and this level of knowledge deepens with time. As understanding improves so does treatment.

— Peter J. Goadsby

Bibliography

The Migraine Trust and Migraine Action Association (UK) and The American Council for Headache Education (USA) publish various information for sufferers and doctors.
Goadsby, P. J. and Silberstein, S. D. (ed.) (1997). Headache. Butterworth-Heinemann, New York.
Lance, J. W. and Goadsby, P. J. (1998). Mechanism and management of headache, (6th edn). Butterworth-Heinemann, London

Migraine
Classification and external resources
The pain of a migraine headache can be debilitating.
ICD-10	G 43
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

Signs and symptoms

Migraines typically present with recurrent severe headache associated with autonomic symptoms. An aura only occurs in a small percentage of people. The severity of the pain, duration of the headache, and frequency of attacks is variable.^[12] A migraine lasting 72 hours is termed status migrainosus and can be treated with intravenous prochlorperazine. The four possible phases to a migraine attack are listed below, although not all the phases are necessarily experienced.^[4] Additionally, the phases experienced and the symptoms experienced during them can vary from one migraine attack to another in the same person:

The prodrome, which occurs hours or days before the headache
The aura, which immediately precedes the headache
The pain phase, also known as headache phase
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), dizziness, hot ears, constipation or diarrhea, increased or decreased urination, and other visceral symptoms.^[13] 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 a migraine attack is near.

Aura

For the 20–30%^[14]^[15] of migraine sufferers who experience migraine with aura, this aura comprises focal neurological phenomena that precede or accompany the attack. They appear gradually over five 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.^[16]

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"^[17]). Some patients complain of blurred or shimmering or cloudy vision, as though they were looking at an area above a heated surface, looking through thick or smoked glass, or, in some cases, tunnel vision and hemianopsia.

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."

Visual symptoms of migraine aura
Enhancements reminiscent of a zigzag fort structure
Negative scotoma, loss of awareness of local structures
Positive scotoma, local perception of additional structures
Mostly one-sided loss of perception

Pain

The typical migraine headache is unilateral, throbbing, and moderate to severe, and can be aggravated by physical activity.^[4] 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 two to 72 hours in adults and one 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, and can be very severe.

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^{[citation needed]}. 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^{[citation needed]}. 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.^[18] According to one summary, "Some people feel unusually refreshed or euphoric after an attack, whereas others note depression and malaise."^[19]

Objective signs

A temporary Horner's syndrome (ptosis-drooping lid, miosis-smaller pupil) may occur during a migraine attack and disappear afterwards.^[20]

Cause

The underlying cause of migraines is unknown.^[21] There are, however, many biological events that have been clinically associated with migraine.

Triggers

Migraines may be induced by triggers, with some reporting it as an influence in a minority of cases^[12] and others the majority.^[22] Many things have been labeled as triggers, however the strength and significance of these relationships are uncertain.^[22]^[23] Common triggers quoted are stress, hunger, and fatigue (these equally contribute to tension headaches).^[22] A 2003 review concluded there was no scientific evidence for an effect of tyramine on migraine.^[24] A 2005 literature review on dietary triggers found the available scientific studies, mostly relying on subjective assessments, were not rigorous enough to prove or disprove any particular triggers.^[25] This is in line with other reviews. A 2009 review of potential triggers in the indoor and outdoor environment concluded the overall evidence was of poor quality, but nevertheless suggested migraineurs take some preventative measures related to indoor air quality and lighting.^[26] While monosodium glutamate (MSG) is frequently reported as a dietary trigger^[27] evidence does not consistently support this.^[28] Migraines are more likely to occur around menstruation.^[29] Other hormonal influences, such as menarche, oral contraceptive use, pregnancy, perimenopause, and menopause, also play a role.^[30]

Depolarization

Animation of cortical spreading depression

The phenomenon known as cortical spreading depression, which is associated with the aura of migraine,^[31] has been theorized as a possible cause of migraines. In cortical spreading depression, neurological activity is initially activated, then depressed over an area of the cerebral cortex. This situation has been suggested to result 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.^[13]

Vascular

Studies have shown 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 some individuals who have migraines experience, because the visual cortex is in the occipital area.^[32]

When the constriction of blood vessels in the brain stops and the aura subsides, the blood vessels of the scalp dilate.^[33] 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.^[32]

Although cerebral vasodilation can trigger migraine attacks, blood vessel diameters return to normal more than an hour before the migraine headaches occur.^[34]

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 and 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.^[32] Serotonergic agonists, such as triptans,^[32] 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 pain,^[35] but this is currently speculation.

Neural

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.^[32]

Unifying theory

Both vascular and neural influences cause migraines.

stress triggers changes in the brain
these changes cause serotonin and/or histamine to be released
blood vessels constrict and dilate
chemicals, including substance P, irritate nerves and blood vessels, causing neurogenic inflammation and pain.^[32]

Pathophysiology

Migraines are believed to be a neurovascular disorder.^[12]

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,^[32] 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 naïve 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."^[36] Some have even attempted to show that vascular changes are of no importance in migraine,^[37]^[38] 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'- J Edmeads^[36]

Pain

Although the initiating factor of migraine remains unknown, copious, irrefutable evidence shows the pain of migraine (the third phase)^[4] 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.^[33]^[39]^[40]^[41]^[42]^[43] Dilatation of the arteries in the brain and dura mater previously was thought to be the origin of the vascular pain, but these vessels have been shown to not dilate during migraine.^[44]^[45] Because these arteries are relatively superficial, it 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 being promoted, largely to the efforts of Dr Elliot Shevel, a South African surgeon, who has reported excellent success using the procedure.^[46]

Pericranial (jaw and neck) muscle tenderness is a common finding in migraine.^[47]^[48]^[49] Muscle tenderness has been shown to be present in 100% of migraine attacks, making muscle tenderness the single most common finding in migraine.^[47] Tender muscle trigger points can be at least part of the cause, and perpetuate most kinds of headaches.^[50]

Diagnosis

Migraines are underdiagnosed,^[51] and often are misdiagnosed.^[52] 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":^[4]

Five or more attacks - for migraine with aura, two attacks are sufficient for diagnosis.
Four hours to three days in duration
Two or more of the following:
- Unilateral (affecting half the head);
- Pulsating;
- "Moderate or severe pain intensity";
- "Aggravation by or causing avoidance of routine physical activity"
One or more of the following:
- Nausea and/or vomiting;
- Sensitivity to both light (photophobia) and sound (phonophobia)

The mnemonic POUNDing (Pulsating, duration of 4–72 hOurs, Unilateral, Nausea, Disabling) can help diagnose migraine. If four of the five criteria are met, then the positive likelihood ratio for diagnosing migraine is 24.^[53]

The presence of either disability, nausea or sensitivity can diagnose migraine with:^[54]

sensitivity of 81%
specificity of 75%

Migraine should be differentiated from other causes of headaches, such as cluster headaches. These are extremely painful, unilateral headaches of a piercing quality. The duration of the common attack is 15 minutes to three hours. Onset of an attack is rapid, and most often without the preliminary signs characteristic of a migraine.^{[citation needed]}

Medical imaging of the head and neck may be used to rule out secondary causes of headaches.^[12]

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).^[4]

According to ICHD-2, there are seven subclasses of migraines (some of which include further subdivisions):

Migraine without aura, or common migraine, involves migraine headaches that are not accompanied by an aura (visual disturbance, see below).
Migraine with aura usually involves migraine headaches accompanied by an aura. Less commonly, an aura can occur without a headache, or with a nonmigraine 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.
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).
Retinal migraine involves migraine headaches accompanied by visual disturbances or even temporary blindness in one eye.
Complications of migraine describe migraine headaches and/or auras that are unusually long or unusually frequent, or associated with a seizure or brain lesion.
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).
Chronic migraine, according to the American Headache Society^[55] and the international headache society,^[56] is a "complication of migraine"s and is a headache fulfilling the diagnostic criteria for "migraine headache", which occurs for a greater time interval. Specifically, greater or equal to 15 days/month for greater than 3 months.

Prevention

Main article: Prevention of migraines

Preventive (also called prophylactic) treatment of migraines can be an important component of migraine management. Such treatments can take many forms, including taking preventive drugs, migraine surgery, taking nutritional supplements, lifestyle alterations, such as increased exercise, and avoidance of migraine triggers.

The goals of preventive therapy are to reduce the frequency, painfulness, and/or duration of migraines, and to increase the effectiveness of abortive therapy.^[57] Another reason to pursue these goals is to avoid medication overuse headache (MOH), otherwise known as rebound headache. This is a common problem among migraineurs, and can result in chronic daily headache.^[58]^[59]

Many of the preventive treatments are quite effective. Even with a placebo, one-quarter of patients find their migraine frequency is reduced by half or more, and actual treatments often far exceed this figure.^[60]

Medication

Preventive migraine drugs are considered effective if they reduce the frequency or severity of migraine attacks by at least 50%.^[61] The major problem with migraine preventive drugs, apart from their relative inefficacy, is that unpleasant side effects are common. So, preventive medication is limited to patients with frequent or severe headaches.^[62]

Many medicines are available to prevent or reduce frequency, duration and severity of migraine attacks. They may also prevent complications of migraine. Beta blockers, such as Propranolol, atenolol, and metoprolol; calcium channel blockers, such as amlodipine, flunarizine and verapamil; the anticonvulsants sodium valproate, divalproex, gabapentin and topiramate; and tricyclic antidepressants are some of the commonly used drugs.^{[citation needed]}

Tricyclic antidepressants have been found to be more effective than SSRIs.^[63] Tricyclic antidepressants have been long established as efficacious prophylactic treatments.^[61] These drugs, however, may give rise to undesirable side effects, such as insomnia, sedation or sexual dysfunction. There is no consistent evidence that SSRI antidepressants are effective for migraine prophylaxis. While amitryptiline (Elavil) is the only tricyclic to have received FDA approval for migraine treatment, other tricyclic antidepressants are believed to act similarly and are widely prescribed, often to find one with a profile of side effects that is acceptable to the patient.^[61] In addition to tricyclics a, the antidepressant nefazodone may also be beneficial in the prophylaxis of migraines due to its antagonistic effects on the 5-HT2A^[64] and 5-HT2C receptors^[65]^[66] It has a more favorable side effect profile than amitriptyline, a tricyclic antidepressant commonly used for migraine prophylaxis. Antidepressants offer advantages for treating migraine patients with comorbid depression.^[61] SSRIs are not approved by the FDA for treatment of migraines, but have been found to be effective by some practitioners.^[61]

There is some evidence that low-dose aspirin has benefit for reducing the occurrence of migraines in susceptible individuals.^[67]^[68]^[69]

Surgery

Migraine surgery which involves decompression of certain nerves around the head and neck may be an option in certain people who do not improve with medications.^[70] It is only effective in those who respond well to Botox injections in specific areas.^[71]^[72] A major advantage of migraine surgery is that, with the correct diagnostic techniques, a definite diagnosis can be made before the surgery is undertaken. Once a positive diagnosis has been made, the results of surgery are outstanding and provide permanent pain relief, as well as relief from the associated symptoms, such as nausea, vomiting, light sensitivity, and sound sensitivity. Surgical cauterization of the superficial blood vessels of the scalp (the terminal branches of the external carotid artery) is only carried out if it has been established with certainty that these vessels are indeed the source of pain. It is a safe and relatively atraumatic procedure which can be performed in a day facility.^[73]

There is also evidence that the correction of a congenital heart defect, patent foramen ovale (PFO), reduces migraine frequency and severity.^[74] Recent studies have advised caution, though, in relation to PFO closure for migraines, as insufficient evidence exists to justify this dangerous procedure.^[75]^[76]

Other therapies

Medical devices, such as biofeedback and neurostimulators, have some advantages in the migraine treatment, mainly when common antimigraine medication is contraindicated or in case of medication over use. Biofeedback helps patient to be conscious of some physiologic parameters to control them and try to relax. This method is considered to be efficient for migraine^[77] and tension-type headache treatment.^[78] A recent clinical trial has demonstrated that simple use of biofeedback as a relaxation technique has similar efficacy for migraine treatment to sophisticated sessions in clinics.^[79] Neurostimulation used initially implantable neurostimulators similar to pacemakers for the treatment of intractable chronic migraines^[80]^[81] with encouraging good results. But the needed surgery with implantable neurostimulators is limiting the indication to sever cases.^[82] A systematic review stated that chiropractic manipulation, physiotherapy, massage and relaxation might be as effective as propranolol or topiramate in the prevention of migraine headaches; however, the research had some problems with methodology.^[83]

"The therapeutic potential of magnesium, coenzyme Q(10), riboflavin, and vitamin B(12) can be cautiously inferred from some published open clinical trials."^[84] A review has concluded that "[c]urrent clinical data support the use of fever-few, butterbur, magnesium, and riboflavin in migraine prophylaxis."^[85]

Migraine diary

A migraine diary allows the assessment of headache characteristics, to differentiate between migraine and tension-type headache and to record the use and efficacy of acute medication. A diary also helps to analyse the relationship between migraine and menstruation.^[86] Finally, the diary can help to identify trigger factors. A trigger may occur up to 24 hours prior to the onset of symptoms;^[12] the majority of migraines, though, are not caused by identifiable triggers.^[12]

Management

There are three main aspects of treatment: trigger avoidance, acute symptomatic control, and pharmacological prevention.^[12] Medications are more effective if used earlier in an attack.^[12] The frequent use of medications may, however, result in medication overuse headache, in which the headaches become more severe and more frequent. These may occur with triptans, ergotamines, and analgesics, especially narcotic analgesics.^[4]

Analgesics

A number of analgesics are effective for treating migraines including:

Non-steroidal anti-inflammatory drugs (NSAIDs): Ibuprofen provides effective pain relief in about half of people.^[87] Naproxen can abort about one third of migraine attacks, which was 5% less than the benefit of sumatriptan.^[88] A 1000 mg dose of aspirin could relieve moderate to severe migraine pain, with similar effectiveness to sumatriptan.^[89]
Paracetamol/acetaminophen, either alone or in combination with metaclopramide, is effective for migraines.^[90]
Simple analgesics combined with caffeine may help.^[91] Even by itself, caffeine can be useful during an attack,^[92]^[93] despite the fact that migraine sufferers are generally advised to limit their caffeine intake.^[93]

Triptans

Triptans such as sumatriptan are effective for both pain and nausea in up to 75% of people.^[12]^[94] The different forms available include oral, injection, nasal spray, and oral dissolving tablets.^[12] Most side effects are mild, such as flushing; however, rare cases of myocardial ischemia have occurred.^[12] They are not addictive, but may cause medication overuse headaches if used more than 10 days per month.^[95]

Ergotamines

Ergotamine^[12] and dihydroergotamine are older medications still prescribed for migraines, the latter in nasal spray and injectable forms.^[12] They were the primary drugs available to abort a migraine prior to the triptans, and are much less expensive than triptans.^{[citation needed]}

Corticosteroids

A single dose of intravenous dexamethasone, when added to standard treatment of a migraine attack, is associated with a 26% decrease in headache recurrence in the following 72 hours.^[96]

Other

Antiemetics by mouth may help relieve symptoms of nausea and help prevent vomiting, which can diminish the effectiveness of orally taken analgesics. In addition, some antiemetics, such as metoclopramide, are prokinetics and help gastric emptying, which is often impaired during episodes of migraine. In the UK, three combination antiemetic and analgesic preparations are available: MigraMax (aspirin with metoclopramide), (paracetamol/codeine for analgesia, with buclizine as the antiemetic) and paracetamol/metoclopramide (Paramax in UK).^[97] The earlier these drugs are taken in the attack, the better their effect.

Prognosis

The risk of stroke may be increased two- to three-fold in migraine sufferers. Young adult sufferers and women using hormonal contraception appear to be at particular risk.^[98] The mechanism of any association is unclear, but chronic abnormalities of cerebral blood vessel tone may be involved. Women who experience auras have been found to have twice the risk of strokes and heart attacks over nonaura migraine sufferers and women who do not have migraines.^[98]^[99] (Note: Women who experience auras and also take oral contraceptives have an even higher risk of stroke).^[100] Migraine sufferers seem to be at risk for both thrombotic and hemorrhagic stroke as well as transient ischemic attacks.^[101] Death from cardiovascular causes was higher in people with migraine with aura in a Women's Health Initiative study, but more research is needed to confirm this.^[99]^[102]

Epidemiology

Disability-adjusted life year for migraines per 100,000 inhabitants in 2002.

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

Incidence of migraine by age and sex

Worldwide, migraines affect more than 10% of people.^[21] In the United States, about 6% of men and 18% of women get a migraine in a given year, with a lifetime risk of about 18% and 43% respectively.^[12] In Europe, migraines affect 12–28% of people at some point in their lives.^[1] Based on the results of a number of studies, one-year prevalence of migraine ranges from 6–15% in adult men and from 14–35% in adult women.^[1] These figures vary substantially with age: approximately 4–5% of children aged under 12 suffer from migraine, with little apparent difference between boys and girls.^[103] A rapid growth in incidence amongst girls occurs after puberty,^[104]^[105]^[106] which continues throughout early adult life.^[107] By early middle age, around 25% of women experience a migraine at least once a year, compared with fewer than 10% of men.^[1]^[108] After menopause, attacks in women tend to decline dramatically, so that in the over 70s, approximately equal numbers of males and females are sufferers, with prevalence returning to around 5%.^[1]^[108]

At all ages, migraine without aura is more common than migraine with aura, with a ratio of between 1.5 and 2.0:1.^[109]^[110] Incidence figures show the excess of migraine seen in women of reproductive age is mainly due to migraine without aura.^[109] Thus, in prepubertal and postmenopausal populations, migraine with aura is somewhat more common than amongst 15–50 year olds.^[107]^[111]

There is a strong relationship between age, sex and type of migraine.^[112]

Studies in Asia and South America suggest the rates there are relatively low,^[113]^[114] but they do not fall outside the range of values seen in European and North American studies.^[1]^[108]

The incidence of migraine is related to the incidence of epilepsy in families, with migraine twice as prevalent in family members of epilepsy sufferers, and more common in epilepsy sufferers themselves.^[115]

History

The Head Ache, George Cruikshank (1819)

Trepanation, the deliberate and (usually) nonfatal drilling of holes into a skull, was practiced 9,000 years ago and earlier.^[116] Some scholars have (controversially) speculated this drastic procedure might have been a migraine treatment, based on cave paintings^[117] and on the fact that trepanation was a historical migraine treatment in 17th-century Europe.^[116]^[118] An early written description consistent with migraines is contained in the Ebers papyrus, written around 1200 BC in ancient Egypt.^[116]

In 400 BC, Hippocrates described the visual aura that can precede the migraine headache, and the relief which can occur through vomiting. 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, with headache-free intervals in between attacks.

Galenus of Pergamon used the term "hemicrania" (half-head), from which the word "migraine" was derived. He thought there was a connection between the stomach and the brain because of the nausea and vomiting that often accompany an attack. For relief of migraine, Andalusian-born physician Abulcasis, also known as Abu El Qasim, suggested application of a hot iron to the head or insertion of garlic into an incision made in the temple.

In the Middle Ages. migraine was recognized as a discrete medical disorder. Followers of Galenus explained migraine as being caused by aggressive yellow bile. Ebn Sina (Avicenna) described migraine in his textbook "El Qanoon fel teb" as "... small movements, drinking and eating, and sounds provoke the pain... the patient cannot tolerate the sound of speaking and light. He would like to rest in darkness alone." Abu Bakr Mohamed Ibn Zakariya Râzi noted the association of headache with different events in the lives of women, "...And such a headache may be observed after delivery and abortion or during menopause and dysmenorrhea."

In Bibliotheca Anatomica, Medic, Chirurgica, published in London in 1712, five major types of headaches are described, including the "Megrim", recognizable as classic migraine. The term "classic migraine" is no longer used, and has been replaced by the term "migraine with aura"^[4] Graham and Wolff (1938) published their paper advocating ergotamine tartrate for relieving migraine. Later in the 20th century, Harold Wolff (1950) developed the experimental approach to the study of headache and elaborated the vascular theory of migraine, which has come under attack as the pendulum again swings to the neurogenic theory. Recently, there has been renewed interest in Wolff's vascular theory of migraine led by Elliot Shevel, a South African headache specialist, who has published a number of articles providing compelling evidence that Wolff was correct.^[40]^[45]^[46]^[119]

Society and culture

Economic impact

Chronic migraine attacks are a significant source of both medical costs and lost productivity. It has been estimated to be the most costly neurological disorder in the European Community, costing more than €27 billion per year.^[120]

Research

Merck Corp new drug, Telcagepant, intended to relieve pain without causing vasoconstriction (narrowing of blood vessels) as current medications such as triptans do, was pulled from the market after clinical trials showed liver function abnormalities in some study subjects. ^ Merck & Co.: Memo to all US study locations involved in protocol MK0974-049

Recently, calcitonin gene related peptides (CGRPs) have been found to play a role in the pathogenesis of the pain associated with migraine, as triptans also decrease its release and action. CGRP receptor antagonists, such as olcegepant and telcagepant, are being investigated both in vitro and in clinical studies for the treatment of migraine.^[121]

In 2010, scientists identified a genetic defect linked to migraines which could provide a target for new drug treatments.^[122]

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^ Derry S, Moore RA, McQuay HJ (2010). Moore, Maura. ed. "Paracetamol (acetaminophen) with or without an antiemetic for acute migraine headaches in adults". Cochrane Database Syst Rev 11 (11): CD008040. doi:10.1002/14651858.CD008040.pub2. PMID 21069700.
^ Goldstein J, Hoffman HD, Armellino JJ et al (September 1999). "Treatment of severe, disabling migraine attacks in an over-the-counter population of migraine sufferers: results from three randomized, placebo-controlled studies of the combination of acetaminophen, aspirin, and caffeine". Cephalalgia 19 (7): 684–91. doi:10.1046/j.1468-2982.1999.019007684.x. PMID 10524663.
^ ""Migraine headaches" information from the Cleveland Clinic". My.clevelandclinic.org. 2006-01-09. http://my.clevelandclinic.org/disorders/Migraine_Headache/hic_Migraine_Headaches.aspx. Retrieved 2011-05-30.
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^ Johnston MM, Rapoport AM (August 2010). "Triptans for the management of migraine". Drugs 70 (12): 1505–18. doi:10.2165/11537990-000000000-00000. PMID 20687618.
^ Tepper Stewart J., S. J.; Tepper, Deborah E. (April 2010). "Breaking the cycle of medication overuse headache". Cleveland Clinic Journal of Medicine 77 (4): 236–42. doi:10.3949/ccjm.77a.09147. PMID 20360117.
^ Colman I, Friedman BW, Brown MD et al (June 2008). "Parenteral dexamethasone for acute severe migraine headache: meta-analysis of randomised controlled trials for preventing recurrence". BMJ 336 (7657): 1359–61. doi:10.1136/bmj.39566.806725.BE. PMC 2427093. PMID 18541610. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2427093.
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External links

Pathology of the nervous system, primarily CNS (G04–G47, 323–349)

Inflammation

Brain	Encephalitis (Viral encephalitis, Herpesviral encephalitis) · Cavernous sinus thrombosis · Brain abscess (Amoebic)

Spinal cord	Myelitis: Poliomyelitis · Demyelinating disease (Transverse myelitis) · Tropical spastic paraparesis · Epidural abscess

Both/either	Encephalomyelitis (Acute disseminated) Meningoencephalitis

Brain/
encephalopathy

Degenerative

Extrapyramidal and movement disorders	Basal ganglia disease: Parkinsonism (PD, Postencephalitic, NMS) · PKAN · Tauopathy (PSP) · Striatonigral degeneration · Hemiballismus · HD · OA Dyskinesia: Dystonia (Status dystonicus, Spasmodic torticollis, Meige's, Blepharospasm) · Chorea (Choreoathetosis) · Myoclonus (Myoclonic epilepsy) · Akathesia Tremor (Essential tremor, Intention tremor) · Restless legs · Stiff person

Dementia	Tauopathy: Alzheimer's (Early-onset) · Frontotemporal dementia/Frontotemporal lobar degeneration (Pick's, Dementia with Lewy bodies) Multi-infarct dementia

Mitochondrial disease	Leigh's

Demyelinating

autoimmune (Multiple sclerosis, Neuromyelitis optica, Schilder's disease) · hereditary (Adrenoleukodystrophy, Alexander, Canavan, Krabbe, ML, PMD, VWM, MFC, CAMFAK syndrome) · Central pontine myelinolysis · Marchiafava-Bignami disease · Alpers' disease

Episodic/
paroxysmal

Seizure/epilepsy	Focal · Generalised · Status epilepticus · Myoclonic epilepsy

Headache	Migraine (Familial hemiplegic) · Cluster · Tension

Cerebrovascular	TIA (Amaurosis fugax, Transient global amnesia) Stroke (MCA, ACA, PCA, Foville's, Millard-Gubler, Lateral medullary, Weber's, Lacunar stroke)

Sleep disorders	Insomnia · Hypersomnia · Sleep apnea (Obstructive, Ondine's curse) · Narcolepsy · Cataplexy · Kleine-Levin · Circadian rhythm sleep disorder (Advanced sleep phase disorder, Delayed sleep phase disorder, Non-24-hour sleep-wake disorder, Jet lag)

CSF

Intracranial hypertension (Hydrocephalus/NPH, Idiopathic intracranial hypertension) · Cerebral edema · Intracranial hypotension

Other

Brain herniation · Reye's · Hepatic encephalopathy · Toxic encephalopathy

Spinal cord/
myelopathy

Syringomyelia · Syringobulbia · Morvan's syndrome · Vascular myelopathy (Foix-Alajouanine syndrome) · Spinal cord compression

Both/either

Degenerative

SA	Friedreich's ataxia · Ataxia telangiectasia

MND	UMN only: PLS · PP · HSP LMN only: PMA · PBP (Fazio-Londe, Infantile progressive bulbar palsy) · Spinal muscular atrophies (SMA, SMARD1, SBMA, SMAX2, SMA-PCH) both: ALS

M: CNS

anat(n/s/m/p/4/e/b/d/c/a/f/l/g)/phys/devp

noco(m/d/e/h/v/s)/cong/tumr, sysi/epon, injr

proc, drug(N1A/2AB/C/3/4/7A/B/C/D)

CNS disease: Headache (G43–G44, 339, 346)

Primary

ICHD 1	Migraine (Familial hemiplegic) · Retinal migraine

ICHD 2	Tension

ICHD 3	Cluster · Chronic paroxysmal hemicrania · SUNCT

ICHD 4	Hemicrania continua · Thunderclap headache · Coital cephalalgia · New daily persistent headache · Hypnic headache

Secondary


ICHD 5	Migralepsy

ICHD 7	Ictal headache · Post-dural-puncture headache

ICHD 8	Hangover · Medication overuse headache

ICHD 13

Trigeminal neuralgia · Occipital neuralgia · External compression headache · Cold-stimulus headache · Optic neuritis · Postherpetic neuralgia · Tolosa-Hunt syndrome

Other

Vascular

M: CNS

anat(n/s/m/p/4/e/b/d/c/a/f/l/g)/phys/devp

noco(m/d/e/h/v/s)/cong/tumr, sysi/epon, injr

proc, drug(N1A/2AB/C/3/4/7A/B/C/D)

Antimigraine preparations (N02C)

Analgesic/abortive

Serotonin modulators

Ergot alkaloids	Dihydroergotamine • Ergotamine • Methysergide • Lisuride

5-HT1 agonists	Triptans (Almotriptan, Avitriptan, Eletriptan, Frovatriptan, Naratriptan, Rizatriptan, Sumatriptan, Zolmitriptan) Alniditan

Other	Dotarizine

Other

Paracetamol^# • Amidrine

Prevention of migraines

Beta blocker	Propranolol^# • Timolol

CCB	verapamil

corticosteroid	flumedroxone

monosaccharide	topiramate

adrenergic agonist	Clonidine

tricyclic antidepressant	amitriptyline • nortriptyline • imipramine

anticonvulsant	valproate • carbamazepine • oxcarbazepine

Ungrouped

Pizotifen • Iprazochrome • Dimetotiazine • Oxetorone • Lomerizine • Telcagepant

^#WHO-EM
^‡Withdrawn from market
Clinical trials:
- ^†Phase III
- ^§Never to phase III

M: CNS

anat(n/s/m/p/4/e/b/d/c/a/f/l/g)/phys/devp

noco(m/d/e/h/v/s)/cong/tumr, sysi/epon, injr

proc, drug(N1A/2AB/C/3/4/7A/B/C/D)

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migraine

mi·graine

migraine

migraine

migraine

migraine

migraine

migraine

migraine

categories related to 'migraine'

migraine

migraine

Migraine

Signs and symptoms

Prodrome

Aura

Pain

Postdrome

Objective signs

Cause

Triggers

Depolarization

Vascular

Serotonin

Melanopsin receptor

Neural

Unifying theory

Pathophysiology

Initiation

Pain

Diagnosis

Classification

Prevention

Medication

Surgery

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Migraine diary

Management

Analgesics

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Ergotamines

Corticosteroids

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Prognosis

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External links

Migraine