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 triggers. The cause of migraine headache is unknown; the most common theory is a disorder of the serotonergic control system.
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.
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). These guidelines constitute arbitrary definitions, and are not supported by scientific data.
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 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.
- 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 and the international headache society, 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.
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. A migraine lasting 72 hours is termed status migrainosus and can be treated with intravenous prochlorperazine.
There are four possible phases to a migraine attack. 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:
- 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.
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. 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.
For the 20–30% 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.
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"). 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.
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."
The typical migraine headache is unilateral, throbbing, and moderate to severe and can be aggravated by physical activity. 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, and a feeling of faintness may occur.
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. According to one summary, "Some people feel unusually refreshed or euphoric after an attack, whereas others note depression and malaise."
Migraines may be induced by triggers, with some reporting it as an influence in a minority of cases and others the majority. Many things have been labeled as triggers, however the strength and significance of these relationships are uncertain. Common triggers quoted are stress, hunger, and fatigue (these equally contribute to tension headaches). A 2003 review concluded that there was no scientific evidence for an effect of tyramine on migraine. A 2005 literature review on dietary triggers found that the available scientific studies, mostly relying on subjective assessments, and thus were not rigorous enough to prove or disprove any particular triggers. This is in line with other reviews. In a 2009 review of potential triggers in the indoor and outdoor environment, concluded that the overall evidence was of poor quality, but nevertheless suggested that migraineurs take some preventative measures related to indoor air quality and lighting. While monosodium glutamate (MSG) is frequently reported as a dietary trigger evidence does not consistently support this. Migraines are more likely to occur around menstruation. Other hormonal influences such as menarche, oral contraceptive use, pregnancy, perimenopause, and menopause also play a role.
It has been theorized that the phenomenon known as cortical spreading depression, which is associated with the aura of migraine, 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. Second, many migraineurs have a prodrome (see above), which occurs up to three days before the 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.
When the constriction of blood vessels in the brain stops and the aura subsides, the blood vessels of the scalp dilate. 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.
Although cerebral vasodilation can trigger migraine attacks, blood vessel diameters return to normal more than an hour before the migraine headaches occur.
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. Another reason to pursue these goals is to avoid medication overuse headache (MOH), otherwise known as rebound headache. This is a common problem among migraneurs, and can result in chronic daily headache.
Many of the preventive treatments are quite effective. Even with a placebo, one-quarter of patients find that their migraine frequency is reduced by half or more, and actual treatments often far exceed this figure.
Preventive migraine drugs are considered effective if they reduce the frequency or severity of migraine attacks by at least 50%. The major problem with migraine preventive drugs, apart from their relative inefficacy, is that unpleasant side effects are common. For this reason, preventive medication is limited to patients with frequent or severe headaches.
There are many medicines 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.
Tricyclics have been found to be more effective than SSRIs. Tricyclic antidepressants have been long established as efficacious prophylactic treatments. 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. In addition to tricyclics a, 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, a tricyclic antidepressant commonly used for migraine prophylaxis. Anti-depressants offer advantages for treating migraine patients with comorbid depression. Selective serotonin reuptake inhibitors (SSRIs) are not approved by the U.S. Food and Drug Administration (FDA) for treatment of migraines, but have been found to be effective by some practitioners.
