Wikia

Psychology Wiki

Migraine headache

Talk2
34,143pages on
this wiki

Assessment | Biopsychology | Comparative | Cognitive | Developmental | Language | Individual differences | Personality | Philosophy | Social |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |

Clinical: Approaches · Group therapy · Techniques · Types of problem · Areas of specialism · Taxonomies · Therapeutic issues · Modes of delivery · Model translation project · Personal experiences ·


This article is in need of attention from a psychologist/academic expert on the subject.
Please help recruit one, or improve this page yourself if you are qualified.
This banner appears on articles that are weak and whose contents should be approached with academic caution
.
Migraine
ICD-10 G43
ICD-9 346
OMIM 157300
DiseasesDB 8207
MedlinePlus 000709
eMedicine neuro/218
MeSH {{{MeshNumber}}}


Migraine is a neurological disorder.[1][2][3] Usually migraine causes episodes of severe or moderate headache (which is often one-sided and pulsating) lasting between several hours to three days, accompanied by gastrointestinal upsets, such as nausea and vomiting, and a heightened sensitivity to bright lights (photophobia) and noise (phonophobia). Approximately one third of people who experience migraine get a preceding aura.[4] The word migraine is French in origin and comes from the Greek hemicrania, as does the Old English term megrim. Literally, hemicrania means "half (the) head".

Migraine is widespread in the population. In the U.S., 18% of women and 6% of men report having had at least one migraine episode in the previous year[5] Wrongdiagnosis.com reports that 10% of people have been diagnosed with migraine and 5% have migraine but have not been diagnosed,[6] with seriousness varying from a rare annoyance to a life-threatening and/or daily experience. Treatments are typically expensive. Periodic or unpredictable disability can cause impoverishment due to patients' inability to work enough or to hold a job at all.

Migraines' secondary characteristics are inconsistent. Triggers precipitating a particular episode of migraine vary widely. The efficacy of the simplest treatment, applying warmth or coolness to the affected area of the head, varies between persons, sometimes worsening the migraine.[7] A particular migraine rescue drug may sometimes work and sometimes not work in the same patient. Some migraine types don't have pain or may manifest symptoms in parts of the body other than the head.

Available evidence suggests that migraine pain is one symptom of several to many disorders of the serotonergic control system, a dual hormone-neurotransmitter with numerous types of receptors. Two disorders — classic migraine with aura (MA, STG) and common migraine without aura (MO, STG) — have been shown to have a genetic factor.[8] Studies on twins show that genes have a 60 to 65% influence on the development of migraine (PMID 10496258 and PMID 10204850 ). Additional migraine types are suspected and could be proven to be genetic. Migraine understood as several or many disorders could explain the inconsistencies, especially if a single patient has more than one genetic type.

However, still other migraine types might be functionally acquired due to hormone organ disease or injury. Three quarters of adult migraine patients are female, although pre-pubertal migraine affects approximately equal numbers of boys and girls. This reveals the strong correlation to hormonal cycling and hormonal-related causes or triggers. Hormonal migraine is a likely consequence of periodically falling hormone levels causing reduction in protein biosynthesis of metabolic components including intestinal tract serotonin.

Signs and symptoms Edit

The signs and symptoms of migraine vary among patients. Therefore, what a patient experiences before, during and after an attack cannot be defined exactly. The four phases of a migraine attack listed below are common but not necessarily experienced by all migraine sufferers. Additionally, the phases experienced and the symptoms experienced during them can vary from one migraine attack to another in the same migraineur:

  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 phaseEdit

Prodromal symptoms occur in 40% to 60% of migraineurs. 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), constipation or diarrhea, increased urination, and other vegetative 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. The headache can range from mild to moderate or intolerable.[1]

Aura phaseEdit

For the 20-30%[9][10] of migraineurs who suffer 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 less 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. Symptoms of migraine aura can be visual, sensory, or motor in nature.[11]

Visual aura is the most common of the neurological events. There is a disturbance of vision consisting usually 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 consists of digitolingual or cheiro-oral paresthesias, a feeling of pins-and-needles experienced in the hand and arm as well as in the ipsilateral nose-mouth area. Paresthesia migrate up the arm and then extend to involve the face, lips and tongue.

Other symptoms of the aura phase can include auditory or olfactory hallucinations, aphasia, vertigo, tingling or numbness of the face and extremities, and hypersensitivity to touch.

Pain phaseEdit

The typical migraine headache is unilateral, throbbing, moderate to severe and can be aggravated by physical activity. Not all of these features are necessary. The pain may be bilateral at the onset or start on one side and become generalized, and usually alternates sides from one attack to the next. The onset is usually gradual. The pain peaks and then subsides, and usually lasts between 4 and 72 hours in adults and 1 and 48 hours in children. The frequency of attacks is extremely variable, from a few in a lifetime to several times a week, and the average migraineur experiences from 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, while vomiting occurs in about one third of patients. Many patients experience sensory hyperexcitability manifested by photophobia, phonophobia, osmophobia and seek a dark and quiet room. Blurred vision, nasal stuffiness, diarrhea, 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. Lightheadedness, rather than true vertigo and a feeling of faintness may occur. The extremities tend to be cold and moist.

Postdrome phaseEdit

The patient may feel tired, "washed out", irritable, or listless and may have impaired concentration, scalp tenderness or mood changes. Some people feel unusually refreshed or euphoric after an attack, whereas others note depression and malaise. Often, some of the minor headache phase symptoms may continue, such as loss of appetite, photophobia, and lightheadedness.

DiagnosisEdit

see also:ICHD classification and diagnosis of migraine

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":

  • 5 or more attacks
  • 4 hours to 3 days in duration
  • 2 or more of - unilateral location, pulsating quality, moderate to severe pain, aggravation by or avoidance of routine physical activity
  • 1 or more accompanying symptoms - nausea and/or vomiting, photophobia, phonophobia

For migraine with aura, only two attacks are required to justify the diagnosis.

The presence of either disability, nausea, or sensitivity can diagnose migraine with[12]:

Pathophysiology Edit

Migraine was once thought to be initiated by problems with blood vessels. This theory is now largely discredited.[13] Current thinking is that a phenomenon known as cortical spreading depression is responsible for the disorder.[14] In cortical spreading depression, neurological activity is depressed over an area of the cortex of the brain. This 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 view is supported by neuroimaging techniques, which appear to show that migraine is primarily a disorder of the brain (neurological), not of the blood vessels (vascular). A spreading depolarization (electrical change) may begin 24 hours before the attack, with onset of the headache occurring around the time when the largest area of the brain is depolarized. 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.

In 2005, research[15] was published indicating that in some people with a patent foramen ovale (PFO), a hole between the upper chambers of the heart, suffer from migraines which may have been caused by the PFO. The migraines end instantly if the hole is patched. Several clinical trials are currently under way in an effort to determine if a causal link between PFO and migraine can be found. Early speculation as to this relationship has centered on the idea that the lungs detoxify blood as it passes through. The PFO allows uncleaned blood to go directly from the right side of the heart to the left without passing through the lungs.

Migraine headaches can be a symptom of Hypothyroidism.

TypesEdit

Migraine without auraEdit

This is the most commonly seen form of migraine; patients who primarily suffer from migraine without aura may also have attacks of migraine with aura. According to the International Classification of Headache Disorders[16] it is a recurrent headache disorder manifesting in attacks lasting 4-72 hours. Typical characteristics of the headache are unilateral location, pulsating quality, moderate or severe intensity, aggravation by routine physical activity and association with nausea and/or photophobia and phonophobia.

In order to diagnose migraine without aura, there must have been at least 5 attacks not attributable to another cause that fulfill the following criteria:

1. Headache attacks lasting 4-72 hours when untreated
2. At least two of the following characteristics:
  • Unilateral location
  • Pulsating quality
  • Moderate or severe pain intensity
  • Aggravation by or causing avoidance of routine physical activity
3. During the headache there must be at least one of the following associated symptom clusters:
  • Nausea and/or vomiting
  • Photophobia and phonophobia

Where these criteria are not fully met, the problem may be classified as "probable migraine without aura" but other diagnoses such as "episodic tension type headache" must also be excluded.

Migraine with auraEdit

This is the second most commonly seen form of migraine: patients who primarily suffer from migraine with aura may also have attacks of migraine without aura. According to the International Classification of Headache Disorders[17] it is a recurrent disorder manifesting in attacks of reversible focal neurological symptoms that usually develop gradually over 5-20 minutes and last for less than 60 minutes. Headache with the features of "migraine without aura" usually follows the aura symptoms. Less commonly, the aura may occur without a subsequent headache or the headache may be non-migrainous in type.

In order to diagnose migraine with aura, there must have been at least 2 attacks not attributable to another cause that fulfill the following criteria:

1. Aura consisting of at least one of the following, but no muscle weakness or paralysis:
  • Fully reversible visual symptoms (e.g. flickering lights, spots, lines, loss of vision)
  • Fully reversible sensory symptoms (e.g. pins and needles, numbness)
  • Fully reversible dysphasia (speech disturbance)
2. Aura has at least two of the following characteristics:
  • Visual symptoms affecting just one side of the field of vision and/or sensory symptoms affecting just one side of the body
  • At least one aura symptom develops gradually over more than 5 minutes and/or different aura symptoms occur one after the other over more than 5 minutes
  • Each symptom lasts from 5-60 minutes

Where these criteria are not fully met, a diagnosis of "probable migraine with aura" may be considered, although other neurological causes must also be excluded. If the picture complies with the criteria but includes one-sided muscular weakness or paralysis, a diagnosis of "sporadic hemiplegic migraine" or "familial hemiplegic migraine" should be considered.

Basilar type migraineEdit

Basilar type migraine (BTM), formerly known as basilar artery migraine (BAM) or basilar migraine (BM), is an uncommon type of complicated migraine with symptoms that result from brainstem dysfunction. Serious episodes of BTM can lead to stroke, coma, or even death. The use of triptans and other vasoconstrictors as abortive treatments in BTM is contraindicated. Abortive treatments for BTM often focus on vasodilation and restoration of normal blood flow to the vertebrobasilar territory and subsequent return of normal brainstem function.

Familial hemiplegic migraineEdit

See also the main article on Familial hemiplegic migraine

Familial hemiplegic migraine 'FHM' is a type of migraine with a possible polygenetic component. These migraine attacks may last 4-72 hours[18] and are apparently caused by ion channel mutations, three types of which have been identified to date. Patients who experience this syndrome have relatively typical migraine headaches preceded and/or accompanied by reversible limb weakness on one side as well as visual, sensory or speech difficulties. A non-familial form exists as well, "sporadic hemiplegic migraine" (SHM). It is often difficult to make the diagnosis between basilar-type migraine and hemiplegic migraine. When making the differential diagnosis is difficult, the deciding symptom is often the motor weakness or unilateral paralysis which can occur in FHM or SHM. While basilar-type migraine can present with tingling or numbness, true motor weakness and/or paralysis occur only in hemiplegic migraine.

Abdominal migraine Edit

According to the International Classification of Headache Disorders[19] abdominal migraine is a recurrent disorder of unknown origin which occurs mainly in children. It is characterised by episodes of moderate to severe central abdominal pain lasting 1-72 hours. There is usually associated nausea and vomiting but the child is entirely well between attacks.

In order to diagnose abdominal migraine, there must be at least 5 attacks, not attributable to another cause, fulfilling the following criteria:

1. Attacks lasting 1-72 hours when untreated
2. Pain must have ALL of the following characteristics:
  • Location in the midline, around the umbilicus or poorly localised
  • Dull or 'just sore' quality
  • Moderate or severe intensity
3. During an attack there must be at least two of the following:
  • Loss of appetite
  • Nausea
  • Vomiting
  • Pallor

Most children with abdominal migraine will develop migraine headache later in life and the two may co-exist during adolescence.

Acephalgic migraine Edit

Acephalgic migraine is a neurological syndrome. It is a variant of migraine in which the patient may experience aura symptoms such as scintillating scotoma, nausea, photophobia, hemiparesis and other migraine symptoms but does not experience headache. Acephalgic migraine is also referred to as amigrainous migraine, ocular migraine, or optical migraine.

Sufferers of acephalgic migraine are more likely than the general population to develop classical migraine with headache.

The prevention and treatment of acephalgic migraine is broadly the same as for classical migraine. However, because of the absence of "headache", diagnosis of acephalgic migraine is apt to be significantly delayed and the risk of misdiagnosis significantly increased.

Visual snow might be a form of acephalgic migraine.

If symptoms are primarily visual, it may be necessary to consult an ophthalmologist to rule out potential eye disease before considering this diagnosis.

Epidemiology Edit

Migraine is an extremely common condition which will affect 12-28% of people at some point in their lives.[20] However this figure — the lifetime prevalence — does not provide a very clear picture of how many patients there are with active migraine at any one time. Typically, therefore, the burden of migraine in a population is assessed by looking at the one-year prevalence — a figure that defines the number of patients who have had one or more attacks in the previous year. The third figure, which helps to clarify the picture, is the incidence — this relates to the number of first attacks occurring at any given age and helps understanding of how the disease grows and shrinks over time.

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.[20] 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.[21] There is then a rapid growth in incidence amongst girls occurring after puberty[22],[23][24] which continues throughout early adult life.[25] By early middle age, around 25% of women experience a migraine at least once a year, compared with fewer than 10% of men.[20][26] After menopause, attacks in women tend to decline dramatically, so that in the over 70s there are approximately equal numbers of male and female sufferers, with prevalence returning to around 5%.[20][26]

At all ages, migraine without aura is more common than migraine with aura, with a ratio of between 1.5:1 and 2:1.[27][28] Incidence figures show that the excess of migraine seen in women of reproductive age is mainly due to migraine without aura.[29] Thus in pre-pubertal and post-menopausal populations, migraine with aura is somewhat more common than amongst 15-50 year olds[30][31]

Geographical differences in migraine prevalence are not marked. Studies in Asia and South America suggest that the rates there are relatively low,[32][33] but they do not fall outside the range of values seen in European and North American studies.[20][34]

Triggers Edit

A migraine trigger is any factor that, on exposure or withdrawal, leads to the development of an acute migraine headache. Triggers may be categorized as behavioral, environmental, infectious, dietary, chemical, or hormonal.

According to the National Library of Medicine's Medical Encyclopedia, Migraine attacks may be triggered by:

  • Allergic reactions
  • Bright lights, loud noises, and certain odors or perfumes
  • Physical or emotional stress
  • Changes in sleep patterns
  • Smoking or exposure to smoke
  • Skipping meals
  • Alcohol or caffeine
  • Menstrual cycle fluctuations, birth control pills
  • Tension headaches
  • Foods containing tyramine (red wine, aged cheese, smoked fish, chicken livers, figs, and some beans), monosodium glutamate (MSG), or nitrates (like bacon, hot dogs, and salami)
  • Other foods such as chocolate, nuts, peanut butter, avocado, banana, citrus, onions, dairy products, and fermented or pickled foods.[35]

Many people report that one or more dietary, physical, hormonal, emotional, or environmental factors precipitate their migraines. The most-often reported triggers include: pesticides (sprayed fruits/vegetables), perfumes or fragrances (30% of sufferers) stress, over-illumination or glare, alcohol, foods, too much or too little sleep, and weather. Some women experience migraines in conjunction with monthly menstrual cycles.

Sometimes the migraine occurs with no apparent "cause". The trigger theory supposes that exposure to various environmental factors precipitates, or triggers, individual migraine episodes. Migraine patients have long been advised to try to identify personal headache triggers by looking for associations between their headaches and various suspected trigger factors. Patients are urged to keep a "headache diary" in which to note what they eat and when they get a headache, to look for correlations, and to try to avoid headache by avoiding factors they identify as triggers. Typically this advice is accompanied by a list of trigger factors.

Food Edit

In 2005, authors who reviewed the medical literature[36] found that the available information about dietary trigger factors relies mostly on the subjective assessments of patients. Some suspected dietary trigger factors appear to genuinely promote or precipitate migraine episodes, but many other suspected dietary triggers have never been demonstrated to trigger migraines. The review authors found that alcohol, caffeine withdrawal, and missing meals are the most important dietary migraine precipitants. The authors say dehydration deserves more attention, and that some patients are sensitive to red wine. The authors found little or no demonstrated evidence that notorious suspected triggers chocolate, cheese, or that histamine, tyramine, nitrates, or nitrites normally present in foods trigger headaches. The artificial sweetener aspartame (NutraSweet®) has not been shown to trigger headache, but in a large and definitive study monosodium glutamate (MSG) in large doses (2.5 grams) was associated with adverse symptoms including headache more often than was placebo. The review authors also note that while general dietary restriction has not been demonstrated to be an effective migraine therapy, it is beneficial for the individual to avoid what has been a definite cause of the migraine.

On the other hand, several headache clinics have had good results with individually tailored dietary restriction as a therapy. Dr. Ian Livingstone, director of the Princeton Headache Clinic, recommends eliminating the following common headache triggers from the diet: aged cheese, monosodium glutamate, processed fish and meats containing nitrates (such as hot dogs), dark chocolate, aspartame, certain alcoholic beverages (including red wine), citrus fruits, and caffeine. After a period of one to two months, these foods can be reintroduced one at a time to determine their trigger potential for that individual. Adding large amounts of the suspected trigger in a short time may generate a response that is easy to observe.

Dr. David Buchholz, a neurologist who treats headaches at Johns Hopkins Hospital, has a longer list of suspected migraine triggers. He also recommends eliminating the triggers from the diet altogether, and then reintroducing them slowly after many weeks to measure the effects. His list includes: coffee (including decaf), chocolate, monosodium glutamate, processed meats and fish (aged, canned, preserved, processed with nitrates, and some meats that contain tyramine), cheese and dairy products (the more aged, the worse), nuts, citrus and some other fruits, certain vegetables (especially onions), fresh risen yeast baked goods, dietary sources of tyramine (including the foods listed above), and whatever gives you a headache.

The National Headache Foundation has a more specific list of triggers, which differs slightly from David Buchholz's list. For example, it says that decaffeinated coffee is allowed. The list details "Allowed", "Use with caution", and "Avoid" triggers.[37]

Weather Edit

Several studies have found some migraines are triggered by changes in weather. One study[38](Prince, 2004) noted that 62% of the subjects in the study thought that weather was a factor, in fact 51% were actually sensitive to weather changes. Among those whose migraines did occur during a change in weather, the subjects often picked a weather change other than the actual weather data recorded. Most likely to trigger a migraine were, in order:

  1. Temperature mixed with humidity. High humidity plus high or low temperature was the biggest cause.
  2. Significant changes in weather
  3. Changes in barometric pressure

Another study[39](Cooke, 2000) researched whether chinook winds (warm westerly winds occurring along the Front Ranges of the Rocky Mountains) are a migraine trigger. Many patients had increased incidence of migraines immediately before and/or during the chinook winds. The number of people reporting migrainous episodes during the chinook winds was higher on high-wind chinook days. The probable cause is "through increased air positive ion concentrations." (Cooke, 2000; full text web search quote)

Hair Wash Headache Edit

Another trigger for Migraine has been proposed by Dr.K.Ravishankar, a neurologist and headache specialist from India. He reported an unusual trigger for migraine seen among Indian women, Hair Wash Headache. It is described as a migraine headache that originates with a head bath. Most Indian women have long hair and so they wash their hair 2-3 times a week. Very often they do not use a hair dryer and often plait their hair when wet. This results in a gradual build up of pain which ultimately results in migraine.[40] (Ravishankar, 2006)

Treatment Edit

Conventional treatment focuses on three areas: trigger avoidance, symptomatic control, and preventive drugs. Patients who experience migraines often find that the recommended treatments are not 100% effective at preventing migraines, and sometimes may not be effective at all.

Trigger avoidance Edit

Patients can attempt to identify and avoid factors that promote or precipitate migraine episodes. Moderation in alcohol and caffeine intake, consistency in sleep habits, and regular meals may be helpful. Beyond an often pronounced placebo effect, general dietary restriction has not been demonstrated to be an effective approach to treating migraine.[2]

Nonetheless, some people fervently claim that they have successfully identified foods that are likely to result in migraines, and by avoiding them, can decrease the likelihood of an episode.

Abortive treatment Edit

Migraine sufferers usually develop their own coping mechanisms for the pain of a migraine attack. A cold or hot shower directed at the head, a hot or cold wet washcloth, a warm bath, or resting in a dark and silent room may be as helpful as medication for many patients, but both should be used when needed.

Some headache sufferers are surprised to learn that a simple cup of coffee is used daily around the world to control minor vascular headaches that are not quite migraines. Minor vascular headaches are frequently associated with the hormonal fluctuations of menstrual periods, irregular eating, and unusually hard work. For migraineurs, a well-timed cup of coffee can prevent outright migraine under the same conditions.

A simple treatment, which has been effective for some, is a counteracting "ice cream headache", briefly provoked by placing spoonfuls of ice cream on the soft palate at the back of the mouth. (Hold them there with your tongue until they melt or become intolerable.) This directs cooling to the hypothalamus, which is suspected to be involved with the migraine feedback cycle, and for some it can stop even a severe headache very quickly. [How to reference and link to summary or text]

For patients who have been diagnosed with recurring migraines, doctors recommend taking migraine abortive medicines to treat the attack as soon as possible. Migraine without aura presenting without prodrome or nausea can present with sudden onset. Many patients avoid taking their medications when an attack is beginning, hoping that "it will go away". However, in many cases once an attack is underway, it can become intensely painful, last for a long time (sometimes even for several days), and become somewhat resistant to medical treatment. In contrast, treating the attack at the onset can often abort it before it becomes serious, and can reduce the near-term frequency of subsequent attacks.

Acetaminophen or NSAIDsEdit

The first line of treatment is over-the-counter (OTC) abortive medication. Patients themselves often start off with paracetamol (known as acetaminophen in the USA), aspirin, ibuprofen, or other simple analgesics that are useful for tension headaches. Some patients find relief from taking Benadryl, an OTC sedative antihistamine, or anti-nausea agents. OTC drugs may provide some relief, although they are typically not effective for most sufferers. It is one of doctors' practical diagnoses of migraine head pain when patients say typical OTC drugs "won't touch it".

If the patient hasn't tried it, doctors may suggest the simple analgesics combined with caffeine. During a migraine attack, emptying of the stomach is slowed, resulting in nausea and a delay in absorbing medication. Caffeine has been shown to partially reverse this effect, and probably accounts for its benefit. Excedrin is an example of an aspirin with caffeine product. Caffeine is recognized by the U.S. FDA as an OTC treatment for migraine[How to reference and link to summary or text].

Serotonin AgonistsEdit

For more details on this topic, see triptans.

Sumatriptan and related selective serotonin receptor agonists are now the therapy of choice for chronic migraine attacks. Triptans are a mid-line treatment suitable for many migraineurs with typical migraines. They may not work for atypical or unusually severe migraines, transformed migraines, or status (continuous) migraines.

Triptans are highly effective, reducing the symptoms or aborting the attack within 30 to 90 minutes in 70-80% of patients. [How to reference and link to summary or text] Many patients have a recurrent migraine later in the day, and only one such recurrence in a day can be treated with a second dose of a triptan.

Triptans have few side effects if used in correct dosage and frequency. Although there is a theoretical risk of coronary spasm in patients with established heart disease, no clinically significant problems have ever been reported in practice.

Evidence is accumulating that these drugs are effective because they act on serotonin receptors in nerve endings as well as the blood vessels. This leads to a decrease in the release of several peptides, including CGRP and Substance P.

These drugs have been available only by prescription (US, Canada and UK), but sumatriptan became available over-the-counter in the UK in June, 2006.[41] The brand name of the OTC product in the UK is Imigran Recovery. Injectable sumatriptan should be available in generic formula in early 2007 as the patent on Imitrex STATDose expires in December, 2006. The patent on Imitrex tablets expires in the USA in 2009, and the generic sumatriptan tablets should be available shortly thereafter. Many migraine sufferers do not use them only because they have not sought treatment from a physician, but others don't because they know that they can't afford them at current prescription prices.

Triptan therapy has been shown to result in a reduction in lost productivity. Sumatriptan has been shown to result in an average of 0.5 fewer missed workdays during the first three months of therapy and 0.7 fewer missed workdays within the first six months, as well as a reduction in the number of days spent working while symptomatic. The average reduction in lost productivity has been estimated at $1,249, at a cost of $25 per day of disability avoided. The annual net savings in reduced health care costs and lost productivity, over the increased cost of triptan therapy, has been estimated at between $114 and $540 per patient; thus the use of these pharmaceuticals represents a cost savings as well as an improvement in the patients' quality of life.

Triptans' cost, typically $20 USD per dose and up to two doses per headache, is a serious problem for low-income patients. In most non-US countries these costs are considerably lower — typically $5-10 per dose. To their credit, drug companies often provide them free to low-income patients in the USA.

Ergot alkaloidsEdit

Until the introduction of sumatriptan in 1991, ergot derivatives (see ergoline) were the primary oral drugs available to abort a migraine once it is established.

Ergot drugs can be used either as a preventive or abortive therapy, though their relative expense and cumulative side effects suggest reserving them as an abortive rescue medicine. However, ergotamine tartrate tablets (usually with caffeine), though highly effective, and long lasting (unlike triptans), have fallen out of favour due to the problem of ergotism. Oral ergotamine tablet absorption is reliable unless the patient is nauseated. Anti-nausea administration is available by ergotamine suppository (or Ergostat sublingual tablets made until circa 1992). Ergotamine-caffeine 1/100 mg fixed ratio tablets (like Cafergot, Ercaf, etc.) are much less expensive per headache than triptans, and are commonly available in Asia. They are difficult to obtain in the USA. Ergotamine-caffeine can't be regularly used to abort evening or night onset migraines due to debilitating caffeine interference with sleep. Pure ergotamine tartrate is highly effective for evening-night migraines, but is rarely or never available in the USA. Dihydroergotamine (DHE), which must be injected or inhaled, can be as effective as ergotamine tartrate, but is much more expensive than $2 USD Cafergot tablets.

Other agentsEdit

If over-the-counter medications do not work, or if triptans are unaffordable, the next step for many doctors is to prescribe fioricet or fiorinal, which is a combination of butalbital (a barbiturate), acetaminophen (in fioricet) or acetylsalicylic acid (more commonly known as aspirin and present in fiorinal), and caffeine. While the risk of addiction is low, butalbital can be habit-forming if used daily, and it can also lead to rebound headaches. Barbiturate-containing medications are not available in many European countries.

Narcotic pain killers (for example, codeine, morphine or other opiates) provide variable relief, but their side effects, the possibility of causing rebound headaches or analgesic overuse headache, and the risk of addiction contraindicates their general use.

Amidrine (a cocktail of a pain reliever, a sedative, and a vasoconstrictor) is sometimes prescribed for migraine headaches.

Anti-emetics by suppository or injection may be needed in cases where vomiting dominates the symptoms. The earlier these drugs are taken in the attack, the better their effect.

Intravenous chlorpromazine has proven very effective in treating status migrainosus—intractable and unremitting migraine. [How to reference and link to summary or text]Status migraine is an extremely rare life-threatening condition.[How to reference and link to summary or text] In otherwise uncomplicated, non-nauseated cases, it can be treated with 20 mg of prednisone tablets every eight hours until the migraine ends, followed by mandatory tapering off doses (the classic steroid taper). Prednisone is a cortisol-like semi-synthetic adrenal hormone, a non-anabolic steroid, which strongly stimulates biosynthesis of proteins from DNA. The replicated proteins include enzymes that cure the migraine through numerous metabolic boosts, including molecular construction of more natural serotonin to be stored in blood platelets.

Prednisone risks include immune system suppression, adrenal axis suppression, non-addictive dependence, and long-term osteoporosis. Vitamin antioxidants taken with calcium and magnesium may reduce the damage caused by the extra free radicals released, and the bone lost, during long term prednisone use.[How to reference and link to summary or text]

Comparative studies Edit

Regarding comparative effectiveness of these drugs used to abort migraine attacks, a 2004 placebo-controlled trial[42] reveals that high dose acetylsalicylic acid (1000 mg), sumatriptan 50 mg and ibuprofen 400 mg are equally effective at providing relief from pain, although sumatriptan was superior in terms of the more demanding outcome of rendering patients entirely free of pain. Acetylsalicylic acid is OTC aspirin, ibuprofen is OTC Advil, and since migraineurs know they don't provide much relief, the results of this study are unexpected. They may be partly related to the dosage of acetylsalicylic acid used, which was considerably higher than the one or two 300 mg tablets normally recommended for OTC use. High doses of aspirin and ibuprofen may cause ringing of the ears, which is a sign of drug toxicity to the inner ear.

Another randomized controlled trial, funded by the manufacturer of the study drug, found that a combination of sumatriptan 85 mg and naproxen sodium 200 mg was better than either drug alone.[43]

Preventive drugs[44] Edit

Following treatment of an acute migraine, it is important to consider preventive measures. Factors that prompt consideration of such measures include: 1) more than two migraines per month with disabilities lasting three or more days per month; 2) failure of acute treatments; 3) contraindications to acute treatments; 4) adverse reactions from acute treatments; 5) use of acute treatments more than twice a week; or 6) presence of uncommon symptoms such as hemiplegia, prolonged, aura, or migraine infarction.

The main goal of preventive therapy is to reduce the frequency, severity, and durations of migraines, and to increase the effectiveness of abortive therapy. Another reason is to avoid medication overuse headache (MOH), otherwise known as rebound headache, which is an extremely common problem among migraneurs. This occurs in part due to overuse of pain medications. MOH results in the development of chronic daily headache due to "transformed" migraine.

Preventive medication has to be taken on a daily basis, usually for a few weeks, before the effectiveness can be determined. Supervision by a neurologist is advisable. A large number of medications with varying modes of action can be used. Selection of a suitable medication for any particular patient is a matter of trial and error, since the effectiveness of individual medications varies widely from one patient to the next. Often preventive medications do not have to be taken indefinitely. Sometimes as little as six months of preventive therapy is enough to "break the headache cycle" and then they can be discontinued.

The most effective prescription medications include several drug classes:

Other drugs:

  • Sansert was withdrawn from the US market by Novartis, but is available in Canadian pharmacies. Although highly effective, it has rare but serious side effects, including retroperitoneal fibrosis.
  • Namenda, memantine HCI tablets, which is used in the treatment of Alzheimer's Disease, is beginning to be used off label for the treatment of migraines. It has not yet been approved by the FDA for the treatment of migraines.
  • ASA or Asprin can be taken daily in low doses such as 80 to 81 mg, the blood thinners in ASA has been shown to help some migrainures, especially those who have an aura.

Physical therapyEdit

Many physicians believe that exercise for 15-20 minutes per day is helpful for reducing the frequency of migraines. [3] (PDF)

Massage therapy and physical therapy are often very effective forms of treatment to reduce the frequency and intensity of migraines. However, it is important to be treated by a well-trained therapist who understands the pathophysiology of migraines. Deep massage can 'trigger' a migraine attack in a person who is not used to such treatments. It is advisable to start sessions as short in duration and then work up to longer treatments.

Frequent migraines can leave the sufferer with a stiff neck which can cause stress headaches that can then exacerbate the migraines. A physical therapy technique called myofascial release claims to be able to relieve this tension and in doing so reduce or eliminate the stress headache element.

Prism eyeglasses Edit

At least two British studies have shown a relationship between the use of eyeglasses containing prisms and a reduction in migraine headaches.

Turville, A. E. (1934) Refraction and migraine. Br. J. Physiol. Opt. 8, 62–89, contains a good review of the literature and theories existing in 1934, and includes the vascular theory of migraine, which is popular today. In that study, Turville suggests that many patients were provided with complete relief from migraine symptoms with proper eyeglass prescriptions, which included prescribed prism.

Wilmut, E. B. (1956) Migraine. Br. J. Physiol. Opt. 13, 93–97, replicated Turville's work. Both studies are subject to criticism because of sample bias, sample size, and the lack of a control group.

Neither study is available online, but another study that found that precision tinted lenses may be an effective migraine treatment and which references the Turville and Wilmut studies can be found at [4] (PDF).

Turville's and Wilmut's conclusions have largely been ignored since 1956 and it is widely believed that vision problems are not migraine triggers.

Most optometrists avoid prescribing prism because, when incorrectly prescribed, it can cause headaches.

Herbal and nutritional supplements Edit

50 mg or 75 mg/day of butterbur (Petasites hybridus) rhizome extract was shown in a controlled trial to provide 50% or more reduction in the number of migraines to 68% of participants in the 75 mg dose group, 56% in the 50 mg dose group and 49% in the placebo group after four months. Native butterbur contains some carcinogenic compounds, but a purified version, Petadolex®, does not.[5]

Cannabis was a standard treatment for migraines from the mid-19th century until it was outlawed in the early 20th century in the USA. It has been reported to help people through an attack by relieving the nausea and dulling the head pain, as well as possibly preventing the headache completely when used as soon as possible after the onset of pre-migraine symptoms, such as aura. There is some indication that semi-regular use may reduce the frequency of attacks. Further studies are being conducted. Some migraine sufferers report that cannabis increases throbbing and pain, especially if smoked. A pharmaceutical company is currently conducting trials of a whole cannabis extract spray for migraine[6]

Supplementation of coenzyme Q10 has been found to have a beneficial effect on the condition of some sufferers of migraines. In a well-controlled trial,[51] Young and Silberstein found that 61.3% of patients treated with 100 mg/day had a greater than 50% reduction in number of days with migraine, making it more effective than most prescription prophylactics. Fewer than 1% reported any side effects.

The plant feverfew (Tanacetum parthenium) is a traditional herbal remedy believed to reduce the frequency of migraine attacks. Clinical trials have been carried out (example), and appear to confirm that the effect is genuine (though it does not completely prevent attacks). [How to reference and link to summary or text]Kudzu root (Pueraria lobata) has been demonstrated to help with menstrual migraine headaches and cluster headaches. While the studies on menstrual migraine assumed that kudzu acted by imitating estrogen, it has since been shown that kudzu has significant effects on the serotonin receptors. Kudzu Monograph at Med-Owl.

Magnesium citrate has reduced the frequency of migraine in an experiment in which the magnesium citrate group received 600 mg per day oral of trimagnesium dicitrate. In weeks 9-12, the frequency of attacks was reduced by 41.6% in the magnesium citrate group and by 15.8% in the placebo group.[52] The supplement Riboflavin or Vitamin B2 has also been used, often with magnesium citrate, to reduce the number of migraines. Its efectiveness is less well documented.

Non-drug medical treatments Edit

Botox is being used by many headache specialists for patients with frequent or chronic migraines with encouraging results.[53] Spinal cord stimulators are an implanted medical device sometimes used for those who suffer severe migraines several days each month.[54]

Transcranial Magnetic Stimulation (TMS): At the 49th Annual meeting of the American Headache Society in June 2006, scientists from Ohio State University Medical Center presented medical research on 47 candidates that demonstrated that TMS — a medically non-invasive technology for treating depression, obsessive compulsive disorder and tinnitus, among other ailments — helped to prevent and even reduce the severity of migraines among its patients. This treatment essentially disrupts the aura phase of migraines before patients develop full-blown migraines.[7] In about 74% of the migraine headaches, TMS was found to eliminate or reduce nausea and sensitivity to noise and light.[8] Their research suggests that there is a strong neurological component to migraines. A larger study will be conducted soon to better assess TMS's complete effectiveness.[55]

Alternatives Edit

Because the conventional approaches to migraine prevention are not 100% effective and can have unpleasant side effects, many seek alternative treatments.

Some migraine sufferers find relief through acupuncture, which is usually used to help prevent headaches from developing. Sometimes acupuncture is used to relieve the pain of an active migraine headache.[How to reference and link to summary or text] In one controlled trial of acupuncture with a sham control in migraine, the acupuncture was not more effective than the sham acupuncture but was more effective than delayed acupuncture.[How to reference and link to summary or text]

Additionally acupressure is used by some for relief. For instance pressure between the thumbs and index finger to help subside headaches if the headache or migraine isn't too severe.[How to reference and link to summary or text]

Incense and scents are shown to help. The smell and incense of peppermint and lavender have been proven to help with migraines and headaches more so than most other scents. Mauskop A, Fox B, What Your Doctor May Not Tell You About Migraines. Warner Books, New York, 2001 Biofeedback has been used successfully by some to control migraine symptoms through training and practice. Mauskop A, Fox B, What Your Doctor May Not Tell You About Migraines. Warner Books, New York, 2001

There is evidence that magnesium supplements can reduce the frequency of migraine headaches. Riboflavin (vitamin B2), co-enzyme Q10 and butterbur extract has been also subjected to double-blind studies suggesting their efficacy in preventing migraine headaches. Mauskop A: Alternative therapies in headache: Is there a role? In: Medical Clinics of North America 85 (4): 1077-1084, 2001.

Sleep is often a good solution if a migraine is not so severe as to prevent it, as when a person awakes the symptoms will have most likely subsided.

Diet, visualization, and self-hypnosis are also alternative treatments and prevention approaches.

Bruxism, clenching or grinding of teeth, especially at night, is a trigger for many migraineurs. A device called a nociceptive trigeminal inhibitor (NTI) takes advantage of a reflex limiting the force of clenching. It can be fitted by dentists and clips over the front teeth at night, preventing contact between the back teeth. It has a success rate similar to butterbur and co-enzyme Q10, although it has not been subjected to the same rigorous testing as the supplements. Massage therapy of the jaw area can also reduce such pain.

Sexual activity has been reported by a proportion of male and female migraine sufferers to relieve migraine pain significantly in some cases.[9]

In many cases where a migraine follows a particular cycle, attempting to interrupt the cycle may prolong the symptoms. Letting a headache "run its course" by not using painkillers can sometimes decrease the length of an episode. This is especially true of cases where vomiting is common, as often the headache will subside immediately after vomiting. Curbing the pain may delay vomiting, and prolong the headache.

History Edit

The history of humanity's suffering from headache dates back to 9000 years ago when basic drastic therapy of that time was trepanation. Headache with neuralgia was recorded in the medical documents of the ancient Egyptians as early as 1200 BC. In 400 BC Hippocrates described the visual aura that can precede the migraine headache and the relief which can be induced by vomiting. Aretaeus of Cappadocia is credited as the discoverer of migraine because of his classic description of the symptoms of a unilateral headache associated with vomiting with headache-free intervals in between attacks in the 2nd century. Galenus of Pergamon used the term "hemicrania", 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, Spanish-born physician Abulcasis, also known as Abu El Quasim, suggested application of a hot iron to the head or insertion of garlic into an incision made in the temple. In the Medieval Ages migraine was recognized as a discrete medical disorder with treatment ranging from hot irons to blood letting and even witchcraft. Followers of Galenus explained migraine as 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. Graham and Wolff (1938) published their paper advocating ergotamine tart 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.

Economic impact Edit

In addition to being a major cause of pain and suffering, chronic migraine attacks are a significant source of both medical costs and lost productivity. Medical costs per migraine sufferer (mostly physician and emergency room visits) averaged $107 USD over six months in one 1988 study,[How to reference and link to summary or text] with total costs including lost productivity averaging $313. Annual employer cost of lost productivity due to migraines was estimated at $3,309 per sufferer. Total medical costs associated with migraines in the United States amounted to one billion dollars in 1994, in addition to lost productivity estimated at thirteen to seventeen billion dollars per year. Employers may benefit from educating themselves on the effects of migraines in order to facilitate a better understanding in the workplace. The workplace model of 9-5, 5 days a week may not be viable for a migraine sufferer. With education and understanding an employer could compromise with an employee to create a workable solution for both.

Migraine and cardiovascular risksEdit

Recent studies have suggested that migraine sufferers may be at increased risk of stroke in later life. A meta-analysis of several such studies published in the British Medical Journal[56] in 2005 appeared to confirm this association, with young adult sufferers and women using hormonal contraception at particular risk. 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 non-aura migraine sufferers and women who do not have migraines.[57]

See alsoEdit

ReferencesEdit

Migraine triggers Edit

  • Federation of American Societies for Experimental Biology [FASEB] [1995]. Analysis of adverse reactions to monosodium glutamate (MSG). Bethesda, MD: Life Sciences Research Office, FASEB.
  • Ravishankar, K (2006). 'Hair wash' or 'Head bath' triggering migraine - observations in 94 Indian patients". Cephalagia 26 (11): 1330-1334. ISSN 0333-1024.

Treatment Edit

Triptans Edit

  • Cohen JA, Beall D, Beck A, et al. Sumatriptan treatment for migraine in a health maintenenace organization: economic, humanistic, and clinical outcomes. Clin Ther 1999;21:190-205.
  • Adelman JU, Sharfman M, Johnson R, et al. Impact of oral sumatriptan on workplace productivity, health-related quality of life, healthcare use, and patient satisfaction with medication in nurses with migraine. Am J Manag Care 1996;2:1407-1416.
  • Cohen JA, Beall DG, Miller DW, Beck A, Pait G, Clements BD. Subcutaneous sumatriptan for the treatment of migraine: humanistic, economic, and clinical consequences. Fam Med 1996;28:171-177.
  • Jhingran P, Cady RK, Rubino J, Miller D, Grice RB, Gutterman DL. Improvements in health-related quality of life with sumatriptan treatment for migraine. J Med Econ 1996;42:36-42.
  • Solomon GD, Nielsen K, Miller D. The effects of sumatriptan on migraine: health-related quality of life. Med Interface 1995;June:134-141.
  • Solomon GD, Skobieranda FG, Genzen JR. Quality of life assessment among migraine patients treated with sumatriptan. Headache 1995;35:449-454.
  • Santanello NC, Polis AB, Hartmaier SL, Kramer MS, Block GA, Silberstein SD. Improvement in migrainespecific quality of life in a clinical trial of rizatriptan. Cephalalgia 1997;17:867-872.
  • Caro JJ, Getsios D. Pharmacoeconomic evidence and considerations for triptan treatment of migraine. Expert Opin Pharmacother 2002;3:237-248.
  • Lofland JH, Johnson NE, Batenhorst AS, Nash DB. Changes in resource use and outcomes for patients with migraine treated with sumatriptan: a managed care perspective. Arch Intern Med 1999;159: 857-863.
  • Cady RC, Ryan R, Jhingran P, O’Quinn S, Pait DG. Sumatriptan injection reduces productivity loss during a migraine attack. Arch Intern Med 1998;158: 1013-1018.
  • Litaker DG, Solomon GD, Genzen JR. Impact of sumatriptan on clinic utilization and costs of care in migraineurs. Headache 1996;36:538-541.
  • Greiner DL, Addy SN. Sumatriptan use in a large group-model health maintenance organization. Am J Health Syst Pharm 1996;53:633-638.
  • Lofland JH, Kim SS, Batenhorst AS, et al. Cost-effectiveness and cost-benefit of sumatriptan in patients with migraine. Mayo Clin Proc 2001;76:1093- 1101.
  • Biddle AK, Shih YC, Kwong WJ. Cost-benefit analysis of sumatriptan tablets versus usual therapy for treatment of migraine. Pharmacotherapy 2000;20: 1356-1364.
  • Caro JJ, Getsios D, Raggio G, Caro G, Black L. Treatment of migraine in Canada with naratriptan: a costeffectiveness analysis. Headache 2001;41:456-464.

General Edit

Economic impact Edit

  • Edmeads J, Mackell JA. The economic impact of migraine: an analysis of direct and indirect costs. Headache 2002;42:501-509.
  • Gerth WC, Carides GW, Dasbach EJ, Visser WH, Santanello NC. The multinational impact of migraine symptoms on healthcare utilisation and work loss. Pharmacoeconomics 2001;19:197-206.
  • Hu XH, Markson LE, Lipton RB, Stewart WF, Berger ML. Burden of migraine in the United States: disability and economic costs. Arch Intern Med 1999;159:813-818.
  • Osterhaus JT, Gutterman DL, Plachetka JR. Healthcare resource and low labour costs of migraine headaches in the US. Pharmacoeconomics 1992;2:2-11.

Clinical pictureEdit

  • Blau JN. Classical migraine: symptoms between visual aura and headache onset. Lancet 1992;340:355-6.
  • Silberstein SD: Migraine symptoms: Results of a survey of self-reported migraineurs. Headache 1995;35:387-96.
  • Silberstein SD, Saper JR, Freitag F. Migraine: Diagnosis and treatment. In: Silberstein SD, Lipton RB, Dalessio DJ, eds. Wolff's headache and other head pain. 7th ed. New York: Oxford University Press, 2001:121-237.

FootnotesEdit

  1. NINDS Migraine Information Page. National Institute of Neurological Disorders and Stroke, National Institutes of Health. URL accessed on 2007-06-25.
  2. Advances in Migraine Prophylaxis: Current State of the Art and Future Prospects. National Headache Foundation (CME monograph). URL accessed on 2007-06-25.
  3. Migraine: diagnosis, management, and new treatment options, Gallagher RM, Cutrer FM, University of Medicine and Dentistry of New Jersey, School of Medicine, Stratford, USA. The American Journal of Managed Care, PMID: 11859906. URL accessed on 2007-06-25.
  4. Guidelines for all healthcare professionals in the diagnosis and management of migraine, tension-type, cluster and medication-overuse headache, Jan 2007,British Association for the Study of Headache. URL accessed on 2007-06-25.
  5. . Silberstein S. Migraine. Lancet 2004;363:381-391
  6. wrongdiagnosis.com
  7. "The Essential Book of Herbal Medicine" (also known as "Out of the Earth") by Simon Y. Mills, Viking Arkana, 1994(1991). Mills is former president of the UK licensed medical herbalists association. Mills' point is the traditional classification of migraines into "hot" and "cold" types, meaning that one's migraine type is determined by whether one's pain is reduced by hot/warm versus cold water.
  8. Ogilvie AD, Russell MB, Dhall P, et al. "Altered allelic distributions of the serotonin transporter gene in migraine without aura and migraine with aura." Cephalalgia. 1998 Jan;18(1):23-6. PMID 9601620
  9. Young, William B. and Silberstein, Stephen D., Migraine and Other Headaches. St. Paul, Minn: AAN Press, 2004.
  10. Evans, Randolph W., MD, and Matthew, Ninan T., MD. Handbook of Headache, Second Edition. Philadelphia: Lippincott Williams & Wilkins. 2005.
  11. Silberstein, Stephen D.; Lipton, Richard B.; Goadsby, Peter J. Headache in Clinical Practice Second Edition. Andover: Thomson Publishing Services. 2002.
  12. Lipton RB, Dodick D, Sadovsky R, et al (2003). A self-administered screener for migraine in primary care: The ID Migraine validation study. Neurology 61 (3): 375-82.
  13. Cohen AS, Goadsby PJ (2005). Functional neuroimaging of primary headache disorders. Curr Pain Headache Rep 45 (9): 141-146.
  14. Lauritzen M. (1994). Pathophysiology of the migraine aura. The spreading depression theory.. Brain 117 (1): 199-210. PMID 7908596.
  15. Schwerzmann M, Wiher S, Nedeltchev K, Mattle HP, Wahl A, Seiler C, Meier B, Windecker S (2004). Percutaneous closure of patent foramen ovale reduces the frequency of migraine attacks. Neurology 62 (8): 1399-401. PMID 15111681.
  16. Cephalalgia 2004;24 (suppl 1):24-5 http://web.archive.org/web/20070729115257/http://216.25.100.131/upload/ct_clas/ihc_II_main_no_print.pdf
  17. Cephalalgia 2004;24 (suppl 1):25-27 http://web.archive.org/web/20070729115257/http://216.25.100.131/upload/ct_clas/ihc_II_main_no_print.pdf
  18. The International Classification of Headache Disorders, 2nd Edition
  19. Cephalalgia 2004;24 (suppl 1):30-31 http://web.archive.org/web/20070729115257/http://216.25.100.131/upload/ct_clas/ihc_II_main_no_print.pdf
  20. 20.0 20.1 20.2 20.3 20.4 Stovner LJ, Zwart J-A, Hagen K, et al. Epidemiology of headache in Europe. Eur J Neurol 2006;13:333-45
  21. 3. Mortimer MJ, Kay J, Jaron A. Epidemiology of headache and childhood migraine in an urban general practice using ad hoc, Vahlquist and IHS criteria. Dev Med Child Neurol 1992;34:1095-1101
  22. Linet MS, Stewart WF, Celentano DD et al. An epidemiologic study of headache among adolescents and young adults. JAMA 1989;261:2211-16
  23. Ziegler DK, Hassanein RS, Couch JR. Characteristics of life headache histories in a nonclinic population. Neurology 1977;27:265-269
  24. Selby G, Lance JW. Observations on 500 cases of migraine and allied vascular headache. J Neurol Neurosurg Psychiat 1960;23:23-32
  25. Anttila P, Metsahonkala L, Sillanpaa M. Long-term trends in the incidence of headache in Finnish schoolchildren. Pediatrics 2006;117:e1197-e1201
  26. 26.0 26.1 Lipton RB,.Stewart WF. Migraine in the United States: a review of epidemiology and health care use. Neurology 1993;43:S6-10
  27. Rasmussen BK,.Olesen J. Migraine with aura and migraine without aura: an epidemiological study. Cephalalgia 1992;12:221-8
  28. Steiner TJ, Scher AI, Stewart WF, et al. The prevalence and disability burden of adult migraine in England and their relationships to age, gender and ethnicity. Cephalalgia 2003; 23:519-27
  29. Rasmussen BK,.Olesen J. Migraine with aura and migraine without aura: an epidemiological study. Cephalalgia 1992;12:221-8
  30. Anttila P, Metsahonkala L, Sillanpaa M. Long-term trends in the incidence of headache in Finnish schoolchildren. Pediatrics 2006;117:e1197-e12017,10
  31. Bigal ME, Liberman JN, Lipton RB. Age-dependent prevalence and clinical features of migraine. Neurology 2006;67:246-51
  32. Wang SJ. Epidemiology of migraine and other types of headache in Asia. Curr Neurol. Neurosci. Rep. 2003;3:104-8
  33. Lavados PM,.Tenhamm E. Epidemiology of migraine headache in Santiago, Chile: a prevalence study. Cephalalgia 1997;17:770-7
  34. Lipton RB,.Stewart WF. Migraine in the United States: a review of epidemiology and health care use. Neurology 1993;43:S6-10
  35. http://www.nlm.nih.gov/medlineplus/ency/article/000709.htm
  36. Holzhammer J, Wober C (2006). [Alimentary trigger factors that provoke migraine and tension-type headache]. Schmerz 20 (2): 151-9. PMID 15806385.
  37. (2004). Low Tyramine Headache Diet. (116 Kb PDF) National Headache Foundation. URL accessed on 2006-10-12.
  38. Prince PB, Rapoport AM, Sheftell FD, Tepper SJ, Bigal ME (2004). The effect of weather on headache. Headache 44 (6): 596-602. PMID 15186304.
  39. Cooke LJ, Rose MS, Becker WJ (2000). Chinook winds and migraine headache. Neurology 54 (2): 302-7. PMID 10668687.
  40. Ravishankar, K (2006). 'Hair wash' or 'Head bath' triggering migraine - observations in 94 Indian patients. Cephalagia 26 (11): 1330-1334. ISSN 0333-1024.
  41. Pharmacies to sell migraine drug. BBC NEWS. URL accessed on 2006-09-05.
  42. Diener H, Bussone G, de Liano H, Eikermann A, Englert R, Floeter T, Gallai V, Göbel H, Hartung E, Jimenez M, Lange R, Manzoni G, Mueller-Schwefe G, Nappi G, Pinessi L, Prat J, Puca F, Titus F, Voelker M (2004). Placebo-controlled comparison of effervescent acetylsalicylic acid, sumatriptan and ibuprofen in the treatment of migraine attacks.. Cephalalgia 24 (11): 947-54. PMID 15482357.
  43. Brandes JL, Kudrow D, Stark SR, et al (2007). Sumatriptan-naproxen for acute treatment of migraine: a randomized trial. JAMA 297 (13): 1443-54.
  44. Modi S, Lowder D (2006). Medications for migraine prophylaxis.. American Family Physician 73 (1).
  45. Linde K, Rossnagel K. Propranolol for migraine prophylaxis.. Cochrane Database Syst Rev: CD003225. PMID 15106196.
  46. Chronicle E, Mulleners W. Anticonvulsant drugs for migraine prophylaxis.. Cochrane Database Syst Rev: CD003226. PMID 15266476.
  47. Steinman M, Bero L, Chren M, Landefeld C (2006). Narrative review: the promotion of gabapentin: an analysis of internal industry documents.. Ann Intern Med 145 (4): 284-93. PMID 16908919.
  48. Moja P, Cusi C, Sterzi R, Canepari C. Selective serotonin re-uptake inhibitors (SSRIs) for preventing migraine and tension-type headaches.. Cochrane Database Syst Rev: CD002919. PMID 16034880.
  49. Tomkins G, Jackson J, O'Malley P, Balden E, Santoro J (2001). Treatment of chronic headache with antidepressants: a meta-analysis.. Am J Med 111 (1): 54-63. PMID 11448661.
  50. Ziegler D, Hurwitz A, Hassanein R, Kodanaz H, Preskorn S, Mason J (1987). Migraine prophylaxis. A comparison of propranolol and amitriptyline.. Arch Neurol 44 (5): 486-9. PMID 3579659.
  51. Rozen T, Oshinsky M, Gebeline C, Bradley K, Young W, Shechter A, Silberstein S (2002). Open label trial of coenzyme Q10 as a migraine preventive.. Cephalalgia 22 (2): 137-41. PMID 11972582.
  52. Peikert A, Wilimzig C, Köhne-Volland R (1996). Prophylaxis of migraine with oral magnesium: results from a prospective, multi-center, placebo-controlled and double-blind randomized study.. Cephalalgia 16 (4): 257-63. PMID 8792038.
  53. Samton JB and Mauskop A. The treatment of headaches with Botulinum Toxin. Expert Review of Neurotherapeutics March 2006, Vol. 6, No. 3, Pages 313-322.
  54. Matharu MS, Bartsch T, Ward N, Frackowiak RS, Weiner R, Goadsby PJ (2004). Central neuromodulation in chronic migraine patients with suboccipital stimulators: a PET study. Brain 127 (Pt 1): 220-30. PMID 14607792.
  55. Mohammad, Yousef (2006-06-22). "Magnets Zap Migraines". 49th Annual Scientific Meeting of the American Headache Society. Retrieved on 2006-07-04. 
  56. Tzourio C, Tehindrazanarivelo A, Iglesias S, Alperovitch A, Chedru F, d'Anglejan-Chatillon J, Bousser MG (1995). Case-control study of migraine and risk of ischaemic stroke in young women. BMJ 310 (6983): 830-3. PMID 7711619.
  57. Kurth, T, Gaziano JM, Cook NR, Logroscino G, Diener HC, Buring JE (July 19 2006). Migraine and risk of cardiovascular disease in women. Journal of the American Medical Association 296 (3): 283-91. PMID 16849661.

External linksEdit

  1. REDIRECT Template:CNS diseases of the nervous system
This page uses Creative Commons Licensed content from Wikipedia (view authors).

Around Wikia's network

Random Wiki