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Migraine

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

Migraine
Classification and external resources

The pain of a migraine headache can be


debilitating.
ICD-10 G43.
ICD-9 346
OMIM 157300
DiseasesD 8207 (Migraine)
B 31876 (Basilar)
4693 (FHM)
MedlinePlu 000709
s
eMedicine neuro/218 neuro/517 emerg/230
neuro/529
MeSH D008881
Migraine is a neurological syndrome characterized by altered bodily perceptions,
severe headaches, and nausea. Physiologically, the migraine headache is a
neurological condition more common to women than to men.[1][2] The word
migraine was borrowed from Old French migraigne (originally as "megrim", but
respelled in 1777 on a contemporary French model). The French term derived from
a vulgar pronunciation of the Late Latin word hemicrania, itself based on Greek
hemikrania, from Greek roots for "half" and "skull".[3]

The typical migraine headache is unilateral (affecting one half of the head) and
pulsating, lasting from 4 to 72 hours;[2] symptoms include nausea, vomiting,
photophobia (increased sensitivity to light), and phonophobia (increased sensitivity
to sound).[4][5][6] 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.[7]

Initial treatment is with analgesics for the headache, an antiemetic for the nausea,
and the avoidance of triggering conditions. The cause of migraine headache is
unknown; the most common theory is a disorder of the serotonergic control system.

There are migraine headache variants, some originate in the brainstem (featuring
intercellular transport dysfunction of calcium and potassium ions) and some are
genetically disposed.[8] Studies of twins indicate a 60 to 65 percent genetic
influence upon their propensity to develop migraine headache.[9][10] 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.[11]

In 2010, scientists identified a genetic defect linked to migraines which could


provide a target for new drug treatments.[12]

Contents
[hide]
1 Classification
2 Signs and symptoms
2.1 Prodrome phase
2.2 Aura phase
2.3 Pain phase
2.4 Postdrome phase
3 Triggers
3.1 Food and Drink
3.2 Weather
4 Pathophysiology
4.1 Depolarization theory
4.2 Vascular theory
4.3 Serotonin theory
4.4 Neural theory
4.5 Unifying theory
5 Diagnosis
6 Prevention
7 Management
7.1 Analgesics
7.2 Analgesics combined with
antiemetics
7.3 Serotonin agonists
7.4 Antidepressants
7.5 Ergot alkaloids
7.6 Steroids
7.7 Other agents
7.7.1 Status migrainosus
7.7.2 Herbal treatment
7.7.3 Cryotherapy and
Thermotherapy
7.8 Exercise
7.9 Comparative studies
7.10 Medication overuse
headaches
8 Prognosis
8.1 Cardiovascular risks
9 Epidemiology
10 History
11 Society and culture
11.1 Economic impact
12 See also
12.1 Organizations
12.2 Other
13 Footnotes
14 References
14.1 Migraine triggers
14.2 Treatment
14.2.1 Triptans
14.3 General
14.4 Economic impact
14.5 Clinical picture
15 External links
15.1 General information
15.2 Organizations
[edit] 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).[13]

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 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.

[edit] Signs and symptoms

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 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.

[edit] Prodrome phase

Prodromal symptoms occur in 40–60% of migraine sufferers. This phase may consist
of altered mood, irritability, depression or euphoria, fatigue, yawning, excessive
sleepiness, craving for certain food (e.g. chocolate), stiff muscles (especially in the
neck), hot ears, constipation or diarrhea, increased urination, and other visceral
symptoms.[14] 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.

[edit] Aura phase

Computer simulation of visual field defects during a migraine with aura based on a
neural network[15][3]

For the 20–30%[16][17] 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). Symptoms of migraine
aura can be visual, sensory, or motor in nature.[18]

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"[19]). 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
nose-mouth area on the same side. Paresthesia 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 Negative scotoma, Positive scotoma,


Mostly one-sided
reminiscent of a loss of awareness of local perception of
loss of perception
zigzag fort structure local structures additional structures
[edit] Pain phase

This section does not cite any references or sources.


Please help improve this article by adding citations to reliable sources.
Unsourced material may be challenged and removed. (September 2009)
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, polyuria, pallor, or sweating may be noted
during the headache phase. There may be localized edema of the scalp or face,
scalp tenderness, prominence of a vein or artery in the temple, or stiffness and
tenderness of the neck. Impairment of concentration and mood are common. The
extremities tend to feel cold and moist. Vertigo may be experienced; a variation of
the typical migraine, called vestibular migraine, has also been described.
Lightheadedness, rather than true vertigo,[citation needed] and a feeling of
faintness may occur.

[edit] Postdrome phase

The patient may feel tired or "hungover" and have head pain, cognitive difficulties,
gastrointestinal symptoms, mood changes, and weakness.[20] According to one
summary, "Some people feel unusually refreshed or euphoric after an attack,
whereas others note depression and malaise."[21]

[edit] Triggers

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. In the medical
literature, these factors are known as 'precipitants.'

The MedlinePlus Medical Encyclopedia, for example, offers the following list of
migraine triggers:

Migraine attacks may be triggered by:

Alcohol

Allergic reactions

Bright lights

Certain odors or perfumes

Changes in hormone levels (which can occur during a woman's menstrual cycle or
with the use of birth control pills)

Changes in sleep patterns

Exercise

Loud noises

Missed meals

Physical or emotional stress


Smoking or exposure to smoke

Certain foods and preservatives in foods may trigger migraines in some


people...This list may not include all triggers...

– MedlinePlus medical encyclopedia.[22]

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 and keeping a migraine journal
recording migraine incidents and diet to look for correlations in order to avoid
trigger foods. It must be mentioned, that some trigger factors are quantitative in
nature, e.g., a small block of dark chocolate may not cause a migraine, but half a
slab of dark chocolate almost definitely will, in a susceptible person. In addition,
being exposed to more than one trigger factor simultaneously will more likely cause
a migraine, than a single trigger factor in isolation, e.g., drinking and eating various
known dietary trigger factors on a hot, humid day, when feeling stressed and having
had little sleep will probably result in a migraine in a susceptible person, but
consuming a single trigger factor on a cool day, after a good night's rest with
minimal environmental stress may mean that the sufferer will not develop a
migraine after all. Nightmares or Traumatic Dreams may also be recorded as
migraine triggers. Migraines can be complex to avoid, but keeping an accurate
migraine diary and making suitable lifestyle changes can have a very positive effect
on the sufferer's quality of life. Some trigger factors are virtually impossible to
avoid, e.g. the weather or emotions, but by limiting the avoidable trigger factors,
the unavoidable ones may have less of an impact on the sufferer.

[edit] Food and Drink

Many migraine sufferers report reduced incidence of migraines due to identifying


and avoiding their individual dietary triggers. However, more studies are needed.

Gluten One food elimination that has proven to reduce or eliminate migraines in a
percentage of patients is gluten. For those with (often undiagnosed) celiac disease
or other forms of gluten sensitivity, migraines may be a symptom of gluten
intolerance. One study found that migraine sufferers were ten times more likely
than the general population to have celiac disease, and that a gluten-free diet
eliminated or reduced migraines in these patients.[23] Another study of 10 patients
with a long history of chronic headaches that had recently worsened or were
resistant to treatment found that all 10 patients were sensitive to gluten. MRI scans
determined that each had inflammation in their central nervous systems caused by
gluten-sensitivity. Seven out of nine of these patients that went on a gluten-free
diet stopped having headaches completely.[24]
MSG Monosodium glutamate (MSG) is frequently reported as a dietary trigger
(12%).[25] In a placebo-controlled trial, MSG in large doses (2.5 grams) taken on an
empty stomach was associated with adverse symptoms including headache more
often than was placebo.[26][27] However another trial found no effect when 3.5g of
MSG was given with food.[28]

Aspartame While some people believe that aspartame triggers migraines, and
anecdotal evidence is present, this has not been medically proven.[29]

Tyramine The National Headache Foundation has a specific list of triggers based on
the tyramine theory, detailing allowed, with caution and avoid triggers.[30]
However, a 2003 review article concluded that there was no scientific evidence for
an effect of tyramine on migraine.[31]

Other A 2005 literature review found that the available information about dietary
trigger factors relies mostly on the subjective assessments of patients.[29] 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, that dehydration[32] deserved more attention, and that some patients
report sensitivity to red wine. Little or no evidence associated notorious suspected
triggers like chocolate, cheese, histamine, tyramine or nitrites with migraines.
However, 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. It must also be
noted that triggers are individual, and what affects one person will not necessarily
affect another. Sufferers are often encouraged to keep a 'migraine diary' to try and
identify common factors that may act as triggers for them. [33]

[edit] Weather

Several studies have found some migraines are triggered by changes in the
weather. One study noted 62% of the subjects thought weather was a factor but
only 51% were sensitive to weather changes.[34] 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:

Temperature mixed with humidity. High humidity plus high or low temperature was
the biggest cause.

Significant changes in weather

Changes in barometric pressure


Another study examined the effects of warm chinook winds on migraines, with
many patients reporting 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 was thought to be an increase in positive ions in the air.[35]

[edit] Pathophysiology

Migraines were once thought to be initiated exclusively by problems with blood


vessels. The vascular theory of migraines is now considered secondary to brain
dysfunction[36] and claimed to have been discredited by others.[37] Trigger points
can be at least part of the cause, and perpetuate most kinds of headaches.[38]

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.

A melanopsin-based receptor has been linked to the association between light


sensitivity and migraine pain.[39]

[edit] Depolarization theory

Animation of cortical spreading depression

A phenomenon known as cortical spreading depression can cause migraines.[40] 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. A study in 2007, using the Positron Emission
Tomography (PET) technique identified the hypothalamus as being critically
involved in the early stages.[41]

[edit] Vascular theory

Migraines can begin when blood vessels in the brain contract and expand
inappropriately. 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.[36][unreliable source?]

When the constriction stops and the blood vessels dilate, they become too wide.
The once solid walls of the 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.[36][unreliable source?]

The vascular theory of migraines is now seen as secondary to brain dysfunction.[36]


[unreliable source?][42]

[edit] Serotonin theory

Serotonin is a type of neurotransmitter, or "communication chemical" which passes


messages between nerve cells. It helps to control mood, pain sensation, sexual
behaviour, sleep, as well as dilation and constriction of the blood vessels among
other things. Low serotonin levels in the brain may lead to a process of constriction
and dilation of the blood vessels which trigger a migraine.[36] Triptans activate
serotonin receptors to stop a migraine attack.[36]

[edit] Neural theory

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.[36]

[edit] Unifying theory

Both vascular and neural influences cause migraines.


stress triggers changes in the brain

these changes cause serotonin to be released

blood vessels constrict and dilate

chemicals including substance P irritate nerves and blood vessels causing


neurogenic inflammation and pain[36]

[edit] Diagnosis

Migraines are underdiagnosed[43] and often misdiagnosed.[44] 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":[45]

5 or more attacks. [For migraine with aura, only two attacks are sufficient for
diagnosis]

4 hours to 3 days in duration.

2 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".

1 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 4 of the 5 criteria are met, then the
positive likelihood ratio for diagnosing migraine is 24.[46]

The presence of either disability, nausea or sensitivity, can diagnose migraine with:
[47]

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 that are characteristic of a
migraine.[citation needed]

[edit] 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 everything from taking certain drugs or nutritional supplements, to
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.[48]
Another reason to pursue these goals is to avoid medication overuse headache
(MOH), otherwise known as rebound headache, which is a common problem among
migraneurs. This is believed to occur in part due to overuse of pain medications,
and can result in chronic daily headache.[49][50]

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.[51] There are many medicines
available to prevent or reduce frequency, duration and severity of migraine attacks.
They may also prevent complications of migraine. Propranolol, atenolol, metoprolol,
flunarizine, sodium valproate, topiramate, and Nortriptyline are some of the
commonly used drugs. But they need to be taken for about 3 months or more.

[edit] Management

Conventional treatment focuses on three areas: trigger avoidance, symptomatic


control, and prophylactic pharmacological drugs. Patients who experience migraines
often find that the recommended migraine treatments are not 100% effective at
preventing migraines, and sometimes may not be effective at all. Pharmacological
treatments are considered effective if they reduce the frequency or severity of
migraine attacks by 50%.[52]

Children and adolescents are often first given drug treatment, but the value of diet
modification should not be overlooked. The simple task of starting a diet journal to
help modify the intake of trigger foods like hot dogs, chocolate, cheese and ice
cream could help alleviate symptoms.[27]

For patients who have been diagnosed with recurring migraines, migraine abortive
medications can be used to treat the attack, and may be more effective if taken
early, losing effectiveness once the attack has begun. Treating the attack at the
onset can often abort it before it becomes serious, and can reduce the near-term
frequency of subsequent attacks.[citation needed]
Although there is a large number of medications to treat migraine, their
effectiveness varies from person to person. What works from one person may not
be effective at all for another one, therefore, early intervention becomes very
important. Dr. Joel Saper, director of the Michigan Headache and Neurological
Institute explains that according to early data untreated headaches can make the
person more vulnerable to pain.[53]

[edit] Analgesics

The first line of treatment is over-the-counter abortive medication.

Some non-steroidal anti-inflammatory drugs (NSAIDs) can effectively alleviate


migraines. In particular:

A randomized controlled trial found that naproxen can abort about one third of
migraine attacks, which was 5% less than the benefit of sumatriptan.[54]

Trials have consistently found that a 1000 mg dose of Aspirin (also called ASA)
could relieve moderate to severe migraine pain, with similar effectiveness to
sumatriptan.[55]

Paracetamol/acetaminophen benefited over half of patients with mild or moderate


migraines in a randomized controlled trial.[56]

Simple analgesics combined with caffeine may help.[57] 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. Excedrin is an
example of an aspirin with caffeine product. Caffeine is recognized by the U.S. Food
and Drug Administration as an Over The Counter Drug (OTC) treatment for migraine
when compounded with aspirin and paracetamol.[58] Even by itself, caffeine can be
helpful during an attack,[59][60] despite the fact that in general migraine-sufferers
are advised to limit their caffeine intake.[60]

Patients themselves often start off with paracetamol, aspirin, ibuprofen, or other
simple analgesics that are useful for tension headaches. OTC drugs may provide
some relief, although they are typically not effective for most sufferers.

In all, the U.S. Food and Drug Administration has approved three OTC products
specifically for migraine: Excedrin Migraine, Advil Migraine, and Motrin Migraine
Pain. Excedrin Migraine, as mentioned above, is a combination of aspirin,
acetaminophen, and caffeine. Both Advil Migraine and Motrin Migraine Pain are
straight NSAIDs, with ibuprofen as the only active ingredient.[61]

[edit] Analgesics combined with antiemetics

Antiemetics by mouth may help relieve symptoms of nausea and help prevent
vomiting, which can diminish the effectiveness of orally taken analgesia. In addition
some antiemetics such as metoclopramide are prokinetics and help gastric
emptying which is often impaired during episodes of migraine. In the UK, there are
three combination antiemetic and analgesic preparations available: MigraMax
(aspirin with metoclopramide), Migraleve (paracetamol/codeine for analgesia, with
buclizine as the antiemetic) and paracetamol/metoclopramide (Paramax in UK).[62]
The earlier these drugs are taken in the attack, the better their effect.

Some patients find relief from taking other sedative antihistamines which have anti-
nausea properties, such as Benadryl which in the US contains diphenhydramine (but
a different non-sedative product in the UK).

[edit] Serotonin agonists

Main article: triptans

Sumatriptan and related selective serotonin receptor agonists are excellent for
severe migraines or those that do not respond to NSAIDs[54] or other over-the-
counter drugs.[56] Triptans are a mid-line treatment suitable for many sufferers of
typical migraines. They may not work for atypical or unusually severe migraines,
transformed migraines, or status (continuous) migraines.

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 clinical consensus.[52]

[edit] Antidepressants

Tricyclic antidepressants have been long established as highly efficacious


prophylactic treatments.[52] These drugs, however, may give rise to undesirable
side effects, such as insomnia, sedation or sexual dysfunction. SSRIs
antidepressants are less established than tricyclics for migraines prophylaxis.
Despite the absence of FDA approval for migraine treatment, antidepressants are
widely prescribed.[52] In addition to tricyclics and SSRIs, the anti-depressant
nefazodone may also be beneficial in the prophylaxis of migraines due to its
antagonistic effects on the 5-HT2A[63] and 5-HT2C receptors[64][65] 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.[52]

[edit] Ergot alkaloids

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). Ergot drugs
themselves can be so nauseating it is advisable for the sufferer to have something
at hand to counteract this effect when first using this drug. 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 and Romania (Cofedol).
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.

[edit] Steroids

Based on a recent meta analysis a single dose of IV dexamethasone, when added to


standard treatment, is associated with a 26% decrease in headache recurrence.[66]

[edit] Other agents

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), paracetamol (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.

Amidrine, Duradrin, and Midrin is a combination of acetaminophen,


dichloralphenazone, and isometheptene often prescribed for migraine headaches.
Some studies have recently shown that these drugs may work better than
sumatriptan for treating migraines.[67]

Antiemetics may need to be given by suppository or injection where vomiting


dominates the symptoms.

Recently it has been found that calcitonin gene related peptides (CGRPs) play a role
in the pathogenesis of the pain associated with migraine as triptans also decrease
its 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.[68]

Merck Corp is developing a new drug called Telcagepant which is intended to


relieve pain without causing vasoconstriction (narrowing of blood vessels) as
current medications such as triptans do. Telcagepant would be a safe therapy for
migraine suffers with risk factors for cardiovascular disease.[69]

[edit] Status migrainosus

Status migrainosus is characterized by migraine lasting more than 72 hours, with


not more than four hours of relief during that period. It is generally understood that
status migrainosus has been refractory to usual outpatient management upon
presentation.

Treatment of status migrainosus consists of managing comorbidities (i.e., correcting


fluid and electrolyte abnormalities resulting from anorexia and nausea/vomiting
often accompanying status migr.), and usually administering parenteral medication
to "break" (abort) the headache.

Although the literature is full of many case reports concerning treatment of status
migrainosus, first line therapy consists of intravenous fluids, metoclopramide, and
triptans or DHE.[70]

[edit] Herbal treatment

The herbal supplement feverfew (more commonly used for migraine prevention, see
below) is marketed by the GelStat Corporation as an OTC migraine abortive,
administered sublingually (under the tongue) in a mixture with ginger.[71] An open-
label study (funded by GelStat) found some tentative evidence of the treatment's
effectiveness,[72] but no scientifically sound study has been done. Cannabis, in
addition to prevention, is also known to relieve pain during the onset of a migraine.
[73]

[edit] Cryotherapy and Thermotherapy

During a migraine the blood vessels in the head tend to dilate as a result of many
chemical changes in the body. Some believe that these vessels become swollen
with blood and thus put pressure on the nerves surrounding the vessels. This
pressure causes the nerve to send pain signals to the brain, resulting in the
debilitating pain most often associated with migraines. Both heat and cooling
therapies uses temperature manipulation to reduce migraine pain. The use of
cooling therapy (cyrotherapy) is believed to cause the swollen blood vessels to
constrict, thus reducing pulsating migraine pain. The use of thermotherapy, on the
other hand, causes blood flow to increase which, in turn, increases the amount of
oxygen and nutrients that are sent to the pain site in the brain. A recent study
published in the Archives of Family Medicine revealed that pressure, heat and cold
can help to relieve headache pain.[74]

[edit] Exercise
Being a neurological syndrome, tense nerves are normally one of the causes that
exacerbate migraine symptoms. Regular exercise is one way to calm nerves.[75]
However, this option may be effective for some people but not for others as in some
cases it may actually be the cause of migraine. According to Lawrence Newman,
MD, director of the Headache Institute at St. Luke's-Roosevelt Hospital Center in
New York migraine sufferers have a heightened neurological system which implies
that they have a tendency to develop migraine when anything is out of the ordinary.
Therefore, such people establish a regular exercise routine. Exercise can benefit
them as it releases endorphins, which are the body's natural painkillers, therefore,
they can lessen the frequency or severity of migraines.[76]

[edit] Comparative studies

Regarding comparative effectiveness of these drugs used to abort migraine attacks,


a 2004 placebo-controlled trial[77] 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 and all other
migraine-related symptoms. [Note that 50 mg of sumatriptan is not a commonly
prescribed full dose (100 mg), so would be expected to not be fully comparable.]

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.[54]

Recently the combination of sumatriptan 85 mg and naproxen sodium 500 mg was


demonstrated to be effective and well tolerated in an early intervention paradigm
for the acute treatment of migraine. Significant pain-free responses in favor of
sumatriptan/naproxen were demonstrated as early as 30 minutes, maintained at 1
hour, and sustained from 2 to 24 hours. At 2 and 4 hours, sumatriptan/naproxen
provided significantly lower rates of traditional migraine-associated symptoms
(nausea, photophobia, and phonophobia) and nontraditional migraine-associated
symptoms (neck pain/discomfort and sinus pain/pressure).[78] An initial study by
Griffith University on Vitamin B supplements for both prevention and management
has yielded promising results.[79]

[edit] Medication overuse headaches

Researchers have learned that the brain's biology can change due to the pain and
the medications used to treat it.[53] Furthermore, the constant use of over-the-
counter or prescription painkillers -two to three days a week after a long period of
time- may cause medication-overuse headaches, also known as rebound
headaches. Such headache may be recognized by its shifting pattern where the
patient experiences migraine-like characteristics and then the symptoms of a
tension-type headache. Such shift can occur during the same day.
Substantial evidence has shown that triptans, ergotamines, simple analgesics,
opioids, butalbital compounds, vicodin as well as other compounds may cause
Medication Overuse Headaches, MOH. To stop MOH, it is necessary to discontinue
the medication causing the MOH. However, withdrawal symptoms will be
experienced from two to ten days including withdrawal headache, tachycardia,
vomiting, anxiety, arterial hypotension, sleep disorders, nervousness and
restlessness.[80]

[edit] Prognosis

[edit] Cardiovascular risks

The risk of stroke may be increased two- to threefold in migraine sufferers. Young
adult sufferers and women using hormonal contraception appear to be at particular
risk.[81] 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.[81][82] (Note: Women
who experience auras and also take oral contraceptives have an even higher risk of
stroke).[4] Migraine sufferers seem to be at risk for both thrombotic and
hemorrhagic stroke as well as transient ischemic attacks.[83] 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.[82][84]

[edit] 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
Age-Gender Incidence

Migraine is an extremely common condition which will affect 12–28% of people at


some point in their lives.[1] 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.[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.[85] There is
then a rapid growth in incidence amongst girls occurring after puberty,[86][87][88]
which continues throughout early adult life.[89] By early middle age, around 25% of
women experience a migraine at least once a year, compared with fewer than 10%
of men.[1][90] 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%.[1][90]

At all ages, migraine without aura is more common than migraine with aura, with a
ratio of between 1.5:1 and 2:1.[91][92] Incidence figures show that the excess of
migraine seen in women of reproductive age is mainly due to migraine without
aura.[91] Thus in pre-pubertal and post-menopausal populations, migraine with
aura is somewhat more common than amongst 15–50 year olds.[89][93]

There is a strong relationship between age, gender and type of migraine.[94]


Geographical differences in migraine prevalence are not marked. Studies in Asia
and South America suggest that the rates there are relatively low,[95][96] but they
do not fall outside the range of values seen in European and North American
studies.[1][90]

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.[97]

[edit] History

The Head Ache. George Cruikshank (1819)

Trepanation, the deliberate and (usually) non-fatal drilling of holes into a skull, was
practiced 9,000 years ago and earlier.[98] Some scholars have (controversially)
speculated that this drastic procedure might have been a migraine treatment,
based on cave paintings[99] and on the fact that trepanation was a historical
migraine treatment in 17th-century Europe.[98][100] An early written description
consistent with migraines is contained in the Ebers papyrus, written around 1200
BC in ancient Egypt.[98]

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 with
treatment ranging from hot irons to bloodletting and even witchcraft[citation
needed]. 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.

[edit] Society and culture

[edit] Economic impact

This section does not cite any references or sources.


Please help improve this article by adding citations to reliable sources.
Unsourced material may be challenged and removed. (August 2008)
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. It has been
estimated to be the most costly neurological disorder in the European Community,
costing more than €27 billion per year.[101] Medical costs per migraine sufferer
(mostly physician and emergency room visits) averaged $107 USD over six months
in one 1988 study,[citation needed] 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.[citation needed]

[edit] See also

Retinal migraine
Carotidynia

Headache (journal)

[edit] Organizations [edit] Other


The City of London Migraine Clinic Migraine (book), a book by neurologist
Migraine Action, a charity dedicated to Oliver Sacks based mainly on his case
individuals affected by migraine studies and geared toward the layman
Migraine Aura Foundation, a German not- Migraine boy, a comic strip featuring a
for-profit organization boy with chronic migraine
Migraine Trust, a British charity Onze Danses Pour Combattre la Migraine
(Eleven Dances for Fighting Migraine), an
album by Belgian band Aksak Maboul
Treatments for chronic headaches
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[edit] References

[edit] Migraine triggers

Federation of American Societies for Experimental Biology [FASEB] [1995]. Analysis


of adverse reactions to monosodium glutamate (MSG). Bethesda, MD: Life Sciences
Research Office, FASEB.

Pashley, H. (2009). About Migraine Triggers. [5]

Radnitz, C. L. (1990). Food-triggered migraine: a critical review. Annals of


Behavioral Medicine, 12, 51–65.

Ravishankar, K (2006). 'Hair wash' or 'Head bath' triggering migraine - observations


in 94 Indian patients". Cephalagia 26 (11): 1330–1334. ISSN 0333-1024.

[edit] Treatment
Pearce, J.M.S. (1994). "Headache. Neurological Management series". Journal of
Neurology Neurosurgery and Psychiatry 57: 134–144.

Mayo Clinic Staff. (2005). Migraine Headache. Retrieved August 14, 2005

Cathy Wong, ND. (2005). Migraine Elimination Diet Retrieved August 14, 2005

Treatment Articles (2005). Butterbur, Co-enzyme Q-10, Melatonin, Folic Acid

Buchholz, D. (2002) Heal your headache: The 1-2-3 Program, New York: Workman
Publishing, ISBN 0-7611-2566-3

Livingstone, I. and Novak, D. (2003) Breaking the Headache Cycle, New York: Henry
Holt and Co. ISBN 0-8050-7221-7

Izecksohn L, and Izecksohn C. . Fluids' Hypertension Syndromes, ISBN 978-85-


906664-0-0.

[edit] Triptans

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.

[edit] General

Sacks, Oliver (1999) Migraine, Vintage ISBN 0-520-08223-0

Relouzat, Raoul & Thiollet, Jean-Pierre, Vaincre la migraine, Anagramme, 2006 ISBN
2-35035046

Blondin, Betsy, (2008) "Migraine Expressions: A Creative Journey through Life with
Migraine, WordMetro Press ISBN 0-615-20197-0

[edit] Economic impact

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.

[edit] Clinical picture


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.

[edit] External links

Migraine at the Open Directory Project

[edit] General information

Migraine Information from the US National Institute of Neurological Disorders and


Stroke

Diagnostic criteriaPDF (1.21 MB)

[edit] Organizations

World Headache Alliance

[show]
v•d•e
Pathology of the nervous system, primarily CNS (G04–G47, 323–349)

Encephalitis (Viral encephalitis, Herpesviral encephalitis) ·


Brain
Cavernous sinus thrombosis · Brain abscess (Amoebic)

Inflamm Spinal Myelitis: Poliomyelitis · Demyelinating disease (Transverse


ation cord myelitis) · Tropical spastic paraparesis · Epidural abscess

Both/eith Encephalomyelitis (Acute disseminated)


er Meningoencephalitis

Brain/ Degenerati Extrapyramidal Basal ganglia disease: Parkinsonism (PD,


encepha ve and Postencephalitic, NMS) · PKAN ·
lopathy movement Tauopathy (PSP) · Striatonigral
disorders 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

Tauopathy: Alzheimer's (Early-onset) ·


Frontotemporal
dementia/Frontotemporal lobar
Dementia
degeneration (Pick's, Dementia with
Lewy bodies)
Multi-infarct dementia

Mitochondrial
Leigh's
disease

autoimmune (Multiple sclerosis, Neuromyelitis optica,


Schilder's disease) · hereditary (Adrenoleukodystrophy,
Demyelinat
Alexander, Canavan, Krabbe, ML, PMD, VWM, MFC,
ing
CAMFAK syndrome) · Central pontine myelinolysis ·
Marchiafava-Bignami disease · Alpers' disease

Seizure/epile Focal · Generalised · Status epilepticus ·


psy Myoclonic epilepsy

Migraine (Familial hemiplegic) · Cluster ·


Headache
Tension

TIA (Amaurosis fugax, Transient global


amnesia)
Cerebrovasc
Episodic/ Stroke (MCA, ACA, PCA, Foville's, Millard-
ular
paroxysmal Gubler, Lateral medullary, Weber's, Lacunar
stroke)

Insomnia · Hypersomnia · Sleep apnea


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

Intracranial hypertension (Hydrocephalus/NPH, Idiopathic


CSF intracranial hypertension) · Cerebral edema · Intracranial
hypotension

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


encephalopathy

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

SA Friedreich's ataxia · Ataxia telangiectasia

UMN only: PLS · PP · HSP


Both/eit Degenerat
LMN only: PMA · PBP (Fazio-Londe, Infantile progressive
her ive MN
bulbar palsy) · SMA (SMN-linked, Kennedy disease,
D
SMAX2, DSMA1)
both: ALS

M: anat(s,m,p,4,e,b,d,c,a,f,l,g noco(m,d,e,h,v,s)/cong/tu proc,drug(N1A/2AB/C/3


C )/phys/devp/cell mr,sysi/epon,injr /4/7A/B/C/D)
N
S

[show]
v•d•e
CNS disease: Headache (G43-G44, 339, 346)

ICHD
Migraine (Familial hemiplegic) · Retinal migraine
1

ICHD
Tension
2
Prima
ry
ICHD
Cluster · Chronic paroxysmal hemicrania
3

ICHD Hemicrania continua · Thunderclap headache · Coital cephalalgia ·


4 New daily persistent headache · Hypnic headache

ICHD
Seco Ictal headache · Post dural puncture headache
7
ndary
ICHD
Hangover · Medication overuse headache
8
Trigeminal neuralgia · Occipital neuralgia · External compression
ICHD
headache · Cold-stimulus headache · Optic neuritis · Postherpetic
13
neuralgia · Tolosa-Hunt syndrome

Other Vascular

M: anat(s,m,p,4,e,b,d,c,a,f,l,g noco(m,d,e,h,v,s)/cong/tu proc,drug(N1A/2AB/C/3


C )/phys/devp/cell mr,sysi/epon,injr /4/7A/B/C/D)
N
S

[show]
v•d•e
Antimigraine preparations (N02C)

Ergot Dihydroergotamine • Ergotamine •


alkaloids Methysergide • Lisuride

Triptans (Almotriptan, Avitriptan,


Serotonin
5-HT1 Eletriptan, Frovatriptan, Naratriptan,
Analgesic/a modulators
agonists Rizatriptan, Sumatriptan,
bortive
Zolmitriptan) Alniditan

Other Dotarizine

Other Paracetamol# • Amidrine

Beta blocker Propranolol# • Timolol

CCB verapamil

corticosteroid flumedroxone

Prevention monosaccharide topiramate


of
migraines adrenergic
Clonidine
agonist

tricyclic
amitriptyline • nortriptyline • imipramine
antidepressant

anticonvulsant valproate • carbamazepine • oxcarbazepine


piperidine (Pizotifen) • adrenochrome (Iprazochrome) •
Ungrouped phenothiazine (Dimetotiazine) • benzoxepin (Oxetorone) •
piperazine (Lomerizine) • azepine (Telcagepant)

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

M: anat(s,m,p,4,e,b,d,c,a,f,l,g noco(m,d,e,h,v,s)/cong/tu proc,drug(N1A/2AB/C/3


C )/phys/devp/cell mr,sysi/epon,injr /4/7A/B/C/D)
N
S
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