Professional Documents
Culture Documents
Migraine
This article is about the disorder. For other uses, see Migraine (disambiguation).
Migraine
Classification and external resources
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]
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
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]
Migraine without aura, or common migraine, involves migraine headaches that are
not accompanied by an aura (visual disturbance, see below).
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 postdrome.
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.
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.
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
The MedlinePlus Medical Encyclopedia, for example, offers the following list of
migraine triggers:
Alcohol
Allergic reactions
Bright lights
Changes in hormone levels (which can occur during a woman's menstrual cycle or
with the use of birth control pills)
Exercise
Loud noises
Missed meals
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.
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.
[edit] Pathophysiology
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.
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?]
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] Diagnosis
5 or more attacks. [For migraine with aura, only two attacks are sufficient for
diagnosis]
Pulsating;
The presence of either disability, nausea or sensitivity, can diagnose migraine with:
[47]
sensitivity of 81%
specificity of 75%
[edit] Prevention
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
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
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]
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]
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).
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
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
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]
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]
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]
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]
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]
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
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
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]
[edit] History
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."
Retinal migraine
Carotidynia
Headache (journal)
^ a b c d e f Stovner LJ, Zwart JA, Hagen K, Terwindt GM, Pascual J (April 2006).
"Epidemiology of headache in Europe". European Journal of Neurology 13 (4): 333–
45. doi:10.1111/j.1468-1331.2006.01184.x. PMID 16643310.
^ "Advances in Migraine Prophylaxis: Current State of the Art and Future Prospects"
(PDF). National Headache Foundation (CME monograph).
http://www.headaches.org/pdf/botoxcme.pdf. Retrieved 2007-06-25.
^ Ogilvie AD, Russell MB, Dhall P, et al. (January 1998). "Altered allelic distributions
of the serotonin transporter gene in migraine without aura and migraine with aura".
Cephalalgia 18 (1): 23–6. doi:10.1046/j.1468-2982.1998.1801023.x. PMID 9601620.
^ Gervil M, Ulrich V, Kaprio J, Olesen J, Russell MB (September 1999). "The relative
role of genetic and environmental factors in migraine without aura". Neurology 53
(5): 995–9. PMID 10496258. http://www.neurology.org/cgi/pmidlookup?
view=long&pmid=10496258.
^ Ulrich V, Gervil M, Kyvik KO, Olesen J, Russell MB (March 1999). "The inheritance
of migraine with aura estimated by means of structural equation modelling". Journal
of Medical Genetics 36 (3): 225–7. PMID 10204850. PMC 1734315.
http://jmg.bmj.com/cgi/pmidlookup?view=long&pmid=10204850.
^ Lay CL, Broner SW (May 2009). "Migraine in women". Neurologic Clinics 27 (2):
503–11. doi:10.1016/j.ncl.2009.01.002. PMID 19289228.
^ [1] Dahlem MA, Engelmann R, Löwel S, Müller SC., Does the migraine aura reflect
cortical organization? Eur J Neurosci. 12:767-70, 2000.
^ Yang WH, Drouin MA, Herbert M, Mao Y, Karsh J (June 1997). "The monosodium
glutamate symptom complex: assessment in a double-blind, placebo-controlled,
randomized study". The Journal of Allergy and Clinical Immunology 99 (6 Pt 1): 757–
62. doi:10.1016/S0091-6749(97)80008-5. PMID 9215242.
^ a b Millichap JG, Yee MM (January 2003). "The diet factor in pediatric and
adolescent migraine". Pediatric Neurology 28 (1): 9–15. doi:10.1016/S0887-
8994(02)00466-6. PMID 12657413.
^ Prince PB, Rapoport AM, Sheftell FD, Tepper SJ, Bigal ME (June 2004). "The effect
of weather on headache". Headache 44 (6): 596–602. doi:10.1111/j.1526-
4610.2004.446008.x. PMID 15186304.
^ Cooke LJ, Rose MS, Becker WJ (January 2000). "Chinook winds and migraine
headache". Neurology 54 (2): 302–7. PMID 10668687.
http://www.neurology.org/cgi/pmidlookup?view=long&pmid=10668687.
^ a b c d e f g h Alexander Mauskop; Fox, Barry (2001). What Your Doctor May Not
Tell You About(TM): Migraines : The Breakthrough Program That Can Help End Your
Pain. New York: Warner Books. ISBN 0-446-67826-0. [page needed]
^ Trigger Point Therapy for Headaches & Migraines, DeLaune, Valerie (New
Harbinger: 2008) [2]
^ Noseda R, Kainz V, Jakubowski M, et al. (February 2010). "A neural mechanism for
exacerbation of headache by light". Nature Neuroscience 13 (2): 239–45.
doi:10.1038/nn.2475. PMID 20062053. Lay summary – ScienceNOW (January 11,
2010).
^ Welch KM; Welch, K.M.A. (November 1993). "Drug therapy of migraine". The New
England Journal of Medicine 329 (20): 1476–83.
doi:10.1056/NEJM199311113292008. PMID 8105379.
^ Lipton RB, Stewart WF, Celentano DD, Reed ML (June 1992). "Undiagnosed
migraine headaches. A comparison of symptom-based and reported physician
diagnosis". Archives of Internal Medicine 152 (6): 1273–8.
doi:10.1001/archinte.152.6.1273. PMID 1599358.
^ van der Kuy PH, Lohman JJ (May 2002). "A quantification of the placebo response
in migraine prophylaxis". Cephalalgia 22 (4): 265–70. doi:10.1046/j.1468-
2982.2002.00363.x. PMID 12100088.
^ a b Lipton RB, Baggish JS, Stewart WF, Codispoti JR, Fu M (2000). "Efficacy and
safety of acetaminophen in the treatment of migraine: results of a randomized,
double-blind, placebo-controlled, population-based study". Archives of Internal
Medicine 160 (22): 3486–92. doi:10.1001/archinte.160.22.3486. PMID 11112243.
http://archinte.ama-assn.org/cgi/pmidlookup?view=long&pmid=11112243.
^ Goldstein J, Hoffman HD, Armellino JJ, et al. (September 1999). "Treatment of
severe, disabling migraine attacks in an over-the-counter population of migraine
sufferers: results from three randomized, placebo-controlled studies of the
combination of acetaminophen, aspirin, and caffeine". Cephalalgia 19 (7): 684–91.
doi:10.1046/j.1468-2982.1999.019007684.x. PMID 10524663.
^ "4.7.4.1 Treatment of acute migraine". British National Formulary (55 ed.). March
2008. pp. 239.
^ Saper JR, Lake AE, Tepper SJ.(2001) "Nefazodone for chronic daily headache
prophylaxis: an open-label study." Headache. 2001 May;41(5):465-74.PMID:
11380644
^ Freitag, Frederick G., Cady, Roger, DiSerio, Frank, Elkind, Arthur, Gallagher, R.
Michael, Goldstein, Jerome, Klapper, Jack A., Rapoport, Alan M., Sadowsky, Carl,
Saper, Joel R. & Smith, Timothy R. "Comparative Study of a Combination of
Isometheptene Mucate, Dichloralphenazone With Acetaminophen and Sumatriptan
Succinate in the Treatment of Migraine." Headache: The Journal of Head and Face
Pain 41 (4), 391-398.
^ Tepper SJ, Stillman MJ (September 2008). "Clinical and preclinical rationale for
CGRP-receptor antagonists in the treatment of migraine". Headache 48 (8): 1259–
68. doi:10.1111/j.1526-4610.2008.01214.x. PMID 18808506.
^ UpToDate.
^ Russo, Ethan (1998). Cannabis for migraine treatment: the once and future
prescription? An historical and scientific review. Pain 76:3-8.
^ a b Kurth, T; Kurth T, Gaziano JM, Cook NR, Logroscino G, Diener HC, Buring JE
(2006). "Migraine and risk of cardiovascular disease in women". JAMA 296 (3): 283–
91. doi:10.1001/jama.296.3.283. PMID 16849661.
^ Becker C, Brobert GP, Almqvist PM, Johansson S, Jick SS, Meier CR. Migraine and
the risk of stroke, TIA, or death in the UK (CME). Headache. 2007;47(10):1374–84.
PMID 18052947
^ Waters WE, Campbell MJ, Elwood PC. Migraine, headache, and survival in women.
BMJ (Clin Res Ed). 1983;287:1442–1443. PMID 6416449
^ Linet MS, Stewart WF, Celentano DD, Ziegler D, Sprecher M (1989). "An
epidemiologic study of headache among adolescents and young adults". JAMA 261
(15): e1197. doi:10.1001/jama.261.15.2211. PMID 2926969.
^ a b Rasmussen BK, Olesen J (1992). "Migraine with aura and migraine without
aura: an epidemiological study". Cephalalgia 12 (4): 221–8; discussion 186.
doi:10.1046/j.1468-2982.1992.1204221.x. PMID 1525797.
^ Steiner TJ, Scher AI, Stewart WF, Kolodner K, Liberman J, Lipton RB (2003). "The
prevalence and disability burden of adult migraine in England and their
relationships to age, gender and ethnicity". Cephalalgia 23 (7): 519–27.
doi:10.1046/j.1468-2982.2003.00568.x. PMID 12950377.
^ Bigal ME, Liberman JN, Lipton RB (2006). "Age-dependent prevalence and clinical
features of migraine". Neurology 67 (2): 246–51.
doi:10.1212/01.wnl.0000225186.76323.69. PMID 16864816.
^ Stewart WF, Linet MS, Celentano DD, Van Natta M, Ziegler D (1991). "Age- and
sex-specific incidence rates of migraine with and without visual aura". Am. J.
Epidemiol. 134 (10): 1111–20. PMID 1746521.
^ Brothwell, Don R. (1963). Digging up Bones; the Excavation, Treatment and Study
of Human Skeletal Remains. London: British Museum (Natural History). pp. 126.
ISBN 0565007041. OCLC 14615536.
[edit] References
[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
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
[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.
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, 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.
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
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
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.
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] Organizations
[show]
v•d•e
Pathology of the nervous system, primarily CNS (G04–G47, 323–349)
Mitochondrial
Leigh's
disease
Spinal
cord/ Syringomyelia · Syringobulbia · Morvan's syndrome · Vascular
myelopa myelopathy (Foix-Alajouanine syndrome) · Spinal cord compression
thy
[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
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
[show]
v•d•e
Antimigraine preparations (N02C)
Other Dotarizine
CCB verapamil
corticosteroid flumedroxone
tricyclic
amitriptyline • nortriptyline • imipramine
antidepressant
#WHO-EM. ‡Withdrawn from market. Clinical trials: †Phase III. §Never to phase III
Hidden categories: All pages needing cleanup | Wikipedia articles needing page
number citations from September 2010 | All articles with dead external links |
Articles with dead external links from September 2010 | Pages with DOIs inactive
since 2010 | Articles needing additional references from September 2009 | All
articles needing additional references | All articles with unsourced statements |
Articles with unsourced statements from September 2009 | All articles lacking
reliable references | Articles lacking reliable references from March 2009 | Articles
with unsourced statements from April 2008 | Articles with unsourced statements
from September 2007 | Articles needing additional references from August 2008 |
Articles with unsourced statements from February 2007 | Articles with unsourced
statements from July 2010
Personal tools
Namespaces
Article
Discussion
Variants
Views
Read
Edit
View history
Actions
Search
Top of Form
Special:Search
Search
Bottom of Form
Navigation
Main page
Contents
Featured content
Current events
Random article
Donate
Interaction
Help
About Wikipedia
Community portal
Recent changes
Contact Wikipedia
Toolbox
Related changes
Upload file
Special pages
Permanent link
Create a book
Download as PDF
Printable version
Languages
العربية
বাংলা
Bosanski
Català
Česky
Cymraeg
Dansk
Deutsch
ް ަދިވެހިބ
ސ
Eesti
Ελληνικά
Español
فارسی
Français
한국어
िहनदी
Hrvatski
Ido
Íslenska
Italiano
עברית
ಕನನಡ
Kurdî
Lietuvių
Magyar
മലയാളം
Nederlands
日本語
Norsk (bokmål)
Norsk (nynorsk)
Polski
Português
Русский
Shqip
Simple English
Slovenčina
Slovenščina
Српски / Srpski
Suomi
Svenska
தமிழ்
ไทย
Türkçe
Українська
Tiếng Việt
Žemaitėška
中文
This page was last modified on 18 November 2010 at 14:40.
Contact us
Privacy policy
About Wikipedia
Disclaimers