Share on Facebook Share on Twitter Email
Answers.com

migraine

 
Medical Encyclopedia: Migraine Headache

Definition

Migraine is a type of headache marked by severe head pain lasting several hours or more.

Description

Migraine is an intense, often debilitating type of headache. Migraines affect as many as 24 million people in the United States, and are responsible for billions of dollars in lost work, poor job performance, and direct medical costs. Approximately 18% of women and 6% of men experience at least one migraine attack per year. More than three million women and one million men have one or more severe headaches every month. Migraines often begin in adolescence, and are rare after age 60.

Two types of migraine are recognized. Eighty percent of migraine sufferers experience "migraine without aura," formerly called common migraine. In "migraine with aura," formerly called classic migraine, pain is preceded or accompanied by visual or other sensory disturbances, including hallucinations, partial obstruction of the visual field, numbness or tingling, or a feeling of heaviness. Symptoms are often most prominent on one side of the body, and may begin as early as 72 hours before the onset of pain.

— Kim A. Sharp, MLn



Search unanswered questions...
Enter a question here...
Search: All sources Community Q&A Reference topics
Dictionary: mi·graine   ('grān') pronunciation
Top
n.

A severe recurring headache, usually affecting only one side of the head, characterized by sharp pain and often accompanied by nausea, vomiting, and visual disturbances. Also called megrim.

[Middle English, from Old French, from Late Latin hēmicrānia, from Greek hēmikrāniā : hēmi-, hemi- + krānion, head.]

migrainous mi·grain'ous adj.

World of the Body: migraine
Top

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

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

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

The cause and incidence of migraine

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

Migraine aura — the flashing lights and zigzags

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

The pain of migraine

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

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

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

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

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

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

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

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

— Peter J. Goadsby

Bibliography

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

See also headache.

Alternative Medicine Encyclopedia: Migraine Headache
Top

Definition

Migraine is a type of headache marked by severe head pain lasting several hours or more.

Description

Migraine is an intense and often debilitating type of headache. The term migraine is derived from the Greek word hemikrania, meaning "half the head," because the classic migraine headache affects only one side of the person's head. Migraines affect as many as 24 million people in the United States, and are responsible for billions of dollars in lost work, poor job performance, and direct medical costs. Approximately 18% of women and 6% of men experience at least one migraine attack per year. Currently, one American in 11 now suffers from migraines, more than three times as many are women, with most of them being between the ages of 30 and 49. Migraines often begin in adolescence, and are rare after age 60.

Two types of migraine are recognized. Eighty percent of migraine sufferers experience "migraine without aura" (common migraine). In "migraine with aura," or classic migraine, the pain is preceded or accompanied by visual or other sensory disturbances, including hallucinations, partial obstruction of the visual field, numbness or tingling, or a feeling of heaviness. Symptoms are often most prominent on one side of the head or body, and may begin as early as 72 hours before the onset of pain.

Causes & Symptoms

Causes

The physiological basis of migraine has proved difficult to uncover. There are a multitude of potential triggers for a migraine attack, and recognizing one's own set of triggers is the key to prevention.

PHYSIOLOGY. The most widely accepted hypothesis of migraine suggests that a migraine attack is precipitated when pain-sensing nerve cells in the brain (called nociceptors) release chemicals called neuropeptides. At least one of the neurotransmitters, substance P, increases the pain sensitivity of nearby nociceptors. This process is called sensitization.

Other neuropeptides act on the smooth muscle surrounding cranial blood vessels. This smooth muscle regulates blood flow in the brain by relaxing or contracting, thus dilating (enlarging) or constricting the enclosed blood vessels. At the onset of a migraine headache, neuropeptides are thought to cause muscle relaxation, allowing vessel dilation and increased blood flow. Other neuropeptides increase the leakiness of cranial vessels, allowing fluid leak, and promote inflammation and tissue swelling. The pain of migraine is thought to result from this combination of increased pain sensitivity, tissue and vessel swelling, and inflammation. The aura seen during a migraine may be related to constriction in the blood vessels that dilate in the headache phase.

GENETICS. Susceptibility to some types of migraine is inherited. A child of a migraine sufferer has as much as a 50% chance of developing migraines. If both parents are affected, the chance rises to 70%. In 2002, a team of Australian researchers identified a region on human chromosome 1 that influences susceptibility to migraine. It is likely that more than one gene is involved in the inherited forms of the disorder. Many cases of migraine, however, have no obvious familial basis. It is likely that the genes that are involved set the stage for migraine, and that full development requires environmental influences, as well.

Two groups of Italian researchers have recently identified two loci on human chromosomes 1 and 14 respectively that are linked to migraine headaches. The locus on chromosome 1q23 has been linked to familial hemiplegic migraine type 2, while the locus on chromosome 14q21 is associated with migraine without aura.

TRIGGERS. A wide variety of foods, drugs, environmental cues, and personal events are known to trigger migraines. It is not known how most triggers set off the events of migraine, nor why individual migraine sufferers are affected by particular triggers but not others.

Common food triggers include:

  • alcohol
  • caffeine products, as well as caffeine withdrawal
  • chocolate
  • foods with an extremely high sugar content
  • dairy products
  • fermented or pickled foods
  • citrus fruits
  • nuts
  • processed foods, especially those containing nitrites, sulfites, or monosodium glutamate (MSG)

Environmental and event-related triggers include:

  • stress or time pressure
  • menstrual periods, menopause
  • sleep changes or disturbances, including oversleeping
  • prolonged overexertion or uncomfortable posture
  • hunger or fasting
  • odors, smoke, or perfume
  • strong glare or flashing lights

Drugs that may trigger migraine include:

  • oral contraceptives
  • estrogen replacement therapy
  • Theophylline
  • Reserpine
  • Nifedipine
  • Indomethicin
  • Cimetidine
  • oversuse of decongestants
  • analgesic overuse
  • benzodiazepine withdrawal

Symptoms

Migraine without aura may be preceded by elevations in mood or energy level for up to 24 hours before the attack. Other pre-migraine symptoms may include fatigue, depression, and excessive yawning.

Aura most often begins with shimmering, jagged arcs of white or colored light progressing over the visual field in the course of 10–20 minutes. This may be preceded or replaced by dark areas or other visual disturbances. Numbness and tingling are common, especially of the face and hands. These sensations may spread, and may be accompanied by a sensation of weakness or heaviness in the affected limb.

Migraine pain is often present only on one side of the head, although it may involve both, or switch sides during attacks. The pain is usually throbbing, and may range from mild to incapacitating. It is often accompanied by nausea or vomiting, painful sensitivity to light and sound, and intolerance of food or odors. Blurred vision is also common.

The pain tends to intensify over the first 30 minutes to several hours, and may last from several hours to a day, or longer. Afterward, the affected person is usually weary, and sensitive to sudden head movements.

Diagnosis

Ideally, migraine is diagnosed by a careful medical history. Unfortunately, migraine is underdiagnosed because many doctors tend to minimize its symptoms as "just a headache." According to a 2003 study, 64% of migraine patients in the United Kingdom and 77% of those in the United States never receive a correct medical diagnosis for their headaches.

So far, laboratory tests and such imaging studies as computed tomography (CT scan) or magnetic resonance imaging (MRI) scans have not been useful for identifying migraine. However, these tests may be necessary to rule out a brain tumor or other structural causes of migraine headache in some patients.

Treatment

At the onset of symptoms, the migraine sufferer should seek out a quiet, dark room and attempt to sleep. Placing a cold, damp cloth or a cold pack on the fore-head may help. Additionally, tying a headband tightly around the head can relieve migraines.

Migraine headaches are often linked with food allergies or intolerances. Identification and elimination of the offending food or foods can decrease the frequency of migraines and/or alleviate these headaches altogether.

Alternative treatments for migraine include:

  • Acupressure. Pressing on the Gates of Consciousness (GB 20) points can relieve migraine.
  • Acupuncture. A National Institutes of Health (NIH) panel concluded that acupuncture may be a useful treatment for headache.
  • Aromatherapy. The essential oil rosemary eases migraine pain.
  • Autogenic training. Autogenic training is a form of self-hypnosis developed in Germany in the 1930s that has been shown in several studies to relieve the pain of migraine.
  • Cognitive behavior therapy.
  • Herbals. Valerian (Valeriana officinalis), passion-flower (Passiflora incarnata), feverfew (Chrysanthemum parthenium), ginger, ginkgo (Ginkgo biloba), goldenseal (Hydrastis canadensis), hawthorn (Crataegus oxyacantha), linden, wood betony (Stachys officinalis), skullcap (Scutellaria lateriflora), or cramp bark (Viburnum opulus) may relieve migraines.
  • Hydrotherapy. Contrast showers, in which a short hot shower is followed by a longer cold shower, may halt an oncoming migraine. A hot enema can temporarily relieve migraine pain.
  • Naturopathy. Migraine headaches are one of the most common reasons for consulting naturopathic practitioners. Naturopaths typically treat migraine with a combination of nutritional therapy and mind/body techniques.
  • Relaxation techniques. Meditation, yoga, hypnosis, visualization, breathing exercises, or progressive muscular relaxation may halt the progression of a migraine.
  • Supplements. Clinical studies have shown that vitamin B2 (riboflavin), magnesium, 5-HTP, or melatonin can reduce the severity of migraines.
  • Transcutaneous electrical nerve stimulation (TENS).

Allopathic Treatments

Nonsteroidal anti-inflammatory drugs (NSAIDs) acetaminophen (Tylenol), ibuprofen (Motrin), and naproxen (Aleve) are helpful for early and mild headache. Excedrin Migraine is a combination product that is indicated for migraine headache.

More severe or unresponsive attacks may be treated with ergotamine (botulinum toxin), dihydroergotamine, sumatriptan (Imitrex), beta-blockers and calcium channel-blockers, antiseizure drugs, antidepressants (SSRIs), meperidine, or metoclopramide. Some of these drugs are also available as nasal sprays, intramuscular injections, or rectal suppositories when vomiting prevents taking the drug by mouth.

Sumatriptan and other triptan drugs (zolmitriptan, rizatriptan, naratriptan, almotriptan, and frovatriptan) should not be taken by people with any kind of vascular disease because they cause coronary artery narrowing. Otherwise these drugs have been shown to be very safe.

Continued use of some antimigraine drugs can lead to "rebound headache," marked by frequent or chronic headaches, especially in the early morning hours. Rebound headache can be avoided by using antimigraine drugs under a doctor's supervision, with the minimum dose necessary to treat symptoms. Tizanidine (Zanaflex) has been reported to be effective in treating rebound headaches when taken together with an NSAID.

Expected Results

Most people can control migraines through recognizing and avoiding triggers, and by using effective treatments. Some people with severe migraines do not respond to preventive or drug therapy. Migraines usually wane in intensity by age 60 and beyond.

Prevention

The frequency of migraine headaches may be lessened by avoiding triggers. It is useful to track these triggers by keeping a headache journal.

One substance that is being studied as a possible migraine preventive is coenzyme Q10, a compound used by cells to produce energy needed for cell growth and maintenance. Coenzyme Q10 has been studied as a possible complementary treatment for cancer. Its use in preventing migraines is encouraging and merits further study.

A study published in early 2003 reported that three drugs currently used to treat disorders of muscle tone are being explored as possible preventive treatments for migraine. They are botulinum toxin type A (Botox), baclofen (Lioresal), and tizanidine (Zanaflex). Early results of open trials of these medications are positive.

Anti-epileptic drugs, which are also known as anti-convulsants, are also being studied as possible migraine preventives. As of 2003, sodium valproate (Epilim) is the only drug approved by the Food and Drug Administration (FDA) for prevention of migraine. Such newer anticonvulsants as gabapentin (Neurontin) and topiramate (Topamax) are presently being evaluated as migraine preventives.

A natural preparation made from butterbur root (Petasites hybridus) has been sold in Germany since the 1970s as a migraine preventive under the trade name Petadolex. Petadolex has been available in the United States since December 1998 and has passed several clinical safety and postmarketing surveillance trials.

Other possible preventive measures include: eating at regular times, not skipping meals, reducing the use of caffeine and pain-relievers, restricting physical exertion (especially on hot days), and keeping regular sleep hours, but not oversleeping. Other measures include:

  • Aerobic exercise, which can reduce the frequency of migraines.
  • Biofeedback thermal control was found to be as effective as medications in preventing migraines.
  • Celery juice consumed twice daily may help to prevent migraines.
  • Feverfew was shown to reduce the severity and frequency of migraines. This herb should not, however, be used during pregnancy or by people taking blood-thinning medications.
  • Ginger may help prevent migraines.
  • Pulsing electromagnetic fields. A preliminary study found that pulsing electromagnetic fields reduced the frequency of migraines.
  • Relaxation techniques can reduce migraine frequency.
  • Supplementation with magnesium and riboflavin was shown to prevent migraines.

Resources

Books

American Council on Headache Education. Migraine: The Complete Guide. New York: Dell, 1994.

"Migraine. " Section 14, Chapter 168 in The Merck Manual of Diagnosis and Therapy, edited by Mark H. Beers, MD, and Robert Berkow, MD. Whitehouse Station, NJ: Merck Research Laboratories, 1999.

Pelletier, Kenneth R., MD. The Best Alternative Medicine, Part II, "CAM Therapies for Specific Conditions: Headaches." New York: Simon & Schuster, 2002.

Periodicals

Bendtsen, L. "Sensitization: Its Role in Primary Headache." Current Opinion in Investigational Drugs 3 (March 2002): 449–453.

Corbo, J. "The Role of Anticonvulsants in Preventive Migraine Therapy." Current Pain and Headache Reports 7 (February 2003): 63–66.

Danesch, U., and R. Rittinghausen. "Safety of a Patented Special Butterbur Root Extract for Migraine Prevention." Headache 43 (January 2003): 76–78.

Diamond, S., and R. Wenzel. "Practical Approaches to Migraine Management." CNS Drugs 16 (2002): 385–403.

Freitag, F. G. "Preventative Treatment for Migraine and Tension-Type headaches : Do Drugs Having Effects on Muscle Spasm and Tone Have a Role?" CNS Drugs 17 (2003): 373–381.

Lea, R. A., A. G. Shepherd, R. P. Curtain, et al. "A Typical Migraine Susceptibility Region Localizes to Chromosome 1q31." Neurogenetics 4 (March 2002): 17–22.

Lipton, R. B., A. I. Scher, T. J. Steiner, et al. "Patterns of Health Care Utilization for Migraine in England and in the United States." Neurology 60 (February 11, 2003): 441–448.

Marconi, R., M. De Fusco, P. Aridon, et al. "Familial Hemiplegic Migraine Type 2 is Linked to 0.9Mb Region on Chromosome 1q23" Annals of Neurology 53 (March 2003): 376–381.

Pryse–Phillips, William E.M., et al. "Guidelines for the Nonpharmacologic Management of Migraine in Clinical Practice." Canadian Medical Association Journal 159 (July 14, 1998): 47–54.

Rozen, T. D., M. L. Oshinsky, C. A. Gebeline, et al. "Open Label Trial of Coenzyme Q10 as a Migraine Preventive." Cephalalgia 22 (March 2002): 137–141.

Sheftell, F. D., and S. J. Tepper. "New Paradigms in the Recognition and Acute Treatment of Migraine." Headache 42 (January 2002): 58–69.

Sinclair, Steven. "Migraine Headaches: Nutritional, Botanical and Other Alternative Approaches." Alternative Medicine Review 4 (1999): 86–95.

Soragna, D., A. Vettori, G. Carraro, et al. "A Locus for Migraine Without Aura Maps on Chromosome 14q21.2-q22.3." American Journal of Human Genetics 72 (January 2003): 161–167.

Stetter, F., and S. Kupper. "Autogenic Training: A Meta-Analysis of Clinical Outcome Studies." Applied Psychophysiology and Biofeedback 27 (March 2002): 45–98.

Tepper, S. J., and D. Millson. "Safety Profile of the Triptans." Expert Opinion on Drug Safety 2 (March 2003): 123–132.

Organizations

American Council for Headache Education. 19 Mantua Road, Mt. Royal, NJ 08061. (609) 423-0043 or (800) 255-2243. .

National Headache Foundation. 428 West St. James Place, Chicago, IL 60614. (773) 388-6399 or (800) 843-2256. .

U. S. Food and Drug Administration (FDA). 5600 Fishers Lane, Rockville, MD 20857. (888) 463-6332. .

Other

"Migraine." American Medical Association. (cited December 2002). .

[Article by: Belinda Rowland; Rebecca J. Frey, PhD]


Recurrent vascular headache, usually on one side of the head. Severe throbbing pain is sometimes accompanied by nausea and vomiting. Some migraine patients have warning symptoms (an "aura") before the headache, including visual disturbance, weakness, numbness, or dizziness. If a stimulus (e.g., a particular food or drink) is found to trigger attacks, avoidance can prevent them. Drugs may be taken as an attack begins (to abort it) or daily by patients with very frequent attacks (to prevent them or reduce their severity).

For more information on migraine, visit Britannica.com.

A severely painful type of headache believed to be caused by the constriction of blood vessels in the head. A migraine typically affects one side of the head and is accompanied by visual disturbances, nausea, and numbness or tingling of the limbs. See also footballer's migraine.

 
Columbia Encyclopedia: migraine
Top
migraine ('grān), headache characterized by recurrent attacks of severe pain, usually on one side of the head. It may be preceded by flashes or spots before the eyes or a ringing in the ears, and accompanied by double vision, nausea, vomiting, or dizziness. The attacks vary in frequency from daily occurrences to one every few years.

Migraine affects women three times as often as men and is frequently inherited. Many disturbances, such as allergy, temporary swelling of the brain, and endocrine disturbances, have been suspected of causing some varieties of the disorder. Although the exact cause is unknown, evidence suggests a genetically transmitted functional disturbance of cranial circulation. The pain is believed to be associated with constriction followed by dilation of blood vessels leading to and within the brain.

Untreated attacks may last for many hours. Mild attacks are often relieved by common sedatives such as aspirin or codeine. Severe attacks may be treated with any of a variety of drugs, including a group called triptans, by injection or in the form of pills or nasal sprays. Certain beta-blockers, antiepileptic drugs, or tricyclic antidepressants may reduce the recurrence of migraines in some patients. Biofeedback is used in training people to recognize the warning symptoms and to practice control over the vascular dilation that initiates attacks.


World of the Mind: migraine
Top
Migraine (from a French word derived from the Greek 'hemi' meaning half and 'kranion' meaning skull) is a transient disorder of brain function which is commonly associated with headache. The diagnosis is usually made when discrete headaches are accompanied by two or more of the following features: unilateral pain, nausea or vomiting, focal cerebral symptoms (e.g. visual phenomena), and a family history of the condition. Attacks usually start to occur before the age of 30 and decrease in frequency with advancing age. Sixty per cent of sufferers are women.

The headache is often preceded by a variety of warnings. Days or hours before its onset there may be a change of mood (usually elation), or an alteration in behaviour, in wakefulness, appetite, bowel activity, or fluid balance. In 'common migraine' these are the only warnings but in 10–15 per cent of patients (those who suffer 'classic migraine') the headache is immediately preceded by disturbances of sensation. These disturbances are usually visual in character, taking the form of flashing coloured lights, zigzag lines, or distortions of visual perception, with or without areas of blindness that begin near the centre of gaze or at the periphery, and then move, usually expanding in size. Less commonly sensations of tingling or numbness occur, usually on one side of the body, particularly in the arm, and even less frequently there can be disturbances of speech and language. In rare forms of migraine other focal neurological deficits may precede the headache: for example, when vertigo, slurred speech, and unsteadiness of gait suggest brain stem dysfunction ('vertebrobasilar migraine'), when there is dysfunction of the nerves that control eye movements ('ophthalmoplegic migraine'), or when there is a unilateral weakness of the limbs (familial 'hemiplegic migraine').

The disturbances, sensory or otherwise, usually last for 20–30 minutes and are followed by a headache which, although often unilateral, may involve both sides of the head, and which is often severe and pulsating in character. When both the sensory disturbances and the pain are unilateral they can involve the same or opposite sides of the body. The pain is often accompanied by nausea (occasionally leading to vomiting) and by an aversion to light and noise. Recovery is almost invariably complete within hours, but can take days. Very rarely an acute attack may result in a permanent neurological disturbance, for example a defect of vision.

Attacks can be precipitated in a number of ways. Perhaps the most common cause is stress of a non-specific kind, as in the case of loss of sleep or overwork, and in some people attacks tend to occur in the period of relaxation that immediately follows the stress. There are many visual triggers, such as glare, flashing lights, and striped patterns. Attacks may also occur in relation to the menstrual cycle and sexual activity. In about 20 per cent of sufferers certain foods, especially chocolate, cheese, and citrus fruit, can precipitate attacks. The agents responsible may include biogenic amines and, when attacks are precipitated by red wine, complex phenols.

The origin and nature of the brain disorder are not known with any certainty. Changes in cerebral blood flow, alterations in neurotransmitter levels, and electrophysiological disturbances found before, during, and after attacks have led to a variety of hypotheses. The fact that attacks are often precipitated by a strong sensory input suggests that a neurological disturbance leads to the development of the attack (and the role of non-specific stress would be consistent with such a viewpoint). The onset and progression of visual disturbances in classical migraine suggest the propagation of a wave through the visual cortex of the brain, at a velocity of 3 mm/min with abnormal excitation at the front of the wave, followed by a depression of activity. It is not clear whether this neurological dysfunction is due to a progressive loss of cortical blood supply or to a disturbance of the neurochemical composition of the environment that surrounds nerve cells (as in the spreading depression of Leao). These two alternatives are not mutually exclusive, but any possible relationship between them is unclear. Specific changes in neurotransmitters have been found during migraine attacks, particularly with regard to serotonin (5-hydroxytryptamine), a vasoactive monoamine. Although these changes relate mainly to reduced levels in circulating plasma, it has been suggested that there is also depletion within the brain, which is of interest in view of the role of serotonin-producing neurons in the perception of pain. Nevertheless it goes without saying that many other neurotransmitters (known and as yet unknown) are undoubtedly involved.

The mechanisms of pain in migraine may involve dilatation of the meningeal and scalp blood vessels, which are known to be pain sensitive. This dilatation is associated with a sterile inflammatory response in and around the vessels and with the release of a number of pain-producing substances such as the neurokines. There are persistent abnormalities in the pulse of scalp arteries in between attacks of unilateral pain on the affected side.

Treatment of migraine is twofold: medication for relief of the acute attack and, for those individuals who suffer frequent attacks, daily treatment to prevent their occurrence. The pain of an acute attack can be reduced by common analgesics or paracetamol, and the nausea by metoclopramide. In addition, it has been common in the past to use the ergot alkaloid derivatives (e.g. ergotamine) which cause constriction of blood vessels and may alleviate pain for this reason. Frequent attacks can be prevented with a variety of drugs, some of which antagonize serotonin (among other neurotransmitters). These drugs include methysergide, pizotifen, amitriptyline, and propranolol. Relaxation therapy and biofeedback may have a role in treatment and claims have been made that the herb feverfew may help prevent attacks.

(Published 1987)

— C. Kennard/Arnold J. Wilkins

    Bibliography
  • Olesen, J. (1985). 'Migraine and regional cerebral blood flow'. Trends in Neurosciences, 8.
  • Pearce, J. M. S. (1984). 'Migraine: a cerebral disorder'. Lancet, 2.
  • Peatfield, R. (1986). Headache.
  • Sacks, O. W. (1999). Migraine.


Wikipedia: Migraine
Top
Migraine
Classification and external resources
ICD-10 G43.
ICD-9 346
OMIM 157300
DiseasesDB 8207 (Migraine)
31876 (Basilar)
4693 (FHM)
MedlinePlus 000709
eMedicine neuro/218 neuro/517 emerg/230 neuro/529
MeSH D008881

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. 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".[1]

The typical migraine headache is unilateral and pulsating, lasting from 4 to 72 hours;[2] symptoms include nausea, vomiting, photophobia (increased sensitivity to light), and phonophobia (increased sensitivity to sound).[3][4][5] Approximately one-third of people who suffer migraine headache perceive an aura—unusual visual, olfactory, or other sensory experiences that are a sign that the migraine will soon occur.[6]

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 idiopathic; the accepted theory is a disorder of the serotonergic control system, as PET scan has demonstrated the aura coincides with diffusion of cortical depression consequent to increased blood flow (up to 300% greater than baseline).

There are migraine headache variants, some originate in the brainstem (featuring intercellular transport dysfunction of calcium and potassium ions) and some are genetically disposed.[7] Studies of twins indicate a 60 to 65 percent genetic influence upon their propensity to develop migraine headache.[8][9] 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.[citation needed]

Contents

Classification

The International Headache Society (IHS) classifies migraine headache.[10]

Defining pain severity

The IHS defines the intensity of pain with a verbal, four-point scale:[11]

Number Name Annotations
0 no pain
1 mild pain does not interfere with usual activities
2 moderate pain inhibits, but does not wholly prevent usual activities
3 severe pain prevents all activities

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 migraineur:

  1. The prodrome, which occurs hours or days before the headache.
  2. The aura, which immediately precedes the headache.
  3. The pain phase, also known as headache phase.
  4. The postdrome.

Prodrome phase

Prodromal symptoms occur in 40–60% of migraineurs (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), constipation or diarrhea, increased urination, and other visceral symptoms.[12] 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.

Aura phase

For the 20–30%[13][14] of individuals who suffer migraine with aura, this aura comprises focal neurological phenomena that precede or accompany the attack. They appear gradually over 5 to 20 minutes and generally last 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. Symptoms of migraine aura can be visual, sensory, or motor in nature.[15]

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"[citation needed]). 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 or olfactory hallucinations, temporary dysphasia, vertigo, tingling or numbness of the face and extremities, and hypersensitivity to touch.

Pain phase

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 usually it alternates 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 migraineur 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, 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.

Postdrome phase

The patient may feel tired or "hungover" and have head pain, cognitive difficulties, gastrointestinal symptoms, mood changes, and weakness.[16] Some people feel unusually refreshed or euphoric after an attack, whereas others note depression and malaise. Often, some of the minor headache phase symptoms may continue, such as loss of appetite, photophobia, and lightheadedness. For some patients, a 5- to 6-hour nap may reduce the pain, but slight headaches may still occur when the patient stands or sits quickly. These symptoms may go away after a good night's rest, although there is no guarantee. Some people may suffer and recover differently than others.

Diagnosis

Migraines are underdiagnosed[17] and misdiagnosed.[18] The diagnosis of migraine without aura, according to the International Headache Society, can be made according to the following criteria, the "5, 4, 3, 2, 1 criteria":

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

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

The 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.[19]

The presence of either disability, nausea or sensitivity, can diagnose migraine with:[20]

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]

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[21] and claimed to have been discredited by others.[22] Trigger points can be at least part of the cause, and perpetuate most kinds of headaches.[23]

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[who?] report impaired thinking for a few days after the headache has passed.

Migraine headaches can be a symptom of Hypothyroidism.[24][citation needed]

Depolarization theory

A phenomenon known as cortical spreading depression can cause migraines.[25] 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 French study in 2007, using the Positron Emission Tomography (PET) technique identified the hypothalamus as being critically involved in the early stages.[26]

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.[21][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.[21][unreliable source?]

The vascular theory of migraines is now seen as secondary to brain dysfunction.[21][unreliable source?][27]

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.[21] Triptans activate serotonin receptors to stop a migraine attack.[21]

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.[21]

Unifying theory

Both vascular and neural influences cause migraines.

  1. stress triggers changes in the brain
  2. these changes cause serotonin to be released
  3. blood vessels constrict and dilate
  4. chemicals including substance P irritate nerves and blood vessels causing pain[21]

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:

MedlinePlus medical encyclopedia[28]

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 "headache diary" 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, i.e., 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. 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.

Food

Many migraine sufferers report reduced incidence of migraines due to identifying and avoiding their individual food 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.[29] 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.[30]

Aspartame While some people believe that aspartame triggers migraines, and anecdotal evidence is present, this has not been medically proven.[31]

MSG In a placebo-controlled trial, monosodium glutamate (MSG) in large doses (2.5 grams) taken on an empty stomach was associated with adverse symptoms including headache more often than was placebo.[32] However another trial found no effect when 3.5g of MSG was given with food.[33]

Tyramine The National Headache Foundation has a specific list of triggers based on the tyramine theory, detailing allowed, with caution and avoid triggers.[34] However, a 2003 review article concluded that there was no scientific evidence for an effect of tyramine on migraine.[35]

Other A 2005 literature review found that the available information about dietary trigger factors relies mostly on the subjective assessments of patients.[31] 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 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, nitrates, 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.

Weather

Several studies have found some migraines are triggered by changes in weather. One study noted 62% of the subjects thought weather was a factor but only 51% were sensitive to weather changes.[36] Among those whose migraines did occur during a change in weather, the subjects often picked a weather change other than the actual weather data recorded. Most likely to trigger a migraine were, in order:

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

Another study 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.[37]

Other

One study found that for some migraineurs in India, washing hair in a bath was a migraine trigger. The triggering effect also had to do with how the hair was later dried.[38]

Strong fragrances have also been identified as potential triggers, and some sufferers report an increased sensitivity to scent as an aura effect.[39]

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%.[40]

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.[41]

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]

Paracetamol or non-steroidal anti-inflammatory drug (NSAIDs)

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

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.[48]

Analgesics combined with antiemetics

Antiemetics by mouth may help relieve symtoms 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).[49] 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).

Serotonin agonists

Sumatriptan and related selective serotonin receptor agonists are excellent for severe migraines or those that do not respond to NSAIDs[42] or other over-the-counter drugs.[43] Triptans are a mid-line treatment suitable for many migraineurs with typical migraines. They may not work for atypical or unusually severe migraines, transformed migraines, or status (continuous) migraines.

Serotonin specific 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.[40]

Antidepressants

Tricyclic antidepressants have been long established as highly efficacious prophylactic treatments.[40] 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.[40] 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[50] and 5-HT2C receptors[51][52] 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.[40]

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.

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.[53]

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.[54]

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.[55]

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.[56]

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.[57] An open-label study (funded by GelStat) found some tentative evidence of the treatment's effectiveness,[58] 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.[59]

Comparative studies

Regarding comparative effectiveness of these drugs used to abort migraine attacks, a 2004 placebo-controlled trial[60] 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.

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.[42]

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).[61]

Epidemiology

Age-Gender Incidence

Migraine is an extremely common condition which will affect 12–28% of people at some point in their lives.[62] 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.[62] 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.[63] There is then a rapid growth in incidence amongst girls occurring after puberty,[64][65][66] which continues throughout early adult life.[67] By early middle age, around 25% of women experience a migraine at least once a year, compared with fewer than 10% of men.[62][68] 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%.[62][68]

At all ages, migraine without aura is more common than migraine with aura, with a ratio of between 1.5:1 and 2:1.[69][70] Incidence figures show that the excess of migraine seen in women of reproductive age is mainly due to migraine without aura.[69] Thus in pre-pubertal and post-menopausal populations, migraine with aura is somewhat more common than amongst 15–50 year olds.[67][71]

There is a strong relationship between age, gender and type of migraine.[72]

Geographical differences in migraine prevalence are not marked. Studies in Asia and South America suggest that the rates there are relatively low,[73][74] but they do not fall outside the range of values seen in European and North American studies.[62][68]

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.[75]

Preventive treatment

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.[76] 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.[77][78]

Many of the preventive treatments described below are quite effective: Even with a placebo (sham treatment), one-quarter of patients find that their migraine frequency is reduced by half or more, and actual treatments often far exceed this figure.[79]

Trigger avoidance

Patients should attempt to identify and avoid factors that promote or precipitate migraine episodes. Moderation in alcohol and caffeine intake, consistency in sleep habits, and regular meals may be helpful. General dietary restriction has not been demonstrated to be an effective approach to treating migraine.[80] However, eliminating particular foods that are known to trigger migraines in an individual can be very effective.

Gluten-Free Diet

Some individuals have a condition called celiac disease (or "gluten intolerance") that results in the body incorrectly processing gluten. Studies have suggested that many migraine sufferers have celiac disease, and for those who do, decreasing gluten intake may significantly reduce migraine frequency.[81] Celiac disease and gluten sensitivity may be an underlying cause of migraines in some patients, and a gluten-free diet has been demonstrated to reduce, if not completely eliminate, migraines in these individuals. A 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.[30] Another study showed that migraneurs were 10 times more likely than the general population to have celiac disease, and that for migraneurs with celiac disease, a gluten-free diet improved blood-flow to the brain and either eliminated migraines or reduced migraine frequency, duration, and intensity.[81]

Prescription drugs

A 2006 review article by S. Modi and D. Lowder offers some general guidelines on when a physician should consider prescribing drugs for migraine prevention:

Following appropriate management of acute migraine, patients should be evaluated for initiation of preventive therapy. Factors that should prompt consideration of preventive therapy include the occurrence of two or more migraines per month with disability lasting three or more days per month; failure of, contraindication for, or adverse events from acute treatments; use of abortive medication more than twice per week; and uncommon migraine conditions (e.g., hemiplegic migraine, migraine with prolonged aura, migrainous infarction). Patient preference and cost also should be considered.

...Therapy should be initiated with medications that have the highest levels of effectiveness and the lowest potential for adverse reactions; these should be started at low dosages and titrated slowly. A full therapeutic trial may take two to six months. After successful therapy (e.g., reduction of migraine frequency by approximately 50 percent or more) has been maintained for six to 12 months, discontinuation of preventive therapy can be considered.

[76]

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

The most effective prescription medications include several drug classes:

A wide range of pharmacological drugs have been evaluated to determine their efficacy in reducing the frequency or severity of migraine attacks.[40] These drugs include beta-blockers, calcium antagonists, neurostabalizers, nonsteroidal anti-inflammatory drugs (NSAIDs),tricyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs), other antidepressants, and other specialized drug therapies.[40] The US Headache Consortium lists five drugs as having medium to high efficacy: amitriptyline, divalproex, timolol, propranolol and topiramate.[40] Lower efficacy drugs listed include aspirin, atenolol, fenoprofen, flurbiprofen, fluoxetine, gabapentin, ketoprofen, metoprolol, nadolol, naproxen, nimodipine, verapamil and Botulinum A.[40] Additionally, most antidepressants (tricyclic, SSRIs and others such as Bupropion) are listed as "clinically efficacious based on consensus of experience" without scientific support.[40] Many of these drugs may give rise to undesirable side-effects, or may be efficacious in treating comorbid conditions, such as depression.

Other drugs:

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

Herbal and nutritional supplements

Butterbur

50 mg or 75 mg/day of butterbur (Petasites hybridus) rhizome extract was shown in a controlled trial to provide 50% or more reduction in the number of migraines to 68% of participants in the 75 mg dose group, 56% in the 50 mg dose group and 49% in the placebo group after four months. Native butterbur contains some carcinogenic compounds, but a purified version, Petadolex, does not.[88]

Cannabis

Cannabis was a standard treatment for migraines from 1874 to 1942.[89] It has been reported to help people through an attack by relieving the nausea and dulling the head pain, as well as possibly preventing the headache completely when used as soon as possible after the onset of pre-migraine symptoms, such as aura.[89]

Coenzyme Q10

Supplementation of coenzyme Q10 has been found to have a beneficial effect on the condition of some sufferers of migraines. In an open-label trial,[90] Young and Silberstein found that 61.3% of patients treated with 100 mg/day had a greater than 50% reduction in number of days with migraine, making it more effective than most prescription prophylactics. Fewer than 1% reported any side effects. A double-blind placebo-controlled trial has also found positive results.[91]

Feverfew

The plant feverfew (Tanacetum parthenium) is a traditional herbal remedy believed to reduce the frequency of migraine attacks. A number of clinical trials have been carried out to test this claim, but a 2004 review article concluded that the results have been contradictory and inconclusive.[92] However, since then, more studies have been carried out.[93] As well as its prophylactic properties, feverfew is also touted as a migraine abortative.

Magnesium citrate

Magnesium citrate has reduced the frequency of migraine in an experiment in which the magnesium citrate group received 600 mg per day oral of trimagnesium dicitrate. In weeks 9–12, the frequency of attacks was reduced by 41.6% in the magnesium citrate group and by 15.8% in the placebo group.[94]

Omega-3 fatty acids

Omega 3 fatty acids have been studied as a method of controlling frequency and intensity of migraines, with a Danish study showing 2/3 of participants who took Omega 3 supplements seeing a decline in intensity and duration of migraines of roughly 30%[95], however another study found Omega 3 treatment to be non-effective[96]

Riboflavin

The supplement Riboflavin (also called Vitamin B2) has been shown (in a placebo-controlled trial)[97] to reduce the number of migraines, when taken at the high dose of 400 mg daily for three months.[98][99]

Vitamin B12

There is tentative evidence that Vitamin B12 may be effective in preventing migraines.[98] In particular, in an open-label pilot study, 1 mg of intranasal hydroxocobalamin (a form of Vitamin B12), taken daily for three months, was shown to reduce migraine frequency by 50% or more in 10 of 19 participants.[100] Although the study was not placebo-controlled, this response is larger than the typical placebo effect in migraine prophylaxis.[79]

Melatonin

Melatonin has been studied in migraine and other headache disorders. In an open label study, migraine patients taking melatonin 3 mg before bedtime with a good headache response and tolerability. Melatonin has multiple mechanisms affecting migraine pathophysiology.[101]

Surgical treatments

Surgical options for reducing or preventing migraines is an active area of research. Treatment of chronic migraines with botulinum neurotoxin (Botox) injections appears to be effective, but the Botox injections do not appear to work for episodic migraines.[102] Several invasive surgical procedures are currently under investigation. One involves the surgical removal of specific muscles or the transection of specific cranial nerve branches in the area of one or more of four identified trigger points.[103] There also appears to be a causal link between the presence of a patent foramen ovale and migraines.[104][105]

Noninvasive medical treatments

Transcranial Magnetic Stimulation (TMS): At the 49th Annual meeting of the American Headache Society in June 2006, scientists from Ohio State University Medical Center presented medical research on 47 candidates that demonstrated that TMS — a medically non-invasive technology for treating depression, obsessive compulsive disorder and tinnitus, among other ailments — helped to prevent and even reduce the severity of migraines among its patients. This treatment essentially disrupts the aura phase of migraines before patients develop full-blown migraines.[106] In about 74% of the migraine headaches, TMS was found to eliminate or reduce nausea and sensitivity to noise and light.[3] Their research suggests that there is a strong neurological component to migraines. A larger study will be conducted soon to better assess TMS's complete effectiveness.[107] In June 2008, a hand-held apparatus designed to apply TMS as a preemptive therapy to avert a migraine attack at the onset of the aura phase was introduced in California.[108]

Biofeedback has been used successfully by some to control migraine symptoms through training and practice.[109]

Hyperbaric oxygen therapy has been used successfully in treating migraines.[110][111][112] This suggests that sufferers might be treated during an attack with a hyperbaric chamber of some sort, such as a Gamow bag (as is done in the treatment of "The Bends" and altitude sickness).

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

There is a speculative connection between vision correction (particular with prism eyeglasses) and migraines. Two British studies, one from 1934[113] and another from 1956[114] claimed that many patients were provided with complete relief from migraine symptoms with proper eyeglass prescriptions, which included prescribed prism. However, both studies are subject to criticism because of sample bias, sample size, and the lack of a control group. A more recent study[115] found that precision tinted lenses may be an effective migraine treatment. (Most optometrists avoid prescribing prism because, when incorrectly prescribed, it can cause headaches.)

Behavioral treatments

Many physicians believe that exercise for 15–20 minutes per day is helpful for reducing the frequency of migraines.[116]

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

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

Sexual activity has been reported by a proportion of male and female migraine sufferers to relieve migraine pain significantly in some cases.[117]

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

Alternative medicine

A number of forms of alternative medicine, particularly bodywork, are used in preventing migraines.

Clinical trials have suggested that chiropractic care may be an efficacious treatment for migraine headaches[118][119] Likewise, Massage therapy, physical therapy, and Bowen Technique[120] are often very effective forms of treatment to reduce the frequency and intensity of migraines.[citation needed] These initial studies are limited by lack of control subjects, poor control subjects, lack of blind study design, small sample sizes, and other methodological flaws.[121] Chiropractic researchers have argued that the current evidence for chiropractic treatment of migraines indicates that "evidence is steadily increasing to the point where there is now seen to be a moderate level of efficacy for chiropractic SMT in the treatment of headaches or migraines".[121] The effect of chiropractic treatment may be mediated by stress release,[121] and may be more efficacious for tension-type headaches than migraines[122] A review of the literature until 2004 found that "Chiropractic manipulation demonstrated a trend toward benefit in the treatment of TTH, but evidence is weak. ... In the absence of clear evidence regarding their role in treatment, physicians and patients are advised to make cautious and individualized judgments about the utility of physical treatments for headache management; in most cases, the use of these modalities should complement rather than supplant better-validated forms of therapy."[122]

Frequent migraines can leave the sufferer with a stiff neck which can cause stress headaches that can then exacerbate the migraines. Claims have been made that Myofascial Release can relieve this tension and in doing so reduce or eliminate the stress headache element.[citation needed]

Some migraine sufferers find relief through acupuncture, which is usually used to help prevent headaches from developing.[123] Sometimes acupuncture is used to relieve the pain of an active migraine headache.[124] In one controlled trial of acupuncture with a sham control in migraine, the acupuncture was not more effective than the sham acupuncture but was more effective than delayed acupuncture.[citation needed]

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

Incense and scents are shown to help. The smell and incense of peppermint and lavender have been proven to help with migraines and headaches more so than most other scents.[125] However, some scents can be a trigger factor.

Large anecdotal evidence suggests that serotonergic psychedelic drugs such as LSD or psilocybin can prevent migraine headaches.

History

The Head Ache. George Cruikshank (1819)

9,000 year old skulls exist with evidence of trepanation. It is hypothesized that this drastic step was taken in response to headaches, though there is no clear evidence proving this.[citation needed]. Headache with neuralgia was recorded in the medical documents of the ancient Egyptians as early as 1200 BC.

In 400 BC Hippocrates described the visual aura that can precede the migraine headache and the relief which can 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 blood letting 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.

Economic impact

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[126]. 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.

Migraine and 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.[127] 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.[127][128] Migraine sufferers seem to be at risk for both thrombotic and hemorrhagic stroke as well as transient ischemic attacks.[129] 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.[130][128]

See also

Organizations

Other

Footnotes

  1. ^ "Etymology of migraine". Online Etymological Dictionary. http://www.etymonline.com/index.php?term=migraine. Retrieved 27 May 2009. 
  2. ^ The International Classification of Headache Disorders, 2nd Edition
  3. ^ "NINDS Migraine Information Page". National Institute of Neurological Disorders and Stroke, National Institutes of Health. http://www.ninds.nih.gov/disorders/migraine/migraine.htm. Retrieved 2007-06-25. 
  4. ^ "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. 
  5. ^ Gallagher RM, Cutrer FM (2002). "Migraine: diagnosis, management, and new treatment options". Am J Manag Care 8 (3 Suppl): S58–73. PMID 11859906. 
  6. ^ "Guidelines for all healthcare professionals in the diagnosis and management of migraine, tension-type, cluster and medication-overuse headache, January 2007, British Association for the Study of Headache" (PDF). http://216.25.100.131/upload/NS_BASH/BASH_guidelines_2007.pdf. Retrieved 2007-06-25. 
  7. ^ Ogilvie AD, Russell MB, Dhall P, et al. (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. 
  8. ^ 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. 
  9. ^ 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". J. Med. Genet. 36 (3): 225–7. PMID 10204850. PMC 1734315. http://jmg.bmj.com/cgi/pmidlookup?view=long&pmid=10204850. 
  10. ^ Headache Classification Subcommittee of the International Headache Society (2004). "The International Classification of Headache Disorders: 2nd edition". Cephalalgia : an international journal of headache 24 Suppl 1: 9–160. doi:10.1111/j.1468-2982.2004.00653.x. PMID 14979299.  Complete supplement online
  11. ^ Headache Classification Subcommittee of the International Headache Society (2004). "The International Classification of Headache Disorders: 2nd edition". Cephalalgia : an international journal of headache 24 Suppl 1: 150. doi:10.1111/j.1468-2982.2004.00653.x. PMID 14979299.  Complete supplement online (see page 150)
  12. ^ Kelman L (October 2004). "The premonitory symptoms (prodrome): a tertiary care study of 893 migraineurs". Headache 44 (9): 865–72. doi:10.1111/j.1526-4610.2004.04168.x. PMID 15447695. http://www.blackwell-synergy.com/openurl?genre=article&sid=nlm:pubmed&issn=0017-8748&date=2004&volume=44&issue=9&spage=865. Retrieved 2008-08-30. 
  13. ^ Silberstein, Stephen D. (2005). Atlas Of Migraine And Other Headaches. London: Taylor & Francis Group. ISBN 1842142739. 
  14. ^ Mathew, Ninan T.; Evans, Randolph W. (2005). Handbook of headache. Hagerstown, MD: Lippincott Williams & Wilkins. ISBN 078175223X. 
  15. ^ Silberstein, Stephen D. (2002). Headache in Clinical Practice, 2nd Edition. London: Taylor & Francis Group. ISBN 1-901865-88-6. 
  16. ^ Kelman L (February 2006). "The postdrome of the acute migraine attack". Cephalalgia 26 (2): 214–20. doi:10.1111/j.1468-2982.2005.01026.x. PMID 16426278. http://www.blackwell-synergy.com/openurl?genre=article&sid=nlm:pubmed&issn=0333-1024&date=2006&volume=26&issue=2&spage=214. Retrieved 2008-08-30. 
  17. ^ Lipton RB, Stewart WF, Celentano DD, Reed ML (1992). "Undiagnosed migraine headaches. A comparison of symptom-based and reported physician diagnosis". Arch. Intern. Med. 152 (6): 1273–8. doi:10.1001/archinte.152.6.1273. PMID 1599358. http://archinte.ama-assn.org/cgi/content/abstract/152/6/1273. Retrieved 2009-10-04. 
  18. ^ Schreiber CP, Hutchinson S, Webster CJ, Ames M, Richardson MS, Powers C (2004). "Prevalence of migraine in patients with a history of self-reported or physician-diagnosed "sinus" headache". Arch. Intern. Med. 164 (16): 1769–72. doi:10.1001/archinte.164.16.1769. PMID 15364670. 
  19. ^ Detsky ME, McDonald DR, Baerlocher MO, Tomlinson GA, McCrory DC, Booth CM (2006). "Does this patient with headache have a migraine or need neuroimaging?". JAMA 296 (10): 1274–83. doi:10.1001/jama.296.10.1274. PMID 16968852. 
  20. ^ Lipton RB, Dodick D, Sadovsky R, et al. (2003). "A self-administered screener for migraine in primary care: The ID Migraine validation study". Neurology 61 (3): 375–82. PMID 12913201. 
  21. ^ 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 (What Your Doctor May Not Tell You About...(Paperback)). New York: Warner Books. ISBN 0-446-67826-0. 
  22. ^ Cohen AS, Goadsby PJ (2005). "Functional neuroimaging of primary headache disorders". Curr Pain Headache Rep 9 (2): 141–6. doi:10.1007/s11916-005-0053-0. PMID 15745626. 
  23. ^ Trigger Point Therapy for Headaches & Migraines, DeLaune, Valerie (New Harbinger: 2008) [1]
  24. ^ http://ecfr.gpoaccess.gov/cgi/t/text/text-idx?c=ecfr&sid=a00605d20ab938aed6a579c5c6d2f5c5&rgn=div6&view=text&node=38:1.0.1.1.5.2&idno=38
  25. ^ Lauritzen M (1994). "Pathophysiology of the migraine aura. The spreading depression theory". Brain 117 (Pt 1): 199–210. doi:10.1093/brain/117.1.199. PMID 7908596. 
  26. ^ Denuelle M, Fabre N, Payoux P, Chollet F, Geraud G (2007). "Hypothalamic activation in spontaneous migraine attacks". Headache 47 (10): 1418–26. doi:10.1111/j.1526-4610.2007.00776.x. PMID 18052951. 
  27. ^ Welch KMA (1993). "Drug therapy of migraine". N Engl J Med 329 (20): 1476–83. doi:10.1056/NEJM199311113292008. PMID 8105379. 
  28. ^ Kantor, D (2006-11-21). "MedlinePlus Medical Encyclopedia: Migraine". http://www.nlm.nih.gov/medlineplus/ency/article/000709.htm. Retrieved 2008-04-04. 
  29. ^ link titleMigraine Linked to Celiac Disease
  30. ^ a b Migraine Headaches: Gluten Triggers Severe Headaches in Sensitive Individuals
  31. ^ a b Holzhammer J, Wöber C (2006). "[Alimentary trigger factors that provoke migraine and tension-type headache]" (in German). Schmerz 20 (2): 151–9. doi:10.1007/s00482-005-0390-2. PMID 15806385. 
  32. ^ Yang WH, Drouin MA, Herbert M, Mao Y, Karsh J (1997). "The monosodium glutamate symptom complex: assessment in a double-blind, placebo-controlled, randomized study". J Allergy Clin Immunol 99 (6 pt 1): 757–62. doi:10.1016/S0091-6749(97)80008-5. PMID 9215242. 
  33. ^ Tarasoff L, Kelly MF (1993). "Monosodium L-glutamate: a double-blind study and review.". Food Chem Toxicol 31 (12): 1019–35. doi:10.1016/0278-6915(93)90012-N. PMID 8282275. 
  34. ^ "Low Tyramine Headache Diet" (PDF). National Headache Foundation. 2004. http://www.headaches.org/pdf/Diet.pdf. Retrieved 2008-04-04. 
  35. ^ Jansen SC, van Dusseldorp M, Bottema KC, Dubois AE (September 2003). "Intolerance to dietary biogenic amines: a review.". Ann Allergy Asthma Immunol. 91 (3): 233–40. PMID 14533654. http://openurl.ingenta.com/content?genre=article&issn=1081-1206&volume=91&issue=3&spage=233&epage=241. 
  36. ^ Prince PB, Rapoport AM, Sheftell FD, Tepper SJ, Bigal ME (2004). "The effect of weather on headache". Headache 44 (6): 596–602. doi:10.1111/j.1526-4610.2004.446008.x. PMID 15186304. http://www.blackwell-synergy.com/openurl?genre=article&sid=nlm:pubmed&issn=0017-8748&date=2004&volume=44&issue=6&spage=596. 
  37. ^ Cooke LJ, Rose MS, Becker WJ (2000). "Chinook winds and migraine headache". Neurology 54 (2): 302–7. PMID 10668687. 
  38. ^ Ravishankar K (2006). "'Hair wash' or 'head bath' triggering migraine - observations in 94 Indian patients". Cephalalgia 26 (11): 1330–4. doi:10.1111/j.1468-2982.2006.01223.x. PMID 17059440. 
  39. ^ link titleFragrance Migraine Triggers
  40. ^ a b c d e f g h i j Kaniecki R, Lucas S. (2004 page=40-52), Treatment of primary headache: preventive treatment of migraine. In: Standards of care for headache diagnosis and treatment., National Headache Foundation 
  41. ^ Millichap JG, Yee MM (2003). "The diet factor in pediatric and adolescent migraine". Pediatr. Neurol. 28 (1): 9–15. doi:10.1016/S0887-8994(02)00466-6. PMID 12657413. 
  42. ^ a b c Brandes JL, Kudrow D, Stark SR, et al. (2007). "Sumatriptan-naproxen for acute treatment of migraine: a randomized trial". JAMA 297 (13): 1443–54. doi:10.1001/jama.297.13.1443. PMID 17405970. 
  43. ^ a b Lipton RB, Baggish JS, Stewart WF, Codispoti JR, Fu M (2000). "Efficacy and safety of paracetamol in the treatment of migraine: results of a randomized, double-blind, placebo-controlled, population-based study". Arch. Intern. Med. 160 (22): 3486–92. doi:10.1001/archinte.160.22.3486. PMID 11112243. 
  44. ^ Goldstein J, Hoffman HD, Armellino JJ, et al. (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 paracetamol, aspirin, and caffeine". Cephalalgia : an international journal of headache 19 (7): 684–91. doi:10.1046/j.1468-2982.1999.019007684.x. PMID 10524663. 
  45. ^ Center for Drug Evaluation and Research (1999-10-07). "Approval Letter, Application 20-802/S802" (PDF). U.S. Food and Drug Administration. http://www.fda.gov/cder/foi/appletter/1999/20802s02ltr.pdf. Retrieved 2008-08-26. 
  46. ^ "Migraine headaches" information from the Cleveland Clinic
  47. ^ a b Mayo Clinic Proceedings 1996;71:1055-1066
  48. ^ Ben (2006). "Managing Migraines". FDA Consumer Magazine.. 
  49. ^ "4.7.4.1 Treatment of acute migraine". British National Formulary (55 ed.). March 2008. pp. 239. 
  50. ^ 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
  51. ^ Mylecharane EJ.(1991)"5-HT2 receptor antagonists and migraine therapy."1: J Neurol. 1991;238 Suppl 1:S45-52.PMID: 2045831
  52. ^ Millan MJ.(2005)"Serotonin 5-HT2C receptors as a target for the treatment of depressive and anxious states: focus on novel therapeutic strategies." 2005 Sep-Oct;60(5):441-60. PMID: 16433010
  53. ^ Colman I, Friedman BW, Brown MD, et al. (June 2008). "Parenteral dexamethasone for acute severe migraine headache: meta-analysis of randomised controlled trials for preventing recurrence". BMJ 336 (7657): 1359–61. doi:10.1136/bmj.39566.806725.BE. PMID 18541610. 
  54. ^ 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.
  55. ^ 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. 
  56. ^ UpToDate.
  57. ^ Migraine News for February 2005, accessed January 4, 2008
  58. ^ RK Cady, CP Schreiber, ME Beach, CC Hart (2005). "Gelstat Migraine (sublingually administered feverfew and ginger compound) for acute treatment of migraine when administered during the mild pain phase". Medical Science Monitor 11 (9): PI65–9. PMID 16127373.  See also summary poster.
  59. ^ Russo, Ethan (1998). Cannabis for migraine treatment: the once and future prescription? An historical and scientific review. Pain 76:3-8.
  60. ^ Diener H, Bussone G, de Liano H, Eikermann A, Englert R, Floeter T, Gallai V, Göbel H, Hartung E, Jimenez M, Lange R, Manzoni G, Mueller-Schwefe G, Nappi G, Pinessi L, Prat J, Puca F, Titus F, Voelker M (2004). "Placebo-controlled comparison of effervescent acetylsalicylic acid, sumatriptan and ibuprofen in the treatment of migraine attacks". Cephalalgia 24 (11): 475. doi:10.1111/j.1468-2982.2004.00783.x. PMID 15482357. 
  61. ^ Silberstein SD, Mannix LK, Goldstein J, et al. (2008). "Multimechanistic (sumatriptan-naproxen) early intervention for the acute treatment of migraine". Neurology 71 (2): 114–21. doi:10.1212/01.wnl.0000316800.22949.20. PMID 18606965. 
  62. ^ a b c d e Stovner LJ, Zwart JA, Hagen K, Terwindt GM, Pascual J (2006). "Epidemiology of headache in Europe". Eur. J. Neurol. 13 (4): 333–45. doi:10.1111/j.1468-1331.2006.01184.x. PMID 16643310. 
  63. ^ Mortimer MJ, Kay J, Jaron A (1992). "Epidemiology of headache and childhood migraine in an urban general practice using Ad Hoc, Vahlquist and IHS criteria". Dev Med Child Neurol 34 (12): 1095–101. PMID 1451940. 
  64. ^ 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. 
  65. ^ Ziegler DK, Hassanein RS, Couch JR (1977). "Characteristics of life headache histories in a nonclinic population". Neurology 27 (3): 265–9. PMID 557763. 
  66. ^ SELBY G, LANCE JW (1960). "Observations on 500 cases of migraine and allied vascular headache". J. Neurol. Neurosurg. Psychiatr. 23: 23–32. doi:10.1136/jnnp.23.1.23. PMID 14444681. 
  67. ^ a b Anttila P, Metsähonkala L, Sillanpää M (2006). "Long-term trends in the incidence of headache in Finnish schoolchildren". Pediatrics 117 (6): e1197–201. doi:10.1542/peds.2005-2274. PMID 16740819. 
  68. ^ a b c Lipton RB, Stewart WF (1993). "Migraine in the United States: a review of epidemiology and health care use". Neurology 43 (6 Suppl 3): S6–10. PMID 8502385. 
  69. ^ 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. 
  70. ^ 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. 
  71. ^ 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. 
  72. ^ 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. 
  73. ^ Wang SJ (2003). "Epidemiology of migraine and other types of headache in Asia". Curr Neurol Neurosci Rep 3 (2): 104–8. doi:10.1007/s11910-003-0060-7. PMID 12583837. 
  74. ^ Lavados PM, Tenhamm E (1997). "Epidemiology of migraine headache in Santiago, Chile: a prevalence study". Cephalalgia 17 (7): 770–7. doi:10.1046/j.1468-2982.1997.1707770.x. PMID 9399008. 
  75. ^ Ottman R, Lipton RB (1994). "Comorbidity of migraine and epilepsy". Neurology 44 (11): 2105–10. PMID 7969967. 
  76. ^ a b Modi S, Lowder D (2006). "Medications for migraine prophylaxis". American Family Physician 73 (1): 72. PMID 16417067. 
  77. ^ Diener H, Limmroth V (2004). "Medication-overuse headache: a worldwide problem". The Lancet Neurology 3: 475. doi:10.1016/S1474-4422(04)00824-5. 
  78. ^ Fritsche G; Diener HC (November 2002). "Medication overuse headaches – what is new?". Expert Opin Drug Saf 1 (4): 331–8. doi:10.1517/14740338.1.4.331. PMID 12904133. http://www.informapharmascience.com/doi/abs/10.1517/14740338.1.4.331. 
  79. ^ a b P-HM van der Kuy, JJHM Lohman (2002). "A quantification of the placebo response in migraine prophylaxis". Cephalalgia 22 (4): 265–270. doi:10.1046/j.1468-2982.2002.00363.x. 
  80. ^ Holzhammer J, Wöber C (2006). "Alimentary trigger factors that provoke migraine and tension-type headache" (in German). Schmerz 20 (2): 151–9. doi:10.1007/s00482-005-0390-2. PMID 15806385. 
  81. ^ a b Migraine Linked to Celiac Disease
  82. ^ Linde K, Rossnagel K (2004). "Propranolol for migraine prophylaxis". Cochrane Database Syst Rev (2): CD003225. doi:10.1002/14651858.CD003225.pub2. PMID 15106196. 
  83. ^ Chronicle E, Mulleners W (2004). "Anticonvulsant drugs for migraine prophylaxis". Cochrane Database Syst Rev (3): CD003226. doi:10.1002/14651858.CD003226.pub2. PMID 15266476. 
  84. ^ Steinman M, Bero L, Chren M, Landefeld C (2006). "Narrative review: the promotion of gabapentin: an analysis of internal industry documents". Ann Intern Med 145 (4): 284–93. PMID 16908919. 
  85. ^ Moja P, Cusi C, Sterzi R, Canepari C (2005). "Selective serotonin re-uptake inhibitors (SSRIs) for preventing migraine and tension-type headaches". Cochrane Database Syst Rev (3): CD002919. doi:10.1002/14651858.CD002919.pub2. PMID 16034880. 
  86. ^ Tomkins G, Jackson J, O'Malley P, Balden E, Santoro J (2001). "Treatment of chronic headache with antidepressants: a meta-analysis". Am J Med 111 (1): 54–63. doi:10.1016/S0002-9343(01)00762-8. PMID 11448661. 
  87. ^ Ziegler D, Hurwitz A, Hassanein R, Kodanaz H, Preskorn S, Mason J (1987). "Migraine prophylaxis. A comparison of propranolol and amitriptyline". Arch Neurol 44 (5): 486–9. PMID 3579659. 
  88. ^ http://www.webmd.com/content/article/98/105003.htm?z=1728_00000_1000_tn_04
  89. ^ a b Russo E (May 1998). "Cannabis for migraine treatment: the once and future prescription? An historical and scientific review". Pain 76 (1-2): 3–8. doi:10.1016/S0304-3959(98)00033-5. PMID 9696453. http://linkinghub.elsevier.com/retrieve/pii/S0304-3959(98)00033-5. Retrieved 2008-08-30. 
  90. ^ Rozen T, Oshinsky M, Gebeline C, Bradley K, Young W, Shechter A, Silberstein S (2002). "Open label trial of coenzyme Q10 as a migraine preventive". Cephalalgia 22 (2): 137–41. doi:10.1046/j.1468-2982.2002.00335.x. PMID 11972582. 
  91. ^ Sándor PS, et al. (2005). "Efficacy of coenzyme Q10 in migraine prophylaxis: A randomized controlled trial". Neurology 64 (4): 713–715. doi:10.1212/01.WNL.0000151975.03598.ED (inactive 2008-06-25). PMID 15728298. http://www.neurology.org/cgi/content/abstract/64/4/713. 
  92. ^ Pittler MH, Ernst E. (2004). "Feverfew for preventing migraine". Cochrane Database of Systematic Reviews (1): CD002286. doi:10.1002/14651858.CD002286.pub2. PMID 14973986. 
  93. ^ For example: Diener HC, Pfaffenrath V, Schnitker J, Friede M, Henneicke-von Zepelin HH (2005). "Efficacy and safety of 6.25 mg t.i.d. feverfew CO2-extract (MIG-99) in migraine prevention—a randomized, double-blind, multicentre, placebo-controlled study". Cephalalgia 25 (11): 1031–41. doi:10.1111/j.1468-2982.2005.00950.x. PMID 16232154. 
  94. ^ Peikert A, Wilimzig C, Köhne-Volland R (1996). "Prophylaxis of migraine with oral magnesium: results from a prospective, multi-center, placebo-controlled and double-blind randomized study". Cephalalgia 16 (4): 257–63. doi:10.1046/j.1468-2982.1996.1604257.x. PMID 8792038. 
  95. ^ http://www.nutraingredients.com/Research/Omega-to-soothe-migraines
  96. ^ http://www.ncbi.nlm.nih.gov/pubmed/11737007?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=6
  97. ^ J Schoenen, J Jacquay, M Lenaerts (1998). "Effectiveness of high dose riboflavin in migraine prophylaxis: A randomized controlled trial". Neurology 150: 466–470. 
  98. ^ a b A Bianchi, S Salomone, F Caraci, V Pizza, R Bernardini, CC D'Amato (2004). "Role of Magnesium, Coenzyme Q10, Riboflavin, and Vitamin B12 in Migraine Prophylaxis". Vitamins and Hormones 69: 297–312. doi:10.1016/S0083-6729(04)69011-X. 
  99. ^ Riboflavin in Prophylactic Treatment of Migraine, EA Balbisi, EM Ambizas, U.S. Pharmacist Vol. 30, No. 05, accessed January 4, 2008.
  100. ^ P-HM van der Kuy, FWHM Merkus, JJHM Lohman, JWM ter Berg, PM Hooymans (2002). "Hydroxocobalamin, a nitric oxide scavenger, in the prophylaxis of migraine: an open, pilot study". Cephalalgia 22 (7): 513–519. doi:10.1046/j.1468-2982.2002.00412.x. 
  101. ^ Peres MF, Zukerman E, da Cunha Tanuri F, Moreira FR, Cipolla-Neto J (August 2004). "Melatonin, 3 mg, is effective for migraine prevention". Neurology 63 (4): 757. PMID 15326268. http://www.neurology.org/cgi/pmidlookup?view=long&pmid=15326268. 
  102. ^ Naumann, M.; So, Y.; Argoff, E.; Childers, K.; Dykstra, D.; Gronseth, S.; Jabbari, B.; Kaufmann, C. et al. (May 2008). "Assessment: Botulinum neurotoxin in the treatment of autonomic disorders and pain (an evidence-based review): Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology". Neurology 70 (19): 1707. doi:10.1212/01.wnl.0000311390.87642.d8. ISSN 0028-3878. PMID 18458231.  edit
  103. ^ Guyuron, B; Kriegler, Js; Davis, J; Amini, Sb (Jan 2005). "Comprehensive surgical treatment of migraine headaches". Plastic and reconstructive surgery 115 (1): 1–9. ISSN 0032-1052. PMID 15622223.  edit
  104. ^ Post, M. C. (Jan 2007). "Patent foramen ovale and migraine". Catheterization and Cardiovascular Interventions 69 (1): 9–9. doi:10.1002/ccd.20931. ISSN 1522-1946. PMID 17143907.  edit
  105. ^ Diener, Hc; Kurth, T; Dodick, D (Jun 2007). "Patent foramen ovale and migraine". Current pain and headache reports 11 (3): 236–40. doi:10.1007/s11916-007-0196-2. ISSN 1531-3433. PMID 17504652.  edit
  106. ^ http://technology.timesonline.co.uk/article/0,,20409-2237003.html
  107. ^ Mohammad, Yousef (2006-06-22). "Magnets Zap Migraines". 49th Annual Scientific Meeting of the American Headache Society. Los Angeles, California. 
  108. ^ http://medicalcenter.osu.edu/mediaroom/press/article.cfm?ID=4059
  109. ^ Nestoriuc Y, Martin A (2007). "Efficacy of biofeedback for migraine: a meta-analysis". Pain 128 (1–2): 111–27. doi:10.1016/j.pain.2006.09.007. PMID 17084028. 
  110. ^ Bennett MH, French C, Schnabel A, Wasiak J, Kranke P (2008). "Normobaric and hyperbaric oxygen therapy for migraine and cluster headache". Cochrane Database Syst Rev (3): CD005219. doi:10.1002/14651858.CD005219.pub2. PMID 18646121. 
  111. ^ Eftedal OS, Lydersen S, Helde G, White L, Brubakk AO, Stovner LJ (2004). "A randomized, double blind study of the prophylactic effect of hyperbaric oxygen therapy on migraine". Cephalalgia 24 (8): 639–44. doi:10.1111/j.1468-2982.2004.00724.x. PMID 15265052. 
  112. ^ Fife William P, Fife Caroline E (1989). "Treatment of Migraine with Hyperbaric Oxygen". J. Hyperbaric Med 4 (1): 7–15. http://archive.rubicon-foundation.org/4386. Retrieved 2008-08-06. 
  113. ^ Turville, A. E. (1934) "Refraction and migraine". Br. J. Physiol. Opt. 8, 62–89
  114. ^ Wilmut, E. B. (1956) "Migraine". Br. J. Physiol. Opt. 13, 93–97
  115. ^ http://www.essex.ac.uk/psychology/overlays/OPO.2002.22%20130-142.pdf
  116. ^ [2] (PDF)
  117. ^ http://www.medscape.com/viewarticle/533713
  118. ^ Nelson CF, Bronfort G, Evans R, Boline P, Goldsmith C, Anderson AV (1998). "The efficacy of spinal manipulation, amitriptyline and the combination of both therapies for the prophylaxis of migraine headache.". Journal of Manipulative and Physiological Therapeutics 21(8) page=511-9. 
  119. ^ Bronfort G, Nilsson N, Haas M, Evans R, Goldsmith CH, Assendelft WJ, Bouter LM (2004). Non-invasive physical treatments for chronic/recurrent headache. Cochrane Database Syst Rev. 3. 
  120. ^ http://www.thebowentechnique.com/content/migraine.htm
  121. ^ a b c Tuchin, PJ, Pollard, H & Bonello, R. (2000). ""A randomized controlled trial of chiropractic spinal manipulative therapy for migraine"". Journal of Manipulative and Physiological Therapeutics 23: 91. doi:10.1016/S0161-4754(00)90073-3. 
  122. ^ a b Biondi, DM (2005). "Physical Treatments for Headache: A Structured Review"". The Journal of Head and Face Pain 45,: 738-746.. 
  123. ^ Facco E, Liguori A, Petti F, et al. (2007). "Traditional Acupuncture in Migraine: A Controlled, Randomized Study". Headache 48 (3): 398. doi:10.1111/j.1526-4610.2007.00916.x. PMID 17868354. 
  124. ^ Melchart D, Thormaehlen J, Hager S, Liao J, Linde K, Weidenhammer W (2003). "Acupuncture versus placebo versus sumatriptan for early treatment of migraine attacks: a randomized controlled trial". J. Intern. Med. 253 (2): 181–8. doi:10.1046/j.1365-2796.2003.01081.x. PMID 12542558. 
  125. ^ Alexander Mauskop; Fox, Barry (2001). What Your Doctor May Not Tell You About: Migraines: The Breakthrough Program That Can Help End Your Pain (What Your Doctor May Not Tell You About...(Paperback)). New York: Warner Books. pp. 130. ISBN 0-446-67826-0. 
  126. ^ Cost of disorders of the brain in Europe
  127. ^ a b Etminan M, Takkouche B, Isorna FC, et al. Risk of ischaemic stroke in people with migraine: Systematic review and meta-analysis of observational studies. BMJ. 2005;330:63. PMID 15596418
  128. ^ 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. 
  129. ^ 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
  130. ^ Waters WE, Campbell MJ, Elwood PC. Migraine, headache, and survival in women. BMJ (Clin Res Ed). 1983;287:1442–1443. PMID 6416449

References

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.
  • Ravishankar, K (2006). 'Hair wash' or 'Head bath' triggering migraine - observations in 94 Indian patients". Cephalagia 26 (11): 1330–1334. ISSN 0333-1024.

Treatment

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.

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 0615201970

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.

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.

External links

General information

Organizations


Translations: Migraine
Top

Dansk (Danish)
n. - migræne

Nederlands (Dutch)
migraine (hoofdpijn- aanvallen)

Français (French)
n. - migraine

Deutsch (German)
n. - Migräne

Ελληνική (Greek)
n. - ημικρανία, πονοκέφαλος

Italiano (Italian)
emicrania

Português (Portuguese)
n. - enxaqueca (f)

Русский (Russian)
мигрень

Español (Spanish)
n. - migraña, jaqueca

Svenska (Swedish)
n. - migrän

中文(简体)(Chinese (Simplified))
偏头痛

中文(繁體)(Chinese (Traditional))
n. - 偏頭痛

한국어 (Korean)
n. - 머리가 부분적으로 아픔

日本語 (Japanese)
n. - 偏頭痛

العربيه (Arabic)
‏(الاسم) صداع نصفي, مرض الشقيقه‏

עברית (Hebrew)
n. - ‮צלחה, פולג, מיגרנה‬


 
 

 

Copyrights:

Medical Encyclopedia. © 2006 through a partnership of Answers Corporation. All rights reserved.  Read more
Dictionary. The American Heritage® Dictionary of the English Language, Fourth Edition Copyright © 2007, 2000 by Houghton Mifflin Company. Updated in 2009. Published by Houghton Mifflin Company. All rights reserved.  Read more
World of the Body. The Oxford Companion to the Body. Copyright © 2001, 2003 by Oxford University Press. All rights reserved.  Read more
Alternative Medicine Encyclopedia. Encyclopedia of Alternative Medicine. Copyright © 2005 by The Gale Group, Inc. All rights reserved.  Read more
Britannica Concise Encyclopedia. Britannica Concise Encyclopedia. © 2006 Encyclopædia Britannica, Inc. All rights reserved.  Read more
Sports Science and Medicine. The Oxford Dictionary of Sports Science & Medicine. Copyright © Michael Kent 1998, 2006, 2007. All rights reserved.  Read more
Columbia Encyclopedia. The Columbia Electronic Encyclopedia, Sixth Edition Copyright © 2003, Columbia University Press. Licensed from Columbia University Press. All rights reserved. www.cc.columbia.edu/cu/cup/ Read more
World of the Mind. The Oxford Companion to the Mind. Second Edition. Copyright © Oxford University Press, 2004. All rights reserved.  Read more
Wikipedia. This article is licensed under the Creative Commons Attribution/Share-Alike License. It uses material from the Wikipedia article "Migraine" Read more
Translations. Copyright © 2007, WizCom Technologies Ltd. All rights reserved.  Read more