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Nursing Diagnosis and Nursing Interventions for Headache
Nursing Diagnosis for Headache 1. Acute Pain related to stess and tension, irritation of nerve pressure, vasospasm, increased intracranial pressure. 2. Ineffective individual coping related to crisis situations, personal vulnerability, not adequat support system, work overload, inadequate relaxation, not adequat coping methods, severe pain. Nursing Intervention for Headache Nursing Diagnosis I Acute Pain related to stess and tension, irritation of nerve pressure, vasospasm, increased intracranial pressure. Nursing Interventions:

Assess complaints of pain, note the intensity with pain scale 0 -10, pain characteristics (eg heavy, throbbing, constant) location, duration, factors that aggravate or relieve. Observation of nonverbal signs of pain, are like: facial expression, posture, restlessness, crying / grimacing, withdrawal, diaphoresis, changes in the frequency of cardiac / respiratory, blood pressure. Note the distinct possibility of pathophysiology, such as brain / meningeal / sinus infection, cervical trauma, hypertension or trauma. Make sure the duration / episode of the problem, who has been consulted, and drug and / or what therapy was used. Instruct patient to report pain immediately if the pain arises. Assess the relationship between physical / emotional state of a person. Note the influence of pain such as: loss of interest in life, decreased activity, weight loss. Suggest to rest in a quiet room. Observation of nausea / vomiting. Instruct the patient to use a positive statement "I am cured, I'm relaxing, I love this life." Advise patient to realize the internal-external dialogue and say "stop" or "delayed" if it appears that negative thoughts. Nursing Diagnosis II Ineffective individual coping related to crisis situations, personal vulnerability, not adequat support system, work overload, inadequate relaxation, not adequat coping methods, severe pain

Nursing Interventions : Approach the patient with a friendly and attentive. Take advantage of activities that can be taught. Assist patients in understanding the changes in the concept of body image. Advise the patient to express his feelings and discussion how the headaches that interfere with the work and pleasures of this life. Ensure the impact of illness on sexual needs. Give information about the causes of headaches, handling, and expected results. Collaboration : Refer to counseling and / or family therapy or class assertiveness training sites as indicated.

2. http://www.uptodate.com/contents/migraine-headaches-in-adults-beyond-the-basics
MIGRAINE HEADACHE OVERVIEW Headaches can be quite debilitating, although the vast majority are not due to life-threatening disorders. Approximately 90 percent of headaches are caused by one of three syndromes (table 1):

Migraine headache Tension-type headaches Cluster headaches

This article discusses migraine headaches in adults. Other types of headaches are discussed separately. (See "Patient information: Headache causes and diagnosis in adults (Beyond the Basics)" and "Patient information: Headache treatment in adults (Beyond the Basics)".) MIGRAINE HEADACHE SYMPTOMS Between 12 and 16 percent of people in the United States experience migraine headaches, making it the second most common type of headache. Pain The pain of a migraine headache usually begins gradually, intensifies over minutes to one or more hours, and resolves gradually at the end of the attack. The headache is typically dull, deep, and steady when mild to moderate in severity; it becomes throbbing or pulsatile when severe. Migraine headaches are worsened by light, sneezing, straining, constant motion, moving the head rapidly, or physical activity. Many migraine sufferers try to get relief by lying down in a darkened, quiet room. In 60 to 70 percent of people, the pain occurs on only one side of the head. In adults, a migraine headache usually lasts a few hours, although it can last from four to 72 hours. Other symptoms Migraine headaches are often accompanied by nausea and vomiting, as well as sensitivity to light and noise. Between 10 and 20 percent of people with migraines also experience nasal stuffiness and runny nose, or teary eyes. The symptoms of a migraine attack may be severe and alarming, but in most cases there are no lasting health effects when the attack ends. Aura About 20 percent of people with migraines experience symptoms before the headache; this is called an aura. The aura may include flashing lights or bright spots, zigzag lines, changes in vision, or numbness or tingling in the fingers of one hand, lips, tongue, or lower face. You may have one or more of these aura symptoms. Auras may also involve other senses and can occasionally cause temporary muscle weakness or changes in speech; these symptoms can be frightening. Aura symptoms typically last five to 20 minutes and rarely last more than 60 minutes. The headache occurs soon after the aura stops. Muscle-related auras may last longer. MIGRAINE HEADACHE TRIGGERS Migraines can be triggered by stress, worry, menstrual periods, birth control pills, physical exertion, fatigue, lack of sleep, hunger, head trauma, and certain foods or drinks that contain chemicals such as nitrites, glutamate, aspartate, tyramine. A partial list of potential triggers appears in the table (table 2). Certain medications and chemicals can also trigger a migraine, including nitroglycerin (used to treat chest pain), estrogens, hydralazine (used to treat high blood pressure), perfumes, smoke, and organic solvents with a strong odor. Headache diary People who have frequent or severe headaches may benefit from keeping a headache diary over the course of one month. This can be used to determine what triggers the migraines and what makes them better. A sample diary is included here (figure 1).

MIGRAINE HEADACHE TREATMENT TYPES Migraine headache treatment depends upon the frequency, severity, and symptoms of your headache. Acute treatment refers to medicines you can take when you have a headache to relieve the pain immediately. Preventive treatment refers to medicines you can take on a regular (usually daily) basis to prevent headaches in the future.

Acute treatment The pain of migraines can be tough to get rid of. Treatment is most likely to work if you take it at the first sign of an attack (eg, at the first sign of aura if one occurs, or when pain begins). In some people, an aura occurs before the migraine (see 'Aura' above). Therefore, an aura can serve as a reliable warning that a migraine headache is on the way, and should be the signal to take migraine medication. (See "Acute treatment of migraine in adults".) Pain relievers Mild migraine attacks may respond to pain relievers, some of which are available without a prescription. These drugs include: Aspirin Acetaminophen (sold as Tylenol) Nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen (sold as Motrin or Advil), indomethacin, or naproxen (sold as Naprosyn or Aleve). Indomethacin is a prescription medicine that comes in a rectal suppository, which may be useful for people who have nausea during their headaches.

Pain relievers are also available in combination with caffeine, which enhances their antimigraine effect. As an example, some pain relievers contain a combination of acetaminophen, aspirin, and caffeine. Pain relievers are often recommended first for mild to moderate migraine attacks. However, they should not be used too often because overuse can lead to medication-overuse headaches or chronic daily headaches. If you respond to a pain reliever, continue taking it with each attack, as long as you do not take it more than once or twice per week. People with gastritis (inflammation of the stomach), ulcers, kidney disease, and bleeding conditions should not take products containing aspirin or NSAIDs. Anti-nausea medications If you have nausea and vomiting with a migraine, you can take an antinausea medicine by injection or rectal suppository. In some cases, antimigraine drugs can be taken in combination with drugs that alleviate nausea and vomiting, such as metoclopramide or prochlorperazine. Anti-nausea medications given by mouth are usually used in combination with other medications to treat acute migraine. However, anti-nausea medications can be given alone in the hospital by intravenous and intramuscular administration to treat acute migraine headache. Triptans If a pain reliever does not control your migraine pain, most healthcare providers will recommend a treatment that is migraine-specific. This includes a class of medications called triptans. Examples of triptans are sumatriptan (also sold as Imitrex), zolmitriptan (sold as Zomig), naratriptan (sold as Amerge), rizatriptan (sold as Maxalt), almotriptan (sold as Axert), eletriptan (sold as Relpax) and frovatriptan (sold as Frova).

Triptans can be used at home or work/school, and are all available in an oral (pill) form. Sumatriptan and zolmitriptan are available as nasal sprays, and sumatriptan is available as an injection. People with familial hemiplegic migraine, basilar migraine, uncontrolled high blood pressure, vascular disease (including ischemic stroke and coronary artery disease), Prinzmetal's angina, pregnancy, and severe kidney or liver disease should not take triptans in most cases. Sumatriptan Sumatriptan is available in many different formulas, including a tablet, nasal spray, and injection. Over 70 percent of people get pain relief within one hour of injecting sumatriptan; by two hours, 90 percent of people notice improvement. Your healthcare provider can help to decide which formula (pill, nasal spray, or shot) is best for you.

Common side effects of injectable sumatriptan include pain at the injection site, dizziness, a feeling of warmth, and tingling in the arms or legs. Most of these reactions occur soon after the injection and resolve within 30 minutes. These drugs are safe for most patients. Sumatriptan nasal spray begins to work faster than the pill form and has fewer side effects than the injection. The most common side effect of the nasal spray is an unpleasant taste. A tablet that contains a combination of sumatriptan-naproxen (sold as Treximet) appears to be more effective than each medication taken alone. It is not known if taking the two medications separately would be as effective as the combination tablet. Ergots Ergotamine is an older, migraine-specific drug. It is often combined with caffeine. Ergots are not usually as effective as triptans and are more likely to cause side effects. Ergots are sometimes recommended for people with migraines of a long duration (greater than 48 hours) or that frequently recur. People with high blood pressure, coronary artery disease, or kidney or liver disease should not use ergotamines. Dihydroergotamine is related to ergotamine, and can be taken by nasal spray for mild or moderate migraine attacks. It can also be given by injection for severe attacks. Other medications Other medications for migraine are not as well studied or are less effective. A small percentage of people with migraine headaches do not respond to routine acute treatments and may require additional treatment for pain. Dexamethasone is a glucocorticoid (steroid) medication that can be given by injection, along with another acute migraine treatment, to reduce the risk of a migraine coming back. Dexamethasone injections may be given in an emergency department or clinic. Preventive treatment Preventive treatment effectively controls migraine headaches in most people, although the benefits of this treatment may not be evident for three to four weeks. In some cases, both acute treatment and preventive treatment are necessary to adequately control migraines. (See"Preventive treatment of migraine in adults".) Beta blockers Beta blockers were originally developed to treat high blood pressure. In addition, beta blockers reduce the frequency of migraine attacks in 60 to 80 percent of people. Commonly used beta blockers include propranolol, nadolol, atenolol, and metoprolol. Beta blockers may cause depression in some people or impotence in some men. Antidepressant medications Tricyclic antidepressants (TCAs) and certain other antidepressant medications are often recommended for migraine prevention. These include amitriptyline, nortriptyline,

and doxepin. Of these, amitriptyline has proven benefit for migraine prevention, while there is less data for the other tricyclics. Side effects are common with tricyclic antidepressants. Most of these drugs cause drowsiness, particularly amitriptyline and doxepin. Therefore, these drugs are usually taken at bedtime and started at a low dose. Additional side effects of tricyclics can include dry mouth, constipation, palpitations, weight gain, blurred vision, and urinary retention. Confusion can occur, particularly in older adults. Anti-seizure medications The anti-seizure medications valproate (also called divalproex or Depakote), gabapentin, and topiramate (sold as Topamax) are sometimes used to prevent migraines. Valproate is an anti-seizure drug that seems to work as well as beta blockers for preventing migraine, and may be better tolerated. However, valproate can cause weight gain and hair loss. Women who are pregnant or sexually active and not using birth control (pills, condoms, etc) should not take valproate. Gabapentin was effective for reducing migraine headache frequency in a small clinical trial. Potential side effects include lightheadedness, drowsiness, dizziness, and balance problems. Topiramate is an anti-seizure drug that can help to prevent migraine. It can cause mild to moderate side effects that may include abnormal sensations (often tingling), fatigue, nausea, changes in taste, loss of appetite, diarrhea, and weight loss. More severe side effects can occur, including difficulty with thinking and concentration.

Calcium channel blockers Calcium channel blockers were developed to treat high blood pressure. Calcium channel blockers are widely used for migraine prevention. Examples of calcium channel blockers include verapamil and nifedipine extended-release. Verapamil is frequently used as a first choice for preventive migraine therapy because it is easy to use and has few side effects. Calcium channel blockers may lose their effectiveness over time, but this can sometimes be remedied by taking a higher dose of the drug or switching to a similar drug. Herbal therapies Herbal therapies have been evaluated for the treatment of migraine headache, including feverfew and butterbur. Of these, feverfew has been the most widely studied. Some studies have found it to be effective for migraine prevention, although most experts agree that the benefits are still unproven. Neither treatment is recommended. Avoiding medication overuse It is essential to use antimigraine medications according to the prescription and clinician's instructions. Overuse of certain medications for migraine, including over-thecounter drugs such as acetaminophen and nonsteroidal antiinflammatory drugs, or prescription drugs such as triptans, can lead to medication-overuse headaches (also called rebound headaches) and to a pattern of daily headaches that require increasing quantities of drugs for relief. A vicious cycle occurs when frequent headaches cause you to take medications, which then cause rebound headaches as the medications wear off, causing you to take more medication, and so on. (See "Patient information: Headache treatment in adults (Beyond the Basics)".) Speak with a healthcare provider if your migraine treatment does not relieve your headaches or if you are having unpleasant medication side effects. Switching to another drug or switching from acute treatment to preventive treatment may be helpful. MENSTRUAL MIGRAINES

Migraines occur about three times more commonly in women than in men. Estrogen has a variable effect on the frequency and severity of a woman's migraines; some women who take birth control pills (which contain estrogen) or hormone replacement therapy experience worsening headaches, while others improve. Similarly, some women have more frequent or severe headaches during pregnancy while others have improvement. (See "Estrogen-associated migraine".) Menstrual migraines are migraine headaches that occur around the beginning of a woman's menstrual period (usually two days before to three days after the period begins). Women with menstrual migraine may also have migraines at other times during the month. Most often, there is no migraine aura associated with menstrual migraines, even if the woman usually has aura at other times. Menstrual migraines are thought to be triggered by the normal decrease in estrogen levels that occurs before the menstrual period begins. Menstrual migraines tend to be longer lasting, more severe, and more resistant to treatment than other types of migraine. Treatment Initial treatment of acute menstrual migraine is the same as treatment for migraine occurring at any other time. (See 'Acute treatment' above.) Preventive therapies for menstrual migraine can be either nonspecific (those that do not address the hormonal trigger) or specific (hormone-based treatments). (See "Estrogen-associated migraine", section on 'Preventive therapies'.) With nonspecific strategies, success requires accurate anticipation of menses for scheduling interventions; therefore, women with irregular cycles are not good candidates for these options. Coexisting problems, such as dysmenorrhea, menorrhagia, endometriosis, as well as contraception needs may influence choice of preventive therapy. A preventive treatment may be useful for women who have menstrual migraines on a predictable schedule. This treatment strategy is called "mini-prophylaxis". Nonsteroidal antiinflammatory drugs (NSAIDs) such as ibuprofen or naproxen are one option for mini-prophylaxis of menstrual migraine. Triptans such as frovatriptan, sumatriptan, or naratriptan are another option. Typically, long-acting triptans are dosed twice daily beginning two days before anticipated menses and continued for five days.

Hormonal treatments may be recommended to prevent menstrual migraines. One approach is to use estrogen-progestin contraceptive pills in an extended cycle; another choice is menstrually-targeted supplemental estrogen. These treatments work by preventing a rapid decline in the level of estrogen in the body before the menstrual period, which is believed to trigger the migraine. However, some experts avoid treatment with estrogen-progestin contraceptives for women who have a menstrual migraine with aura. Others consider the use of such treatment only for healthy women younger than age 35 who do not have focal neurologic signs and who do not smoke. WHERE TO GET MORE INFORMATION Your healthcare provider is the best source of information for questions and concerns related to your medical problem.

This article will be updated as needed on our web site (www.uptodate.com/patients). Related topics for patients, as well as selected articles written for healthcare professionals, are also available. Some of the most relevant are listed below. Patient level information UpToDate offers two types of patient education materials. The Basics The Basics patient education pieces answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Patient information: Headache (The Basics) Beyond the Basics Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are best for patients who want in-depth information and are comfortable with some medical jargon. Patient information: Headache causes and diagnosis in adults (Beyond the Basics) Patient information: Headache treatment in adults (Beyond the Basics) Professional level information Professional level articles are designed to keep doctors and other health professionals up-to-date on the latest medical findings. These articles are thorough, long, and complex, and they contain multiple references to the research on which they are based. Professional level articles are best for people who are comfortable with a lot of medical terminology and who want to read the same materials their doctors are reading. Acute treatment of migraine in adults Basilar-type migraine Chronic migraine Estrogen-associated migraine Evaluation of headache in adults Headache syndromes other than migraine Headache, migraine, and stroke Preventive treatment of migraine in adults The following organizations also provide reliable health information. National Library of Medicine

(www.nlm.nih.gov/medlineplus/migraine.html, available in Spanish) National Institute of Neurological Disorders and Stroke

(www.ninds.nih.gov/disorders/migraine/migraine.htm) American Headache Society

(www.achenet.org/resources/information_for_patients/) [1-4]

Literature review current through: Aug 2012. | This topic last updated: Dec 16, 2011.
Find Print The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care p

http://www.jaoa.org/content/107/suppl_6/ES10.full

Diagnosing and Managing Migraine Headache

1. Loretta L. Mueller, DO + Author Affiliations 1. Dr Mueller is an associate professor of family medicine and director of the University Headache Center at the University of Medicine and Dentistry of New JerseySchool of Osteopathic Medicine in Stratford. Dr Mueller has been principal investigator in clinical trials for Merck & Co, Inc; GlaxoSmith Kline, Vernalis, Ortho-McNeil, and AstraZeneca. She is a national consultant for Merck & Co, Inc, and on speakers bureaus for Merck & Co, Inc, and GlaxoSmithKline. 1. Address correspondence to Loretta L. Mueller, DO, University Headache Center, 42 E Laurel Rd, University Doctors Pavilion, Ste 1700, Stratford, NJ 08084-1354. E-mail:SOMPhysicians@umdnj.edu Next Section

Abstract
Headache is one of the chief complaints among patients visiting primary care physicians. Diagnosis begins with exclusion of secondary causes for headache. More than 90% of patients will have a primary-type headache, so diagnosis can often be completed without further testing. Although tension-type headaches are the most common kind of headache, patients with this type of headache rarely seek treatment unless occurrence is daily. Migraine, which affects more than 30 million people in the United States, is the most common headache diagnosis for which patients seek treatment. Migraine is a chronic, often inherited condition involving brain hypersensitivity and a lowered threshold for trigeminal-vascular activation. Intermittent debilitating attacks are characterized by autonomic, gastrointestinal, and neurologic symptoms. Migraine results in a marked decrease in a patient's quality of life, as measured by physical, mental, and social health-related instruments. Accurate assessment of a patient's disability will guide physicians in prescribing appropriate modes of therapy. However, migraine remains underdiagnosed, and patients with migraine remain undertreated. A comprehensive treatment approach to migraine may include nonpharmacologic measures, as well as abortive and prophylactic medications. Informing patients about realistic treatment expectations, possible delayed efficacy of medications, and avoidance of caffeine and overuse of medications is critical for successful outcomes. Management of migraine is a dynamic process, because headaches evolve over time and medication tachyphylaxis may occur, necessitating changes in therapy. Pathologic findings in the neck constitute an accepted etiology or precipitant for headache. Osteopathic manipulative treatment may reduce pain input into the trigeminal nucleus caudalis, favorably altering neuromuscularautonomic regulatory mechanisms to reduce discomfort from headache. Previous SectionNext Section

Migraine is a common condition, annually affecting 12% of the United States population, including 18% of women, 6% of men, and 4% of children.1-3 Lifetime prevalence of migraine in women in the United States exceeds 25%.1-3 The prevalence of migraine has not changed since 1989, based on evidence from three large studies: American Migraine Study I,1 American Migraine Study II,2 and American Migraine Prevention and Prevalence Study.3 Migraine in the United States is more prevalent in Caucasians than in African Americans, and the lowest prevalence in the United States is among Asian Americans.2 Migraine is generally more common in people who are in lower socioeconomic groups.2 Migraine typically begins affecting individuals when they are in their teens or twenties, with peak prevalence occurring at approximately age 40 years.2 First onset of migraine after age 50 years should raise suspicion of secondary headache causes. One quarter of adults with migraine will experience four or more severe attacks per month, each with a mean duration of about 24 hours.2 Previous SectionNext Section

Diagnosis of Migraine
Migraine is a diagnosis strongly linked to a patient's medical history. Typical characteristics of migraine headache include unilateral throbbing pain associated with moderate to severe disability, nausea, vomiting, phonophobia, photophobia, and increased pain with physical exertion.4 Migraine in children is generally shorter in duration than migraine in adults, with less pronounced associated symptoms and possible presentation as cyclic vomiting, abdominal symptoms, or paroxysmal vertigo rather than head pain.4 It is important to note that no isolated characteristic is necessary to make the diagnosis of migraine. The three most predictive characteristics for a migraine diagnosis are disability, nausea, and photophobia.5 An abbreviated set of diagnostic criteria for migraine is available in a validated screening instrument called ID Migraine.5

Less than a third of patients with migraine have focal neurologic signs, termed auras, just before or during some headaches.4 The diagnosis for these patients is migraine with aura (formerly called classic migraine), in contrast to migraine without aura (formerly called common migraine).4Auras are most commonly visual and less commonly sensory or motor in nature. Migraines associated with motor auras are called hemiplegic migraines and may occur on a hereditary basis within families and a sporadic basis among individuals.4Triptans are contraindicated for patients with hemiplegic migraine because of a lack of adequate testing of these medications in this small population. Migraine is often mistaken for sinus or tension headache. Migraine is confused with sinus headaches because the autonomic symptoms of migraine include nasal stuffiness or discharge, occurring in 87% of patients with migraine.6 In addition, the headache in these patients may be located above the sinuses.6 Migraine often is confused with tension headache because 75% of patients with migraine have neck pain during or immediately before or after a migraine.7 The diagnosis of migraine is based on criteria developed by the International Headache Society in 1988 and revised by the society in 2004the International Classification of Headache Disorders II (ICHD II).4 Similar to the Diagnostic and Statistical Manual of Mental Disorders (DSM IV) used in psychiatric evaluations, the ICHD II requires that patients' headaches must have certain characteristics for each kind of diagnosis (Figures 1 and 2). Headaches are categorized by primary or secondary headaches, with four broad groups of primary headaches, including migraine, tension, cluster, and miscellaneous headaches, and 10 broad groups of secondary headaches (Figure 2).4 Although necessary for medical research, the ICHD II criteria4may be cumbersome for use by physicians in the primary care setting. Nevertheless, the criteria do offer a process for organizing a differential diagnosis; if patients have the symptoms listed in the criteria, physicians are more comfortable that the patient truly has that primary headache diagnosis and is less likely to have a brain tumor or other grave condition.

Any abnormalities in a patient's medical history or physical examination suggesting secondary headache must be carefully evaluated before making a primary headache diagnosis. However, recommendations by the US Headache Consortium8 state that neuroimaging is generally not necessary in adult patients presenting with typical migraine, normal findings on neurologic examination, and no recent change in headache characteristics.9 These recommendations are based on data indicating that only 0.18% of this patient group show a clinically significant intracranial pathologic lesion on neuroimaging.9

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Figure 1. The International Classification of Headache Disorders II (ICHD-II) criteria for migraine without aura. (Source: Headache Classification Subcommittee of the International Headache Society. The international classification of headache disorders. Cephalalgia. 2004;24(suppl 1):14160.) Previous SectionNext Section

Triggers of Migraine
Migraine is believed to be an inherited condition of cortical hyperexcitability.10 Some patients with migraine are able to identify headache triggers. Triggers may be inconsistent or additive and are not specific to migraine. For example, menses is a trigger for 60% of female migraineurs and is also a trigger for tension-type headache.11 Stress or let-down after a stressful event, change in sleep or meal schedules, and such environmental factors as loud noise, odors, or flickering lights may also precipitate migraine headache.11

Approximately a quarter of patients with migraine recognize certain food as migraine triggers.12 Such triggers include monosodium glutamate (also known as hydrolyzed yeast extract, natural flavoring, hydrolyzed vegetable protein), often found in soups and Chinese food.12 Nitrites (a preservative found in lunch meats and hot dogs), tyramines (found in wines and such aged foods as cheeses), and phenylethylamine (found in chocolate, garlic, nuts, raw onions, and seeds) are other potential migraine triggers.12 Alcohol of any kind, artificial sweeteners, citrus fruits, pickled products, and vinegars are additional likely triggers.12 It should be noted that not all patients have these food triggers, so a diet totally eliminating these items is not warranted in all migraineurs. Daily consumption of caffeine can lead to caffeine withdrawal headaches or rebound headaches interfering with or negating the effects of migraine preventive medications. Daily caffeine consumption is much greater than many people expect, with a typical cup (8 oz) of drip coffee containing about 135 mg of caffeine.13 Patients should be advised that caffeine is used in combination with many over-the-counter (OTC) pain medications because it enhances analgesia.14,15 Caffeine has a half-life of up to 9.5 hours; and the body transforms it into more than 25 metabolites.14 Overuse of caffeine is a risk factor for progression of occasional migraine to a chronic daily pattern. Additional considerations for such a progression include acute medication overuse, depression, obesity, sleep disorders, and stressful life events.16 Head trauma may cause or exacerbate headaches. Based on ICHD II criteria,4 new onset of headaches within 7 days of head trauma is diagnosed as posttraumatic headache, while continued headache after 3 months is termed chronic posttraumatic headache. Even mild head trauma without loss of consciousness or objective findings can cause new onset or exacerbation of headaches, necessitating long-term management.4 The proposed neurophysiologic basis for cervicogenic headache is nocioceptive input from trigeminal and cervical (C1-C3) afferent neurons converging on second-order neurons in the trigeminocervical

nucleus.17 In addition, several recent anatomic discoveries identify direct neuronal connections between extracranial structures and the dura mater.18 Hack et al19 found a neuronal connection between the rectus capitis posterior minor muscle and dorsal spinal dura mater at the atlanto-occipital junction, which appears to restrict dural movement toward the spinal cord. Abnormalities in the cervical spine, such as muscular spasm, may transmit forces to the pain-sensitive dura mater. Theoretically, alleviating accessible causes of pain through such modalities as osteopathic manipulative treatment (OMT) should increase a patient's headache thresholds. However, because of a lack of controlled studies on OMT and other modalities, biofeedback is the only nonpharmacologic therapy for migraine that is considered to be evidence-based by the US Headache Consortium.8 Previous SectionNext Section

Pharmacologic Management of Migraine

Abortive Medications More than 90% of patients with migraine have disability with their attacks, and half these patients require bed rest.20Despite this high level of disability, less than 60% of patients with migraine have their headache diagnosed as such by a physician.20 Thus, many patients are not adequately treated with abortive or prophylactic medications for migraine. A major obstacle in diagnosing headache in a primary care setting is time constraint. An average office visit by a patient to a primary care physician lasts 9 minutes and usually addresses multiple complaints.2 Scheduling additional visits specifically to address the headache complaint and having patients keep diaries of headache frequency, severity, and medications may help overcome obstacles to proper diagnosis and treatment.

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Figure 2. The International Classification of Headache Disorders II (ICHD II) outline of primary headache disorders and secondary headache disorders, developed by the International Headache Society in 1988 and revised by the society in 2004. (Source: Headache Classification Subcommittee of the International Headache Society. The international classification of headache disorders. Cephalalgia. 2004;24(suppl 1):14160.) Patients are usually not adept at initiating accurate descriptions of disability experienced during migraine attacks, and physicians may not accurately assess migraine-related disability of their patients, many of whom may be healthy young individuals between headache attacks. In light of these problems, a clinically useful, validated instrument for disability assessment is the Migraine Disability Assessment (MIDAS) tool,21 which can be used to assess the number of work or school days lost during a 3-month period due to migraine. Studies show that healthcare providers are more likely to treat patients with effective, migraine-specific therapeutic modalities if they are aware of the patients' migraine disabilities.22,23 The Disability in Strategies of Care (DISC) trial22 confirmed that patients with moderate to severe migraine-caused disability are more likely to respond to high-end modes of therapy. In the DISC trial, 75% of patients had a failed response to high-dose aspirin (800-1000 mg/d) and metoclopramide (10 mg/d) therapy, requiring zolmitriptan (2.5 mg/d) as effective high-end therapy. The US Headache Consortium recommends serotonin 5HT1B/D agonists (ie, triptans) as first-line therapy in a stratified-care approach for patients with migraine who experience moderate to severe disability (Figure 3).23 Seven triptans are available for migraine, all in tablet formulation.23Two of these triptans (rizatriptan, zolmitriptan) are available as oral wafers that may be taken without water; two (sumatriptan, zolmitriptan) are available as nasal sprays; and one (sumatriptan) is available in a subcutaneous formulation.23 Headache

relief with triptans is not pathognomonic to migraine; migraine, tensiontype, and secondary headaches may all respond to these drugs.24Conversely, not all migraines respond to triptans.24 Triptans have the same contraindications in patients with known or suspected ischemic cardiac, cerebrovascular, peripheral vascular, or uncontrolled hypertensive disease.25However, the Triptan Cardiovascular Safety Expert Panel concluded that chest symptoms occurring with triptan use are generally not serious or ischemic; the incidence of serious cardiovascular events with triptan use appears to be extremely low; and the cardiovascular risk-benefit profile of triptans favors their use in the absence of contraindications.25One type of triptan should not be combined with another type or with a vasoconstrictor within 24 hours of administration. Rizatriptan, sumatriptan, and zomitriptan should not be used within 2 weeks of administration of a monoamine oxidase (MAO) inhibitor; rizatriptan should be dosed at 5 mg per dose for patients using propranolol hydrochloride; and eletriptan should not be used within 3 days of the use of strong cytochrome P4503A inhibitors, such as clarithromycin. Labels on all triptans carry a cautionary statement noting that these drugs may cause the serotonin syndrome when used in combination with other serotonergic drugs such as serotonin reuptake inhibitors (SSRIs, including the antidepressant fluoxetine hydrochloride).26 Symptoms of serotonin syndrome may include autonomic hyperactivity such as tremor, diarrhea, hypertension and tachycardia. Neuromuscular abnormalities or mental status changes such as rigidity, hyperreflexia, hyperthermia, anxiety, or akathisia are additional symptoms. Although all triptans have documented efficacy for migraine with and without aura (including menstrual migraine), naratriptan and frovatriptan generally have slower onset of action as demonstrated by 2 hours' pain relief data.

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Figure 3. Prophylactic medication considerations for patients with migraine, as recommended by the United States Headache Consortium. (Source: Silberstein SD. Practice parameter: evidence-based guidelines for migraine headache (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology [published erratum appears in Neurology.2000;56:142]. Neurology. 2000;55: 754-762.) Interpatient variability also exists for triptan efficacy, with different patients responding differently to particular triptans, and some patients requiring transition from one triptan to another to maintain efficacy.23 Assessment of efficacy of triptans and other abortive medications should be repeated at each patient visit, with several questions asked of patients and various target endpoints addressed (Figure 4). Alternative abortive medications to triptans include ergots and their synthetic derivative, dihydroergotamine; butalbital-containing analgesics or other analgesic combinations; isometheptene mucate combination; nonsteroidal anti-inflammatory drugs (NSAIDs); and opioids.23 Administration of butalbital-containing products is controversial because there are no placebo-controlled trials supporting their efficacy for migraine. In addition, the potential exists for butalbital overuse resulting in rebound headaches, and some patients may use butalbital-containing products to treat underlying comorbid anxiety.23 Opioid therapy is also controversial, with several studies reporting activation of pronociceptive mechanisms with long-term use of opioids.27,28 Rescue treatment options when first-line agents fail in an outpatient or emergency department setting include the following: dihydroergotamine, divalproex sodium,29droperidol,30 intranasal lidocaine,31 ketorolac, magnesium sulfate,32 opioids, parenteral sumatriptan, prochlorperazine,

propofol,33 and steroids. All of these medications except sumatriptan and dihydroergotamine are used off-label for migraine. Abortive polytherapy is an option when single agents do not provide adequate relief for patients with migraine. An NSAID and/or a gastrokinetic drug (eg, metoclopramide) may be used in addition to a triptan.34 Researchers have found that cutaneous allodynia (a condition in which such nonnoxious stimuli as mechanical pressure and thermal changes cause skin pain) develops in nearly 80% of patients with migraine.35 Studies indicate that cutaneous allodynia is a marker for central sensitization and abortive medications are less likely to produce complete pain relief after this phenomenon develops.35 Providing abortive treatment during the early mild phase of migraine results in higher pain-free rates among patients.35However, for patients with frequent headaches who consistently require treatment more than 2 days per week, prophylactic medication may be needed to reduce headache frequency. The potential for headache rebound exists with frequent use of most abortive medications, including butalbitalcombination products, caffeine-containing products, and triptans.23

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Figure 4. Factors to assess and target endpoints for assessment of efficacy of abortive medications in treatment of patients with migraine. Prophylactic Medications Generally, prophylactic medications (Figure 3) are taken daily to reduce headache frequency, decrease headache intensity, and/or allow for improved abortive management of migraine. However, more subtle

improvements in quality of life may warrant continuation of prophylactic therapy, even if a high level of headache reduction is not achieved. Serial MIDAS tests can monitor improvements for such measures as lost work or school days and loss of productivity related to home chores or social functions.21 More than one prophylactic medication may be used in combination when only a partial response is achieved with one drug and when that drug's dosage cannot be increased because of maximal dose or drug intolerance. Prophylactic modes of therapy may be used intermittently for headaches occurring at predictable times, such as during menses, exercise, or sexual activity.23 Physicians should keep in mind that prophylactic medications are not a cure for headache, and abortive therapy will remain necessary for breakthrough attacks. In addition, patient education about medication use is important for compliance. No prophylactic medication was originally developed to treat patients with migraine, and only four medications have US Food and Drug Administration (FDA) indication for migraine: divalproex sodium, propranolol, timolol maleate, and topiramate. Major classes of prophylactic medications for migraine include antiepileptics, -blockers, calcium-channel blockers, and tricyclic antidepressants (Figure 3).23 The exact physiologic mechanisms of these varied drugs are not known, but the mechanisms are believed to involve suppression of central hyperexcitability and/or enhancement of antinociceptive pathways.10 Comorbidities (eg, angina, depression, epilepsy) generally will influence prescribing considerations for prophylactic medications (Figure 3). The US Headache Consortium has published evidence-based guidelines for selecting a prophylactic medication for patients with migraine.23 There are conflicting reports regarding the efficacy of botulinum toxin A for migraine or chronic daily headache prophylaxis, with most studies not achieving primary endpoint efficacy.36 For patients with infrequent migraines and those who are reluctant or unable to use prescription prophylactic medications, alternative agents

may be considered. Dietary supplements that may be effective for migraine prevention, based on results of placebo-controlled trials, include butterbur root (Petasites hybridus), coenzyme Q10, feverfew, magnesium, melatonin, and riboflavin (vitamin B2).37,38 Many combination products are available, such as MigreLief (feverfew, magnesium, riboflavin) and Migravent (butterbur root, feverfew, magnesium, riboflavin; Vita Sciences, Airmont, NY). The following anecdotal case presentation describes a typical patient whose case illustrates the diagnosis and management of migraine. Previous SectionNext Section

Case Presentation
Cheryl is a 44-year-old woman with perimenopausal symptoms of hot flashes interrupting sleep. She is seen by her physician because of an exacerbation of headaches that are unilateral, hemicranial, throbbing, and associated with nausea and photophobia. At times she must lie in a dark quiet room to try to help ease her headache pain. She denies having associated neurologic symptoms such as vision loss, but she says that she often yawns for several hours before headaches, and she has some nasal congestion and neck ache during the pain phase. Cheryl's headaches started at age 14 years, typically occurring only during her menses and persisting for 1 day. She now complains of a gradual increase in headache frequency and duration during the previous 2 years, with her typical bad headaches (ie, migraine without aura) occurring both during menses (lasting 4 days) and outside of menses (two attacks lasting 1 day each). Sumatriptan succinate tablets (100 mg/d) no longer provide her with adequate relief. On further questioning, Cheryl admits to milder headaches occurring on a daily basis for at least the entire previous year. She says she manages those headaches daily with six OTC combination analgesics containing caffeine, accounting for 390 mg of caffeine (65 mg/tablet) per day. She had not initially noted this analgesic use on her medication list because she believed she could control these milder headaches on her own. She

also admits to drinking two cups of coffee daily (20 oz each), accounting for approximately 675 mg of additional caffeine (135 mg/8 oz)13 per day. Cheryl reports that all previous preventive treatments had failed, including divalproex sodium (1000 mg/d for 3 wk), topiramate (25 mg/d for 2 mo), and verapamil (240 mg/d for 1 mo). She notes that she could not tolerate propranolol hydrochloride (60 mg/d) because it made her too tired. Management of Cheryl's Headaches Make the Proper DiagnosisTake a detailed headache history of the patient, including all prescription and OTC medications used and the frequency of their use. Cheryl's headache diagnosis is migraine without aura, in addition to probable medication overuse headache. She has a long history of typical migraines. However, the character of her headaches has changed. They have become more frequent and more difficult to manage, requiring additional medications. These changes may indicate the need for further testing, such as brain MRI, though there are certain known reasons for escalation of Cheryl's headaches. She is overusing caffeine and analgesics, substances that may cause, worsen, or maintain her daily headache pattern. She is also perimenopausal, with hormonal fluctuations and sleep disturbance. Thus, it may be reasonable to withdraw the overused agents with close follow-up before conducting further testing. Educate the Patient About Nonpharmacologic Management Cheryl should understand that her diagnosis is migraine, that there are no objective markers for this disorder, and that it is usually inherited, chronic, and biochemical in nature. There is no single definitive cause of migraine or definitive treatment for patients with migraine. However, the disorder can be successfully managed. It is important for the patient to stay regimented in her daily schedule, including meals and

sleep. Fluid intake should be maintained, because dehydration is a trigger for migraine. Any identified food triggers for migraine should be avoided, though food may not consistently trigger headaches and may be additive with other stimuli. The patient should be especially careful to avoid migraine triggers during her most vulnerable time for headaches (ie, during menses). Regular exercise may have beneficial effects on headaches. Relaxation activities, including biofeedback training, listening to relaxation tapes, and performing yoga, may also be beneficial. Furthermore, OMT for paravertebral cervical spasm associated with headaches may be beneficialthough some patients have cutaneous allodynia during acute migraine and may prefer not to be touched at such times.

Educate the Patient About Pharmacologic Management Use of all analgesics and caffeine was terminated. Cheryl was warned that she would probably have more intense headaches while withdrawing from these substances and that any prescribed abortive medications may not work as effectively as a caffeine product for the next few weeks. Removal of offending agents alone may markedly improve headaches, but most patients still require prophylactic therapy. Treatment with prophylactic medications was initiated immediately, and Cheryl was made aware that medication doses are started low and gradually increased, depending on observed efficacy and adverse effects. It may take 3 months for prophylactic medications to achieve complete benefit at the full therapeutic doses. In the past, this patient did not achieve effective doses of prophylactic medications or did not use these medications long enough. In addition, she had been overusing caffeine and abortive

medications during prophylactic medication trials, rendering the medications ineffective. Initiate Treatment Cheryl was educated; weaned off caffeine and an OTC proprietary acetaminophenacetylsalicylic acid (ASA)-caffeine formulation; started on an alternative triptan for first-line acute treatment; and given a second-line abortive medication (a phenothiazine) for nausea and/or rescue pain when the triptan did not provide complete relief. Rescue therapy is often sedating, but the goal of rescue therapy is alleviation of pain and associated symptoms rather than restoring full function. Cheryl was encouraged to not take any OTC medications for her daily milder headaches, but she was given an NSAID as needed for up to 2 days per week. A daily regimen of lowdose amitriptyline (10 mg/d for 1 wk; then 20 mg/d) at bedtime was started for headache prevention; this medication also helped Cheryl sleep. She was provided with detailed written instructions on her treatment and a diary to keep track of her headache frequency, severity, and medications. Have the Patient Follow Up Headaches change with time, and secondary headaches may develop in patients who have had life-long headaches. In addition, abortive and prophylactic medications need to be continually assessed and adjusted to achieve maximal benefit. Physicians should review headache diaries, any medication adverse effects, and any changes in medical condition that may warrant changes in therapy. Generally, prophylactic medications are continued for approximately 6 months if a beneficial response is achieved, then attempts are made to wean the patient away from the medications.

Prophylactic medications may be stopped with continued observed benefits, or headaches may worsen. If headaches worsen, the lowest dose that adequately controls headache should be maintained. Cheryl had severe headaches during the first week she was off caffeine and the acetaminophen-ASA-caffeine formulation. She then noticed a lessening of headache intensity, with some headache-free days by the third week of therapy. At her next visit, 1 month later, amitriptyline was increased to 40 mg/d. Two months after her second visit, Cheryl had only one migraine with menses per month. The use of her triptan during these episodes provided complete pain relief within 2 hours. Recurrence of headache 24 hours later was again relieved with her triptan. After 2 months, Cheryl rarely had mild tension-type headaches and did not require abortive treatment for such headaches. Previous SectionNext Section

Comment
Migraine is the most common type of headache seen in primary care. Yet, migraine is often not properly diagnosed, and patients with migraine are often inadequately treated because of physician time constraints, lack of physician understanding of migraine-related disabilities, incorrect patient self-diagnosis, and/or incomplete patient medication history. Successful management of migraine requires intensive patient education and thorough physician knowledge about available treatment options and strategies. These treatment options and strategies include stratified care with a migraine-specific abortive medication for patients with moderate to severe disability; early intervention with an abortive medication before central sensitization occurs; and the use of a

prophylactic medication to reduce headache frequency, severity, and risk for rebound. Previous Section

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Pathophysiology: What Happens in Your Brain During a Migraine

First, what is pathophysiology? Pathophysiology refers to the changes that occur in the body's systems, resulting in abnormal function, as a result of an illness, a disease, or an abnormal condition such as migraine. Scientists are constantly learning new information about what happens in your brain at the start of a migraine and during a headache. Most of us have probably heard about changes in blood vessels associated with migraine headaches. It might seem that blood vessels constrict during a migrainethat would seem logical, wouldn't it? And so they do, some of thembut the entire situation is not as simple as originally thought. Initially, it was thought that the blood vessels on the surface of your brain dilate, and with each heartbeat, the blood surging through throws the dilated blood vessel wall up against your skull, resulting in that throbbing pounding pain you are so familiar with. And migraines were termed vascular headaches. Recently, that phenomenon has been thrown into doubt, although various experts disagree. Certainly, though, it is not as simple as just blood vessel changes. Migraine mostly happens within your brain. Several things happen at the beginning of a migraine attack, and we are not yet sure exactly what happens first, or whether one leads to another.

CHANGES IN YOUR BRAINCORTICAL SPREADING DEPRESSION

We know that there are waves of electrical changes that go across the brain, starting at the back and moving slowly towards the front. First there is a wave of excitation, followed by what is called spreading cortical depression. This has been known since the 1940s, when it was discovered in rabbits by a Brazilian neurologist named Leo, although it wasn't immediately associated with migraine at that time. Interestingly, though, there was another neurologist at about that time (named Lashley) who tracked the spread of his ownvisual auras, and found that they moved at about 2-3 mm/minute. This is about the same speed as cortical spreading depression.

We have since made an association between cortical spreading depression and migraine aura. And, in fact, we have been able to demonstrate very slow changes moving across the brain during migraine aura on both blood oxygen level dependent (BOLD) MRI studies and magnetoencephalography. These changes move at a rate consistent with the speed of cortical spreading depression. Although most of these studies have been done in migraine with aura, there is one PET study done in a single patient who has migraine without aura showing slowing of blood flow in a similar pattern, suggesting that cortical spreading depression may occur in migraine without aura as well. Obviously, it is much harder to study in migraine without aura, as it is more difficult to determine when the beginning of the attack is in order to test it. Recent studies of blood vessels in the brain during cortical spreading depression show that there is constriction of the blood vessels as the waves of spreading depression pass over the brain. There is also a drop in oxygenation of that segment of the brain as a consequence. Yes, youre rightthats not a good thing. Fortunately, it does not last long until the wave passes along.

Brainstem Activation
There is also evidence of brainstem activation at the beginning of a migraine. Areas of the brainstem show up as brightly active on PET scans in the beginning of a migraine attack. These studies have indicated that brainstem activation occurs in both migraine with and without aura. If you like, take a look at diagrams of the brainstem and other brain areas. So is this what causes the pain? Well, yes and no. We know that these areas of the brainstemthe raph nucleus, and the locus cruleusare important in the maintenance of mood and the processing of pain. Other brainstem areas, the substantia nigra and the red nucleus, were previously thought to be more important for normal movement, and we have found recently that they have a role in headache pain as well.

But that's not the whole migraine pain story. We still haven't gotten to the inside of your head, really. Everything we have talked about so far has happened at the base of the brain or on its surface. And we haven't really covered that in detail yet.

EXCITABLE NEURONS
Based on research, the best understanding we now have is that migraine arises from abnormally excitable neurons in the brain and trigeminal nerve. What causes the neurons to be abnormally excitable? Various things can do this, including low magnesium, abnormal calcium channels on the surface of the neuron, mitochondrial abnormalities, or other inherited brain chemical abnormalities. The newest things in the migraine story are the gliathe support cells in the brainwhich also appear to have a role in transmitting pain, perhaps moreso in chronic headache, although their story is still being determined. The trigeminal nerves start in the brainstem in the trigeminal nucleus caudalis, and travel to your face, teeth, eyes, sinuses, and forehead. They also go to the blood vessels on the surface of the brain. So, now we have excitable neurons, and (maybe) dilating blood vessels. These make up what we call thetrigeminovascular system, or trigeminovascular theory of migraine. Now, why maybe? A recent study has shown that this may not actually be the case, and that vascular headaches may not even be vascular at all! A study in Brain conducted by Schoonman et al induced experimental migraine in both migraine sufferers and control subjects with intravenous nitroglycerine. The controls developed dilation of the meningeal vessels (the ones on the surface of the brain); the migraineurs did not. This result casts some doubt on the trigeminovascular theory, particularly if these results are replicated by other similar studies. While there is still some controversy over the "vascular" part of migraine, the situation was recently summed up by Dr. Andrew Charles, UCLA migraine researcher. Dr. Charles indicated that while it is clear that vascular

changes occur in migraine, it does not mean migraine is triggered by vascular processes, and that the dilation of blood vessels is neither necessary nor sufficient for causing migraine pain. According to existing trigeminovascular theory, once the messages come from the activated cells in the trigeminal nucleus in the brainstem, and travel to the trigeminal nerves that go to the dural blood vessels on the brain's surface, it causes dilation. However, the trigeminal activation also causes the release of brain chemicals called neuropeptides (substance P, CGRP or calcitonin gene-related peptide, neurokinin A, 5HT or serotonin, and noradrenalin.)
ALLODYNIA

The release of these chemicals causes inflammation, and what is called peripheral sensitization. This is most likely what results in the throbbing pain most people experience. As the attack progresses, something can occur called central sensitization. When this occurs, it causes what is known as cutaneous allodynia. This means that things that are usually just a normal touch are now felt as painful. Many headache patients withallodynia cannot continue to wear earrings, necklaces or neckties, or their glasses. Some find that they cannot lie down on the side of the head pain, or report that "even their hair hurts." Up to 80% of migraine sufferers are affected by some degree of cutaneous allodynia, and it generally occurs in the late stages of a migraine attack when the pain is severe. This is why it is important to treat early when the pain is mild or moderate. When central sensitization becomes advanced, it can involve areas beyond the head, and simple touch on the arms or shoulder can be perceived as painful. For example, I am aware of one migraine sufferer who is bothered by the seams in her clothing during such an attack. At this stage of the migraine, migraine-specific medication is less likely to be helpful, and studies have shown that while they will reduce the pain and relieve the throbbing, they cannot abort the attack, and allodynic pain remains as well as other migraine symptoms.

In late-stage migraine, other medications may be necessary in order to end the attack. We do not yet have migraine-specific medications designed for the late stage of the migraine attack, although research into migraine pathophysiology is ongoing. As we learn more, it should lead to better developments in the treatment of migraine.
References: 1. Leo, APP. Spreading depression of activity in the cerebral cortex. J. Neurophysiol. 1944; 7:359-90. 2. Leo, APP, Morison, RS. Propagation of spreading cortical depression. Neurophysiol.1945; 8:33-45. 3. Lashley K. Patterns of cerebral integration indicated by scotomas of migraine. Arch. Neurol. Psychiatry 1941; 46: 331-339. 4. Charles A, Brennan K. Cortical Spreading DepressionNew Insights and Persistent Questions. Cephalalgia. 2009;29(10):1115 -1124. 5. Malick A, Burstein R. Peripheral and central sensitization during migraine. Funct. Neurol. 2000;15 Suppl 3:28-35. 6. Olesen J, Larsen B, Lauritzen M. Focal hyperemia followed by spreading oligemia and impaired activation of rCBF in classic migraine. Annals of Neurology. 1981; 9,344-352. 7. Burstein R, Cutrer MF, Yarnitsky D. The development of cutaneous allodynia during a migraine attack clinical evidence for the sequential recruitment of spinal and supraspinal nociceptive neurons in migraine. Brain. 2000;123 ( Pt 8):1703-1709. 8. Burstein R, Yarnitsky D, Goor-Aryeh I, Ransil BJ, Bajwa ZH. An association between migraine and cutaneous allodynia. Ann. Neurol. 2000;47(5):614-624. 9. Charles, A. Intercellular calcium waves in glia. Glia. 1998; 24:39-49. 10. Schoonman GG, van der Grond J, Kortmann C, et al. Migraine headache is not

associated with cerebral or meningeal vasodilatationa 3T magnetic resonance angiography study. Brain. 2008;131(8):2192 -2200. 11. Hadjikhani N, Sanchez del Rio M, Wu O, Schwartz D, Bakker D, Fischl B, Kwong KK,

Cutrer, FM, Rosen BR, Tootell RBH, Sorensen AG, Moskowitz MA. Mechanisms of migraine aura revealed by functional MRI in human visual cortex. PNAS. 2011; ,9:4687-4692. by Christina Peterson, M.D. Updated June 25, 2011

http://en.wikipedia.org/wiki/Migraine

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

Migraine is a chronic disorder characterized by recurrent moderate to severe headaches often in association with a number of autonomic nervous system symptoms. The word derives from the Greek (hemikrania), "pain on one side of the head",[1] from - (hemi-), "half", and (kranion), "skull".[2] Typically the headache is unilateral (affecting one half of the head) and pulsating in nature, lasting from 2 to 72 hours. Associated symptoms may include nausea, vomiting,photophobia (increased sensitivity to light), phonophobia(increased sensitivity to sound) and the pain is generally aggravated by physical activity.[3] Up to one-third of people with migraine headaches perceive an aura: a transient visual, sensory, language, or motor disturbance which signals that the headache will soon occur.[3] Migraines are believed to be due to a mixture of environmental and genetic factors.[4] About two-thirds of cases run in families.[5] Fluctuating hormone levels may also play a role: migraine affects slightly more boys than girls before puberty, but about two to three times more women than men.[6][7] Propensity for migraines usually decreases during pregnancy.[6] The exact mechanisms of migraines are not known. It is,

however, believed to be a neurovascular disorder.[5] The primary theory is related to increased excitability of the cerebral cortex and abnormal control of pain neurons in the trigeminal nucleus of thebrainstem.[8] Initial recommended management is with simple analgesics such as ibuprofen and acetaminophen for the headache, an antiemetic for the nausea, and the avoidance of triggers. Specific agents such as triptans orergotamines may be used by those for whom simple analgesics are not effective. Globally, more than 10% of the population is affected by migraine at some point in life.

Signs and symptoms

Migraines typically present with selflimited, recurrent severe headache associated with autonomicsymptoms.[5][9] About 15-30% of people experience migraines with an aura[10][11] and those who have migraines with aura also frequently have migraines without aura.[12] The severity of the pain, duration of the headache, and frequency of attacks is variable.[5] A migraine lasting longer than 72 hours is termed status migrainosus.[13] There are four possible phases to a migraine, although not all the phases are necessarily experienced:[3]
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, the effects experienced following the end of a migraine attack

[edit]Prodrome

phase

Prodromal or premonitory symptoms occur in ~60% of those with migraines[14][15] with an onset of two hours to two days before the start of pain or the aura [16] These symptoms may include a wide variety of phenomena[17]including: altered mood, irritability, depression or euphoria, fatigue, craving for certain food, stiff muscles (especially in the neck), constipation or diarrhea, and sensitivity to smells or noise.[14] This may occur in those with either migraine with aura or migraine without aura.

Aura phase

An aura is a transient focal neurological phenomenon that occurs before or during the headache.[15] They appear gradually over a number of minutes and generally last fewer than 60 minutes.[19] Symptoms can be visual, sensory or motor in nature and many people experience more than one.[20] Visual effects are the most common, occurring in up to 99% of cases and exclusively in more than half.[20] Vision disturbances often consists of a scintillating scotoma (an area of partial alteration in the field of vision which flickers.)[15] These typically start near the center of vision and then spread out to the sides with zigzagging lines which have been described to look like fortifications or walls of a castle.[20] Usually the lines are in black and white but some people also see colored lines.[20] Some people lose part of their field of vision known as hemianopsia while others experience blurring.[20] Sensory aura are the second most common occurring in 30-40% of people with auras.[20] Often a feeling of pins-and-needles begins on one side in the hand and arm and spreads to the nose-mouth area on the same side.[20] Numbness usually occurs after the tingling has passed with a loss of position sense.[20] Other symptoms of the aura phase can include: speech or language disturbances, world spinning, and less commonly motor problems.[20] Motor symptoms indicate that this is a hemiplegic migraine, and weakness often lasts longer than one hour unlike other auras.[20] An aura rarely occurs without a subsequent headache,[20] known as a silent migraine.

Pain phase

Classically the headache is unilateral, throbbing, and moderate to severe in intensity.[19] It usually comes on gradually[19] and is aggravated by physical activity.[3] In more than 40% of cases however the pain may be bilateral, and neck pain is commonly associated.[21] Bilateral pain is particularly common in those who have migraines without an aura.[15] Less commonly pain may occur primarily in the back or top of the head.[15] The pain usually lasts 4 to 72 hours in adults[19] however in young children frequently lasts less than 1 hour.[22] The frequency of attacks is variable, from a few in a lifetime to several a week, with the average being about one a month. [23][24] The pain is frequently accompanied by nausea, vomiting, sensitivity to light, sensitivity to sound, sensitivity to smells, fatigue and irritability.[15] In a basilar migraine, a migraine with neurological symptoms related to thebrain stem or with neurological symptoms on both sides of the body,[25] common effects include: a sense of the world spinning, lightheadedness, and confusion.[15] Nausea occurs in almost 90% of people, and vomiting occurs in about one-third.[26] Many thus seek a dark and quiet room.[26] Other symptoms may include: blurred vision, nasal stuffiness, diarrhea, frequent urination, pallor, or sweating.[27] Swelling or tenderness of the scalp may occur as can neck stiffness.[27] Associated symptoms are less common in the elderly.[28] [edit]Postdrome The effects of migraine may persist for some days after the main headache has ended; this is called the migraine postdrome. Many report a sore feeling in the area where the migraine was, and some report impaired thinking for a few days after the headache has passed. The patient may feel tired or "hung over" and have head pain, cognitive difficulties, gastrointestinal symptoms, mood changes, and weakness.[29] According to one summary, "Some people feel unusually refreshed or euphoric after an attack, whereas others note depression and malaise."[30] [edit]Cause The underlying cause of migraines is unknown[31] however they are believed to be related to a mix of environmental and genetic factors.[4] They run in families in about two-thirds of cases[5] and rarely occur due to a single gene defect.[32] A number of psychological conditions are associated including: depression, anxiety, and bipolar disorder[33] as are many biological events or triggers. [edit]Genetics

Studies of twins indicate a 34 to 51% genetic influence of likelihood to develop migraine headaches.[4] This genetic relationship is stronger for migraines with aura than for migraines without aura.[12] A number of specific variants of genes increase the risk by a small to moderate amount.[34] Single gene disorders that result in migraines are rare.[34] One of these is known as familial hemiplegic migraine, a type of migraine with aura, which is inherited in a autosomal dominant fashion.[35][36] It is related to disorders of gene coding for proteins involved in ion transport.[15] Another is CADASIL syndrome or cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. [15] [edit]Triggers Migraines may be induced by triggers, with some reporting it as an influence in a minority of cases[5] and others the majority.[37] Many things have been labeled as triggers, however the strength and significance of these relationships are uncertain.[37][38] A trigger may occur up to 24 hours prior to the onset of symptoms.[5]
[edit]Physiological

Common triggers quoted are stress, hunger, and fatigue (these equally contribute to tension headaches).[37]Migraines are more likely to occur around menstruation.[39] Other hormonal influences, such as menarche, oral contraceptive use, pregnancy, perimenopause, and menopause, also play a role.[40] These hormonal influences seem to play a greater role in migraine without aura.[41] Migraines typically do not occur during thesecond and third trimesters or following menopause.[15]
[edit]Dietary

Reviews of dietary triggers have found that evidence mostly relies on subjective assessments and is not rigorous enough to prove or disprove any particular triggers.[42][43] Regarding specific agents there does not appear to be evidence for an effect of tyramine on migraine[44] and while monosodium glutamate (MSG) is frequently reported as a dietary trigger[45] evidence does not consistently support this.[46]
[edit]Environmental

Potential triggers in the indoor and outdoor environment concluded the overall evidence was of poor quality, but nevertheless suggested people with migraines take some preventive measures related to indoor air quality and lighting.[47] While once believed to be more common in those of high intelligence this does not appear to be true.[41]

[edit]Pathophysiology

Animation of cortical spreading depression

Migraines are believed to be a neurovascular disorder[5] with evidence supporting its mechanisms starting within the brain and then spreading to the blood vessels. [48] Some researchers feel neuronal mechanisms play a greater role,[49] while others feel blood vessels play the key role.[50] Others feel both are likely important.[51] High levels of the neurotransmitterserotonin, also known as 5-hydroxytryptamine, is believed to be involved.[48] [edit]Aura Cortical spreading depression or spreading depression of Leo is bursts of neuronal activity followed by a period of inactivity, which is seen in those with migraines with an aura.[52] There are a number of explanations for its occurrence including activation of NMDA receptors leading to calcium entering the cell.[52] After the burst of activity blood flow to the cerebral cortex in the area affected is decreased for two to six hours.[52] It is believed that when depolarization travels down the underside of the brain nerves that sense pain in the head and neck are triggered.[52] [edit]Pain The exact mechanism of the head pain which occurs during a migraine is unknown.[53] Some evidence supports a primary role for central nervous system structures (such as the brainstem and diencephalon)[54]while other data support the role peripheral activation (such as via the sensory nerves that surround blood vessels of the head and neck).[53] The potential candidates vessels include: dural

arteries, pial arteries and extracranial arteries such as those of the scalp.[53] The role of vasodilatation of the extracranial arteries, in particular, is believed to be significant.[55] [edit]Diagnosis The diagnosis of a migraine is based on signs and symptoms.[5] Imaging test are occasionally performed to exclude other causes of headaches.[5] It is believed that a substantial number of people with the condition have not been diagnosed. [5] 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":[3]

Five or more attacks for migraine with aura, two attacks are sufficient for diagnosis. Four hours to three days in duration Two or more of the following:

Unilateral (affecting half the head); Pulsating; "Moderate or severe pain intensity"; "Aggravation by or causing avoidance of routine physical activity"

One or more of the following:

Nausea and/or vomiting; Sensitivity to both light (photophobia) and sound (phonophobia)

If someone experiences two of the following: photophobia, nausea, or inability to work / study for a day the diagnosis is more likely.[56] In those with four out of five of the following: pulsating headache, duration of 472 hours, pain on one side of the head, nausea, or symptoms that interfere with the person's life, the probability that this is a migraine is 92%.[11] In those with less than three of these symptoms the probability is 17%.[11] [edit]Classification
Main article: ICHD classification and diagnosis of migraine

Migraines were first comprehensively classified in 1988.[12] The International Headache Society most recently updated their classification of headaches in 2004.[3] According to this classification migraines are primary headaches along with tension-type headaches and cluster headaches, among others.[57]

Migraines are divided into seven subclasses (some of which include further subdivisions):

Migraine without aura, or "common migraine", involves migraine headaches that are not accompanied by an aura Migraine with aura, or "classic migraine", usually involves migraine headaches accompanied by an aura. Less commonly, an aura can occur without a headache, or with a nonmigraine headache. Two other varieties are familial hemiplegic migraine and sporadic hemiplegic migraine, in which a person has migraines with aura and with accompanying motor weakness. If a close relative has had the same condition, it is called "familial", otherwise it is called "sporadic". Another variety is basilar-type migraine, where a headache and aura are accompanied by difficulty speaking, world spinning, ringing in ears, or a number of other brainstem-related symptoms, but not motor weakness. This type was initially believed to be due to spasms of the basilar artery, the artery that supplies the brainstem.[25]

Childhood periodic syndromes that are commonly precursors of migraine include cyclical vomiting(occasional intense periods of vomiting), abdominal migraine (abdominal pain, usually accompanied by nausea), and benign paroxysmal vertigo of childhood (occasional attacks of vertigo).

Retinal migraine involves migraine headaches accompanied by visual disturbances or even temporary blindness in one eye. Complications of migraine describe migraine headaches and/or auras that are unusually long or unusually frequent, or associated with a seizure or brain lesion. Probable migraine describes conditions that have some characteristics of migraines, but where there is not enough evidence to diagnose it as a migraine with certainty (in the presence of concurrent medication overuse).

Chronic migraine is a complication of migraines, and is a headache that fulfills diagnostic criteria formigraine headache and occurs for a greater time interval. Specifically, greater or equal to 15 days/month for longer than 3 months.[58]

[edit]Abdominal

migraine

The diagnosis of abdominal migraines is controversial.[59] Some evidence indicates that recurrent episodes of abdominal pain in the absence of a headache may be a type of migraine.[59][60] Or are at least a precursor to migraines.[12] These episodes of pain may or may not follow a migraine like prodrome and typically last minutes to hours.[59] They often occur in those with either a personal or family history of typical migraines.[59]Other

syndromes that are believed to be precursors include: cyclical vomiting syndrome and benign paroxysmal vertigo of childhood.[12] [edit]Differential

diagnosis

Other conditions that can cause similar symptoms to a migraine headache include: temporal arteritis, cluster headaches, acute glaucoma, meningitis and subarachnoid hemorrhage.[11] Temporal arteritis typically occurs in people over 50 years old and presents with tenderness over the temple, cluster headaches presents with one-sided nose stuffiness, tears and severe pain around the orbits, acute glaucoma is associated with vision problems, meningitis with fevers, and subaracchnoid hemorrhage with a very fast onset. [11] Tension headachestypically occur on both sides, are not pounding, and are less disabling. [11] [edit]Prevention
Main article: Prevention of migraines

Preventive treatments of migraines include: medications, nutritional supplements, lifestyle alterations, and surgery. Prevention is recommended in those who have headaches more than two days a week, cannot tolerate the medications used to treat acute attacks, or those with severe attacks that are not easily controlled.[11] The goal is to reduce the frequency, painfulness, and/or duration of migraines, and to increase the effectiveness of abortive therapy.[61] Another reason prevention is to avoid medication overuse headache. This is a common problem and can result in chronic daily headache.[62][63] [edit]Medication Preventive migraine medications are considered effective if they reduce the frequency or severity of the migraine attacks by at least 50%.[64] Guidelines are fairly consistent in rating topiramate, divalproex/sodium valproate, propranolol, and metoprolol as having the highest level of evidence for first-line use.[65]Recommendations regarding effectiveness varied however for gabapentin.[65] Timolol is also effective for migraine prevention and in reducing migraine attack frequency and severity, while frovatriptan is effective for prevention of menstrual migraine.[65] Amitriptyline and venlafaxine are probably also effective.[66] Botox has been found to be useful in those with chronic migraines but not those with episodic ones.[67] [edit]Alternative

therapies

Petasites hybridus(butterbur) root extract has proven effective for migraine prevention.[68]

Acupuncture is effective in the treatment of migraines.[69] The use of "true" acupuncture is not more efficient than sham acupuncture, however, both "true" and sham acupuncture appear more effective than routine care, with fewer adverse effects than prophylactic drug treatment.[70] Chiropractic manipulation, physiotherapy, massage and relaxation might be as effective as propranolol ortopiramate in the prevention of migraine headaches; however, the research had some problems with methodology.[71] There is some tentative evidence of benefit for: magnesium, coenzyme Q(10), riboflavin, vitamin B(12),[72] and Fever-few, although better quality trials must be done to confirm these preliminary results.[73]Of the alternative medicines butterbur has the best evidence for its use.[74] [edit]Devices

and surgery

Medical devices, such as biofeedback and neurostimulators, have some advantages in migraine prevention, mainly when common anti-migraine medications are contraindicated or in case of medication overuse. Biofeedback helps people be conscious of some physiological parameters so as to control them and try to relax and may be efficient for migraine treatment.[75][76] Neurostimulation uses implantable neurostimulators similar to pacemakers for the treatment of intractable chronic migraines with encouraging results for severe cases.[77][78] Migraine surgery, which involves decompression of certain nervesaround the head and neck, may be an option in certain people who do not improve with medications.[79] [edit]Management There are three main aspects of treatment: trigger avoidance, acute symptomatic control, and pharmacological prevention.[5] Medications are more effective if used earlier

in an attack.[5] The frequent use of medications may result in medication overuse headache, in which the headaches become more severe and more frequent.[3] This may occur with triptans, ergotamines, and analgesics, especially narcotic analgesics.[3] [edit]Analgesics Recommended initial treatment for those with mild to moderate symptoms are simple analgesics such as non-steroidal anti-inflammatory drugs (NSAIDs) or the combination of acetaminophen, acetylsalicylic acid, andcaffeine.[11] A number of NSAIDs have evidence to support their use. Ibuprofen has been found to provide effective pain relief in about half of people.[80] Diclofenac has been found effective.[81] Aspirin can relieve moderate to severe migraine pain, with an effectiveness similar to sumatriptan.[82]Ketorolac is available in an intravenous formulation.[11] Paracetamol (also known as acetaminophen), either alone or in combination with metoclopramide, is another effective treatment with a low risk of adverse effects.[83] In pregnancy acetaminophen and metoclopramide are deemed safe as are NSAIDs until the third trimester.[11] [edit]Triptans Triptans such as sumatriptan are effective for both pain and nausea in up to 75% of people.[5][84] They are the initially recommended treatments for those with moderate to severe pain or those with milder symptoms who do not respond to simple analgesics.[11] The different forms available include oral, injectable, nasal spray, and oral dissolving tablets.[5] In general, all the triptans appear equally effective, with similar side effects. However, individuals may respond better to specific ones.[11] Most side effects are mild, such as flushing; however, rare cases of myocardial ischemia have occurred.[5] They are thus not recommended for people with cardiovascular disease.[11] While historically not recommended in those with basilar migraines there is no specific evidence of harm from their use in this population to support this caution.[25] They are not addictive, but may cause medication overuse headaches if used more than 10 days per month.[85] [edit]Ergotamines Ergotamine and dihydroergotamine are older medications still prescribed for migraines, the latter in nasal spray and injectable forms.[5] They appear equally effective to the triptans,[86] are less expensive,[87] and experience adverse effects that typically are

benign.[88] In the most debilitating cases, such as those with status migrainosus, they appear to be the most effective treatment option.[88] [edit]Other Intravenous metoclopramide or intranasal lidocaine are other potential options.[11] Metoclopramide is the recommended treatment for those who present to the emergency department.[11] A single dose of intravenousdexamethasone, when added to standard treatment of a migraine attack, is associated with a 26% decrease in headache recurrence in the following 72 hours.[89] Spinal manipulation for treating an ongoing migraine headache is not supported by evidence.[90] It is recommended that opioids and barbiturates not be used.[11] [edit]Prognosis Long term prognosis in people with migraines is variable.[9] Most people with migraines have periods of lost productivity due to their disease[5] however typically the condition is fairly benign[9] and is not associated with an increased risk of death.[91] There are four main patterns to the disease: symptoms can resolve completely, symptoms can continue but become gradually less with time, symptoms may continue at the same frequency and severity, or attacks may become worse and more frequent.[9] Migraines with aura appears to be a risk factor for ischemic stroke[92] doubling the risk.[93] Being a young adult, being female, using hormonal contraception, and smoking further increases this risk.[92] There also appears to be an association with cervical artery dissection.[94] Migraines without aura do not appear to be a factor.[95] The relationship with heart problems is inconclusive with a single study supporting an association.[92]Overall however migraines do not appear to increase the risk of death from stroke or heart disease.[91]Preventative therapy of migraines in those with migraines with auras may prevent associated strokes.[96] [edit]Epidemiology

Disability-adjusted life year for migraines per 100,000 inhabitants in 2002

no data <45 4565 6585 85105 105125 125145

145165 165185 185205 205225 225245 >245

Worldwide, migraines affect more than 10% of people.[31] In the United States, about 6% of men and 18% of women get a migraine in a given year, with a lifetime risk of about 18% and 43% respectively.[5] In Europe, migraines affect 1228% of people at some point in their lives with about 615% of adult men and 1435% of adult women getting at least one yearly.[7] Rates of migraines are slightly lower in Asia and Africa than in Western countries.[41][97] Chronic migraines occur in approximately 1.4 to 2.2% of the population.[98]

Incidence of migraine by age and sex

These figures vary substantially with age: migraines most commonly start between 15 and 24 years of age and occur most frequently in those 35 to 45 years of age. [5] In children, about 1.7% of 7 year olds and 3.9% of those between 7 and 15 years have migraines, with the condition being slightly more common in boys before puberty.[99] During adolescence migraines becomes more common among women[99] and this persists for the rest of the lifespan, being two times more common among elderly females than males.[100] In women migraines without aura is more

common than migraines with aura, however in men the two types occur with similar frequency.[41] During perimenopause symptoms often get worse before decreasing in severity.[100] While symptoms resolve in about two thirds of the elderly, in between 3 and 10% they persist.[28] [edit]History

The Head Ache, George Cruikshank (1819)

An early description consistent with migraines is contained in the Ebers papyrus, written around 1200 BCE in ancient Egypt.[101] In 200 BC, writings from the Hippocratic school of medicine described the visual aura that can precede the headache and a partial relief occurring through vomiting.[102]

A trepanated skull, from theIron age. The perimeter of the hole in the skull is rounded off by ingrowth of new bony tissue, indicating that the person survived the operation.

A second-century description byAretaeus of Cappadocia divided headaches into three types: cephalalgia, cephalea, and heterocrania.[103] Galen of Pergamonused the term hemicrania (half-head), from which the word migraine was eventually derived.[103] He also proposed that the pain arose from the meninges and blood vessels of the head.[102] Migraines were first divided into the two now used types - migraine with aura (migraine ophthalmique) and migraine without aura (migraine vulgaire) in 1887 by Louis Hyacinthe Thomas a French Librarian.[102] Trepanation, the deliberate drilling of holes into a skull, was practiced as early as 7,000 BCE.[101] While sometimes people survived, many would have died from the procedure due to infection.[104] It was believed to work via "letting evil spirits escape".[105] William Harvey recommended trepanation as a treatment for migraines in the 17th century.[106] While many treatments for migraines have been attempted, it was not until 1868 that use of a substance which eventually turned out to be effective began. [102] This substance was the fungus ergot from which ergotamine was isolated in 1918.[107] Methysergide was developed in 1959 and the first triptan, sumatriptan, was developed in 1988.[107] During the 20th century with better study design effective preventative measures where found and confirmed.[102] [edit]Society and culture Migraines are a significant source of both medical costs and lost productivity. It has been estimated that they are the most costly neurological disorder in the European Community, costing more than 27 billion per year.[108] In the United States direct costs have been estimated at 17 billion USD.[109] Nearly a tenth of this cost is due to the cost of triptans.[109] Indirect costs are around 15 Billion USD, of which missed work is the greatest component.[109] In those who do attend work with a migraine effectiveness is decreased by around a third.[108]Negative impacts also frequently occur for a person's family.[108] [edit]Research Calcitonin gene related peptides (CGRPs) have been found to play a role in the pathogenesis of the pain associated with migraine.[11] CGRP receptor antagonists, such as olcegepant and telcagepant, have been investigated both in vitro and in clinical studies for the treatment of migraine.[110] In 2011, Merck stoppedphase III clinical

trials for their investigational drug telcagepant.[111][112] Transcranial magnetic stimulation also shows promise.[11]