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Migraine
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Posted March 17, 2016 FRIDAY, March 11, 2016 (HealthDay News) -- Severe migraines are associated with an increased risk of complications during pregnancy and childbirth, especially among older women, new research  ...
Head Injuries Tied to Higher Migraine Risk for Veterans
Posted June 21, 2014 THURSDAY, June 19, 2014 (HealthDay News) -- U.S. veterans of the Iraq and Afghanistan wars who suffered brain injuries are at a much higher risk for headaches, especially migraines, a new study  ...
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Migraine's Link to Higher Heart Disease Risk May Not Be Genetic
Posted July 7, 2015 THURSDAY, July 2, 2015 (HealthDay News) -- People who have migraines have a greater risk for heart disease, but their genes may not be to blame for the connection, new research suggests.  ...

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Migraine



Related terms
Background
Risk factors and causes
Treatment
Author information
Bibliography
Types of headaches

Related Terms
  • Abortive, anticonvulsant, antiviral, arrhythmia, arteriovenous malformations, artery, aura, basilar, artery, beta-blocker, caffeine, calcium channel blocker, carotid, carotidynia, cerebrovascular, cluster headache, computer tomography, constriction, cranial, CT, dilation, EEG, electroencephalography, epidural hematoma, ergot, estrogen, headache, heredity, herpes simplex encephalitis, hormone, intracerebral, magnetic resonance imaging, menopause, MRI, neuropeptides, nociceptors, norepinephrine, ophthalmoplegic migraine, opiate, pallor, parasthesia, photophobia, PMS, postdrone, premenstrual syndrome, preventative, primary headache, prodrome, progesterone, prophylactic, ptosis, rebound headache, scintillating scotomas, secondary headache, serotonin, stroke, subarachnoid hemorrhages, subdural hematoma, tension headache, TIA, transient ischemic attack, trauma, tricyclic antidepressant, triptan, vertigo.

Background
  • A migraine is not just headache pain. Migraine is thought to be a genetic neurological disease characterized by flare-ups often called "migraine attacks" or "migraine episodes." A headache can be one symptom of a migraine attack. Some individuals with migraine disease often have migraine attacks without having a headache.
  • Migraine attacks, or episodes, occur in phases or parts. A typical migraine attack consists of four phases. Not every individual experiencing a migraine has all four phases. The four phases of a migraine attack are prodrome, aura, headache, and postdrome (see Signs and Symptoms).
  • Individuals suffering from migraines tend to have recurring attacks triggered by a lack of food or sleep, certain food allergies, exposure to light, or hormonal changes in women, including puberty, menopause, and premenstrual syndrome (PMS). Anxiety, stress, or relaxation after stress can also be triggers. Exposure to a trigger does not always lead to a headache. Conversely, avoidance of triggers cannot completely prevent headaches. Different migraine sufferers respond to different triggers, and any one trigger will not induce a headache in every person who has migraine headaches.
  • Attacks tend to become less severe as the migraine sufferer ages. The uncertainty of when attacks may occur leads to additional patient anxiety. Symptoms, incidence, and severity of migraine headaches vary by individual.
  • Migraine headaches are the second most common type of primary headache. An estimated 28 million people in the United States (about 12% of the population) will experience migraine headaches at one time in their lives.
  • In the United States, migraine headaches often go undiagnosed or are misdiagnosed as tension or sinus headaches. As a result, many migraine sufferers do not receive effective treatment.
  • Treatments for migraine attacks involve prevention of the attack and treatment of acute (immediate) symptoms such as the headache.

Risk factors and causes
  • Central nervous system disorder: The precise cause of a migraine attack is not completely understood. There appears to be general agreement, however, that a key element is changes in the blood flow within the brain due to a variety of triggers. The most widely accepted theory suggests that a migraine attack is precipitated when pain-sensing nerve cells in the brain (called nociceptors) release chemicals called neuropeptides (nerve proteins) in response to stimulation of the trigeminal nerve system. At least one of the neurotransmitters (chemicals that transmit impulses to the brain), substance P, increases the pain sensitivity of other nearby nociceptors. Other neuropeptides act on the smooth muscle surrounding cranial (skull) blood vessels, causing inflammation. This smooth muscle regulates blood flow in the brain by causing vasodilation (relaxation of blood vessels) or vasoconstriction (contracting the blood vessel). 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 permeability of cranial (skull) blood vessels, allowing fluid containing inflammatory chemicals to leak and promote inflammation and tissue swelling. The pain of migraine is though to result from this combination of increased pain sensitivity, tissue, and vessel swelling, and inflammation.
  • Heredity: Susceptibility to migraine may be inherited. A child of a migraine sufferer has as much as a 50% chance of developing a migraine attack in their lifetime. If both parents are affected, the chance rises to 70%. However, the gene or genes responsible have not been identified. Genetics also increase the chances of having migraine attacks that are chronic (or long-term).
  • Neurotransmitters: Neurotransmitters are chemical messengers in the brain. Two important ones, serotonin and dopamine, appear to be critical in the processes leading to a migraine attack. Serotonin (also called 5-hydroxytryptamine or 5-HT) is involved in regulation of pain perception and mood, among other important functions. A number of studies have suggested that serotonin can stop the migraine process. To support this observation, higher-than-normal levels of a serotonin compound are excreted in urine and levels of serotonin in the blood drop during a migraine attack. Also, drugs that target receptors in the brain for serotonin are generally effective in stopping a migraine. The receptors for serotonin implicated in a migraine attack are found on the trigeminal nerve endings. Serotonin appears to block the peptides (including substance P) involved in over-stimulating nerves and producing inflammation.
  • Dopamine, another important neurotransmitter, may act as a stimulant or accelerator of the migraine process. Some evidence suggests that certain genetic factors make people over-sensitive to the effects of dopamine, which include nerve cell excitation. Such nerve-cell over-activity could trigger the events in the brain leading to migraine. The prodromal symptoms (including mood changes, yawning, or drowsiness), for example, have been associated with increased dopamine activity. Dopamine receptors are also involved in regulation of blood flow in the brain, which may be of importance when dealing with vasoconstriction and vasodilation.
  • Calcium-channels: Some migraines may be due to abnormalities in the channels within cells that transport the electrical ions calcium, magnesium, sodium, and potassium. Calcium-channels regulate the release of serotonin, an important neurotransmitter in the migraine process. Magnesium interacts with calcium-channels and magnesium deficiencies have been detected in the brains of migraine patients. Calcium-channels also play a major role in cortical spreading depression (CSD), a brain event that includes a "wave" of nerve impulses (firing) that spreads across the surface of the brain, moving from the back (occipital region) of the cerebral cortex toward the front at about one-eighth to three-sixteenth inches (three to five millimeters) per minute. After the nerve excitation, a depression in nerve cell function occurs that can last for minutes. CSD is thought to be one of the causes of a migraine attack. Some individuals with migraine may inherit one or more factors that impair calcium-channels, making them susceptible to headaches. For example, mutations in a gene that encodes calcium channels appears to be responsible for familial hemiplegic migraine.
  • Gender and Age: A migraine attack is three times more common in women than in men. Although the exact relationship between hormones and headaches is not clear, fluctuations in estrogen and progesterone seem to trigger headaches in many women with migraine headaches, including those with premenstrual syndrome (PMS) and menopause. It seems to be hormonal fluctuations, or changes, that trigger migraine attacks, not the presence of the hormone. Prepubescent females, or females prior to reproductive maturity, can also suffer from migraines. Women with a history of migraines often have reported headaches immediately before or during their periods. Others report more migraines during pregnancy or menopause. Hormonal medications, such as oral contraceptives (birth control pills) and hormone replacement therapy (HRT, including estrogen and progesterone therapy), may also worsen migraines. In children younger than 10 years, boys appear to have migraines more often than girls. After puberty starts, migraine headaches are much more common in females (female-to-male ratio, 3:1), most likely due to hormonal changes.
  • In general, the rate of migraine occurrence in males drops to a low by age 28-29 years, with one case per 1,000 people in this age group.
  • Migraine occurrence among females increases sharply up to age 40 years and then declines gradually.
  • The age when migraine headache with aura begins appears to peak at or before age 4-5 years (6.6 cases per 1000 people in that age group), while the highest rate for migraine without aura occurs at age 10-11 years (10.1 cases per 1000 people in that age group).
  • The severity and frequency of attacks tend to lessen with age. Data suggests that migraine attacks are a chronic (long-term) condition, although long remissions (illness-free periods) are common. One study showed that 62% of young adults were free of migraine headaches for more than two years, but only 40% continued to be free of them after 30 years.
  • Diet: Certain foods and beverages appear to trigger headaches in sensitive individuals. Common dietary triggers include alcohol (especially beer and red wine), aged cheeses, chocolate, fermented, pickled, or marinated foods (tofu, kim chee, miso), aspartame (an artificial sweetener), caffeine, monosodium glutamate (MSG, a key flavor enhancer in some Asian foods), and many canned and processed foods. Skipping meals or fasting also can trigger migraines. Eating proper food is very important in migraine prevention because a continuous supply of proper nutrients is essential to keeping chemical balance in the brain. Brain chemistry can be changed significantly by a single meal and, in turn, some changes in food composition can rapidly affect brain function. While all foods eaten modify brain function, some specifically alter mood or energy, such as caffeine or refined sugars. Eating unhealthy foods that do not supply adequate nutrients for proper brain function, or foods that alter brain function can cause migraine attacks in susceptible individuals
  • Magnesium deficiency: Because levels of magnesium (a mineral involved in nerve cell function) also drop right before or during a migraine headache, it is possible that low amounts of magnesium may cause nerve cells in the brain to misfire. About 20% of the population consumes less than two-thirds of the RDA (recommended dietary allowance) for magnesium.
  • Stress: A period of hard work followed by relaxation may lead to a "weekend migraine" headache. Acute (immediate) or chronic (long-term) stress at work or home also can set off a migraine.
  • Sensory stimulus: Bright lights, sun glare, and unusual smells, including pleasant scents (such as perfume or flowers), and unpleasant odors (such as paint thinner and secondhand smoke) can trigger a migraine attack.
  • Physical factors: Intense physical exertion, including sexual activity, may provoke migraines. Changes in sleep patterns, including too much or too little sleep, also can initiate a migraine headache. Sleep changes are usually seen in both adults and children with migraines. Healthcare professionals recommend eight hours of uninterrupted sleep nightly for adults. Sleep helps regulate certain neurochemicals (brain chemicals), including serotonin. Decreases in serotonin may cause a migraine attack.
  • Environmental changes: A change of weather, season, altitude level, barometric pressure, or time zone can prompt a migraine headache. Environmental changes such as moving to a new area where the plants and pollens are different may also trigger a migraine attack.
  • Medications: Taking certain medications can aggravate migraines, including oral contraceptives (birth control pills), estrogen replacement therapy, nitrates (nitroglycerin), theophylline (Slobid®), reserpine (Serpasil®), nifedipine (Procardia® or Adalat®), indomethicin (Indocin®), cimetidine (Tagamet®), decongestant overuse (such as pseudoephedrine or Sudafed®), and anti-anxiety drug withdrawal, including alprazolam (Xanax®) and diazepam (Valium®). Caffeine withdrawal and the discontinuation of pain medications can trigger a migraine.

Treatment
  • Many factors may contribute to the occurrence of migraine attacks, including diet, sleep, hormonal changes, changes in brain chemistry, and heredity. They are known as trigger factors. When identified, avoidance of trigger factors reduces the number of headaches a patient may experience. Trigger factors may be targets of drug therapy also.
  • Treatment for migraine attacks is divided into two categories, including acute (immediate) or prophylactic (preventative). Acute treatment is used during a migraine to stop or slow the progress of the attack, and preventative (or prophylactic) treatment tries to prevent migraine attacks from occurring.
  • Preventive (Prophylactic):
  • Preventative medication may be prescribed for patients who have frequent migraine attacks (three or more a month), those who do not respond consistently to acute treatment, and when specific medicines are contraindicated because of other medical conditions (such as stroke or bleeding in the brain). Studies have reported that as many as 40% of these patients may benefit from preventative treatment. The U.S. Food and Drug Administration (FDA) has approved four prescription drugs for migraine prevention. These include the beta-blockers propranolol (Inderal®) and timolol (Blocadren®), and the anticonvulsants topiramate (Topamax®) and divalproex sodium (Depakote®).
  • Anticonvulsants: Anticonvulsant medicines, normally used for seizures, have been used to prevent migraine headaches. Examples of anticonvulsants that have been used are valproic acid (Depakote®, Depakote ER®, Depakene®), phenobarbital, gabapentin (Neurontin®), and topiramate (Topamax®). Control of the cortical spreading depression (CSD), is thought to be the reason for anticonvulsant effectiveness in preventing migraine attacks. Side effects include fatigue (tiredness), nausea, vomiting, and trembling.
  • Beta-blockers: Beta-blockers are a class of drugs that safely slow the heart beat and decrease blood pressure. Beta-blockers have been used for many years to prevent migraine headaches. In migraine prevention, beta-blockers help dilate (open) blood vessels in the brain, which may prevent the vascular (blood vessel) symptoms associated with a migraine attack, including vasoconstriction (blood vessel narrowing) and vasodilation (blood vessel widening). Beta-blockers can also help reduce physical symptoms associated with migraine attacks, such as anxiety, heart palpitations, and shaking,
  • Beta-blockers used in migraine prevention include propranolol (Inderal®), atenolol (Tenormin®), metoprolol (Lopressor®, Toprol XL®), and nadolol (Corgard®). Beta-blockers generally are well tolerated in most individuals. They can aggravate breathing difficulties in patients with asthma, chronic bronchitis (inflammation of the bronchial tubes), or emphysema (loss of lung function). In patients who already have slow heart rates (bradycardia) and heart block (defects in electrical conduction within the heart), beta-blockers can cause dangerously slow heartbeats. Beta-blockers can aggravate symptoms of heart failure. Other side effects include drowsiness, diarrhea, constipation, fatigue (tiredness), insomnia, nausea, depression, dreaming, memory loss, and impotence (loss of sexual performance).
  • Calcium channel blockers (CCBs): CCBs are a class of drugs normally used for high blood pressure, angina (chest pain), and arrhythmias (abnormal heart rhythms). CCBs also appear to alter serotonin (a brain chemical). Serotonin imbalances are a causative factor in developing a migraine. CCBs used in preventing migraine headaches are diltiazem (Cardizem®, Dilacor®, Tiazac®), and verapamil (Calan®, Verelan®, Isoptin®).The most common side effects of CCBs are constipation, nausea, headache, rash, edema (swelling of the legs with fluid), low blood pressure, drowsiness, and dizziness. Drinking grapefruit juice or eating grapefruit may cause levels of CCBs to rise, potentially leading to life threatening arrhythmias (irregular heart beats). Healthcare professionals recommend that individuals taking CCBs not consume grapefruit juice.
  • Hormone replacement therapy (HRT): For women with hormonal imbalances that may be causing the migraines, hormone replacement therapy (HRT) may be used, including estrogen and progesterone. HRT, however, may cause side effects such as blood clots, an increased risk of developing some types of cancers, and heart disease. Menstruating women at risk for migraines may be placed on oral contraceptives for HRT. Pre-pubescent girls that are at risk for migraine attacks will not be treated with HRT, but with other methods such as beta-blockers and anticonvulsants.
  • Lifestyle: Lifestyle changes, including decreasing stress levels, increasing exercise levels, and controlling the diet, have a major impact on migraine prevention and development. Lifestyle factors that are important in the prevention of migraines include regular sleep patterns, regular exercise (level depends upon the individual), limiting stress, limiting caffeine consumption to less than two caffeine-containing beverages a day, avoiding bright or flashing lights, and wearing sunglasses if sunlight is a trigger. Identifying and avoiding foods that trigger headaches is important. Healthcare professionals recommend keeping a food journal, where the individual writes down everything they have for each meal of the day. Then review the diary with a healthcare professional. It is impractical to adopt a diet that avoids all known migraine triggers; however, it is reasonable to avoid foods that consistently trigger migraine headaches. Triggers vary from one individual to another.
  • Tricyclic antidepressants (TCAs): TCAs are thought to prevent migraine headaches by altering the balance of serotonin, a neurotransmitter in the brain. Low levels of serotonin are thought to be a causative agent in migraine attacks. Chronic stress and depression can cause elevated levels of the stress hormone cortisol, which is produced in the adrenal glands. Cortisol can in turn cause imbalances in serotonin, leading to a migraine attack. The tricyclic antidepressants that have been used in preventing migraine headaches include amitriptyline (Elavil®), nortriptyline (Pamelor®, Aventyl®), doxepin (Sinequan®), and imipramine (Tofranil®). Side effects include constipation, dry mouth, low blood pressure (hypotension), increased heart rate, (tachycardia), urinary retention, sexual dysfunction, and weight gain. TCAs may cause excessive sedation and fatigue (tiredness).
  • Others: Other drugs less commonly used for migraine prevention include anti-serotonin medications, including methysergide (Sansert®), which prevent migraine headaches by constricting (making smaller) blood vessels and reducing inflammation of the blood vessels. Cyproheptadine (Periactin®) is an antihistamine that increases serotonin activity and is used occasionally in migraine prevention. Low levels of serotonin are a cause of migraine attacks.
  • Acute (Immediate):
  • Over-the-counter (OTC) treatments: The U.S. Food and Drug Administration (FDA) has approved three over-the-counter (OTC) products to treat migraine attacks. Excedrin® Migraine (a combination of aspirin, acetaminophen, and caffeine) is indicated for migraine and its associated symptoms such as head pain. Advil® Migraine and Motrin® Migraine Pain (both are ibuprofen) have anti-inflammatory action and are approved to treat migraine headache and its pain.
  • Triptans: The triptans attach to serotonin receptors on the blood vessels and nerves and thereby reduce inflammation and constrict (narrow) the blood vessels. A reduction in inflammation decreases pressure on nerves in the trigeminal nerve system (nerves in the cranium or head), which decreases the pain signals to the brain and stops the headache. Traditionally, triptans, which are prescription medicines, were prescribed for moderate or severe migraines after over-the-counter (OTC) analgesics such as ibuprofen (Advil®) and other simple measures failed. Newer studies suggest that triptans can be used as the first treatment for patients with migraines that are causing disability. Significant disability is defined as more than ten days of at least 50% disability during a three month period.
  • Triptans should be used early after the migraine begins, before the onset of pain or when the pain is mild. Using a triptan early in an attack increases its effectiveness, reduces side effects, and decreases the chance of recurrence of another headache during the following 24 hours. Used early, triptans can be expected to abort more than 80% of migraine headaches within two hours. Triptans include sumatriptan (Imitrex®), almotriptan (Axert®), naratriptan (Amerge®), rizatriptan (Maxalt®), zolmitriptan (Zomig®), frovatriptan (Frova®), and eletriptan (Relpax®).
  • The most common side effects of triptans are facial flushing, tingling of the skin, and a sense of tightness around the chest and throat. Other less common side effects include drowsiness, fatigue (tiredness), and dizziness. These side effects are short-lived and are not considered serious. Triptans are not used in pregnant women and are not generally used in young children.
  • In patients with severe nausea, a combination of a triptan and an anti-nausea medication, such as prochlorperazine (Compazine®), may be used.
  • Ergots: Ergots, like triptans, are medications that abort migraine headaches. Examples of ergots include ergotamine preparations (Cafergot®) and dihydroergotamine preparations (Migranal®, DHE-45®). Ergots, like triptans, cause constriction (narrowing) of blood vessels, but ergots tend to cause more constriction of vessels in the heart and other parts of the body than the triptans, and the produce more negative effects on the heart than the triptans. Therefore, the ergots are not as safe as the triptans. Ergots are used to help stop the vasodilation (blood vessel widening) associated with a migraine attack. The ergots also are more prone to cause nausea and vomiting than the triptans. The ergots can cause prolonged contraction of the uterus and miscarriages in pregnant women.
  • Midrin: Midrin is used to abort migraine and tension headaches. It is a combination of isometheptene (a blood vessel constrictor), acetaminophen (a pain reliever), and dichloralphenazone (a mild sedative). The combination medication can help take care of three potential factors associated with a migraine attack, including vasodilation, pain, and anxiety. Midrin® is most effective if used early during a headache. However, because of its potent blood vessel constricting effect, it should not be used in patients with high blood pressure, kidney disease, glaucoma (increased pressure in the eyes), atherosclerosis (hardening of the arteries), liver disease, or in patients taking monoamine oxidase inhibitors (MAOIs) including phenelzine (Nardil®), isocarboxazid (Marplan®), and tranylcypromine sulfate (Parnate®).
  • Other prescription medications: Some attacks may not be eliminated by acute therapy, and the individual requires pain-relieving measures. Due to the severity of the headaches, some patients may require a narcotic analgesic, including oxycodone (Percocet®), codeine, or meperidine (Demerol®). If the individual is experiencing frequent migraine attacks, the habitual use of opiate analgesics should be avoided. Opiates can cause addiction (both physical and mental) and may also cause rebound headaches, which are headaches that occur when the pain medicine no longer provides relief.
  • Butorphanol (Stadol NS®) is an opiate-like drug available for injection and intranasal (in the nose) administration. The normal dosage of Stadol NS® is one spray into the nostril, which usually relieves migraine symptoms in 15-30 minutes. This drug can be used every hour for relief. The use of Stadol NS® may result in dependency if used regularly for pain relief. Side effects include nausea and vomiting, nasal irritation, and sedation.
  • Butalbital, a barbiturate medication, is also used for the immediate relief of migraine headache pain. It is used in various prescription combinations with aspirin, acetaminophen, caffeine, or codeine (an opiate pain medication). These medications are potentially addicting and are not used as initial treatment. They are sometimes used for patients whose headaches fail to respond to over-the-counter (OTC) medications but who are not candidates for triptans either due to pregnancy or the risk of heart attack and stroke. Products include butalbital and acetaminophen (Axocet®, Bupap®, Cephadyn®, Phrenilin®, or Sedapap®); butalbital, acetaminophen, and caffeine (Fioricet®, Esgic®); butalbital and aspirin (Axotal®); butalbital, aspirin, and caffeine (Fiorinal®); butalbital, acetaminophen, caffeine, and codeine (Fioricet #3 with Codeine® or Fioricet w/ Codeine®); and butalbital, aspirin, caffeine, and codeine (Fiorinal #3 with Codeine® or Fiorinal w/ Codeine®).

Author information
  • This information has been edited and peer-reviewed by contributors to the Natural Standard Research Collaboration (www.naturalstandard.com).

Bibliography
  1. American Academy of Family Physicians. .
  2. Blanchard EB, Appelbaum KA, Radnitz CL, et al. Placebo-controlled evaluation of abbreviated progressive muscle relaxation and of relaxation combined with cognitive therapy in the treatment of tension headache. J Consult Clin Psychol. 1990;58(2):210-5. .
  3. Estevez M, Gardner KL. Update on the genetics of migraine. Hum Genet. 2004;114(3):225-35. .
  4. Hershey AD, Tang Y, Powers SW, et al. Genomic abnormalities in patients with migraine and chronic migraine: preliminary blood gene expression suggests platelet abnormalities. Headache. 2004;44(10):994-1004. .
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Types of headaches
  • A headache is pain in occurring in the head. There are two types of headaches: primary headaches and secondary headaches. Primary headaches are not associated with (caused by) other diseases. Examples of primary headaches are migraine headaches, tension headaches, and cluster headaches. Secondary headaches are caused by associated disease, such as brain tumors. The associated disease may be minor or serious and life threatening. Seven in ten people have at least one type of headache a year.
  • Migraine headaches:
  • Migraine with aura: Migraine with aura is a migraine headache characterized by a neurological (nervous system) experience originating in the brain called an aura. Most auras appear as bright shimmering lights around objects (halos) or at the edges of the field of vision (called scintillating scotomas), zigzag lines, wavy images, or other visual hallucinations. Other individuals may experience temporary vision loss. An aura is usually experienced 10-30 minutes before the headache.
  • Non-visual auras include muscle weakness, speech or language abnormalities, dizziness, and paresthesia (tingling or numbness) of the face, tongue, or extremities.
  • Migraine without aura: Migraine without aura, or "silent" migraine, is the most prevalent type of migraine headache and may occur on one or both sides of the head. Tiredness or mood changes may be experienced the day before the headache. Nausea, vomiting, and sensitivity to light (also called photophobia) often accompany migraine without aura.
  • Basilar migraine: Basilar migraine or basilar artery migraine, involves a disturbance of the basilar artery (blood vessel) in the brainstem. Symptoms include severe headache, vertigo (dizziness), double vision, slurred speech, and poor muscle coordination. Basilar migraines pain is usually bilateral, or on both sides of the head. This type occurs in any age, but mostly occurs in females.
  • Carotidynia: Carotidynia is also called lower-half headache or facial migraine. It produces deep, dull, aching, and sometimes piercing pain in the jaw or neck. There is usually tenderness and swelling over the carotid artery (blood vessel) in the neck. Episodes can occur several times weekly and last a few minutes to hours. This type occurs more commonly in older people.
  • Headache-free migraine: A headache-free migraine is characterized by the presence of aura without a headache. This occurs in patients with a history of migraine with aura.
  • Ophthalmoplegic migraine: Ophthalmoplegic migraine begins with a headache felt in the eye and is accompanied by vomiting. As the headache progresses, the eyelid droops (ptosis), and the nerves responsible for eye movement become paralyzed. Eyelid dropping may persist for days or weeks.
  • Status migraine: Status migraine is a rare type involving intense pain that usually lasts longer than 72 hours. The patient may require hospitalization.
  • Other primary headaches:
  • Tension headaches: Tension headaches are the most common type of primary headache. As many as 90% of adults have had or will have tension headaches. Tension headaches are more common among women than men, possibly due to hormonal changes. Tension headaches often begin in the back of the head and upper neck as a band-like tightness or pressure. Tension headaches also are described as a band of pressure surrounding the head with the most intense pain over the eyebrows. The pain of tension headaches usually is mild (not disabling) and bilateral (affecting both sides of the head). Tension headaches are not associated with an aura or visual disturbances, and the patient normally has proper vision. Tension headaches are seldom associated with nausea, vomiting, or sensitivity to light and sound. Tension headaches usually occur sporadically (infrequently and without a pattern) but can occur frequently and even daily in some people. Most people are able to function despite their tension headaches. Tension headaches do not have a clear cause. Many healthcare professionals attribute tension headaches to excess stress during daily activities and anxiety.
  • Cluster headaches: Cluster headaches are headaches that come in groups lasting weeks or months, separated by pain-free periods of months or years. During the period in which the cluster headaches occur, pain typically occurs once or twice daily, but some patients may experience pain more than twice daily. Each episode of pain lasts from 30 minutes to one and one-half hours. Attacks tend to occur at about the same time every day and often awaken the patient at night from a sound sleep. The pain typically is excruciating and located unilaterally around or behind one eye. Some patients describe the pain as feeling like a hot poker in the eye. The affected eye may become red, inflamed, and watery. The nose on the affected side may become congested and runny. Unlike patients with migraine headaches, patients with cluster headaches tend to be restless. They often pace the floor, bang their heads against a wall, and can be driven to desperate measures. Cluster headaches are much more common in males than females. Cluster headaches do not have a clear cause, although alcohol and cigarettes can precipitate attacks. Many healthcare professionals believe that cluster and migraine headaches share a common cause that begins in the nerve that carries sensation from the head to the brain (trigeminal nerve) and ends with the blood vessels that surround the brain dilating (widening) and contracting (narrowing), which causes pain. Others believe that the pain arises in the deep vascular channels in the head and does not involve the trigeminal nerve. Cluster headaches are a rare type primary headache, affecting 0.1% of the population. An estimated 85% of cluster headache sufferers are men. The average age of cluster headache sufferers is 28-30 years, although headaches may begin in childhood.
  • Secondary headaches:
  • Secondary headaches are headaches caused by conditions other than those related to primary headaches, such as migraine. Secondary headaches have diverse causes, ranging from serious and life threatening conditions such as intracranial hemorrhage (bleeding within the skull), cerebral venous sinus thrombosis (blood clot within the membrane that covers the brain), cerebral stroke or infarct (lack of oxygen to the brain causing neurological damage), cerebral aneurysm (bulging blood vessel in the brain), Lyme disease (a bacteria from ticks), excess cerebrospinal fluid in the brain (hydrocephalus), meningitis (inflammation of the membranes of the brain or spinal cord), low level of cerebral spinal fluid (CSF), nasal sinus blockage, postictal headache (occurs after a stroke or seizure), temporomandibular joint dysfunction(TMJ), and brain tumor. Secondary headache pain can vary in severity.
  • Less serious but common conditions may also cause headaches, such as withdrawal from caffeine and the discontinuation of pain medications. Overuse of pain relievers causes the pain relievers to become less effective. As the effect of the pain reliever wears off, headaches recur (rebound headache). These drugs include Over-The-Counter (OTC) or prescription pain relievers, such as acetaminophen (Tylenol®), ibuprofen (Advil®, Motrin®), or opiates such as oxycodone (Percocet®, Oxycontin®) and hydrocodone (Lortab®, Vicodin®). Medications such as estrogen, progestins, calcium channel blockers (commonly used for treating high blood pressure), and selective serotonin reuptake inhibitors (SSRIs, commonly used to treat depression) can cause secondary headaches.
  • Individuals with a subarachnoid hemorrhage typically report having a sudden onset of severe headache. The pain of recurrent migraine headaches tends to build up gradually. Sometimes the headache of subarachnoid hemorrhage is triggered by exertion, such as exercise or sex.
  • Musculoskeletal problems, such as injuries or poor posture, can cause or contribute to headaches such as tension and migraine headaches.
  • Headaches soon after trauma (injury) to the head may be caused by subdural (inner layer of the brain) or epidural (outer layer of the brain) hematomas (blood clots).
  • Headaches that persistently occur on the same side are often secondary headaches associated with conditions such as brain tumors or arteriovenous malformations (abnormal clusters of blood vessels in the brain).
  • Bacterial meningitis is a rapidly progressive and life-threatening disease with fever, headaches, stiff neck, and deterioration in mental function. Herpes simplex encephalitis (brain swelling caused by a herpes virus) is an infection of the brain that causes death of brain tissue. Symptoms include fever, headache, and deterioration in mental function. Early treatment with antibiotics and anti-viral agents can decrease the extent of brain damage and improve survival.
  • Associated temporary weakness of the extremities or facial muscles can be symptoms of transient ischemic attacks (TIAs, or temporary lack of oxygen to the brain). TIAs are warning signals for future strokes that can cause permanent brain damage. Headache also can accompany strokes and intracerebral bleeding (bleeding into the brain).

Copyright © 2011 Natural Standard (www.naturalstandard.com)


The information in this monograph is intended for informational purposes only, and is meant to help users better understand health concerns. Information is based on review of scientific research data, historical practice patterns, and clinical experience. This information should not be interpreted as specific medical advice. Users should consult with a qualified healthcare provider for specific questions regarding therapies, diagnosis and/or health conditions, prior to making therapeutic decisions.



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