Headache

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).



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.