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What's the Deal With Alcohol and Ibuprofen?

FitSugar — Wed, 04 Mar 2009 10:00:57 -0800

If you wake up with a headache after a night of overindulging, sometimes figuring out what painkiller to take can make the headache even worse. I've heard that it's bad to take acetaminophen (aka Tylenol), because it can lead to liver damage, but take note: you're also not supposed to drink while taking ibuprofen.

Ibuprofen is part of the anti-inflammatory drug family known as NSAIDs, which can cause tears in the stomach lining if taken on an empty tummy. Add alcohol to the mix, and the potential danger is heightened. If you take ibuprofen when drinking more than the recommended amount for women (about two to three drinks), you increase your risk of stomach irritation and bleeding. This is especially true for people who are prone to ulcers.

But wait! Taking Tylenol when you're hungover isn't such a good idea either. To find out why, read more.

Acetaminophen can lead to liver damage if you take it in large doses (that's 4,000 milligrams, or eight extra-strength Tylenol) for more than a couple of days. Heavy drinkers who take acetaminophen and don't eat enough can overtax their livers. However, the risks associated with taking Tylenol after recreational drinking are somewhat blurry. According to The Straight Dope:

I'll spare you the biochemistry, but basically acetaminophen and alcohol in combination overwhelm the liver's ability to remove toxins from your bloodstream. . . . It's not clear from the medical literature what happens if you take acetaminophen after a one-time bender (as opposed to chronic alcohol abuse). But don't substitute some other painkiller - aspirin and ibuprofen can have side effects too. Better to be suffering than dead.

So what's a hungover, headache-plagued gal to do - besides not drinking so much in the first place? Since the jury is still out on the exact effects of combining Advil or Tylenol with booze, probably best just to tough it out. Maybe even try a natural remedy like yoga. Got one that works for you? Share it in the comments.

Source

Alcoholism

FitSugar — Wed, 08 Oct 2008 17:35:36 -0700

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Drug Research

Topiramate (Topamax), an anticonvulsant drug used to treat epilepsy, is showing promise as a treatment for alcohol dependence. In a 2007 study published in the Journal of the American Medical Association, patients who took topiramate had fewer heavy drinking days, fewer drinks per day, and more days of not drinking at all than patients who received placebo.

Alcohol and Heart Disease

Heart disease is one of the leading causes of death among people who are heavy drinkers. Alcohol abuse and dependence increase the risks for unhealthy cholesterol levels, high blood pressure, heart failure, and stroke. Although the heart benefits of moderate alcohol use are widely discussed in the popular media, to date there are no definitive scientific studies that prove that alcohol consumption is beneficial to overall health.

The American Heart Association recommends that people who drink alcohol do so in moderation (one to two drinks a day for men, one drink a day for women). If you don’t drink, the American Heart Association advises against starting to drink to reduce the risk of heart disease. The best methods for preventing heart disease are exercise, healthy diet, and avoiding all forms of tobacco exposure.

Alcohol and Cancer

Long-term heavy alcohol use may increase the risks for many types of cancer including stomach, colorectal, mouth, tongue, throat, liver, and breast cancers. To reduce breast cancer risk, the American Cancer Society recommends that women limit their amount of alcohol consumption. Women who are at high risk for breast cancer should consider not drinking at all.

Introduction

Alcoholism is a chronic, progressive, and often fatal disease. It is a primary disorder and not a symptom of other diseases or emotional problems. The chemistry of alcohol allows it to affect nearly every type of cell in the body, including those in the central nervous system. After prolonged exposure to alcohol, the brain becomes dependent on it. The severity of this disease is influenced by factors such as genetics, psychology, culture, and response to physical pain.

Alcoholism is a chronic illness marked by dependence on alcohol consumption. It interferes with physical or mental health, and social, family, or job responsibilities. This addiction can lead to liver, circulatory, and neurological problems. Pregnant women who drink alcohol in any amount may harm the fetus.

Alcoholism, alcohol dependence, and alcohol abuse are associated with the following:

The only indication of early alcoholism may be the unpleasant physical responses to withdrawal that occur during even brief periods of abstinence.
Alcoholics have little or no control over the quantity they drink or the duration or frequency of their drinking.
Alcoholics are preoccupied with drinking, deny their own addiction, and continue to drink even though they are aware of the dangers.
Over time, some alcoholics become tolerant to the effects of drinking and require more alcohol to become intoxicated, creating the illusion that they can "hold their liquor."
Alcoholics may have blackouts after drinking and have frequent hangovers that cause them to miss work and other normal activities.
Alcoholics might drink alone and start their drinking early in the day.
Alcoholics periodically quit drinking or switch from hard liquor to beer or wine, but these periods rarely last.
Severe alcoholics often have a history of accidents, marital and work instability, and alcohol-related health problems.
Episodic violent and abusive incidents involving spouses and children and a history of unexplained or frequent accidents are often signs of drug or alcohol abuse.

Alcoholism can develop insidiously, and often there is no clear line between problem drinking and alcoholism. Eventually alcohol dominates thinking, emotions, and actions and becomes the primary means through which a person can deal with people, work, and life.

In addition to alcohol dependence, experts are now defining alcohol use by levels of harm that it may be causing. This information is useful to determine possible interventions at earlier stages. The following categories of alcohol use and abuse use a definition of one drink as 12 ounces of beer, 5 ounces of wine, or 1.5 ounces (a jigger) of 90-proof liquor.

Moderate Drinking. Moderate drinking, particularly red wine, appears to offer health benefits. Moderate drinking is defined as equal to or less than two drinks a day for men and one drink a day for women.

Hazardous (Heavy) Drinking. Hazardous drinking puts people at risk for adverse health events. People who are heavy drinkers consume:

More than 14 drinks per week, or four to five drinks at one sitting, for men
More than seven drinks per week, or three drinks at one sitting, for women
Frequent intoxication

Harmful Drinking. Drinking is considered harmful when alcohol consumption has actually caused physical or psychologic harm. This is determined by:

Clear evidence that alcohol is responsible for such harm.
The nature of that harm can be identified.
Alcohol consumption has persisted for at least a month or has occurred repeatedly for the past year.

Certain people are at much higher risk for harmful drinking, such as older individuals with high blood pressure or those taking medications for arthritis or pain.

Alcohol Abuse. People with alcohol abuse have one or more of the following alcohol-related problems over a period of 1 year:

Failure to fulfill work or personal obligations
Recurrent use in potentially dangerous situations
Problems with the law
Continued use in spite of harm being done to social or personal relationships

Alcohol Dependence. People who are alcohol dependent have three or more of the following alcohol-related problems over a year:

Increased amounts of alcohol are needed to produce an effect
Withdrawal symptoms or drinking alcohol is used to avoid these symptoms
Drinks more over a given period than intended
Unsuccessful attempts to quit or cut down
Gives up significant leisure or work activities
Continues to drink in spite of the knowledge of its physical or psychological harm to oneself or others

Two-thirds of those with alcohol dependence continued to be dependent on alcohol after 5 years.

Causes

People have been drinking alcohol for about 15,000 years. Drinking steadily and consistently over time can produce dependence and cause withdrawal symptoms during periods of abstinence. This physical dependence, however, is not the sole cause of alcoholism. To develop alcoholism, other factors usually come into play, including biology, genetics, culture, and psychology.

Genetic factors play a significant role in alcoholism and may account for about half of the total risk for alcoholism. The role that genetics plays in alcoholism is complex, however, and it is likely that many different genes are involved. Research suggests that alcohol dependence, and other substance addictions, may be associated with genetic variations in 51 different chromosomal regions.

Researchers are investigating a number of inherited traits that make particular individuals susceptible to this disorder:

The amygdala is an area of the brain thought to play a role in the emotional aspects of craving, which can lead to addiction. Some studies indicate that the amygdala is smaller in subjects with family histories of alcoholism, suggesting that inherited differences in brain structure may affect risk. Other studies suggest that certain brain chemicals (neurotransmitters) and proteins in the amygdala region may be involved in the link between anxiety and alcoholism.
Some studies indicate that people may inherit a lack of the warning signals that ordinarily make people stop drinking. Research suggests this factor may contribute to 40 - 60% of alcoholism cases related to genetic factors. (Even in the absence of genetic factors, repeated exposure to alcohol increases the ability to tolerate larger amounts before experiencing behavioral impairment.)
Some people with alcoholism may have an inherited dysfunction in the transmission of serotonin. Serotonin is a brain chemical messenger (neurotransmitter). It is important for well-being and associated behaviors (eating, relaxation, and sleep). Abnormal serotonin levels are associated with high levels of tolerance for alcohol. They are also linked to impulsivity and aggressiveness. These behaviors can predispose people to drink and can increase the risk for dangerous behaviors and suicide in people who are alcohol dependent.
Dopamine is another neurotransmitter associated with alcoholism and other addictions. Research indicates that high levels of the D2 dopamine receptor may help inhibit behavioral responses to alcohol, and protect against alcoholism, in people with a family history of alcohol dependence.

Even if genetic factors can be identified, however, they are unlikely to explain all cases of alcoholism. It is important to understand that whether they inherit the disorder or not, people with alcoholism are still legally responsible for their actions. Inheriting genetic traits does not doom a child to an alcoholic future. Environment, personality, and emotional factors also play a strong role.

Alcohol has widespread effects on the brain and can affect neurons (nerve cells), brain chemistry, and blood flow within the frontal lobes of the brain. Researchers are particularly interested in systems of neurotransmitters (chemical messengers) in the brain that are affected by alcohol. Some research is focusing on the way these neurotransmitters are employed in the brain after long-term alcohol use in order to adapt to the cravings and pain of withdrawal. Such chemical changes may lead to dependency or to relapse after quitting in two ways:

They increase the need to reduce agitation
They increase the desire to restore pleasurable feelings

When a person who is dependent on alcohol stops drinking, chemical responses create an overexcited nervous system and agitation by changing the level of chemicals that inhibit impulsivity or stress and excitation. High norepinephrine levels, a chemical the brain produces more of when drinking is stopped, in fact, may be the primary factor in withdrawal symptoms, such as an increase in blood pressure and heart rate. This hyperactivity in the brain produces an intense need to calm down and to use more alcohol. One study suggested that the need to relieve agitation may be the more important factor in causing a relapse than restoring mood.

Drinking alcohol stimulates the release of neurotransmitters (serotonin, dopamine, and opioid peptides) that produce pleasurable feelings such as euphoria, a sensation of being rewarded, and a sense of well-being.

Over time, however, heavy alcohol use appears to deplete the stores of dopamine and serotonin. Persistent drinking, therefore, eventually fails to restore mood, but by then the drinker has been conditioned to believe that alcohol will improve spirits (even though it does not).

Between 80 - 90% of people treated for alcoholism relapse, even after years of abstinence. Patients and their caregivers should understand that relapses of alcoholism are analogous to recurrent flare-ups of chronic physical diseases. Factors that place a person at high risk for relapse include:

Frustration and anger
Social pressure
Internal temptation

Mental and Emotional Stress. Alcohol blocks out emotional pain and is often perceived as a loyal friend when human relationships fail. It is also associated with freedom and with a loss of inhibition that offsets the tedium of daily routines. When the alcoholic tries to quit drinking, the brain seeks to restore what it perceives to be its equilibrium. The brain's best weapons to achieve this are depression, anxiety, and stress (the emotional equivalents of physical pain), which are produced by brain chemical imbalances. These negative moods continue to tempt alcoholics to return to drinking long after physical withdrawal symptoms have abated.

It is important to realize that any life change, even changes for the better, may cause temporary grief and anxiety. With time and the substitution of healthier pleasures, this emotional turmoil weakens and can be overcome.

Co-dependency. Many aspects of the ex-drinker's relationships change when drinking stops, making it difficult to remain abstinent:

One of the most difficult problems that occur is being around other people who are able to drink socially without danger of addiction. A sense of isolation, a loss of enjoyment, and the ex-drinker's belief that pity, not respect, is guiding a friend's attitude can lead to loneliness, low self-esteem, and a strong desire to drink again.
Friends may not easily accept the sober, perhaps more subdued, ex-drinker. Close friends and even intimate partners may have difficulty in changing their responses to this newly sober person and, even worse, may encourage a return to drinking.
To preserve marriages, spouses of alcoholics often build their own self-images on surviving or handling their mates' difficult behavior and then discover that they find it difficult to adjust to new roles and behaviors.

In such cases, separation from these "enablers" may be necessary for survival. It is no wonder that, when faced with such losses, even if they are temporary, a person returns to drinking. The best course in these cases is to encourage close friends and family members to seek help as well. Fortunately, groups such as Al-Anon exist for this purpose.

Social and Cultural Pressures. The media portrays the pleasures of drinking in advertising and programming. The medical benefits of light-to-moderate drinking are frequently publicized, giving ex-drinkers the spurious excuse of returning to alcohol for their health. These messages must be categorically ignored and acknowledged for what they are: An industry's attempt to profit from potentially great harm to individuals.

Risk Factors

About 90% of adults in the U.S. drink alcohol. Every day, more than 700,000 Americans are being treated for alcoholism. In addition, up to half of American men have problems that are caused by alcohol.

Some researchers have categorized people with alcoholism as Type 1 or Type 2.

Type 1 individuals are more often women. They typically become alcoholic at a later age, have less severe symptoms or fewer psychiatric problems, and have a better outlook on life than those classified as type 2.
Type 2 people are more likely to be male. They tend to become alcoholic at an early age and have a high family risk for alcoholism, more severe symptoms, and a negative outlook on life.

Not only do these two groups tend to respond differently to psychotherapeutic approaches, but they may also respond differently to medications.

Drinking in Adolescence. About half of under-age Americans have used alcohol. About 2 million people ages 12 - 20 are considered heavy drinkers, and 4.4 million are binge drinkers. Anyone who begins drinking in adolescence is at risk for developing alcoholism. The earlier a person begins drinking, the greater the risk. A 2006 survey of over 40,000 adults indicated that among those who began drinking before age 14, nearly half had become alcoholic dependent by the age of 21. In contrast, only 9% of people who began drinking after the age of 21 developed alcoholism.

Young people at highest risk for early drinking are those with a history of abuse, family violence, depression, and stressful life events. People with a family history of alcoholism are also more likely to begin drinking before the age of 20 and to become alcoholic. Such adolescent drinkers are also more apt to underestimate the effects of drinking and to make judgment errors, such as going on binges or driving after drinking, than young drinkers without a family history of alcoholism.

Drinking in the Elderly Population. Although alcoholism usually develops in early adulthood, the elderly are not exempt. In fact, doctors may overlook alcoholism when evaluating elderly patients, mistakenly attributing the signs of alcohol abuse to the normal effects of the aging process. A survey of adults over 60 reported that 15% of men and 12% of women were hazardous drinkers, and 9% of men and 3% of women were alcohol dependent.

Alcohol also affects the older body differently. People who maintain the same drinking patterns as they age can easily develop alcohol dependency without realizing it. It takes fewer drinks to become intoxicated, and older organs can be damaged by smaller amounts of alcohol than those of younger people. Also, up to one-half of the 100 most prescribed drugs for older people react adversely with alcohol. Medications used for arthritis or pain pose a particular danger for interaction with alcohol.

Most alcoholics are men, but the incidence of alcoholism in women has been increasing over the past 30 years. Studies indicate that about 7% of men and 2.5% of women abuse alcohol. However, studies suggest that women are more vulnerable than men to many of the long-term consequences of alcoholism. For example, women are more likely than men to develop alcoholic hepatitis and to die from cirrhosis, and women are more vulnerable to the brain cell damage caused by alcohol.

Individuals who were abused as children have a higher risk for substance abuse later on. In one study, 72% of women and 27% of men with substance abuse disorders reported physical or sexual abuse or both. They also had worse response to treatment than those without such a history.

Overall, there is no difference in alcoholic prevalence among African-Americans, Caucasians, and Hispanic-Americans. Some population groups, however, such as Native Americans, have an increased incidence of alcoholism while others, such as Jewish and Asian Americans, have a lower risk. Although the biological or cultural causes of such different risks are not known, certain people in these population groups may have a genetic susceptibility or invulnerability to alcoholism because of the way they metabolize alcohol.

Psychiatric Disorders. Severely depressed or anxious people are at high risk for alcoholism, smoking, and other forms of addiction. Likewise, a large proportion of alcohol-dependent people suffer from an accompanying psychiatric or substance abuse disorder. Either anxiety or depression may increase the risk for self-medication with alcohol. Depression is the most common psychiatric problem in people with alcoholism or substance abuse.

Depression is less reported in the male population, but this may be caused by male tendency to mask emotional disorders with behavior such as alcohol abuse.

Specific anxiety disorders, such as panic disorders and social phobia, may pose particular risks for alcohol and substance abuse. Social phobia causes an intense fear of being publicly scrutinized and humiliated. Panic disorders cause intense anxiety and panic attacks. People with these disorders may use alcohol as a way to become less inhibited in public situations or to calm feelings of panic. While anxiety disorders are found in about 15% of adults overall, over 50% of people with alcohol abuse problems suffer from these conditions. People who have anxiety disorders are more likely to resume drinking after treatment for alcohol dependence. [For more information, see In-Depth Report #28: Anxiety.]

Long-term alcoholism itself may cause chemical changes that produce anxiety and depression. In fact, a study on elderly people with depression reported that when even moderate drinkers reduced consumption, their mood improved. Studies also indicate that alcohol use may promote panic attacks. It is not always clear, then, whether people with emotional disorders are self-medicating with alcohol, or whether alcohol itself is producing mood swings.

Behavioral Disorders and Lack of Impulse Control. Studies are also finding that alcoholism is strongly related to impulsive, excitable, and novelty-seeking behavior, and such patterns are established early on. Children who later become alcoholics or who abuse drugs are more likely to have less fear of new situations than others, even if there is a greater risk for harm than in nonalcoholics. Specifically, children with attention deficit hyperactivity disorder (ADHD), a condition that shares these behaviors, have a higher risk for alcoholism in adulthood. The risk is especially high in children with ADHD and conduct disorder.

Alcoholism is not restricted to any social or economic levels. For example, a thorough 1996 study reported no higher prevalence of alcoholism among adult welfare recipients than in the general population (about 7%). There was also no difference in prevalence between African-Americans and Caucasians in low-income groups. On the other hand, people in low-income groups who drank did display some tendencies that differed from the general population of drinkers. For instance, in one study as many women as men were heavy drinkers in lower income groups. Excessive drinking may also be more dangerous in lower income groups. One study found that alcohol was a major factor in the higher death rate of people, particularly men, in lower socioeconomic groups compared with those in higher groups.

Complications

Alcoholism reduces life expectancy by 10 - 12 years. Next to smoking, it is the most common preventable cause of death in America. Although studies indicate that adults who drink moderately (about one drink a day for women and two drinks a day for men) have a lower mortality rate than their nondrinking peers, their risk for untimely death increases with heavier drinking. The earlier a person begins drinking heavily, the greater their chance of developing serious illnesses later on. Once one becomes dependent on alcohol, it is very difficult to quit.

Alcohol can affect the body in so many ways that researchers have a hard time determining exactly what the consequences are from drinking. Interestingly, although heavy drinking is associated with earlier death, studies suggest it is not from a higher risk of the more common serious health problems, such as heart attack, heart failure, diabetes, lung disease, or stroke. It is well known, however, that chronic consumption leads to many problems that can increase the risk for death:

In general, people who drink regularly have a higher rate of death from injury or violence.
Alcohol overdose can lead to death. This is a particular danger for adolescents who may want to impress their friends with their ability to drink alcohol but cannot yet gauge its effects. However, alcohol overdose doesn't only occur from any one heavy drinking incident, but may also occur from a constant infusion of alcohol in the bloodstream.
Severe withdrawal and delirium tremens. Delirium tremens occurs in about 5% of alcoholics. It includes progressively severe withdrawal symptoms and altered mental states. In some cases, it can be fatal.
Frequent, heavy alcohol use directly harms many areas in the body and produce dangerous health conditions (liver damage, pancreatitis, anemia, upper gastrointestinal bleeding, nerve damage, and impotence).
Alcohol abusers who need surgery have an increased risk of postoperative complications, including infections, bleeding, insufficient heart and lung functions, and problems with wound healing. Alcohol withdrawal symptoms after surgery may impose further stress on the patient and hinder recuperation.

Although not traditionally thought of as a medical problem, a review of studies found that hangovers have significant consequences that include changes in liver function, hormonal balance, and mental functioning and an increased risk for depression and cardiac events. Hangovers can impair job performance, increasing the risk for mistakes and accidents. Interestingly, hangovers are generally more common in light-to-moderate drinkers than heavy and chronic drinkers, suggesting that binge drinking can be as threatening as chronic drinking. Any man who drinks more than five drinks or any woman who has more than three drinks is at risk for a hangover.

Alcohol plays a large role in accidents, suicide, and crime:

Alcohol plays a major role in more than half of all automobile fatalities.
Alcohol-related automobile accidents are the leading causes of death in young people.
Fewer than two drinks can impair the ability to drive. Even one drink may double the risk of injury, and more than four drinks increases the risk by 11 times.
Alcoholism is the primary diagnosis in one-quarter of all people who commit suicide.
Alcohol is implicated in 67% of all murders.

Alcoholic households are less cohesive and have more conflicts, and their members are less independent and expressive than households with nonalcoholic or recovering alcoholic parents. Domestic violence is a common consequence of alcohol abuse.

Effect on Women. Research suggests that for women, the most serious risk factor for injury from domestic violence may be a history of alcohol abuse in her male partner.

Effect on Children. Alcoholism in parents also increases the risk for violent behavior and abuse toward their children. Children of alcoholics tend to do worse academically than others, have a higher incidence of depression, anxiety, and stress and lower self-esteem than their peers. In addition to their own inherited risk for later alcoholism, many children of alcoholics have serious coping problems that may last their entire life.

Adult children of alcoholic parents are at higher risk for divorce and for psychiatric symptoms. One study concluded that the only events with greater psychological impact on children are sexual and physical abuse.

Researchers are finding common genetic factors in alcohol and nicotine addiction, which may explain, in part, why alcoholics are often smokers. Alcoholics who smoke compound their health problems. More alcoholics die from tobacco-related illnesses, such as heart disease or cancer, than from chronic liver disease, cirrhosis, or other conditions that are more directly tied to excessive drinking. Abuse of other substance is also common among alcoholics.

Alcoholic Hepatitis and Cirrhosis. Alcohol is absorbed in the small intestine and passes directly into the liver, where it becomes the preferred energy source. The liver, then, is particularly endangered by alcoholism. In the liver, alcohol converts to toxic chemicals, notably acetaldehyde, which trigger the production of immune factors called cytokines. In large amounts, these factors cause inflammation and tissue injury.

Cirrhosis is a chronic liver disease that causes damage to liver tissue, scarring of the liver (fibrosis; nodular regeneration), progressive decrease in liver function. Consequences of a failing liver include excessive fluid in the abdomen (ascites), bleeding disorders (coagulopathy), increased pressure in the blood vessels (portal hypertension), and brain function disorders (hepatic encephalopathy). Excessive alcohol use is the leading cause of cirrhosis.

Even moderate alcohol intake can produce pain in the upper right quarter of the abdomen -- a possible symptom of liver involvement. In many cases, such symptoms may be an indication of fatty liver or alcohol hepatitis, which are reversible liver conditions.

Between 10 - 20% of people who drink heavily (five or more drinks a day) develop cirrhosis, a progressive and irreversible scarring of the liver that can eventually be fatal. Alcoholic cirrhosis (also sometimes referred to as portal, Laennec’s, nutritional, or micronodular cirrhosis) is the primary cause of cirrhosis in the U.S. [For more information, see In-Depth Report #75: Cirrhosis.]

Not eating when drinking and consuming a variety of alcoholic beverages increase the risk for liver damage. Nevertheless, the amount of alcohol consumed and the patterns of drinking are only weak predictions of risk. Up to 90% of heavy drinkers do not develop advanced irreversible liver disease. Other risk factors have been identified that may increase the danger to the liver in heavy drinkers:

Obesity is a major factor for all stages of liver disease.
Women develop liver disease at lower quantities of alcohol intake than men.
Genetic factors that regulate the immune responses also play role.

Viral Hepatitis B and C. People with alcoholism tend to have lifestyles that put them at higher risk for hepatitis B and C, which are caused by viruses. Chronic forms of viral hepatitis pose risks for cirrhosis and liver cancer, and alcoholism significantly increases these risks. People with alcoholism should be immunized against hepatitis B. They may need a higher-than-normal dose of the vaccine for it to be effective. There is no vaccine for hepatitis C. [For more informaiton, see In-Depth Report #59: Hepatitis.]

Alcoholism can cause many problems in the gastrointestinal tract. Violent vomiting can produce tears in the junction between the stomach and esophagus. Alcoholism poses a high risk for diarrhea and hemorrhoids. It increases the risk for ulcers, particularly in people taking the painkillers known as nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin or ibuprofen. It can also lead to swollen veins in the esophagus (esophagitis), called varices, which can lead to bleeding.

Click the icon to see an image of ulcer emergencies.

Alcohol can contribute to serious and chronic inflammation of the pancreas (pancreatitis) in people who are susceptible to this condition. There is some evidence of a higher risk for pancreatic cancer in people with alcoholism, although this higher risk may occur only in people who are also smokers.

Click the icon to see an image of the pancreas.

Moderate amounts (one to two drinks a day) of alcohol can improve some heart disease risk factors, such as increasing HDL (“good cholesterol”) levels. However, at this time there is no definitive proof that moderate drinking improves overall health, and the American Heart Association does not recommend drinking alcoholic beverages solely to reduce cardiovascular risk.

Excessive drinking clearly has negative effects on heart health. In fact, heart disease is one of the leading causes of death for alcoholics. Alcohol abuse increases levels of triglycerides (unhealthy fats) and increases the risks for high blood pressure, heart failure, and stroke. In addition, the extra calories in alcohol can contribute to obesity, a major risk factor for many heart problems.

Click the icon to see an image of the heart.

Alcohol abuse and dependence may increase the risk for certain type of cancers. In particular, heavy alcohol use appears to increase the risks for mouth, throat, esophageal, gastrointestinal, liver, colorectal, and breast cancers. Women who are at high risk for breast cancer should consider not drinking at all.

Pneumonia. Over time, chronic alcoholism can cause severe reductions in white blood cells, which increase the risk for community-acquired pneumonia (pneumonia acquired outside of hospitals or nursing homes). Patients who abuse alcoholism have a greater risk for developing severe pneumonia. Doctors recommend that patients with alcohol dependence should receive an annual pneumococcal pneumonia vaccination. The initial signs of pneumococcal pneumonia are high fever, cough, and stabbing chest pains. Immediately contact your doctor if you experience these symptoms.

Click the icon to see an image of pneumonia.

Severe alcoholism is associated with osteoporosis (loss of bone density), muscular deterioration, skin sores, and itching. Alcohol-dependent women seem to face a higher risk than men for damage to muscles, including muscles of the heart, from the toxic effects of alcohol.

Click the icon to see an image of osteoporosis.

Effects Sexual Function and Fertility. Alcoholism increases levels of the female hormone estrogen and reduces levels of the male hormone testosterone, factors that possibly contribute to impotence in men and infertility in women. Such changes may also be responsible for the higher risks for absent periods and abnormal uterine bleeding in women with alcoholism.

Drinking During Pregnancy and Effects on the Infant. Even moderate amounts of alcohol can have damaging effects on the developing fetus, including low birth weight and an increased risk for miscarriage. High amounts can cause fetal alcohol syndrome, a condition that can cause mental and growth retardation. Although there is no specific amount of alcohol intake, the risk of developing the syndrome is increased depending on the time of alcohol exposure during pregnancy, a patter of drinking (four or more drinks per occasion), and how often alcohol consumption occurs.

Moderate alcohol consumption may help protect the hearts of adults with type 2 diabetes. Heavy drinking however is associated with obesity, which is a risk factor for this form of diabetes. In addition, alcohol can cause hypoglycemia, a drop in blood sugar, which is especially dangerous for people with diabetes who are taking insulin. Intoxicated diabetics may not be able to recognize symptoms of hypoglycemia, a potentially hazardous condition.

Drinking too much alcohol can cause immediate mild neurologic problems in anyone, including insomnia and headache. Long-term alcohol use may even physically affect the brain. Depending on length and severity of alcohol abuse, neurologic damage may not be permanent, and abstinence nearly always leads to eventual recovery of normal mental function.

Effect on Mental Functioning. Studies have reported less blood flow in the frontal lobes of the brain, which may reflect links to deeper levels. In one study, even recent high alcohol use (within the last 3 months) was associated with some loss of verbal memory and slower reaction times. Over time, chronic alcohol abuse can impair so-called "executive functions," which include problem solving, mental flexibility, short-term memory, and attention. These problems are usually mild to moderate and can last for weeks or even years after a person quits drinking. In fact, such persistent problems in judgment are possibly one reason for the difficulty in quitting. Alcoholic patients who have co-existing psychiatric or neurologic problems are at particular risk for mental confusion and depression.

Wernicke-Korsakoff Syndrome. Wernicke-Korsakoff syndrome is a serious consequence of severe thiamin (vitamin B1) deficiency in alcoholism. Symptoms of this syndrome include severe loss of balance, confusion, and memory loss. Eventually, it can result in permanent brain damage and death. Once the syndrome develops, oral supplements have no effect, and only adequate and rapid intravenous vitamin B1 can treat this serious condition.

Peripheral Neuropathy. Vitamin B1 deficiencies can also lead to peripheral neuropathy, a condition that causes pain, tingling, and other abnormal sensations in the arms and legs.

Click the icon to see an image of the nervous system.

People with alcoholism should be sure to take vitamin and mineral supplements. Even apparently well-nourished people with alcoholism may be deficient in important nutrients. Deficiencies in vitamin B are particularly health risks in people with alcoholism. Other vitamin and mineral deficiencies, however, can also cause widespread health problems.

Folate Deficiencies. Alcohol interferes with the metabolism of folate, a very important B vitamin, called folic acid when used as a supplement. Folate deficiencies can cause severe anemia. Deficiencies during pregnancy can lead to birth defects in the infant.

Vitamin B1 Deficiencies. Many of the B vitamins are essential for nerve protection. Severe deficiencies are common in alcoholism and can have serious consequences on the central nervous system, notably peripheral neuropathy and, in very severe cases, Wernicke-Korsakoff syndrome.

The effects of many medications are strengthened by alcohol, while others are inhibited. Of particular importance is alcohol's reinforcing effect on anti-anxiety drugs, sedatives, antidepressants, and antipsychotic medications. Alcohol also interacts with many drugs used by people with diabetes. It interferes with drugs that prevent seizures or blood clotting. It increases the risk for gastrointestinal bleeding in people taking aspirin or other nonsteroidal inflammatory drugs (NSAIDs) including ibuprofen and naproxen. Chronic alcohol abusers have a particularly high risk for adverse side effects from consuming alcohol while taking certain antibiotics. These side effects include flushing, headache, nausea, and vomiting. In other words, taking almost any medication should preclude drinking alcohol.

Diagnosis

Even when people with alcoholism experience withdrawal symptoms, they nearly always deny the problem, leaving it up to co-workers, friends, or relatives to recognize the symptoms and to take the first steps toward encouraging treatment. Denial, in fact, may be an important warning signal for alcoholism.

Family members cannot always rely on a doctor to make an initial diagnosis. Although 15 - 30% of people who are hospitalized have alcoholism or alcohol dependence, doctors often fail to screen for the problem. In addition, doctors themselves often do not recognize the symptoms. Even when doctors identify an alcohol problem, however, they are frequently reluctant to confront the patient with a diagnosis that might lead to treatment for addiction.

A doctor who suspects alcohol abuse should ask the patient questions about current and past drinking habits to distinguish moderate from heavy, or hazardous, drinking. Screening tests for alcohol problems in older people should account for possible medical problems or medications that might place them at higher risk for hazardous drinking than younger individuals.

A number of short screening tests are available, which a person can even take on their own. Because people with alcoholism often deny their problem or otherwise attempt to hide it, the tests are designed to elicit answers related to problems associated with drinking rather than the amount of liquor consumed or other specific drinking habits.

CAGE Test. The CAGE test is an acronym for the following questions and is the quickest test:

Attempts to CUT (C) down on drinking
ANNOYANCE (A) with criticisms about drinking
GUILT (G) about drinking
Use of alcohol as an EYE-OPENER (E) in the morning

This test and another called the Self-Administered Alcoholism Screening Test (SAAST) appear to be most useful in detecting possible alcoholism in white, middle-aged males. They are not very accurate for identifying alcohol abuse in older people, white women, and African-Americans and Mexican Americans.

T-ACE Test. The T-ACE test is a four-question test that appears to be quite accurate in identifying alcoholism in both men and women. It asks the following questions:

Does it TAKE (T) more than three drinks to make you feel high?
Have you ever been ANNOYED (A) by people's criticism of your drinking?
Are you trying to CUT DOWN (C) on drinking?
Have you ever used alcohol as an EYE OPENER (E) in the morning?

A positive response to two of these four questions is considered to indicate possible alcohol abuse or dependence.

AUDIT Test. A more effective and important test for most people may be the Alcohol Use Disorders Identification Test (AUDIT), which is the only test specifically designed to identify hazardous or harmful drinking. It asks three questions about amount and frequency of drinking, three questions about alcohol dependence, and four questions about problems related to alcohol consumption.

A Single-Question. One simple question may be as sensitive as the CAGE or AUDIT: "When was the last time you had more than five drinks (for men) or four drinks (for women) in one day?" An answer of "within 3 months" accurately identified about half of people who were problem drinkers. Problem drinking is defined as hazardous drinking within the last month or some alcohol-use disorder during the past year.

Other Screening Tests. Other short screening tests are the Michigan Alcoholism Screening Test (MAST) and the Alcohol Dependence Scale (ADS).

Some symptoms of alcoholism may be attributed to other disorders, particularly in the elderly, where symptoms of confusion, memory loss, or falling may be attributed to the aging process alone. Heavy drinkers may be more likely to complain to their doctors about so-called somatization symptoms, which are vague ailments, such as joint pain, intestinal problems, or general weakness, that have no identifiable physical cause. Such complaints should signal the doctor to follow-up with screening tests for alcoholism.

Alcoholism is particularly less likely to be recognized in elderly women. In fact, only 1% of older women who need treatment for alcoholism are diagnosed accurately and treated appropriately. Instead, they are often diagnosed with depression and may even be prescribed anti-anxiety drugs or antidepressants that can have dangerous interactions with alcohol.

Physical Examination. A physical examination and other tests should be performed to uncover any related medical problems.

Laboratory Tests. Tests for alcohol levels in the blood are not useful for diagnosing alcoholism because they reflect consumption at only one point in time and not long-term usage. Certain blood tests, however, may provide biologic markers that suggest medical problems associated with alcoholism or indications of alcohol abuse:

Carbohydrate-deficient transferrin (CDT). This compound is a marker for heavy drinking and can be helpful in monitoring patients for progress towards abstinence.
Gamma-glutamyltransferase (GGT). This liver enzyme is very sensitive to alcohol and can be elevated after moderate alcohol intake and in chronic alcoholism.
Aspartate (AST) and alanine aminotransaminases (ALT). These are liver enzymes and are markers for liver damage.
Testosterone. Male hormone levels in men with alcoholism may be low. (Such results sometimes persuade men with alcoholism to seek help.)
Mean corpuscular volume (MCV). This blood test measures the size of red blood cells, which increase with alcohol use over time.

Treatment for Alcoholism

Once a diagnosis of alcoholism is made, the next major step is getting the patient to seek treatment. The main reasons alcoholics do not seek treatment are:

Lack of confidence in successful therapies
Denial of their own alcoholism
Social stigma attached to the condition and its treatment

The alcoholic patient and everyone involved should fully understand that alcoholism is a disease. Furthermore, the responses to this disease (need, craving, fear of withdrawal) are not character flaws but symptoms, just as pain or discomfort are symptoms of other illnesses. They should also realize that treatment is difficult and sometimes painful, just as are treatments for other life-threatening diseases, such as cancer, but that treatment is the only hope for a cure.

Interventions by family members, employers, and therapists can be very effective in motivating a person to quit and in reducing drinking over the short term. Even brief interventions from a primary care doctor and self-help information can be helpful in reducing harmful drinking. Studies report, however, that only regular follow-up and reinforcement will sustain quit rates and possibly even improve survival rates.

Personal Intervention Meetings. The best approaches for motivating a patient to seek treatment are interventional group meetings between people with alcoholism and their friends and family members who have been affected by the alcoholic behavior. Using this approach, each person affected offers a compassionate but direct and honest report describing specifically how they have been hurt by their loved one's alcoholism. The family and friends should express their affection for the patient and their intentions for supporting the patient through recovery, but they must strongly and consistently demand that the patient seek treatment. Children may even be involved in this process, depending on their level of maturity and ability to handle the situation.

Employer Intervention. Employers can be particularly effective. Their approach should also be compassionate but strong, threatening the employee with loss of employment if they do not seek help. Some large companies provide access to inexpensive or free treatment programs for their workers. Studies suggest that such interventions are effective at helping the worker at least to cut back on drinking.

The ideal goals of long-term treatment by many doctors and organizations such as Alcoholics Anonymous (AA) are total abstinence. Patients who secure total abstinence have better survival rates, mental health, and marriages, and they are more responsible parents and employees than those who continue to drink or relapse. To achieve this, the patient aims to avoid high-risk situations and replace the addictive patterns with satisfying, time-filling behaviors.

Because abstinence is so difficult to attain, however, many professionals choose to treat alcoholism as a chronic disease. In other words, patients should expect and accept relapse but should aim for as long a remission period as possible. Even merely reducing alcohol intake can lower the risk for alcohol-related medical problems.

AA and other alcoholic treatment groups are greatly worried by treatment approaches that do not aim for strict abstinence, however. Many people with alcoholism are eager for any excuse to start drinking again. There is also no way to determine which people can stop after one drink and which ones cannot.

Evidence strongly suggests that seeking total abstinence and avoiding high-risk situations are the optimal goal for people with alcoholism.

A number of treatment options now exist for alcoholism. It is first important to determine whether inpatient or outpatient care would best benefit the individual. A variety of treatment options exist that do not require overnight stay in a hospital. Structured programs exist that involve anywhere from a couple of hours a day for several days a week to 20 or more hours per week (sometimes called partial hospitalization) of monitoring. Withdrawal and subsequent abstinence monitoring using outpatient visits to a doctor is occasionally tried for select, low-risk patients.

Inpatient care may also be performed in a general or psychiatric hospital or in a center dedicated to treatment of alcohol and other substance abuse. Factors that indicate a need for this type of treatment include:

Coexisting medical or psychiatric disorder
Delirium tremens
Potential harm to selves or others
Failure to respond to conservative treatments
Disruptive home environment

A typical inpatient regimen may include the following stages:

A physical and psychiatric work-up for any physical or mental disorders
Detoxification -- this phase involves initiating abstinence, managing withdrawal symptoms and complications, and ensuring that the patient remains in treatment
On-going treatment with medications in some cases
Psychotherapy, usually cognitive behavioral therapy
An introduction to Alcoholics Anonymous

Some -- but not all -- studies have reported better success rates with inpatient treatment of patients with alcoholism. However, newer studies strongly suggest that alcoholism can be effectively treated in a doctor’s office.

The new approach to outpatient treatment uses “medical management” -- a disease management approach that is used for chronic illnesses such as diabetes. With medical management, patients receive regular 20-minute sessions with a health care provider. The provider monitors the patient’s medical condition, medication, and alcohol consumption.

A medical management approach generally involves one or both of the following:

Drug treatment with naltrexone (ReVia, Vivitrol)
Behavioral counseling with a therapy technique called combined behavioral intervention (CBI)

Outpatient Treatment Options. People with mild-to-moderate withdrawal symptoms are usually treated as outpatients. Treatments are similar to those in inpatient situations and include:

Psychotherapy or counseling
Medications that target brain chemicals involved in addiction
Social support groups such as Alcoholics Anonymous
Cognitive therapies
Quitting smoking (smoking interferes with the brain’s recovery from alcoholism)
Involvement of family and other significant people in patient's life

After-Care and Work Therapy. After-care employs services that help alcoholics maintain sobriety. For example, in some cities, sober-living houses provide residences for people who are trying to stay sober. They do not offer formal treatment services, but the people living there offer each other support and maintain an abstinent environment. One study reported that work therapy improved the outcome for homeless veterans who were being treated for substance abuse.

About 25% of people are continuously abstinent following treatment, and another 10% use alcohol moderately and without problems. Most studies strongly suggest that intensive and prolonged treatment is important for successful recovery, whether the patient is treated within or outside a treatment center.

Certain factors play a role in success or failure. Patients from low-income groups tend to have worse results in general. Their difficulties are often intensified by lack of insurance, low self-esteem, and minimal social support.

Severe alcoholism is often complicated by the presence of serious medical illnesses. People with alcoholism should try at least to maintain a healthy diet and take vitamin supplements. Such deficiencies are a major cause of health problems in people with alcoholism. Women are particularly endangered.

A program called integrated outpatient treatment (IOT) may be specifically helpful for medically ill alcoholics. The patient visits a clinic once a month and receives both intensive alcohol treatment and a physical check-up, which includes tracking factors, such as liver function, that are affected by drinking.

Treatment for patients with both alcoholism and mental illness is particularly difficult. The greater the psychiatric distress a person is experiencing, the more the person is tempted to drink, particularly in negative situations.

There has been some concern that self-help programs, such as Alcoholics Anonymous (AA), are not effective for patients with dual diagnoses of mental illness and alcoholism, because the focus of the organization is on addiction, not psychiatric problems. Studies, however, have reported that they are also effective in many of these patients. (AA may not be as helpful for people with schizophrenia and schizoaffective disorder.) In one study, individuals with a dual diagnosis achieved better abstinence rates after being treated only for alcoholism compared to patients treated for the mental disorder as well. (Cognitive-behavioral therapy was used for both groups.)

Newer antidepressants such as selective serotonin reuptake inhibitors (SSRIs) are proving to be very useful complements to AA or counseling sessions. Anti-anxiety medications are also available for people with anxiety. People with alcoholism and more severe problems such as schizophrenia or severe bipolar disorder may require other types of medications.

Treatment for Alcohol Withdrawal

When a person with alcoholism stops drinking, withdrawal symptoms begin within 6 - 48 hours and peak about 24 - 35 hours after the last drink. During this period, the inhibition of brain activity caused by alcohol is abruptly reversed. Stress hormones are overproduced, and the central nervous system becomes overexcited. Common symptoms include:

Anxiety
Irritability
Agitation
Insomnia

Additional symptoms may include:

Extremely aggressive behavior
Fever
Rapid heartbeat
Changes in blood pressure (either higher or lower)
Mental disturbances
Seizures occur in about 10% of adults during withdrawal. In about 60% of these patients, the seizures are multiple. The time between the first and last seizure is usually 6 hours or less.
Delirium tremens (DTs) are withdrawal symptoms that become progressively severe and include altered mental states (hallucinations, confusion, severe agitation) or generalized seizures. DTs are potentially fatal. They develop in up to 5% of alcoholic patients, usually 2 - 4 days after the last drink, although it may take 2 or more days to peak.

It is not clear if older people with alcoholism are at higher risk for more severe symptoms than younger patients. However, several studies have indicated that they may suffer more complications during withdrawal, including delirium, falls, and a decreased ability to perform normal activities.

Upon entering a hospital due to alcohol withdrawal, patients should be given a physical examination for any injuries or medical conditions. They should be treated, if possible, for any potentially serious problems, such as high blood pressure, anemia, liver damage, or irregular heartbeat.

The immediate goal of treatment is to calm the patient as quickly as possible. Patients should be observed for at least 2 hours to determine the severity of withdrawal symptoms. Doctors may use assessment tests, such as the Clinical Institute Withdrawal Assessment (CIWA) scale, to help determine treatment and whether the symptoms will progress in severity.

About 95% of people have mild-to-moderate withdrawal symptoms, including agitation, trembling, disturbed sleep, and lack of appetite. In 15 - 20% of people with moderate symptoms, brief seizures and hallucinations may occur, but they do not progress to full-blown delirium tremens. Such patients often can be treated as outpatients. After being examined and observed, the patient is usually sent home with a 4-day supply of anti-anxiety medication, scheduled for follow-up and rehabilitation, and advised to return to the emergency room if withdrawal symptoms increase in severity. If possible, a family member or friend should support the patient through the next few days of withdrawal.

Benzodiazepines. Anti-anxiety drugs known as benzodiazepines inhibit nerve-cell excitability in the brain and are considered to be the treatment of choice. They relieve withdrawal symptoms, help prevent progression to delirium tremens, and reduce the risk for seizures. Long-acting drugs, such as chlordiazepoxide (Libritabs, Librium), oxazepam (Serax), and halazepam (Paxipam) are preferred. They pose less risk for abuse than the shorter-acting drugs, which include diazepam (Valium), alprazolam (Xanax), and lorazepam (Ativan).

Assessing symptoms frequently and administering benzodiazepine doses as needed (instead of giving to a fixed dose at regular intervals) may reduce the incidence of withdrawal symptoms and other adverse events, including delirium, seizures, and transfer to the intensive care unit.

Some doctors question the use of any anti-anxiety medication for mild withdrawal symptoms, since these drugs are subject to abuse. Others believe that repeated withdrawal episodes, even mild forms, that are inadequately treated may result in increasingly severe and frequent seizures with possible brain damage. In any case, benzodiazepines are usually not prescribed for more than 2 weeks or administered for more than 3 nights per week. Problems with benzodiazepines include:

Side Effects. Common side effects of benzodiazepines are daytime drowsiness and a hung-over feeling. In rare cases, they actually cause agitation. Respiratory problems may be worsened. The drugs stimulate eating and can cause weight gain. Benzodiazepines can interact with certain drugs, including cimetidine (Tagamet), antihistamines, and oral contraceptives. Benzodiazepines are potentially dangerous when used in combination with alcohol. Overdoses are serious, although rarely fatal. Elderly people are more susceptible to side effects and should usually start at half the dose prescribed for younger people. Benzodiazepines are associated with birth defects and should not be used by pregnant women or nursing mothers.
Loss of Effectiveness and Dependence. The primary problem with these drugs is their loss of effectiveness over time with continued use at the same dosage. As a result, patients may increase their dosage level to prevent anxiety. Patients then can become dependent. In fact, some evidence suggests that people with alcoholism, or even a family history of alcoholism, may be more susceptible to benzodiazepine abuse than nonalcoholics. This is a common danger and can occur after as short a time as 3 months. (These drugs do not cause euphoria, a so-called "high," so such drugs are not addictive in the same way narcotics are.)
Withdrawal Symptoms. People who discontinue benzodiazepines after taking them for even 4 weeks can experience mild rebound symptoms. The longer the drugs are taken and the higher the dose, the more severe the symptoms. They include sleep disturbance and anxiety, which can develop within hours or days after stopping the medication. Some patients experience withdrawal symptoms, including stomach distress, sweating, and insomnia, that can last from 1 - 3 weeks. Sleep changes, in fact, can persist or months or years after quitting and may be a major factor in relapse.

Antiseizure Medications. Antiseizure drugs, such as carbamazepine (Tegretol) or divalproex sodium (Depakote), may be useful for reducing the requirements of a benzodiazepine. When used by themselves, however, they do not appear to reduce seizures or delirium associated with withdrawal.

Other Supportive Drugs. Beta-blockers, such as propranolol (Inderal) and atenolol (Tenormin), are sometimes used in combination with benzodiazepines. They slow heart rate and reduce tremors. They may also reduce cravings.

Note on Treating Alcohol Withdrawal with Alcohol. Some medical centers give patients alcohol to help with withdrawal. Experts do not recommend this approach. There is no evidence that this approach is safe or effective, while there is substantial evidence on the safety and effectiveness of benzodiazepines.

Treating Delirium Tremens. People with symptoms of delirium tremens must be treated immediately. Untreated delirium tremens has a fatality rate that can be as high as 20%. Treatment usually involves intravenous anti-anxiety medications. It is extremely important that fluids be administered. Restraints may be necessary to prevent injury to the patient or to others.

Treating Seizures. Seizures are usually self-limited and treated with a benzodiazepine. Intravenous phenytoin (Dilantin) along with a benzodiazepine may be used in patients who have a history of seizures, who have epilepsy, or in those with ongoing seizures. Because phenytoin may lower blood pressure, the patient's heart should be monitored during treatment. Chlormethiazole, a derivative of vitamin B1, is used in Europe for reducing agitation and seizures.

Psychosis. For hallucinations or extremely aggressive behavior, antipsychotic drugs, particularly haloperidol (Haldol), may be administered. Korsakoff's psychosis (Wernicke-Korsakoff syndrome) is caused by severe vitamin B1 (thiamine) deficiencies, which cannot be replaced orally. Rapid and immediate injection of the B vitamin thiamin is necessary.

Therapy

Standard forms of therapy for alcoholism include:

Cognitive-behavioral therapy
Combined behavioral intervention
Interactional group psychotherapy based on the Alcoholics Anonymous (AA) 12-step program

Comparison studies have reported that these approaches are equally effective when the program is competently administered. Specific people may do better with one program than another. One study, for example, examined the differences in success rates on type 1 or type 2 alcoholics:

People in the type 1 group did well with the 12-step approach. They did not do as well with cognitive-behavioral therapy. (Type 1 individuals become alcoholic at a later age, have less severe symptoms or fewer psychiatric problems, and have a better outlook on life than those classified as type 2. They are more likely to be women.)
The people in the type 2 group tended to do better with cognitive-behavioral therapy. (Type 2 people are more likely to be male, become alcoholic at an early age, have a high family risk for alcoholism, have more severe symptoms, and have a negative outlook on life.)

This difference in response to the two forms of treatment held up after 2 years. Other studies have also reported that people with fewer psychiatric problems do best with the AA approach.

AA, founded in 1935, is an excellent example of interactional group psychotherapy and remains the most well-known program for helping people with alcoholism. It offers a very strong support network using group meetings open 7 days a week in locations all over the world. A buddy system, group understanding of alcoholism, and forgiveness for relapses are AA's standard methods for building self-worth and alleviating feelings of isolation.

AA's 12-step approach to recovery includes a spiritual component that might deter people who lack religious convictions. Prayer and meditation, however, have been known to be of great value in the healing process of many diseases, even in people with no particular religious assignation. AA emphasizes that the "higher power" component of its program need not refer to any specific belief system. Associated membership programs, Al-Anon and Alateen, offer help for family members and friends.

We admit we were powerless over alcohol -- that our lives have become unmanageable.
We have come to believe that a Power greater than ourselves could restore us to sanity.
We have made a decision to turn our will and our lives over to the care of God, as we understand what this Power is.
We have made a searching and fearless moral inventory of ourselves.
We have admitted to God, to ourselves and to another human being the exact nature of our wrongs.
We are entirely ready to have God remove all these defects of character.
We have humbly asked God to remove our shortcomings.
We have made a list of all persons we had harmed and have become willing to make amends to them all.
We have made direct amends to such people wherever possible, except when to do so would injure them or others.
We have continued to take personal inventory and when we were wrong promptly admitted it.
We have sought through prayer and meditation to improve our conscious contact with God as we understand what this higher Power is, praying only for knowledge of God's will for us and the power to carry that out.
Having had a spiritual awakening as the result of these steps, we have tried to carry this message to alcoholics and to practice these principles in all our affairs.

Cognitive-behavioral therapy (CBT) uses a structured teaching approach and may be better than AA for people with severe alcoholism. Patients are given instruction and homework assignments intended to improve their ability to cope with basic living situations, control their behavior, and change the way they think about drinking. The following are examples of approaches:

Patients might write a history of their drinking experiences and describe what they consider to be risky situations.
They are then assigned activities to help them cope when exposed to "cues" (places or circumstances that trigger their desire to drink).
Patients may also be given tasks that are designed to replace drinking. An interesting and successful example of such a program was one that enlisted patients in a softball team. This gave them the opportunity to practice coping skills, develop supportive relationships, and engage in healthy alternative activities.

CBT may be especially effective when used in combination with opioid antagonists, such as naltrexone. CBT that addresses alcoholism and depression also may be an important treatment for patients with both conditions.

Combined behavioral intervention (CBI) is a new form of therapy that uses special counseling techniques to help motivate people with alcoholism to change their drinking behavior. CBI combines elements from other psychotherapy treatments such as cognitive behavioral therapy, motivational enhancement therapy, and 12-step programs. Patients are taught how to cope with drinking triggers. Patients also learn strategies for refusing alcohol so that they can achieve and maintain abstinence. In a 2006 study in the Journal of the American Medical Association, CBI -- combined with regular doctor’s office visits (medical management) -- worked as well as naltrexone in successfully treating alcoholism.

Partners of people with alcoholism can also benefit greatly from behavioral approaches that help them cope with their mate. Children of an alcoholic mother or father may do better if both parents participate in couples-based therapy, rather than just treating the parent with alcoholism.

Nearly all patients who are alcohol dependent suffer from insomnia and sleep problems, which can last months to years after abstinence. Sleep disturbances may even be important factors in relapse. Available therapies include sleep hygiene, bright light therapy, meditation, relaxation methods, and other nondrug approaches. Many medications for inducing sleep are not recommended in people with alcoholism. [For more information, see In-Depth Report #27: Insomnia.]

Some people try alternative methods, such as acupuncture or hypnosis. Such approaches are not harmful. In one study, acupuncture reduced the desire for alcohol in nearly half of people, although it was not significantly more helpful than conventional treatments.

Medications

In the U.S., three drugs are specifically approved to treat alcohol dependence:

Naltrexone (ReVia, Vivitrol)
Acamprosate (Campral)
Disulfiram (Antabuse)

Naltrexone and acamprosate are categorized as anticraving drugs. Disulfiram is an aversion drug. Other types of medications, such as antidepressants, may also be used to treat patients with alcoholism.

Anticraving drugs are opioid antagonists. These drugs reduce the intoxicating effects of alcohol and the urge to drink

Naltrexone. Naltrexone (ReVia, Vivitrol) is approved for the treatment of alcoholism and helps reduce alcohol dependence in the short term for people with low-to-moderate alcohol dependency. ReVia is a pill that is taken daily by mouth. In 2006, the FDA approved Vivitrol, a once-a-month injectable form of naltrexone.

Naltrexone is usually prescribed along with psychotherapy. The most common side effect is nausea, which is usually mild and temporary. High doses can cause liver damage. The drug should not be given to anyone who has used narcotics within 7 - 10 days. For ReVia, it is important that patients take the pill on a daily basis. Because many patients have difficulty sticking to this daily regimen, a monthly injection of Vivitrol may be an easier option.

Naltrexone does not work in all patients. Some studies suggest that people with a specific genetic variant may respond better to the drug than those without the gene. The gene regulates receptors that affect the response to opioids. A 2005 study indicated that naltrexone works best for patients who have a family history of alcoholism, began drinking at an early age, and abuse other drugs.

Research is being conducted on the effects of combining naltrexone with acamprosate (Campral), particularly for individuals who have not responded to single drug treatment. In a 2006 study in the Journal of the American Medical Association that examined various outpatient drug and behavioral treatments, naltrexone worked as well as psychotherapy in preventing relapse to heavy drinking for patients who had recently abstained from alcohol. However, the study showed no benefit for acamprosate either when combined with naltrexone or used alone.

Acamprosate. Acamprosate (Campral) is the newest drug to be approved for treatment of alcoholism. Acamprosate calms the brain and reduces cravings by inhibiting the transmission of the neurotransmitter gamma aminobutyric acid (GABA). Studies indicate that it reduces the frequency of drinking and, in concert with psychotherapy, improves quality of life even in patients with severe alcohol dependence. One study reported that 60% of patients remained abstinent for 12 weeks, and in another 43% were still abstinent after nearly a year. The drug may cause occasional diarrhea and headache. It also can impair certain memory functions but does not alter short-term working memory or mood. People with kidney problems should use acamprosate cautiously. For some patients, combination therapy with naltrexone or disulfiram may provide greater benefit than acamprosate alone.

Disulfiram. Some drugs have properties that interact with alcohol to produce distressing side effects. Disulfiram (Antabuse) causes flushing, headache, nausea, and vomiting if a person drinks alcohol while taking the drug. The symptoms can be triggered after drinking half a glass of wine or half a shot of liquor and may last from half an hour to 2 hours, depending on dosage of the drug and the amount of alcohol consumed. One dose of disulfiram is usually effective for 1 - 2 weeks. Overdose can be dangerous, causing low blood pressure, chest pain, shortness of breath, and even death. The drug is more effective if patients have family or social support, including AA "buddies," who are close by and vigilant to ensure that they take it.

Topiramate. Topiramate (Topamax) is an anti-seizure drug used to treat epilepsy. It also helps control impulsivity. Studies indicate it may be a promising treatment for alcohol dependence. In one well-designed study, patients who took topirimate had fewer heavy drinking days, fewer drinks per day, and more continuous days of abstinence than patients who received placebo. Side effects included burning and itching skin sensations, change in taste sensation, loss of appetite, and difficulty concentrating.

Resources

www.niaaa.nih.gov -- National Institute on Alcohol Abuse and Alcoholism
www.samhsa.gov -- Substance Abuse and Mental Health Services Administration
www.ncadi.samhsa.gov -- National Clearinghouse for Alcohol and Drug Information
www.aca-usa.org -- American Council on Alcoholism
www.ncadd.org -- National Council on Alcoholism
www.alcoholics-anonymous.org -- Alcoholics Anonymous
www.al-anon-alateen.org -- Al-Anon Family Group Headquarters
www.nofas.org -- National Organization on Fetal Alcohol Syndrome

References

Anton RF, O'Malley SS, Ciraulo DA, Cisler RA, Couper D, Donovan DM, et al. Combined pharmacotherapies and behavioral interventions for alcohol dependence: the COMBINE study: a randomized controlled trial. JAMA. 2006 May 3;295(17):2003-17.

Chudley AE, Conry J, Cook JL, Loock C, Rosales T, LeBlanc N. Fetal alcohol spectrum disorder: Canadian guidelines for diagnosis. CMAJ. 2005 Mar 1;172(5 Suppl):S1-S21.

de Roux A, Cavalcanti M, Marcos MA, Garcia E, Ewig S, Mensa J, et al. Impact of alcohol abuse in the etiology and severity of community-acquired pneumonia. Chest. 2006 May;129(5):1219-25.

Gazdzinski S, Durazzo T, Jahng GH, Ezekiel F, Banys P, Meyerhoff D. Effects of chronic alcohol dependence and chronic cigarette smoking on cerebral perfusion: a preliminary magnetic resonance study. Alcohol Clin Exp Res. 2006 Jun;30(6):947-58.

Hingson RW, Heeren T, Winter MR. Age at drinking onset and alcohol dependence: age at onset, duration, and severity. Arch Pediatr Adolesc Med. 2006 Jul;160(7):739-46.

Johnson C, Drgon T, Liu QR, Walther D, Edenberg H, Rice J, et al. Pooled association genome scanning for alcohol dependence using 104,268 SNPs: Validation and use to identify alcoholism vulnerability loci in unrelated individuals from the collaborative study on the genetics of alcoholism. Am J Med Genet B Neuropsychiatr Genet. 2006 Aug 7; [Epub ahead of print]

McKenna W. In: Goldman L and Ausiello DA, eds. Cecil Medicine. 23rd edition. Saunders; 2007.

O'Connor PG. In: Goldman L and Ausiello DA, eds. Cecil Medicine. 23rd edition. Saunders; 2007.

Volkow ND, Wang GJ, Begleiter H, Porjesz B, Fowler JS, Telang F, et al. High levels of dopamine D2 receptors in unaffected members of alcoholic families: possible protective factors. Arch Gen Psychiatry. 2006 Sep;63(9):999-1008.

Review Date:
12/28/2007
Reviewed By:
Harvey Simon, MD, Editor-in-Chief, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

A.D.A.M., Inc. is accredited by URAC, also known as the American Accreditation HealthCare Commission (www.urac.org). URAC's accreditation program is an independent audit to verify that A.D.A.M. follows rigorous standards of quality and accountability. A.D.A.M. is among the first to achieve this important distinction for online health information and services. Learn more about A.D.A.M.'s editorial policy, editorial process and privacy policy. A.D.A.M. is also a founding member of Hi-Ethics and subscribes to the principles of the Health on the Net Foundation (www.hon.ch).

A.D.A.M. Copyright

The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 for all medical emergencies. Links to other sites are provided for information only -- they do not constitute endorsements of those other sites. © 1997-2009 A.D.A.M., Inc. Any duplication or distribution of the information contained herein is strictly prohibited.

adam.com

Headaches - tension

FitSugar — Wed, 08 Oct 2008 17:35:00 -0700

In This Report

Highlights
Introduction
Prognosis
Causes
Risk Factors
Diagnosis
Managing Tension-Type Heada...
Medications
Treatment
Lifestyle Changes
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Global Prevalence of Tension-Type Headache

Tension-type headaches account for nearly half of all headaches, according to a 2007 study in Cephalagia. The researchers estimated that more people are disabled by tension-type headache than by migraine.

Causes of Tension-Type Headaches

Doctors are not really sure why tension-type headaches occur. Possible causes include muscle contractions or changes in brain chemicals. Several studies in 2006 and 2007 presented the theory that tension-type headaches may be due to myofascial trigger points in the shoulders and neck, as well as poor head posture. Some researchers suggest that tension-type headaches may be related to fibromyalgia, a condition that is also characterized by myofascial pain.

Tension-type headaches may be triggered by:

Chronic poor posture
Overwork and stress
Lack of sleep
Dental problems, including temporomandibular joint disorder (TMJ)
Certain types of foods
Skipping meals
Medication overuse
Hormonal changes related to menstruation

Managing Tension-Type Headaches

Acetaminophen (Tylenol) or non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen (Motrin, Advil), naproxen (Aleve), or ketoprofen (Actron, Orudis KT) can usually provide pain relief for tension-type headache attacks. Patients who have chronic headaches sometimes take amitriptyline (Elavil), a prescription tricyclic antidepressant, to help prevent attacks. Exercise, stress reduction, and relaxation techniques are very important lifestyle approaches for controlling tension-type headaches.

Introduction

Most people are familiar with headaches, the all too common affliction marked by throbbing, piercing, or vise-like pain around much or a part of the head. There are many different kinds of headaches, and they range from being an infrequent annoyance to a persistent, severe, and disabling medical condition.

The brain itself is insensitive to pain, so that is not what hurts when a headache arises. The pain, instead, occurs in the following locations:

The tissues covering the brain
The attaching structures at the base of the brain
Muscles and blood vessels around the scalp, face, and neck

Doctors categorize headaches as either primary or secondary, which helps to distinguish the many different kinds of headaches and to determine appropriate treatments for each.

Primary Headaches. A headache is considered primary when a disease or other medical condition does not cause it. Most primary headaches fall into three main types: Tension-type, migraine, and cluster headaches.

Tension headache is the most common primary headache and accounts for 90% of all headaches.
Neurovascular headaches are the second most frequently occurring primary headaches and include migraines (the more common) and cluster headaches. Such headaches are caused by an interaction between blood vessel and nerve abnormalities. [See In-Depth Report #97: Migraine headaches and In-DepthReport #99: Cluster headaches.]

Headaches are usually caused by muscle tension, vascular problems, or both. Migraines are vascular in origin, and may be preceded by visual disturbances, loss of peripheral vision, and fatigue. Over-the-counter pain medications can relieve most headaches.

Symptoms of migraine and tension-type headaches often overlap, and a diagnosis is sometimes difficult.

Secondary Headaches. Secondary headaches are caused by other medical conditions, such as sinus infections, neck injuries, and strokes. About 2% of headaches are secondary to abnormalities or infections in the nasal or sinus passages, and they are commonly referred to as sinus headaches.

Chronic Daily Headaches. The International Headache Society's classification system includes a category called chronic daily headaches. They may originate as tension headaches, migraines, or a combination of these or other headache types. Chronic daily headaches affect 4 - 5% of the population.

Click the icon to see an image of the different types of headache.

Chronic daily headaches are defined as any benign headache that occurs at least 15 days a month and is not associated with a serious neurologic abnormality. Most people with these headaches have them daily, or almost daily, and they can be quite debilitating.

Chronic daily headaches are, in turn, subdivided into two categories:

Short-duration headaches last fewer than 4 hours. The most common short-acting chronic headaches are cluster headaches.
Long-duration headaches last more than 4 hours. Tension-type headaches are the most common type of long-duration chronic (recurring) headaches and, in fact, the most common type of chronic headaches in general.

General Description. Tension-type headaches, also called muscle contraction headaches or simply tension headaches, are the most common of all headaches. Tension-type headaches can last minutes to days and have the following characteristics:

The pain is commonly described as a tight feeling, as if the head were in a vise. It usually occurs on both sides of the head and is often experienced in the forehead, in the back of the head and neck, or in both regions. Soreness in the shoulders or neck is common.
Depression, anxiety, and sleeping problems may accompany persistent headaches.
Sufferers of tension-type headaches may also have migraine-like symptoms, including being sensitive to light or noise (but not both). Some patients also may suffer from visual disturbances. (Such symptoms in tension headaches, however, tend to be less severe than in migraine. Tension headaches also do not cause nausea or limit activities to the degree that migraines do.)

Types of Tension Headache. In 2004, the International Headache Society updated its original 1988 classification criteria. Tension-type headaches are now divided into the following four classifications:

Frequent episodic tension-type headache. Headaches occur at least once but not more than 15 days per month for at least 3 months (a minimum of 12 days but not more than 180 days per year). Headaches last from at least 30 minutes to 7 days.
Infrequent episodic tension-type headache. At least 10 episodes of headache that occur less than 1 day per month (12 days per year). Because these headaches occur infrequently, they do not impact a patient's quality of life as severely as frequent episodic headaches and may not require attention from a medical professional.
Chronic tension-type headache. Headaches occur at least 15 days per month for at least 3 months (180 days per year). The headache persists for hours at a time and may be continuous.
Probable tension-type headache. Probable tension headaches may be classified as probable frequent episodic, probable infrequent episodic, or probable chronic. They have most, but not all, of the symptoms of tension-type headaches and are not attributed to migraine without aura or other neurological disorders. Probable chronic tension-type headache may be related to medication overuse.

Migraine Headache: General Description of Its Course. Migraine is now recognized as a chronic illness, not simply as a headache. These headaches are often classified by whether or not auras accompany them:

Common migraines are without auras. About 75% of migraines are the common type.
Classic migraines are those with auras.

A person may experience one or the other at different times.

In general, there are four symptom phases to a migraine (although they may not all occur in every patient): the prodrome phase, auras, the attack, and the postdrome phase.

Prodrome. The prodrome phase is a group of vague symptoms that may precede a migraine attack by several hours, or even a day or two. Prodrome symptoms include:

Sensitivity to light or sound
Changes in appetite
Fatigue and yawning
Malaise
Mood changes
Food cravings

Auras. Auras are sensory disturbances that occur before the migraine attack in between 20 - 25% of patients. Visually, auras are referred to as being positive or negative:

Positive auras include bright or shimmering light or shapes at the edge of their field of vision called scintillating scotoma. They can enlarge and fill the line of vision. Other positive aura experiences are zigzag lines or stars.
Negative auras are dark holes, blind spots, or tunnel vision (inability to see to the side).
Patients may have mixed positive and negative auras. This is a visual experience that is sometimes described as a fortress with sharp angles around a dark center.

Other neurologic symptoms may occur at the same time as the aura, although they are less common. They include:

Speech disturbances
Tingling, numbness, or weakness in an arm or leg
Perceptual disturbances such as space or size distortions
Confusion

Migraine Attack. If untreated, attacks usually last from four to 72 hours. A typical migraine attack produces the following symptoms:

Throbbing pain on one side of the head. The word migraine, in fact, is derived from the Greek word hemikrania, meaning "half of the head" because the pain of migraine often occurs on one side. Pain also sometimes spreads to affect the entire head.
Pain worsened by physical activity.
Nausea, sometimes with vomiting.
Visual symptoms.
Facial tingling or numbness.
Extreme sensitivity to light and noise.
Looking pale and feeling cold.
Less common symptoms include tearing and redness in one eye, swelling of the eyelid, and nasal congestion, including runny nose. (Such symptoms are more common in certain other headaches, notably cluster headaches. In one study, however, they occurred in over 40% of migraine sufferers.)

Postdrome. After a migraine attack, there is usually a postdrome phase, in which patients may feel exhausted and mentally foggy for a while.

Cluster Headache. Cluster headaches are very painful events. Patients typically awaken a few hours after they go to sleep with the following symptoms:

Very severe, stabbing pain centered in one eye.
Excessive tearing, a drooping eyelid, and one stuffy or runny nostril, all on the same side as the pain.
Feelings of intense restlessness are common. People in the throes of a cluster headache may pace the floor or may even bang their heads against the wall in an attempt to cope with the pain.
Cluster headaches often have a cycle with the following pattern:
Attacks themselves are usually brief, lasting 30 - 90 minutes, although they can persist for up to 3 hours.
During an active period, sufferers can experience as few as one attack every other day to one or more daily. In a rare form of cluster headache, known as chronic paroxysmal hemicrania, as many as six attacks per day can occur.
An active period of recurrent cluster attacks typically extends over 4 - 12 weeks.
Headache-free periods last several months to even years.

Hemicrania Continua. Hemicrania continua is a rare form of chronic headache. Such headaches occur on one side of the face, mostly in women. The patient generally experiences continuous low-level headache with periodic attacks that can last days to weeks. (About 10% of patients experience remissions.) The actual attacks can be mild to severe, and may resemble migraines. The headaches can usually be treated successfully with NSAIDs such as indomethacin (Indocin). Migraine medications are typically not as helpful.

Prognosis

Both episodic tension-type headache and chronic daily headache affect quality of life. Tension-type headache episodes are rarely disabling, however, and rarely require emergency treatment. If they do, usually there is a migraine component occurring with the tension-type headache.

Nevertheless, although they are not medically dangerous, chronic tension headaches have a negative impact on quality of life, families, and work productivity. Several studies have reported lower quality of life with any chronic daily headache compared to those with no headaches or who have only episodic ones. In one study, people with tension-type headaches tended to have higher anxiety and lower quality of life during a headache attack than people with migraines (who, however, were less able to cope during a migraine attack).

In one study, two-thirds of patients with chronic tension-type headaches reported daily or near daily headaches for an average of 7 years. Only 12% reported headaches occurring less than 20 days a month. In the study, 74% of the patients had to take some time off from work because of the headaches, and about a third reported impaired sleep, less energy, and reduced emotional well-being on 10 or more days a month. Most were able to carry out their daily responsibilities even when in pain, although at lower than normal capacity. This and other studies report a strong association between anxiety and depression and chronic tension-type headaches.

Causes

There does not appear to be a single cause of chronic tension-type headache. Many factors are likely involved.

One of the most popular theories on the cause of tension-type headaches involves muscle contraction in the head, neck, and shoulders. There are several ideas about how muscle tension may produce these headaches.

The most common cause of tension-type headaches is muscle contraction in the head, neck or shoulders.

Studies have suggested that tension-type headache sufferers may have higher-than-average muscle tenderness in the face and head that make them more susceptible to headache after muscle contractions. A few studies suggest that some patients with chronic headaches may be overly sensitive to pain in general or may overestimate muscle contraction pain.

One theory suggests that sustained tension or stress that produces muscle contractions in the tender areas around the skull constrict blood vessels. Blood flow is reduced so oxygen is blocked and waste matter builds up, resulting in pain.

Still, pain can last long after the muscles have relaxed, and clear evidence is lacking on how or even if muscle contractions are a major cause of tension headache.

Researchers are increasingly finding evidence to support factors that are common to both migraine and tension-type headache. Some research suggests that both problems may result from a continuum of abnormalities in the central nervous system (the nerves in the brain and spine). Such changes trigger a progression of symptoms starting with mild sensations, developing into tension headache, and finally, progressing in some people to a migraine.

Serotonin and Other Neurotransmitter Levels. Neurotransmitters are chemical messengers in the brain. Serotonin is a neurotransmitter (chemical messenger in the brain) that is important for sleep, well-being, and other factors that affect quality of life. Abnormalities in serotonin levels have been observed in both tension-type and migraine headache sufferers. Altered levels of other neurotransmitters, importantly dopamine and stress hormones, also occur with migraine and tension-type headaches.

Dopamine, for example, may act as a stimulant of the migraine process. Some evidence suggests that certain genetic factors make people oversensitive 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 (mood changes, yawning, drowsiness), for example, have been associated with increased dopamine activity. Dopamine receptors are also involved in regulation of blood flow in the brain.

Reduced Magnesium Levels. Magnesium deficiencies have been observed in people with both tension-type and migraine headaches. Researchers have noted a drop in magnesium levels before or during a migraine attack. Magnesium plays a role in nerve cell function. Reduced levels could be a destabilizing factor, causing the nerves in the brain to misfire, possibly even accounting for the auras that many sufferers experience.

Nitric Oxide. Other research suggests that over-excitable neurons release nitric oxide, a small molecular messenger, which may be important in triggering in most primary headaches (tension-type, cluster, and migraines). Elevated levels have been observed in blood cells of patients with tension-type headache. Some evidence suggests that the release of this molecule in blood vessels may activate nerve pathways in the brain, muscles, or elsewhere and increase pain.

Estrogen Fluctuations in Women. Tension-type headaches and migraine headaches are more common in females during adolescence and adulthood. Most likely hormone fluctuations, rather than whether levels are elevated or low, trigger headaches. Some research suggests that fluctuations in estrogen levels may impact levels of serotonin and other pain-modulating substances that affect these headaches.

Inflammation in the Maxillary Nerve. Early studies suggest that some chronic tension-type and migraine headaches may be caused by inflammation in the nerve that runs behind the cheekbone (the maxillary nerve) -- not around the covering of the brain. In fact, some work using ice water for reducing swelling in areas of the gums above the last upper molars has relieved some severe migraine and tension-type headaches.

Genetic factors appear to play a role in predisposing people to recurrent tension headaches. One study of twins suggested that the chances of inheriting the susceptibility to recurring headaches (both migraine and tension) were about 70% in close relatives. The trait is equal in both boys and girls. Because such headaches tend to occur more in females, however, hormonal, social, psychological, or other factors must play a role in their development.

Tension-type headache has been highly associated with an intense response to stress. Some studies suggest that patients with chronic tension-type headaches have more general feelings of anxiety or depression and are less able to express their emotions. One study indicated that patients with tension headaches tend to perceive everyday events as more stressful than those without headaches. Some research even suggests that tension-type headache victims may have some biological predisposition for translating stress into muscle contraction. Still, the link between stress and tension-type headaches is not fully understood, and some evidence challenges any causal association.

Whiplash, concussions, and other head and neck injuries, even mild ones, may result in persistent tension-type or migraine headaches in both adults and children. Such headaches should be treated as if they were the primary types. The risk for tension headaches may persist for years after the injury.

Myofascial pain involves the fascia (connective tissue) and muscles. Some researchers think that tension-type headaches may be linked to myofascial trigger points in the neck and shoulder muscles. Trigger points are knots in the muscle tissue that can cause tightness, weakness, and intense pain in various areas of the body. (For example, a trigger point in the shoulder may result in headache.) Because fibromyalgia is also characterized by myofascial pain, researchers are exploring whether there may be an association between this condition and tension-type headache. [See In-Depth Report #76: Fibromyalgia.]

Medication Overuse (Rebound) Headache. About a third of persistent headaches -- whether chronic migraine or tension-type -- are medication-overuse headaches. These are the result of a rebound effect caused by the regular overuse of headache medications. Nearly any headache medication can produce this effect. In one study of headache sufferers, medication-overuse headaches developed after an average of 1.7 years of regular use of triptans (18 doses a month), after 2.7 years of ergot use (37 doses as month), and after 4.8 years using painkillers (114 doses a month). Regular use of painkillers for any chronic problem (such as arthritis) poses a 2% risk for medication-overuse headache, with risk being highest in people who already have primary headaches, especially migraines.

Chronic Migraines. In some cases, migraines naturally evolve into chronic, daily headaches referred to as transformed migraines.

About 90% of people seeking help for headaches have a primary headache. The rest are secondary headaches, caused by an underlying disorder that produces headache as a symptom. More than 300 conditions can cause headaches. Some of the most common are listed below.

Sinus Headaches. Many primary headaches, including migraines, are misdiagnosed as sinus headaches. Sinus headaches can occur in the front of the face, usually around the eyes, across the cheeks, or over the forehead. They are usually mild in the morning and increase during the day and are usually accompanied by fever, runny nose, congestion, and general debilitation. Sinus headaches spread over a larger area of the head than migraines, but it is often difficult to tell them apart, particularly if headache is the only symptom of sinusitis. They even coexist in many cases. Often, the visual changes associated with migraine can rule out sinusitis, but such visual changes do not occur with all migraines. (In rare cases, sinusitis can cause double vision and even vision loss, a sign of very serious infection.)

Headaches that Originate in the Neck. Some headaches may be caused by abnormalities of the neck muscles (called cervicogenic headaches). Nerves in the neck converge in the trigeminal nerve, which is the largest nerve in the skull. It originates in the brain stem and supplies sensation to the face. This nerve can generate pain signals to the facial area that the brain may interpret as headache. Pain is usually on one side. Even if it affects both sides of the head it is usually more severe on one side. The quality of the headache may be difficult to distinguish from an aching tension headache or a mild migraine without aura. Cervicogenic headaches can result from prolonged poor posture (such as that caused by sitting in front of a computer keyboard or driving daily for long periods), arthritis, injuries of the upper spine, or abnormalities in the cervical spine (the spinal bones in the neck).

Temporomandibular Joint Disorder. Muscle contractions that cause headaches may be a result of temporomandibular joint dysfunction (TMJ, also known as TMD), which is caused by clenching the jaws or grinding the teeth (usually during sleep), or by abnormalities in the jaw joints themselves. The diagnosis is easy if chewing produces pain or if jaw motion is restricted or noisy. TMJ pain can occur in the ear, cheek, temples, neck, or shoulders. This condition often coexists with chronic tension headache.

Click the icon to see an image of temporomandibular joint dysfunction.

Glaucoma. Acute glaucoma is caused by increased pressure in the eye and requires immediate medical attention. Throbbing pain may be felt around or behind the eyes or in the forehead. Patients have redness in the eye and may see halos or rings around lights.

Brain Tumor. Fear of brain tumor is common among people with headaches, but headache is almost never the first or only sign of a tumor. Changes in personality and mental functioning, vomiting, seizures, and other symptoms are more likely to appear first. When the headache does develop, it is often worse early in the morning or may awaken sufferers during the night.

Neuralgia. Neuralgia is pain due to nerve abnormalities, which can occur in the facial area and resemble migraines or sinus headaches.

Hypertension. Although many people attribute headaches to high blood pressure, evidence suggests that hypertension does not cause headaches. An exception is malignant hypertension, an uncommon medical emergency in which the blood pressure abruptly rises to extreme levels, causing damage to blood vessels in the brain, heart, and kidneys.

Strokes Caused by Blood Clots or Hemorrhages. A blood clot or hemorrhage in the brain leading to a stroke can cause a severe headache, sometimes referred to as a thunderclap headache when it is very sudden and severe. The onset of such a headache, particularly if it is associated with confusion, stupor, or other neurologic symptoms, mandates prompt medical attention.

Epilepsy. Severe headaches that can last 12 hours or longer are very common in epilepsy. Migraine is particularly associated with epilepsy.

Head Injuries. It is obvious that a significant blow to the head will cause pain. In most cases, the pain is similar to tension-type headache and is treated in the same way as the primary headache. Post-injury headaches, however, can reflect serious damage, ranging from skull fractures to internal bleeding, and monitoring is important.

Disorders of the Meninges. The meninges are the membranes covering the brain and the spinal cord. Meningitis, which is an infection or irritation of these membranes, is an uncommon but potentially serious cause of severe headache. Other symptoms include nausea and stiffness or pain in the neck.

Gynecologic Problems. Many clinicians have anecdotally linked gynecologic problems, such as ovarian cysts and menstrual disorders, to chronic headaches, and new data are emerging to support this association.

Temporal (Giant Cell) Arteritis. Certain causes of headaches are unique to the elderly, such as temporal arteritis, also called giant cell arteritis. Inflammation in arteries that carry blood to the head, neck, and sometimes the upper part of the body can cause very severe headaches. The risk for this headache is highest in people over age 70, especially among women, people of European heritage, and patients with polymyalgia rheumatica.

Miscellaneous Causes of Benign Headaches. Rapid consumption of ice cream or other very cold foods or beverages is the most common trigger of sudden headache pain, which may be prevented by warming the food or drink for a few seconds in the front of the mouth before swallowing. Other common benign causes of headache include eyestrain, dental problems, allergies, systemic infections, and caffeine withdrawal. Headaches may be induced by sexual activity or intense physical exertion. Leakage from spinal cord fluid is rare but can cause headaches that may be mistaken for brain tumors.

Risk Factors

Tension-type headaches are the most common headaches, accounting for nearly half of all headaches. According to one study, nearly 40% of Americans have at least one episode of tension headache during the course of a year. Some reports estimate that over 85% of women and about 63% of men will have a tension-type headache at some point during a year. Nearly everyone has at least one tension-type headache during their lifetime.

Surveys indicate that about 3 - 5% of the general population has chronic tension-type headache, with the prevalence being higher in women.

About 40% of people with tension-type headaches first have them before they are age 20, and another 40% first experience them between ages 20 - 40. Most of the remaining headache sufferers first have tension-type headaches in the decade between ages 40 - 50. Chronic tension-type headache tends to occur in older adults.

Headaches in Children. Headaches are rare before age 4 but increase in prevalence throughout childhood, reaching a peak around age 13. In one large study, about 7% of seven year olds and 15% of 11 year olds had headaches. Ten percent of these childhood headaches were recurrent. In many of these patients, chronic headaches persist into adulthood. In addition, as adults these patients have a tendency to develop multiple physical or psychiatric complaints, such as back pain, muscle aches, digestive complaints, and depression.

Studies have found that only a minority of chronic childhood headaches are due to physical conditions, such as head injuries or medical problems. In one study, over 62% of children with tension-type headache episodes suffered some form of emotional disorder. In the study, every child reported the presence of a stress factor.

Psychological factors associated with childhood tension-type headaches include:

Sleep problems. According to one study, more than two-thirds of children who experience chronic daily headaches suffer from sleep disturbances, especially difficulty falling asleep.
Moderate or severe depression.
Emotional rigidity in a child and more repressed anger than their peers.
Family stress. This includes maternal illness or separation, family bereavement, relationship problems, mental illness in a family member, and other stressful family events.
Problems at school. According to a National Headache Foundation survey, nearly 30% of children miss school because of headaches. For many children, the start of the school season can be a particularly stressful time.

The National Headache Foundation recommends these tips for parents:

Keep a diary of child’s headaches noting time of onset, length and intensity of attack, location of pain, and food triggers.
Make sure child gets plenty of sleep at regular times.
Avoid changes in child’s eating routing (hunger and eating at irregular times can trigger headaches).
Discuss any headache concerns with child’s doctor.

The following conditions can make people susceptible to tension-type headaches.

Chronic poor posture
Chronic overwork
Upper respiratory tract infections, such as colds and flu
Sleep disorders. Sleep problems, such as insomnia, sleep apnea, or habitual snoring, are common in all primary headaches. Headache can disturb sleep, but sleep disorders may also contribute directly to tension headache, particularly those that occur at night or early morning. (In one study, treating people who had chronic headaches for sleep apnea cured the headaches in many cases.)
Obesity
Hypothyroidism (decreased thyroid function)
Dental problems
Allergies
Substance or alcohol abuse
Temporomandibular joint dysfunction (TMJ, also called TMD). This is a condition in which there are abnormalities in the jaw joints. TMJ itself can cause headache, and it also often coexists with chronic tension headache.

Certain triggers, including the following, may cause headache episodes in people with chronic tension-type headaches:

Specific stressful events
Not eating on time
Fatigue or lack of sleep
Crying. In one study, only stress, anxiety, and menstruation were more important headache triggers in women.
Withdrawal from over-used substances (caffeine, nicotine, alcohol, pain relievers)
Eyestrain
Intense physical exertion, including sexual activity. Athletes are at higher risk for headaches. Patients with tension-type headaches should not avoid exercise, however. Ordinary levels of physical activity do not usually precipitate these headaches. Furthermore, a sedentary lifestyle may increase the risks for stress and obesity and thereby for tension headaches in susceptible people.
Certain foods, such as chocolate, cheese, and the flavor enhancer monosodium glutamate (MSG), are commonly cited as triggers for tension headaches as they are for migraines.
Medications (overuse of headache medications, nitrates, certain anti-depressants, some drugs used to treat high blood pressure, and many others.)
Hormonal changes, such as specific menstrual phases, in women.

Weather conditions, certain smells, smoke, and light, which can set off migraines, are not common triggers for tension-type headaches.

The rapid consumption of ice cream or other very cold foods or beverages is a well-known trigger of sudden headache pain -- the so-called "ice cream" headache. It can be easily prevented by warming the food or drink for a few seconds in the front of the mouth before swallowing. Drinking a glass of room-temperature water quickly relieves the pain.

Diagnosis

Diagnosing the cause of persistent daily headache is difficult, even for expert doctors. Studies report that people who visit the emergency room with disabling headache are often misdiagnosed as tension-type headaches instead of migraines. It is important to choose a doctor who is sensitive to the needs of headache sufferers and aware of the latest advances in treatment.

Extensive testing may be advised for anyone with a chronic, daily headache. Tracking times of medications, withdrawal, and headache, using the headache diary, is usually very helpful in diagnosis.

According to the International Headache Society, a diagnosis of tension-type headache is suggested by the following symptoms:

Pressing or tightening (but non-pulsating) feeling
Mild-to-moderate pain on both sides of the head
Not aggravated by routine physical activity (walking, etc.)

In episodic tension-type headaches:

No nausea or vomiting
Photophobia (intolerance of light) or phonophobia (intolerance of sound) may be absent or one of these symptoms (but not both) may be present

In chronic tension-type headaches:

No vomiting
No moderate or severe nausea
No more than one of the following symptoms: Mild nausea, photophobia, or phonophobia
Some types of chronic tension headache may include tenderness upon manual palpitation of the head (pericranial tenderness).

Differentiating Medication-Overuse (Rebound) Headache from Tension-Type Headache. About a third of persistent headaches are the result of the rebound effect caused by the overuse of headache medications (formerly called rebound headaches).

Usually in such cases, medications have been taken on an ongoing basis for more than 3 days each week. If patients stop taking these drugs, the headaches come back. The patient then starts taking the drugs again. Eventually the headache simply persists and medications are no longer effective. Even after successful medication withdrawal, relapse is common, particularly with drugs that contain caffeine, so doctors should check for this type of headache even in patients who have previously been treated.

Medications implicated in medication-overuse headache include barbiturates, sedatives, narcotics, and migraine medications, particularly those that also contain caffeine. (Heavy caffeine use can also cause this condition.) Simple painkillers, such as aspirin or ibuprofen, are less likely causes of medication-overuse headaches.

Differentiating Tension Headaches from Chronic Migraines. It is often difficult to differentiate between chronic migraine and chronic tension-type headaches. The McGill Pain Questionnaire may be useful for ruling out migraine. According to a 2003 study, patients with migraine who answer the questionnaire report significantly more severe specific symptoms (throbbing, stabbing, gnawing, hot, sickening, exhausting) than those with tension-type headaches. There is very little difference between these headaches, however, in scores of overall severity of the pain.

For an accurate diagnosis, the patient should describe the following:

Duration and frequency of headaches
Recent changes in their character
Location of the pain
Type of pain (throbbing or steady pressure)
Intensity of the headache
Associated symptoms, such as visual disturbances or nausea and vomiting. (These are seen most often with migraines.)
Behaviors during a headache. Different behaviors may help distinguish between migraine and tension headaches. People with tension headaches tend to relieve pain by massaging the scalp, temples, or the nape of the neck. People with migraines are more likely to compress the forehead and temples (tying a scarf around the head) or to apply cold to the area. They also tend to isolate themselves, lie down, induce vomiting, and use more pillows than usual. (None of these maneuvers do much good in relieving either headache, unfortunately.)

The patient should try to recall what seems to bring on the headache and anything that relieves it. Keeping a headache diary is a useful way to identify triggers that bring on headaches. Be sure to include all events preceding an attack. Often two or more triggers interact to produce a headache.

Researchers are investigating triggers of headaches to determine if certain ones are more likely to set off different primary headaches. In general, however, the same stimuli seem to trigger any of the primary headaches, although people with migraines may be more sensitive to some of them (weather, certain smells, light, and smoke) than people with tension headaches.

Tracking medications is an important way of identifying medication-overuse headache or transformed migraine.

Be sure to attempt to define the intensity of the headache. There are different scoring symptoms available that help communicate the severity of the pain to the doctor. For instance, the following is a number system that can be helpful:

1 = Mild, barely noticeable

2 = Noticeable, but does not interfere with work/activities

3 = Distracts from work/activities

4 = Makes work/activities very difficult

5 = Incapacitating

The patient should report any other conditions that might be associated with headache, including but not limited to the following:

Any chronic or recent illness and their treatments
Any injuries, particularly head or back injuries
An uncharacteristic dietary changes
Any current medications or recent withdrawal from any drugs, including over-the-counter or natural remedies
Any history of caffeine, alcohol, or drug abuse
Any serious stress, depression, and anxiety
The doctor will also need the patient's general medical and family history, particularly concerning headaches or other diseases such as epilepsy. Migraine, in particular, tends to run in families.

In order to diagnose a chronic headache, the doctor will examine the head and neck and will usually perform a neurologic examination, which includes a series of simple exercises to test strength, reflexes, coordination, and sensation. The doctor will also examine the eyes to rule out pressure build-up in the eye as a cause of headache. The doctor may ask questions to test short-term memory and related aspects of mental function.

Imaging tests of the brain may be recommended under the following circumstances:

If the results of the history and physical examination suggest neurologic problems.
For patients with headache that wakes them at night.
For new headaches in the elderly. In this age group, it is particularly important to first rule out age-related disorders, including stroke, hypoglycemia, hydrocephalus, and head injuries (usually from falls).
For patients with worsening headache.

They are not recommended for patients with migraine and with no other abnormal indications.

The following tests may be used:

A CT (computed tomography) scan may be ordered to rule out other conditions, particularly chronic sinusitis, which, in one study, occurred in 20% of patients with chronic headache. Other findings include aneurysms, benign or cancerous growths, and other abnormalities in the brain.
X-rays and other tests may also be used if sinusitis is strongly suspected.
A neck x-ray can reveal arthritis or spinal problems.
Other tests include an MRI (magnetic resonance imaging), EEG (electroencephalogram), lumbar puncture, ultrasound testing, and cerebral angiography, which are only performed if there is reason to suspect an underlying disease.

Headaches indicating a serious underlying problem, such as cerebrovascular disorder or malignant hypertension, are uncommon. (It should again be emphasized that a headache is not a common symptom of a brain tumor.) People with existing chronic headaches, however, might miss a more serious condition believing it to be one of their usual headaches. Such patients should immediately call a doctor if the quality of a headache or accompanying symptoms has changed. Everyone should call a doctor for any of the following symptoms:

Sudden, severe headache that persists or increases in intensity over the following hours, sometimes accompanied by nausea, vomiting, or altered mental states (possible hemorrhagic stroke).
Sudden, very severe headache, worse than any headache ever experienced (possible indication of hemorrhage or a ruptured aneurysm).
Chronic or severe headaches that begin after age 50.
Headaches in the back of the head accompanied by other symptoms, such as memory loss, confusion, loss of balance, changes in speech or vision, or loss of strength in or numbness or tingling in arms or legs (possibility of small stroke in the base of the skull).
Headaches after head injury, especially if drowsiness or nausea are present (possibility of hemorrhage).
Headaches accompanied by fever, stiff neck, nausea, and vomiting (possibility of spinal meningitis).
Headaches that increase with coughing or straining (possibility of brain swelling).
A throbbing pain around or behind the eyes or in the forehead accompanied by redness in the eye and perceptions of halos or rings around lights (possibility of acute glaucoma).
A one-sided headache in the temple in elderly people; the artery in the temple is firm and knotty and has no pulse; scalp is tender (possibility of temporal arteritis, which can cause blindness or even stroke if not treated).
Sudden onset and then persistent, throbbing pain around the eye possibly spreading to the ear or neck unrelieved by pain medication (possibility of blood clot in one of the sinus veins of the brain).

Managing Tension-Type Headaches

Given the very high prevalence of tension-type headaches, some experts express frustration over the lack of serious scientific attention given to this problem. Unfortunately, few tension headache sufferers seek medical help for their problem, and 60% of those with severe headaches use only over-the-counter medications. Many patients fear that they will not be taken seriously by their doctor or believe the widespread misperceptions that their problem is due solely to stress. With medications, relaxation training, lifestyle changes, and other therapies, over 90% of patients can be helped.

Fortunately, most acute tension-type headaches get better without any treatment, and simple over-the-counter pain relievers such as acetaminophen or non-steroidal anti-inflammatory drugs (NSAIDs) can treat mild symptoms.

The most common pain relievers are:

Acetaminophen (Tylenol, Anacin-3, Panadal, Phenaphen, Valadol)
Over-the-counter NSAIDs include aspirin, ibuprofen (Motrin IB, Advil, Nuprin, Rufen), naproxen (Aleve), ketoprofen (Actron, Orudis KT)
Prescription NSAIDs include ibuprofen (Motrin), naproxen (Naprosyn, Anaprox), diclofenac (Voltaren), tolmetin (Tolectin), ketoprofen (Orudis, Oruvail)

Acetaminophen may be effective for moderate-to-severe headaches only at high doses (1,000 mg), while NSAIDs can be effective at lower doses. One study indicated that ibuprofen and naproxen were more effective than aspirin or acetaminophen.

There are few proven therapies for treating or preventing chronic tension-type headaches, and studies are weak. To date, the major treatments used for chronic tension-type headache are a group of antidepressants called tricyclics, and cognitive-behavior therapy. Used alone either of these approaches achieves modest benefits, at best. A combination, however, may be very helpful in some cases.

Some research suggests the following steps in treating this condition:

Because many chronic daily headaches are due to over-use of headache medications, withdrawal from such drugs is the first action. (NSAIDs or other painkillers should not be used to prevent chronic tension-type headaches.)
Cognitive behavioral therapies, including relaxation and stress-reduction techniques, should be used next for managing headaches. They should be the first option for children and adolescents with chronic headaches.
If medication withdrawal and psychological methods fail to bring improvement, tricyclic antidepressants are tried next in combination with cognitive therapy.
Physical therapy, massage therapy, or acupuncture may help some people.

If headaches develop because of medication overuse, the patients cannot recover without stopping the drugs. (If caffeine is the culprit, a person may only need to reduce coffee or tea drinking to a reasonable level, not necessarily stop drinking it altogether.) The patient usually has the option of stopping abruptly or gradually and should expect the following course:

Most headache drugs can be stopped abruptly, but the patient should be sure to check with the doctor before withdrawal. Certain non-headache medications, such as anti-anxiety drugs or beta-blockers, require gradual withdrawal.
If the patient chooses to taper off standard headache medications, withdrawal should be completed within three days or shorter. Otherwise the patient may become discouraged.
No matter which approach is used for stopping medication, the patient must expect a period of worsening headache for a few days afterward. Alternative pain relievers may be administered during the first days to help withdrawal.
Most people feel better within 2 weeks, although headache symptoms can persist up to 16 weeks (and in rare cases even longer).

Studies suggest that nearly half of patients with medication-overuse headaches relapse. According to one study, the relapse rate may be much higher for tension headaches (73%) than for migraine headaches (22%). More research is needed to determine the optimal methods for drug withdrawal. On the encouraging side, some patients experience dramatic long-term relief from all headaches afterward.

Medications

The standard treatments for tension-type headaches are non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin and ibuprofen, and tricyclic antidepressants, usually amitriptyline (Elavil, Endep).

Several pain relievers are helpful for mild-to-moderate headaches. They should not be used to prevent headaches, however.

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs). NSAIDs are common pain relievers that block prostaglandins, substances that dilate blood vessels and cause inflammation and pain. NSAIDs are usually the first drugs tried for almost any kind of headache. There are dozens of NSAIDs. Aspirin is the most common, but it is not as effective for acute tension-type headache as other NSAIDs. Common NSAIDs include:

Over-the-counter NSAIDs. Aspirin, ibuprofen (Motrin), naproxen (Aleve), ketoprofen (Actron, Orudis KT)
Prescription NSAIDs. Diclofenac (Voltaren, Cataflam, Solaraze), tolmetin (Tolectin), indomethacin (Indocin)

Patients should be aware that long-term use of high-dose NSAIDs may increase the risk for stomach bleeding and heart problems, including heart attack and stroke.

Acetaminophen. Acetaminophen (Tylenol) is a good alternative to NSAIDs when stomach distress, ulcers, or allergic reactions prohibit their use. A high dose (1,000 mg), however, is needed for this drug to be effective for headaches. Midrin (a combination of a drug that narrows blood vessels, a mild sedative, and acetaminophen) may be very helpful for tension-type headaches.

Acetaminophen does have some adverse effects, however, and the daily dose should not exceed 4 grams (4,000 mg). Patients who take high doses of this drug for long periods are at risk for liver damage, particularly if they drink alcohol and do not eat regularly. Acetaminophen may cause serious kidney problems in people who already have kidney disease. It also may interact with certain medications, including the blood thinner warfarin.

Antidepressants known as tricyclics are most often used for prevention of severe chronic tension-type headaches. Newer selective serotonin-reuptake inhibitors (SSRIs) antidepressants are also sometimes used in milder cases.

Tricyclic Antidepressants. Tricyclics are not only useful for depression but also appear to help relieve muscle pain and improve sleep. They are sometimes classified in one of two categories: tertiary or secondary amines:

Tertiary amines include amitriptyline (Elavil) and imipramine (Tofranil). Amitriptyline is the tricyclic most commonly used for tension-type headache. These drugs tend to cause more drowsiness than secondary amines, which may be helpful for patients with sleep problems.)
Secondary amines include desipramine (Norpramin) and nortriptyline (Pamelor, Aventyl). Secondary amines may have fewer side effects than tertiary amines, but they are just as toxic in high amounts.

Less commonly used tricyclics include doxepin (Sinequan), amoxapine (Asendin), maprotiline (Ludiomill), protriptyline (Vivactil), trimipramine (Surmontil), mianserin (Bolvidon), and dothiepin (Prothiaden).

Unfortunately, these drugs can lose effectiveness over time. Side effects are also fairly common with these medications. Drowsiness is the most common, but may vary by specific drug. In addition, side effects most often reported include dry mouth, constipation, blurred vision, sexual dysfunction, weight gain, trouble urinating, heart rhythm problems, and dizziness. Blood pressure may also drop suddenly when sitting up or standing.

Tricyclics can have serious, although rare, side effects, including heart rhythm problems, which can be dangerous for some patients with certain heart diseases. These drugs can be fatal with overdose.

Selective Serotonin-Reuptake Inhibitors. Selective serotonin-reuptake inhibitors (SSRIs) work by increasing levels of serotonin in the brain. SSRIs include fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil), fluvoxamine (Luvox), and citalopram (Celexa). Because they act on serotonin specifically, they have fewer side effects than the older antidepressants, such as monoamine oxidase inhibitors (MAOIs), which affect a number of chemicals in the body. SSRIs take 2 - 4 weeks to be effective in most adults and sometimes longer, up to 12 weeks, so their value for treating headaches is limited.

Side effects may include nausea, stomach problems, agitation, insomnia, mild tremor, impulsivity, temporary weight gain or loss, and sexual dysfunction. Death from overdose is extremely rare. Serious interactions can occur with other antidepressants, such as tricyclics and MAOIs.

Designer Antidepressants. Several drugs target other neurotransmitters, such as norepinephrine, alone or in addition to serotonin, and are showing promise for prevention of tension-type headache. The following are some examples:

In one study, bupropion (Wellbutrin) was as effective as a tricyclic in preventing tension-type headaches.
Nefazodone (Serzone), a fast-acting designer antidepressant, was particularly beneficial in a study of patients with chronic daily headaches. After 3 months of treatment, symptoms were reduced by half in over 70% of patients. Nearly 60% of them said their symptoms improved over 75%.
Venlafaxine (Effexor), a designer antidepressant that targets both serotonin and the brain chemical norepinephrine, is showing promise for preventing chronic tension-type headaches (as well as migraines). In one study, patients who took the extended-release form of the drug for 6 months went from an average of 24 tension headaches a month to 15.
Mirtazapine (Remeron) is a unique antidepressant known as a 5-HT2 blocker. It may indirectly enhance the affects of both serotonin and norepinephrine. In one study, it was as effective in treating chronic tension-type headache as the tricyclic Elavil. Mirtazapine has significantly fewer side effects than tricyclics, although it may slightly raise cholesterol and triglyceride levels. It may also cause blurred vision and slight weight gain.

Mild anti-anxiety drugs are occasionally used as an adjunct in treating chronic headaches to decrease muscle contraction or to calm anxiety symptoms during periods of extreme stress. They include alprazolam (Xanax) and clonazepam (Klonopin). They tend to be highly addictive, however, and patients should therefore use them only on a short-term basis.

Tramadol. Tramadol (Ultram) is a pain reliever that has been used as an alternative to opioids. It has opioid-like properties but is not as addictive. (Dependence and abuse have been reported, however.) It can cause nausea, but does not cause severe gastrointestinal problems, as NSAIDs can. Some patients experience severe itching. A combination of tramadol and acetaminophen (Ultracet) is now available and provides more rapid pain relief than tramadol alone and more durable relief than acetaminophen alone. Side effects are the same as for each of these drugs.

Opioids. Opioids, such as codeine or hydrocodone, are sometimes prescribed for severe headaches, although their use is controversial because of the risk for addiction. Methadone is showing promise for patients who do not respond to standard treatments. These drugs are narcotics, however, and may be subject to abuse. Patients must be monitored and reevaluated regularly. Overuse of these drugs can reduce their effectiveness and lead to medication-overuse headaches, so it is important for a doctor to supervise this type of medication. Long-term, high-dosage use of some of these drugs can also lead to kidney disease and ulcers. Other, less serious side effects include gastrointestinal upset, dizziness, and ringing in the ears (tinnitus).

Sedatives. Barbiturates, particularly butalbital (Butalan) and its combinations (Fioricet, Axocet), are occasionally prescribed if other medications fail to provide relief. These drugs are sedatives that also contain pain relievers. Because they pose a very high risk for alcohol-like intoxication, dependence and drug-induced headaches during withdrawal, they should be used very sparingly. Some experts believe they should not be used at all for headaches.

Valproate. In some studies, the anticonvulsant medication valproate has been effective for stopping headaches in some patients with persistent migraines and tension-type chronic daily headaches. In one study, 75% of patients with either type of headache experienced at least a 50% reduction in headache frequency and severity. Minor side effects occurred in a third of the patients. Other anti-seizure medications are under investigation.

Botulinum Toxin. Botulinum toxin A (Botox) injections are now widely used to relax muscles and reduce skin wrinkles. They are also being investigated for chronic daily headaches, which include tension-type headache. This potentially deadly toxin is very safe when tiny amounts are injected into small muscles. In a 2003 study of various headache types (including tension-type headache), over 85% of all the patients had fewer headaches per month and the intensity of the pain. Several 2005 studies reported that Botox injections every 3 months might help patients with chronic daily headaches have fewer headaches. However, other studies have reported no benefit. Botox is not approved for headache treatment.

It should be noted that Botox also causes headaches in about 1% of cases. In some cases, the headaches can be very severe and long lasting (from 8 days to a month). Some researchers suggest that either a contaminated batch of Botox or a specific injection technique may be the cause, but additional investigation is needed.

Tizanidine. Tizanidine (Zanaflex) is a muscle relaxant that is emerging as a possible effective preventive drug in chronic tension-type headaches. Called an alpha2-adrenergic agonist, it blocks the release and effectiveness of a stress chemical in the body called norepinephrine and may also help prevent muscle spasms. Studies have reported that nearly 70% of patients with chronic tension-type headaches experienced a reduction in headache symptoms of 50% or more. It also appears to help patients experiencing medication-overuse headache to withdraw from medications. Side effects are usually minor and include fatigue and dry mouth, although patients taking the drug need to be monitored periodically for potential liver damage.

Nitric Oxide Synthase Inhibitors. Nitric oxide synthase inhibitors block nitric oxide, which may play a role in increasing nerve activity that leads to headache. Drugs being investigated include L-NG methyl arginine hydrochloride (L-NMMA) and L-NG-nitro-arginine. Studies suggest they may be very helpful in reducing chronic tension-type pain.

Treatment

In cases where abnormalities or injuries in the cervical spine (the spinal bones in the neck) cause headaches, a cervical epidural nerve block may be beneficial in treating and preventing further pain. This procedure involves injecting small amounts of a corticosteroid and anesthetic into spaces between the vertebrae in the neck to block the nerves. Some patients have reported significant pain relief from this procedure.

Dental Adjustment. Some reports suggest that dental adjustment to help teeth bite down evenly might help some people with temporomandibular joint disorder and chronic headaches. The results indicated that dental adjustments may be helpful. A systematic review in 2003, however, reported no headache relief from this approach.

Nociceptive Trigeminal Inhibition. A dental device called the NTI (nociceptive trigeminal inhibition) tension suppression system has been approved for relief of headaches due to jaw clenching during the night. The small plastic mouthpiece is fitted by a dentist and slips over the two front teeth, preventing teeth clenching at night. Preliminary studies report some benefits for relief of migraines and associated tension-type headaches.

Techniques using acupuncture points on the body have become popular for managing pain. Studies do show some benefits.

Standard Acupuncture. A major 2001 analysis of 26 trials of acupuncture suggested that it may have some benefit for tension headache, but the evidence to date is not completely convincing. Some studies comparing short-term acupuncture to sham (dummy) procedures report no benefits. A 2005 study suggested that acupuncture may help tension-type headache, but needling at non-acupuncture points worked just as well. This suggests a placebo effect may account for the headache relief experienced by acupuncture patients.

Acupuncture, hypnosis and biofeedback are all alternative ways to control pain. Acupuncture involves the insertion of tiny sterile needles, slightly thicker than a human hair, at specific points on the body.

Percutaneous Electrical Nerve Stimulation. A technique called percutaneous electrical nerve stimulation (PENS) uses low-level electrical pulses delivered through acupuncture needles into soft tissue. Patients are barely aware of the sensation. Some studies are showing some benefits, but strong evidence is still lacking to confirm or refute its benefits.

Acupressure. One acupressure practitioner reports that pressing for 60 seconds on the web space between the forefinger and thumb of the dominant hand erases headache in patients with migraine and tension-type headaches. The specific spot pressed should be the most tender point in the web area. The patient should then lie down for about 15 minutes.

Two investigational procedures called automated or electrical twitch obtaining intramuscular stimulation (ATOIMS or ETOIMS) are showing promise. ATOIMS uses an automated mechanical device that vibrates the muscle using a tiny pin. (The sensation is described as similar to a mosquito bite.) ETOIMS uses an extremely mild electrical current. They can also be used together. Both approaches cause the muscles to twitch and relax, and then the process is stopped. Discomfort is minimal. Small studies are reporting some help in relieving a number of conditions that cause chronic pain, including tension headache.

Spinal manipulation by chiropractors or osteopaths may have some benefits for preventing tension-type headaches. Evidence is stronger on benefits of spinal manipulation for patients with headaches originating from nerve or muscular problems in the neck. Some researchers believe that tension-type headaches relieved by spinal manipulation are probably really caused by neck problems.

In a small 2006 study, daily relaxation exercises combined with three sessions of osteopathic treatment helped reduce the frequency -- but not the intensity -- of tension-type headaches. Another 2006 study suggested that physical therapy that incorporates a craniocervical (head and neck) training program may help reduce tension-type headache frequency, intensity, and duration as well as reduce the need for pain medication. In the 6-week program, patients performed 10-minute exercises twice a day. The exercises were designed to retrain muscles in the head, neck, and shoulders. The benefits of these exercises lasted up to 6 months after the program had ended.

Lifestyle Changes

Good health habits -- including adequate sleep, healthy diet, regular exercise, and good stress management -- are important, along with the following specific measures for headache management. Quitting smoking is essential in reducing the risks for all headaches.

An ancient and potentially effective remedy for tension headaches uses pressure applied to the head (such as a headband or a towel wrapped around the head) plus either heat or cold. In one study, 87% of headache sufferers experienced significant relief, and the rest reported moderate relief while they were wearing special headbands that could be tightened. They applied packs that were frozen or heated in a microwave. (Either heat or cold packs were useful, although people with tension headaches generally preferred cold packs.)

A healthy diet rich in fresh fruits and vegetables and whole grains and low in saturated fats (animal fats) is important to everyone. Fish (particularly oily fish, such as salmon and tuna) and soy are protein sources that may be a good alternative to red meats.

Caffeine. In some people with headaches, caffeine appears to be an excellent companion to medications. One study found that the caffeine equivalent of two and a half of cups of coffee can help treat a tension-type headache by itself. Many medications contain combinations of pain or anxiety relievers and caffeine, which boosts pain-relieving potency and counters drowsiness. Taking ibuprofen along with caffeine is even more effective than either substance alone. (It should be noted that in some people with migraines, the tannin found in coffee or tea may be a trigger for the headache. In addition, withdrawal from caffeine is a major cause of headache.)

Headaches that occur during the night and early morning may be related to sleep disorders. One study reported that treating an underlying sleep disorder, such as sleep apnea or insomnia, in patients who also had headaches resulted in headache cure or improvement in all patients except those who suffered from restless legs syndrome.

Several stress-reduction methods are available that may help counteract the tendency for muscle contraction and uneven blood flow associated with some headaches. Such approaches may be especially helpful for children and pregnant women with chronic headaches. (For information on acupuncture and spinal manipulation, see the Treatment section of this report.)

Among the stress reduction techniques that may be helpful are:

Guided imagery. (This uses body awareness and visualization of pleasant or positive images.)
Biofeedback. This technique works when patients develop awareness of their physical responses and learn to feed this information back to the brain for the purpose of replicating that response. It is often used to reduce muscle tension. One interesting and sometimes effective technique for headaches is called thermal biofeedback. It is based on the concept that hand-warming reduces blood flow to the brain and so relieves headache. The patient learns techniques (such as using specific images) that can raise the temperatures of the hand during a headache. Studies suggest the approach has been helpful in children with tension and migraine headaches.
Autogenic training. This approach combines elements of meditation, relaxation, and self-hypnosis. In one study, it reduced headache frequency and use of medications in patients with tension-type and migraine headaches. It was more successful for tension-type headache.
Massage therapy. In one study, massage therapy of the neck and shoulder muscles reduced the frequency of chronic daily tension-type headaches within the first week of treatment. (It did not have any effect on the intensity of headaches, however.)
Reflexology, an alternative massage method that manipulates the feet, was associated with improvement in 81% of patients with tension or migraine headaches. Patients reported an improvement in energy, well-being, and increased ability to understand the cause of the headaches. In the study, 19% went off medication.
Muscle relaxation exercises.
Self-hypnosis.
Breathing exercises. Studies have reported that correct and rhythmic breathing from the diaphragm can sometimes relieve tension-type headaches. Such breathing exercises may be particularly beneficial when performed with physical movements. (Yoga, in fact, is a practice that combines both and has been helpful in people with headaches.)

Any of these therapies may be used in conjunction with drug therapy.

Numerous herbal remedies are promoted for tension-type headache. It is important that anyone taking herbal or so-called natural remedies be aware of the lack of regulations governing their quality and effectiveness.

Essential Oils. Some patients find relief using two drops of peppermint, eucalyptus, or lavender oil added to one cup of water. The patient soaks a cloth in the solution and applies it as a compress to the head.

Herbs. Generally, manufacturers of herbal remedies and dietary supplements do not need approval from the Food and Drug Administration (FDA) to sell their products. Just like a drug, herbs and supplements can affect the body's chemistry, and therefore have the potential to produce side effects that may be harmful. There have been several reported cases of serious and even lethal side effects from herbal products. Always check with your doctor before using any herbal remedies or dietary supplements.

The following are special concerns for people taking natural remedies for headache:

Feverfew is the most studied herbal remedy for headaches. It does appear to help some people. However, like all effective headache remedies, long-term use can cause a rebound effect. Some experts recommend purchasing feverfew in dried leaf form. Feverfew is generally safe, but side effects can be distressing, particularly canker sores in the mouth (5 - 15% of cases) and stomach distress. Pregnant women or women hoping to become pregnant should not take this herb. People with any blood-clotting disorders should not take it.
Valerian has sedative qualities and is listed on the FDA's list of generally safe products. However, its effects can be dangerously increased if it is used with pharmaceutical sedatives. High doses of valerian can cause blurred vision, excitability, vivid dreams, and changes in heart rhythm.
Comfrey is an herbal remedy used to treat several inflammatory problems. Evidence suggests that comfrey is toxic to the liver. Animal studies have reported a possible cancer risk. It is banned in several countries.

Resources

www.headaches.org -- National Headache Foundation
www.americanheadachesociety.org -- American Headache Society
www.aan.com -- American Academy of Neurology
www.ninds.nih.gov -- National Institute of Neurological Disorders and Stroke
www.i-h-s.org -- International Headache Society

References

Anderson RE, Seniscal C. A comparison of selected osteopathic treatment and relaxation for tension-type headaches. Headache. 2006 Sep;46(:1273-80.

Fernandez-de-Las-Penas C, Alonso-Blanco C, Cuadrado ML, Gerwin RD, Pareja JA. Myofascial trigger points and their relationship to headache clinical parameters in chronic tension-type headache. Headache. 2006 Sep;46(:1264-72.

Fernandez-de-Las-Penas C, Cuadrado ML, Pareja JA. Myofascial trigger points, neck mobility, and forward head posture in episodic tension-type headache. Headache. 2007 May;47(5):662-72.

Lenaerts ME, Gill PS. At the crossroads between tension-type headache and fibromyalgia. Curr Pain Headache Rep. 2006 Dec;10(6):463-6.

Stovner Lj, Hagen K, Jensen R, Katsarava Z, Lipton R, Scher A, et al. The global burden of headache: a documentation of headache prevalence and disability worldwide. Cephalalgia. 2007 Mar;27(3):193-210.

van Ettekoven H, Lucas C. Efficacy of physiotherapy including a craniocervical training programme for tension-type headache; a randomized clinical trial. Cephalalgia. 2006 Aug;26(:983-91.

Zissis NP, Harmoussi S, Vlaikidis N, Mitsikostas D, Thomaidis T, Georgiadis G, et al. A randomized, double-blind, placebo-controlled study of venlafaxine XR in out-patients with tension-type headache. Cephalalgia. 2007 Apr;27(4):315-24. Epub 2007 Mar 7.

Review Date:
10/29/2007
Reviewed By:
Harvey Simon, MD, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital.

A.D.A.M. Copyright

adam.com

Gout

FitSugar — Wed, 08 Oct 2008 17:35:16 -0700

In This Report

Highlights
Introduction
Symptoms
Causes and Risk Factors
Triggers
Diagnosis
Treatment: Acute Gout Attac...
Treatment: Preventing Attac...
Other Treatments
Lifestyle Changes
Complications
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Types of Gout:

There are two types of gout -- primary and secondary.

Primary gout: The cause is usually unknown. However, primary gout is likely the result of a combination of genetic, hormonal, and dietary factors.
Secondary gout: Secondary gout is caused by medications or medical conditions that cause an increase in the serum (blood) levels of uric acid.

Risk Factors:

Risk factors for gout include:

Advancing age
Male gender
Family history of the condition
Obesity
Use of certain drugs, including diuretics, aspirin, cyclosporine, or levodopa
Drinking a large amount of alcohol, particularly beer
Exposure to lead
Organ transplants
Thyroid problems

Symptoms of a Gout Attack:

Symptoms of a gout attack include:

Severe pain at and around the joint
- May feel like "crushing" or a dislocated bone
- Walking and the weight of bed sheets may be unbearable
- Usually takes 8 - 12 hours to develop
- Occurs late at night or early in the morning and may wake you up
Swelling that may extend beyond the joint
Red, shiny, tense skin over the affected area, which may peel after a few days
Chills and mild fever, loss of appetite, and feelings of ill health

Research News

A large study found that people with gout are at an increased risk of having metabolic syndrome. Metabolic syndrome is a collection of problems, such as abdominal obesity, high blood pressure, and low "good" cholesterol. This syndrome increases a person's risk of heart disease and diabetes.

Introduction

Gout is a painful and common type of arthritis. About 1 in 100 people develop gout. The condition is usually associated with a long-lasting, abnormally high amount of uric acid in the blood, called chronic hyperuricemia.

The rate of gout has increased in recent decades, not only in America but also in other developed countries. The increase is possibly due to dietary and lifestyle changes, greater use of medications that cause hyperuricemia, and aging populations. Gout is very uncommon in developing countries.

Click the icon to see an animation about gout.

Metabolism of Purines. The process leading to hyperuricemia and gout begins with the metabolism of purines, nitrogen-containing compounds that are important for energy. Purines can be divided into two types:

Endogenous purines are manufactured within human cells.
Exogenous purines are obtained from foods.

The process of breaking down purines results in the formation of uric acid in the body. Most mammals have an enzyme called uricase, which breaks down uric acid so it can be easily removed from the body. Because humans lack uricase, uric acid is not as easily removed, and can build up in body tissues.

Uric Acid and Hyperuricemia. Purines in the liver produce uric acid. The uric acid enters the bloodstream, and most of it eventually goes through the kidneys and is excreted in the urine. The remaining uric acid travels through the intestines, where bacteria help break it down.

Normally these actions keep the level of uric acid in the blood plasma (the liquid part of the blood) at a healthy level, which is below 6.8 mg/dL. But under certain circumstances, the body produces too much uric acid or removes too little. In either case, concentrations of uric acid increase in the blood. This condition is known as hyperuricemia.

If concentrations of uric acid reach 7 mg/dL and above, needlelike crystals of a salt called monosodium urate (MSU) form. As MSU crystals build up in the joints, they trigger inflammation and pain, the characteristic symptoms of gout.

Symptoms

The specific symptoms of gout depend on the stage of the disease. Gout is often divided into four stages:

Asymptomatic hyperuricemia
Acute gouty arthritis
Intercritical gout
Chronic tophaceous gout

Asymptomatic means there are no symptoms. Asymptomatic hyperuricemia is considered the first stage of gout. MSU levels slowly increase in the body. This stage lasts for an average of 30 years.

Note: Hyperuricemia does not inevitably lead to gout. In fact, less than 20% of cases develop the full-blown arthritic gout disease.

Acute gouty arthritis occurs when the first symptoms of gout appear. Sometimes the first signs of gout are brief twinges of pain (petit attacks) in an affected joint. These attacks can precede the actual full-blown condition by several years.

MSU crystals form at normal body temperature when the concentration of uric acid in the blood reaches 7 mg/dL. At lower temperatures, MSU crystals form at lower concentrations of uric acid. Since blood temperature falls the further blood gets from the heart, gout strikes the toes and fingers first.

Symptoms of acute gouty arthritis include:

Severe pain at and around the joint
- May feel like "crushing" or a dislocated bone
- Walking and the weight of bed sheets may be unbearable
- Usually takes 8 - 12 hours to develop
- Occurs late at night or early in the morning and may wake you up
Swelling that may extend beyond the joint
Red, shiny, tense skin over the affected area, which may peel after a few days
Chills and mild fever, loss of appetite, and feelings of ill health

Most often symptoms start in one joint.

Monoarticular Gout. Gout that occurs in one joint is called monoarticular gout. About 60% of all first-time monoarticular gout attacks in middle-aged adults occur in the big toe. This occurrence is known as podagra. Symptoms can also occur in other locations, such as the ankle or knee.

Polyarticular Gout. If more than one joint is affected, the condition is known as polyarticular gout. Multiple joints are affected in only 10 - 20% of first attacks. Older people are more likely to have polyarticular gout. The most frequently affected joints are the foot, ankle, knee, wrist, elbow, and hand. The pain usually occurs in joints on one side of the body and it is usually, although not always, in the lower legs and the feet. People with polyarticular gout are more likely to have a slower onset of pain and a longer delay between attacks. People with polyarticular gout are also more likely to experience low-grade fever, loss of appetite, and a general feeling of poor health.

An untreated attack will typically peak 24 - 48 hours after the first appearance of symptoms, and go away after 5 - 7 days. However, some attacks last only hours, while others persist as long as several weeks.

Intercritical gout is the term used to describe the periods between attacks. The first attack is usually followed by a complete remission of symptoms, but, if left untreated, gout nearly always returns. Over two-thirds of patients will have at least one further attack within 2 years of the first attack. By 10 years, over 90% of the patients are likely to have repeat attacks.

Chronic Tophaceous Gout and Tophi. After several years, persistent gout can develop into a condition called chronic tophaceous gout. This long-term condition often produces tophi, which are solid deposits of MSU crystals that form in the joints, cartilage, bones, and elsewhere in the body. In some cases, tophi break through the skin and appear as white or yellowish-white, chalky nodules that have been described as looking like crab eyes.

Click the icon to see an image of tophi gout.

Without treatment, tophi develop about 10 years after the initial onset of gout, although the occurence can range from 3 to 42 years. Tophi are more likely to appear early in the course of the disease in older people. In the elderly population, women appear to be at higher risk for tophi than men. Certain people, such as those who are receiving cyclosporine after a transplant, have a high risk of developing tophi.

Development of Chronic Pain. When gout remains untreated, the intercritical periods typically become shorter and shorter, and the attacks, although sometimes less intense, can last longer. Over the long term (about 10 - 20 years) gout becomes a chronic disorder characterized by constant low-grade pain and mild or acute inflammation. Gout may eventually affect several joints, including those that may have been free of symptoms at the first appearance of the disorder. In rare cases, the shoulders, hips, or spine are affected.

Location of Tophi. Tophi generally form in the following locations:

Curved ridge along the edge of the outer ear
Forearms
Elbow or knee
Hands or feet -- older patients, particularly women, are more likely to have gout in the small joints of the fingers.
Around the heart and spine (rare)

Tophi are generally painless. However, they can cause pain and stiffness in the affected joint. Eventually, they can also erode cartilage and bone, ultimately destroying the joint. Large tophi under the skin of the hands and feet can give rise to extreme deformities.

Uric Acid Nephrolithiasis (Kidney Stones). Persons who have kidney stones that formed from uric acid are more likely to have higher levels of uric acid in their blood than in their urine. This suggests that gout is responsible for this type of kidney stones. Uric acid stones and other forms of kidney stones are present in 10 - 25% of patients with primary gout, a rate of more than 1,000 times that of the general population. In gout caused by other conditions (called secondary gout), the reported rate reaches 42%.

Click the icon to see an image of nephrolithiasis.

Not all of the kidney stones in patients with gout are made of uric acid. Some are made from calcium oxalate, calcium phosphate, or substances combined with uric acid. Uric acid stones can also form when you do not have gout or hyperuricemia.

Chronic Uric Acid Interstitial Nephropathy. Chronic uric acid interstitial nephropathy occurs when crystals slowly form in the structures and tubes that carry fluid from the kidney. It is reversible and not likely to injure the kidneys.

Kidney Failure. Sudden overproduction of uric acid can occasionally block the kidneys and cause them to fail. This occurrence is very uncommon but can develop after any of the following:

Chemotherapy for leukemia or lymphoma
Severe heat stress from vigorous exercise
Epileptic seizures
Corticosteroid therapy for severe allergic reactions

Causes and Risk Factors

Gout is classified as either primary or secondary, depending on what causes the high levels of uric acid in the blood (hyperuricemia).

More than 99% of primary gout cases are referred to as idiopathic, meaning that the cause of the hyperuricemia cannot be determined. Primary gout is most likely the result of a combination of genetic, hormonal, and dietary factors. Secondary gout is caused by drug therapy or by medical conditions other than a metabolic disorder.

The following factors increase your risk for gout:

Advancing age
Male gender
Family history of the condition
Obesity
Use of certain drugs, including diuretics ("water pills"), aspirin, cyclosporine, or levodopa
Drinking a large amount of alcohol, particularly beer
Exposure to lead
Organ transplants
Thyroid problems
Other serious illness

Each risk factor is discussed in more detail below.

Middle-Aged Adults. Gout usually occurs in middle-aged men, peaking in the mid-40s. It is most often associated in this age group with obesity, high blood pressure, unhealthy cholesterol levels, and heavy alcohol use.

Elderly. Gout can also develop in older people, when it occurs equally in men and women. In this group, gout is most often associated with kidney problems and the use of diuretics. It is less often associated with alcohol use.

Children. Except for rare inherited genetic disorders that cause hyperuricemia, gout in children is rare.

Men. Men are significantly at higher risk for gout. In males, uric acid levels rise substantially at puberty. In about 5 - 8% of American men, levels exceed 7 mg/dL (indicating hyperuricemia). However, gout typically strikes after 20 - 40 years of persistent hyperuricemia, so men who develop it usually experience their first attack between the ages of 30 and 50.

Women. Before menopause, women have a significantly lower risk for gout than men, possibly because of the actions of estrogen. This female hormone appears to facilitate uric acid excretion by the kidneys. (Only about 15% of female gout cases occur before menopause.) After menopause the risk increases in women. At age 60 the incidence is equal in men and women, and after 80, gout occurs more often in women.

According to the National Institute of Arthritis and Musculoskeletal and Skin Diseases, up to 18% of people with gout have a family history of the condition. Some people with a family history of gout have a defective protein (enzyme) that interferes with the way the body breaks down purines.

Researchers report a clear link between body weight and uric acid levels. In one Japanese study, overweight people had two to more than three times the rate of hyperuricemia as those who maintained a healthy weight. Children who are obese may have a higher risk for gout in adulthood.

Thiazide diuretics are "water pills" used to control hypertension. The drugs are strongly linked to the development of gout. In fact, 75% of patients who develop gout at an older age report the use of diuretics.

Several other medications can increase uric acid levels and raise your risk for gout. These include:

Aspirin -- low doses of aspirin reduce uric acid excretion and increase the chance for hyperuricemia. This may be a problem for older people who take baby aspirin (81 mg) to protect against heart disease.
Niacin (used to treat cholesterol problems)
Pyrazinamide (used to treat tuberculosis)

Drinking excessive amounts of alcohol can raise your risk of gout. Beer is the kind of alcohol most strongly linked with gout, followed by spirits. Moderate wine consumption does not appear to increase the risk of developing gout.

Alcohol use is highly associated with gout in younger adults. Binge drinking particularly increases uric acid levels. Alcohol appears to play less of a role among elderly patients, especially among women with gout.

Alcohol increases uric acid levels in the following three ways:

Providing an additional dietary source of purines (the compounds from which uric acid is formed)
Intensifying the body's production of uric acid
Interfering with the kidneys' ability to excrete uric acid

Chronic occupational exposure to lead is associated with build-up of uric acid and a high incidence of gout.

Kidney transplantation poses a high risk for renal insufficiency and gout. In addition, other transplantation procedures, such as heart and liver, increase the risk of gout. The procedure itself poses a risk of gout, as does the medication (cyclosporine) used to prevent rejection of the transplanted organ. Cyclosporine also interacts with indomethacin, a common gout treatment.

The kidneys are responsible for removing waste from the body, regulating electrolyte balance and blood pressure, and stimulating red blood cell production.

Treatment of several other conditions can cause significant elevations of uric acid in the blood, and therefore a gout attack. These conditions include:

Leukemia
Lymphoma
Psoriasis

Triggers

Triggers are events or conditions that can set off a gout attack. Certain risk factors, including a purine-rich diet, are also considered a trigger. Triggers include:

Joint injury
Overindulging in alcohol or purine-rich foods
Over-strenuous exercise
Severe illness or infection
Stress
Sudden weight loss
Surgery
Using certain drugs

Hot and humid weather may also be strongly associated with recurrent gout attacks. Such weather can cause sweating and, ultimately, dehydration, which has long been recognized as a potential trigger for gout attacks.

Drinking more water and fluids when it's warm outside could help persons with gout prevent future attacks.

Diagnosis

The first step in diagnosing the disease is to determine which joints are affected. A physical examination and medical history can help confirm or rule out gout. For example, gout is more likely if arthritis first appears in the big toe.

The speed of the onset of pain and swelling is also important. Symptoms that take days or weeks (rather than hours) to develop probably indicate a disorder other than gout.

Abnormal enlargements in joints that had been affected by previous injury or osteoarthritis are possible signs of gout. This is particularly significant in older women who take diuretics ("water pills").

A blood test is usually done to measure uric acid levels and detect hyperuricemia. A low level of uric acid in the blood makes a diagnosis of gout much less probable, and a very high level increases the likelihood of gout, especially if patient has symptoms of gout. Nevertheless, uric acid levels in the blood during an attack of gout can be within or below the normal range, and the presence of hyperuricemia does not necessarily mean someone has gout. However, most doctors feel that closer monitoring of blood uric acid levels in people with gout may help reduce gout flares.

Synovial fluid examination is the most accurate method for diagnosing gout. The synovial fluid is the lubricating liquid that fills the synovium (the membrane that surrounds a joint and creates a protective sac). The fluid cushions joints and supplies nutrients and oxygen to the cartilage surface that coats the bones. This exam also helps detect gout during intercritical periods.

The health care provider uses a needle attached to a syringe to draw out fluid from the affected joint. This is called aspiration. Local anesthesia is not used because it can reduce the effectiveness of the procedure. However, the procedure is usually only mildly uncomfortable. Afterwards, there can be some minor discomfort in the area where the needle was inserted, but it usually goes away quickly.

The fluid sample is sent to a laboratory for analysis. Testing can reveal the presence of monosodium urate (MSU) crystals, which will nearly always confirm a diagnosis of gout. The laboratory can also test the sample for infection.

The procedure itself can cause infection, though this occurs in less than 0.1% of patients. Aspiration sometimes eases the patient's symptoms by reducing swelling and pressure on the tissue surrounding the joint.

Synovial fluid analysis is a method to look at the fluid that cushions a joint. It is done to help diagnose and treat joint-related problems such as gout.

It is sometimes helpful to gauge the amount of uric acid found in a patient's urine, particularly if the patient is young and has pronounced hyperuricemia that might be related to a metabolic disorder. If uric acid in the urine exceeds a particular value, further tests for an enzyme defect or other identifiable cause of gout should be performed. Greater-than-normal amounts of uric acid in the urine also mean that the patient is more likely to develop uric acid kidney stones.

Typically, a 24-hour urine test is performed. The patient discards the first urination sample on the day of the test. Afterward all urine passed over the next 24 hours is collected into a special container, including the first urination on the morning of day two. The container is delivered to the patient's health care provider or sent directly to the laboratory.

The urine is collected during an intercritical period, after the patient has been placed on a purine-reduced diet. The patient is also asked to temporarily stop using alcohol and any medications that can interfere with the test. The patient should not change any of his or her usual eating or drinking patterns when performing this test.

Click the icon to see an image of a uric acid test.

X-Rays. For the most part, x-rays do not reveal any problems during the early stages of gout. Their usefulness lies in assessing the progress of the disorder in its chronic phase and identifying other health problems with symptoms similar to gout. Tophi can be seen on x-rays before they become apparent on physical examination.

Advanced Imaging Techniques. Advanced imaging techniques being investigated for identifying tophi include computed tomography (CT), magnetic resonance imaging (MRI), and Doppler ultrasonography.

As part of the diagnosis, other disorders that produce gout-like symptoms or cause hyperuricemia should be ruled out. In general, it is easy to distinguish acute gout that occurs in one joint from other arthritic conditions. The two disorders that may confuse this diagnosis are pseudogout and septic arthritis. Pseudogout is a condition most likely to be confused with gout.

Chronic gout can often resemble rheumatoid arthritis. Several other conditions may at some point in their course resemble gout.

Pseudogout (also called calcic gout and calcium pyrophosphate dihydrate deposition disease) is a common inflammatory arthritis among older adults. It is very similar to gout, but is caused by deposits of calcium pyrophosphate dihydrate crystals in and around the joints.

Although symptoms of pseudogout resemble gout in some ways, there are differences:

The first attack typically strikes the knee. Other joints commonly affected are the shoulders, wrists, and ankles. At least two-thirds of cases affect more than one joint during a first attack. Pseudogout may involve any joint, although the small joints in the fingers or toes are not commonly affected.
The symptoms of pseudogout also appear more slowly than those of gout, taking days rather than hours to develop.
Pseudogout is more likely to first develop in elderly people, particularly those with osteoarthritis. (It affects 10 - 15% of people over 65.)

Pseudogout is more likely to occur in the autumn while gout attacks are most common in the spring.

Conditions that are associated with a higher risk for pseudogout in elderly patients include underlying acute medical conditions, trauma, or surgery. Medical conditions associated with pseudogout include hypothyroidism, diabetes, gout, and osteoarthritis. Liver transplantation also may increase the risk.

There is no cure for pseudogout. It is a progressive disorder that can eventually destroy joints. Treatments for pseudogout are similar to those for gout and are aimed at relieving the pain and inflammation and reducing the frequency of attacks.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are effective for treating inflammation and pain from pseudogout.
For acute attacks in large joints, fluid aspiration alone or with corticosteroids may help.
Colchicine may be used for acute attacks.
Magnesium carbonate may help dissolve crystals, but existing hard deposits may remain.
Surgery may be required for joint replacement.

Rheumatoid Arthritis. Rheumatoid arthritis can distort the joints of the finger and cause inflammation and pain that may mimic gout. In older people, it is particularly difficult to distinguish chronic gout from rheumatoid arthritis. A proper diagnosis can be made with a detailed medical history, laboratory tests, and identification of MSU crystals.

Osteoarthritis. Gout can coincide and be confused with osteoarthritis in older people, particularly when it occurs in arthritic finger joints in women. In general, gout should be suspected if the joints in the fingertips are unusually enlarged.

Click the icon to see an image of osteoarthritis.

Infections. Joint infections can have features that resemble gout. A correct diagnosis is critical for appropriate treatment. For example, some cases of gout have been confused with infection after joint replacement. On the other hand, joint infection not associated with surgery might indicate sepsis, which is a widespread and potentially life-threatening bacterial infection that can cause inflamed joints, chills, and a spiking fever. The severity of the fever and a high white blood cell count in the joint fluid helps diagnose a septic infection, while urate crystals in the joint are a good indicator of gout.

Charcot Foot. Between 1 - 2.5% of people with diabetes have Charcot foot or Charcot joint (medically referred to as neuropathic arthropathy). This condition is caused by problems in the nerves in the feet. Early changes may resemble gout, with the foot becoming swollen, red, and warm. Recognition and treatment of this condition is very important. A seriously affected foot can become deformed. The bones may crack, splinter, and erode, and the joints may shift, change shape, and become unstable.

Bunions. A bunion is a foot deformity that usually occurs at the head of the first of five long bones (the metatarsal bones) that extend from the arch and connect to the toes, and may be confused with gout. The first metatarsal bone is the one that attaches to the big toe. A bunion begins to form when the big toe is forced in toward the rest of the toes, causing the head of the first metatarsal bone to jut out and rub against the side of the shoe. The underlying tissue becomes inflamed, and a painful bump forms. As this bony growth develops, the bunion is formed as the big toe is forced to grow at an increasing angle towards the rest of the toes.

Click the icon to see an illustrated series detailing bunion removal.


Disease	Specific Subtypes
Osteoarthritis
Infectious Arthritis	Lyme disease, septic arthritis, bacterial endocarditis, mycobacterial and fungal arthritis, viral arthritis, osteomyelitis
Postinfectious or Reactive Arthritis	Reiter syndrome (a disorder characterized by arthritis and inflammation in the eye and urinary tract), rheumatic fever, inflammatory bowel disease
Pseudogout
Rheumatic Autoimmune Diseases	Rheumatoid arthritis, systemic vasculitis, systemic lupus erythematosus, scleroderma, Still's disease (also called juvenile rheumatoid arthritis)
Fibromyalgia
Other Diseases	Chronic fatigue syndrome, hepatitis C, familial Mediterranean fever, cancers, AIDS, leukemia, bunions, Whipple's disease, dermatomyositis, Behcet's disease, Henoch-Schonlein purpura, Kawasaki's disease, erythema nodosum, erythema multiforme, pyoderma gangrenosum, pustular psoriasis

Treatment: Acute Gout Attack

Acute attacks of gout and long-term treatment of gout and hyperuricemia require different approaches. Treatment usually involves medication. After the first attack, some health care providers advise their patients to keep a supply of medications on hand so that self-medication can begin at the first sign of symptoms of a second acute attack. There are also specific treatments for conditions associated with gout, including uric acid nephropathy and uric acid nephrolithiasis.

Many patients do not require medications. During the period between gout attacks, patients are advised to avoid foods high in purines and to maintain a healthy weight. Patients should also avoid alcohol and reduce any stress.

Drug treatments for acute attacks of gout are aimed at relieving pain and reducing inflammation. They should be started as early as possible.

Medications used in the treatment of gout include:

NSAIDs (nonsteroidal anti-inflammatory drugs)
Colchicine
Corticosteroids

Powerful forms of nonsteroidal anti-inflammatory drugs (NSAIDs) are the drugs of choice for an acute attack in younger, healthy patients with no serious health problems, particularly problems that affect the kidneys, liver, or heart. Usually indomethacin is prescribed for 2 - 7 days.

There are dozens of NSAIDs available. Over-the-counter NSAIDs include:

Low-dose Ibuprofen (Motrin IB, Advil, Nuprin)
Naproxen (Aleve)
Ketoprofen (Actron, Orudis KT)

Prescription NSAIDs include:

Ibuprofen (Motrin)
Naproxen (Naprosyn, Anaprox)
Flurbiprofen (Ansaid)
Diclofenac (Voltaren)
Tolmetin (Tolectin)
Ketoprofen (Orudis, Oruvail)
Dexibuprofen (Seractil)
Indomethacin (Indocin)

Indomethacin (Indocin) is typically the first choice of treatment for patients who have no medical conditions that would interfere with its use. Usually 2 - 7 days of high-dose indomethacin is enough to treat a gout attack. The first dose of indomethacin usually begins to act against the pain and inflammation within 24 hours and often much sooner.

Ibuprofen, naproxen, sulindac, or NSAIDs are good alternatives, particularly for elderly patients who might experience confusion or bizarre sensations with indomethacin. (Aspirin is an NSAID, but is associated with a higher risk for gout and should be avoided.)

Regular use of even over-the-counter NSAIDs can cause certain health problems, such as:

Ulcers and gastrointestinal bleeding
Increased blood pressure -- people with hypertension, severe vascular disease, kidney, or liver problems and those taking diuretics must be closely monitored if they need to take NSAIDs.
Delayed emptying of the stomach, which could interfere with the actions of other drugs. The elderly are at special risk.
Dizziness
Tinnitus (ringing in the ear)
Headache
Skin rash
Depression
Confusion or bizarre sensation (in some higher-potency NSAIDs, notably indomethacin)
Kidney damage

NSAIDs can cause kidney problems, especially in the elderly and those with kidney disease. When caught early enough, these problems generally resolve if the drugs are stopped. Any sudden weight gain or swelling should be reported to a physician. Anyone with kidney disease should avoid these drugs.

Patients with diabetes who take hypoglycemics by mouth may need to adjust their medication dosage if they also take NSAIDs, because of possible harmful interactions between these classes of drugs.

Some studies reported that ibuprofen (but not other NSAIDs) may reduce the heart-protective effects of low-dose aspirin. Additional research is needed to confirm these findings.

Long-term use of NSAIDs is a common cause of ulcers. NSAID-related bleeding and stomach problems may be responsible for over 100,000 hospital admissions and over 15,000 deaths each year. Because there are usually no gastrointestinal symptoms from NSAIDs until bleeding begins, health care providers cannot predict which patients taking these drugs will develop bleeding.

Those at high risk for NSAID-related bleeding include the elderly, anyone with a history of an ulcer or gastrointestinal bleeding, patients with serious heart conditions, those who drink too much alcohol, and persons on certain medications, such anticoagulants (blood thinners), corticosteroids, or bisphosphonates (drugs used for osteoporosis).

Preventing NSAID-Related Ulcers. Switching to alternative pain relievers is the first step in preventing or healing ulcers caused by NSAIDs. If people cannot change drugs, they should use the lowest NSAID dose possible.

In addition, medications are available that may help prevent ulcers in people who need to take NSAIDs. Proton-pump inhibitors (PPIs) are the first drug of choice for preventing ulcers in high-risk individuals. They have been shown to reduce NSAID-ulcer rates by as much as 80% compared with no treatment. Types of these drugs include omeprazole (Prilosec), esomeprazole (Nexium), lansoprazole (Prevacid), rabeprazole (AcipHex ), and pantoprazole (Protonix). Prevacid is the first proton-pump inhibitor specifically approved for protecting against ulcers in chronic NSAID users.

Arthrotec is a combination of an ulcer-protective drug called misoprostol and the NSAID diclofenac. It too may reduce the risk for gastrointestinal bleeding.

Colchicine is a derivative of the autumn crocus (also called the meadow saffron). It has been used against gout attacks for centuries. It is highly effective, although it is no longer the first drug of choice because of its frequent, unpleasant, and sometimes very serious side effects.

Colchicine may be given to a healthy adult within 48 hours of an attack. It should not be used by elderly patients or those with kidney, liver, or bone marrow disorders. It can also affect fertility and should not be used during pregnancy. The drug can cause gastrointestinal side effects at high dose, including nausea, vomiting, diarrhea, and abdominal cramps. Low doses do not pose as high a risk for gastrointestinal symptoms, and can prevent further attacks, including attacks in patients who are starting anti-hyperuricemic therapies.

Colchicine may be taken by mouth or given by an intravenous line. Those who take it by mouth need doses every hour until either symptoms improve or side effects develop. Improvement should be seen by the tenth dose. It usually eliminates the pain of an acute attack within 48 hours. The intravenous route has some serious side effects, however, and poses an increased risk for injury to the kidney, liver, central nervous system, and bone marrow.

The antibiotic erythromycin, or H2 blockers such as famotidine (Pepcid AC), cimetidine (Tagamet), or ranitidine (Zantac) may intensify the gastrointestinal side effects of colchicine.

Warning Note: Overdose of colchicine can be dangerous, and there have even been reports of death. The drug may also suppress blood cell production and cause nerve and muscular injury in certain people, sometimes even in those not taking high doses.

Corticosteroids may be used in patients who cannot tolerate NSAIDs and they may be particularly beneficial for elderly patients. Injections into an affected joint provide effective relief for many patients, but this is not useful for patients who have multiple affected joints. Steroids taken by mouth may be used for patients who cannot take NSAIDs or colchicine and who have gout in more than one joint. Corticosteroids include triamcinolone and prednisone.

Treatment: Preventing Attacks

After an acute attack some patients remain at high risk for another attack for several weeks during the intercritical period. Such patients include those with kidney insufficiency or those with congestive heart failure who are on diuretics. Low doses of colchicine or NSAIDs may be used to during this period for prevention of another attack. They should be taken in low doses for 1 - 2 months after an attack, or for longer periods in patients who have experienced frequent attacks.

Antihyperuricemic medications reduce levels of uric acid in the body. The decision whether to use an antihyperuricemic medicine and at what point is not entirely clear. Some health care providers do not prescribe them if hyperuricemia is mild, or until a patient has had two gout attacks. Others prescribe them immediately after a single attack. Most of the time, antihyperuricemic therapy means taking a drug routinely throughout life, which many people find difficult.

Experts do not recommend treatment for hyperuricemia that causes no symptoms. Asymptomatic hyperuricemia often does not lead to gout or other health problems. In addition, the drugs used to treat it are expensive and carry certain risks. In unusual circumstances treatment may be justified, for example in patients with very high uric acid levels that threaten the kidney or those with a personal or strong family history of gout, kidney stones, or kidney damage.

Before treatment, some experts recommend a 24-hour urine collection sample in patients with frequent gout attacks to determine whether they are over-producers or under-excreters of uric acid. Also, before starting one of these drugs, any previous acute attack should be completely controlled and the joints should not be inflamed. Some health care providers prefer to wait about a month after an attack.

Low doses of NSAIDs or colchicine are used during several months after introducing anti-hyperuricemic therapies to prevent gout attacks. It should be noted that NSAIDs, particularly aspirin and similar drugs, reduce the effectiveness of uricosurics. These are drugs given to under-excreters of uric acid (see below). Patients taking uricosurics should avoid NSAIDs, if possible.

Long-term treatment of hyperuricemia may be recommended for people who have:

A risk for tophaceous gout
Had more than two or three acute attacks of gout in the past
Unusually severe attacks, or attacks that affect more than one joint
Joint damage from gout, as shown on x-rays
Hyperuricemia caused by an identifiable inborn metabolic deficiency

Uricosurics. These drugs prevent the kidney from reabsorbing uric acid, and therefore increase the amount excreted in the urine. They are appropriate when gout is caused by under-excretion of uric acid, which occurs in about 80% of gout cases. They are not used for patients with reduced kidney function or those with tophaceous gout. Uricosurics are usually the choice for preventing gout in the following patients:

Those under 60 years of age
Those with normal diets
Those who have normal kidney function
Those who have no risk of kidney stones

Uricosuric drug candidates should produce no more than 700 - 800 mg of uric acid in the urine over a 24-hour period.

Probenecid (Benemid, Probalan) and sulfinpyrazone (Anturane) are the standard uricosurics. A more potent uricosuric, benzbromarone, may work for people with severe tophaceous gout and kidney impairment when other drugs do not. In some studies, benzbromarone was equal to or even more effective than allopurinol, another type of antihyperuricemic drug. Because benzbromarone can cause liver failure in some patients, it is available in the U.S. only with special authorization. A uricosuric combined with allopurinol may be beneficial in some cases.

Probenecid is taken two to three times a day, and sulfinpyrazone begins at twice a day and increases to three or four times daily. The initial doses should be low and gradually increased. Probenecid combined with colchicine is more effective than probenecid alone, but everyone responds differently, so the dose should be carefully individualized.

The possible side effects of probenecid and sulfinpyrazone include skin rashes, gastrointestinal problems, anemia, and kidney stone formation. To help reduce acidity and the risk for kidney stones, patients should drink plenty of fluids (ideally water, not caffeinated beverages). Sodium bicarbonate supplemented by acetazolamide can also reduce acidity and the risk for stones.

NSAIDs, particularly aspirin, as well as other salicylate drugs, interfere with uricosuric drugs and reduce effectiveness. Patients who require minor pain relief should instead take acetaminophen (Tylenol). Uricosurics interact with many other drugs, and a patient should be sure to inform their health care provider of all medications they are taking.

People who take these drugs should have normal kidney function. This therapy may not be as beneficial in many elderly patients, who often have some kidney insufficiency.

Allopurinol (Lopurin, Zyloprim). Allopurinol blocks uric acid production. It is the drug most often used in long-term gout treatment for older patients and those who overproduce uric acid.

Allopurinol is taken by mouth once a day in doses of 100 - 600 mg, depending on the patient's response to treatment. When it is first used, allopurinol can trigger further attacks of gout. Therefore, during the first months (or longer) of therapy, the patient also takes an NSAID or colchicine to reduce that possibility.

Allopurinol has positive effects on "bad" cholesterol levels, so it may be better than other drugs for patients with both gout and coronary artery disease.

Side effects, which can be severe, include:

Rash
Diarrhea
Headache
Fever
Leukopenia (a reduction in the number of white blood cells)
Thrombocytopenia (a reduction in the number of platelets)
Cataracts

In rare cases, the rash can become severe and widespread enough to be life threatening (this condition is called toxic epidermal necrolysis, or TEN). Allergic individuals who experience only a mild rash may be able to build up their tolerance for the drug by undergoing a desensitization process.

Allopurinol interacts with certain other drugs, such as azathioprine.

Puricase (PEG-Uricase). This is an experimental drug that has been shown to rapidly reduce excess uric acid. If approved, it may help those who have failed other treatments.

It should be noted that many drugs used for gout can also precipitate acute gout symptoms and so should not be used until symptoms have subsided. The patient should then start treatment with small doses that gradually increase.

Hypertensive Agents. People with gout have a higher risk for high blood pressure. Some of the drugs used to treat hypertension, such as thiazide diuretics, can increase the risk for gout attacks. Newer agents, such as losartan (an angiotensin II receptor antagonist), and amlodipine (a calcium channel blocker), may have beneficial effects on both high blood pressure and gout.

Febuxostat. Febuxostat is the first drug to emerge in many decades as a potential new treatment for chronic gout. It may prove to be an alternative for patients who are allergic to allopurinol. The drug is awaiting approval from the U.S. Food and Drug Administration (FDA).

Other Treatments

Surgery. Large tophi that are draining, infected, or interfering with the movement of joints may need to be surgically removed. When infection is present, the procedure carries a high risk for complications. People most likely to have surgery also tend to have other medical conditions that might worsen their outlook. In one study, experts suggested that better preventive measures, such as the use of allopurinol, could reduce the need for surgery.

Several other surgical procedures are available for relieving pain and improving the function of affected joints. It is sometimes necessary to replace joints.

Hot and Cold Therapy. Rest and protecting the affected joint with a splint can also promote recovery. One study reported that applying ice packs for 30 minutes four times daily significantly reduced pain. However, a different study recommended applying warm water continuously and moving the joint. The theory behind this advice was that the pain in a gout attack is due to grinding from the crystals and that warmth would help dissolve the crystals and relieve pain.

Lifestyle Changes

Any activities that increase energy demands on the body also increase metabolism of purines, which produces uric acid. Avoiding stress and staying healthy are important for the prevention of attacks.

Because uric acid levels are only mildly affected by diet, dietary therapy does not play a large role in the prevention of gout. Still, people who have had an attack of gout may benefit from reducing their intake of purine-rich foods, particularly if they eat unusually large quantities of such foods.

While meat and certain types of seafood and shellfish do produce high levels of purines in the blood, research has suggested that not all purine-rich foods are associated with gout. Eating a moderate amount of purine-rich vegetables (spinach, cauliflower, mushrooms, legumes) does not appear to increase the risk of gout.

Dairy products, especially low-fat products (low-fat yogurt and skim milk), may actually protect against gout. Researchers have also found that taking 500 mg a day of vitamin C significantly reduces uric acid levels. They are investigating whether vitamin C can be used to prevent or treat gout.

Foods to Avoid:

Organ meats (liver, kidneys, sweetbreads)
Red meat (beef, pork, lamb)
Meat extracts (soup, broth, gravies)
Seafood (anchovies, sardines, herring, fish roe, canned tuna fish, shrimp, lobster, scallops, mussels)
Yeast products (beer and baked goods)

A supervised weight-loss program may be a very effective way to reduce uric acid levels in overweight patients. Crash dieting, on the other hand, is counterproductive because it can increase uric acid levels and may cause an acute attack.

Drinking plenty of water and other nonalcoholic beverages helps remove MSU crystals from the body.

Alcohol should be avoided, since it promotes purine metabolism and uric acid production. It also may reduce excretion of uric acid. Heavy drinking, especially binge drinking of beer or distilled spirits, should be avoided.

People with gout should also attempt to avoid activities that cause repetitive joint trauma, such as wearing tight shoes.

Travel is an example of an activity that increases the risk for gout. It not only increases stress, but eating and drinking patterns may change. Before traveling, patients should discuss preventive measures with their health care providers. The doctor may prescribe a prednisone tablet to be taken immediately at the first sign of a gout attack. In most cases, this stops the episode.

Complications

Properly treated gout rarely poses a long-term health threat, though it can be a cause of short-term pain and incapacity for thousands of Americans.

Left untreated, gout can develop into a painful and disabling chronic disorder. Persistent gout can destroy cartilage and bone, causing irreversible joint deformities and loss of motion. Survey results released in 2006 show that two-thirds of persons with gout consider the pain of attacks among the worst they've ever experienced. An estimated 75% of those surveyed said flare-ups made walking very difficult, and about 70% reported trouble putting on shoes or playing sports.

Tophi are firm chalky, gritty clumps of uric acid crystals that build up in tissue surrounding a joint. If gout is not treated, tophi can grow to the size of golf balls and can destroy bone and cartilage in the joints, similar to the process in rheumatoid arthritis. If they lodge in the spine, tophi can cause serious damage including compression, although this is very rare. In extreme cases, joint destruction results in complete disability.

Kidney Stones. Kidney stones occur in 10 - 40% of gout patients, and can occur at any time after the development of hyperuricemia. Although the stones are usually composed of uric acid, they may also be mixed with other materials.

Kidney stones result when urine becomes too concentrated, and substances in the urine crystallize to form stones. Symptoms occur when the stones begin to move down the ureter and cause intense pain. Kidney stones may form in the pelvis or calyces of the kidney or in the ureter.

Kidney Disease. About 25% of patients with chronic hyperuricemia develop progressive kidney disease, which sometimes ends in kidney failure. It should be noted, however, that many experts believe that chronic hyperuricemia is unlikely to be a common cause of kidney disease. In most cases, the kidney disease comes first and causes high concentrations of uric acid.

Gout is found in higher rates in people with high blood pressure, coronary artery disease, and heart failure. Hyperuricemia, in fact, has been associated with a higher risk of death from heart conditions. A large study published in 2007 found an association between gout and having the metabolic syndrome -- a collection of problems, such as abdominal obesity, high blood pressure, high triglycerides levels, and low "good" cholesterol levels. This syndrome increases a person's risk of heart disease and diabetes.

A study published in the August 2006 journal Arthritis & Rheumatism found that gout increases the risk of heart attacks in men with no previous history of heart problems. According to some studies, hyperuricemia may be associated with heart disease, but there is not enough data to confirm such an association.

Click the icon to see an image of coronary artery blockage.

The following are some conditions that are associated with long-term gout:

Cataracts
Dry eye syndrome
Complications in the lungs (in rare cases, uric acid crystals occur in the lungs)

Resources

www.niams.nih.gov -- National Institute of Arthritis and Musculoskeletal and Skin Diseases
www.rheumatology.org -- American College of Rheumatology
www.arthritis.org -- The Arthritis Foundation
www.gouteducation.org -- The Gout & Uric Acid Education Society

References

Choi HK, Ford ES, Li C, Curhan G. Prevalence of the metabolic syndrome in patients with gout: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 2007;57(1):109-15.

Huang HY, Appel LJ, Choi MJ et al. The effects of vitamin C supplementation on serum concentrations of uric acid: results of a randomized controlled trial. Arthritis Rheum. 2005 Jun;52(6):1843-7.

Krishnan E, Baker JF, Furst DE, Schumacher HR. Gout and the risk of acute myocardial infarction. Arthritis Rheum. 2006 Aug;54(:2688-96.

Underwood M. Diagnosis and management of gout. BMJ. 2006;332(7553):1315-9.

Zhang W, Doherty M, Bardin T, et al. EULAR evidence based recommendations for gout. Part I: Diagnosis. Report of a task force of the Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2006;65(10):1301-11.

Zhang W, Doherty M, Bardin T, et al. EULAR evidence based recommendations for gout. Part II: Management. Report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2006;65(10):1312-24.

Zhang YQ, Chaisson CE, Chen CA, McAlindon TE, Hunter DJ. High Humidity and High Temperature Increase the Risk of Recurrent Gout Attacks: The Online Case-crossover Gout Study. Presentation Number 707. American College of Rheumatology Annual Scientific Meeting, Washington, DC, November 2006.

Review Date:
1/21/2008
Reviewed By:
Harvey Simon, MD, Editor-in-Chief, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

A.D.A.M. Copyright

adam.com

Menstrual disorders

FitSugar — Wed, 08 Oct 2008 17:34:59 -0700

In This Report

Highlights
Introduction
Menstrual Disorders
Causes
Risk Factors
Complications
Diagnosis
Treatment
Medications
Surgery
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

“No-Period” Pill Approved

In May 2007, the FDA approved Lybrel, the first birth control pill that completely eliminates monthly menstrual periods. Lybrel contains low doses of the estrogen estradiol and the progesterone levonorgestrol. The active pills are taken 365 days a year -- with no inactive pill breaks. In clinical trials, 59% of women who took Lybrel completely stopped menstrual periods by the end of the first year. Some women, however, continued to have occasional unscheduled bleeding or spotting during the first 3 - 6 months.

Other Options for Eliminating Menstrual Periods

In addition to Lybrel, women with menstrual problems have several other options for stopping periods:

Levonorgestrol-Releasing Intrauterine System (LNG-IUS). The LNG-IUS is an intrauterine device (IUD) that is placed in the uterus. The LNG-IUS releases levonorgestrol for up to 5 years. Over the course of the first year, it reduces menstrual bleeding. Many women find that their periods completely stop. Doctors often recommend this contraceptive device as a treatment for menorrhagia (heavy bleeding) and an alternative to hysterectomy. In the U.S., the LNG-IUS is marketed as Mirena.
Depo-Provera. Depo-Provera is an injectable progestin contraceptive. Most women who use Depo-Provera stop menstruating after a year. However, Depo-Provera is associated with serious side effects, including loss of bone density. Because of this risk, the FDA recommends that Depo-Provera should not be used for more than 2 years. Weight gain is also a common side effect.
Hysterectomy. Hysterectomy, the surgical removal of the uterus, is a permanent cure for menorrhagia, but it is an invasive procedure that also ends fertility.

Menstruation in Girls and Adolescents

According to a 2006 report from the American Academy of Pediatrics and the American College of Obstetricians and Gynecologists:

Most girls begin to menstruate when they are between 12 - 13 years old.
Menstruation usually starts 2 - 3 years after initial breast development.
Girls who have not begun menstruation by the age of 15 should see a doctor for an evaluation.

Introduction

The Primary Organs and Structures in the Reproductive System.

The uterus is a pear-shaped organ located between the bladder and lower intestine. It consists of two parts, the body and the cervix.
When a woman is not pregnant the body of the uterus is about the size of a fist, with its walls collapsed and flattened against each other. During pregnancy, the walls of the uterus are pushed apart as the fetus grows.
The cervix is the lower portion of the uterus. It has a canal opening into the vagina with an opening called the os, which allows menstrual blood to flow out of the uterus into the vagina.
Leading off each side of the body of the uterus are two tubes known as the fallopian tubes. Near the end of each tube is an ovary.
Ovaries are egg-producing organs that hold 200,000 - 400,000 follicles (from folliculus, meaning "sack" in Latin). These cellular sacks contain the materials needed to produce ripened eggs, or ova.
The inner lining of the uterus is called the endometrium, and during pregnancy it thickens and becomes enriched with blood vessels to house and support the growing fetus. If pregnancy does not occur, the endometrium is shed and a woman starts her menstrual flow (or "period"). Menstrual flow also consists of blood and mucus from the cervix and vagina.

The uterus is a hollow muscular organ located in the female pelvis between the bladder and rectum. The ovaries produce the eggs that travel through the fallopian tubes. Once the egg has left the ovary it can be fertilized and implant itself in the lining of the uterus. The main function of the uterus is to nourish the developing fetus prior to birth.

Reproductive Hormones. The hypothalamus (an area in the brain) and the pituitary gland control the reproductive hormones. In women, six hormones help regulate the reproductive system:

Click the icon to see an image of the hypothalamus and pituitary gland.

Gonadotropin-releasing hormone (GnRH) is released by the hypothalamus.
GnRH stimulates the pituitary gland to produce follicle-stimulating hormone (FSH) and luteinizing hormone (LH).
Estrogen, progesterone, and the male hormone testosterone are secreted by the ovaries at the command of FSH and LH.

Click the icon to see an image of the pituitary gland.

Ovulation. The process leading to fertility is very intricate. It depends on the healthy interaction of two sets of organs and hormone systems in both the male and female. In addition, reproduction is limited by the phases of female fertility. Nevertheless, this astonishing process results in conception within a year for about 80% of couples. Only 15% conceive within a month of their first attempts, however, and about 60% succeed after 6 months.

A woman's ability to produce children occurs after she enters puberty and begins to menstruate. The process to conception is complex:

With the start of each menstrual cycle, FSH stimulates several follicles to mature over a two-week period until their eggs nearly triple in size. Only one follicle becomes dominant, however, during a cycle.
FSH signals this dominant follicle to produce estrogen, which enters the bloodstream and reaches the uterus. There, estrogen stimulates the cells in the uterine lining to reproduce, therefore thickening the walls.
Estrogen levels reach their peak around the 14th day of the cycle (counting days beginning with the first day of a period). At that time, they trigger a surge of LH.

LH serves two important roles:

First, the LH surge around the 14th cycle day stimulates ovulation. It does this by causing the dominant follicle to burst and release its egg into one of the two fallopian tubes. Once in the fallopian tube, the egg is in place for fertilization.
Next, LH causes the ruptured follicle to develop into the corpus luteum. The corpus luteum provides a source of estrogen and progesterone during pregnancy.

Fertilization. The so-called "fertile window" is 6 days long and starts 5 days before ovulation and ends the day of ovulation. Fertilization occurs as follows:

The sperm can survive for up to 3 days once it enters the fallopian tube. The egg survives 12 - 24 hours unless it is fertilized by a sperm.
If the egg is fertilized, it moves about 2 - 4 days later from the fallopian tube into the uterus where it is implanted in the uterine lining and begins its nine-month incubation.
The placenta forms at the site of the implantation. The placenta is a thick blanket of blood vessels that nourishes the fertilized egg as it develops.
The corpus luteum (the yellow tissue formed from the ruptured follicle) continues to produce estrogen and progesterone during pregnancy.

Click the icon to see an image of the placenta.

Click the icon to see an image of the corpus luteum.

If the egg is not fertilized, the corpus luteum degenerates into a form called the corpus albicans, and estrogen and progesterone levels drop. Finally, the endometrial lining sloughs off and is shed during menstruation.


Menstrual Phases	Typical No. of Days	Hormonal Actions
Follicular (Proliferative) Phase	Cycle Days 1 through 6: Beginning of menstruation to end of blood flow.	Estrogen and progesterone start out at their lowest levels. FSH levels rise to stimulate maturity of follicles. Ovaries start producing estrogen and levels rise, while progesterone remains low.
	Cycle Days 7 - 13: The endometrium thickens to prepare for the egg implantation.
Ovulation	Cycle Day 14:	Surge in LH. Largest follicle bursts and releases egg into fallopian tube.
Luteal (Secretory) Phase, also known as the Premenstrual Phase	Cycle Days 15 - 28:	Ruptured follicle develops into corpus luteum, which produces progesterone. Progesterone and estrogen stimulate blanket of blood vessels to prepare for egg implantation.
	If fertilization occurs:	Fertilized egg attaches to blanket of blood vessels that supplies nutrients for the developing placenta. Corpus luteum continues to produce estrogen and progesterone.
	If fertilization does not occur:	Corpus luteum deteriorates. Estrogen and progesterone levels drop. The blood vessel lining sloughs off and menstruation begins.

Click the icon to see an animation about the menstrual cycle.

What is Menstruation? Menstruation, also called a "period," is the cyclical flow of blood from the uterus in women between the ages of puberty and menopause.

Onset of Menstruation (Menarche). The onset of menstruation, called the menarche, typically begins between the ages of 12 - 13 years. Menarche generally occurs 2 - 3 years after initial breast development (breast budding). African-American and Hispanic girls tend to mature slightly earlier than Caucasian girls. A higher body mass index (BMI) during childhood is associated with an earlier onset of puberty. Environmental factors and nutrition may also affect menarche timing.

Length of Monthly Cycle. The menstrual cycle can be very irregular during the first 1 - 2 years, ranging from 21 - 45 days. The length then generally stabilizes to an average of 28 days, although the cycle length may range from 21 - 34 days and still be considered normal. A variation of 10 days or more -- either more or fewer days -- may have an impact on fertility, however. The cycle lengthens when a woman is in her 40s, reaching an average of 31 days by age 49. A number of factors can affect cycle length at any age.


Shorter Cycles	Longer Cycles
Regular alcohol use.	Being under 21 and over 44.
Stressful jobs.	Being very thin (also at risk for short bleeding periods).
	Competitive athletics (also at risk for short bleeding periods).

Length of Periods. Periods average 6.6 days in adolescent girls. By the age of 21, menstrual bleeding averages 6 days until women approach menopause. However, about 5% of healthy women menstruate fewer than 4 days and 5% menstruate more than 8 days.

Normal Absence of Menstruation. Normal absence of periods can occur in any woman under the following circumstances:

Menstruation stops during the duration of pregnancy. Some women continue to have irregular bleeding during the first trimester. This bleeding may indicate a threatened miscarriage and requires immediate attention by the doctor.
When women breastfeed they are unlikely to ovulate. After that time, menstruation usually resumes and they are fertile again.
Perimenopause starts when the intervals between periods begin to lengthen, and it ends with menopause itself (the complete cessation of menstruation). Menopause usually occurs at about age 51, although smokers often go through menopause earlier.

Menstrual Disorders

There are a number of different menstrual disorders. Problems can range from heavy, painful periods to no period at all.

Dysmenorrhea is severe, frequent cramping during menstruation. Pain occurs in the lower abdomen but can spread to the lower back and thighs. Dysmenorrhea is usually referred to as primary or secondary.

Primary dysmenorrhea. Cramps occur from contractions in the uterus. These contractions are a normal part of the menstrual process. With primary dysmenorrhea, cramping pain is directly related to and caused by menstruation. About half of menstruating women experience primary dysmenorrhea. It usually begins 2 - 3 years after a women begins to menstruate. The pain typically develops when the bleeding starts and continues for 32 - 48 hours. Cramps are generally most severe during heavy bleeding.

Secondary dysmenorrhea. Secondary dysmenorrhea is menstrually related pain that accompanies another medical or physical condition, such as endometriosis or uterine fibroids.

During a normal menstrual cycle, the average woman loses about 1 ounce (30 mL) of blood. Most women change their tampons or pads around 3 - 6 times per day. Menorrhagia is the medical term for significantly heavier bleeding. Menorrhagia occurs in 9 - 14% of all women and can be caused by a number of factors. Women often overestimate the amount of blood lost during their periods. Clot formation is fairly common during heavy bleeding and is not a cause for concern. However, women should consult their doctor if any of the following occurs:

Soaking through at least one pad or tampon every 1 - 2 hours for several hours
Heavy periods that regularly last 10 or more days
Bleeding between periods or during pregnancy. Spotting or light bleeding between periods is common in girls just starting menstruation and sometimes during ovulation in young adult women, but it is still a good idea to speak with a doctor.

Amenorrhea is the absence of menstruation. There are two categories: primary amenorrhea and secondary amenorrhea. These terms refer to the time when menstruation stops:

Primary amenorrhea occurs when a girl does not begin to menstruate. Girls who show no signs of sexual development (breast development and pubic hair) by age 13 should be evaluated by a doctor. Any girl who does not have her period by age 15 should be evaluated for primary amenorrhea.
Secondary amenorrhea occurs when periods that were previously regular become absent for at least three cycles.

Oligomenorrhea is a condition in which menstrual cycles are infrequent. It is very common in early puberty and does not usually indicate a medical problem. When girls first menstruate they often do not have regular cycles for a couple of years. Even healthy cycles in adult women can vary by a few days from month to month. In some women, periods may occur every 3 weeks and in others, every 5 weeks. Flow also varies and can be heavy or light. Skipping a period and then having a heavy flow may occur; this is most likely due to missed ovulation rather than a miscarriage. Women should be concerned when periods come less than 21 days or more than 3 months apart, or if they last more than 10 days. Such events may indicate ovulation problems.

Premenstrual syndrome (PMS) is a set of physical, emotional, and behavioral symptoms that occur during the last week of the luteal phase (a week before menstruation) in most cycles. The symptoms typically do not start until at least day 13 in the cycle, and resolve within 4 days after bleeding begins. Women may begin to experience premenstrual syndrome symptoms at any time during their reproductive years. Once established, the symptoms tend to remain fairly constant until menopause, although they can vary from cycle to cycle. About 100 symptoms have been identified with the premenstrual phase. [See In-Depth Report #79: Premenstrual syndrome.]

Causes

Menstrual disorders can be triggered by a number of different factors, such as hormone imbalances, genetic factors, clotting disorders, and pelvic diseases.

Contraction-Causing Chemicals. Powerful chemicals known as prostaglandins and arachidonic acid can induce uterine muscle contractions. Prostaglandins also play a large role in the heavy bleeding that causes dysmenorrhea.
Abnormal Nervous System Response. Some women with primary dysmenorrhea may have autonomic nervous systems that are overly sensitive to menstrual cycle changes. The autonomic nervous system regulates heart rate and blood pressure, and it contains the pain receptors in nerve fibers in the uterus and pelvic area. As a result, women with autonomic nervous system abnormalities may have a more intense response to pain.
Abnormalities in the Arteries in the Uterus.Impaired blood flow through the arteries in the uterus may cause severe dysmenorrhea for some women.
Genetic Factors. Genetic factors may play an important role in over half of primary dysmenorrhea cases.
Endometriosis. Endometriosis is a chronic and often progressive disease that develops when the tissue that lines the uterus (endometrium) grows onto other areas, such as the ovaries, bowels, or bladder. [See In-Depth Report #74: Endometriosis.]

Endometriosis is the condition in which the tissue that normally lines the uterus (endometrium) grows on other areas of the body causing pain and irregular bleeding.

Uterine Fibroids. Fibroids are noncancerous growths that grow on the walls of the uterus. They can cause heavy bleeding during menstruation and cramping pain. [See In-Depth Report #73: Uterine fibroids.]
Other Causes. Pelvic inflammatory disease, ovarian cysts, and ectopic pregnancy. The intrauterine device (IUD) contraceptive can also cause dysmenorrhea.

Hormonal imbalances and uterine fibroids are the most common causes of menorrhagia. Other causes of menorrhagia include:

Dysfunctional Uterine Bleeding (DUB). DUB is a general term for abnormal bleeding. It is usually caused by hormonal problems and is one of the primary causes of menorrhagia. DUB usually occurs either when girls begin to menstruate or when women approach menopause, but it can occur at any time in during a woman's reproductive life. About 90% of DUB events occur when ovulation is not occurring (anovulatory DUB). In such cases, women do not properly develop and release a mature egg. When this happens, the corpus luteum does not form. As a result, estrogen is produced continuously, causing an overgrowth of the uterus lining. The period is delayed in such cases, and when it occurs menstruation can be very heavy and prolonged. The other 10% of DUB cases occur in women who are ovulating (ovulatory DUB), but progesterone secretion is prolonged because estrogen levels are low. This causes irregular shedding of the uterine lining and break-through bleeding.
Von Willebrand Disease and Other Bleeding Disorders. Bleeding disorders that stop blood from clotting can cause heavy menstrual bleeding. Most of these disorders have a genetic basis. Von Willebrand disease is the most common of these bleeding disorders and may be underdiagnosed in many women with unexplained menorrhagia.
Abnormal Blood Vessel Growth. Every month, blood vessels regrow in the uterus to replace the blood-rich uterine lining lost during menstruation. Abnormalities in this growth process (called arteriogenesis or angiogenesis) may occur in some women with menorrhagia.
Abnormalities in the Uterus. Structural problems or other abnormalities in the uterus may cause bleeding. They include uterine polyps (small benign growths in the uterus), uterine fibroids, endometriosis, adenomyosis, and miscarriage. Infections or inflammation in the vagina or pelvic area can also cause heavy bleeding.
Medications. Certain drugs, including anticoagulants and anti-inflammatory medications, can cause heavy bleeding.
Cancer. Uterine, ovarian, and cervical cancer can cause excessive bleeding but these are rare causes.
Other Medical Conditions. Systemic lupus erythematosus, diabetes, pelvic inflammatory disorder, and thyroid disorders can cause heavy bleeding. Women who have migraine headaches may be more likely to experience menorrhagia and endometriosis.

Fibroid tumors may not need to be removed if they are not causing pain, bleeding excessively, or growing rapidly.

Normal causes of skipped or irregular periods include pregnancy, breastfeeding, hormonal contraception, and perimenopause. Skipped periods are also common during adolescence, when it may take a while before ovulation occurs regularly. Consistently absent periods may be due to the following factors:

Delayed Puberty. The most common cause of primary amenorrhea is delayed puberty due to some genetic factor that delays physical development.
Weight Loss and Eating Disorders. Extreme weight loss and reduced fat stores lead to hormonal changes that include low thyroid levels (hypothyroidism) and elevated stress hormone levels (hypercortisolism). These changes produce a reduction in reproductive hormones. A syndrome known as the female athlete triad is associated with hormonal changes that occur with eating disorders in young women who excessively exercise. It comprises anorexia (severe weight loss), amenorrhea, and osteoporosis (decrease in bone density).
Polycystic Ovarian Syndrome (PCOS). PCOS is a condition in which the ovaries produce high amounts of androgens (male hormones), particularly testosterone. PCOS occurs in about 6% of women, and amenorrhea or oligomenorrhea (infrequent menses) is quite common. According to some studies, nearly 30% of obese women with PCOS have amenorrhea.
Elevated Prolactin Levels (Hyperprolactinemia). Prolactin is a hormone produced in the pituitary gland that stimulates breast development and milk production in association with pregnancy. High levels of prolactin (hyperprolactinemia) in women who are not pregnant or nursing can reduce gonadotropin hormones and inhibit ovulation, thus causing amenorrhea. It is the cause of between 10 - 40% of cases of secondary amenorrhea.
Premature Ovarian Failure (POF). POF is the early depletion of follicles before age 40. In most cases it leads to premature menopause. POF is a significant cause of infertility.
Structural Problems. In some cases, structure problems or scarring in the uterus may prevent menstrual flow. Inborn genital tract abnormalities may also cause primary amenorrhea. A specific malformation called Mullerian agenesis, in which no vagina or uterus develops, is rare but still causes about 16% of primary amenorrhea cases.
Stress. Physical and emotional stress may block the release of luteinizing hormone, causing temporary amenorrhea
Other Medical Conditions. Epilepsy, thyroid problems, celiac sprue, metabolic syndrome, and Cushing's disease are associated with amenorrhea.

If the ovaries produce too much androgen (hormones such as testosterone) a woman may develop male characteristics. This ovarian imbalance can be caused by tumors in the ovaries or adrenal glands, or polycystic ovarian disease. Virilization may include growth of excess body and facial hair, amenorrhea (loss of menstrual period) and changes in body contour.

Risk Factors

Age plays a key role in menstrual disorders. Girls who start menstruating at age 11 or younger are at higher risk for severe pain, longer periods, and longer menstrual cycles. Between 20 - 90% of teenage girls report menstrual pain and about 15% report that it is severe. Adolescents may experience amenorrhea before their ovulating cycles become regular.

Women who are approaching menopause (perimenopause) may also skip periods. Occasional episodes of heavy bleeding are also common as women approach menopause.

Other risk factors include:

Weight. Being either excessively overweight or underweight can increase the risk for dysmenorrhea and amenorrhea.
Smoking and Alcohol Use. Smokers have a 50% higher risk than nonsmokers for menstrual pain. Alcohol does not cause menstrual pain, but in women with existing dysmenorrhea, alcohol consumption may prolong the pain.
Stress. Physical and emotional stress may block the release of luteinizing hormone, causing temporary amenorrhea. Emotional problems, including history of sexual abuse, may predispose to dysmenorrhea.
Menstrual Cycles and Flow. Longer and heavier menstrual cycles can cause dysmenorrhea.
Pregnancy History. Women who have had a higher number of pregnancies are at increased risk for menorrhagia. Women who have never given birth are at increased risk of dysmenorrhea, while women who first gave birth at a young age are at lower risk.
Chronic Pelvic Pain. Many women experience chronic pain in the pelvic area. This pain can be due to gynecologic reasons (fibroids, endometriosis, pelvic inflammatory disease) or non-gynecologic causes (irritable bowel syndrome, interstitial cystitis, diverticulitis).

Exercise and oral contraceptive use may help protect against dysmenorrhea.

Complications

An estimated 10 - 15% of all women in their reproductive years have chronic gynecologic problems. Nearly 30% of women reporting such problems spend one or more days in bed per year because of them. In fact, menstrual pain is the primary cause of short-term absences in school age girls. In adult women, who have not received treatment, it is an important cause of reduced work productivity.

Menorrhagia is the most common cause of anemia in premenopausal women. A blood loss of more than 80mL per menstrual cycle can trigger anemia. According to one report, 10% of women in their reproductive years have iron deficiencies, and between 2 - 5% have iron levels low enough to cause anemia. Although poor diets play a role in many cases, the problem is compounded in women who have heavy periods.

Most cases of anemia are mild. Nevertheless, even mild anemia can reduce oxygen transport in the blood, causing fatigue and a diminished physical capacity. (Some studies indicate that even iron deficiency without anemia can produce a subtle but still lower capacity for exercise.) Moderate-to-severe iron-deficiency anemia is known to reduce endurance.

Moderate-to-severe anemia can also cause shortness of breath, rapid heart rate, lightheadedness, headaches, ringing in the ears (tinnitus), irritability, pale skin, restless legs syndrome, and mental confusion. Heart problems can occur in prolonged and severe anemia that is not treated. Pregnant women who are anemic, particularly in the first trimester, have an increased risk for a poor pregnancy outcome. [See In-Depth Report #57: Anemia.]

Amenorrhea caused by reduced estrogen levels increases the risk for osteoporosis (loss of bone density). Conditions that are associated with low estrogen levels include eating disorders, the female-athlete triad (excessive exercise and weight loss), pituitary tumors, and premature ovarian failure. Because bone growth is at its peak in adolescence and young adulthood, losing bone density at that time is very dangerous, and early diagnosis and treatment is essential for long-term health. [See In-Depth Report #18: Osteoporosis.]

Osteoporosis is a condition characterized by progressive loss of bone density, thinning of bone tissue, and increased vulnerability to fractures. Osteoporosis may result from disease, dietary or hormonal deficiency, or advanced age. Regular exercise and vitamin and mineral supplements can reduce and even reverse loss of bone density.

Some conditions associated with heavy bleeding, such as ovulation abnormalities, fibroids, or endometriosis, are important contributors to infertility. Many conditions that cause amenorrhea, such as ovulation abnormalities and polycystic ovary syndrome, can also cause infertility. Irregular periods from any cause may make it more difficult to conceive. In some cases treating the underlying condition can restore fertility. In other cases, specific fertility treatments that use assisted reproductive technologies may be beneficial. [See In-Depth Report #22: Infertility in women.]

Diagnosis

A doctor needs to have a complete history of any medical or personal conditions that might be causing menstrual disorders. This information can help determine whether a menstrual problem is caused by another medical condition. For example, non-menstrual conditions that may cause abdominal pain include appendicitis, urinary tract infections, ectopic pregnancy, and irritable bowel syndrome. Endometriosis and fibroids may cause heavy bleeding and pain. Doctors may ask questions concerning:

Menstrual cycle patterns -- length of time between periods, number of days that periods last, number of days of heavy or light bleeding
The presence or history of any medical conditions that might be causing menstrual problems
Any family history of menstrual problems
History of pelvic pain
Regular use of any medications (including vitamins and over-the-counter drugs)
Diet history, including caffeine and alcohol intake
Past or present contraceptive use
Any recent stressful events
Sexual history (it is very important that patients trust their doctor enough to describe any sexual activity that might be risky)

Menstrual Diary. A menstrual diary is a helpful way to keep track of changes in menstrual cycles. Patients can record when their period starts, how long it lasts, and the amount of bleeding and pain that occurs during the course of menstruation.

Pelvic Examination. A pelvic exam is a standard part of diagnosis. A Pap test may be done during this exam.

Blood tests can help rule out other conditions that cause menstrual disorders. For example, a doctor may test thyroid function to make sure that low thyroid (hypothyroidism) is not present. Blood tests can also check follicle-stimulating hormone, estrogen, and prolactin levels. Patients who have menorrhagia may get tests for bleeding disorders. If patients are losing a lot of blood, they should also get tested for anemia.

Patients who have amenorrhea may need to receive special hormonal tests. The progestational challenge test uses oral or injected progesterone to test for a functional uterine lining (endometrium):

Bleeding that occurs up to 3 weeks after the progesterone dose suggests that the woman has normal estrogen levels but is not ovulating, particularly if thyroid and prolactin levels are normal. In such cases, the doctor will check for stress, recent weight loss, and any medications. Such results could also suggest polycystic ovaries or stress.
A failure to bleed could indicate an abnormal uterus that prevents outflow or insufficient estrogen. In such cases, the next step may be to administer estrogen followed by progestin. If bleeding occurs after that, then the cause of amenorrhea is related to low estrogen levels. The doctor will then check for ovarian failure, anorexia, or other causes of low estrogen. If bleeding does not occur, then the doctor would check for obstructions that are preventing outflow of menstruation.

Imaging techniques are often used to detect certain conditions that may be causing menstrual disorders. Imaging can help diagnose fibroids, endometriosis, or structural abnormalities of the reproductive organs.

Ultrasound and Sonohysterography. Ultrasound is the standard imaging technique for evaluating the uterus and ovaries, detecting fibroids, ovarian cysts and tumors, and finding obstructions in the urinary tract. It uses sound waves to produce an image of the organs. Ultrasound carries no risk and causes very little discomfort.

Transvaginal sonohysterography uses ultrasound along with saline injected into the uterus to enhance the visualization of the uterus.

Hysteroscopy. Hysteroscopy is a procedure that may be used to detect the presence of fibroids, polyps, or other causes of bleeding. It may miss cases of uterine cancer, however, and is not a substitute for more invasive procedures, such as D&C or endometrial biopsy, if cancer is suspected.

It is done in the office setting and requires no incisions. The procedure uses a long flexible or rigid tube called a hysteroscope, which is inserted into the vagina and through the cervix to reach the uterus. A fiber optic light source and a tiny camera in the tube allow the doctor to view the cavity. The uterus is filled with saline or carbon dioxide to inflate the cavity and provide better viewing. This can cause cramping.

Hysteroscopy is non-invasive, but 30% of women report severe pain with the procedure. The use of an anesthetic spray such as lidocaine may be highly effective in preventing pain from this procedure. Other complications include excessive fluid absorption, infection, and uterine perforation. Hysteroscopy is also performed as part of surgical procedures.

Laparoscopy. Diagnostic laparoscopy, an invasive surgical procedure, is currently the only definitive method for diagnosing endometriosis. Laparoscopy normally requires a general anesthetic, although the patient can go home the same day. The procedure is as follows:

Click the icon to see an image of laparoscopy.

The surgeon makes tiny abdominal incisions through which a fiber optic tube, equipped with small camera lenses, is inserted. The doctor uses these devices to view the uterus, ovaries, tubes, and peritoneum (lining of the pelvis) on a video monitor.
Carbon dioxide gas is injected into the abdomen, distending it and pushing the bowel away so that the doctor has a wider view.
A blue dye may be flushed through the fallopian tubes to determine blockage; if there is an obstruction, the dye will not flow through the tube.
If the surgeon needs to remove small endometrial cysts or other lesions during the procedure (operative laparoscopy), tiny surgical instruments are passed through a tube.

The procedure is used for detecting and staging endometriosis to determine its severity. In some cases, the procedure itself will restore fertility in women with endometriosis.

Transvaginal Hydrolaparoscopy. Transvaginal hydrolaparoscopy is a new and less invasive approach than laparoscopy, since the instruments are inserted through the vagina, not through incisions in the abdomen. It requires only sedation, does not use CO2 to distend the abdomen, and has a much shorter and easier recovery than with standard laparoscopy. When used by a skilled professional, it is as accurate as laparoscopy, but is not yet widely available.

Endometrial Biopsy With or Without Dilation and Curettage (D&C). When heavy or abnormal bleeding occurs, an endometrial (uterine) biopsy can be performed in the office along with an ultrasound. It is usually used with a procedure called dilation and curettage (D&C), which is particularly important to rule out uterine (endometrial) cancer. A D&C is a somewhat invasive procedure:

A D&C is usually done in an outpatient setting so that the patient can return home the same day, but it sometimes requires a general anesthetic. It may need to be performed in the operating room to rule out serious conditions or treat some minor ones that may be causing the bleeding.
The cervix (the neck of the uterus) is dilated (opened).
The surgeon scrapes the inside lining of the uterus and cervix.

The procedure is used to take samples of the tissue and to relieve heavy bleeding in some instances. D&C can also be effective in scraping off small endometrial polyps, but it is not very useful for most fibroids, which tend to be larger and more firmly attached.

Click the icon to see an image of a D&C.

Treatment

Making dietary adjustments starting about 14 days before a period may help some women with certain mild menstrual disorders, such as cramping. The general guidelines for a healthy diet apply to everyone; they include eating plenty of whole grains, fresh fruits and vegetables, and avoiding saturated fats and commercial junk foods.

Dietary Fats. A 2000 study reported that women who followed a low-fat vegetarian diet for two menstrual cycles experienced less pain and bloating and a shorter duration of premenstrual symptoms than those who ate meat. Women who are losing too much blood, however, may need meat to help maintain iron levels. Choosing more fish and eggs may be a helpful alternative.

More than one study has reported less menstrual pain with a higher intake of omega 3 fatty acids (fat compounds found in oily fish, such as salmon and tuna). In one study, supplements of fish oil also appeared to reduce heavy bleeding in adolescent girls.

Salt Restriction. Limiting salt may help bloating.

Reducing Caffeine, Sugar, and Alcohol. Reducing caffeine, sugar, and alcohol intake may be beneficial. The effects of alcohol are mixed. One study found that women who drank less wine had less menstrual pain than those who drank more wine. Another reported that regular consumption of alcohol lowered the risk for developing cramps, but it actually increased the length of cramping time in certain women. In any case, alcohol is certainly not recommended for relieving menstrual disorders.

Forms of Iron. Women who have heavy menstrual bleeding can sometimes become anemic. Eating iron-rich foods can help prevent anemia. Iron found in foods is either in the form of heme or non-heme iron. Heme iron is better absorbed than non-heme iron.

Foods containing heme iron are the best for increasing or maintaining healthy iron levels. Such foods include (in order of iron-richness) clams, oysters, organ meats, beef, pork, poultry, and fish.
Non-heme iron is less well absorbed. About 60% of iron in meat in non-heme (although meat itself helps absorb non-heme iron). Eggs, dairy products, and iron-containing vegetables only have the non-heme form. Such vegetable products include dried beans and peas, iron-fortified cereals, bread, and pasta products, dark green leafy vegetables (chard, spinach, mustard greens, kale), dried fruits, nuts, and seeds.

The absorption of non-heme iron often depends on the food balances in meals. The following are foods that enhance absorption of non-heme iron:

Meat and fish not only contain heme iron, the best form for maintaining stores, but they also help absorb non-heme iron.
Increasing intake of vitamin C rich foods can enhance absorption of non-heme iron during a single meal. In any case, vitamin C rich foods are healthful and include broccoli, cabbage, citrus fruits, melon, tomatoes, and strawberries. One orange or six ounces of orange juice can double the amount of iron the body absorbs from plant foods. (Taking vitamin C supplements does not appear to have any significant effect on iron stores.)

Exercise may help reduce menstrual pain. It is not clear, however, how intense the exercise should be to reduce dysmenorrhea. For example young female athletes in a 2001 study were only half as likely to suffer from dysmenorrhea as their non-active peers. However, they were also three times more likely to experience an absence of periods. Exercise may be very helpful for women with menstrual pain due to endometriosis. It relieves stress and tension and may reduce hormonal levels that could contribute to endometrial growth.

Sexual Activity. There have been reports that orgasm reduces the severity of menstrual cramps.

Applying Heat. One study found that continuously applying a heated abdominal pad for 12 hours 2 days in a row was as effective in reducing menstrual cramps as ibuprofen (Advil). A warm bath may also be helpful.

Menstrual Hygiene. Tampons should be changed every 4 - 6 hours. Scented pads and tampons should be avoided; feminine deodorants can irritate the genital area. Women should not douche during or between periods. Women who douche on a weekly basis are more likely to contract cervical cancer than those who do not. Douching may destroy the natural bacteria normally present in the vagina. Bathing regularly is sufficient.

Acupuncture and Acupressure. Some studies, including a small well-conducted trial, have reported relief from pelvic pain after acupuncture or acupressure, a technique that applies small pins or pressure to specific points on the body. Some women report relief with reflexology, an acupuncture technique that uses manual pressure on acupuncture points on the ears, hands, and feet.

Yoga and Meditative Techniques. Yoga and meditative techniques that promote relaxation may help relieve menstrual cramps.

Chiropractic. Some women with primary dysmenorrhea have sought help from chiropractors trained in spinal manipulation. One study compared a high-force spinal manipulation technique with a low-force maneuver used as a placebo technique. Both showed lower scores on tests that measure pain, perhaps indicating that a simple back rub by a sympathetic partner or friend may be helpful.

Herbs and Supplements. Studies have not generally found herbal or natural remedies to be any more effective than placebos for reducing menstrual disorders. Natural remedies for menstrual symptoms include:

Evening primrose oil. Evening primrose oil contains a polyunsaturated fatty acid known as gamma linolenic acid. This compound seems to block the release of cytokines and prostaglandins, immune system factors that are manufactured by the endometrium. These factors are involved in uterine muscle contraction and cramping. Foods that contain gamma linolenic acid include black currant oil and cold-water fish.
Omega-3 fatty acids. There is some evidence that the fatty acids found in fish oil have anti-inflammatory properties that may help relieve menstrual cramps. Omega-3 fatty acids are available in supplement pill form, but diets that include cold-water fish (tuna, salmon, mackerel) provide the best source for these nutrients.
Ginger. Ginger tea or capsules may help to relieve nausea and bloating.
Aromatherapy. Aromatherapy with topically-applied lavender, sage, and rose oils may help ease menstrual cramps, according to a small 2006 study.
Pycnogenol. Pycnogenol, an extract from the bark of the French maritime pine tree, may help reduce menstrual pain and discomfort, according to some small studies.

Generally, manufacturers of herbal remedies and dietary supplements do not need FDA approval to sell their products. Just like with drugs, herbs and supplements can affect the body's chemistry, and therefore have the potential to produce side effects that may be harmful. There have been a number of reported cases of serious and even lethal side effects from herbal products. Patients should check with their doctor before using any herbal remedies or dietary supplements.

The following are special concerns for people taking natural remedies for menstrual disorders:

Valerian has been used by some women for menstrual cramps. This herb is listed on the FDA's list of generally safe products. However, its calming effects can be dangerously increased if it is used with sedative drugs. Other interactions and long-term side effects are unknown.
Black cohosh (also known as Cimicifuga racemosa or squawroot) contains a plant estrogen and is the most studied herbal remedy for treating menopausal symptoms, although a 2006 study indicated it is ineffective. Some women also use it for dysmenorrhea. Black cohosh has been used for decades in Germany and appears to be safe, but because its actions resemble estrogen more clinical studies are needed to confirm both long-term safety and effectiveness. Headaches and gastrointestinal problems are common side effects. At this time, experts do not recommend taking it for more than 6 months.

Medications

There are a number of different medicines prescribed for menstrual disorders.

Nonsteroidal Anti-inflammatory Drugs (NSAIDs). Nonsteroidal anti-inflammatory drugs (NSAIDs) block prostaglandins, the substances that increase uterine contractions. They are effective painkillers that also help control the inflammatory factors that may be responsible for heavy menstrual bleeding. Aspirin is the most common NSAID, but there are dozens of others available over the counter or by prescription.

Among the most effective NSAIDs for menstrual disorders are ibuprofen (Advil, Motrin, Midol PMS), naproxen (Aleve, Naprosyn, Naprelan, Anaprox), and mefenamic acid (Ponstel). In a comparison study of ibuprofen and naproxen, both were effective, but the effects of naproxen lasted longer. Naproxen, however, may carry a higher risk for gastrointestinal (GI) effects than ibuprofen. Long-term use of any NSAID can increase the risk for GI bleeding and ulcers. Long-term NSAID use can also increase the risk for heart attack and stroke.

An ulcer is a crater-like lesion on the skin or mucous membrane caused by an inflammatory, infectious, or malignant condition. To avoid irritating an ulcer a person can try eliminating certain substances from their diet such as caffeine, alcohol, aspirin, and avoid smoking. Patients can take certain medicines to suppress the acid in the stomach causing the erosion of the stomach lining. Endoscopic therapy can be used to stop bleeding from the ulcer.

Acetaminophen. Some evidence suggests that acetaminophen (Tylenol) reduces levels of female hormones (gonadotropins and estradiol, an estrogen), which may have some beneficial effect on menstrual disorders. A combination of acetaminophen and pamabrom (Women's Tylenol Menstrual Relief) is specifically aimed at treating menstrual pain and bloating. (Pamabrom is a diuretic, a drug used to reduce fluid build-up and bloating.) One study indicated that acetaminophen is less effective than NSAIDs for dysmenorrhea, but does not have the same potentially harmful effects on the gastrointestinal tract.

Oral contraceptives (OCs), commonly called "the Pill" collectively, contain combinations of an estrogen and a progestin (either a natural progesterone or the synthetic form called progestogen). The estrogen compound used in most combination OCs is estradiol. There are many different progestins, but commonly used types include levonorgestrol, drospirenone, norgestrol, norethindrone, and desogestrel. (Combination contraceptives are also available in other forms, including patches and vaginal rings, but they may increase the risk for menstrual cramping and bleeding.)

Click the icon to see an image of hormone-based contraceptives.

OCs are often used to regulate periods in women with menstrual disorders, including menorrhagia (heavy bleeding), dysmenorrhea (severe pain), and amenorrhea (absence of periods). Oral contraceptives are as effective for treating pain from endometriosis as the more potent gonadotropin releasing hormone agonists. They also protect against ovarian and endometrial cancers.

High-dose OCs have been specifically helpful for adolescents with severe dysmenorrhea. Studies with low-dose OCs have also shown they can reduce menstrual pain for adolescents and adults.

OCs may be taken in cycles that include pills of the same or different strengths. These are categorized as monophasic (one-phase), biphasic (two-phase), or triphasic (three-phase). Monophasic pills contain the same amount of hormones in each dose. Biphasic and triphasic pills contain different dosages of hormones with the pill packs. The monophasic regimen is the most studied regimen and is usually recommended for dysmenorrhea as well as premenstrual symptoms.

Continuous-Dosing OCs. Standard OCs usually come in a 28-pill pack with 21 days of “active” (hormone) pills and 7 days of “inactive” (placebo) pills. Newer “continuous-dosing” (also called “continuous-use”) oral contraceptives aim to reduce -- or even eliminate -- monthly menstrual periods. These OCs contain a combination of estradiol and the progesterone levonorgestrel, but use extending dosing of active pills.

Seasonale, the first continuous-dosing contraceptive, was approved in 2003. It contains 81 days of active pills followed by 7 days of inactive pills. Women who take Seasonale have on average a period every 3 months. Seasonique, a follow-up to Seasonale, was approved in 2006. As with Seasonale, it produces about 4 periods a year. With Seasonique, a woman takes 84 days of levonorgestrol-estradiol pills followed by 7 days of pills that contain only low-dose estradiol.

In 2007, the FDA approved Lybrel, which supplies a daily low dose of levonorgestrol and estradiol with no inactive pills. Because Lybrel contains only active pills, which are taken 365 days a year, it completely eliminates monthly menstrual periods. In clinical trials, 59% of women who took Lybrel completely stopped menstrual periods by the end of the first year. Some women, however, experienced occasional unscheduled bleeding or spotting during the first 3 - 6 months.

Side effects. Common side effects of combination OCs include headache, nausea, bloating, breast tenderness, and bleeding between periods. The estrogen component in combination OCs is usually responsible for these side effects. In general, today’s OCs are much safer than OCs of the past because they contain much lower dosages of estrogen.

However, all OCs can increase the risk for migraine, stroke, heart attack, and blood clots. The risk is highest for women who smoke or who have a history of heart disease risk factors (such as high blood pressure or diabetes) or past cardiac events. Women who have certain metabolic disorders, such as polycystic ovary syndrome (PCOS), are also at higher risk for the heart-related complications associated with these pills.

Progestins (either natural progesterone or synthetic progestogen) are used by women with irregular or skipped periods to restore regular cycles. Because of this, they may also help menstrual pain. They also reduce heavy bleeding and may protect against uterine and ovarian cancers. Progestin-only contraceptives may be a good option for women who are not candidates for estrogen-containing OCs, such as women smokers over the age of 35.

Progestins can be delivered in various forms:

Levonorgestrel-Releasing Intrauterine System (LNG-IUS). An intrauterine device (IUD) that releases progestin can be very beneficial for menstrual disorders, regardless of its contraceptive effects. In the United States, a levonorgestrel-releasing intrauterine system, also called an LNG-IUS, is sold under the brand name Mirena. The LNG-IUS has been proven to reduce heavy bleeding and pain in many women who suffer from menorrhagia and dysmenorrhea. In a 3-year study, the proportion of women with dysmenorrhea using the LNG-IUS dropped from 60% to about 30%. Some studies suggest that the LNG-IUS is more effective than oral contraceptives for controlling heavy menstrual bleeding.

Many experts now recommend the LNG-IUS as a first-line treatment for menorrhagia, particularly for women who may face hysterectomy (removal of uterus), conservative surgery such as endometrial resection (removal of endometrial lining), or endometrial ablation (destruction of endometrial lining). Studies report that about 60% of women with menorrhagia who use the LNG-IUS are able to avoid hysterectomy. Some clinical trials suggest that endometrial resection or ablation may be better at reducing menstrual bleeding than the LNG-IUS. Other studies report that the device is as effective as conservative surgery. Research also indicates that women who choose the LNG-IUS are as satisfied with their quality of life as those who choose surgery.

The LNG-IUS remains in place in the uterus and releases the progestin levonorgestrel for up to 5 years. Progestin released by an IUD mainly affects the uterus and cervix, and so it causes fewer widespread side effects than progestin pills do. (However, the other major IUD -- the Copper T -- may increase bleeding.)

After the LNG-IUS is inserted, heaver periods may occur during the first 3 - 6 months as the lining of the uterus is shed. This shedding may also cause irregular periods and light bleeding (“spotting”) between menstrual cycles. Eventually, the LNG-IUS results in a shorter period, with little or no blood flow. For many women, the LNG-IUS completely stops menstrual periods.

Common side effects include cramping, acne, back pain, breast tenderness, headache, mood changes, and nausea. The LNG-IUS may increase the risk for ovarian cysts, but such cysts usually cause no symptoms and resolve on their own. Women who have a history of pelvic inflammatory disease or who have had a serious pelvic infection should not use the LNG-IUS.

Injections (Depo-Provera). Depo-Provera uses a progestin called medroxyprogesterone. Most women who use Depo-Provera stop menstruating altogether after a year. Depo-Provera may be beneficial for women with heavy bleeding, severe cramps, or both. Women who eventually want to have children should be aware that Depo-Provera can cause persistent infertility for up to 22 months after the last injection, although the average is 10 months.

Weight gain can be a problem, particularly in women who are already overweight. Women should not use Depo-Provera if they have a history of liver disease, blood clots, stroke, or cancer of the reproductive organs.

Long-term (more than 2 years) use of Depo-Provera can cause loss of bone density. In 2004, the FDA added a “black box” warning to the Depo-Provera label advising of this risk. The warning notes that the decline in bone density increases with duration of use and may not be completely reversible even after the drug is discontinued. Based on this information, the FDA recommends that Depo-Provera should not be used for longer than 2 years unless other birth control methods are inadequate. [See In-Depth Report #91: Birth control options for women.]

Gonadotropin releasing hormone (GnRH) agonists are sometimes used to treat menorrhagia. GnRH agonists block the release of the reproductive hormones LH (luteinizing hormone) and FSH (follicular-stimulating hormone). As a result, the ovaries stop ovulating and no longer produce estrogen. GnRH agonists include goserelin (Zoladex), buserelin, a monthly injection of leuprolide (depot Lupron), and a nasal spray, Nafarelin (Synarel). Such drugs may be used alone or in preparation for procedures used to destroy the uterine lining. They are not generally suitable for long-term use.

Commonly reported side effects, which can be severe in some women, include menopausal-like symptoms. These symptoms include hot flashes, night sweats, changes in the vagina, weight change, and depression. The side effects vary in intensity depending on the GnRH agonist. They may be more intense with leuprolide and persist after the drug has been stopped.

The most important concern is possible osteoporosis from estrogen loss. Women ordinarily should not take these drugs for more than 6 months. Certain approaches may preserve enough estrogen to protect bones and still effectively relieve endometriosis symptoms:

Add-back therapy, which provides doses of estrogen and progestin that are high enough to maintain bone density, but are too low to offset the beneficial effects of the GnRH agonist.
Intermittent leuprolide, which uses repeated 6-month courses of GnRH agonists followed by an average of 9 months of symptom control only.
Taking GnRH agonists in very low doses is an alternate approach, but is still largely untested.
Adding a bone-protective drug called a bisphosphonate (alendronate or etidronate) may be helpful.
Other drugs are being tested in combination with a GnRH agonist to preserve bone. They include parathyroid hormone or selective estrogen-receptor modulators (SERMs).

GnRH treatments used alone do not prevent pregnancy. Furthermore, if a woman becomes pregnant during their use, there is some risk for birth defects. Women who are taking GnRH agonists should use non-hormonal birth control methods, such as the diaphragm, cervical cap, or condoms while on the treatments.

Danazol (Danocrine) is a synthetic substance that resembles a male hormone. It suppresses estrogen, and therefore menstruation, and is used (sometimes in combination with an oral contraceptive), to help prevent heavy bleeding. It may also improve surgical success rates in women with menorrhagia when used before ablation or resection to destroy the uterine lining. It is not suitable for long-term use.

Adverse side effects include facial hair, deepening of the voice, weight gain, acne, and dandruff. It may also increase the risk for unhealthy cholesterol levels. Pregnant women or those trying to become pregnant should not take this drug because it may cause birth defects. [See In-Depth Report #74: Endometriosis or In-Depth Report #63: Uterine fibroids.]

Surgery

Women with heavy menstrual bleeding, dysmenorrhea, or both have medical and surgical options available to them. Most procedures eliminate the possibility for childbearing, however. Hysterectomy removes the entire uterus while ablation and resection destroy most or all of uterine lining.

For some women, an intrauterine device (IUD) that releases hormones is proving to be a good medical alternative to surgery. The levonorgestrel-releasing intrauterine system, or LNG-IUS (Mirena), is increasingly being used to treat menorrhagia. Many experts recommend it as a first-line treatment for heavy bleeding. Studies have found the LNG-IUS to work just as well as ablation and resection. Women should be sure to ask their doctors about all medical options before undergoing surgical procedures.

In either standard endometrial resection or ablation, the entire lining of the uterus (the endometrium) is removed or destroyed. The standard endometrial ablation and resection techniques are equally effective in reducing bleeding. In general, either one reduces bleeding by about half. About 15% of women require a hysterectomy later on. Some recent studies report that microwave endometrial ablation may work better than resection, and considerably reduce the need for future hysterectomy. Women should discuss with their surgeon which procedure may be best for them.

Hormonal Pretreatment. Hormonal drugs, such as GnRH analogs or danazol, are sometimes used before the procedures to help prepare the uterus by thinning the endometrial lining. However, a 2005 study suggested that drug preparation may not be required before microwave endometrial ablation.

Postoperative Effects of Endometrial Ablation or Resection Procedures. Postoperative effects of either procedure include the following:

Anesthesia may cause nausea and even vomiting for a few hours following the operation.
Cramping and pain occurs but can usually be relieved using over-the-counter painkillers.
Patients may experience frequent urination for the first day after the procedure and blood-tinged, watery vaginal discharge for more than a month.

Complications of Endometrial Ablation or Resection Procedures. Complications from either procedure may include perforation of the uterus, injury to the intestine, hemorrhage, or infection.

In standard resection and ablation, the uterine cavity is expanded by filling it with fluid. In rare instances, excess glycine from the fluid instilled in the uterus builds up in the bloodstream and causes an abnormal drop in sodium levels. This can be a serious event resulting in mental confusion, convulsions, and, very rarely, death. General anesthesia may pose a lower risk for this complication than local. Some of the newer ablation procedures do not require fluid instillation.

In a 2002 study, 10% of patients who were given standard ablation using the roller ball technique experienced blockage or blood build-up in the fallopian tubes that require a follow-up procedure or a hysterectomy later on.

Resection procedures benefit those women who have very heavy menstrual bleeding but do not have any other underlying uterine problems, such as polyps, hyperplasia of the endometrium, or cancer. Resection also seems to have a higher success rate in reducing bleeding and relieving pain in older women than younger women.

Resection procedures typically involve the following:

The patients are given a local or general anesthesia.
The surgeon dilates (widens) the cervix and fills the uterine cavity with fluid to improve visualization.
The surgeon then removes the uterine lining.

Endometrial ablation involves the destruction of the uterine lining using a number of approaches that include heat, electricity, laser energy, and other methods. The standard ablation approach uses hysteroscopy to allow the doctor to view the uterus.

A typical procedure uses the following approach:

The doctor uses hysteroscopy to view the uterine cavity. This is a fiber optic light source inside a long flexible or rigid tube, which is inserted into the uterus in order to view the cavity. The image of the uterine cavity is transmitted by camera lenses to a video screen.
The uterine cavity is filled with fluid for better visualization. A special substance such as glycine, sorbitol, or mannitol may be added to the fluid so that it does not conduct electricity. This process prevents accidental burns.
With ablation, uterine tissue is usually vaporized using a thin powerful laser beam or high electric voltage. One ablation technique, known as electrocautery with roller ball diathermy, uses a device that looks like a tiny steamroller. This device applies heat and destroys endometrial tissue as it rolls across the uterine lining.
The procedure typically takes 15 - 45 minutes. Although a general anesthetic is usually required, the patient can go home the same day.

It takes about 3 months to determine whether the procedure has been effective. There should be a follow-up appointment about 2 weeks after the procedure. One study revealed 80% of the women were satisfied with ablation. However, this was lower than the 89% satisfaction rate reported by women who had hysterectomy. About 30% of women who have this procedure still require additional surgeries, including hysterectomies, within 5 years. The risk is higher in younger women. The risk for complications increases with repeat ablations.

Newer endometrial ablation techniques (described below) do not use the hysteroscopy. These “second-generation” procedures are technically easier to perform than standard ablation and may be less dependent on the skill of the surgeon. A 2005 review found that second-generation procedures reduce surgery time. Women who had the newer procedures were less likely to experience fluid buildup, perforation of the uterus, cervical cuts and tears, or accumulation of blood in the uterus. However, women did experience more nausea, vomiting, and cramping.

Balloon Endometrial Ablation. Balloon ablation (ThermaChoice in the U.S., Cavaterm in Europe) is proving to be very effective:

A balloon at the tip of a catheter tube is filled with fluid and inflated until it conforms to the walls of the uterus.
A probe in the balloon heats the fluid to destroy the endometrial lining.
After 8 minutes the fluid is drained out and the balloon is removed.

Studies show that bleeding is controlled in 70 - 90% of patients for at least 5 years. It is fast, simple to perform, and comparison studies suggest that it is as effective as resection and standard ablation.

Treatment is less likely to succeed in younger women, those with a tipped uterus, when the uterine lining is 4 mm or thicker, and when menstrual bleeding is prolonged. Pregnancy is possible if some of the lining is maintained, but generally women should not depend on it to preserve fertility.

Electric Wand Ablation. This approach involves inserting a slender wand up through the cervix (the NovaSure System). A triangular mesh-like device is then passed through the wand and expands to fit the uterus. Electrical energy is passed through it for about 90 seconds and the mesh and wand are then withdrawn. As with many other second-generation ablation techniques, it is quick, effective, and does not require pretreatment to expand the uterus. In a 2003 study, it achieved significantly lower bleeding rates than balloon ablation.

Freezing (Cryoablation). With cryoablation (Her Option Uterine Cryoablation Therapy System), the uterine tissue is frozen, which destroys the lining. The procedure takes about 10 minutes to destroy the lining, and it requires no fluid to expand the uterus and little anesthetic. Ultrasound is used to guide the procedure so that the surgeon can view the depth of the ablation. In a 2003 study, cryoablation was slightly less successful than a standard ablation procedure. However, bleeding still declined by 92% with the freezing technique, and quality of life significantly improved.

Hot Saline. Another recently approved technique [Hydro-Therm-Ablator (HTA) system] uses hot saline (salt water) to destroy the lining. It takes about 10 minutes to do this. This is not a "blind" procedure but uses hysteroscopy so that the surgeon can view the uterus.

Laser Ablation. Endometrial laser intrauterine thermotherapy (ELITT) is an ablation technique that does not require either fluid or devices for expanding the uterus or direct contact with the endometrium. This appears to be a very effective approach.

Microwave Endometrial Ablation. Microwave endometrial ablation applies very low-power microwaves to the uterus, which limits tissue destruction only to the lining without causing any unnecessary harm to other tissues. It takes about 3 minutes. Studies report success rates equal to standard ablation and resection procedures.

Until recently, hysterectomy was the only surgical option for uterine fibroids. Other procedures, however, are now available:

Myomectomy. Myomectomy is the surgical removal of only one or more fibroids. Myomectomy usually involves a laparotomy (a procedure that uses a wide abdominal incision) or less invasive surgical techniques, such as laparoscopy and hysteroscopy. In such cases, unlike with hysterectomy, this technique may preserve fertility.
Uterine Artery Embolization (UAE). UAE, also called uterine fibroid embolization (UFE), is a non-surgical radiology procedure. An interventional radiologist injects small plastic particles through a catheter placed in the uterine artery. The particles block the blood supply to the fibroids and cause them to shrink.
Other Procedures. Endometrial ablation (destruction of the lining of the uterus) may be useful in women with small fibroids and heavy bleeding. Myolysis is another procedure best suited for women with specific types of small fibroids. Magnetic resonance-guided focused ultrasound (MRgFUS) is the newest type of fibroid procedure. Myolysis and MRgFUS use heat to cut off the blood supply to fibroids.

Women should discuss each option with their doctor. Deciding on the surgical procedure depends on the location, size, and number of fibroids. Certain procedures affect a women’s fertility and are recommended only for women who are past childbearing age or who do not want to become pregnant. The risk for bleeding increases with the surgeon's inexperience, so patients are urged to investigate the surgeon's track record. [See In-Depth Report #73: Uterine fibroids.]

Hysterectomy is the surgical removal of the uterus and is the second most frequently performed surgery in premenopausal women (Cesarean sections are first). About 600,000 hysterectomies are performed each year in the U.S., which is among the highest rate of all countries. By age 60, about a third of American women have had this procedure. The highest hysterectomy rates are in women age 40 - 44. Women in the southern and midwestern areas of the United States are more likely to have the operation than those in the northeast and west.

Click the icon to see an illustrated series detailing a hysterectomy.

A 2007 study suggested that a combination of factors predicts whether a woman will decide to have a hysterectomy. A woman who meets all three of these factors has a 95% chance of having a hysterectomy:

Presence of symptoms (pelvic pain, bleeding, symptomatic fibroids)
Lack of symptom improvement or resolution despite treatment
Previous use of GnRH agonist drugs

Heavy bleeding, often from fibroids, is the reason for about two-thirds of all hysterectomies. However, in about half of these hysterectomies, no abnormalities are detected to explain the bleeding. In one European study, women with menorrhagia were more likely to choose hysterectomy over conservative treatment if they also had pelvic pain and were inconvenienced by the heavy bleeding. The number of procedures has continued to increase, but the rise has slowed substantially in recent years.

In its support, hysterectomy, unlike medical treatments and less invasive procedures, cures menorrhagia completely, and most women are satisfied with the procedure. Less invasive hysterectomy procedures are also improving recovery rates and increasing satisfaction afterward.

Still, in one study in 70% of cases when doctors recommended hysterectomies, they did not give their patients alternative choices or adequate diagnostic evaluations. Some studies suggest that the levonorgestrel-releasing intrauterine system (Mirena) might help avoid hysterectomy in 80% of cases. Any woman, even one who has reached menopause, uncertain about a recommendation for a hysterectomy for fibroids or heavy bleeding should certainly seek a second opinion.

[See In-Depth Report #73: Uterine fibroids or In-Depth Report #74: Endometriosis.]

Some evidence suggests that surgically cutting the pain-conducting nerve fibers leading from the uterus diminishes the pain from dysmenorrhea. Two procedures, uterine nerve ablation and laparoscopic presacral neurectomy, can block such nerves. Small studies have shown benefits from these procedures, but stronger evidence is needed before they can be recommended for women with severe primary dysmenorrhea.

Laparoscopic Uterosacral Nerve Ablation (LUNA). LUNA is a recent approach that uses either laser or cauterization to destroy nerves in a small segment of the ligaments that connect the cervix with the lower back. The ligaments do not appear to provide any structural support. There are few side effects from the procedure. The patient does not lose any sensations associated with sexual activity.

Laparoscopic Presacral Neurectomy (LPSN). LPSN uses laser techniques to sever a web of nerves between the lower spine and tail bone that transmit pain from the uterus. The procedure does not affect fertility. Studies suggest that it may work better than LUNA in the long term, but it also poses a higher risk of complications. These complications include constipation, diarrhea, and urinary problems. However, many women find that these symptoms eventually improve.

Resources

www.acog.org -- American College of Obstetricians and Gynecologists
www.resolve.org -- National Infertility Association
www.asrm.com -- American Society for Reproductive Medicine
www.endometriosisassn.org -- Endometriosis Association
www.pelvicpain.org -- International Pelvic Pain Society

References

American Academy of Pediatrics Committee on Adolescence; American College of Obstetricians and Gynecologists Committee on Adolescent Health Care; Diaz A, Laufer MR, Breech LL. Menstruation in girls and adolescents: using the menstrual cycle as a vital sign. Pediatrics. 2006 Nov;118(5):2245-50.

Archer DF, Jensen JT, Johnson JV, Borisute H, Grubb GS, Constantine GD. Evaluation of a continuous regimen of levonorgestrel/ethinyl estradiol: phase 3 study results. Contraception. 2006 Dec;74(6):439-45. Epub 2006 Sep 18.

Han SH, Hur MH, Buckle J, Choi J, Lee MS. Effect of aromatherapy on symptoms of dysmenorrhea in college students: A randomized placebo-controlled clinical trial. J Altern Complement Med. 2006 Jul-Aug;12(6):535-41.

Learman LA, Kuppermann M, Gates E, Gregorich SE, Lewis J, Washington AE. Predictors of hysterectomy in women with common pelvic problems: a uterine survival analysis. J Am Coll Surg. 2007 Apr;204(4):633-41. Epub 2007 Feb 23.

Review Date:
6/16/2007
Reviewed By:
Harvey Simon, MD, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital.

A.D.A.M. Copyright

adam.com

Hepatitis

FitSugar — Wed, 08 Oct 2008 17:35:31 -0700

In This Report

Highlights
Introduction
Diagnosis
Hepatitis A
Hepatitis B and D
Hepatitis C
Autoimmune Hepatitis
Symptom Management
Outlook
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Drug Approvals

In 2006, the FDA approved telbivudine (Tyzeka), a new type of nucleoside analog drug, for treatment of chronic hepatitis B. There are now six drugs approved for hepatitis B treatment.
In 2007, the FDA approved HepaGam B, an intravenous immune globulin drug, for preventing hepatitis B recurrence following liver transplantation.

Drug Warning

In 2007, the FDA revised the prescribing label for entecavir (Baraclude), a drug used to treat hepatitis B. The new label advises against using entacavir in patients infected with both hepatitis B and HIV who are not receiving antiretroviral (anti-HIV) therapy.

Hepatitis C May Increase Lymphoma Risk

Hepatitis C infection increases the risk for developing non-Hodgkin’s lymphoma (NHL) by 20 - 30%, according to a 2007 study of male war veterans published in the Journal of the American Medical Association.

Causes of Death in Hepatitis B and C

Liver disease in general, and liver cancer in particular, is the leading cause of death in patients infected with hepatitis B, according to a 2006 study in the Lancet. Hepatitis B is the leading cause of liver cancer.
Patients with hepatitis C are also at high risk for death from liver disease. However, the Lancet study indicated that young women with hepatitis C face an even higher risk of dying from illegal intravenous drug use.

Drug Research

Adefovir (Hepsera) is commonly used to treat hepatitis B, but many patients eventually develop drug resistance. A 2006 study suggested that adefovir works well for about 5 years, with resistance occurring in about 20% of patients.
Combination treatment with pegylated interferon and ribavirin is an effective treatment for hepatitis C, but causes many side effects. Researchers are studying whether some patients may be able to succeed with a shorter course of treatment. Unfortunately, a 2007 New England Journal of Medicine study suggested that 16 weeks of treatment does not work as well as the standard 24-week course.

Introduction

Hepatitis is a disorder in which viruses or other mechanisms produce inflammation in liver cells, resulting in their injury or destruction. The liver is the largest organ in the body, occupying the entire upper right quadrant of the abdomen. It performs over 500 vital functions including:

The liver processes all of the nutrients the body requires, including proteins, glucose, vitamins, and fats.
The liver manufactures bile, the greenish fluid stored in the gallbladder that helps digest fats.
One of the liver's major contributions is to render harmless potentially toxic substances, including alcohol, ammonia, nicotine, drugs, and harmful by-products of digestion.
Old red blood cells are removed from the blood by the liver and spleen, and the iron contained in them is recycled to the bone marrow to make new red blood cells.

The esophagus, stomach, large and small intestine -- aided by the liver, gallbladder, and pancreas -- convert the nutritive components of food into energy and break down the non-nutritive components into waste to be excreted.

Damage to the liver can impair these and many other processes. Hepatitis varies in severity from a self-limited condition with total recovery to a life-threatening or life-long disease. It can occur from many different causes:

In the most common hepatitis cases (viral hepatitis), specific viruses incite the immune system to fight off infections. Specific immune factors become over-produced that cause injury.
Hepatitis can also result from an autoimmune condition, in which abnormal immune factors attack the body's own liver cells.
Inflammation of the liver can also occur from medical problems, drugs, alcoholism, chemicals, and environmental toxins.

No matter what the cause of hepatitis, it can take either an acute (short term) or chronic (long term) form. In some cases, acute hepatitis develops into a chronic condition, but chronic hepatitis can also occur on its own. Although chronic hepatitis is generally the more serious condition, patients having either condition can experience varying degrees of severity.

Acute Hepatitis. Acute hepatitis can begin suddenly or gradually, but it has a limited course and rarely lasts beyond 1 or 2 months. Usually, there is only spotty liver cell damage and evidence of immune system activity. Rarely, acute hepatitis can cause severe, even life-threatening, liver damage.

Chronic Hepatitis. The chronic forms of hepatitis last for prolonged periods. Doctors usually categorize chronic hepatitis by indications of severity:

Chronic persistent hepatitis is usually mild and nonprogressive or slowly progressive, causing limited damage to the liver.
Chronic active hepatitis involves extensive liver damage and cell injury beyond the portal tract.

Click the icon to see an image of aggressive hepatitis.

Most cases of hepatitis are caused by viruses that infect liver cells and begin replicating. They are defined by the letters A through G:

Hepatitis A, B, and C are the most common viral forms of hepatitis. Investigators are still looking for additional viruses that may be implicated in hepatitis unexplained by the current known viruses.
Other hepatitis viruses include hepatitis E and hepatitis G. Like hepatitis A, hepatitis E is caused by contact with contaminated food or water. It is not serious except in pregnant women, when it can be life threatening. Hepatitis G is always chronic and most likely has the same modes of transmission as hepatitis C. It does not appear to have serious effects.

Scientists do not know exactly how these viruses actually cause hepatitis (inflammation in the liver). As the virus reproduces in the liver, several proteins and enzymes, including many that attach to the surface of the viral protein, are also produced. Some of these may be directly responsible for liver damage. Researchers are investigating elevated levels of specific immune factors, including T cell sub-types in the liver of hepatitis C and B patients. T cells are important infection fighters in the immune system that in some cases release powerful inflammatory substances (tumor necrosis factor and interferon gamma) that can cause considerable damage leading to hepatitis B or C.

Autoimmune chronic hepatitis accounts for about 20% of all chronic hepatitis cases. Like other autoimmune disorders, this condition develops because a genetically defective immune system attacks the body's own cells and organs (in this case the liver). The attack is triggered by an environmental factor, probably a virus. Suspects include the measles virus, a hepatitis virus, or the Epstein-Barr virus, which causes mononucleosis. It is also possible that a reaction to a drug or other toxin that affects the liver also triggers an autoimmune response in susceptible individuals. In about 30% of cases, autoimmune hepatitis is associated with other disorders that involve autoimmune attacks on other parts of the body.

Alcohol. About 10 - 35% of heavy drinkers develop alcoholic hepatitis. In the body, alcohol breaks down into various chemicals, some of which are very toxic to the liver. After years of drinking, liver damage can be very severe, leading to cirrhosis in about 10 - 20% of cases. Although heavy drinking itself is the major risk factor for alcoholic hepatitis, genetic factors may play a role in increasing a person's risk for alcoholic hepatitis. Women who abuse alcohol are at higher risk for alcoholic hepatitis and cirrhosis than are men who drink heavily. High-fat diets may also increase the risk in heavy drinkers.

Drugs. Because the liver plays such a major role in metabolizing drugs, hundreds of medications can cause reactions that are similar to those of acute viral hepatitis. Symptoms can appear anywhere from 2 weeks to 6 months after starting drug treatment. In most cases, they disappear when the drug is withdrawn, but in rare circumstances they may progress to serious liver disease. Drugs most noted for liver interactions include halothane, isoniazid, methyldopa, phenytoin, valproic acid, and the sulfonamide drugs. Very high doses of acetaminophen (Tylenol) have been known to cause severe liver damage and even death, particularly when used with alcohol.

Nonalcoholic fatty liver disease (NAFLD) affects between 10 - 24% of the population. It covers several conditions, including nonalcoholic steatohepatitis (NASH). NAFLD has features similar to alcoholic hepatitis, particularly a fatty liver, but it occurs in individuals who drink little or no alcohol. Severe obesity and diabetes are the major risk factors for NAFLD as well as complications from NAFLD. NAFLD is usually benign and very slowly progressive. In certain patients, however, it can lead to cirrhosis, liver failure, or liver cancer. [For more information, see In-Depth Report #75: Cirrhosis.]

Diagnosis

In people suspected of having or carrying viral hepatitis, doctors will measure certain substances in the blood.

Bilirubin. Bilirubin is one of the most important factors indicative of hepatitis. It is a red-yellow pigment that is normally metabolized in the liver and then excreted in the urine. In patients with hepatitis, the liver cannot process bilirubin, and blood levels of this substance rise. (High levels of bilirubin cause the yellowish skin tone, known as jaundice.)
Liver Enzymes (Aminotransferases). Enzymes known as aminotransferases, including aspartate (AST) and alanine (ALT), are released when the liver is damaged. Measurements of these enzymes, particularly ALT, are the least expensive and most noninvasive tests for determining severity of the underlying liver disease and monitoring treatment effectiveness. Enzyme levels vary, however, and are not always an accurate indicator of disease activity. (For example, they are not useful in detecting progression to cirrhosis.)

Blood is drawn from a vein (venipuncture), usually from the inside of the elbow or the back of the hand. A needle is inserted into the vein, and the blood is collected in an air-tight vial or a syringe. Preparation may vary depending on the specific test.

Radioimmunoassays. To identify the particular virus causing hepatitis, blood tests called radioimmunoassays are performed. Typically, radioimmunoassays identify particular antibodies, which are molecules in the immune system that attack specific antigens. (Antigens are any molecules that the body considers threatening or dangerous and which can be targeted by antibodies.) Some of these tests can pinpoint hepatitis antigens directly. These tests, however, have limitations:

There may not be sufficient numbers of antibodies to be detectable by blood tests for up to weeks or months after hepatitis develops. Blood tests that are taken too early may miss these signs of infection.
Antibodies also linger after patients recover, so a positive antibody test can indicate a previous infection but does not necessarily determine if the infection is active.

The assays for individual hepatitis viruses may differ.

Polymerase Chain Reaction. In some cases of hepatitis C, a polymerase chain reaction (PCR), may be performed. PCR is able to make multiple copies of the virus’ genetic material to the point where it is detectable.

A liver biopsy may be performed for acute viral hepatitis caught in a late stage or for severe cases of chronic hepatitis. No laboratory tests for enzyme or viral levels can truly determine the actual damage to the liver. A biopsy helps determine treatment possibilities, the extent of damage, and the long-term outlook.

The biopsy requires abdominal surgery, most often laparoscopy. This procedure takes about an hour. It requires general anesthesia and involves the following steps:

The surgeon makes one or more small incisions (about 0.5 - 1.0 inch) in the abdomen.
Carbon dioxide or nitrous oxide is delivered through the incision to inflate the abdomen so that the involved area is visible.
The surgeon inserts a thin tube, called a laparoscope, which contains a tiny camera. Surgical instruments are also inserted through the incision to remove the liver tissue for biopsy.

Click the icon to see an explanation of liver biopsy.

A less invasive procedure, called a minilaparoscopy, uses a smaller scope and may prove to reduce the time of the procedure.

Patients with cirrhosis are usually screened for liver cancer using tests for a substance called alpha-fetoprotein (AFP) and ultrasound. It is not known, however, if such screening has much impact on survival, since it is not very sensitive and has a high rate of false positives (suggesting the presence of cancer when it is not actually present). Screening is not necessary in patients without cirrhosis.

Hepatitis A

About a third of the U.S. population has antibodies to hepatitis A, indicating previous infection by the virus. The hepatitis A virus infects up to 200,000 Americans every year and causes symptoms in about 134,000 of them. Almost 30% are children under age 15.

Hepatitis A (formerly called infectious hepatitis) is excreted in feces and transmitted by contaminated food and water. Eating shellfish taken from sewage-contaminated water is a common means of contracting hepatitis A. Infected people can transmit it to others if they do not take strict sanitary precautions. Hepatitis A is infectious for 2 - 4 weeks before symptoms develop and for a few days afterward.

People at risk for passing the infection along or being infected include:

International travelers. Hepatitis A is the hepatitis strain people are most likely to encounter in the course of international travel. In fact, in spite of the availability of a vaccine, the increase in travel to underdeveloped countries has kept the incidence of hepatitis A steady in Western nations. The incidence may even be increasing.
Day care employees and children. It is estimated that between 11 - 16% of hepatitis A cases occur among day care employees and children who attend day care. The risk for children attending day care is very low, however, if hygienic precautions are used, particularly when changing babies and handling diapers.
Sexually active homosexual men.
Intravenous drug users.
Health care, food industry, and sewage workers.

A fly may act as a mechanical vector of diseases such as hepatitis A, which means the fly carries the infective organism on its feet or mouth parts and contaminates food or water which a person then consumes. A biological vector actually develops an infective organism in its body and passes it along to its host, usually through its saliva. A fly can be a biological vector, as in the transmission of leishmaniasis by the sandfly.

Symptoms of acute viral hepatitis may begin suddenly or develop gradually. They may be so mild that patients mistake the disease for the flu. They include:

Nearly all patients experience some fatigue and often have mild fever.
Gastrointestinal problems are very common, including nausea, vomiting, a general feeling of discomfort in the abdomen, or a sharper pain that may occur in the upper right area of the abdomen. This pain tends to increase during jerking movements, such as climbing stairs or riding on a bumpy road.
Gastrointestinal problems can also lead to loss of appetite, weight loss, and dehydration.
After about 2 weeks, dark urine and jaundice (a yellowish color in the skin and whites of the eyes) develops in some, but not all, patients. (Children tend not to develop jaundice.)
About half of all patients have light colored stools, muscle pain, drowsiness, irritability, and itching, usually mild.
Diarrhea and joint aches occur in about a quarter of patients.
The liver may be tender and enlarged, and most people have mild anemia.
In about 10% of patients, the spleen is enlarged.

Travelers should take the following precautions:

Get vaccinated against hepatitis A and possibly B if traveling for long periods of time to countries where epidemics occur.
Use only carbonated bottled water for brushing teeth and drinking. (Remember that ice cubes can carry infection.) Boiling water is the best method for eliminating infectious organisms. Bringing the water to a good boil for at least a minute generally renders it safe to drink.
Heated food should be hot to the touch and eaten promptly.
Don’t buy food from street vendors.
Beware of sliced fruit that may have been washed in contaminated water. Travelers themselves should peel all fresh fruits and vegetables.
Avoid dairy products.
Avoid raw or undercooked meat and fish.

Two vaccines (Havrix, Vaqta) are now available, both very safe and effective for preventing hepatitis A (HAV). They can be given along with immune globulin and other vaccines. A combination Hep A - Hep B vaccine (Twinrix) that contains both Havrix and Engerix-B (a hepatitis B vaccine) is also available.

Click the icon to see a discussion of hepatitis A vaccine.

Candidates for HAV Vaccinations. Vaccinations for hepatitis A are recommended for:

Children age 12 - 23 months (the U.S. Centers for Disease Control and Prevention recommends that children receive the first dose of the hepatitis A vaccine when they are 12 months old, and a second dose 6 months later). Hepatitis A used to affect mostly children, but now occurs mostly in adults.
Travelers to developing countries. (Travelers should also receive immune globulin if they are visiting high-risk areas within 4 weeks of the vaccination.)
Sexually active homosexual men
Illegal drug users, especially those who inject drugs
Health care workers
People with chronic liver disease
People with hemophilia or other blood-clotting disorders

Side Effects. Although there are few side effects, allergic responses from the vaccination can occur. Hair loss has been reported in very few people after a second administration. There may be pain at the injection site. (Havrix causes more pain at the injection site than Vaqta.)

Symptoms are usually mild, especially in children, and generally appear between 2 - 6 weeks after exposure to the virus. Adult patients are more likely to have fever, jaundice, and itching that can last up to several months.

Hepatitis A is the least serious of the common hepatitis viruses. It does not directly kill liver cells, and there is no risk for a chronic form. Severe (fulminant) hepatitis is the only major concern, but even if it develops, it is almost always less dangerous than with other viral types. Only 1 in a 1,000 patients is at risk for death from this complication. If hepatitis A infection occurs in patients with hepatitis C, however, superinfections can occur, even without cirrhosis, leading to a life-threatening form of fulminant hepatitis. (Infection of patients with hepatitis B who do not have cirrhosis does not appear to be as dangerous.)

Radioimmunoassays are generally used to identify IgM antibodies, first produced to fight hepatitis A. They appear early in the course of the disease and usually can be identified as soon as symptoms appear. IgM antibodies disappear during recovery, but those known as IgG antibodies persist, and their presence can be used to indicate a previous infection.

The primary goals for managing acute viral hepatitis are to provide adequate nutrition, to prevent additional damage to the liver, and to prevent transmission to others.

Precautions for Preventing Transmission of Hepatitis A. Because hepatitis A and hepatitis E are usually passed through contaminated food, people with these viruses should not prepare food for others. Unfortunately, these viruses are most contagious before symptoms appear.

Using hot water when cleaning utensils or clothing is essential. Heating a contaminated article for 1 minute kills the virus. Simple household bleach is effective for disinfecting hard surfaces. Sterilizing is not necessary. Still, even with strong precautions, utensils used by the patient for eating and cooking should be kept separate from those used by others.
Abstain from sexual activity or take strict precautions.
Abstain from alcohol. Moderate drinking after recovery is not harmful for most people.

Hepatitis B and D

Hepatitis B and D were formerly called serum hepatitis. Hepatitis B is mainly transmitted through blood transfusions, contaminated needles, and sexual contact. Blood screening has reduced the risk from transfusions. It can also be passed from cuts, scrapes, and other breaks in the skin. Hepatitis D virus can replicate only by attaching to hepatitis B and therefore cannot exist without the B virus being present.

Risk Factors for Hepatitis B. About 1.2 million Americans are chronically infected with hepatitits B and between 20 - 30% acquired the infection when they were children. Men are at higher risk than women. Among ethnic groups living in the United States, Asians are at highest risk, due to the high rate of hepatitits B in Asian countries. Fortunately, in the US the number of new infections has declined dramatically -- by 67% between 1990 and 2002. In 2003, 7,526 cases were reported compared to over 20,000 in 1990. The greatest decrease has occurred in children. Among young adults and people living in the Northeast, however, the incidence has increased since 1999. This may indicate that sexual activity is an important route for viral transmission and that the protective effect of the vaccine has not yet reached older, high-risk groups. Also, as with hepatitis A, the increase in travelers to underdeveloped nations may be responsible for the steady rate.

Hepatitits B is far more common overseas and about 600,000 people die each year from conditions, such as liver cancer or cirrhosis, that are related to chronic hepatitis B. Nearly 70% of these infections were acquired during infancy or early childhood.

People at risk include:

Drug users who share needles.
Children of infected mothers. Pregnant women with hepatitis B can transmit the virus to their babies. Even if they are not infected at birth, unvaccinated children of infected mothers run a 60% risk of developing hepatitits B before age 5. Children are more likely than adults to become chronic carriers, although between 6 - 12% of children spontaneously recover each year.
People with multiple sex partners or other high-risk sexual behavior.
Hospital workers and others exposed to blood products. Contaminated medical instruments, including fingerstick devices used for more than one individual, have been known to transmit the virus.
Staff members and clients of institutions for the developmentally disabled.
Prisoners.
Immigrants from areas where the disease rate is high. (International travelers who spend long periods in such areas may also be at risk.)

People at highest risk for becoming chronic carriers of the virus include:

Children infected before age 5, including newborns, most of whom become carriers.
Infected people with damaged immune systems, such as AIDS patients.

Risk Factors for Hepatitis D. Hepatitis D occurs only in people with hepatitis B. It is not common in the U.S. and the incidence of this hepatitis is declining rapidly overseas. Experts anticipate that it will be extremely rare in the near future. Those who recover from hepatitis B are immune to further infection from both hepatitis B and D viruses.

The following are some precautions for preventing the transmission of hepatitits B or hepatitits C:

All objects contaminated by blood from patients with hepatitis B or C must be handled with special care. (Restrictions on food preparation are not necessary for these hepatitis viruses.)
Patients with viral hepatitis should abstain from sexual activity or take strict precautions. Infected patients should use condoms and contraceptives that prevent passage of the virus, possibly even in relationships that last for years. Women partners or infected women should abstain from sexual activity during menstruation. Either partner with infections that cause bleeding in the genital or urinary areas should avoid sexual activity until the infection is no longer active.
Couples with an infected partner or people sharing household with an infected person should avoid sharing personal items, such as razors or toothbrushes.

Note: There is no evidence that the viruses can be passed through casual contact, or other contact without exposure to blood, including kissing, hugging, sneezing, or coughing or by sharing eating utensils or drinking glasses. People infected with chronic hepatitis B or C should not be excluded from work, school, play, childcare or any social or work settings on the basis of their infection.

Symptoms appear long after the initial infection, usually 4 - 24 weeks. Many patients may not even experience them or they may be mild and flu-like. About 10 - 20% of patients have a fever and rash. Nausea is not common. Sometimes there is general aching in the joints. The pain can resemble arthritis, affecting specific joints and accompanied by redness and swelling.

Most people with hepatitis B recover from the virus. The risk of progressing to the chronic form of hepatitis B is age dependent. Only 2 - 6% of people who are older than 5 years old when they acquire the virus will develop chronic hepatitis B. The risk for chronic hepatitis in children age 1 - 5 years is 30%, and the risk for infants under the age of 1 is up to 90%. In the U.S., about 1.25 million people are chronically infected with hepatitis B. Worldwide, about 400 million people are chronically infected.

Chronic hepatitis B infection significantly increases the risk for liver damage, including cirrhosis and liver cancer. In fact, hepatitis B is the leading cause of liver cancer worldwide. According to a 2006 Lancet study, liver disease, especially liver cancer, is the main cause of death in people with chronic hepatitis B. Because of these high risks, it is very important that patients with chronic hepatitis B receive regular screenings for liver cancer.

Patients with hepatitis B who are co-infected with hepatitis D may develop a more severe form of acute infection than those who have only hepatitis B. Co-infection with hepatitis B and D increases the risk of developing acute liver failure. Patients with chronic hepatitis B who develop chronic hepatitis D also face high risk for cirrhosis. Hepatitis D occurs only in people who are already infected with hepatitis B.

A diagnosis of hepatitis B relies on measuring the liver enzymes aspartate (AST) and alanine (ALT) -- released when the liver is damaged -- assays to identify the viral DNA, and a liver biopsy.

Doctors must then determine if the condition is chronic but inactive or whether it is more aggressive. This is done by identifying a specific antigen called HBsAg, which is a protein that is found in the blood in early stages of hepatitis B and suggests the presence of a viral replication. Most people develop antibodies to this antigen during convalescence. Their condition is referred to as HBeAG negative, or anti-HBe, and suggests that infection is on the wane. About 5 - 10% of people do not clear the infection but become carriers of the antigen (called HBsAG-positive). Evidence of its persistence for more than 6 months suggests that the condition is chronic.

Tests can identify specific genetic types of hepatitis B virus (designated A to G). It is not clear how significant they are in treating patients with hepatitits B.

It is important to remember, however, that viral levels are not an accurate measure of actual liver damage. Only a biopsy can determine this.

To diagnose hepatitis D using an antibody test, hepatitis B must already have been identified.

General precautions for preventing hepatitis B when traveling are the same as those for hepatitis A. In infected people, precautions for preventing transmission are similar to those for hepatitis C.

Vaccinations for Prevention of Hepatitis B. Several inactivated virus vaccines, including Recombivax HB, GenHevac B, Hepagene, and Engerix-B, can prevent hepatitis B and are safe even for infants and children. A triple-antigen hepatitis B vaccine (Hepacare) is proving to be effective for people who do not respond to the standard vaccines. Vaccination programs are also helping to reduce the risk for liver cancer. A combination vaccine (Twinrix) that contains Engerix-B and Havrix, a hepatitis A vaccine, is now approved for people with risk factors for both hepatitis A and B.

Click the icon to see an image discussing hepatitis B vaccine.

Until recently, the vaccine contained a mercury-based preservative called thimerosal. In response to concerns, professional organizations recommended suspending vaccinations in infants with noninfected mothers. In 1999, a thimerosal-free vaccine became available, and medical centers are now urged to continue vaccinations. Unfortunately, even after the thimerosal-free vaccine became available, a number of hospitals still have not restored vaccination of all infants. This is a safe vaccine. Parents should be sure their children are immunized.

Candidates for Hepatitits B Vaccinations. Experts now recommend that all infants and children not previously vaccinated be immunized by the time they reach seventh grade.

Typical schedules for hepatitis B vaccinations in childhood are as follows:

All infants should receive the hepatitis B vaccine soon after birth and before hospital discharge. (The first dose may be given by age 2 months if the mother has no evidence of infection. Infants of mothers infected with hepatitits B should be treated with immune globulin plus the hepatitis vaccine within 12 hours of birth. Vaccinating the newborn prevents infection from being transmitted from mother to child.)
The second dose should be given at least 4 - 6 weeks after the first dose. The third dose is given at least 8 weeks after the second dose (typically when the baby is 6 - 23 months old).
Children who are 11 - 12 years old and who have not been immunized should receive two or three doses of the vaccine (depending on the brand) given over a few months.

Hepatitis B vaccine protection lasts at least 10 years. Booster shots after that may be recommended, depending on continuing risk such as sexual exposure.

The following adults are at very high risk and should be vaccinated:

Health care and public safety workers who may be exposed to blood products. Such individuals have a risk for hepatitis B virus that ranges from 15 - 30%.
People in the same household as hepatitits B infected individuals. (Unvaccinated people who have had intimate exposure to people with hepatitits B may be protected with immune globulin, which is sometimes administered with the vaccine.)
Travelers to developing countries.
Patients who require transfusions and have not been infected with hepatitits B. (Those with blood clotting disorders should have the vaccination administered under the skin, not injected in the muscle.)
Sexually active homosexual or heterosexual individuals with multiple partners or who engage in high-risk sexual behavior.
People with any sexually transmitted diseases.

Other people at risk who may benefit from vaccinations include:

Patients and workers in mental institutions and morticians.
Patients on hemodialysis. (People on hemodialysis may need larger doses or boosters. They also may need to be re-vaccinated if blood tests indicate they are losing immunity.)
People who use injected drugs.
Pregnant women at risk for the virus should be vaccinated. There is no evidence that the vaccine is dangerous to the fetus.
People receiving treatments or who have conditions that suppress the immune system may need the vaccination, although its benefits for this group are unclear except for those at high risk, such as people with HIV or spleen abnormalities.

The regimen in adults is typically three doses given over 6 months. People with alcoholism may need high doses.

Soreness at the injection site is the most common side effect. There have been some reports of nerve inflammation after vaccinations for hepatitis B, and there has been some concern about three small studies associating the vaccine with an insignificant increase in multiple sclerosis. Recent studies, however, have found no evidence to support these concerns. Nonetheless, some groups oppose the vaccination in children who are not in high-risk groups. It should be strongly stressed that worldwide 65 million people with chronic hepatitis are expected to die from liver disease. Vaccinations save lives. For example, in Taiwan, where infection rates are high and infants are at risk for hepatitis B from infected mothers, vaccination programs have significantly reduced the risk for liver cancer.

Six drugs are currently approved in the United States for treatment of chronic hepatitis B:

Peginterferon alfa-2a (Pegasys)
Interferon-alfa-2b (Intron)
Adefovir (Hepsera)
Lamivudine (Epivir)
Entecavir (Baraclude)
Telbivudine (Tyzeka)

These drugs block the replication of hepatitits B in the body. Some also help boost the immune system. A doctor will decide which drug to prescribe based on a patient’s age, disease severity, and other factors. Each drug has various advantages and disadvantages in terms of cost, efficacy, side effects, and likelihood of drug resistance. A combination of drugs may also be prescribed.

Peginterferon alfa-2a. Peginterferon alfa-2a (Pegasys) was approved in 2005 for treatment of chronic hepatitis B. (Peginterferon is also called pegylated interferon.) The drug was previously approved in 2002 for treatment of chronic hepatitis C. Pegasys prevents the hepatitis B virus from replicating and also helps boost the immune system. It is given as a weekly injection. Peginterferon is sometimes prescribed in combination with lamivudine (Epivir).

Interferon Alpha. For many years, interferon alfa-2b (Intron) was the standard drug for hepatitis B. The drug is usually taken by injection every day for 16 weeks. (It does not appear to help hepatitis D.) Unfortunately, even in hepatitis B, the virus recurs in almost all cases, although this recurring mutation may be weaker than the original strain. Administering the drug for longer periods may produce sustained remission in more patients while still being safe. Interferon is also effective in eligible children, although long-term effects are unclear.

Lamivudine,Entecavir, and Telbivudine. These drugs are classified as nucleoside analogs. Lamivudine (Epivir or 3TC) is an antiretroviral drug that is used to treat human immunodeficiency virus (HIV) as well as hepatitis B. Studies suggest that lamivudine reduces viral count in over half of hepatitis B patients who take it as sole therapy for about a year. It is less expensive than interferon-alfa and has fewer side effects, but may not work as well as interferon-alfa for long-term therapy. A major problem with lamivudine is the development of mutated viral strains that become resistant to the drug, particularly in areas where the virus is common. About 20% of patients who take lamivudine develop drug resistance.

In 2005, the FDA approved entecavir (Baraclude) for treatment of adults with chronic hepatitis B. In clinical trials, entecavir worked better than lamivudine for treating hepatitits B. Entecavir appears to have less risk of drug resistance than lamivudine. Studies also suggest that it may be a good alternative treatment for patients who have developed resistance to lamivudine. Questions have been raised about the drug’s possible cancer risks. Ongoing studies are evaluating this risk.

In 2006, the FDA approved telbivudine (Tyzeka), the newest nucleoside analog drug, for treatment of chronic hepatitis B.

Adefovir. Adefovir (Hepsera) belongs to a class of antiviral drugs called nucleotide analogs. (Nucleotides are related to nucleosides but have a slightly different chemical structure.) Nucleotide analogs block an enzyme involved in the replication of viruses. Adefovir costs more than lamivudine, but may be effective against lamivudine-resistant strains of hepatitits B. The drug must be taken on a long-term basis. A 2006 study indicated that when patients stopped taking adefovir after 48 weeks, the hepitatis B virus resumed replication. Patients who took the drug for a longer period (144 weeks) continued to benefit from treatment. Another 2006 study indicated that for some patients, adefovir remains effective for up to 5 years, although resistance occurs in about 20% of patients.

Drug Warnings. In 2004, the FDA issued two drug warnings for patients with hepatitits B. The HIV drug tenofovir (Viread) should not be used to treat patients with HIV who are co-infected with hepatitits B as the drug may increase hepatitis severity. The lymphoma drug rituximab (Rituxan) may reactivate hepatitits B. Patients with lymphoma should be screened for hepatitits B. In 2007, the FDA revised the label for entecavir (Baraclude); patients who are co-infected with hepatitits B and HIV should take entecavir only if they are also taking antiretroviral HIV drugs.

Investigational Drugs.

Emtricitabine is a nucleoside analog drug used to treat HIV and AIDS. It is being investigated for chronic hepatitits B.
Pegylated interferon alfa-2b (Peg-Intron) and alfa-2a (Pegasys) are approved for treatment of chronic hepatitis C. They are being investigated alone and in combination with other drugs, such as ribavirin (Copegus, Rebetol), for treatment of hepatitits B. The combination of pegylated interferon and ribavirin is the standard treatment for hepatitis C.
Thymosin Alpha 1 (Zadaxin), also called thymalfasin, is a synthetic version of a substance derived from the thymus gland (which is responsible for maturation of immune factors called T-cells). It appears to be safe for hepatitis B patients when used alone or in combination with interferon. It is approved in many countries, but not the United States.

Liver Transplantation. If the disease progresses to liver failure, liver transplantation may be an option. It is not foolproof, however. Viral recurrence is high in patients with hepatitis B. However, regular, lifelong injections of hepatitis B immune globulin (HepaGam B) can reduce the risk for re-infection following liver transplantation.

Hepatitis C

Hepatitis C is spread by contact with infected human blood. It is the most common blood-borne infection in the country. Until blood screening began in 1990, the hepatitis C virus was primarily transmitted through blood transfusions. Now, hepatitis C is transmitted mainly through intravenous drug use and sharing needles. Nearly half of people infected with hepatitis C have a history of injecting drugs. People who received a blood transfusion before 1992 are also at high risk, as are people who have had 20 or more sexual partners. Hepatitis C can also be passed from an infected mother to her baby during birth. (Breast-feeding does not increase the risk of transmission.)

Click the icon to see an image discussing hepatitis C.

About 4 million Americans have had an initial hepatitis C infection and an estimated 3.2 million have chronic hepatitis C. Hepatitis C affects about 170 million people worldwide. Most people with chronic hepatitis C are unaware that they have it. It is not possible to predict which patients will develop the chronic form of hepatitis C.

Ethnic Groups. In general, hepatitis C occurs most commonly in non-Caucasian men ages 30 - 49 years. Over 6% of African-Americans are infected with hepatitis C, about two to three times the risk for Caucasians.

Most patients with hepatitis C do not experience symptoms. If they appear at all, symptoms develop about 1 – 2 months after a person is infected. Symptoms of progressive chronic viral hepatitis may be very subtle. In some patients, itchy skin is the first symptom. Overall, fatigue is the most common symptom. Many patients do not experience any symptoms at all. Chronic hepatitis C can be present for 10 - 30 years, and cirrhosis or liver failure can sometimes develop before patients experience any clear symptom.

Some evidence suggests, however, that patients with chronic hepatitis C often experience an impaired quality of life, mostly from fatigue. Fatigue can impair daily function, vitality, and mood in ways that are similar to other chronic diseases. The severity of the fatigue is not necessarily related to the degree of liver injury. Some patients develop pain in small joints in the body (such as the hand) that may be nearly indistinguishable from symptoms of rheumatoid arthritis, fibromyalgia, or carpal tunnel syndrome. Recent research suggests that sexual dysfunction may be common among men with chronic hepatitis C. Other nonspecific symptoms include abdominal discomfort, loss of appetite, depression, and difficulty concentrating.

Acute Form. Acute hepatitis C is rarely recognized, since there are no symptoms in up to 80% of patients. About 15 - 45% of acute cases clear up on their own without becoming chronic. Early treatment with interferon drugs can significantly reduce the risk for progression to chronic hepatitis.

Chronic Form. About 55 - 85% of infected people develop chronic hepatitis. Chronic hepatitis C poses a risk for cirrhosis, liver cancer, or both.

Five - 20% of patients with chronic hepatitis C develop cirrhosis over a period of 20 – 30 years. The longer the patient has had the infection, the greater the risk. Patients who have had hepatitis C for more than 60 years have a 70% chance of developing cirrhosis.
Seventy percent of patients with chronic hepatitis C eventually develop chronic liver disease.
Of these patients, 4% eventually develop liver cancer. (Liver cancer rarely develops without cirrhosis first being present.)

About 1 - 5% of people with chronic hepatitis C eventually die from liver diseases (cirrhosis or liver cancer). However, according to a 2006 Lancet study, intravenous drug-related deaths are more common than liver-related deaths among younger female patients (ages 15 - 24) infected with hepatitis C or hepatitis C and B.

Patients with chronic hepatitis C may also be at higher risk for non-liver disorders, including the following:

Cryoglobulinemia (a disorder in which protein clumps form in the blood). This can cause skin rash and ulcers, kidney problems, arthritis, and sensations (such as tingling or pain) in the hands and feet. People with such symptoms may have particular difficulties with interferon, which can have similar side effects.
Porphyria cutanea tarda (a disorder that causes skin color and texture changes and sensitivity to light).
Certain autoimmune disorders, particularly hypothyroidism and rheumatoid arthritis.
Type 2 diabetes, particularly among younger people with hepatitis C who are overweight.
Some experts believe that hepatitis C may infect the central nervous system in certain patients, possibly accounting for the fatigue, depression, or both experienced by patients who have even relatively mild cases.
Certain types of lymphomas (cancers of the lymphatic system). According to a 2007 study in the Journal of the American Medical Association, hepatitis C infection increases the risk of developing non-Hodgkin’s lymphoma by 20 - 30%. The risk for a particular type of non-Hodgkin’s lymphoma, Waldenstrom’s macroglobulinemia, increases by 300%. However, this study only evaluated male Vietnam War veterans, so these risks may not apply to the general public.

Tests for Liver Enzymes. Blood tests showing elevated liver enzymes, particularly alanine aminotransferase (ALT), plus symptoms of hepatitis (jaundice, fatigue) are often first signs of acute hepatitis. In chronic hepatitis, however, liver enzymes may be normal or fluctuate. They also can be elevated even after the virus has cleared.

Tests to Identify the Virus. The standard first test for diagnosing hepatitis C is known as enzyme-linked immunosorbent assay (ELISA or EIA). The antibody for hepatitis C is used to identify the virus. The antibody may not show up for 6 weeks to 1 year after the onset of the disease, however, so its absence is not necessarily an indication of a healthy liver. A test called an immunoblot assay (called RIBA) may also be used to confirm the presence of the virus. An accurate home test (Hepatitis C Check) is now available. It supplies a lancet for obtaining a drop of blood, which is sent to the laboratory for EIA and possibly RIBA analysis. Results take about a week.

Tests to Identify Genetic Types and Viral Load. Additional tests called hepatitis C RNA assays may be used to confirm the diagnosis. They use a polymerase chain reaction (PCR) to detect the RNA (the genetic material) of the virus. Such tests may be performed if there is some doubt about a diagnosis but the doctor still firmly believes the virus is present.

hepatitis C RNA assays also determine virus levels (called viral load). Such levels do not reflect the severity of the condition or speed of progression, as they do for other viruses, such as HIV. However, high viral loads suggest a poorer response to treatment with interferons.

Such techniques may also help determine the genotype of the virus, which can be helpful in determining a treatment approach. There are six main genetic types of hepatitis C and more than 50 subtypes. They do not appear to affect the rate of progression of the disease itself, but they can differ significantly in their effects on response to treatment. Genotype 1 is the most difficult to treat and is the cause of up to 75% of the cases in the U.S. The other common genetic types are types 2 (15%) and 3 (7%), which are more responsive to treatment. People with hepatitis C need to have their genotype tested so that doctors can make appropriate treatment recommendations.

Researchers are working on developing a genetic test to identify patients with chronic hepatitis C who are most at risk of developing cirrhosis. In 2007, scientists announced they had made progress on a test that measures variations in seven genes to calculate a “Cirrhosis Risk Score.” The researchers hope that this experimental test may eventually help doctors decide which patients should receive early treatment with alpha-interferon and ribavirin.

Liver Biopsy. Only a biopsy can determine the extent of injury in the liver. Some doctors now recommend biopsies for all patients with chronic hepatitis C, regardless of severity, because of the risk for liver damage even in patients without symptoms. If a biopsy does not show any scarring and liver enzymes are normal, patients can be assured that the outlook is very favorable.

No vaccines are available, but immune globulin helps protect against developing hepatitis C after transfusions. Periodic doses of immune globulin in sexual partners of infected people also appear to be protective. In infected people, preventing transmission is similar to those for hepatitis B.

Interferons. Interferons are natural proteins that activate certain immune functions in the body and have anti-viral properties. The natural interferons used for chronic hepatitis B and C are called type I interferons. They are given by injection, need to be taken three times a week, and include the following:

Interferon alfa 2b (Intron A). Used for both hepatitis B and C.
Interferon alfa 2a (Roferon-A). Mostly used for hepatitis C.
Interferon alfa-n1 (Wellferon). Approved but mostly used in Canada for hepatitis C.

Newer synthetic interferons have been developed that are showing some advantages over the natural forms:

Pegylated interferon (PegINF). Pegylated interferons use a small molecule called polythelene glycol (PEG), which attaches to a protein and extends the activity of the interferon. This action allows the drug to be taken only once a week. Drugs available include pegylated interferon alfa-2b (Peg-Intron) and alfa-2a (Pegasys).
Interferon alfacon-1 (Infergen). This drug is called a consensus interferon (CIFN) because it was genetically developed using the most commonly occurring amino acid sequences from each of the natural type 1 alpha interferons. It is 5 - 10 times more biologically active than natural type 1 interferons. CIFN is usually given three times a week when used as initial treatment for hepatitis C.

Interferon Candidates. The best candidates for interferon treatments are patients who are at greatest risk for cirrhosis. Factors suggesting a higher risk for cirrhosis include:

Detectable virus levels as determined by an assay test.
High levels of aminotransferase enzyme for more than 6 months.
Indication of liver scarring on biopsy.

Patients who are not good candidates for interferon and are usually ineligible include:

Women who are pregnant or planning to become pregnant soon.
Patients with advanced cirrhosis. (It is unclear if the drug improves survival in patients with advanced cirrhosis and, in any case, it may be dangerous for them.)
Patients with fluid in the abdomen (ascites).
Patients with anemia or risk factors for anemia should not take the combination treatments, although they may be candidates for interferon alone.

Several kinds of patients are ineligible for treatment because of the high risk for noncompliance and the severe psychiatric effects of the drugs. They include patients with psychiatric and medical problems and substance abusers. Some doctors believe that these patients could benefit from treatment.

Side Effects and Complications of Treatment with Interferon. Common side effects of any interferon are flu-like symptoms (fever, chills, muscle aches) that usually occur within 6 hours and gradually decline over 1 - 2 weeks. (Pegylated interferon may pose a higher risk for these symptoms than the natural interferons.)

Chronic or more serious effects include:

Emotional and mental changes. Depression can be very severe, and cases of suicidal thoughts have been reported. Other mental and emotional symptoms include anxiety, amnesia, confusion, irritability, impaired concentration, decreased alertness, memory problems, and mental slowing.
Changes in sensation.
Weight loss.
Skin rashes.
Hair loss.
Gastrointestinal problems, including nausea, vomiting, and diarrhea, and, in severe cases intestinal bleeding and ulcers.
Fatigue and general weakness.
Back pain.
Complications in the lungs, including worsening of asthma. In severe cases, interferon can cause shortness of breath, inflammation in the lungs, and pneumonia.
Possible negative effects on cholesterol and lipid levels.
Heart rhythm disturbances, which, in rare cases, can be serious.
Mild anemia.
Drop in platelet and white blood cell counts, increasing susceptibility to bacterial infections.
May trigger an autoimmune response, possibly causing anemia, diabetes, lupus-like symptoms, hypothyroidism, or even autoimmune hepatitis.
Complications in the eye, including bleeding that, in some cases, may lead to loss of vision if not detected promptly.
Rare reports of acute pancreatitis.
In children, interferon therapy temporarily disrupts growth.

Patients have a difficult time with prolonged therapy. Over 20% drop out if treatment lasts longer than 2 years. Depression is the most common reason for stopping the treatment.

Several different methods of administering interferons are under investigation to help reduce some of the problems associated with injections. These methods include pills, pumps, and controlled release implants.

Interferons in Combination with Ribavirin. Ribavirin, a nucleoside analog drug, does not work alone, but it can double sustained response rates when combined with an interferon.

Pegylated interferon combined with ribavirin is the gold standard treatment for chronic hepatitis C in both adults and children. It achieves response rates of up to 50% for patients infected with hepatitis C genotype 1 (the most common genotype form in the U.S.) and up to 80% for patients infected with genotypes 2 or 3. Interferon alone is usually reserved for patients who cannot tolerate ribavirin.

A 2005 study suggested that some patients with hepatitis C genotypes 2 or 3 may be able to benefit from a shorter course of combination treatment (12 weeks) than the standard 24-week treatment duration. A shorter treatment time may reduce the risk of side effects. However, a 2007 study in the New England Journal of Medicine found that 16 weeks of combination therapy in patients with these genotypes did not work as well as the 24-week regimen. Given the significant side effects associated with combination pegylated interferon and ribavirin treatment, particularly anemia, researchers are actively investigating how to identify which patients may be able to succeed with shorter treatment duration.

PegINF combinations may help slow progression of scarring, and have even achieved improvement in some patients who already have cirrhosis. Whether the combination treatment protects against future liver cancer is still unclear. (A higher total dose, rather than a longer duration of treatment, may be the critical factor for protection.)

Side Effects of Combination Treatment. The side effects of the combination include those of both interferon and ribavirin. Interferon side effects may occur more often in the combination treatment. Combination treatment side effects may include:

Anemia occurs in about 22% of patients who take combination treatment versus 1% who take interferon alone. This complication is reversible and usually stabilizes after 1 - 2 months of treatment. However, some patients may become so anemic that they have to stop the medication. Since anemia can worsen heart disease, patients with a history of significant heart problems should not be treated with ribavirin. Other nucleoside analogues are being investigated that may have a lower risk for anemia than ribavirin.
Flu-like symptoms such as fever, headaches, and muscle aches are the most common side effect.
Reduced white blood cell count.
Skin disorders such as dry skin and rash.
Coughing and shortness of breath.
Gastrointestinal symptoms (nausea, indigestion, lack of appetite).
Emotional and psychological symptoms, such as severe sleep disturbances, depression, irritability, and anxiety.
Combination treatment in pregnant women poses a very high risk for birth defects.

Determining Treatment Success. Doctors measure treatment success and approaches based on the patient’s response to the treatments:

Early Response. These are patients who respond to the drug right away. This means that their viral count drops very rapidly within the first few weeks of treatment and is still undetectable at 12 weeks. (One difficulty in deciding when to stop treatment, even in responders, is the inability to predict at 12 weeks which of these patients will relapse and which ones will have a sustained response.)
Sustained Response. Patients who are free of the virus longer than 6 months are considered to be sustained responders. The overall sustained response rates with the current standard combination of pegylated interferon and ribavirin is over 50%, with certain factors predicting higher or lower response rates.
Relapse. In relapse, the virus comes back again and requires retreatment. This is usually due to the development of mutant strains that are resistant to the drugs or because the original dose was too low.
Nonresponse. Patients are considered to be nonresponders if the virus is still detectable 12 weeks after interferon alone or after 24 weeks of combination therapy. Treating these patients again has achieved only a 15% response.

People at Risk for Poor Response to Combination Treatment. The following patients have a greater risk for not responding to combination treatment with interferon and ribavirin:

People at high risk for aggressive hepatitis C.
Having a high viral count.
Having a specific genetic type of the virus. Patients with genotype 1 do not respond as well to combination treatment as patients with genotypes 2 or 3.
Older age (especially older than 60 years).
African-Americans are less responsive to treatment than Caucasians or Asians. The reasons for this are unclear.

Failure can be due to other, modifiable factors, which should be assessed before stopping treatment, particularly in patients who had interferon alone. They include:

Interferon dose was too low.
Patient did not comply fully with the treatment.
Patient was consuming alcohol.
Treatment time was too short. Some evidence suggests that response can significantly improve for many patients with genotype 1 if treatment time is extended to 48 weeks.

Even if viral levels linger, interferon treatment may still have benefits. For example, patients with normal liver enzyme levels appear to have almost no risk for liver damage, even if viral levels persist after treatment. Evidence also suggests that interferon reduces liver scarring and may reduce the risk for liver cancer in some patients, even if the treatment does not eliminate the virus. More research is needed, however, to confirm these findings.

Investigational Drugs for Hepatitis C. The current drugs used for hepatitis C still do not meet the needs of all patients. They are expensive, have significant side effects, do not work in half the patients who take them, and are unsuitable in many others. Investigation is ongoing to find better solutions. Drugs that may show promise include:

Albinterferon alfa-2b (Albuferon). This long-acting form of interferon-alfa may have fewer side effects and require less dosing than pegylated interferons. It is currently being tested in combination with ribavirin in Phase II trials for patients with genotype 1 chronic hepatitis C.
Thymosin Alpha 1 (Zadaxin), also called thymalfasin, is a synthetic version of a peptide derived from the thymus gland (which is responsible for maturation of immune factors called T cells). It is being used for hepatitis B and is under investigation for hepatitis C in combinations interferon.
Celgosivir. Celgosivir is a new type of antiviral drug, which blocks alpha-glucosidase, an enzyme involved in viral replication. Celgosivir is being studied in combination with pegylated interferon alfa-2b and ribavirin. The drug is derived from the Australian chestnut tree.
Eltrombopag (Revolade). Thrombocytopenia, reduced production of blood platelets, is a condition that affects patients with hepatitis C and cirrhosis. Patients with thrombocytopenia cannot tolerate standard antiviral therapy. Researchers hope that eltrombopag, a drug that stimulates platelet production, may help normalize platelet levels so that they can start antiviral drug treatment.
Statins. Statin drugs are used for the treatment and management of cholesterol. Researchers are studying whether they may help improve liver enzyme levels in patients with hepatitis C.

Other drugs under investigation include vaccines, genetic therapies known as antisense oligonucleotides or monoclonal antibodies, and drugs that will help prevent or reduce progression of liver scarring or progression to liver cancer. Even if successful, none of these drugs will be available for many years.

Liver Transplantation for Hepatitis C. If the disease progresses to the point where it becomes life-threatening, liver transplantation may be an option. Nearly 40% of liver transplant patients are infected with hepatitis C. However, liver transplantation is not a cure for hepatitis C. The virus nearly always returns. One study of patients with hepatitis C reported 5-year risks for viral recurrence of 80% and for cirrhosis of 10%. A 2004 study found that the hepatitis C virus comes back with more severity in livers from living donors than livers taken from cadavers. Researchers are investigating retreatment with antiviral drugs.

In both hepatitis B and C, the disease often persists or returns despite treatment. The virus continually generates many “mutant viruses” that differ just slightly from the parent virus. These mutated viruses may be resistant to interferons and so, over time, the drugs become ineffective.

Autoimmune Hepatitis

Autoimmune chronic hepatitis typically occurs in women ages 20 - 40 who have other autoimmune diseases, including:

Systemic lupus erythematosus
Rheumatoid arthritis
Sjögren's syndrome
Inflammatory bowel disease
Glomerulonephritis
Hemolytic anemia

Some research indicates that the postmenopausal period may be another peak in incidence of autoimmune hepatitis among women. About 30% of patients are men, however, and in both genders there is often no relationship to another autoimmune disease. In general, researches have not discovered major risk factors for this condition.

About 85% of people with chronic active autoimmune hepatitis do not have severe symptoms. When symptoms occur, they range from minimal to severe, and include fatigue, jaundice, fever, and weight loss. The liver and spleen are often enlarged. In addition, patients with this condition may experience skin disorders, including palmar erythema (red palms) and spider angioma (a blood-red spot, the size of a pinhead, from which tiny blood vessels radiate like spider legs). Itching is not common, however. The abdomen or legs may be swollen due to the accumulation of fluid.

If a patient has symptoms of chronic active hepatitis for 6 months or more and a virus cannot be identified, doctors usually suspect autoimmune hepatitis. Other autoimmune liver diseases, however, can confuse a diagnosis. To help confirm this condition, test results may show high levels of immune factors called serum globulins or certain antibodies to liver proteins. In some cases, a successful trial of steroid drugs may be the only way to diagnose autoimmune hepatitis.

Autoimmune hepatitis is usually benign and causes little trouble. There is a very small risk that it can evolve into the active form. One study reported a 10-year survival rate of 95%, which was similar to the same age group in the general population. However, it the condition evolves into the chronic active form, 5-year survival may be only 50% if the disease is not treated. (The survival rate can be higher in people with milder symptoms and less liver damage.)

Although very uncommon, severe autoimmune hepatitis can be life-threatening and require intensive therapy, possibly including liver transplantation. The risk for liver failure and bleeding in the stomach and esophagus is highest in the early years after disease onset. This risk diminishes over time but is replaced by an increase in liver cancer rates and bleeding in the stomach and intestines. The risk for liver cancer is not as high, however, as with chronic viral hepatitis.

Patients with autoimmune hepatitis who have mild symptoms and slight inflammation of the liver do not require any treatment except to relieve symptoms. They should be monitored, however, for any signs of disease progression. Severe autoimmune hepatitis is a life-threatening condition and requires intensive therapy.

Because of effective treatment options and in spite of a high rate of relapse, long-term survival rates in patients with autoimmune hepatitis are excellent. Drugs that block factors in the immune system and help reduce inflammation and symptoms of autoimmune hepatitis are most often used.

Corticosteroids. The corticosteroid prednisone (Deltasone, Orasone, Sterapred, generic) is the standard drug for treating autoimmune hepatitis. It produces remission of symptoms in about 80% of patients with autoimmune hepatitis. For most patients, steroids also reduce symptoms within 3 months, improve liver function within 6 months, and restore liver health within 2 years. Between 10 - 20% of patients continue to deteriorate despite steroid treatment, although higher doses may help some of these people. (Steroids are generally not useful for chronic hepatitis B or C. Suppressing the immune system in these patients can actually encourage the viruses to multipy more quickly.)

Treatment usually needs to continue for about 2 years before the disease is in complete remission. Usually, steroids are stopped when disease symptoms have disappeared, when blood tests show that aminotransferase (AST) levels are less than two times normal, and liver biopsies reveal no active cell damage. Steroid medications must be withdrawn very slowly. Patients who are very elderly or who have advanced (decompensated) cirrhosis are not good candidates for this treatment.

Unfortunately, remission rarely lasts more than 3 years. About half of patients relapse within 6 months, and only about 20% of patientsare disease-free for more than 5 years. A 2007 study indicated that AST, gamma-globulin, and immunoglobulin-G (IgG) levels are helpful in predicting which patients may relapse and which patients have the best chance for maintaining remission. Still, most patients with autoimmune hepatitis will eventually have a relapse. Re-administering prednisone therapy after relapse achieves another remission in about 80% of patients.

Corticosteroid side effects can be very distressing and sometimes serious. They include weight gain, skin problems, moon-shaped face, high blood pressure, diabetes, cataracts, mental disturbances, infections, and osteoporosis.

Azathioprine. Doctors often prescribe the drug azathioprine (Imuran) along with steroids to help reduce severe side effects caused by using steroids alone. When azathioprine is given in combination with prednisone, the prednisone dose can be reduced, thereby lowering the corticosteroid’s side effects. Azathioprine also suppresses the immune system and helps prevent relapse, but the drug will not induce remission by itself.

Other Drugs. Other immunosuppressant drugs, such as mycophenylate mofetil (MMF), cyclosporine (Neoral), or tacrolimus (Prograf) are sometimes prescribed for patients who are not helped by standard treatment.

Liver Transplantation and Autoimmune Hepatitis. If all therapies fail and the disease becomes life threatening, liver transplantation may be performed. Liver transplantation can be a successful option for many people. Survival rates are about 90% after 1 year, and 70 - 80% after 5 years.

Symptom Management

The primary goals for managing viral hepatitis are to provide adequate nutrition, to prevent additional damage to the liver, and to prevent transmission to others. For mild cases of acute viral hepatitis, no drug therapy or other treatment is either available or necessary. Hospitalization is needed only for people at high risk for complications such as pregnant women, elderly people, patients with other serious conditions, or those who have severe nausea and vomiting and need to have fluids administered intravenously.

The following tips may be useful:

All patients should abstain from alcohol and sexual contact during the acute phase.
Although most patients with hepatitis experience fatigue and require more rest than usual, they can be as physically active as they want without affecting recovery. In fact, patients should be encouraged to be as active as they can.
Depression is common, particularly in people used to an active life. Patients should be reassured that in the majority of hepatitis cases, recovery is complete.
The liver processes many types of medications. As soon as hepatitis is diagnosed, patients should stop taking all drugs (including over-the-counter-medication) except those prescribed or recommended by their doctors. Specific nonsteroidal anti-inflammatory drugs (NSAIDs) that should be avoided include ibuprofen (Advil, Motrin) and acetaminophen (Tylenol). Ibuprofen (Advil, Motrin) may increase liver enzymes and cause liver damage in patients with hepatitis C. Acetaminophen (Tylenol) may cause sudden liver failure in patients with hepatitis A or B. Acetaminophen can also damage the liver if taken in combination with alcohol.

After the onset of acute hepatitis, periodic visits to the doctor for repeat blood tests are necessary, the frequency of which depends on how well the patient feels. If symptoms still occur after 3 months and laboratory tests still indicate active presence of the virus, the patient should be evaluated every month. If symptoms persist beyond 6 months, a liver biopsy may be required to determine any liver damage.

Dietary Factors to Protect the Liver. In general, no vitamins or special diets have been proven to be particularly beneficial. The following may be helpful, however:

Eating many small snacks during the day, with larger ones in the morning, may help prevent weight loss while reducing the severity of nausea. Patients might be able to tolerate high-caloric drinks to supplement their regular diet.
One small Japanese study suggested that vitamin E might help protect against liver damage in patients with hepatitis C.
Thiamine binds to iron and helps reduce iron load in the liver. One small study suggested it may be helpful for patients with chronic hepatitis B. Pork is high in the vitamin, but more healthy sources include dried fortified cereals, oatmeal, corn, nuts, cauliflower, sunflower seeds and vitamin pills.
Some research suggests that supplements of omega-3 fatty acids (found in fish oil and evening primrose oil) may help protect the diseased liver.
Higher coffee intake has been shown to reduce the risk for cirrhosis.

Manufacturers of herbal remedies and dietary supplements do not need FDA approval to sell their products. Just like a drug, herbs and supplements can affect the body's chemistry, and therefore have the potential to produce side effects that may be harmful. There have been several reported cases of serious and even lethal side effects from herbal products. Patients should always check with their doctors before using any herbal remedies or dietary supplements.

Popular herbal remedies for hepatitis include ginseng, glycyrrhizin (a compound in licorice), catechin (found in green tea), and silymarin (found in milk thistle). Aside from milk thistle, there has been no evidence that these herbs are helpful for hepatitis. Studies on milk thistle’s benefit have been mixed. Some studies have indicated that milk thistle may help improve liver enzyme levels. However, a 2005 review found that the herb did not reduce deaths from liver disease caused by hepatitis B or C.

Patients with hepatitis should be aware that some herbal remedies may cause liver damage. In particular, kava (an herb used to relieve anxiety and tension) may be dangerous for people with chronic liver disease.

Outlook

In most cases of acute viral hepatitis, recovery is complete and the liver returns to normal within 2 - 8 weeks. In a small number of cases of hepatitis B or C, the condition can be prolonged and recovery may not occur for a year. About 5 - 10% of these patients will have a flare-up of milder symptoms before full recovery. A few of these patients may go on to develop chronic hepatitis. People who have been infected with a hepatitis virus continue to produce antibodies to that specific virus. This means that they cannot be reinfected with the same hepatitis virus again. Unfortunately, they are not protected from other types.

Serious consequences of acute viral hepatitis are rare, but can be life threatening if they occur. Pregnant women with acute hepatitis B, C, or E are at higher risk for complications of acute hepatitis.

In very rare cases, within 2 months of onset of acute hepatitis, a very serious condition known as fulminant hepatitis can develop. In this event, the liver fails with catastrophic consequences. The following events may develop:

A large swollen abdomen (known as ascites) and a peculiar hand-flapping tremor (called asterixis).
These symptoms may be followed by stomach and intestinal bleeding and mental confusion, stupor, or coma caused by brain injury (encephalopathy).

No medications, including corticosteroids, have any effect against the condition itself. Liver transplantation is currently the only life-saving treatment for fulminant acute hepatitis and has survival rates of up to 60%. Without liver transplantation, the chance of survival is only 20%.

Other serious and rare consequences of acute viral hepatitis are aplastic anemia (which can be fatal), pancreatitis, hypoglycemia, and polyarteritis, a serious inflammation of blood vessels.

Chronic Persistent Hepatitis. Chronic persistent hepatitis is usually mild and nonprogressive or slowly progressive, causing limited damage to the liver. Cell injury in such cases is usually limited to the region of portal tracts, which contains vessels that carry blood to the liver from the digestive tract. In some cases, however, more extensive liver damage can occur over long periods of time and progress to chronic active hepatitis.

Chronic Active Hepatitis. If damage to the liver is extensive and cell injury occurs beyond the portal tract, chronic active hepatitis can develop. Significant liver damage has usually occurred by this time. Nearly every bodily process is affected by a damaged liver, including digestive, hormonal, and circulatory systems. Symptoms can significantly impair daily life.

Cirrhosis. If liver cells are destroyed between the portal tract and the central veins in the liver, progressive cell damage can build a layer of scar tissue over the liver, resulting in the condition known as cirrhosis. In such cases, the entire liver is threatened with malfunction and failure. If cirrhosis develops, the average survival time is about 10 years. The risk for cirrhosis is much higher in patients with hepatitis C than in those with hepatitis B. [For more information, see In-Depth Report #75: Cirrhosis.]
Liver Cancer. The risk for liver cancer in patients with cirrhosis is about 14% but varies widely depending on the cause of hepatitis. (Liver cancer is rare in patients who do not develop cirrhosis.)

Click the icon to see an image of cirrhosis of the liver.

Liver transplantation may be indicated for the following patients:

Those who have developed life-threatening cirrhosis and who have a life expectancy of more than 12 years.
Patients with liver cancer that has not spread beyond the liver.

Current 5-year survival rates after liver transplantation are 55 - 80%, depending on different factors. Patients report improved quality of life and mental functioning after liver transplantation. Unfortunately, in about half of all patients with chronic hepatitis, the disease recurs after transplantation.

Patients should consider medical centers that have performed more than 50 transplants per year and produced better-than-average results. Unfortunately, there are far more people waiting for liver donors than there are available organs. [For more information on liver transplantation, see In-Depth Report #75: Cirrhosis.]

Resources

www.cdc.gov/hepatitis -- Centers for Disease Control and Prevention
www.hepfi.org -- Hepatitis Foundation International
www.hepb.org -- Hepatitis B Foundation
www.liverfoundation.org -- American Liver Foundation
www.aasld.org -- American Association for the Study of Liver Diseases
www.gastro.org -- American Gastrointestinal Association
www2.niddk.nih.gov -- National Institute of Diabetes and Digestive and Kidney Diseases
www.immunize.org -- Immunization Action Coalition
www.hivandhepatitis.com -- Hepatitis and HIV
www.unos.org -- United Network for Organ Sharing

References

Amin J, Law MG, Bartlett M, Kaldor JM, Dore GJ. Causes of death after diagnosis of hepatitis B or hepatitis C infection: a large community-based linkage study. Lancet. 2006 Sep 9;368(9539):938-45.

Giordano TP, Henderson L, Landgren O, Chiao EY, Kramer JR, El-Serag H, et al. Risk of non-Hodgkin lymphoma and lymphoproliferative precursor diseases in US veterans with hepatitis C virus. JAMA. 2007 May 9;297(18):2010-7.

Hadziyannis SJ, Tassopoulos NC, Heathcote EJ, Chang TT, Kitis G, Rizzetto M, et al. Long-term therapy with adefovir dipivoxil for HBeAg-negative chronic hepatitis B for up to 5 years. Gastroenterology. 2006 Dec;131(6):1743-51. Epub 2006 Sep 20.

Huang H, Shiffman ML, Friedman S, Venkatesh R, Bzowej N, Abar OT, et al. A 7 gene signature identifies the risk of developing cirrhosis in patients with chronic hepatitis C. Hepatology. 2007 Aug;46(2):297-306.

Montano-Loza AJ, Carpenter HA, Czaja AJ. Improving the end point of corticosteroid therapy in type 1 autoimmune hepatitis to reduce the frequency of relapse. Am J Gastroenterol. 2007 May;102(5):1005-12. Epub 2007 Feb 23.

Shiffman ML, Suter F, Bacon BR, Nelson D, Harley H, Sola R, et al. Peginterferon alfa-2a and ribavirin for 16 or 24 weeks in HCV genotype 2 or 3. N Engl J Med. 2007 Jul 12;357(2):124-34.

Wang CS, Wang ST, Yao WJ, Chang TT, Chou P. Hepatitis C virus infection and the development of type 2 diabetes in a community-based longitudinal study. Am J Epidemiol. 2007 Jul 15;166(2):196-203. Epub 2007 May 11.

Review Date:
8/31/2007
Reviewed By:
Harvey Simon, MD, Editor-in-Chief, In-Depth Reports; Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital.

A.D.A.M. Copyright

adam.com

Ear infections

FitSugar — Wed, 08 Oct 2008 17:35:31 -0700

In This Report

Highlights
Introduction
Causes
Risk Factors
Symptoms
Prognosis
Diagnosis
Prevention
Treatment
Home Remedies
Medications
Surgery
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Ear Infections

Middle ear (otitis media) infections are very common in young children. They include:

Acute otitis media (AOM) is an inflammation caused by bacteria that travel to the middle ear from fluid trapped in the Eustachian tube. Children with AOM exhibit signs of an ear infection including pain, fever, and tugging at the ear.
Otitis media with effusion (OME) refers to fluid that accumulates in the middle ear without obvious signs of infection. OME usually produces no symptoms, but some children will have difficulty hearing or complain of “plugged up” ears.

Prevention

Preventing colds and influenza (“flu”) is the best way to prevent ear infections. Make sure children wash their hands frequently and receive an influenza vaccine annually. The pneumococcal vaccine is also very helpful for preventing ear infections.

Treatment

Most ear infections resolve without antibiotic treatment.
For most children with AOM, doctors recommend waiting 48 - 72 hours before prescribing antibiotics. However, children younger than 6 months should receive immediate antibiotic treatment. Parents can give children 6 months and older ibuprofen or acetaminophen to help relieve pain.
Antibiotics are not helpful for most cases of OME. Doctors usually monitor children with OME for 3 months to see if their condition improves. Some children with hearing loss and developmental problems may eventually need surgery. Inserting tubes into the ear drum (tympanostomy) is the usual surgery for this problem.

Introduction

The ear is the organ of hearing and balance. It has three parts: the outer, middle, and inner ear.

The outer ear collects sound waves, which move through the ear canal to the tympanic membrane, commonly called the eardrum.
The tympanic membrane, or ear drum, is lined with mucus. When incoming sound waves strike this membrane, it vibrates like a drum, and converts the sound waves into mechanical energy.
This energy echoes through the middle ear. The middle ear is a complex structure filled with air and made of tiny bones. These bones vibrate to the rhythm of the eardrum and pass the sound waves on to the inner ear.
The inner ear is filled with fluid. Here, hair-like structures stimulate nerves to change sound waves into electrochemical impulses that are carried to the brain, which senses these impulses as sounds.
The inner ear also contains three semi-circular canals that function as the body's gyroscope, regulating balance.
The Eustachian tube, an important structure in the ear, runs from the middle ear to the passages behind the nose and the upper part of the throat. This tube helps equalizes the air pressure in the middle ear to the outside air pressure. Problems here are primary factors in most cases of ear infection.

The ear consists of external, middle, and inner structures. The eardrum and the three tiny bones conduct sound from the eardrum to the cochlea.

Acute Otitis Media (AOM). An inflammation in the middle ear is known as "otitis media." AOM is a middle ear infection caused by bacteria that traveled to middle ear from fluid build-up in the Eustachian tube. AOM may develop during or after a cold or the flu.

Middle ear infections are extremely common in children, but they are infrequent in adults.
In children, ear infections often recur, particularly if they first develop in early infancy.

Otitis Media with Effusion (OME). This condition occurs when fluid, called an effusion, becomes trapped behind the eardrum in one or both ears, even when there is no infection. In chronic and severe cases, the fluid is very sticky and is commonly called "glue ear."

It is usually not painful. Sometimes the only clue that it is present is a feeling of stuffiness in the ears, which can feel like "being under water."
It may impair children's hearing.
Children who are susceptible to OME can have frequent episodes for more than half of their first 3 years of life.
Most episodes will resolve within 3 months, but 30 - 40% of children may have recurrent episodes. Only 5 - 10% of episodes last longer than 1 year.

Chronic Otitis Media. This condition refers to persistent fluid behind the tympanic membrane without any infection present. It is called suppurative chronic otitis when there is persistent inflammation in the middle ear or mastoids, or chronic rupture of the eardrum with drainage.

Swimmer’s Ear (Acute Otitis Externa). Acute otitis externa (AOE) is an inflammation or infection of the outer ear and ear canal. It can be triggered by water that gets trapped in the ear. The trapped water can cause bacteria to breed. AOE can also be precipitated by overly aggressively scratching or cleaning ears or when an object gets stuck in the ears.

In 2006, the American Academy of Otolaryngology -- Head and Neck Surgery Foundation (AAO-HNSF) issued their first guidelines for management of AOE. A key recommendation is that AOE should be treated with topical (not oral) antibiotics. For pain relief, over-the-counter remedies such as acetaminophen or nonsteroidal anti-inflammatory drugs (such as ibuprofen) usually help, but in severe cases opioid drugs may be prescribed. With eardrops, most cases of AOE will clear up within 2 - 3 days.

Causes

Bacteria. Certain bacteria are the primary causes of acute otitis media (AOM). They are detected in about 60% of cases. The bacteria most commonly causing ear infections are:

Streptococcus pneumoniae (also called S. pneumoniae or pneumococcus) is the most common bacterial cause of acute otitis media, causing about 40 - 80% of cases in the U.S.
Haemophilus influenzae, the next most common culprit, is responsible for 20 - 30% of acute infections.
Moraxellacatarrhalis is responsible for 10 - 20% of infections.
Other bacteria include Streptococcus pyogenes and Staphylococcus aureus.

Viruses. Rhinovirus is a common virus that causes a cold and plays a leading role in the development of ear infections. It is not the direct infecting organism, however. But other viruses, such as respiratory syncytial virus (RSV, a virus responsible for childhood respiratory infections) and influenza (flu), may be the actual causes of some ear infections. Increasing evidence suggests that both viruses and bacteria play a role in ear infections. Viruses can increase middle ear inflammation and interfere with antibiotics’ efficacy in treating bacterial-causes ear infections. HIV or other immunocompromised states also increase the risk for ear infections.

Acute otitis media (middle ear infection) is usually due to a combination of factors that increase susceptibility to infections by specific organisms in the middle ear. The infection typically evolves as follows:

The primary setting for ear infections is in a child's Eustachian tube, which runs from the middle ear to the nose and upper throat. The Eustachian tube is shorter and smaller in children than adults, and therefore more vulnerable to blockage. It is also more horizontal in younger children and therefore does not drain as well.
Changes in middle ear pressure occur in about two-thirds of children with colds. Colds and respiratory infections are caused by viruses, such as the rhinovirus. Viruses play an important role in many ear infections, and can set the scene for a bacterial infection.
However, many bacteria normally thrive in the passages of the nose and throat. Most are not harmful. In fact, some can even block harmful bacteria from getting out of control. An additional defense system in the airways, such as mucus, prevents the harmful bacteria from spreading and infecting deeper passages, such as those in the ear.
If a cold does occur, the virus can cause the membranes along the walls of the inner passages to swell and obstruct the airways. If this inflammation blocks the narrow Eustachian tube, the middle ear may not drain properly. Fluid builds up. The defense systems described above become inefficient, and the fluid becomes a breeding ground for bacteria and subsequent infection.

Respiratory viruses may also contribute directly to the infection. Allergens can also produce inflammation and blockage in the Eustachian tube, which creates an environment favorable to bacteria.

The rise in ear infections has paralleled the increasing incidences of other upper and lower airway disorders such as asthma, allergies, and sinusitis. For example, the same bacteria are often responsible for both ear infections and sinusitis. In one study, 38% of children with ear infections also had sinusitis, and other studies have reported that nearly half of children with OME have concurrent sinusitis. Data indicate that nearly a third of infants and toddlers with upper respiratory infections go on to develop acute otitis media.

Medical or Physical Conditions that Affect the Middle Ear. Any medical or physical condition that reduces the ear's defense system can increase the risk for ear infections. Children with shorter than normal and relatively horizontal Eustachian tubes are at particular risk for initial and recurrent infections. Inborn structural abnormalities, such as cleft palate, increase risk. Genetic conditions, such as Kartagener's syndrome in which the cilia (hair-like structures) in the ear are immobile and cause fluid build up, also increase the risk. Children with Down syndrome or Fetal Alcohol Syndrome may also be at increased risk due to anatomical abnormalities.

Otitis media with effusion (OME) may occur spontaneously following an episode of acute otitis media. Susceptibility to OME may also be due to an abnormal or malfunctioning Eustachian tube that causes a negative pressure in the middle ear, which allows fluid to leak in through capillaries.

Risk Factors

Acute ear infections account for 15 - 30 million visits to the doctor each year in the U.S. In fact, ear infections are the most common reason why an American child sees the doctor. Furthermore, the rate of acute otitis media has been rising over the past decades.

Acute Otitis Media (AOM). About two-thirds of children will have a least one attack of AOM by age 3, and a third of these children will have at least 3 episodes. Boys are more likely to have infections than girls.

AOM generally affects children ages 6 - 18 months. The earlier a child has a first ear infection, the more susceptible they are to recurrent episodes (for instance, 3 or more episodes within a 6-month period).

As children grow, however, the structures in their ears enlarge and their immune systems become stronger. By 16 months, the risk for recurrent infections is rapidly declining. After age 5, most children have outgrown their susceptibility to any ear infections.

Otitis Media with Effusion. OME is very common in children aged 6 months to 4 years, with about 90% of children having OME at some point. More than 50% of children have OME before the age of 1, and more than 60% by age 2.

Ear infections are more likely to occur in the fall and winter. The following conditions also put children at higher risk for ear infection:

Allergies. Some experts believe that an increase in allergies is also partially responsible for the higher number of ear infections, which is unlikely to be related to day care attendance. Studies indicate that 40 - 50% of children over 3 years old who have chronic otitis media also have allergic rhinitis (hay fever). Allergies can cause inflammation in the airways, which may contribute to ear infections. Allergies are also associated with asthma and sinusitis. However, a causal relationship between allergies and ear infections has not been definitively established.
Enrollment in day care. Although ear infections themselves are not contagious, the respiratory infections that precipitate them can pose a risk for children with close and frequent exposure to other children. Some experts believe that the increase in ear and other infections may be due to the higher attendance of very small children, including infants, in day care centers beginning in the 1970s.
Exposure to second-had cigarette smoke. Parents who smoke pose a significant risk for both otitis media with effusion (OME) and recurrent acute otitis media (AOM) in their children. (Passive smoking does not appear to be a cause of initial ear infections, however.)
Being bottle-fed as infants. Babies who are bottle-fed may have a higher risk for otitis media than breastfed babies. The American Academy of Pediatrics recommends breastfeeding for at least the baby's first 6 months.
Pacifier use. Several studies have found that the use of pacifiers place children at even higher risk for ear infections. Sucking increases production of saliva, which helps bacteria travel up the Eustachian tubes to the middle ear.
Obesity. Obesity has been associated with the occurrence of OME.
Having siblings with recurrent ear infections.
Anatomical abnormalities of upper airways.

Symptoms

Symptoms of acute otitis media usually develop suddenly and can include:

Pain or discomfort in the ear. However, it is difficult to determine if an infant or child who hasn't yet learned to speak has an ear infection. Some children may indicate pain if they have trouble swallowing food and rejecting it. Some parents believe that tugging on the ear indicates an infection, but this gesture is more likely to indicate pain from teething.
Coughing
Nasal congestion
Fever
Irritability
Sleeplessness
Loss of appetite
Vomiting
Diarrhea
Listlessness

If the ear infection is severe, the tympanic membrane may rupture, causing the parent to notice pus draining from the ear. (This usually brings relief from pain.) Pus in the ear may cause hearing loss in some children.

Fevers and colds often make children irritable and fussy, so it is difficult to determine if acute otitis media is present as well. Symptoms are not apparent in about a third of children with acute middle ear infection.

OME often has no symptoms at all. Some hearing loss may occur, but it is often fluctuating and hard to detect, even by observant parents. The only sign to a parent that the condition exists may be when a child complains of "plugged up" hearing. Other symptoms can include loud talking, not responding to verbal commands, and turning up the television or radio.

Older children with OME may have difficulty targeting specific sounds in a noisy room. In such cases, some parents or teachers may attribute their behavior to lack of attention or even to an attention deficit disorder. OME is often diagnosed during a regular pediatric visit.

Prognosis

Doctors should carefully evaluate ear infections in infants fewer than 3 months old, and consider more serious infections, such as meningitis.

While severe cases of recurrent acute otitis media or persistent otitis media with effusion (OME) are associated with impaired hearing for a period of time, the long-term consequences resulting from this hearing loss may not be significant in most children.

Hearing loss in children may temporarily slow down language development and reading skills. However, results from a high quality study strongly indicate that uncomplicated chronic middle ear effusion poses no danger for developmental delays. Researchers evaluated children who had either prompt insertion of ear tubes to drain fluid when they were younger than age 3, or delayed insertion of tubes many months later. When the children were tested at ages 9 - 11, researchers found no differences in speech and language, auditory processing, attention, behavior, social skills, and academic achievement. As the majority of chronic ear effusion cases eventually clear up on their own, many experts now recommend against surgical intervention for most children.

Occasionally, patients with chronic otitis media develop involvement of the inner ear. In these situations hearing loss can potentially be permanent. Most of these patients will also have problems with vertigo.

Serious complications or permanent physical injuries from ear infections are very uncommon, but may include:

Structural damage. Certain children with severe or recurrent otitis media may be at risk for structural damage in the ear, including erosion of the ear canal.
Cholesteatomas. Cysts in the ear called cholesteatomas are an uncommon complication of recurrent or severe ear infections.
Calcifications. In rare cases, even after a mild infection, some children develop calcification and hardening in the middle and, occasionally, in the inner ear. This may be due to immune abnormalities.

Before the introduction of antibiotics, mastoiditis (an infection in the bones located in the skull), was a serious, albeit rare, complication of otitis media. This condition is difficult to treat and requires intravenous antibiotics and drainage procedures. Surgery may be necessary.

If pain and fever persist in spite of antibiotic treatment of otitis media, the doctor should check for mastoiditis. Most cases of mastoiditis are generally not associated with ear infections.

If an infection of the mastoid air cells cannot be controlled with antibiotics, surgery may be needed.

Impaired Balance. Some studies have indicated that children with chronic OME have problems with motor development and balance.

Facial Paralysis. Very rarely, a child with acute otitis media may develop facial paralysis, which is temporary and usually relieved by antibiotics or possibly drainage surgery. Facial paralysis may also occur for patients with chronic otitis media and a cholesteatoma (cyst in the middle ear). Surgery is often necessary to correct this condition.

Diagnosis

The doctor should be sure to ask the parent if the child has had a recent cold, flu, or other respiratory infection. If the child complains of pain or has other symptoms of otitis media, such as redness and inflammation, the doctor should rule out any other causes. These may include, but are not limited to, the following:

Otitis media with effusion. OME is commonly confused with acute otitis media. It must be ruled out because it does not respond to antibiotics.
Dental problems (such as teething).
Infection in the outer ear. Symptoms include pain, redness, itching, and discharge. Infection in the outer ear, however, can be confirmed by wiggling the ears, which will produce pain. (This movement will have no significant effect if the infection is in the middle ear.)
Foreign objects in the ear. This can be dangerous. A doctor should always check for this first when a small child indicates pain or problems in the ear.
Viral infection can produce redness and inflammation. Such infections, however, are not treatable with antibiotics and resolve on their own.
A parent's or child's attempts to remove earwax.
Intense crying can cause redness and inflammation in the ear.

Instruments Used for Examining the Ear. An ear examination should be part of any routine physical examination in children, particularly because the problem is so common and may not cause symptoms.

The doctor first removes any ear wax (called cerumen) in order to get a clear view of the middle ear.
The doctor uses a small flashlight-like instrument called an otoscope to view the ear directly. This is the most important diagnostic step. The otoscope can reveal signs of acute otitis media, bulging eardrum, and blisters.

An otoscope is a tool that shines a beam of light to help visualize and examine the condition of the ear canal and eardrum. Examining the ear can reveal the cause of symptoms such as an earache, the ear feeling full, or hearing loss.

To determine an ear infection, the doctor should always use a pneumatic otoscope. This device detects any reduction in eardrum motion. It has a rubber bulb attachment that the doctor presses to push air into the ear. Pressing the bulb and observing the action of the air against the eardrum allows the doctor to gauge the eardrum's movement.
Some doctors may use tympanometry to evaluate the ear. In this case, a small probe is held to the entrance of the ear canal and forms an airtight seal. While the air pressure is varied, a sound with a fixed tone is directed at the eardrum and its energy is measured. This device can detect fluid in the middle air and also obstruction in the Eustachian tube.
A procedure similar to tympanometry, called reflectometry, also measures reflected sound. It can detect fluid and obstruction, but does not require an airtight seal at the canal.

Neither tympanometry nor reflectometry are substitutes for the pneumatic otoscope, which allows a direct view of the middle ear.

Findings Indicating AOM or OME. A diagnosis of AOM requires all three of the following criteria:

History of recent sudden symptoms. Symptoms may include fever, pulling on the ear, pain, irritability, or discharge (otorrhea) from the ear.
Presence of fluid in the middle ear. This may be indicated by fullness or bulging of the eardrum or limited mobility.
Signs and symptoms of inflammation. These may include redness of the eardrum as well as assessment of the child's discomfort. Ear pain that is severe enough to interfere with sleep may indicate inflammation.

AOM (fluid and infection) is often difficult to differentiate from OME (fluid without infection). It is important for a doctor to make this distinction as OME does not require antibiotic treatment. In patients with OME, an air bubble may be visible and the eardrum is often cloudy and very immobile. A scarred, thick, or opaque eardrum may make it difficult for the doctor to distinguish between acute otitis media and OME.

Parents can also use a sonar-like device, such as the EarCheck Monitor, to determine if there is fluid in their child's middle ear. EarCheck uses acoustic reflectometry technology, which bounces sound waves off the eardrum to assess mobility. When fluid is present behind the middle ear (a symptom of AOM and OME), the eardrum will not be as mobile. The device works like an ear thermometer and is painless. Results indicate the likelihood of the presence of fluid and may help patients decide whether they need to contact their child's doctor. However, it is not recommended that children be treated with antibiotics based on the findings using this device.

On rare occasions the doctor may need to draw fluid from the ear using a needle for identifying specific bacteria, a procedure called tympanocentesis. This procedure can also relieve severe ear pain. This is most often performed by an ear, nose, and throat (ENT) specialist, and usually only in severe or recurrent cases. In most cases, tympanocentesis is not necessary in order to obtain an accurate enough diagnosis for effective treatment.

Hearing tests performed by an audiologist are usually recommended for children with persistent otitis media with effusion. A hearing loss below 20 decibels usually indicates problems.

Determining Impaired Hearing in Infants and Small Children. Unfortunately, it is very difficult to test children under 2 years old for hearing problems. One way to determine hearing problems in infants is to gauge the baby's language development:

At 4 - 6 weeks most babies with normal hearing make cooing sounds.
By around 5 months, infants should be laughing out loud and making one-syllable sounds with both a vowel and consonant.
Between 6 - 8 months, babies should be able to make word-like sounds with more than one syllable.
Usually starting around 7 months, and by 10 months, babies babble (making many word-like noises).
Around 10 months, babies can identify and use some term for a parent, such as dada, baba, or mama.
Babies speak their first word usually by the end of their first year.

If a child's progress is significantly delayed beyond these times, a parent should suspect possible hearing problems.

Determining Impaired Hearing in Older Children. Hearing loss in older children may be detected by the following behaviors:

They may not respond to speech spoken beyond 3 feet away.
They may have difficulty following directions.
Their vocabulary may be limited.
They may have social and behavioral problems.

Prevention

The best way to prevent ear infections is to prevent colds and flu.

Good Hygiene. Colds and flus are spread primarily when an infected person coughs or sneezes near someone else. A very common method for transmitting a cold is by shaking hands. Everyone should always wash their hands before eating and after going outside. Ordinary soap is sufficient. Waterless hand cleaners that contain an alcohol-based gel are also effective for everyday use and may even kill cold viruses. (They are less effective, however, if extreme hygiene is required. In such cases, alcohol-based rinses are needed.) Antibacterial soaps add little protection, particularly against viruses. In fact, one study suggests that common liquid dish washing soaps are up to 100 times more effective than antibacterial soaps in killing respiratory syncytial virus (RSV), which is known to cause pneumonia and has been associated with ear infections. Wiping surfaces with a solution that contains 1 part bleach to 10 parts water is very effective in killing viruses.

The American Academy of Pediatrics (AAP) and the U.S. Centers for Disease Control (CDC) recommend annual influenza vaccination for all children 6 months to 5 years of age. Preventing influenza (the "flu') may be a more important protective measure against ear infections than preventing bacterial infections. For example, studies report that children who are vaccinated against influenza experience a third fewer ear infections during flu season than unvaccinated children.

Flu Vaccines. Flu vaccines produce an immune response that attacks the active virus. Vaccines are typically given by injection, usually between October and December. Antibodies to the influenza virus generally develop within 2 weeks of vaccination, and immunity peaks within 4 - 6 weeks, then gradually wanes. An intranasal vaccine called FluMist is approved for children ages 2 years and older. FluMist is made from a live but weakened influenza virus; flu shots use inactivated (not live) viruses. Children younger than 2 years old, and children younger than age 5 who have asthma or recurrent wheezing, should not receive FluMist.

Possible side effects include:

Allergic Reaction. Newer vaccines contain very little egg protein, but an allergic reaction still may occur in people with strong allergies to eggs.
Soreness at the Injection Site. Up to two-thirds of people who receive the influenza vaccine develop redness or soreness at the injection site for 1 - 2 days afterward.
Flu-like Symptoms. Other side effects include mild fatigue and muscle aches and pains. They tend to occur between 6 - 12 hours after the vaccination and last up to 2 days. These symptoms are not influenza itself but an immune response to the virus proteins in the vaccine. Anyone with a fever, however, should not be vaccinated until the ailment has subsided.

Antiviral Drugs. Antiviral drugs are available to treat influenza. One such drug, oseltamivir (Tamiflu), is approved for use in children age 1 year and older. Studies report significant reduction in symptoms and in the incidence of ear infections with this drug. In another study, when the antiviral drug, zanamivir (Relenza), was administered in the nasal passages of adults with influenza, middle ear abnormalities were reduced by more than half, to 32%. This drug is available for children older than 7 years for treatment of influenza, but no research has determined its value for preventing or treating otitis media in children.

[For more information, see In-Depth Report #94: Colds and influenza.]

Preventive Antibiotics. Antibiotics have been used to prevent bacterial infections in children with recurrent ear infections (4 or more episodes a year). Studies suggest, however, that overall they only prevent 1 episode a year, and are not generally recommended for prevention, except for specific situations.

Pneumococcal Vaccine. The pneumococcal conjugate vaccine (PCV) protects against S. pneumoniae (also called pneumococcal) bacteria in children, the most common cause of middle ear infections, pneumonia, and other respiratory infections. It is included in the Recommended Childhood Immunization Schedule and is specifically approved for preventing otitis media. High quality evidence indicates these vaccinations could result in over 1.5 million fewer office visits, over 20% fewer procedures for tube implants, and significantly fewer antibiotic prescriptions. The recommended schedule of pneumococcal immunization is four doses, given at 2, 4, 6, and 12 - 15 months of age.

Still, the pneumococcal vaccine does not completely protect against otitis media. The current pneumococcal vaccine does not protect against all subtypes of S. pneumoniae. Also, other types of bacteria can cause the problem. Scientists are working on developing a new type of pneumococcal vaccine that combines S. pneumoniae and H. influenzae strains that are not influenced by the currently available H. influenzae vaccine. Researchers hope this investigational vaccine may eventually help prevent middle ear infection caused by these organisms.

Healthy Diet. Daily diets should include foods such as fresh, dark-colored fruits and vegetables, which are rich in antioxidants and other important food chemicals that help boost the immune system.

Probiotics ("Good" Bacteria). Researchers are studying the possible protective value of certain strains of lactobacilli, bacteria found in the intestines. Some of these strains, particularly acidophilus, are used to make yogurt. Studies have been mixed on probiotics’ benefits for preventing ear infections.

Xylitol. Xylitol, a sugar alcohol produced naturally in birch, strawberries, and raspberries, has properties that fight Streptococcal pneumonia bacteria. A few studies have reported that children who chew gum or swallow a syrup containing xylitol experience fewer ear infections, but other studies have not shown that xylitol is helpful.

Parents or others should not smoke around children. Several studies have found that children who live with smokers have a significant risk for ear infections.

Breastfeeding offers protection against many early infections, including ear infections. Mother's milk provides immune factors that help protect the child from infections. Also, infants are held during breast-feeding in a position that allows the Eustachian tubes to function well. In addition, a 2006 study suggested that breastfeeding can help protect even those children who are genetically susceptible to ear infections.

If possible, new mothers should breast-feed their infants for at least 4 - 6 months. According to the American Academy of Pediatrics, exclusively breast-feeding for a baby’s first 6 months helps to prevent ear and other respiratory infections. For bottle-fed babies, to improve protection mothers should not lay babies down with their bottle; they should hold the infants in the same way they would to breast-feed them.

Treatment

Treatments for ear infections cost the U.S. $3 - 4 billion each year, and many of these treatments, particularly heavy antibiotic use and surgical procedures, are often unnecessary in many children.

Experts continue to argue about the best approach for treating ear infections. The major debates rest on the use of antibiotics, surgery, and watchful waiting in both acute otitis media (AOM) and otitis media with effusion (OME).

Until recently, nearly every American child with an ear infection who visited a doctor received antibiotics. In one region of the U.S., more than 70% of children received antibiotics before they were 7 months old, and the most common reason for these medications was acute otitis media.

Major studies now indicate that antibiotics are unnecessary in most cases of acute otitis media. Between 80 - 90% of all children with uncomplicated ear infections recover within a week without antibiotics. Likewise, receiving antibiotics for an acute ear infection does not seem to prevent children from having fluid behind the ears after the infection is cleared up. Antibiotics are rarely recommended for otitis media with effusion.

Antibiotic Resistance. The intense and widespread use of antibiotics is leading to a serious global problem of bacterial resistance to common antibiotics. In the U.S., nearly a quarter of S. pneumoniae are currently resistant to at least three antibiotics. High rates of resistance strains are even being observed in infants. In general, regions and institutions with the highest rate of resistance are those in which antibiotics are the most heavily prescribed.

Watchful Waiting for AOM. Because of the high rate of antibiotic resistance, and the fact that non-severe AOM usually resolves on its own without antibiotics, many pediatric guidelines recommend a “watchful waiting” period before antibiotics are prescribed. Current guidelines released by the American Academy of Pediatrics and the American Academy of Family Physicians recommend an initial observation period of 48 - 72 hours for select children. Pain relief can initially be given with acetaminophen (Tylenol), ibuprofen (Advil), or topical benzocaine drops.

If there is no improvement or symptoms worsen, parents can schedule an appointment with the child's doctor to determine if antibiotics are needed. (Parents should contact the doctor within the first 24 hours if their child is 6 months or younger and has fever or other severe symptoms.) Another option is to ask the doctor for a Safety Net Antibiotic Prescription (SNAP) that can be filled if symptoms do not improve within 48 - 72 hours

While children with non-severe AOM given antibiotics may recover slightly more quickly, they often have a high number of side effects and antibiotic-resistant bacterial strains. Studies have found that giving parents the option of delaying antibiotic treatment helps to reduce the unnecessary use of antibiotics without causing any health problems for the children. Unfortunately, surveys indicate that although medical guidelines recommend watchful waiting, few doctors regularly practice it.

The American Academy of Pediatrics (AAP) and the American Academy of Family Physicians (AAFP) guidelines and recent evidence support the following recommendations:

Accurate diagnosis of AOM including differentiation from OME.
Children fewer than 6 months of age should receive immediate antibiotic treatment.
Children 6 months or older should be treated for pain within the first 24 hours with either acetaminophen or ibuprofen.
An initial observation period of 48 - 72 hours is recommended for select children to determine if the infection will resolve on its own without antibiotic treatment. (Most children do improve within 72 hours.)
For children aged 6 months - 2 years, criteria for recommending an observation period are an uncertain diagnosis of AOM and a determination that the AOM is not severe. For children older than 2 years, the observation period criteria are non-severe symptoms or uncertain diagnosis. Severe AOM symptoms include moderate to severe pain and a fever of at least 102.2° F (39° C).
Antibiotic prophylaxis may be recommended for recurrent acute otitis media. Which children should be treated this way, as well as which antibiotics and for how long, have not been clearly determined.

The American Academy of Pediatrics (AAP), the American Academy of Family Physicians (AAFP), and the American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS) released updated clinical practice guidelines for OME in 2004. These guidelines include the following treatment recommendations:

Watchful Waiting for OME. The child is typically monitored for the first 3 months. Antibiotics are not helpful for most patients with OME. For one, the condition resolves without treatment in nearly all children, especially those whose OME followed an acute ear infection. About 75 - 90% of OME cases that result from AOM resolve within 3 months. If OME last longer than 3 months, a hearing test should be conducted. Even if OME lasts for longer than 3 months, the condition generally resolves on its own without any long term effects on language or development and intervention may not be necessary. The doctor will re-evaluate the child at periodic intervals to determine if there is risk for hearing loss.

Drug Treatment. It is important for parents to recognize that persistent fluid behind the eardrum after treatment for acute otitis media does not indicate failed treatment. Antibiotics, decongestants, antihistamines and corticosteroids do not help and are not recommended for routine management of OME. These drugs are not effective for OME, either when used alone or in combination. Antihistamines and decongestants may cause more harm than good by provoking side effects such as stomach upset and drowsiness. At present, there is no compelling evidence to indicate that allergy treatment can assist with OME management nor has a causal relationship between allergies and OME been established.

Surgery. The decision to pursue surgery must be determined on an individual basis. Children with OME lasting longer than 4 months may be considered candidates for surgery if they have:

Hearing loss greater than 40 dB
Hearing loss between 21 - 39 dB (Children in this group may be observed or considered for surgery)
Hearing loss of 20 dB or less, when speech, language, or developmental problems are observed
OME and structural damage to the ear canal, eardrum, or middle ear

Tympanostomy (the insertion of tubes into the eardrum) is the first choice for surgical intervention. Adenoidectomy (removal of adenoids) plus myringotomy (removal of fluid), with or without tube insertion, is sometimes recommended as a repeat surgical procedure. (Myringotomy alone is not recommended for OME treatment. Between 20 - 50% of children who undergo this procedure may have OME relapse and need additional surgery). Tube insertion may be advised for children younger than 4 years of age. Adenoidectomy is not recommended as an initial procedure unless some other condition (chronic sinusitis, nasal obstruction, adenoiditis) is present.

Tonsillectomy (removal of tonsils) is not recommended for OME treatment.

Home Remedies

Careful monitoring of the child's condition (watchful waiting) along with home remedies may be a viable alternative to antibiotic treatment for many children with a first episode of acute otitis media. However, in some situations parents should contact their medical professional immediately:

Seek immediate medical attention for high fever, severe pain, or other signs of complications.
Parents of infants should contact their doctor immediately if they have any fever, regardless other symptoms.

Before antibiotics, parents used home remedies to treat the pain of ear infections. Now, with current concern over antibiotic overuse, many of these remedies are again popular.

Depending on regional cultures, parents may have pressed a warm water bottle or warm bag of salt against the ear. Such old-fashioned remedies may still help to ease ear pain.
Due to the high risk of burns, ear candles should not be used to remove wax from ears. There is no evidence to indicate that these candles are safe or effective for treatment of AOM or other ear conditions.

Herbal remedies are not standardized or regulated, and their quality and safety are largely unknown. Parents should never give their child herbal remedies, including oral remedies, without approval from a doctor.

Valsalva's Maneuver. A simple technique called the Valsalva's maneuver is useful in opening the Eustachian tubes and providing occasional relief from the chronic stuffy feeling accompanying otitis media with effusion. It may also be useful for unplugging ears during air travel descent as well. It works as follows:

The child takes a deep breath and closes the mouth.
The child then blows the nose gently while, at the same time, pinching it firmly shut.
The parent should be sure to instruct the child not to blow too hard or the eardrum could be harmed.

Do not use this technique if an infection is present.

A number of pain relievers are available to help relieve symptoms.

Either acetaminophen (Tylenol) or ibuprofen (Advil) is the pain-reliever of choice in children.
Older children may be able to take prescription pain relievers that contain codeine if the pain is severe.
Eardrops containing anesthetics (Auralgan) are also available by prescription. Auralgan provides short-acting pain relief and may help children endure ear discomfort until an oral pain reliever takes effect. Parents should check with a doctor before using them. Eardrops could cause damage in children who have a ruptured eardrum. This might be indicated by fluid drainage from the ear canal.

Note: Aspirin and aspirin-containing products are not recommended for children or adolescents. Reports of Reye syndrome, a very serious condition, have been associated with aspirin use in children who have chicken pox or flu.

Many non-prescription products are available that combine antihistamines, decongestants, and other ingredients, and some are advertised as cold remedies for children. Researchers have found little or no benefits for acute otitis media or for otitis media with effusion using decongestants (either oral or nasal sprays or drops), antihistamines, or combination product. Their use is not recommended for AOM or OME. Recent research has questioned the general safety of these products and they are currently banned for use in children under age 2 years.

Swimming can pose specific risks for children with current ear infections or previous surgery. Water pollutants or chemicals may exacerbate the infection, and underwater swimming causes pressure changes that can cause pain. The following precautions should be taken:

Children with ruptured acute otitis media (drainage from ear canal) should not go swimming until their infections are completely cured.
Children with AOM that is not ruptured should not dive or swim underwater.
Some doctors recommend that children with implanted ear tubes should use earplugs or cotton balls coated in petroleum jelly when swimming to prevent infection. Others say earplugs are only necessary if the child will be diving underwater. Parents should consult their child's doctor.

Medications

When antibiotics are needed, a number of different classes are available for treating acute ear infections. Amoxicillin is a penicillin antibiotic and the drug of first choice. Other antibiotics are available for children who are allergic to penicillin or who do not respond within 2 - 3 days.

Duration. If a child needs antibiotics for acute otitis media, experts recommend they be taken for the following periods of time:

A 10-day course of antibiotics is usually recommended for children younger than 6 years of age, and for those with severe AOM.
Antibiotic therapy for 5 - 7 days is recommended for children 6 years of age or older with mild-to-moderate symptoms.

Parents should be sure their child finishes the entire course of therapy. Failure to finish is a major factor in the growth of bacterial strains that are resistant to antibiotics.

What to Expect. Earaches usually resolve within 24 hours after taking an antibiotic, although about 10% of children who are treated do not respond. This may occur when a virus is present or if the bacteria causing the ear infection is resistant to the prescribed antibiotic. A different antibiotic may be needed.

In some children whose treatment is successful, fluid will still remain in the middle ear for weeks or months, even after the infection has resolved. During that period, children may have some hearing problems, but eventually the fluid almost always drains away. Antibiotics should not be used to treat residual fluid.

Follow-Up. Your child should return to the doctor's office:

Two to 3 weeks after therapy, if initial therapy cleared up the infection and the child is less than 15 months old, or has risk factors for reinfection
Three to 6 weeks after treatment, if initial therapy cleared up the infection and the child is older than 15 months old and has no specific risk factors
Within 48 hours of taking the last antibiotic dose if signs of infection are still present (for example, there is still pus in the ear)

When suspecting complications, consult with an ear, nose, and throat specialist (otolaryngologist) . This specialist may perform a tympanocentesis or myringotomy, procedures in which fluid is drawn from the ear and examined for specific organisms. But, this is reserved for severe cases.

The selection of an antibiotic is determined in part by the severity of the child's condition as well as a history of response/non-response to antibiotic therapy. Treatment decisions take into account whether the child's condition is severe or non-severe.

Amoxicillin is generally recommended for first-line treatment of AOM. The combination drug amoxicillin-clavunate is prescribed for patients who have severe pain or a fever higher than 102.2° F(39° C). Other drug classes may be prescribed if a child is allergic to penicillin or does not respond to the initial therapy.

The following treatment guidelines provide general recommendations based on the severity of a child's AOM.

First-line treatment for non-severe AOM:

Amoxicillin 80 - 90 mg/kg per day orally. Amoxicillin is a penicillin antibiotic.

If the patient has an allergy or a history of non-response to penicillin drugs, one of the following antibiotics may be prescribed:

Azithromycin or clarithromycin. These drugs are in the macrolide class and are administered orally.
Cefdinir, cefuroxime, or cefpodoxime. These drugs, classified as cephalosporins, are taken by mouth. They may cause reactions in penicillin-allergic patients.

If the patient does not respond to amoxicillin or alternative antibiotic drugs after 48 - 72 hours, one of the following drugs may be prescribed:

Amoxicillin-clavulanate, clindamycin, or ceftriaxone. Ceftriaxone is injected intramuscularly. The other two drugs are administered orally. Each of these drugs is a different type of antibiotic. Amoxicillin-clavulanate (Augmentin) is classified as a penicillin; ceftriaxone (Rocephin) is a cephalosporin; clindamycin (Cleocin) is a lincosamide.

First-line treatment for severe AOM:

Amoxicillin-clavulanate (Augmentin). This antibiotic is known as an augmented penicillin. It works against a wide spectrum of bacteria and is administered orally.

Second-line treatment for severe AOM:

Ceftriaxone. Ceftriaxone (Rocephin) is an injectable cephalosporin that may be prescribed as an alternative to amoxicillin-clavulanate, especially for children who have vomiting or other conditions that hamper oral administration.
Tympanocentesis or clindamycin. Patients with severe AOM who have failed to respond to amoxicillin-clavulanate after 48 - 72 hours may require the withdrawal of fluid from the ear (tympanocentesis) in order to identify the bacterial strain causing the infection. If tympanocentesis cannot be performed, clindamycin may be prescribed orally to treat penicillin-resistant pathogens that have not responded to prior drug therapy.

The most common side effects of nearly all antibiotics are gastrointestinal problems, including cramps, nausea, vomiting, and diarrhea. This can be a significant problem in infants and small children. One study reported that giving such children a soy-based formula that contained fiber (Isomil DF) was helpful in reducing these side effects.
Amoxicillin use during infancy may lead to enamel defects and discolorations of permanent teeth.
Allergic reactions can also occur with all antibiotics but are most common with medications derived from penicillin or sulfa. These reactions can range from mild skin rashes to rare but severe, even life-threatening, anaphylactic shock.
Some drugs, including certain over-the-counter medications, interact with antibiotics. Parents should tell the doctor about all medications their children are taking.

Surgery

A tympanostomy involves the insertion of tubes to allow fluid to drain from the middle ear. The procedure involves:

A general anesthetic (asleep, no pain). Children typically recover completely within a few hours.
Myringotomy (removal of fluid) is performed first.
After myringotomy, the doctor inserts a tube to allow continuous drainage of the fluid from the middle ear.

Click the icon to see an illustrated series detailing ear tube insertion.

Postoperative Effects. Tympanostomy is a simple procedure, and the child almost never has to spend the night in the hospital. Acetaminophen (Tylenol) or ibuprofen (Advil) is sufficient for any postoperative pain in most children. Some children, however, may need codeine or other powerful pain relievers.

Generally, the tubes stay in the eardrum for at least several months before coming out on their own. On rare occasions, they will need to be surgically removed.

Complications. Otorrhea, drainage of secretion from the ear, is the most common complication after surgery and can be persistent in some children. It is usually treated with antibiotic eardrops. One study suggests that wearing earplugs may help the problem.

More serious complications from the operation are very uncommon, but may include:

General anesthetic risks. Rarely, allergic reactions or other complications, such as throat spasm or obstruction, may occur. The risk is highest in children who have other medical conditions, most commonly upper respiratory infections, lung disease, or GERD. Anesthetic-related risks are nearly always easily treated.
Tube blockage. Sometimes the tubes become blocked from sticky secretions or clotted blood after the operation.
Persistent eardrum perforation. This condition occurs when the eardrum does not close after the tubes have come out. It is the most common serious complication, but it is very rare.
Scarring can also occur, particularly in children who need more than one procedure, but it almost never affects hearing.
Small keratin (skin cell) containing cysts called cholesteatomas develop around the tube site in around 1% of patients.

Success Rates. Hearing is almost always restored following tympanostomy. Failure to achieve normal or near-normal hearing is usually due to complicated conditions, such as preexisting ear problems or persistent OME in children who have had previous multiple tympanostomies. Persistent fluid is the main reason for continued impaired hearing. Only a small percentage of hearing loss cases can be attributed to complications of the operation itself.

Earplugs as a Precaution. Many doctors feel that children should use earplugs when swimming while the tubes are in place in order to prevent infection. Others feel that as long as the child does not dive or swim underwater, earplugs may not be necessary. Parents should talk to their child's doctor about this subject. Cotton balls coated with petroleum jelly are effective alternatives to ear plugs. Children do not need to wear earplugs while showering.

Follow-Up. Eventually, the tubes fall out as the hole in the eardrum closes. This may happen after several months or more than a year later. It is painless. In fact, the patient and parents may not even be aware that the tubes are out.

About 20 - 50% of children may have OME relapse and need additional surgery that involves adenoidectomy and myringotomy. Tube reinsertion may be recommended for children younger than 4 years of age.

Myringotomy is used to drain the fluid and may be used (with or without ear tube insertion) in combination with adenoidectomy as a repeat surgical procedure if initial tympanostomy is not successful. It is not effective as a sole surgical procedure. Myringotomy involves the following steps:

The surgeon makes a very small incision in the eardrum.
Fluid is sucked out using a vacuum-like device.
The fluid is usually examined for identifying specific bacteria.
The eardrum heals in about a week.

Adenoids are collections of spongy lymph tissue in the back of the throat, similar to the tonsils. Removal of the adenoids, called adenoidectomy, is usually only considered for OME if a pre-existing condition exists such as chronic sinusitis, nasal obstruction, or chronic adenoiditis (inflammation of the adenoids). Unless these conditions exist, adenoidectomy is not recommended for treatment of OME.

Adenoidectomy plus myringotomy (removal of fluid) may be performed if an initial tympanostomy (tube insertion) procedure is unsuccessful in resolving OME. This combination procedure works best in children ages 4 years or older. Tube insertion is recommended for children under 4 years of age. It is not necessary to perform an adenoidectomy along with tube insertion for children under 4 years of age.

Click the icon to see an image of the adenoids.

Laser-assisted myringotomy is a technique that is being investigated as an alternative to conventional tympanostomy and myringotomy. At present, there is not enough evidence to say whether it is as good as ear tubes, the standard procedure. Some clinical trials have suggested that the success rate for laser-assisted myringotomy is half that of standard tympanostomy/myringotomy. Many insurance companies consider laser-assisted myringotomy to be an investigational procedure and will not pay for it.

Resources

www.nidcd.nih.gov -- National Institute on Deafness and Other Communication Disorders
www.aap.org -- American Academy of Pediatrics
www.entnet.org -- American Academy of Otolaryngology, Head and Neck Surgery

References

American Academy of Family Physicians; American Academy of Otolaryngology-Head and Neck Surgery; American Academy of Pediatrics Subcommittee on Otitis Media With Effusion. Otitis media with effusion. Pediatrics. 2004 May;113(5):1412-29.

American Academy of Pediatrics Committee on Infectious Diseases. Recommended immunization schedules for children and adolescents -- United States, 2007. Pediatrics. 2007 Jan;119(1):207-8.

American Academy of Pediatrics Subcommittee on Management of Acute Otitis Media. Diagnosis and management of acute otitis media. Pediatrics. 2004 May;113(5):1451-65.

Belshe RB, Edwards KM, Vesikari T, Black SV, Walker RE, Hultquist M, et al. Live attenuated versus inactivated influenza vaccine in infants and young children. N Engl J Med. 2007 Feb 15;356(7):685-96.

Dohar J, Giles W, Roland P, Bikhazi N, Carroll S, Moe R, et al. Topical ciprofloxacin/dexamethasone superior to oral amoxicillin/clavulanic acidin acute otitis media with otorrhea through tympanostomy tubes. Pediatrics. 2006 Sep;118(3):e561-9.

Griffin GH, Flynn C, Bailey RE, Schultz JK. Antihistamines and/or decongestants for otitis media with effusion (OME) in children. Cochrane Database Syst Rev. 2006 Oct 18;(4):CD003423.

Hatakka K, Blomgren K, Pohjavuori S, Kaijalainen T, Poussa T, Leinonen M, et al. Treatment of acute otitis media with probiotics in otitis-prone children-a double-blind, placebo-controlled randomised study. Clin Nutr. 2007 Jun;26(3):314-21. Epub 2007 Mar 13.

Hautalahti O, Renko M, Tapiainen T, Kontiokari T, Pokka T, Uhari M. Failure of xylitol given three times a day for preventing acute otitis media. Pediatr Infect Dis J. 2007 May;26(5):423-7.

Koopman L, Hoes AW, Glasziou PP, Cees L, Appelman L, Burke P, et al. Antibiotic therapy to prevent the development of asymptomatic middle ear effusion in children with acute otitis media: a meta-analysis of individual patient data. Arch Otolaryngol Head Neck Surg. Feb 2008;134(2):128-132.

Leach AJ, Morris PS. Antibiotics for the prevention of acute and chronic suppurative otitis media in children. Cochrane Database Syst Rev. 2006 Oct 18;(4):CD004401.

Little P. Delayed prescribing -- a sensible approach to the management of acute otitis media. JAMA. 2006 Sep 13;296(10):1290-1.

Paradise JL, Feldman HM, Campbell TF, Dollaghan CA, Rockette HE, Pitcairn DL, et al. Tympanostomy tubes and developmental outcomes at 9 to 11 years of age. N Engl J Med. 2007 Jan 18;356(3):248-61.

Prymula R, Peeters P, Chrobok V, Kriz P, Novakova E, Kaliskova E, et al. Pneumococcal capsular polysaccharides conjugated to protein D for prevention of acute otitis media caused by both Streptococcus pneumoniae and non-typable Haemophilus influenzae: a randomised double-blind efficacy study. Lancet. 2006 Mar 4;367(9512):740-8.

Ramakrishnan K, Sparks RA, Berryhill WE. Diagnosis and treatment of otitis media. Am Fam Physician. 2007 Dec 1;76(11):1650-8.

Smith JA, Danner CJ. Complications of chronic otitis media and cholesteatoma. Otolaryngol Clin North Am. 2006 Dec;39(6):1237-55.

Rosenfeld RM, Brown L, Cannon CR, Dolor RJ, Ganiats TG, Hannley M, et al. Clinical practice guideline: acute otitis externa. Otolaryngol Head Neck Surg. 2006 Apr;134(4 Suppl):S4-23.

Rosenfeld RM, Singer M, Wasserman JM, Stinnett SS. Systematic review of topical antimicrobial therapy for acute otitis externa. Otolaryngol Head Neck Surg. 2006 Apr;134(4 Suppl):S24-48.

Rovers MM, Glasziou P, Appelman CL, Burke P, McCormick DP, Damoiseaux RA, et al. Antibiotics for acute otitis media: a meta-analysis with individual patient data. Lancet. 2006 Oct 21;368(9545):1429-35.

Ruohola A, Meurman O, Nikkari S, Skottman T, Salmi A, Waris M, et al. Microbiology of acute otitis media in children with tympanostomy tubes: prevalences of bacteria and viruses. Clin Infect Dis. 2006 Dec 1;43(11):1417-22.

Spiro DM, Tay KY, Arnold DH, Dziura JD, Baker MD, Shapiro ED. Wait-and-see prescription for the treatment of acute otitis media: a randomized controlled trial. JAMA. 2006 Sep 13;296(10):1235-41.

Review Date:
2/19/2008
Reviewed By:
Harvey Simon, MD, Editor-in-Chief, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

A.D.A.M. Copyright

adam.com

Migraine headaches

FitSugar — Wed, 08 Oct 2008 17:35:00 -0700

In This Report

Highlights
Introduction
Prognosis
Causes
Risk Factors
Diagnosis
Treatment Approaches
Medications Used for Treatm...
Prevention
Medications Used for Preven...
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Migraine Surveys

About 17.1% of women and 5.6% of men suffer migraines, according to the 2007 American Migraine Prevalence and Prevention survey. Nearly a third of respondents reported 3 or more migraine attacks per month. Over half were severely impaired or needed bed rest during attacks. Although many patients met the criteria for preventive medication, only a small percentage actually received it.
About 20% of patients with migraine take potentially addictive opioid and barbiturate drugs, even though these drugs have not been approved by the Food and Drug Administration (FDA) for migraine treatment, according to a 2007 survey commissioned by the U.S. National Headache Foundation.

FDA Actions

The opioid drug fentanyl (Fentora) should not be prescribed "off-label" to patients with migraine or other severe headaches, warns the FDA, following several reports of drug-related deaths. Fentanyl is approved only for treating cancer pain.
In 2007, the FDA pulled 15 unapproved ergotamine preparations off the market because they lacked a warning label describing the risks for serious drug interactions.

Migraines in Adolescents

Many adolescents may stop having migraines, or transition to less severe types of headaches, when they reach adulthood, suggests a small 2006 study in Neurology.
Zolmitriptan (Zomig) nasal spray appears to be safe and effective for adolescent migraine, indicates a 2007 study in Pediatrics. Zolmitriptan, like all migraine drugs, is currently approved only for adults.

Sumatriptan-Naproxen Combination

A combination of the triptan drug sumatriptan (Imitrex) and the nonsteroidal anti-inflammatory drug naproxen (Aleve) works better for migraine pain relief than either drug alone, according to a 2007 study in the Journal of the American Medical Association.

Introduction

The pain from a headache does not start from inside the brain. (The brain itself can not feel pain.) Instead, headache pain begins in one or more of the following locations:

The tissues covering the brain
The structures at the base of the brain
Muscles and blood vessels around the scalp, face, and neck

Headache is generally categorized as primary or secondary.

Primary Headache. A headache is considered primary when a disease or other medical condition does not cause it.

Tension headache is the most common primary headache and accounts for 90% of all headaches. [See In-Depth Report # 11: Tension headaches.]
Neurovascular headaches are the second most common primary headaches. This type includes migraines and cluster headaches. [See In-Depth Report # 99: Cluster headaches.] Such headaches are caused by an interaction between blood vessel and nerve abnormalities.

Click the icon to see a depiction of migraine cause.

Secondary Headache. Secondary headaches are caused by other medical conditions, such as sinusitis, neck injuries or abnormalities, and stroke. About 2% of headaches are secondary headaches caused by abnormalities or infections in the nasal or sinus passages. [See "Causes of Secondary Headaches," in this report.]

It is not uncommon for someone to experience a combination of headache types.

Click the icon to see a comparison of headache symptoms.

Migraine is now recognized as a chronic illness, not simply as a headache. About 28 million people suffer from migraines annually. They are often classified by whether or not auras (seeing bright "spots" or "stars") accompany them:

Common migraines are without auras. About 75% of migraines are the common type.
Classic migraines are those with auras.

A person may experience one or the other at different times.

In general, there are four phases to a migraine (although they may not all occur in every patient): The prodrome phase, auras, the attack, and the postdrome phase.

Prodrome. The prodrome phase is a group of vague symptoms that may precede a migraine attack by several hours, or even a day or two. Prodrome symptoms include:

Sensitivity to light or sound
Changes in appetite
Fatigue and yawning
Malaise
Mood changes
Food cravings

Auras. Auras are sensory disturbances that occur before the migraine attack in 1 in 5 patients. Visually, auras are referred to as being positive or negative:

Positive auras include bright or shimmering light or shapes at the edge of their field of vision called scintillating scotoma. They can enlarge and fill the line of vision. Other positive aura experiences are zigzag lines or stars.
Negative auras are dark holes, blind spots, or tunnel vision (inability to see to the side).
Patients may have mixed positive and negative auras. This is a visual experience that is sometimes described as a fortress with sharp angles around a dark center.

Other neurologic symptoms may occur at the same time as the aura, although they are less common. They include:

Speech disturbances
Tingling, numbness, or weakness in an arm or leg
Perceptual disturbances such as space or size distortions
Confusion

Migraine Attack. If untreated, attacks usually last from 4 - 72 hours. A typical migraine attack produces the following symptoms:

Throbbing pain on one side of the head. The word migraine, in fact, is derived from the Greek word hemikrania, meaning "half of the head" because the pain of migraine often occurs on one side. Pain also sometimes spreads to affect the entire head.
Pain worsened by physical activity
Nausea, sometimes with vomiting
Visual symptoms
Facial tingling or numbness
Extreme sensitivity to light and noise
Looking pale and feeling cold

Less common symptoms include tearing and redness in one eye, swelling of the eyelid, and nasal congestion, including runny nose. (Such symptoms are more common in certain other headaches, notably cluster headaches. In one study, however, they occurred in over 40% of migraine sufferers.)

Postdrome. After a migraine attack, there is usually a postdrome phase, in which patients may feel exhausted and mentally foggy for a while.

In some cases, patients eventually experience on-going and chronic headaches. In fact, in an analysis using two different diagnostic methods, between 87 - 90% of daily chronic headaches were actually migraines. Some doctors believe that, unless otherwise demonstrated, any chronic headache consisting of episodes of disabling pain that recur regularly over years should be considered as a migraine.

Chronic migraines may occur from overuse of migraine medications (called a rebound headache) or may develop over time (called transformed migraine).

Rebound Headache. The most common cause of chronic migraine is the rebound effect, which is a cycle caused by overuse of migraine medications. The process involves the following:

Patients typically have taken pain medication for more than 3 days a week on an ongoing basis.
When the patients stop taking medication, they experience a rebound headache.
They start taking the drugs again.
Eventually the headache simply persists, and medications are no longer effective.

Medications implicated in rebound migraines include nonprescription painkillers (acetaminophen, aspirin, ibuprofen), barbiturates, sedatives, narcotics, and migraine medications, particularly those that also contain caffeine. (Heavy caffeine use can also cause this condition.)

Transformed Migraines. In some cases, migraines themselves evolve into chronic, daily headaches called transformed migraines. Such headaches resemble tension headaches but are more likely to be accompanied by gastrointestinal distress and mental or visual disturbances and, in women, to be affected by menstrual cycles. In one study, the risk for transformed migraines were associated with other factors, including allergies, asthma, hypothyroidism, hypertension, and a daily intake of caffeine.

Migraines are defined by the number and length of attacks and whether an aura is present.

Definition of Migraines without Auras (Common Migraine). To be defined as a migraine without aura, a patient should have at least five attacks that have the following characteristics:

A. Each untreated, or unsuccessfully treated, attack must last 4 - 72 hours.

B. It must have at least two of the following four characteristics:

Pain on one side of the head
Pulsing or throbbing pain
Pain severe enough to impair or prevent daily activities
Pain must be intensified by exertion, such as walking up stairs

C. During a headache at least one of the following symptoms must also be present:

Nausea, vomiting or both
Sensitivity to light and noise

In addition, other neurologic or medical conditions that might be causing this pain must be ruled out, or, if they do occur, they are not related in time to the suspected migraine.

Definition of Migraines with Auras (Classic Migraine). To be defined as a migraine with aura, the patients must have at least two attacks that have three out of four of the following events.

At least one fully reversible aura symptom suggesting the headache starts in the cerebral cortex or brain stem.
At least one aura symptom that develops gradually over more than 4 minutes ,or two or more aura symptoms that occur in succession.
No single aura symptom that lasts more than 1 hour. (There may be successive aura symptoms that extend that time, but each one should not last more than 60 minutes.)
The headache itself may begin before, at the same time, or at an interval of no more than an hour after the aura.

As with common migraines, other neurologic or medical conditions that might be causing this pain must be ruled out or if they occur, they are not related in time to the suspected migraine.

Click the icon to see a definition of a migraine.

Although migraine is considered to be a specific chronic illness, it has various presentations that occur in different individuals.

Menstrual Migraines. Migraines are often tied to a woman’s menstrual cycle. Researchers think that estrogen plays a role. About half of women with migraines report an association with menstruation. Compared to migraines that occur at other times of the month, menstrual migraines tend to be more severe, last longer, and not have auras. Triptan drugs can provide relief and may also help prevent these types of migraines.

The highest incidence of migraines typically occurs during the early follicular phase, (beginning of menstruation). A 2005 study found that women are 1.7 times more likely to have a migraine during the 2 days before menstruation begins. But, women are 2.5 times more likely to have a migraine during the first 3 days of menstruation. During this time, migraines are more likely to be severe, with symptoms that include vomiting.

Ophthalmoplegic Migraine. This very rare headache tends to occur in younger adults. The pain centers around one eye and is usually less intense than in a standard migraine. It may be accompanied by vomiting, double vision, a droopy eyelid, and paralysis of eye muscles. Attacks can last from hours to months. A computed tomography (CT) or magnetic resonance imaging (MRI) scan may be needed to rule out an aneurysm (a rupture blood vessel) in the brain.

Retinal Migraine. Symptoms of retinal migraine are short-term blind spots or total blindness in one eye that lasts less than an hour. A headache may precede or occur with the eye symptoms. Sometimes retinal migraines develop without headache. Other eye and neurologic disorders must be ruled out.

Basilar Migraine. Considered a subtype of migraine with aura, this migraine starts in the basilar artery, which forms at the base of the skull. It occurs mainly in young people. Symptoms may include vertigo (the room spins), ringing in the ears, slurred speech, unsteadiness, possibly loss of consciousness, and severe headaches.

Familial Hemiplegic Migraine. This is a very rare inherited genetic migraine disease. It can cause temporary paralysis on one side of the body, vision problems, and vertigo. These symptoms occur about 10 - 90 minutes before the headache.

Status Migrainosus. This is a serious and rare migraine. It is so severe and lasts so long that it requires hospitalization.

About 90% of people seeking help for headaches have a primary headache disorder. The balance of secondary headaches is caused by an underlying disorder that produces the headache as a symptom. Many conditions cause headaches as a symptom. Some of the most common are listed below.

Sinus Headache. Many primary headaches, including migraine, are misdiagnosed as sinus headaches. Nearly 9 in 10 patients who think they have sinus headaches actually have or probably have had a migraine. Sinus headaches occur in the front of the face, usually around the eyes, across the cheeks, or over the forehead. They are usually mild in the morning and increase during the day and are usually accompanied by fever, runny nose, congestion, and general debilitation. Sinus headaches spread over a larger area of the head than migraines, but telling the difference between these two kinds of headache is difficult, particularly if a headache is the only symptom of sinusitis. The two may even coexist in many cases. Often, the visual changes associated with migraine can rule out sinusitis, but such visual changes do not occur with all migraines. (Rarely, sinusitis can cause double vision and even vision loss, a sign of very serious infection.)

Headache Due to Neck Problems. Some headaches may be caused by abnormalities of the neck muscles resulting from prolonged poor posture (such as that caused by sitting in front of a computer keyboard or driving daily for long periods), arthritis, injuries of the upper spine, or abnormalities in the cervical spine (the spinal bones in the neck). Nerves in the neck converge in the trigeminal nerve in the face and can generate pain signals that the brain may interpret as headache. Pain is usually on one side. Even if it affects both sides of the head, it is usually more severe on one side. The quality of the headache may be similar to an aching tension headache or a mild migraine without aura.

Temporomandibular Joint Dysfunction. Temporomandibular joint dysfunction (TMJ) is caused by clenching the jaws or grinding the teeth (usually during sleep), or by abnormalities in the jaw joints themselves. The diagnosis is easy if chewing produces pain or if jaw motion is restricted or noisy. TMJ pain can occur in the ear, cheek, temples, neck, or shoulders.

Brain Tumor. Fear of having a brain tumor is common among people with headaches, but a headache is almost never the first or only sign of a tumor. Changes in personality and mental functioning, vomiting, seizures, and other symptoms are more likely to appear first. When the headache does develop, it is often worse early in the morning or may awaken sufferers during the night.

Neuralgia. Neuralgia is pain due to nerve abnormalities, which can occur in the facial area and resemble migraine or sinus headaches.

Hypertension. Although many people attribute headaches to high blood pressure, the two are rarely associated. An exception is malignant hypertension, an uncommon medical emergency, in which the blood pressure abruptly rises to extreme levels, causing damage to blood vessels in the brain, heart, and kidneys.

Head Injuries. It is obvious that a significant blow to the head will cause pain. Post-injury headaches, however, can reflect serious damage, ranging from skull fractures to internal bleeding.

Disorders of the Meninges. The meninges are the membranes covering the brain and the spinal cord. In very rare instances, ordinary physical strain may injure or weaken the meninges, causing a leakage of cerebrovascular fluid (the fluid that bathes the brain). This can cause severe headache and nausea, which are relieved by lying flat. The condition is very treatable. Meningitis, which is an infection or irritation of these membranes, is an uncommon but potentially serious cause of severe headache. Other symptoms include nausea and stiffness or pain in the neck.

Miscellaneous Causes of Benign Headaches. Rapid consumption of ice cream or other very cold foods or beverages is the most common trigger of sudden headache pain. (It may be prevented by warming the food or drink for a few seconds in the front of the mouth before swallowing.) Other common benign causes of headache include eyestrain, dental problems, allergies, systemic infections, and caffeine withdrawal. Headaches may be induced by sexual activity or intense physical exertion. Leakage from spinal cord fluid is rare but can cause headaches that may be mistaken for brain tumors.

Click the icon to see an image of the sinuses.

Prognosis

For many people, migraines eventually go into remission and sometimes disappear completely, particularly as they age. Estrogen decline after menopause may be responsible for remission in some older women. One study reported that the following people with migraines (called migraineurs) have a better chance of remission if they have:

A family history of migraine with aura
Migraines that are not triggered by light
No other primary headaches

According to another study, a history of head trauma or oral contraceptive use predicted a poorer long-term outlook.

Migraine or severe headache is a risk factor for stroke in both men and women, especially before age 50. About 19% of all strokes occur in people with a history of migraine. Research indicates that migraine also increases the risk for other types of heart problems.

Migraine with aura carries a higher risk for stroke than without auras. A 2005 analysis of over 12,000 participants from an atherosclerosis risk study found that migraine with aura was significantly associated with higher risk for stroke and transient ischemic attacks. Another 2005 study suggested that people who experience migraine with aura tend to have more cardiovascular risk factors than people without migraine. These risk factors included worse cholesterol profile, higher blood pressure, early history of heart disease and stroke, and greater likelihood of using oral contraceptives.

Results from a 2005 study showed that women who have migraine with aura are at increased risk of ischemic stroke compared with those who do not have auras and those who have non-migraine headaches. Women under age 55 had the highest risk, with more than double the risk. A 2006 Women’s Health Study of women ages 45 and older found that migraine with aura also increases women’s risk for heart attack, angina, and death due to ischemic heart disease (in which blood flow is decreased due to narrowing of coronary arteries). Migraine without aura did not increase heart disease and stroke risks.

Studies suggest specific stroke risk factors for younger women with migraines, particularly those with auras. Smoking, high blood pressure, and birth control pills considerably raise one's risk 10 - 20 times.

Researchers are also studying the relationship between patent foramen ovale (PFO) and migraine. A PFO is a hole in the wall dividing the upper left and right heart chambers. About half of patients with PFO have severe migraines with aura. Researchers are investigating whether surgical repair of the PFO may help control migraines in patients with this heart condition.

Migraine and other headaches associated with aura may increase the risk for retina damage (retinopathy) among middle-aged people, suggests a 2007 study.

The negative impact of migraines on quality of life, families, and even work productivity is significant and often underrated as a serious complication. Studies indicate that people with migraines have poorer social interactions and emotional health than patients with chronic medical illnesses, including asthma, diabetes, and arthritis. Anxiety (particularly panic disorders) and major depression are also strongly associated with migraines.

A 2005 National Headache Foundation-sponsored survey of migraine sufferers reported that:

90% of people with migraines could not function normally on the day of a migraine attack
80% experienced abnormal sensitivity to light and noise
75% experienced nausea and vomiting
30% required bed rest
25% missed at least 1 day of work due to migraine in past 3 months

Effect of Pregnancy on Migraines. In one study, pregnant women with tension or migraine headaches experienced 80% fewer headaches, usually after the end of the first trimester.

Effect of Migraine on the Pregnant Woman or Fetus. Migraine headaches do not pose any added risks during pregnancy to the mother or the fetus, although women with migraines may be at higher risk for having smaller (but not premature) babies.

Causes

Until recently, the general theory on the migraine process rested solely on the idea that abnormalities of blood vessel (vascular) systems in the head were responsible for migraines. Now, however, doctors tend to believe that migraine starts with an underlying central nervous system disorder. When triggered by various stimuli, this disorder sets off a chain of neurologic and biochemical events, some of which subsequently affect the brain's vascular system. No experimental model fully explains the migraine process.

There is certainly a strong genetic component in migraine with or without auras. Researchers have located a single genetic mutation responsible for the very rare familial hemiplegic migraine, but several genes are likely to be involved in the great majority of migraine cases. Numerous chemicals, structures, nerve pathways, and other players involved in the process are under investigation.

Central Nervous Disorder. One theory that attempts to integrate many of the known events in the migraine process is as follows:

Stress or some unknown factor triggers the release of certain protein fragments called peptides (Substance P, calcitonin gene-related peptide, and others).
These peptides dilate blood vessels and produce an inflammatory response that triggers over-excitation of the nerve cells in the trigeminal pathway. [This nerve pathway runs from the brain stem to the head and face. These nerves spread to the meninges (the membrane covering of the brain).]
While the brain itself is insensitive to pain, the meninges and blood vessels around the brain are sensitive to pain. Some doctors suggest that pain occurs when blood drains from the center of the head to the blood vessels around the brain.
Auras are believed to be a response to blood flow changes that cause a rapid reduction in brain activity that reaches the cerebral cortex (the outer layer of the brain), referred to as spreading depression. This effect may be visualized as an electrical wave spreading through the brain just as a wave of water is caused by the dropping of a pebble. Some research suggests that in people with auras, the cortical spreading depression itself activates the inflammation in the trigeminal nerves that triggers pain in the meninges.

One theory of the cause of migraine is a central nervous system (CNS) disorder. The CNS consists of the brain and spinal cord. In migraine, various stimuli may cause a series of neurologic and biochemical events that affect the brain's vascular system.

Abnormal 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 appear to play a particularly critical role in migraine:

Calcium channels regulate the release of serotonin, an important neurotransmitter in the migraine process. (A neurotransmitter is a chemical messenger that allows communication between nerves in the brain.)
Magnesium interacts with calcium channels, and magnesium deficiencies have been detected in the brains of patients with migraine.
Calcium channels also play a major role in cortical spreading depression, the brain event that appears to be important in migraine symptoms.

Some patients with migraines 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.

Researchers are also investigating factors that are common to both migraines and tension-type headaches. Some research suggests that both problems may result from a continuum of abnormalities in the central nervous system (the nerves in the brain and spine). Such changes trigger a progression of symptoms starting with mild sensations, developing into tension headache, and finally, progressing in some people to a migraine.

Dopamine, for example, may act as a stimulant 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 (mood changes, yawning, drowsiness), for example, have been associated with increased dopamine activity. Dopamine receptors are also involved in regulation of blood flow in the brain.

Nitric Oxide. Other research suggests that over-excitable neurons release nitric oxide, a small molecular messenger that may be important in triggering in most primary headaches (tension-type, cluster, and migraines). Elevated levels have been observed in blood cells of patients with tension-type headache. Some evidence suggests that the release of this molecule in blood vessels may activate nerve pathways in the brain, muscles, or elsewhere and increase pain.

Estrogen Fluctuations in Women. Tension-type headaches and migraine headaches are slightly more common in females during adolescence and adulthood. Most likely hormone fluctuations, rather than whether levels are elevated or low, trigger headaches. Some research suggests that fluctuations in estrogen levels may impact levels of serotonin and other pain-modulating substances that affect these headaches.

A wide range of events and conditions can alter conditions in the brain that bring on nerve excitation and trigger migraines. They include, but are not limited to:

Emotional stress
Intense physical exertion (exercise, lifting, and even bowel movements or sexual activity)
Abrupt weather changes
Bright or flickering lights
High altitude
Travel motion
Lack of sleep
Low blood sugar and fasting
Chemicals found in certain foods. More than 100 foods may potentially trigger migraine headache. Caffeine is one such trigger. Caffeine withdrawal can also trigger migraines in people who are accustomed to caffeine. Experts recommend that patients keep a headache diary to track which foods trigger migraine.

Risk Factors

About 30 million Americans suffer from migraine headaches. They affect about 17% of all women and 6% of men. In fact, 70% of all migraine sufferers are women. Migraine is more prevalent among women throughout the world and in every culture. Although the incidence of migraine is similar for boys and girls during childhood, it increases in girls after puberty. Most people with migraine have 1 - 4 attacks per month.

Hormone Fluctuations in Women. Most migraines in women develop during the hormonally active years between adolescence and menopause. Fluctuations of estrogen and progesterone, rather than their presence, appear to increase the risk for migraines and their severity in some women.

About half of women with migraines report headaches associated with their menstrual cycle, although true menstrual migraines may actually be less common. True menstrual migraines tend not to have auras and to increase in prevalence between 2 days before and 5 days after the onset of period.
The first 3 months of pregnancy can worsen migraines in some women, although one study reported that pregnancy had little effect one way or the other on severity in most women with chronic headaches.
Women whose migraines are affected by pregnancy or menstruation are also likely to have worse migraines if they take oral contraceptives or hormone replacement therapies.

General Age of Onset. More than 20% of adults with migraines report that their headaches started before age 10, and over 45% say they started before age 20. The incidence of migraine declines in both men and women after age 40.

Migraine in Children. Migraine headaches occur in all ages and can appear in children as young as 4 years of age. Migraines in children are equally prevalent in boys and girls. Studies estimate that about 4 – 10% of all children suffer from migraine. Research indicates that overweight children may be especially susceptible to headaches, although this association is most likely due to poor nutrition and lack of exercise rather than excess weight. Children who have sleep problems, especially difficulty falling asleep, may also be more prone to migraines.

A small 2006 study indicated that some adolescents with migraine may eventually grow out of their condition. By the end of the 10-year study, 38% of patients had stopped having migraines, and 20% had transitioned into less severe tension-type headache. Children with a family history of migraine were more likely to continue having migraines.

Migraine Onset in Older Adults. Although uncommon, late-life migraine occurs in about 1% of the population, usually in men. In such cases, it often occurs as migraine with visual disturbances but without headache.

Migraine headaches can be inherited. If both parents suffer from migraines, their children have a 75% chance of getting them. When only one parent gets migraines, there is a 50% chance that children will be afflicted.

Caucasians have a higher risk than either African-Americans or Asians. Worldwide, one study reported that migraines are most common in North America. They are slightly less prevalent in South America and Europe and far less common in Asia and Africa. Investigators believe that the differences are due to genetic variations, not lifestyle factors.

People with migraine have a higher incidence of other medical conditions, including:

Asthma and allergies. These conditions have also been associated with a higher risk for conversion from having periodic migraines attacks to a chronic form (transformed migraines).
H. pylori infection. People who are infected with the bacteria H. pylori, the major cause of peptic ulcers, are at higher risk for migraines.
Epilepsy. Patients with epilepsy are twice as likely to have migraines as the general population.
Fibromyalgia
Systemic lupus erythematosus
Raynaud syndrome
Mitral valve prolapse
Narcolepsy

One study suggested that women with migraines tend to over-respond to stressful situations. In the study, they were more likely than other women to be diligent, conscientious, and overly sensitive to pressure from others. More likely, however, a person's family history of migraine, rather than any personality trait, is the important risk factor.

Diagnosis

Anyone, including children, who has recurring or persistent headaches should consult a doctor. There are no blood tests or imaging techniques that can be used to diagnose migraine headaches. A diagnosis will be made on the basis of history and physical exam, and, if necessary, tests may be necessary to rule out other diseases or conditions that may be causing the headaches. It is important to choose a doctor who is sensitive to the needs of headache sufferers and aware of the latest advances in treatment.

For an accurate diagnosis, the patient should describe:

Duration and frequency of headaches
Recent changes in their character
Location of pain
Type of pain (throbbing or steady pressure)
Intensity of the headache
Associated symptoms, such as visual disturbances or nausea and vomiting
Behaviors during a headache. This may help distinguish between migraine and tension headaches. The predominant behavior with tension headaches is massaging the scalp, temples, or the nape of the neck. A person with migraines is more apt to use compression (such as tying a scarf around the forehead and temples) or to apply cold. They also tend to isolate themselves, lie down, induce vomiting, and use more pillows than usual. (None of these maneuvers do much good in relieving either headache, unfortunately.)

The presence of auras or other visual disturbances do not always identify migraine:

Patients with severe sinus infections may experience double vision or visual loss. (This is an emergency condition, since it indicates the infection has spread to areas around the eyes.)
Many migraine sufferers have no auras.
Many elderly people with late-onset migraine have auras but no pain.

Note all conditions, including any foods eaten, preceding an attack. Often two or more triggers interact to produce a headache. For example, a combination of weather changes and fatigue can make headaches more likely than the presence of just one of these events.
Keep a migraine record for at least three menstrual cycles. For women, this can help to confirm or refute a diagnosis of menstrual migraine.
Track medications. This is important for identifying possible rebound headache or transformed migraine.
Attempt to define the intensity of the headache using a number system, such as:

1 = Mild, barely noticeable

2 = Noticeable, but does not interfere with work/activities

3 = Distracts from work/activities

4 = Makes work/activities very difficult

5 = Incapacitating

The patient should report any other conditions that might be associated with headache, including but not limited to:

Any chronic or recent illness and their treatments
Any injuries, particularly head or back injuries
Any uncharacteristic dietary changes
Any current medications or recent withdrawals from any drugs, including over-the-counter or natural remedies.
Any history of caffeine, alcohol, or drug abuse.
Any serious stress, depression, and anxiety.

The doctor will also need a general medical and family history of headaches or diseases, such as epilepsy, that may increase their risk. Migraine tends to run in families.

In order to diagnose a chronic headache, the doctor will examine the head and neck and will usually perform a neurologic examination, which includes a series of simple exercises to test strength, reflexes, coordination, and sensation. The doctor may ask questions to test short-term memory and related aspects of mental function.

Extensive testing may be advised for anyone with a chronic, daily headache. Tracking times of medications, withdrawal, and headache, using the headache diary, is usually very helpful in diagnosis.

Differentiating Rebound Headaches from Transformed Migraines. Migraines that evolve to chronic headaches must be first differentiated between natural transformed migraines and rebound headaches (the most common cause of persistent migraines):

A transformed migraine is usually more consistent in its severity and its location than a rebound headache.
Transformed migraines are less sensitive to triggers than rebound headaches.

Differentiating Transformed from Tension Headaches. Once rebound headache is ruled out, the doctor must then differentiate natural transformed migraines from tension headaches:

In most cases of transformed migraine (but not tension headache), gastrointestinal or neurologic symptoms are present.
Transformed migraine is also frequently associated with menstrual fluctuations in women.

Imaging tests of the brain may be recommended under the following circumstances:

If the results of the history and physical examination suggest neurologic problems.
For patients with headaches that wake them at night.
For new headaches in the elderly. In this age group, it is particularly important to first rule out age-related disorders, including stroke, hypoglycemia, hydrocephalus, and head injuries (usually from falls).
For patients with worsening headaches.

They are not recommended for patients with migraine and with no other abnormal indications.

The following tests may be used:

A CT (computed tomography) scan may be ordered to rule out brain disorders or headaches caused by chronic sinusitis.
X-rays and other tests may also be used if sinusitis is strongly suspected.
A neck x-ray can reveal arthritis or spinal problems.
Other imaging tests include an MRI (magnetic resonance imaging), EEG (electroencephalogram), lumbar puncture, ultrasound testing, and cerebral angiography, positron emission tomography (PET), and single-photon emission computed tomography (SPECT). These tests are only performed if there is reason to suspect an underlying disease or as part of clinical studies.

A CT (computed tomography) scan is a much more sensitive imaging technique than x-ray, allowing high definition of not only the bony structures but also the soft tissues. Clear images of organs and structures, such as the brain, muscles, joints, veins and arteries, as well as of tumors and hemorrhages, may be obtained with or without the injection of contrasting dye.

Headaches indicating a serious underlying problem, such as cerebrovascular disorder or malignant hypertension, are uncommon. (It should again be emphasized that a headache is not a common symptom of a brain tumor.) People with existing chronic headaches, however, might miss a more serious condition by believing it to be one of their usual headaches. Such patients should call a doctor promptly if the quality of a headache or accompanying symptoms has changed. Everyone should call a doctor for any of the following symptoms:

Sudden, severe headache that persists or increases in intensity over the following hours, sometimes accompanied by nausea, vomiting, or altered mental states (possible hemorrhagic stroke).
Sudden, very severe headache, worse than any headache ever experienced (possible indication of hemorrhage or a ruptured aneurysm).
Chronic or severe headaches that begin after age 50.
Headaches in the back of the head accompanied by other symptoms, such as memory loss, confusion, loss of balance, changes in speech or vision, or loss of strength in or numbness or tingling in arms or legs (possibility of small stroke in the base of the skull).
Headaches after head injury, especially if drowsiness or nausea are present (possibility of hemorrhage).
Headaches accompanied by fever, stiff neck, nausea and vomiting (possibility of spinal meningitis).
Headaches that increase with coughing or straining (possibility of brain swelling).
A throbbing pain around or behind the eyes or in the forehead accompanied by redness in the eye and perceptions of halos or rings around lights (possibility of acute glaucoma).
A one-sided headache in the temple in elderly people; the artery in the temple is firm and knotty and has no pulse; scalp is tender (possibility of temporal arteritis, which can cause blindness or even stroke if not treated).
Sudden onset and then persistent, throbbing pain around the eye possibly spreading to the ear or neck unrelieved by pain medication (possibility of blood clot in one of the sinus veins of the brain).

Treatment Approaches

Many effective headache remedies are available for treating a migraine attack. Still, a study that analyzed over 800,000 cases of migraine reported that most migraines are not treated according to any recommended guidelines. In the study, 30% of patients were treated with potentially addictive opioids -- most often merepidine (Demerol). Furthermore, 70% of these patients were not offered effective and available anti-migraine drugs. Anti-nausea drugs that have no effect on headaches were used six times more often than drugs that reduce headaches.

A 2007 survey of migraine sufferers, commissioned by the U.S. National Headache Foundation, reported that 20% of patients are prescribed non-approved medications containing opioids or barbiturates. The survey also indicated that patients who take non-approved drugs are more likely to experience drug-related side effects. For mild migraines, non-prescription treatments (Excedrin Migraine, Advil Migraine, Motrin Migraine Pain) are the best first choice. For severe migraines, doctors recommend starting with a triptan drug.

Preventive treatment, used to stop migraine attacks before they happen, may help many patients. According to another 2007 survey, more than 1 in 4 patients with migraine are candidates for preventive therapy but most do not receive it.

As many as 30% of patients with migraine also have accompanying headaches resulting from tension, drugs, infections, or other causes. It is important to distinguish between headache types in order to determine appropriate treatment.

General Guidelines. The general goals of treatment are:

Choose drugs with as few side effects as possible. Patients should talk to their doctors about various methods for administering the medication (pills, injections, nasal spray, or rectal suppositories) and begin with the one they believe will be the least distressing.
Treat the attack rapidly, within an hour of symptom onset if possible. Start with low doses, and build up dosage slowly.
Try to minimize the use of back-up or "rescue medications." (A rescue medication is typically a narcotic opiate drug, which is used for pain relief when other medications fail.)
Try to guard against rebound effect. Nearly all drugs used for migraine can cause rebound headache, and patients should not take any the drugs for longer than 2 days per week.
It may take 2 - 4 months for any drug to be effective.

Stepped-Up Treatment Approach. Some doctors recommend a stepped-up treatment course for an acute migraine attack. This involves starting with the least potent treatments and taking increasingly more powerful drugs until the pain stops. In this approach, patients may need up to five different medications to achieve pain relief. A typical stepped-up approach is the following:

The patient should first use nonprescription pain relievers (NSAIDs, Excedrin Migraine) and stress-reduction techniques.
If these are not effective within 2 hours, the patient should take migraine-specific drugs. Triptans are the first choice, then ergot derivatives.
Patients with migraines associated with severe nausea or vomiting may use injected or rectally administered drugs. Nausea itself should be treated with specific anti-nausea drugs, such as metoclopramide (Reglan).
If migraine medications fail to relieve symptoms within 4 hours, rescue drugs (opioids, corticosteroids) may be used.

Stratified Approach. Many doctors and patients now prefer the stratified approach. The doctor first estimates the severity of the patient's condition based on his or her history. Then, depending on the severity of a typical attack, the doctor decides whether the patient should start with more or less powerful drugs at the first signs of the migraine:

Patients with less disabling migraines start with general pain relievers.
Patients with a history of moderate-to-severe migraines start with migraine-specific prescription medicine, such as a triptan, at the onset of mild pain.

Some studies report dramatic relief with the stratified approach. In one study, zolmitriptan, a newer triptan, reduced the intensity of headaches within 2 hours in 70% of patients with moderate pain but only in 44% of those with severe headaches.

Side effects can be severe with many migraine drugs, although newer drugs, such as the recent generation triptans, may provide effective early relief without significant side effects.

Studies estimate that between 5 - 10% of children have migraines but that the disorder is underdiagnosed in children. An interesting study reported that when children drew pictures in response to their doctors' questions about their migraines, the doctors were able to tell the difference between migraine and non-migraine headaches in the majority of cases.

Symptoms in Children. The standard diagnostic criteria for migraine in adults may apply to only about two-thirds of migraines in children and adolescents. For example, doctors have seen the following differences:

Headaches tend to last for a shorter time (as little as an hour) in children.
Migraine pain tends to occur in the face and on both sides of the head in two-thirds of child patients.
Children often have a form of migraine known as a migraine equivalent or abdominal migraine, which does not cause a headache at all. Instead, children experience periodic bouts of nausea and vomiting (called cyclic vomiting syndrome) or other secondary symptoms found in adult migraine, such as a reaction against light or sound. Cyclic vomiting may occur in nearly 2% of school-aged children with or without a migraine association.
Migraine triggers in children are similar to those in adults, but common ones in children are anxiety and fear, and eating ice cream.

Outlook in Children. Migraine in children is disabling, as it is in adults, and they tend to lose more school days than other children. Children with frequent headaches may also be at higher risk for headaches in adulthood and also for other physical and psychiatric problems. However, some children who have migraine eventually stop having attacks when they reach adulthood, or have less severe types of headaches.

Treatments in Children. Most children with migraines may need only mild pain relievers and home remedies (such as ginger tea) to treat their headaches. The American Academy of Neurology’s 2004 practice guidelines for children and adolescents recommend the following drug treatments:

For children age 6 years and older, ibuprofen (Advil) is recommended. Acetaminophen (Tylenol) may also be effective. Acetaminophen works faster than ibuprofen, but the effects of ibuprofen last longer.
For adolescents age 12 years and older, sumaptriptan (Imitrex) nasal spray is recommended.

Preventive Measures in Children. Non-medication methods, including biofeedback and muscle relaxation techniques may be helpful. In one study of children with migraines and poor sleep habits, who were taught how to sleep better instructions without using medications had significantly fewer migraine attacks.

If these methods fail, then preventive drugs may be used, although evidence is weak on the effectiveness of standard migraine preventive drugs in children.

If medication overuse causes rebound migraines develop, the patients cannot recover without stopping the drugs. (If caffeine is the culprit, a person may need only to reduce coffee or tea drinking to a reasonable level, not necessarily stop drinking it altogether.) The patient can usually stop abruptly or gradually. The patient should expect the following:

Most headache drugs can be stopped abruptly, but the patient should talk to their doctor first. Certain non-headache medications, such as anti-anxiety drugs or beta-blockers, require gradual withdrawal.
If the patient chooses to taper off standard headache medications, withdrawal should be completed within three days.
The patient may take other pain medicines during the first days. Examples of drugs that may be used include dihydroergotamine (with or without metoclopramide), NSAIDs (in mild cases), corticosteroids, or valproate.
The patient must expect their headache to get worse after they stop taking their medications, no matter which method they use. Most people feel better within 2 weeks, although headache symptoms can persist up to 16 weeks (and in rare cases even longer).
If the symptoms do not respond to treatment and cause severe nausea and vomiting, the patient may need to be hospitalized.

On the encouraging side, some patients experience dramatic long-term relief from all headaches afterward, and one study reported that 82% of patients significantly improved 4 months after medication withdrawal.

Medications Used for Treatment

Many different medications are used to treat migraines. However, the Food and Drug Administration (FDA) has specifically approved only the following types of drugs for migraine treatment:

Non-prescription drugs: Excedrin Migraine, Advil Migraine, Motrin Migraine Pain
Prescription drugs: Triptans and ergotamine

Other types of drugs, including opioids and barbiturates, are sometimes prescribed off-label for migraine treatment. Opioids and barbiturates have not been approved by the FDA for migraine relief, and they can be addictive.

All FDA-approved migraine treatments are approved only for adults. No migraine products have officially been approved for use in children.

Some patients with mild migraines respond well to over-the-counter (OTC) painkillers, particularly if they take the medicine at the very first sign of an attack.

The Food and Drug Administration has approved three OTC (nonprescription) products to treat migraine. Excedrin Migraine (a combination of aspirin, acetaminophen, and caffeine) was the first such medication approved for the temporary relieve of migraine and its symptoms. Studies have reported significant relief in nearly 70% of patients. It may also help menstrual migraines. Advil Migraine and Motrin Migraine Pain, both containing ibuprofen, are also approved to treat migraine headache.

Cooling Pads. Cooling pads may help during an attack. Some products (Migraine Ice, TheraPatch Headache Cool Gel) use a pad containing a gel that cools the skin for up to 4 hours and can be placed on the forehead, temple, or back of the neck.

Non-steroidal anti-inflammatory drugs (NSAIDs) include aspirin, ibuprofen, and naproxen. They were among the first types of drugs tried to treat mild-to-moderate migraines. Aspirin, ibuprofen (Advil, Motrin), and naproxen (Anaprox, Aleve) are all available without prescription. Naproxen may have specific benefits for migraine. A 2007 study indicated that a combination of naproxen and sumatriptan provides better migraine pain relief than either drug alone.

Other types of NSAIDs are available only by prescription. Some studies indicate that the NSAID combination diclofenac-potassium (Cataflam) may work faster than the migraine drug sumatriptan (Imitrex) and help reduce nausea. The combination is not appropriate for people allergic to aspirin or at risk for bleeding.

Injectable NSAIDs, particularly ketorolac (Toradol), may be very effective for severe and persistent migraines. A 2003 study found that intravenous ketorolac provided greater pain relief than nasal sumatriptan (Imitrex). A 2005 study presented at the annual meeting of the American Headache Society reported that intravenous ketorolac was more effective than opioid drugs for late-stage treatment of severe migraine attacks.

COX-2s are a class of prescription drugs that have the anti-inflammatory effects of NSAIDs, but do not upset most people's stomachs. However, most of these drugs have been withdrawn from the U.S. market due to increased risk for heart attack and stroke. Celecoxib (Celebrex) is the only available COX-2, and it has a strong warning label alerting users of the potential for heart attack, stroke, and serious gastrointestinal problems. (The warning is the same one the Food and Drug Administration recommended for the labels of prescription NSAIDs in 2005.)

NSAID Side Effects. High dosages and long-term use of NSAIDs can increase the risk for heart problems, kidney problems, and stomach bleeding. In April 2005, the FDA asked drug manufacturers of prescription NSAIDs to include with their products the same boxed warning used for the COX-2 inhibitor celecoxib (Celebrex). This boxed warning emphasizes an increased risk for cardiovascular events and gastrointestinal bleeding in people taking these drugs. The FDA also requested manufacturers of over-the-counter NSAIDs to revise their labels to include more specific language concerning potential cardiovascular and gastrointestinal risks. Due to its proven heart benefits, aspirin was excluded from these labeling revisions.

Triptans (also referred to as serotonin agonists) were the first drugs specifically developed for use against migraine. They are the most important migraine drugs currently available. They help maintain serotonin levels in the brain, and so specifically target one of the major components in the migraine process.

Triptans are recommended as first-line drugs for adult patients with moderate-to-severe migraines when NSAIDs are not effective. Triptans have the following benefits:

They are effective for most patients with migraine, as well as patients with combination tension and migraine headaches.
They do not have the sedative effect of other migraine drugs.
Withdrawal after overuse appears to be shorter and less severe than with other migraine medications

Sumatriptan. Sumatriptan (Imitrex) has the longest track record and is the most studied of all triptans. It is available as a fast-dissolving pill, nasal spray, or injection. Injected sumatriptan works the fastest of all the triptans and is the most effective, but it can cause pain at the injection site. The nasal spray form bypasses the stomach and is absorbed more quickly than the oral form. Some patients report relief as soon as 15 minutes after administration. The spray tends to work less well when a person has nasal congestion from cold or allergy. It may also leave a bad taste. Sumatriptan is effective for many patients, but headache recurs in 20 - 40% of people within 24 hours after taking the drug.

A 2007 study in the Journal of the American Medical Association suggested that a combination of sumatriptan and naproxen works better than either drug alone.

Other Triptans. Newer triptans include almotriptan (Axert), zolmitriptan (Zomig), naratriptan (Amerge), rizatriptan (Maxalt), frovatriptan (Frova), and eletriptan (Relpax). Comparison studies with sumatriptan suggest that some of the newer drugs have fewer side effects and are superior to sumatriptan for providing immediate, sustained, and consistent pain relief. Recurrence rates are also lower. They are also being investigated for prevention under certain circumstances, such as menstrual migraines, but benefits appear limited.

Studies on newer triptans indicate:

Almotriptan is as effective as oral sumatriptan and may have fewer side effects, particularly chest pain, than most other triptans.
Rizatriptan may have the most rapid effects of all oral triptans. Zolmitriptan also has a more rapid effect than sumatriptan (although there appears to be no significant difference in adverse effects). Both rizatriptan and zolmitriptan are also available as rapidly dissolving wafers.
Eleptriptan is also very rapidly effective at high doses, but at those levels may have significant adverse effects. (To date, it does not seem to have any advantages over other triptans in head-to-head comparisons.)
Naratriptan and frovatriptan have a delayed response but long duration, few side effects, and lower risk for recurrence than with sumatriptan. Some evidence suggests that they may have specific benefits for stopping prolonged migraines and may even play a role in prevention.
Frovatriptan: A large study of more than 500 women with an average 12-year history of menstrual migraines examined the use of frovatriptan for the short-term prevention of such headaches. Researchers found that the migraines disappeared in over half of the women on the higher dose (5 mg) of frovatriptan.
Zolmitriptan (Zomig): Several studies indicate that zomitriptan nasal spray may be safe and effective for adolescents. In one study, zolmitriptan relieved pain within 2 hours for nearly half of the children (aged 12 - 17 years) enrolled in the trial. Zolmitriptan nasal spray is approved only for adults.

Side Effects. Many of the newer triptans may have fewer severe side effects than sumatriptan. Side effects of most triptans, however, can include:

Tingling and numbness in the toes
Sensations of warmth
Discomfort in the ear, nose, and throat
Nausea
Drowsiness
Dizziness
Muscle weakness
Heaviness, pain, or both in the chest. (About 40% of patients taking sumatriptan experience these symptoms, and they are major factors in discontinuing the drug. Newer drugs, such as almotriptan, produce fewer chest symptoms.)
Rapid heart rate

Complications of Triptans. The following are potentially serious problems.

Complications of heart and circulation. Triptans narrow (constrict) blood vessels. Because of this effect, spasms in the blood vessels may occur and cause serious side effects, including stroke and heart attack. Such events are rare, but patients with an existing history or risk factors for these conditions should generally avoid triptans.
Serotonin syndrome. Serotonin syndrome is a life-threatening condition that occurs from an excess of the brain chemical serotonin. Triptan drugs used to treat migraine, as well as certain types of antidepressant medications, can increase serotonin levels. These antidepressant drugs include serotonin reuptake inhibitors (SSRIs) -- such as fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft) -- and selective serotonin/norepinephrine reuptake inhibitors (SNRIs), such as duloxetine (Cymbalta) and venlafaxine (Effexor). It is very important that patients not combine a triptan drug with a SSRI or SNRI drug. Serotonin syndrome is most likely to occur when starting or increasing the dose of a triptan or antidepressant drug. Symptoms include restlessness, hallucinations, rapid heartbeat, tremors, increased body temperature, diarrhea, nausea, and vomiting. You should seek immediate medical care if you have these symptoms.

The following people should avoid triptans or take them with caution and only with the advisement of a doctor:

Anyone with a history or any risk factors for stroke, uncontrolled diabetes, high blood pressure, or heart disease.
People taking antidepressants that increase serotonin levels.
Children and adolescents. They may be safe, but controlled studies are needed to confirm this. (Triptans should not, in any case, be the first-line treatment for children.)
People with basilar or hemiplegic migraines. (Triptans are not indicated for these migraineurs.)
There is no evidence to date of any higher risk for birth defects in pregnant women who take triptans. Still, women should be cautious about taking any medications during pregnancy and discuss any possible adverse effects with their doctors.

Drugs containing ergotamine (commonly called ergots) constrict smooth muscles, including those in blood vessels, and are useful for migraine. They were the first anti-migraine drugs available. Ergotamine is available by prescription in the following preparations:

Dihydroergotamine (DHE) is an ergot derivative. It is administered as a nasal spray form (Migranal) or by injection, which can be performed at home.
Ergotamine is available tablets taken by mouth, tablets taken under the tongue (sublingual), and rectal suppositories. Some of the tablet forms of ergotamine contain caffeine.

Ergotamine’s role since the introduction of triptans is now less certain. Only the rectal forms of ergotamine are superior to rectal triptans. Injected, oral, and nasal-spray forms are all inferior to the triptans. Ergotamine may still be helpful for patients with status migrainous or those with frequent recurring headaches.

Side Effects. Side effects of ergotamine include:

Nausea
Dizziness
Tingling sensations
Muscle cramps
Chest or abdominal pain

The following are potentially serious problems:

Toxicity. Ergotamine is toxic at high levels.
Adverse effects on blood vessels. Ergot can cause persistent blood vessel contractions, which may pose a danger for people with heart disease or risk factors for heart attack or stroke.

Internal scarring (fibrosis). Scarring can occur in the areas around the lungs, heart, or kidneys. It is often reversible if the drug is stopped.

The following patients should avoid ergots:

Pregnant women. Ergots can cause miscarriage.
People over age 60.
Patients with serious, chronic health problems, particularly those of the heart and circulation.

Ergotamine can interact with other medications, such as antifungal drugs and some antibiotics. All ergotamine products approved by the Food and Drug Administration (FDA) contain a "black box" warning in the prescription label explaining these drug interactions. In 2007, the FDA pulled 15 unapproved older ergotamine products off the market, in part because they lacked this warning label. The five FDA-approved ergotamine products that remain on the market are:

Migergot suppository (marketed by G and W Labs)
Ergotamine Tartrate and Caffeine tablets (marketed by Mikart and West Ward)
Cafergot tablets (marketed by Sandoz)
Ergomar sublingual tablets (marketed by Rosedale Therapeutics)

Nasal drops containing lidocaine, a local anesthetic, can provide effective and quick pain relief within 15 minutes for many migraine sufferers. However, lidocaine has certain downsides:

It is rather difficult to administer. Patients must be lying down with their head dangling.
The headache often relapses in an hour, and other drugs must then be used.
Side effects include unpleasant taste, burning sensation, and facial numbness.

However, the drug does not cause drowsiness or heart rhythm disturbances as some other migraine treatments do. It should not be used for any other form of headache.

If the pain is very severe and does respond to other drugs, doctors may try painkillers containing opioids. Opioid drugs include morphine, codeine, meperidine (Demerol), and oxycodone (Oxycontin)]. Butorphanol is an opioid in nasal spray form that may be useful as a rescue treatment when others fail.

Opioids are not approved for migraine treatment and should not be used as first-line therapy. Nevertheless, many opioid products are prescribed to patients with migraine, sometimes with dangerous results. In 2007, following reports of several drug-related deaths, the Food and Drug Administration warned that the cancer pain pill fentanyl (Fentora) should not be used to treat patients with migraine or others conditions for which the drug is not specifically approved.

Side Effects. Side effects for all opioids include drowsiness, impaired judgment, nausea, and constipation. There is a risk for addiction, and these drugs can become ineffective with long-term use for chronic migraines. Doctors should not prescribe opioids to patients at risk for drug abuse, including those with personality or psychiatric disorders.

Metoclopramide (Reglan) is used in combinations with other drugs to treat the nausea and vomiting that occurs with other drugs and with migraine itself. Metoclopramide and other anti-nausea drugs, such as domperidone (Motilium), may help the intestine better absorb migraine medications.

New drugs in clinical trials include tonabersat (a gap junction blocker), trexima (a combination triptan and non-steroidal anti-inflammatory drug), GW274150 (a nitric oxide synthase inhibitor), and MK-0974 (a calcitonin gene-related peptide antagonist). Researchers are also investigating a nasal spray containing capsaicin, the chemical found in cayenne peppers.

Prevention

There are several ways to prevent migraine attacks. You should try a healthy diet, the right amount of sleep, and non-drug approaches, such as biofeedback, first for prevention.

Behavioral techniques that reduce stress and empower the patient may help some people with migraines. Studies report between 35 - 50% reduction in migraine and tension-type headaches with these approaches. They generally include:

Biofeedback therapy
Cognitive-behavioral therapy
Relaxation techniques

Behavioral methods may help counteract the tendency for muscle contraction and uneven blood flow associated with some headaches. They may be particularly beneficial for children, adolescents, and pregnant and nursing women, and anyone who cannot take most migraine medications.

Biofeedback. Studies have demonstrated some effectiveness from biofeedback for migraine headaches. Biofeedback training teaches the patient to monitor and modify physical responses, such as muscle tension, using special instruments for feedback.

Cognitive Behavioral Therapy. Behavioral therapy may be useful alone but is particularly beneficial for patients who are on preventive drug treatments. It typically uses the headache diary to track activities and headaches. The patient then works with the therapist to change or add behaviors or medications that will reduce the frequency and severity of attacks.

Alternative non-drug therapies used for headache management and prevention include hypnosis, meditation, visualization and guided imagery, acupuncture, acupressure, yoga, and other relaxation exercises. There is no clear evidence that any of these techniques have specific value for migraines.

Some studies report the following:

Acupuncture. Acupuncture is a Chinese medicine technique that uses thin needles to stimulate specific points aligned with energy pathways in the body. Studies have showed mixed results on the benefits of acupuncture for migraine. A 2005 study published in the Journal of the American Medical Association reported that acupuncture was no more effective than sham acupuncture (needles placed at non-acupuncture points) in preventing migraines. More than 300 people were enrolled in this randomized trial. A 2006 study of 960 people, published in Lancet Neurology, found that real acupuncture, sham acupuncture, and standard drug treatment were all equally effective in preventing migraine attacks.
Relaxation Techniques. Muscle relaxation techniques may be helpful. One study reported that relaxation treatments appeared to help adolescents with migraine but not tension headaches.

Hormonal drugs, such as oral contraceptives or hormone replacement therapy, have a mixed effect on women with migraines. Oral contraceptives have been associated with worse headaches in 18 - 50% of women and have also been linked to a higher risk for stroke in women with classic migraines (with auras). Young women should avoid or stop oral contraception if they have classic migraines, migraines that worsen or change character after oral contraceptives , if they have close relatives with stroke or heart disease, or if they smoke.

Some evidence suggests, however, that oral contraceptives may help prevent true menstrual migraines (which do not have auras). In such cases, their benefits may outweigh the low risk of a serious adverse event. Keeping a migraine record for at least three menstrual cycles can help confirm whether a woman actually has a true menstrual migraine.

Making a few minor changes in your lifestyle can make your migraines more bearable. Improving sleep habits is important for everyone, and especially those with headaches. What you eat also has a huge impact on migraines, so dietary changes can be extremely beneficial, too.

Avoiding Food Triggers. Avoiding foods that trigger migraine is an important preventive measure. Common food triggers include monosodium glutamate (MSG), processed lunch meats that contain nitrates, dried fruits that contain sulfites, aged cheese, alcohol and red wine, chocolate, and caffeine. However, people’s responses to triggers differ. Keeping a headache diary that tracks diet and headache onset can help identify individual food triggers.

Healthy Diet. One study indicated that a diet low in fat and high in complex carbohydrates may significantly reduce the frequency, severity, and duration of migraine headaches. Such a diet is healthy in general, in any case.

Eating Regularly. Eating regularly is important to prevent low blood sugar. People with migraines who fast periodically for religious reasons might consider taking preventive medications.

Fish Oil. Some studies suggest that omega-3 fatty acids, which are found in fish oil, have anti-inflammatory and nerve protecting actions. These fatty acids can be found in oily fish, such as salmon, mackerel, or sardines. They can also be obtained in supplements of specific omega-3 compounds (DHA-EPA).

Exercise is certainly helpful for relieving stress. An analysis of several studies reported that aerobic exercise in particular might help prevent migraines. It is important, however, to warm up gradually before beginning a session, since sudden, vigorous exercise might actually precipitate or aggravate a migraine attack.

Manufacturers of herbal remedies and dietary supplements do not need Food and Drug Administration approval to sell their products. Just like a drug, herbs and supplements can affect the body's chemistry, and therefore have the potential to produce side effects that may be harmful. There have been several reported cases of serious and even lethal side effects from herbal products. Patients should always check with their doctors before using any herbal remedies or dietary supplements.

Riboflavin (Vitamin B2). There is reasonable evidence on the benefits of vitamin B2 for migraine sufferers. In one study, patients who took 400 mg of vitamin B2 (riboflavin) reduced their migraine attacks by half, although the vitamin had no effect on the severity or duration of migraines that did occur. In another study, it helped increase the effectiveness of beta-blockers, drugs used to prevent migraines in some people. Vitamin B2 is generally safe, although some people taking high doses develop diarrhea.

Magnesium Supplements. Studies have reported a higher rate of magnesium deficiencies in some patients with migraine, such as those with menstrual migraines. Magnesium helps relax blood vessels. Some patients report relief from supplements.

Feverfew. Feverfew is the most studied herbal remedy for headaches and is effective in some cases. However, like all effective headache remedies, overuse can cause a rebound effect.

Ginger. In general, herbal medicines should never be used by children or pregnant or nursing women without medical counsel. One exception may be ginger, which has no side effects and can be eaten in powder or fresh form, as long as quantities are not excessive. Some people have reported less pain and frequency of migraines while taking ginger, and children can take it without danger.

Medications Used for Prevention

The Food and Drug Administration has approved four drugs for prevention of migraine:

Propanolol (Inderal)
Timolol (Blacadrene)
Divalproex sodium (Depakote)
Topiramate (Topamax)

Propanolol and timolol are beta-blocker drugs. Divalproex and topiramate are anti-seizure drugs. Many other drugs are also being used or investigated for preventing migraines.

Beta-blockers are usually prescribed to reduce high blood pressure. Some beta-blockers, however, are also useful in reducing the frequency of migraine attacks and their severity when they occur. Propranolol (Inderal) and timolol (Blocadren) have been approved specifically for prevention of migraine. Metoprolol (Toprol), atenolol (Tenormin), and nadolol (Corgard) are also being studied for migraine prevention.

Side Effects. Side effects may include:

Fatigue and lethargy are common.
Some people experience vivid dreams and nightmares, depression, and memory loss.
Dizziness and lightheadedness may occur upon standing.
Exercise capacity may be reduced.
Other side effects may include cold extremities, asthma, decreased heart function, gastrointestinal problems, and sexual dysfunction.

If side effects occur, the patient should call a doctor, but it is extremely important not to stop the drug abruptly. Some evidence suggests that people with migraines who have had a stroke should avoid beta-blockers.

Anti-seizure drugs, also called anti-epileptic drugs or anticonvulsants, affect the neurotransmitter gamma aminobutyric acid (GABA), which helps prevent nerve cells from over-firing. GABA may also have a role in migraines. These drugs are commonly used for epilepsy and bipolar disease. Anti-seizure drugs are more expensive than other drugs. They also have significant side effects. Divalproex sodium (Depakote) and topiramate (Topamax) are the only anti-seizure drugs that are approved for migraine prevention. However, if patients do not respond to either of these drugs, doctors may try other types of anti-seizure medications.

Divalproex Sodium (Depakote). Divalproex sodium (Depakote) was first approved in 1996 for migraine prevention. A once-a-day formulation of divalproex (Depakote ER) was approved in 2000. Doctors sometimes prescribe a similar drug, valproate (Depakene). Pregnant patients should not use these drugs, as they may cause birth defects.

Topiramate (Topamax). In 2004, the Food and Drug Administration approved topiramate for prevention of migraines in adults. Studies from 2006 indicated that the drug works well when used on a long-term basis. Patients in these studies experienced significantly fewer migraines for up to 14 months. Topiramate’s most common side effect is a tingling sensation in the arms and legs. Weight loss is also a side effect. In clinical trials, patients lost an average of 3.8% of their body weight.

Other Anti-Seizure Drugs Under Investigation. Researchers are studying other types of anti-seizure drugs for migraine prevention. These include levetiracetam (Keppra), gabapentin (Neurontin), pregabalin (Lyrica), zonisamide (Zonegran), tiagabine (Gabitril), and the investigational drug lacosamide (LCM).

Side Effects. Anti-seizure medication's side effects vary by drug but may include:

Nausea and vomiting
Diarrhea
Cramps
Hair loss
Dizziness
Sleepiness
Blurred vision
Weight gain
Valproate and divalproex can cause serious side effects of inflammation of the pancreas (pancreatitis) and damage to the liver

Amitriptyline (Elavil, Endep), a tricyclic antidepressant drug, has been used for many years as a first-line treatment for migraine prevention. It may work best for patients who also have depression or insomnia. Tricyclics can have significant side effects, including disturbances in heart rhythms, and can be fatal in overdose. Although other tricyclic antidepressants may have fewer side effects than amitritpyline, they do not appear to be particularly effective for migraine prevention.

Researchers have investigated newer types of antidepressants, including serotonin-reuptake inhibitors(SSRIs), such as fluoxetine (Prozac). However, studies to date do not indicate that SSRIs are helpful for migraine prevention.

Muscle Relaxants. Botulinum toxin A (Botox) injection, a common wrinkle treatment, causes small muscles to relax. This approach is now being used with some success for treating disorders that involve over-excited muscle activity, including myofascial pain syndrome and migraine. One study reported complete migraine relief in more than half of patients being tested and improvement of more than 50% in another 35% of patients. Relief lasted 3 - 4 months with no adverse effects. A study presented at the 2005 meeting of the American Headache Society reported that patients who regularly received Botox injections every 3 months reduced both the frequency of migraine attacks and their reliance on pain medications

Angiotensin Converting Enzyme Inhibitors. Commonly used for treating high blood pressure, angiotensin converting enzyme (ACE) inhibitors block the production of the protein angiotensin, which constricts blood vessels and may be involved in migraine. Studies using the ACE inhibitor lisinopril (Prinivil, Zestril) are reporting significant reduction in migraine attacks.

Angiotensin-Receptor Blockers. Angiotensin-receptor blockers (ARBs) have actions similar to ACE inhibitors, but may have fewer side effects. In one study, patients who took the ARB candesartan (Atacand) had significantly fewer headaches compared to patients who received placebo.

Neurostimulation Devices. Researchers are investigating a transcranial magnetic stimulation (TMS) device to help stop migraines before they occur. The hair dryer-size device is held to the back of the head and delivers quick magnetic pulses. The device is used when a patient experiences the first signs of a migraine. Other types of nerve stimulation devices are also under investigation.

Inhalation Devices. These devices use heat to vaporize a drug so that it can be inhaled into the lungs. Clinical trials are currently testing this device with procholorperazine (Compazine), a tranquilizer drug that is used to treat nausea and vomiting.

Nasal Devices. New types of nasal sprays and powders are being researched. Some of them use capsaicin, the chemical found in cayenne peppers, to help relieve pain.

Skin Patches. The Actyve transdermal patch uses a small battery-powered system to deliver a triptan drug through the skin.

Drugs. New drugs in development include tonabersat (gap junction blocker), trexima (combination triptan and non-steroidal anti-inflammatory drug), and GW274150 (nitric oxide synthase inhibitor).

Resources

www.headaches.org -- National Headache Foundation
www.americanheadachesociety.org -- American Headache Society
www.aan.com -- American Academy of Neurology
www.ninds.nih.gov -- National Institute of Neurological Disorders and Stroke
www.clinicaltrials.gov -- Find clinical trials
www.migraineinfo.org -- National Migraine Association

References

Brandes JL, Kudrow D, Stark SR, O'Carroll CP, Adelman JU, O'Donnell FJ, et al. Sumatriptan-naproxen for acute treatment of migraine: a randomized trial. JAMA. 2007 Apr 4;297(13):1443-54.

Lewis DW, Winner P, Hershey AD, Wasiewski WW; Adolescent Migraine Steering Committee. Efficacy of zolmitriptan nasal spray in adolescent migraine. Pediatrics. 2007 Aug;120(2):390-6.

Lipton RB, Bigal ME, Diamond M, Freitag F, Reed ML, Stewart WF; AMPP Advisory Group. Migraine prevalence, disease burden, and the need for preventive therapy. Neurology. 2007 Jan 30;68(5):343-9.

Monastero R, Camarda C, Pipia C, Camarda R. Prognosis of migraine headaches in adolescents: a 10-year follow-up study. Neurology. 2006 Oct 24;67(:1353-6.

Rose KM, Wong TY, Carson AP, Couper DJ, Klein R, Sharrett AR. Migraine and retinal microvascular abnormalities: the Atherosclerosis Risk in Communities Study. Neurology. 2007 May 15;68(20):1694-700.

Review Date:
11/1/2007
Reviewed By:
Harvey Simon, MD, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital.

A.D.A.M. Copyright

adam.com

Foot pain

FitSugar — Wed, 08 Oct 2008 17:35:02 -0700

In This Report

Highlights
Introduction
Causes
Risk Factors
Treatment: Corns and Callus...
Treatment: Bunions
Treatment: Hammertoes
Treatment: Ingrown Toenails...
Treatment: Forefoot Pain...
Treatment: Heel Pain
Treatment: Flat Feet
Treatment: Abnormally High ...
Treatment: Tarsal Tunnel Sy...
Treatment: Foot Injury
Prevention
Shoes
Insoles and Orthotics
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Treatment for Ingrown Toenail:

Orthonyxia, a surgical technique that implants a small metal brace into the top of the nail, was as effective as traditional surgical techniques for preventing ingrown toenail from recurring, according to one study.
A nonsurgical method for treating ingrown toenail with chemicals uses either sodium hydroxide or phenol, but one study shows that sodium hydroxide procedures have a better outcome and faster recovery than phenol procedures.

Treatment for Forefoot Pain:

Ultrasound-guided injection of alcohol might provide relief from Morton's neuroma, according to one study. Symptoms improved in 94% of patients who had the treatment, a success rate comparable to that of surgery.

Treatment for Heel Pain:

NSAIDs reduce pain and disability in people with plantar fasciitis when used with other techniques, such as night splints and stretching.
Studies show that extracorporeal shockwave therapy provides a very small reduction in heel pain without side effects. It may be a good option for patients who haven't responded well to conservative treatment.

Work-related Foot Problems:

An estimated 120,000 job-related foot injuries occur every year, about a third of them involving the toes. A number of foot problems -- including arthritis of the foot and ankle, toe deformities, pinched nerves between the toes, plantar fasciitis, adult-acquired flat foot, and tarsal tunnel syndrome -- have been attributed to repetitive use at work.

Introduction

Foot pain is very common. About 75% of people in the United States have foot pain at some time in their lives. Most foot pain is caused by shoes that do not fit properly or that force the feet into unnatural shapes (such as pointed-toe, high-heeled shoes).

The foot is a complex structure of 26 bones and 33 joints, layered with an intertwining web of more than 120 muscles, ligaments, and nerves. It serves the following functions:

Supports weight
Acts as a shock absorber
Serves as a lever to propel the leg forward
Helps maintain balance by adjusting the body to uneven surfaces

Because the feet are very small compared with the rest of the body, the impact of each step exerts tremendous force upon them. This force is about 50% greater than the person's body weight. During a typical day, people spend about 4 hours on their feet and take 8,000 - 10,000 steps. This means that the feet support a combined force equivalent to several hundred tons every day.

Foot pain generally starts in one of three places: the toes, the forefoot, and the hindfoot.

The Toes. Toe problems most often occur because of the pressure imposed by ill-fitting shoes.

The Forefoot. The forefoot is the front of the foot. Pain originating here usually involves one of the following bone groups:

The metatarsal bones (five long bones that extend from the front of the arch to the bones in the toe)
The sesamoid bones (two small bones embedded at the top of the first metatarsal bone, which connects to the big toe)

The Hindfoot. The hindfoot is the back of the foot. Pain originating here can extend from the heel, across the sole (known as the plantar surface), to the ball of the foot (the metatarsophalangeal joint).

Condition	Location	Symptoms	Recommended Footwear
Toe Pain
Corns and calluses	Around toes, usually little toe, bottom of feet or areas exposed to friction.	Hard, dead, yellowish skin.	Wide (box-toed) shoes; soft cushions under heel or ball of foot, or customized or gel insoles for calluses. Doughnut-shaped pads for corns.
Ingrown toenails	Toenails.	Nail curling into skin causes pain, swelling, and, in extreme cases, infection.	Sandals, open-toed shoes.
Bunions and bunionettes (tailor's bunion)	Big toe (bunions) or little toe (bunionettes).	The following can occur alone or in combination: Metatarsus primus varus. The first (big toe) metatarsal bone shifts away from the second, and the big toe points inward. Medial exostosis. This is a bony bump at the base of the big toe, which protrudes outward. Area next to bony bump is red, tender, and occasionally filled with fluid. Toe joint may be inflamed. Hallux valgus. This is a deformity in which the bone and joint of the big toe shift and grow inward, so that the second toe crosses over the big toe.	Soft, wide-toed shoes or sandals. Bunion shields or splints. Thick doughnut-shaped moleskin pads, custom-made orthotics or foot slings, if necessary. Avoid shoes with stitching along the side of the "bump."
Morton's neuroma (also called interdigital neuroma)	Inflammation of the nerve, usually between the third and fourth toes and bottom of the foot near these toes.	Cramping and burning pain, or electric-shock sensation. The condition may produce a thick protective sheath around the nerve that feels like a ball. This may be detected by pressing top to bottom on the top of the foot using one hand and moving the other hand from side to side. Morton's neuroma is aggravated by prolonged standing and relieved by removal of the shoes and forefoot massage.	Wide (box-toed) shoes. Orthotic or insole with pad that reduces stress on the painful area.
Hammertoe or claw toe	Usually second toe, but may develop in any or all of the three middle toes.	Toes form hammer or claw shape. In hammertoe, the first knuckle of the toe is mainly affected. In claw toe the entire toe is deformed. No pain at first, but pain increases as tendon becomes tighter and toes stiffen.	Wide (box-toed) shoes. Toe pads or specially designed shields, splints, caps, or slings. (Splints or slings are not for people with diabetes.)
Front-of-the-Foot Pain
Metatarsalgia	Ball of the foot.	Acute, recurrent, or chronic pain without a known cause.	Wide (box-toed) shoes. Orthotic with pad that reduces metatarsal pressure. Gel cushions. Metatarsal bandage.
Stress fracture	Most often in the area beneath the second or third toe.	Sudden pain (which persists) when injury occurs.	Low-heeled shoes with stiff soles.
Sesamoiditis	Ball of foot beneath big toe.	Pain and swelling.	Low-heeled shoe with stiff sole and soft padding inside.
Heel and Back-of-the-Foot Pain
Plantar fasciitis or heel spurs	Back of the arch right in front of heel.	At onset, some people report a tearing or popping sound. Pain is most severe with first steps after getting out of bed. Pain decreases after stretching, returns after inactivity.	Over-the-counter foot insole (cut quarter-size hole surrounding painful area). Possible night splints. Orthotics if necessary.
Bursitis of the heel	Center of the heel.	Pain, with warmth and swelling. Increases during the day.	Heel cup.
Haglund's deformity (pump bump)	Fleshy area on the back of the heel.	Tender swelling aggravated by shoes with stiff backs.	Soft shoes. Heel pads. Possible orthotic to support heel.
Achilles tendinitis	Achilles tendon: area along the back between calf muscles and heel.	Pain worsens during physical activities (particularly running), after which the tendon usually swells and stiffens. If it ruptures, popping sound may occur followed by acute pain similar to a blow at the back of the leg.	Insoles, tendon strap, heel cups.
Arch and Bottom-of-the Foot Pain
Tarsal tunnel syndrome	Anywhere along the bottom of the foot.	Numbness, tingling, or burning sensations, pain, most commonly felt at night.	Specially designed orthotics to relieve pressure.
Flat feet or posterior tibial tendon dysfunction (PTTD)	The arch.	No arch. Often no pain or discomfort. Three stages in PTTD: Pain and weakness in the tendon. The arch flattens but is still flexible. The foot becomes rigid and possibly painful at the ankle. Sometimes people report fatigue, pain, or stiffness in the feet, legs, and lower back.	For children, possible custom-made insoles.
High arches (hollow feet)	The arch.	High arches. Lower back pain, possible tendency to lower limb injuries.

Causes

Nearly all causes of foot pain can be grouped under one of the following:

Ill-fitting shoes. Poorly fitting shoes are a frequent cause of foot pain. High-heeled shoes concentrate pressure on the toes and can aggravate, if not cause, problems with the toes.
Certain medical conditions. Any medical condition that causes a disturbance in the way a person walks can contribute to foot pain. This may include diseases or conditions that lead to pain or numbness in the feet (such as diabetes), leg and foot deformities, spinal problems, and neurological disorders such as Parkinson's disease or cerebral palsy.
High-impact exercise. High-impact exercising, such as jogging or strenuous aerobics, can injure the feet. Common injuries include corns, calluses, blisters, muscle cramps, acute knee and ankle injuries, plantar fasciitis, and metatarsalgia.

Arthritic Conditions. Arthritic conditions, particularly osteoarthritis and gout, can cause foot pain. Although rheumatoid arthritis almost always develops in the hand, the ball of the foot can also be affected.

Diabetes. Diabetes is an important cause of serious foot disorders. [For more information, see In-Depth Report #9: Diabetes - type 1 and In-Depth Report #60: Diabetes - type 2.]

Obesity. Obesity can cause foot and ankle pain.

Pregnancy. Pregnancy can cause fluid buildup and swollen feet. The increased weight and imbalance of pregnancy contributes to foot stress.

Medications. Some medications, such as calcitonin and drugs used for high blood pressure, can cause foot swelling.

Click the icon to see an image of foot inspection.

Risk Factors

A risk factor is anything that increases your chances of getting a disease or condition. The following are factors that increase your risk for foot pain:

Elderly people are at very high risk for foot problems. As you age, your feet widen and flatten, and the fat padding on the sole of the foot wears down. The skin on the feet also becomes dryer. Foot pain in older adults may be the first sign of age-related conditions, such as arthritis, diabetes, and circulatory disease. Foot problems can also impair balance and function in this age group.

Taking fashion to extreme limits, some people have turned to cosmetic surgery as a drastic way to fit into high-heeled shoes. Procedures include surgical shortening of the toes, narrowing of feet, or injecting silicone into the pads of the feet. Such methods may increase your risk for future foot pain. The American Orthopaedic Foot and Ankle Society (AOFAS) and other foot-related medical associations have expressed concern over this trend. The AOFAS strongly advises against cosmetic foot surgery and urges consumers to carefully consider the relative risks and benefits of undergoing unnecessary surgical procedures.

Women are at higher risk than men for severe foot pain, probably because of high-heeled shoes. Severe foot pain appears to be a major cause of general disability in older women.

An estimated 120,000 job-related foot injuries occur every year, about a third of them involving the toes. A number of foot problems -- including arthritis of the foot and ankle, toe deformities, pinched nerves between the toes, plantar fasciitis, adult-acquired flat foot, and tarsal tunnel syndrome -- have been attributed to repetitive use at work.

For example, in a study of New York police officers who walked an average of 3 miles a day, 20% experienced foot pain at the end of their workday. (Insoles can relieve much of this pain.) No studies, however, have scientifically distinguished between injuries due to work versus those due to regular use. This is an important issue because of its potential impact on disability claims.

Pregnant women have an increased risk of foot problems due to weight gain, swelling in their feet and ankles, and the release of certain hormones that cause ligaments to relax. These hormones help when bearing the child, but they can weaken the feet.

People who engage in regular high-impact aerobic exercise are at risk for plantar fasciitis, heel spurs, sesamoiditis, shin splints, Achilles tendon, and stress fractures. Women are at higher risk for stress fractures than are men.

Gaining weight puts added stress on the feet and can lead to foot or ankle injuries. The added pressure on the soft tissues and joints of the foot in overweight people increases the likelihood of developing tendinitis and plantar fasciitis.

Treatment: Corns and Calluses

A corn is a protective layer of dead skin cells that forms due to repeated friction. It is cone-shaped and has a knobby core that points inward. This core can put pressure on a nerve and cause sharp pain. Corns can develop on the top of, or between, toes. If a corn develops between the toes, it may be kept pliable by the moisture from perspiration and is therefore called a soft corn.

Corns develop as a result of friction from the toes rubbing together or against the shoe. They often occur from the following:

Shoes, socks, or stockings that fit too tightly around the toes
Pressure on the toes from high-heeled shoes
Shoes that are too loose, due to the friction of the foot sliding within the shoe
Deformed and crooked toes

Calluses are composed of the same material as corns. Calluses, however, develop on the ball or heel of the foot. The skin on the sole of the foot is ordinarily about 40 times thicker than the skin anywhere else on the body, but a callus can even be twice as thick. A protective callus layer naturally develops to guard against excessive pressure and chafing as people get older and the padding of fat on the bottom of the foot thins out. If calluses get too big or too hard, they may pull and tear the underlying skin.

Risk factors for calluses include the following:

Poorly fitting shoes
Walking regularly on hard surfaces
Flat feet

Of note, in people with diabetes, the presence of calluses is a strong predictor of ulceration, particularly in those who have a history of foot ulcers.

Preventing Corns and Calluses and Relieving Discomfort. To prevent corns and calluses and relieve discomfort if they develop:

Do not wear shoes that are too tight or too loose. Wear well-padded shoes with open toes or a deep toe box (the part of the shoe that surrounds the toes). If necessary, have a cobbler stretch the shoes in the area where the corn or callus is located.
Wear thick socks to absorb pressure, but do not wear tight socks or stockings.
Apply petroleum jelly or lanolin hand cream to corns or calluses to soften them.
Use doughnut-shaped pads that fit over a corn and decrease pressure and friction. They are available at most drug stores.
Place cotton, lamb's wool, or mole skin between the toes to cushion any corns in these areas.

Removing Corns and Calluses. To remove a corn or callus, soak it in very warm water for 5 minutes or more to soften the hardened tissue, then gently sand it with a pumice stone. Several treatments may be necessary. Do not trim corns or calluses with a razor blade or other sharp tool. Unsterile cutting tools can cause infection, and it is easy to slip and cut too deep, causing excessive bleeding or injury to the toe or foot.

Medicated Solutions and Pads. There are numerous over-the-counter pads, plasters, and medications for removing corns and calluses. These treatments commonly contain salicylic acid, which may cause irritation, burns, or infections that are more serious than the corn or callus. Use caution with these medications. The following people should not use them:

Patients with diabetes
Patients with reduced feeling in the feet due to circulation problems or neurological damage
Patients who do not have the flexibility or eyesight to use them properly

Treatment: Bunions

A bunion is a deformity that usually occurs at the head of one of the five long bones (the metatarsal bones) that extend from the arch of the foot and connect to the toes. A bunion typically develops in the following way:

Most often it occurs in the first metatarsal bone (the one that attaches to the big toe). A bunion may also develop in the bone that joins the little toe to the foot (the fifth metatarsal bone), in which case it is known as either a bunionette or a tailor's bunion.
A bunion begins to form when the big or little toe is forced in toward the rest of the toes, causing the head of the metatarsal bone to jut out and rub against the side of the shoe.
The underlying tissue becomes inflamed, and a painful bump forms.
As this bony growth develops, the bunion is formed as the big toe is forced to grow at an increasing angle toward the rest of the toes. One important bunion deformity, hallux valgus, causes the bone and joint of the big toe to shift and grow inward, so that the second toe crosses over it.

Several conditions can cause bunions:

Narrow high-heeled shoes with pointed toes can put enormous pressure on the front of the foot.
Injury in the joint may cause a bunion to develop over time.
Genetics play a role in 10 - 15% of all bunions.

Flat feet, gout, arthritis, and occupations (such as ballet) that place undue stress on the feet can also increase the risk for bunions.

Shoes and Protective Pads. Pressure and pain from bunions and bunionettes can be relieved by wearing appropriate shoes, such as the following:

Soft, wide, low-heeled leather shoes that lace up
Athletic shoes with soft toe boxes
Open shoes or sandals with straps that don't touch the irritated area

A thick doughnut-shaped, moleskin pad can protect the protrusion. In some cases, an orthotic can help redistribute weight and take pressure off the bunion. Nonsteroidal anti-inflammatory drugs (NSAIDs) or corticosteroid injections may offer some pain relief.

Surgery. If discomfort persists, surgery may be necessary, particularly for more serious conditions, such as hallux valgus. There are more than 100 surgical variations, ranging from removing the bump to realigning the toes.

The most common surgery, an office procedure known as bunionectomy, involves shaving down the bone of the big toe joint. In one procedure the surgeon uses a very small incision, through which the bone-shaving drill is inserted. The physician shaves off the bone, guided by feel or x-ray. This technique is not a cure, but patient satisfaction is high and results are long-lasting.

Click the icon to see an illustrated series detailing bunion removal.

More extensive surgeries may be required to realign the toe joint. Although there are variations of each, they generally involve one or more of the following:

Osteotomy (cutting and realigning the joint). Long-term studies on osteotomies report that 90% of patients are satisfied with the procedure.
Exostetectomy (removal of the large bony growth). This technique is only useful when there is no shift in the toe bone itself.
Arthrodesis (removal of damaged portion of the joint, followed by implantation of screws, wires, or plates to hold the bones together until they heal). This is the gold standard procedure for very severe cases or when previous procedures have failed. Most patients report good results.
Arthroplasty (removal of damaged portion of the joint with the goal of achieving a flexible scar). This technique offers symptom relief and faster rehabilitation than arthrodesis, but it can cause deformity and some foot weakness. Arthroplasty tends to be used in older patients. Biologic or synthetic implants for supporting the toes are showing promise as part of this procedure.
Tendon and Ligament Repair. If tendons and ligaments have become too loose, the surgeon may tighten them.

In severe cases, surgeons are testing bone grafts to restore bone length in patients who have had previous bunion surgeries or damage from osteoarthritis.

Complications, though uncommon in even the most complex procedures, can include:

Continued pain
Infection
Possible numbness
Irritation from implants used to support the bone
An excessively shortened metatarsal bone

Recovery from more invasive procedures, such as arthrodesis or osteotomy, may take 6 - 8 weeks, and it can be that long before a patient can put full weight on the foot. In such cases, the patient will need to wear a cast or use crutches. Elderly patients may need wheelchairs.

Treatment: Hammertoes

A hammertoe is a permanent deformity of the toe joint, in which the toe bends up slightly and then curls downward, resting on its tip. When forced into this position long enough, the tendons of the toe shrink, and the toe stiffens into a hammer- or claw-like shape.

Hammertoe is most common in the second toe, but it can develop in any or all of the three middle toes if they are pushed forward and do not have enough room to lie flat in the shoe. The risk is increased when the toes are already crowded by the pressure of a bunion. Risks include:

Lying down for long periods
Diabetes
Diseases that affect the nerves and muscles

Click the icon to see an image of a hammertoe.

Treatment for Hammertoe. At first, a hammertoe is flexible, and any pain it causes can usually be relieved by putting a toe pad, sold in drug stores, into the shoe. To help prevent and ease existing discomfort from hammertoes, shoes should have a deep, wide toe area. As the tendon becomes tighter and the toe stiffens, other treatments, including exercises, splints, and custom-made shoe inserts (orthotics) may help redistribute weight and ease the position of the toe.

Surgery. Patients with severe cases of hammertome may need surgery. If the toe is still flexible, only a simple procedure that releases the tendon may be involved. Such procedures sometimes require only a single stitch and a Band-Aid. If the toe has become rigid, surgery on the bone is necessary, but it can still be performed in the doctor's office. A procedure called PIP arthroplasty involves releasing the ligaments at the joint and removing a small piece of toe bone, which restores the toe to its normal position. The toe is held in this position with a pin for about 3 weeks, and then the pin is removed. One study reported that 92% of patients who had arthroscopy were still pain free after 5 years.

Treatment: Ingrown Toenails

Ingrown toenails can occur on any toe but are most common on the big toes. They usually develop when tight-fitting or narrow shoes put too much pressure on the toenail and force the nail to grow into the flesh of the toe. Incorrect toenail trimming can also contribute to the risk of developing an ingrown toenail. Other causes are:

Fungal infections
Injuries
Abnormalities in the structure of the foot
Repeated impact on the toenail from high-impact aerobic exercise

An ingrown toenail is a condition in which the edge of the toenail grows into the skin of the toe. The big toe is most commonly affected. Symptoms include pain, redness, and swelling around the toenail.

Caring for Toenails. Trim toenails straight across and keep them long enough so that the nail corner is not visible. If the nail is cut too short, it may grow inward. If the nail does grow inward, do not cut the nail corner at an angle. This only trains the nail to continue growing inward. When filing the nails, file straight across the nail in a single movement, lifting the file before the next stroke. Do not saw back and forth. A cuticle stick can be used to clean under the nail.

Treatments. To relieve pain from ingrown toenails, try wearing sandals or open-toed shoes. Soaking the toe for 5 minutes twice a day in a warm water solution of Domeboro or Betadine can help. People who are at increased risk for infections, such as those with diabetes, should have professional treatment.

Antibiotic ointments can treat ingrown toenails that are infected. Apply the ointment by working a wisp of cotton under the nail, especially the corners, to lift the nail up and drain the infection. The cotton will also help force the toenail to grow out correctly. Change the cotton daily, and use the antibiotic consistently.

In severe cases, more intensive treatments are needed. Surgery involves simply cutting away the sharp portion of ingrown nail, removing the nail bed, or removing a wedge of the affected tissue. One study found that orthonyxia, a newer surgical technique that implants a small metal brace into the top of the nail, is as effective as traditional surgical techniques for preventing ingrown toenails from recurring.

Nonsurgical methods can also treat ingrown toenails. One technique uses chemicals to remove the skin. Both sodium hydroxide and phenol may be used, but research shows that sodium hydroxide produces a better outcome and faster recovery than phenol. Other nonsurgical methods include using cauterization (heating), or lasers, to remove the skin.

Treatment: Forefoot Pain

Forefoot pain refers to pain and discomfort felt toward the top of the foot. The rate of forefoot pain and deformity increases with age. When a cause cannot be determined, any pain on the ball of the foot is generally referred to as metatarsalgia.

Forefoot pain may be due to:

Morton's neuroma
Sesamoiditis
Stress fractures

A neuroma usually means a benign tumor of a nerve. However, Morton’s neuroma, also called interdigital neuroma, is not actually a tumor. It is a thickening of the tissue surrounding the nerves leading to the toes. Morton’s neuroma usually develops when the bones in the third and fourth toes pinch together, compressing a nerve. It can also occur in other locations. The nerve becomes enlarged and inflamed. The inflammation causes a burning or tingling sensation and cramping in the front of the foot. Other causes of this condition include:

Tight, poorly-fitting shoes
Injury
Arthritis
Abnormal bone structure

Treatment for Neuromas. Pain from Morton's neuroma can be reduced by massaging the affected area. Roomier shoes (box-toed shoes), pads of various sorts, and cortisone injections in the painful area are also helpful. A combination of cortisone injections and shoe modifications provides better immediate relief than changes in footwear alone. Ultrasound-guided injection of alcohol might also provide relief from Morton's neuroma, research finds.

If these treatments are not effective, the enlarged area may need to be surgically removed. In one long-term study of one surgeon's experience, 85% of patients reported good to excellent satisfaction nearly 6 years after surgery. About 65% were pain free. Some numbness is common afterward, but it rarely bothers patients. Occasionally, the nerve tissue may re-grow and form another neuroma.

Sesamoiditis is an inflammation of the tendons around the small, round bones that are embedded in the head of the first metatarsal bone, which leads to the big toe. Sesamoid bones bear much stress under ordinary circumstances; excessive stress can strain the surrounding tendons. Often there is no clear-cut cause, but sesamoid injuries are common among people who participate in jarring, high-impact activities, such as ballet, jogging, and aerobic exercise.

Treatment for Sesamoiditis. Rest and reducing stress on the ball of the foot are the first lines of treatment for sesamoiditis. A low-heeled shoe with a stiff sole and soft padding inside is all that is usually required. In severe cases, surgery may be necessary.

A stress fracture in the foot, also called fatigue or march fracture, usually results from a break or rupture in any of the five metatarsal bones (mostly the second or third). These fractures are caused by overuse during strenuous exercise, particularly jogging and high-impact aerobics. Women are at higher risk for stress fracture than men.

A fracture in the first metatarsal bone, which leads to the big toe, is uncommon because of the thickness of this bone. If it occurs, however, it is more serious than a fracture in any of the other metatarsal bones because it dramatically changes the pattern of normal walking and weight bearing.

Treatment for Stress Fractures. Patients should seek treatment if pain persists for 3 weeks. In a study of young athletes, treatment after that time reduced the chance that they could return to their sport. Surgery may be needed if conservative measures fail. In most cases, however, stress fractures heal by themselves if you avoid rigorous activities. Some health care providers recommend moderate exercise, particularly swimming and walking. It is best to wear low-heeled shoes with stiff soles. Occasionally, a health care provider may recommend wearing a special wooden shoe and a compressive wrap to make walking more comfortable.

Treatment: Heel Pain

The heel is the largest bone in the foot. Heel pain is the most common foot problem and affects 2 million Americans every year. It can occur in the front, back, or bottom of the heel. Types of heel pain include:

Achilles tendinitis
Bursitis of the heel
Excess pronation
Haglund's deformity
Heel spur syndrome
Plantar fasciitis

Each type of heal pain is described in more detail below. General treatment guidelines are as follows:

The American Orthopaedic Foot and Ankle Society (AOFAS) suggests shoe inserts, medications, and stretching as a first line of therapy for heel pain. One study found that 95% of women who used an insert and did simple stretching exercises for the Achilles tendon and plantar fascia experienced improvement after 8 weeks.
If these treatments fail, the patient may need prescription heel orthotics and extended physical therapy. Surgery may be an option if other methods have failed.

Achilles tendinitis is an inflammation of the tendon that connects the calf muscles to the heel bone. It is caused by small tears in the tendon from overuse or injury. This condition is most common in people who engage in high-impact exercise, particularly jogging, racquetball, and tennis.

People at highest risk for this disorder from these activities are those with a shortened Achilles tendon. Such people tend to roll their feet too far inward when walking, and may bounce when they walk. A shortened tendon can be due to an inborn structural abnormality, or it can develop from regularly wearing high heels.

An inflamed or torn Achilles tendon causes intense pain and affects mobility.

Evidence is uncertain about the best way to treat either acute or chronic Achilles tendinitis. Some approaches include:

Treatments to Relieve Pain and Reduce Inflammation. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin or ibuprofen (Advil), may help ease pain and reduce inflammation. It is also helpful to apply ice for 20 - 30 minutes, four or five times a day. (Note: Corticosteroid injections are sometimes used, although evidence suggests they don't help very much, and they can pose a risk for rupture of the tendon.)

Gentle Stretching. Gentle calf muscle stretches may also help reduce pain and spasms. If the calf is swollen, elevate the leg. Exercise is safe when the heel is no longer swollen or tender, even if pain is still present. If pain increases with exercise, stop immediately.

Laser Therapy. Low-level laser therapy that emits energy directed at pain trigger points has helped some patients. No strong evidence supports its use to date, however.

Surgery vs. Nonsurgical Treatment. Chronic inflammation may lead to rupture of the Achilles tendon. If pain continues, the ruptured tendon will require a cast and perhaps surgery, called tendon transfer. Although some experts believe a cast without surgery is a sufficient treatment for such rupture, there is a chance the tendon may rupture again in the future, even after it heals. Some experts suggest surgery for active people and nonsurgical treatment for older people.

Surgery requires a long incision with a postoperative period of immobilization that can average 6 weeks. Complications can include a significant surgical scar, infection, and muscle atrophy, although surgery reduces pain and preserves foot function in the long term. Less invasive techniques are being tested. In one study, selected patients with ruptured tendons were hospitalized for about 5 days and fitted with special footgear (Variostabil, which continuously raised the back of the foot). The footgear was effective for most patients, and the tendon ruptured again in only 5% of cases.

Bursitis of the heel is an inflammation of the bursa, a small sack of fluid beneath the heel bone. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin or ibuprofen (Advil), and steroid injections will help relieve pain from bursitis. Applying ice and massaging the heel are also beneficial. A heel cup or soft padding in the heel of the shoe reduces direct impact when walking.

Pronation is the normal motion that allows the foot to adapt to uneven walking surfaces and to absorb shock. Excessive pronation occurs when the foot has a tendency to turn inward and stretch and pull the fascia. It can cause not only heel pain, but also hip, knee, and lower back problems.

Haglund's deformity, known medically as posterior calcaneal exostosis, is a bony growth surrounded by tender tissue on the back of the heel bone. It develops when the back of the shoe repeatedly rubs against the back of the heel, aggravating the tissue and the underlying bone. It is commonly called pump bump because it frequently occurs with high heels. (It can also develop in runners, however.)

Treatment for Haglund's Deformity. Applying ice followed by moist heat will help ease discomfort from a pump bump. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin or ibuprofen (Advil), will also reduce pain. Your doctor may recommend an orthotic device to control heel motion. Corticosteroid injections are not recommended because they can weaken the Achilles tendon.

In severe cases, surgery may be necessary to remove or reduce the bony growth. According to one study, however, surgery was not effective for more than 30% of patients and, in fact, the condition worsened in 14% of patients who had surgery. A more recent study reported that surgery cured 90% of cases, but patients took 6 months to 2 years to fully recover. Experts advise patients to try all conservative measures before choosing surgery.

Plantar fasciitis is a common foot problem that accounts for 1 million office visits per year. Plantar fasciitis occurs from small tears and inflammation in the wide band of tendons and ligaments that stretches from the heel to the ball of the foot. This band, much like the tensed string in a bow, forms the arch of the foot and helps serve as a shock absorber for the body.

The term plantar means the sole of the foot, and fascia refers to any fibrous connective tissue in the body. Most people with plantar fasciitis experience pain in the heel with their first steps in the morning. The pain also often spreads to the arch of the foot. The condition can be temporary, or it may become chronic if ignored. Resting can provide relief, but only temporarily.

Heel spurs are calcium deposits that can develop under the heel bone as a result of the inflammation that occurs with plantar fasciitis. Heel spurs and plantar fasciitis are sometimes blamed interchangeably for pain, but plantar fasciitis can occur without heel spurs, and spurs commonly develop without causing any symptoms at all.

Causes of Plantar Fasciitis. The cause of plantar fasciitis is often unknown. It is usually associated with overuse during high-impact exercise and sports. Plantar fasciitis accounts for up to 9% of all running injuries. Because the condition often occurs in only one foot, however, factors other than overuse are likely to be responsible in many cases. Other causes of this injury include poorly-fitting shoes, lack of calf flexibility, or an uneven stride that causes an abnormal and stressful impact on the foot.

Treatment Goals. The three major treatment goals for plantar fasciitis are:

Reducing inflammation and pain
Reducing pressure on the heel
Restoring strength and flexibility

Embarking on an exercise program as soon as possible and using NSAIDs, splints, or heel pads as needed can help relieve the problem. Pain that does not subside with NSAIDs may require more intensive treatments, including leg supports and even surgery.

Exercises to Restore Strength and Flexibility. Stretching the plantar fascia is the mainstay therapy for restoring strength and flexibility. One exercise involves the following:

Put the hands on a wall and lean against them.
Place the uninjured foot on the floor in front of the injured foot.
Raise the heel of the injured foot.
Gently stretch the injured leg and foot.

With stretching treatments, the plantar fascia nearly always heals by itself but it may take as long as a year, with pain occurring intermittently. A moderate amount of low-impact exercise (such as walking, swimming, or cycling) also seems to be beneficial.

Treatment. Inflammation and pain is most commonly treated with ice and over-the-counter nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin or ibuprofen. NSAIDs reduce pain and disability in people with plantar fasciitis when used with other techniques, such as night splints and stretching.

Corticosteroids are powerful anti-inflammatory agents. An injection of a steroid plus a local anesthetic (such as xylocaine) may provide relief in severe cases of plantar fasciitis. (Steroid injections are not used for pain that is only due to heel spurs). For athletes or performers who need immediate relief, an effective method is to administer the steroid dexamethasone using a procedure called iontophoresis, which introduces the drug into the foot's tissue using an electrical current.

Several non-drug approaches can relieve pressure on the heel, including:

Sturdy Shoes and Insoles. It is important to wear comfortable but sturdy shoes that have thick soles, rubber heels, and a sole insole to relieve pressure. (An insole with an arch support might also be helpful.) Cutting a round hole about the size of a quarter in the sole cushion under the painful area may help support the rest of the heel while relieving pressure on the painful spot. Heel cups are not very useful. When combined with exercises that stretch the arch and heel cord, over-the-counter insoles may offer the same relief as prescribed orthotics.
Night Splints. Some evidence suggests that splints worn at night may be helpful for some people. One device, for example, uses an Ace bandage and an L-shaped fiberglass splint to keep the foot stretched while the patient is sleeping. This allows the muscle to heal. One study reported that nearly any splint, regardless of cost, is equally effective in about three-quarters of patients. Although patient compliance may be better with custom-made prescribed orthotics than with tension night splints, one study found they are equally effective in improving pain.
Elevated Heels. Some people report relief from mild symptoms with the use of shoes or cowboy boots that have elevated heels. This approach, however, may not work in some people and is not recommended for anyone with a moderate-to-severe condition. (Heel cups have not been proven to be very useful.)
Orthotics. For severe conditions, such as fallen arches or structural problems that cause imbalance, insoles, called orthotics, molded from a plaster cast of the patient's foot may be needed. (See "Insoles and Orthotics" section).
Extracorporeal Shock Wave Therapy (ESWT). ESWT may be used as an alternative to surgery for patients who have not responded to other treatments. The therapy uses low-dose sound waves to injure the surrounding tissues in the heel, which is believed to trigger healing of the tissues that are causing the pain. Studies show that the treatment provides a very small reduction in heel pain without side effects. It can be considered as an option for patients who haven't responded well to extensive conservative treatment.
Surgery. Surgery may be needed for some patients, typically those who have disabling heel pain that does not respond to other treatments for at least a year. A typical surgery is called instep plantar fasciotomy. It relieves pressure on the nerves that are causing pain by removing and therefore releasing part of the plantar fascia. A less invasive method uses a procedure called endoscopy, which requires smaller incisions. Wearing a below-the-knee walking cast after surgery for 2 weeks may reduce the need for pain relief and speed recovery time compared to the use of crutches.
Botox. Small studies show that injections of botulinum toxin (Botox), a protein used to temporarily paralyze certain muscles, reduces pain and improves patients' future ability to walk. More research is needed on this treatment.

Treatment: Flat Feet

Flat foot, or pes planus, is a defect of the foot that eliminates the arch. The condition is most often inherited. Arches, however, can also fall in adulthood, in which case the condition is sometimes referred to as posterior tibial tendon dysfunction (PTTD). This occurs most often in women over age 50, but it can occur in anyone. The following are risk factors for PTTD:

Wearing high heels for long periods of time is a particular risk for flat feet. Over the years, the Achilles tendon in the back of the calf shortens and tightens, so the ankle does not bend properly. The tendons and ligaments running through the arch then try to compensate. Sometimes they break down, and the arch falls.
Some studies have indicated that the earlier a person starts wearing shoes, particularly for long periods of the day, the higher the risk for flat feet later on.
Other conditions that can lead to PTTD include obesity, diabetes, surgery, injury, rheumatoid arthritis, or the use of corticosteroids.

Some research suggests that flat feet in adults can, over time, actually exert abnormal pressure on the ankle joint that can cause damage. One indirect complication of flat arches may be urinary incontinence or leakage during exercise. The less flexible the arch, the more force reaches the pelvic floor, jarring the muscles that affect urinary continence. Nevertheless, whether flat feet pose any significant problems in adults is unknown. For example, one study on athletes with flat feet indicated that they had no higher risk for leg or foot injuries than did athletes with normal arches.

Treatment for Flat Feet in Children. Doctors usually can't diagnose flat feet until a child is 6 years old. Children with flat feet typically don't have symptoms, and often outgrow the condition. Children who are experiencing symptoms might need to change shoes or wear arch supports. In rare cases, minimally invasive joint insert surgery may be an option.

Treatment for Flat Feet in Adults. In general, conservative treatment for flat feet acquired in adulthood (posterior tibial tendon dysfunction) involves pain relief and insoles or custom-made orthotics to support the foot and prevent progression.

In severe cases, surgery may be required to correct the foot posture, usually with procedures called osteotomies or arthrodesis that typically lengthen the Achilles tendon and adjust tendons in the foot. One procedure uses an implant to support the arch. These procedures have potential complications. Conservative methods should be tried first.

Treatment: Abnormally High Arches

An overly-high arch (hollow foot) can cause problems. Army studies have found that recruits with the highest arches have the most lower-limb injuries and that flat-footed recruits have the least. Contrary to the general impression, the hollow foot is much more common than the flat foot.

Clawfoot, or pes cavus, is a deformity of the foot marked by very high arches and very long toes. Clawfoot is a hereditary condition, but can also occur when muscles in the foot contract or become unbalanced due to nerve or muscle disorders.

Claw toe is a deformity of the foot in which the toes are pointed down and the arch is high, making the foot appear claw-like. Claw toe can be a condition from birth or develop as a consequence of other disorders.

Treatment: Tarsal Tunnel Syndrome

Tarsal tunnel syndrome results from compression of a nerve that runs through a narrow passage behind the inner ankle bone down to the heel. It can cause pain anywhere along the bottom of the foot. It can occur with:

Diabetes
Back pain
Arthritis
Injury to the ankle
Abnormal blood vessels
Scar tissue that press against the nerve

Magnetic resonance imaging (MRI) and the dorsiflexion-eversion test can diagnose this syndrome.

Treatment for Tarsal Tunnel Syndrome. Specially designed shoe inserts called orthotics can relieve pain from tarsal tunnel syndrome, because they help redistribute weight and take pressure off the nerve. Corticosteroid injections may also help. Surgery is sometimes performed, particularly if symptoms persist for more than a year, although its benefits are a matter of debate. Tarsal tunnel syndrome caused by known conditions, such as tumors or cysts, may respond better to surgery than tarsal tunnel syndrome of unknown cause. It can take months after this surgery for a person to recover and resume normal activities. Only experienced surgeons should perform tarsal tunnel syndrome surgery.

Treatment: Foot Injury

If you suspect that you have broken or fractured bones in a toe or foot, call a doctor, who will probably order x-rays. Even if you can walk, you still might have a fracture. People are often able to walk even if a foot bone has been fractured, particularly if it is a chipped bone or a toe fracture.

Over-the-counter nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used to treat mild pain caused by muscle inflammation. Aspirin is the most common NSAID. Others include ibuprofen (Motrin, Advil, Nuprin, Rufen), ketoprofen (Actron, Orudis KT), naproxen (Aleve, Naprelan), and tolmetin (Tolectin). A gel containing ibuprofen can be applied to sore joints. Acetaminophen (Tylenol) is not an NSAID, and although it is a mild pain reliever, it will not reduce inflammation. It is important to note that high doses or long-term use of any NSAID can cause gastrointestinal disturbances with sometimes serious consequences, including dangerous bleeding. No one should take NSAIDs for prolonged periods of time without consulting a doctor.

The acronym RICE stands for rest, ice, compression, and elevation -- the four basic elements of immediate treatment for an injured foot.

Rest. Patients should get off injured foot as soon as possible.
Ice. This is particularly important to reduce swelling and promote recovery during the first 48 hours. Wrap a bag or towel containing ice around the injured area on a repetitive cycle of 20 minutes on, 40 minutes off.
Compression. Lightly wrap an Ace bandage around the area.
Elevation. Elevate the foot on several pillows.

Minor injuries like sprains may be treated at home if broken bones are not suspected. The acronym RICE is helpful for remembering how to treat minor injuries: "R" stands for rest, "I" is for ice, "C" is for compression, and "E" is for elevation. Pain and swelling should decrease within 48 hours, and gentle movement may be beneficial, but don't put pressure on a sprained joint until the pain is completely gone (one to several weeks).

Prevention

The American Podiatric Medical Association offers the following tips for preventing foot pain:

Don't ignore foot pain -- it's not normal. If the pain persists, see a doctor who specializes in podiatry.
Inspect feet regularly. Pay attention to changes in color and temperature. Look for thick or discolored nails (a sign of developing fungus), and check for cracks or cuts in the skin. Peeling or scaling on the soles of feet could indicate athlete's foot. Any growth on the foot is not considered normal.
Wash feet regularly, especially between the toes, and dry them completely.
Trim toenails straight across, but not too short. (Cutting nails in corners or on the sides increases the risk for ingrown toenails.)
Make sure shoes fit properly. Purchase new shoes later in the day when feet tend to be at their largest, and replace worn out shoes as soon as possible.
Select and wear the right shoe for specific activities (such as running shoes for running).
Alternate shoes. Don't wear the same pair of shoes every day.
Avoid walking barefoot, which increases the risk for injury and infection. At the beach or when wearing sandals, always use sunblock on your feet, as you would on the rest of your body.
Be cautious when using home remedies for foot ailments. Self-treatment can often turn a minor problem into a major one.
It is critical that people with diabetes see a podiatric physician at least once a year for a checkup. People with diabetes, poor circulation, or heart problems should not treat their own feet, including toenails, because they are more prone to infection.

Skin creams can help maintain skin softness and pliability. A pumice stone or loofah sponge can help get rid of dead skin.

Taking a warm footbath for 10 minutes two or three times a week will keep the feet relaxed and help prevent mild foot pain caused by fatigue. Adding 1/2 cup of Epsom salts increases circulation and adds other benefits. Taking footbaths only when the feet are painful is not as helpful.

In addition to wearing proper shoes and socks, walking often -- and properly -- can prevent foot injury and pain. The head should be erect, the back straight, and the arms relaxed and swinging freely at the side. Step out on the heel, move forward with the weight on the outside of the foot, and complete the step by pushing off the big toe.

Exercises specifically for the toe and feet are easy to perform and help strengthen them and keep them flexible. Helpful exercises include the following:

Raise and curl the toes 10 times, holding each position for a count of five.
Put a rubber band around both big toes and pull the feet away from each other. Count to five. Repeat 10 times.
Pick up a towel with the toes. Repeat five times.
Pump the foot up and down to stretch the calf and shin muscles. Perform for 2 or 3 minutes.

Early Development. The first year of life is important for foot development. Parents should cover their babies' feet loosely, allowing plenty of opportunity for kicking and exercise. Change the child's position frequently. Children generally start to walk at 10 - 18 months. They should not be forced to start walking early. Wearing just socks or going barefoot indoors helps the foot develop normally and strongly and allows the toes to grasp. Going barefoot outside, however, increases the risk for injury and other conditions, such as plantar warts.

Shoes. Children should wear shoes that are light and flexible, and since their feet tend to perspire, their shoes should be made of materials that breathe. Replace footwear every few months as the child's feet grow. Footwear should never be handed down. Protect children's feet if they participate in high-impact sports.

Shoes

In general, the best shoes are well cushioned and have a leather upper, stiff heel counter, and flexible area at the ball of the foot. The heel area should be strong and supportive, but not too stiff, and the front of the shoe should be flexible. New shoes should feel comfortable right away, without a breaking-in period.

Well-fitted shoes with a firm sole and soft upper are the best way to prevent many problems with the feet. They should be purchased in the afternoon or after a long walk, when the feet have swelled. There should be 1/2 inch of space between the longest toe and the tip of the shoe (remember, the longest toe is not always the big toe), and the toes should be able to wiggle upward.

Stand when being measured, and have both feet sized, buying shoes that fit whichever foot is largest. Wear the same socks as you would regularly wear with the new shoes. Women who are accustomed to wearing pointed-toe shoes may prefer the feel of tight-fitting shoes, but with wear their tastes may adjust to shoes that are less confining and properly fitted.

Ideally, the shoe should have a removable insole. Thin, hard soles may be the best choice for older people. Elderly people wearing shoes with thick inflexible soles may be unable to sense the position of their feet relative to the ground, significantly increasing the risk for falling.

High heels are the major cause of foot problems in women. Although people believe that foot binding is a problem limited to Chinese women of the past, many fashionable high heels are designed to constrict the foot by up to an inch. Women who insist on wearing high-heeled shoes should at least look for shoes with wide toe room, reinforced heels that are relatively wide, and cushioned insoles. They should also keep the amount of time they spend wearing high heels to a minimum.

The way shoes are laced can be important for preventing specific problems. Laces should always be loosened before putting shoes on. People with narrow feet should buy shoes with eyelets farther away from the tongue than people with wider feet. This makes for a tighter fit for narrower feet and a looser fit for wider feet. If, after tying the shoe, less than an inch of tongue shows, the shoes are probably too wide. Adjust tightness both at the top and bottom of the shoe. When shoes with high arches cause pain, skip eyelets when lacing them to relieve pressure.

If shoes need breaking in, place moleskin pads next to areas on the skin where friction is likely to occur. Once a blister occurs, moleskin is not effective. Change shoes during the day, and rotate between different pairs of shoes. As soon as the heels show noticeable wear, replace the shoes or their heels.

Avoid extreme variations between exercise, street, and dress shoes.

Exercise and Sports. Shoes purchased for exercise should be specifically designed for a person's preferred sport. For instance, a running shoe should especially cushion the forefoot, while tennis shoes should emphasize ankle support. Athletic socks are almost as important as shoes. Experts often recommend padded acrylic socks.

Occupational Footwear. Because a number of occupations put the feet in danger, workers in high-risk jobs should be sure their footwear is protective. For example, non-electric workers at risk for falling or rolling objects or punctures should wear shoes with steel toes and possibly other metal foot guards. Electric workers should wear footgear with no metal parts (or insulated steel toes) and rubber soles and heels. Chemical workers should wear shoes made of synthetics or rubber, not leather.


Aerobic Dancing	Sufficient cushioning to absorb shock and pressure, which should be many times greater than shock from walking. Arches that maintain side-to-side stability. Thick upper leather support. Box toe. Orthotics may be required for people with ankles that over-turn inward or outward. Soles should allow for twisting and turning.
Cycling	Rigid support across the arch to prevent collapse during pedaling. Heel lift. Cross-training or combo hiking/cycling shoes may be sufficient for the casual biker. Toe clips or specially designed shoe cleats for serious cyclers. In some cases, orthotics may be needed to control arch and heel and balance the forefoot.
Running	Sufficient cushioning to absorb shock and pressure. Fully bendable at the ball of the foot. Enough traction on the sole to prevent slipping. Consider insole or orthotic with arch support for problem feet.
Tennis	Allows side-to-side sliding. Low-traction sole. Snug fitting heel with cushioning. Padded toe box with adequate depth. Soft-support arch.
Walking	Lightweight. Breathable upper material (leather or mesh). Wide enough to accommodate ball of the foot. Firm padded heel counter that does not bite into heel or touch anklebone. Low heel close to ground for stability. Good arch support. Front provides support and flexibility.

Insoles and Orthotics

Insoles are flat cushioned inserts that are placed inside the shoe. They are designed to reduce shock, provide support for heels and arches, and absorb moisture and odor. In general, they can be very helpful for many people.

People respond very differently to specific insoles. What may work for one person may not for another. Consider the thickness of socks when purchasing insoles to be sure they do not squeeze the toes up against the shoes. Insoles can be purchased in athletic and drug stores. Shoe stores that specialize in foot problems often sell customized, but more expensive, insoles. In general, over-the-counter insoles offer enough support for most people's foot problems. Most well-known brands of athletic shoes have built-in insoles.

Brands and Materials. There are many types of insoles available. They are composed of various materials, such as cork, leather, plastic foam, and rubber. Very effective insoles are now made from viscoelastic polymers (such as Sorbothane, Airplus, Spenco, Dr. Scholl's Massaging Gel, and others), which are gel-like materials that act both as liquids and solids.

Heel Cushions for Shortened Achilles Tendons. People who have developed short, tightened Achilles tendons (usually women who have worn high-heeled shoes for prolonged periods) should consider using heel cushions. Like insoles, heel cushions are inserted inside the shoes. They should be at least 1/8 inch thick, but not more than 1/4 inch thick.

For severe conditions, such as fallen arches or structural problems that cause imbalance, podiatrists or physicians may need to fit and prescribe orthotics, or orthoses, which are insoles molded from a plaster cast of the patient's foot. Orthotics are usually categorized as rigid, soft, or semi-rigid.

Before seeking prescription orthotics, people with less severe problems should consider testing the lower-priced, over-the-counter insoles.

Types of orthotics include:

Rigid Orthotics. Rigid orthotics are used to control motion in two major foot joints that lie directly below the ankle. They are often used to prevent excessive pronation (the turning in of the foot) and are useful for people who are very overweight or have uneven leg lengths. Some experts warn that rigid orthotics may cause sesamoiditis or benign tumors from pinched nerves.
Soft Orthotics. Soft orthotics are designed to absorb shock, improve balance, and remove pressure from painful areas. They are made from a lightweight material and are often beneficial for people with diabetes or arthritis. Soft orthotics need to be replaced periodically, and because they are bulkier than rigid orthotics, they may require larger shoes.
Semi-Rigid Orthotics. Semi-rigid orthotics are designed to provide balance, often for a specific sport. They are typically made of layers of leather and cork reinforced by silastic.

Resources

www.apma.org -- American Podiatric Medical Association
www.aofas.org -- American Orthopaedic Foot and Ankle Society
www.acfas.org -- American College of Foot and Ankle Surgeons
www.aapsm.org -- American Academy of Podiatric Sports Medicine
www.apta.org -- American Physical Therapy Association
www.diabetes.org -- American Diabetes Association
http://ndep.nih.gov/campaigns/Feet/Feet_overview.htm -- National Diabetes Education Program
www.arthritis.org -- Arthritis Foundation
www.podiatrynetwork.com -- Podiatry Network

References

Bostanci S, Kocyigit P, Gurgey E. Comparison of phenol and sodium hydroxide chemical matricectomies for the treatment of ingrowing toenails. Dermatol Surg. 2007;33:680-685.

Donley BG, Moore T, Sferra J, Gozdanovic J, Smith R. The efficacy of oral nonsteroidal anti-inflammatory medication (NSAID) in the treatment of plantar fasciitis: a randomized, prospective, placebo-controlled study. Foot Ankle Int. 2007;28:20-23.

Frey C, Zamora J. The effects of obesity on orthopaedic foot and ankle pathology. Foot Ankle Int. 2007;28:996-999.

Gollwitzer H, Diehl P, von Korff A, Rahlfs VW, Gerdesmeyer L. Extracorporeal shock wave therapy for chronic painful heel syndrome: a prospective, double blind, randomized trial assessing the efficacy of a new electromagnetic shock wave device. J Foot Ankle Surg. 2007;46:348-357.

Hughes RJ, Ali K, Jones H, Kendall S, Connell DA. Treatment of Morton's neuroma with alcohol injection under sonographic guidance: follow-up of 101 cases. Am J Roentgenol. 2007;188:1535-1539.

Kruijff S, van Det RJ, van der Meer GT, van den Berg IC, van der Palen J, Geelkerken RH. Partial matrix excision or orthonyxia for ingrowing toenails. J Am Coll Surg. 2008;206:148-153.

Malay DS, Pressman MM, Assili A, Kline JT, York S, Buren B, Heyman ER, Borowsky P, LeMay C. Extracorporeal shockwave therapy versus placebo for the treatment of chronic proximal plantar fasciitis: results of a randomized, placebo-controlled, double-blinded, multicenter intervention trial. J Foot Ankle Surg. 2006;45:196-210.

Review Date:
12/14/2007
Reviewed By:
Harvey Simon, MD, Editor-in-Chief, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

A.D.A.M. Copyright

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Ibuprofen (By mouth)

admin — Thu, 04 Sep 2008 19:47:24 -0700

Overview

Introduction
Brand Name(s)
When This Medicine Should Not Be Used
How to Use This Medicine
How to Store and Dispose of This Medicine
Drugs and Foods to Avoid
Warnings While Using This Medicine
Possible Side Effects While Using This Medicine

HEALTH GUIDE REFERENCE FROM A.D.A.M

Introduction

Ibuprofen (eye-byoo-PROE-fen)

Treats fever and pain, including pain caused by headache, toothache, arthritis, cold or flu, migraine, or menstrual cramps. This is a non-steroidal anti-inflammatory medicine (NSAID).

Brand Name(s)

Motrin, Advil, Motrin Children's, Motrin IB, Advil Children's, Motrin Infants', Motrin Junior, QC Ibuprofen, Rite Aid Ibuprofen, I-Prin, Ibuprohm, Bufen, The Medicine Shoppe Medi-profen, Ibu-2, Medi-First Ibuprofen

There may be other brand names for this medicine.

When This Medicine Should Not Be Used

You should not use this medicine if you have had an allergic reaction (including asthma) to ibuprofen, aspirin, or other NSAID medicines, such as aspirin, diclofenac, naproxen, Aleve®, Celebrex®, Ecotrin®, or Voltaren®. You should not use this medicine if you have a stomach ulcer, a bleeding disorder. Do not take this medicine if you have advanced kidney disease. Do not use this medicine right before or right after having coronary artery bypass graft (CABG), a type of heart surgery.

How to Use This Medicine

Tablet, Liquid, Chewable Tablet, Capsule, Liquid Filled Capsule

Your doctor will tell you how much of this medicine to use and how often. Do not use more medicine or use it more often than your doctor tells you to.
If you are using prescription-strength ibuprofen: This medicine should come with a Medication Guide. Read and follow these instructions carefully. Ask your doctor or pharmacist if you have any questions. Ask your pharmacist for the Medication Guide if you do not have one. Your doctor might ask you to sign some forms to show that you understand this information.
If you are using this medicine without a prescription, follow the instructions on the medicine label.
It is best to take this medicine with food or milk, so it does not upset your stomach.
Shake the oral liquidwell just before using. Measure the oral liquid medicine with a marked measuring spoon, oral syringe, or medicine cup.
You must chew the chewable tablet completely before you swallow it. Drink some water afterwards to make sure you swallow all of the medicine.
For a Child: If you are not sure how much medicine to give, ask your pharmacist or health caregiver. It is best to figure a child's dose based on how much the child weighs, not the child's age. For most kinds of ibuprofen, do not give this medicine more than 4 times in 1 day (24 hours) unless the doctor tells you to.
For an Adult: Follow your doctor's instructions for how much medicine to take. If you are taking this medicine without a prescription, follow the directions on the package, but do not take more than 6 pills in 1 day (24 hours) unless your doctor tells you to.
Use this medicine for the shortest time possible and in the smallest dose possible. This will help lower the risk of side effects.

If a dose is missed:

If you miss a dose or forget to use your medicine, use it as soon as you can. If it is almost time for your next dose, wait until then to use the medicine and skip the missed dose. Do not use extra medicine to make up for a missed dose.

How to Store and Dispose of This Medicine

Store the medicine in a closed container at room temperature, away from heat, moisture, and direct light. Do not freeze the oral liquid.
Ask your pharmacist, doctor, or health caregiver about the best way to dispose of any outdated medicine or medicine no longer needed.
Keep all medicine away from children and never share your medicine with anyone.

Drugs and Foods to Avoid

Ask your doctor or pharmacist before using any other medicine, including over-the-counter medicines, vitamins, and herbal products.

Make sure your doctor knows if you are also using aspirin, methotrexate (Rheumatrex®), lithium (Eskalith®), a blood thinner such as warfarin (Coumadin®), a steroid such as cortisone, dexamethasone, hydrocortisone, methylprednisolone, prednisolone, prednisone, Orapred®, or a diuretic ("water pill") such as furosemide, hydrochlorothiazide (HCTZ), torsemide, Demadex®, Lasix®.
Do not use any other NSAID medicine unless your doctor says it is okay. Some other names are aspirin, diclofenac, naproxen, Aleve®, Celebrex®, Ecotrin®, or Votaren®.
Do not drink alcohol while you are using this medicine.

Warnings While Using This Medicine

Make sure your doctor knows if you are pregnant or breast feeding. You should not use this medicine during the later part of pregnancy.
Make sure your doctor knows if you have high blood pressure, congestive heart failure (CHF), or other heart or circulation problems. Tell your doctor if you have kidney disease, liver disease, a bleeding problem, or lupus or a similar connective tissue disease
This medicine might cause bleeding in your stomach or intestines. This is more likely if you have had a stomach ulcer in the past, if you smoke or drink alcohol regularly, if you are over 60 years old, if you are in poor health, or if you are using certain other medicines (a steroid or a blood thinner). Tell your doctor if you have ongoing or repeat stomach problems such as heartburn, indigestion, upset stomach, or pain.
This medicine may raise your risk of having a heart attack or stroke. This is more likely in people who already have heart disease. People who use this medicine for a long time might also have a higher risk.
This medicine should not be given to a child younger than 6 months old unless your doctor tells you otherwise. If your child has a severe or ongoing sore throat, high fever, headache, nausea, and vomiting, call your child's doctor right away.
If your symptoms do not improve or if they get worse, call your doctor.Call your doctor if the pain gets worse or lasts longer than 10 days, or if the fever lasts longer than 3 days.
Tell your doctor if you have been vomiting or had diarrhea. You might be dehydrated.
This medicine might contain phenylalanine (aspartame). This is only a concern if you have a disorder called phenylketonuria (PKU), which is a problem with amino acids. Talk to your doctor before using this medicine if you have PKU.
This medicine might contain sugar. If you have diabetes, you might need to count this in your diet.
When treating a migraine headache: Talk to your doctor if you have a headache that feels different from your usual headache, if the pain is much worse than usual, if you have a fever and stiff neck, if you have a headache every day, if this is your first migraine headache, or if the pain is so bad you cannot get up. Call your doctor if your headache was caused by a recent head injury, physical effort, coughing, or bending down.
Make sure any doctor or dentist who treats you knows that you are using this medicine.

Possible Side Effects While Using This Medicine

Call your doctor right away if you notice any of these side effects:

Allergic reaction: Itching or hives, swelling in your face or hands, swelling or tingling in your mouth or throat, chest tightness, trouble breathing.
Blistering, peeling, red skin rash.
Bloody or black, tarry stools.
Change in how much or how often you urinate, blood in your urine.
Chest pain, shortness of breath, or coughing up blood.
Fever, neck pain, stiff neck.
Numbness or weakness in your arm or leg, or on one side of your body.
Pain in your lower leg (calf).
Problems with vision, speech, or walking.
Redness or swelling of the body area where you have pain.
Severe stomach pain.
Shortness of breath, cold sweat, and bluish-colored skin.
Sudden or severe headache.
Swelling in your hands, ankles, or feet.
Trouble seeing, change in how you see colors.
Vomiting blood or something that looks like coffee grounds.

If you notice these less serious side effects, talk with your doctor:

Dizziness
Mild nausea, stomach pain, or heartburn.
Ringing in your ears.

Review Date: 8/4/2008

A.D.A.M. Copyright

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