FitSugar

Diet Tip: Switch Hands

FitSugar — Wed, 16 Jul 2008 13:00:00 -0700

Eating quickly is a habit. Mealtimes have become a speedy endeavor, rather than a time to sit down and enjoy eating food. A good meal is truly one of the simple pleasures of life and we get to do it at least three times a day. If you need to slow down, I have an idea for you.

Try eating an entire meal with your less-dominant hand. If you're right handed, eat with your left. Yes, it will feel weird, but that's a good thing. The struggle to coordinate reaching a fork or spoon to your mouth will force you to eat more slowly. You will savor the effort and the taste. Surely, using your nondominant hand will help you take 20 minutes to eat a meal. Try it and tell me how it goes.

Source

Back pain and sciatica

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

In This Report

Highlights
Introduction
Causes
Risk Factors
Diagnosis
Medications
Complementary and Alternati...
Exercise and Physical Thera...
Surgery
Other Treatments
Specific Treatment for Acut...
Specific Treatment for Chro...
Prognosis
Complications
Prevention
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Surgery

Kyphoplasty, a surgical technique used to treat spinal fractures, does not improve a person's back pain or quality of life, according to a review published in 2006 by a nonprofit health services research agency. Kyphoplasty should only be done if bed rest, medicines, and physical therapy do not relieve back pain.

Ultrasound

Therapeutic ultrasound uses sound waves to deliver gentle vibrations to an area of the body. Scientists in England are studying whether therapeutic ultrasound may help relieve pain and disability due to sciatica.

Acupuncture

Studies continue to show that acupuncture helps some patients with low back pain. Now, research published in the British Medical Journal online says the alternative treatment seems to be worth the price in the long run.

Stem Cells

Researchers in England have pioneered a new technique to grow new spinal tissue using stem cells. Stem cells are the building blocks of specific cells. Every cell in the human body starts (or "stems") from a stem cell. Researchers say a patient's stem cells may someday be used to grow new tissue that can replace damaged discs.

Back pain tied to brain changes

Chronic back pain appears to be linked to tiny structural changes in the brain. German researchers have found that persons with chronic back pain have more activity in the parts of the brain involved in pain processing and emotional responses. It is unclear if the brain changes came before the pain or if they occurred in response to the pain. The scientists presented their findings at the 2006 Radiological Society of North American annual meeting.

Introduction

Back pain is one of the most common reasons people visit their doctor. According to the National Institute of Arthritis and Musculoskeletal and Skin Diseases, 8 out of 10 people have some type of backache.

Back pain can be acute or chronic.

Acute pain develops suddenly and goes away within 6 weeks. Acute pain is the most common type of back pain.
Chronic pain can come on fast or slow, but it lasts longer than 3 months. Back pain can occur in any area of the back, but it is more common in the lower part, which supports most of the body’s weight.

The back is highly complex, and pain may result from damage or injury to any of various bones, nerves, muscles, ligaments, and other structures. Still, despite sophisticated techniques that provide detailed anatomical images of the spine and other tissues, the cause of most cases of back pain remain elusive.

Vertebrae. The spine is a column of small bones, or vertebrae, that support the entire upper body. The column is grouped into three sections.

The cervical (C) vertebrae are the seven spinal bones that support the neck.
The thoracic (T) vertebrae are the twelve spinal bones that connect to the rib cage.
The lumbar (L) vertebrae are the five lowest and largest bones of the spinal column. Most of the body's weight and stress falls on the lumbar vertebrae.

Click the icon to see an image of the spine.

Below the lumbar region is the sacrum, a shield-shaped bony structure that connects with the pelvis at the sacroiliac joints.

At the end of the sacrum are two to four tiny, partially fused vertebrae known as the coccyx or "tail bone."

Click the icon to see an image of the sacrum.

Each vertebra is designated by using a letter and number, which allows the doctor to determine where it is in the spine.

The letter reflects the spinal region where the vertebra is located: C=cervical (neck region), T=thoracic (chest, or middle back, region), and L=lumbar (lower back).
The number signifies the vertebra's place within that spinal region. The numbers start with 1 at the top of a region and count up as the vertebrae descend within the region. For example, C4 is the fourth bone down in the cervical region and T8 is the eighth thoracic vertebrae.

The Disks. Vertebrae in the spinal column are separated from each other by small cushions of cartilage known as intervertebral disks. The disks have no blood supply of their own. They need to rely on nearby blood vessels to keep them nourished.

Click the icon to see an image of an intervertebral disk.

Each disk is 80% water and contains two structures.

Inside each disk is a jelly-like substance called the nucleus pulposus.
The nucleus pulposus is surrounded by a tough, fibrous ring called the annulus.

Click the icon to see an image of the nucleus pulposus.

Processes. Each vertebra in the spine has a number of bony projections called processes. The spinal and transverse processes attach to the muscles in the back and act like little levers, allowing the spine to twist or bend. The particular processes form the joints between the vertebrae themselves, meeting together and interlocking at the zygapophysial joints (more commonly known as facet or z joints ).

Spinal Canal. Each vertebra and its processes surround and protect an arch-shaped central opening. These arches, aligned to run down the spine, form the spinal canal, which encloses the spinal cord.

Click the icon to see an image of the vertebrae and spinal cord.

Spinal Cord. The spinal cord is the central trunk of nerves that connects the brain with the rest of the body. Each nerve root passes from the spinal column to other parts of the body through small openings bounded on one side by the disk and the other by the facets. When the spinal cord reaches the lumbar region, it splits into four bundled strands of nerve roots called the cauda equina (meaning horsetail in Latin).

Click the icon to see an image of the cauda equina.

Causes

In about 85% of back pain cases, the origin of the pain is unknown, and imaging studies usually fail to determine the cause. Disk herniation and disk degeneration due to aging are the most common causes of low back pain. Other problems can also cause this pain, however.

Over the years, the disk can wear away (degenerate), causing inflammation and irritation. This age-related condition is a major source of chronic low back pain.

A herniated disk, sometimes, but incorrectly, called a slipped disk, is widely held to be the most common cause of severe back pain and sciatica. A disk in the lumbar area becomes herniated when it ruptures or thins out and degenerates to the point that the gel within the disk (nucleus pulposus) pushes outward. The damaged disk can take many forms.

A bulge -- The gel has been pushed out slightly from the disk and is evenly distributed around the circumference.
Protrusion -- The gel has pushed out slightly and asymmetrically in different places.
Extrusion -- The gel balloons extensively into the area outside the vertebrae or breaks off from the disk.

There is some debate, however, about how pain develops from a herniated disk and how frequently it causes low back pain. Many people have disks that bulge or protrude and do not suffer back pain. Extrusion (which is less common than the other two conditions) is highly associated with back pain, since the gel is likely to extend out far enough to press against the nerve root, most often the sciatic nerve. Extrusion is very uncommon, however, while sciatic and low-back pain are very common. But there may be other causes of low back pain

Ordinarily, at the time of any injury, the immune system triggers key factors that are designed to promote healing. Evidence is now pointing to an abnormal and persistent immune response in the cells of the nucleus pulposus that may be responsible for nerve injury and pain in the lower back. In such cases, the nucleus pulposus in the herniated disk overproduces certain factors known as cytokines -- notably tumor necrosis factor (TNF) -- that, in high levels, cause inflammation and cell damage. Evidence now suggests that such cytokines cause a biochemical reaction in the regions surrounding the bulging or protruded nucleus pulposus, which results in pain.

Abnormalities in the Annular Ring. Research has also focused on tears in the annular ring -- the fibrous band that surrounds and protects the disk. The annular ring contains a dense nerve network and high levels of peptides that heighten perception of pain. Tears in the annular ring are a frequent finding in patients with degenerative disk disease. Some cases of chronic low back pain may be caused by inward growth of nerve fibers into the annular ring, which triggers pain within the intervertebral disk.

At some time, up to 40% of people have pain called sciatica. This condition occurs when the sciatic nerve is trapped or inflamed.

The Sciatic Nerve. The sciatic nerve has an extensive pathway.

It first branches from the nerve roots that descend off the lowest part of the spinal cord (in the lumbar and sacral areas). Each of the two branches of the sciatic nerve is about as wide as a thumb.
Each branch of the nerve threads through the pelvis and deep into either side of the buttocks.
The nerve branches then pass down each hip and along the back of each thigh to the foot.

Causes of Sciatica. A herniated disk pressing on the sciatic nerve is the most common cause of sciatica, although spinal stenosis or other vertebral abnormalities that press on the sciatic nerve can also cause pain.

The main nerve traveling down the leg is the sciatic nerve. Pain associated with the sciatic nerve usually originates when nerve roots in the spinal cord become compressed or damaged. Symptoms can include tingling, numbness, or pain that radiates to the buttocks, legs, and feet.

Symptoms of Sciatica

Pain due to sciatica can vary widely. It may feel like a mild tingling, dull ache, or a burning sensation. In some cases, the pain is severe enough to cause immobility.

The pain most often occurs on one side. Some people have sharp pain in one part of the leg or hip and numbness in other parts. The affected leg may feel weak.

The pain often starts slowly. Sciatica pain may get worse:

At night
After standing or sitting for long periods of time
When sneezing, coughing, or laughing
After bending backwards or walking more than 50 - 100 yards (particularly if it is caused by spinal stenosis)

Sciatica pain usually goes away within 6 weeks, unless there are serious underlying conditions. Pain that lasts longer than 30 days, or gets worse with sitting, coughing, sneezing, or straining may indicated a longer recovery.

Other than age-related degenerative disk disorders, injuries in the muscles and ligaments supporting the back are the major causes of low back pain. Of note, is the iliac crest pain syndrome (iliolumbar syndrome), in which there are tears in the ligaments that help support the pelvic bone.

Spinal stenosis is the narrowing of the spinal canal. This typically develops as a person ages and the disks become drier and start to shrink. At some point in this process, any disruption, such as a minor injury that results in disk inflammation, can cause impingement on the nerve root and trigger pain. Pain from spinal stenosis can occur in both legs, or it can be felt as sciatica. Spinal stenosis occurs mostly in the elderly with degenerative osteoarthritis, but it can sometimes be caused by other problems, including infection and birth defects.

Spondylosis is a condition in which the fourth or fifth lumbar vertebrae degenerate or develop small fractures. This condition affects 4 - 6% of the general population, and the rates may be higher in certain populations. As it progresses, the spine can become unstable and lead to spondylolisthesis, in which one vertebra slips forward over the other and causes sciatica. The condition most often occurs in older individuals with women having a higher risk than men. It is also a common cause of back pain from stress fractures in young athletes and can also be due to inherited problems, injury, or bone disease.

Some cases of sciatica pain may occur when a muscle located deep in the buttocks pinches the sciatic nerve. This muscle is called the piriformis. The resulting condition is called piriformis syndrome. Piriformis syndrome usually develops after an injury. In rare cases leg swelling, deep-vein blood clots, or both may occur. Piriformis syndrome is sometimes difficult to diagnose.

Ankylosing spondylitis is a chronic inflammation of the spine that may gradually result in a fusion of vertebrae. Symptoms include a slow development of back discomfort, with pain lasting for more than 3 months. The back is usually stiff in the morning; pain improves with exercise. In severe cases, the patient must continually stoop over. It can be quite mild, however, and it rarely affects a person's ability to work. It occurs mostly in young Caucasians in their mid-20s. The disease is more common in men, but about 30% of the cases are in women. Researchers believe that in most cases it is hereditary. About 20% of people with inflammatory bowel disease and about 20% of people with psoriasis develop a form of ankylosing spondylitis. There are few effective treatments for this potentially disabling disease, although etanercept (Enbrel) and infliximab (Remicade), anti-inflammatory agents known as TNF-blockers, are proving to be beneficial.

Any abnormality in joints, vertebrae, or nerve roots can cause back pain:

The facet (z-joints) joints can wear down. In such cases, pain occurs on arching the back or when walking.
In some cases a segment (consisting of two vertebrae and their common joint and disk) becomes unstable when its parts wear down.
Injury to nerve roots, notably deep root ganglia (nerve cells in the spine whose fibers extend from skin to muscle tissue), may be important in some cases. Some patients may have scar tissue that traps the nerve roots in the lower spine and causes sciatica.

Risk Factors

In most known cases, pain begins with an injury, after lifting a heavy object, or after making a sudden movement. Not all people have back pain after such events, however. In the majority of back pain cases, the causes are unknown.

Some evidence suggests that after episodes of back pain, some people may experience changes in brain structure and chemicals that produce an exaggerated response in nerve cells. In fact, a 2005 study suggested that chronic back pain actually shrinks the brain by as much as 11%. Such brain changes may cause a persistent perception of pain even though the actual injury has healed.

German researchers have found that chronic back pain appears to be linked to tiny structural changes in the brain. Using a specialized imaging method, they learned that persons with chronic back pain seemed to have a different, more complex structure to their brain and more activity in the areas involved in pain processing and emotional responses. It is unclear if the brain changes occurred before the pain or in response to the pain.

A number of conditions may make people more or less susceptible to low back pain.

Intervertebral disks begin deteriorating and growing thinner by age 30. One-third of adults over 20 show signs of herniated disks (although only 3% of these disks cause symptoms). As people continue to age and the disks lose moisture and shrink, the risk for spinal stenosis increases. The incidence of low back pain and sciatica increases in women at the time of menopause as they lose bone density. In older adults, osteoporosis and osteoarthritis are also common. However, the risk for low back pain does not mount steadily with ever-increasing age, which suggests that at a certain point, the conditions causing low back pain plateau.

Inherited Spinal Structure Abnormalities. Many people have a genetic susceptibility to low back pain, usually from inheriting spinal structural abnormalities.

Inherited Weakened Disks. Studies are finding that specific mutations of the COL9A gene may play a role in about 10% of sciatica cases. The gene is normally involved in producing collagen, the protein building block in all structural tissue in the body. When defective, it may cause the disk to be less able to resist compressive forces. One 2001 study found the defective gene was present in twice as many patients with disk problems as in patients without back pain.

The likelihood of experiencing back pain increases as children age. Some studies suggest that pain is more common among girls than boys. A common cause of temporary back pain is carrying backpacks that are too heavy for children. Backpacks should not weigh more than 20% of the child's body weight. They should weigh even less for very young children. Emotional or behavioral problems may also contribute to back pain in children.

Jobs that involve lifting, bending, and twisting into awkward positions, as well as those that cause whole-body vibration (usually due to long-distance truck driving), place workers at particular risk for low back pain. The longer a person continues such a job, the higher the risk. Some workers wear back support belts, but evidence strongly suggests that they are useful only for people who are currently have low back pain. The belts offer little added support for the back and do not prevent back injuries. In one study, workers who wore the belt for prevention reported more back pain than the workers who did not wear them.

A number of companies are developing programs to protect against back injuries. Although studies are mixed on the outcome of company interventions, one analysis suggested that they do have a positive effect. Employers and workers should make every effort to create a safe working environment. Office workers should have chairs, desks, and equipment that support the back or help maintain good posture.

Infections. A number of common and uncommon infections are a cause of back pain. Chronic uterine or pelvic infections can cause low back pain in women. Osteomyelitis is infection in the spine, a rare cause of back pain. Other infections that cause back pain include Lyme disease, septic arthritis, bacterial endocarditis, Reiter syndrome, mycobacterial, fungal arthritis, and viral arthritis. Chlamydia pneumonia, an atypical organism that is a common cause of mild pneumonia in young adults, is now believed to cause widespread inflammation in the body's tissue, including blood vessels, and may be responsible for a number of chronic conditions, including heart disease. Some evidence further suggests it may cause inflammation in arteries of the lower spine and contribute to spinal stenosis.

Many medical conditions are associated with back pain.

Osteoporosis is a disease of the skeleton in which the amount of calcium present in the bones slowly decreases to the point where the bones become fragile and prone to fracture. It usually does not cause pain unless the vertebrae collapse suddenly, in which case the pain is often severe. Studies indicate, however, that the incidence of low back pain and sciatica increase around the time of menopause, and very tiny fractures in the vertebrae caused by osteoporosis may be an undetected cause of back pain in many elderly women.
Osteoarthritis occurs in joints where cartilage is damaged and then destroyed, usually as a result of aging. In reaction to this destruction, the bones associated with the joints develop abnormalities. When osteoarthritis affects the spine, it may damage the cartilage in the disks, the moving joints of the spine, or both. The nerves may become pinched, causing pain and in advanced cases, numbness and muscle weakness. The patient may also experience muscle spasms and diminished mobility.
Inflammatory disorders, such as Crohn's disease and rheumatoid arthritis, can produce inflammation in the spine (sacroiliitis), although the spine is less commonly affected than other locations.
Other conditions that can directly cause pain include fibromyalgia, Paget's disease, Parkinson's disease, abscesses, blood clots, and cancer.
Other medical conditions cause referred back pain, which occurs in conjunction with problems in organs unrelated to the spine (although usually located near it). Such conditions include ulcers, kidney disease (including kidney stones), ovarian cysts, and pancreatitis.

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.

It should be noted, however, that a number of medical conditions, such as lung and heart problems and chronic headaches, commonly occur with low back pain. A causal relationship among them, however, is uncertain.

Persistent low back pain in children is more likely to have a serious cause that requires treatment than back pain in adults. According to one small study, one third of children being treated at a hospital for back pain were found to have serious underlying problems.

Stress fractures (spondylolysis) in the spine are a common cause of back pain in young athletes. Sometimes a fracture may not show up for a week or two after an injury. Spondylolysis can cause spondylolisthesis, a condition in which the spine becomes unstable and the vertebrae slip over each other.

Hyperlordosis is an inborn exaggerated inward curve in the lumbar area. Scoliosis, an abnormal curvature of the spine in children, does not usually cause back pain.

Juvenile chronic arthropathy is an inherited form of arthritis. It can cause pain in the sacrum and hip joints of children and young people. It used to be grouped under juvenile rheumatoid arthritis, but is now defined as a separate problem.

Injuries, benign tumors such as osteoblastoma or neurofibroma and cancers, including leukemia, can also cause back pain in children.

Medications may trigger back pain. For example, anticoagulants can cause bleeding or an internal bruise. Long-term steroid use can cause infection or compression fractures.

Some research is suggesting that some people have motor control abnormalities in the deep muscles near the spine. Such lack of control causes instability in the spine that can lead to pain.

Pregnant women are prone to back pain due to a shifting of abdominal organs, the forward redistribution of body weight, and the loosening of ligaments in the pelvic area as the body prepares for delivery. Tall women are at higher risk than short women. Although some earlier research had suggested that the use of epidurals for pain relief during labor could lead to chronic back pain, studies in 2002 reported no increased risk.

Psychological factors are known to play a strong influential role in three phases of low back pain:

Some evidence suggests preexisting depression and the inability to cope may be more likely to predict the onset of pain than physical problems. For example, a British study reported that people who showed emotional distress at age 23 were nearly twice as likely to suffer from back pain 10 years later. A 2005 study found that a “passive” coping style (not wanting to confront problems) was strongly associated with the risk of developing disabling neck or low back pain.
The perception of pain. Social and psychological factors play a role in the severity of a person's perception of back pain. For example, one study compared truck drivers and bus drivers. Nearly all the truck drivers liked their work. Half of them reported low back pain but only 24% lost time at work. Bus drivers, on the other hand, reported much lower job satisfaction than truck drivers, and these workers with back pain had a significantly higher absentee rate than truck drivers in spite of less stress on their backs. Similarly, another study found that pilots, who generally reported "loving their jobs," reported far fewer back problems than their flight crews. And yet another study reported that low rank, low social support, and high stress in soldiers was associated with a higher risk for disabling back pain.
Chronic pain. Depression and a tendency to develop physical complaints in response to stress also increase the likelihood that acute back pain will become a chronic condition. The way a patient perceives and copes with pain at the beginning of an acute attack may actually condition the patient to either recover or develop a chronic condition. Those who over-respond to pain and fear for their long-term outlook tend to feel out of control and become discouraged, increasing their risk for long-term problems.

Studies also suggest that patients who reported prolonged emotional distress have less favorable outcomes after back surgeries. It should be strongly noted that the presence of psychological factors in no way diminishes the reality of the pain and its disabling effects. Recognizing it as a strong player in many cases of low back pain, however, can help determine the full range of treatment options.

Diagnosis

Because nearly all cases of low back pain clear up in a short time and are not due to serious problems, a medical history and a brief physical examination are almost always sufficient.

Still, with very severe or chronic back pain, it is important that any serious medical causes as well as cauda equina syndrome and progressive nerve damage be ruled out first. If the doctor suspects a serious underlying cause, the approach to determining the origin of back pain involves answering three questions:

Is some general medical disorder present that could be causing the pain?
Are there social or emotional factors that might be intensifying the pain?
Are the nerves in the spine involved in the pain (such as in sciatica)?

Such questions can usually be answered with a medical history and physical examination.

A patient should report any serious health problems and concerns during a medical and family history, especially those listed below.

Previous episodes of back pain
Any injuries or accidents involving the neck, back, or hips
History of cancer
Unexplained weight loss or chronic infection
The frequency, duration, and nature of the back pain
When the back pain occurs
What triggered the pain (such as lifting a heavy object)
Conditions that make the pain worse such as coughing
Any situation that relieves the pain
Urination of bowel movement problems
Other relevant symptoms such as morning stiffness, weakness, or numbness in the legs.

The main goal of a physician exam is to try and determine the source of the pain and to determine limits of movement.

Patients are asked to sit, stand, and walk in different ways (flat-footed, on the toes, and on their heels).
In some cases they are asked to walk on a treadmill to test for weakness in toe or heel walking (which may indicate stenosis).
Patients will be requested to bend forward, backward, and sideways and to twist.
Patients will be asked to lift their leg straight up while lying down. The doctor will also move the patient's legs in different positions and bend and straighten the knees. (Pain caused by sciatica can be intensified by lifting the affected leg straight in the air. It is usually sharp, localized, and accompanied by numbness or tingling. Pain caused by inflammation is duller and more generalized and not affected by lifting a straight leg.)
The doctor may measure the circumference of the calves and thighs to look for muscle deterioration.
To test nerve function and reflexes, doctors will tap the knees and ankles with a rubber hammer. The doctor may also touch parts of the body lightly with a pin, cotton swab, or feather to test for numbness and nerve sensitivity.

Because most patients with back pain are on the mend or completely recovered within 6 weeks, imaging techniques such as x-rays or scans are rarely recommended in the first month unless a tumor, fracture, infection, cauda equina syndrome, or progressive neurologic disease is suspected.

Patients who have the following symptoms or experienced certain events may need imaging studies.

Pain that lasts more than a month
Very severe or progressive pain, numbness
Muscle weakness
A previous accident or injury that might have affected the back
A history of cancer
Indications of an underlying disease such as fever or unexplained weight loss
Pain that occurs in patients over 65 years of age

If these conditions exist, usually an x-ray is used first. If results are inconclusive, either computed tomography (CT) or magnetic resonance imaging (MRI) may be performed. (Ultrasound is not useful.)

X-Rays. Although many patients with acute and uncomplicated low back pain believe that plain x-rays of the spinal column are important in a diagnosis, they are not very helpful in most patients except for reducing anxiety. If pain persists after 6 - 8 weeks, then x-rays are usually warranted. In such cases, x-rays may reveal signs of injury, infection, tumors, stenosis, or changes in the vertebrae that may be causing inflammation or compression on the nerve. There are many different types of x-rays for the spine.

A diskography is an x-ray of the disk. This procedure requires injections into disks suspected of being the source of pain and disks nearby. It can be painful and is generally only used for patients who are undergoing back surgery to identify the location of the injured disk.
An x-ray myelogram is an x-ray of the spine that requires a spinal injection of a special dye and the need to lie still for several hours to avoid a very painful headache. It has value only for select patients with pain on moving and standing. It has largely been replaced by CT and MRI scans.

CT stands for computerized tomography. In this procedure, a thin x-ray beam is rotated around the area of the body to be visualized. Using very complicated mathematical processes called algorithms the computer is able to generate a 3-D image of a section through the body. CT scans are very detailed and provide excellent information for the doctor.

Magnetic Resonance Imaging (MRI). Magnetic resonance imaging (MRI) can provide very well-defined images of soft tissue and bone. It is not painful, but some people may feel claustrophobic in scanners that are fully enclosed. MRIs can detect annular tears, or disk fragments, and non-spinal causes of back pain, including infection and cancer. However, MRIs are no more effective than x-rays in identifying arthritis, and they are more expensive. Some medical evidence suggests that relying on MRI images of disk abnormalities to determine treatment has resulted in many unnecessary surgeries. At least 40% of all adults have bulging or protruding vertebral disks, and most have no back pain. The degree of disk abnormalities revealed by MRIs often have very little to do with the severity of the pain or the need for surgery. Disk abnormalities in people who have back pain may simply be a coincidence rather than an indication for treatment.

Click the icon to see an image of a MRI machine.

Advanced imaging techniques should be used only when underlying infection, cancer, or nerve involvement is suspected.

Magnetic Resonance Neurography. This imaging exam looks at the nerves in the pelvic area. Researchers reporting in the Journal of Neurosurgery found that it helped reveal pinched nerves that can cause leg pain. The findings could lead to new ways to diagnose sciatica and piriformis syndrome.

Bone Scintigraphy and SPECT Imaging.In rare cases, doctors may use bone scintigraphy (bone scanning) to determine abnormalities in the bones. The technique may be useful for early detection of spinal fractures, cancer that has spread to the bone, or osteoarthritis. During this exam, a small amount of radioactive material is injected into a vein. It circulates through the body, and is absorbed by the bones. The bones can then be visualized using x-rays or single photon emission computed tomography (SPECT). A study in the February 2006 journal Radiology found that SPECT can help determine which patients would get low back pain relief from spinal injections. Forty-seven patients were randomly divided into two groups: One group received SPECT before they were scheduled for an injection, the other group did not. Those who showed spinal problems on the SPECT images received an injection in the area of the abnormalities. Those who had a normal SPECT, as well as those who did not have the test at all, received injections in the area recommended by their referring physician. After a month, those who had targeted injections using the SPECT images had greater pain relieve than those who did not.

Electrodiagnostic tests that analyze the electric waveforms of nerves and muscles may be useful for detecting nerve abnormalities that may be causing back pain and identifying possible injuries. They are also useful to determine if any abnormal structural findings on an MRI or other imaging test have real significance as a cause of the back pain. It should be noted that any nerve injuries that affect these tests may not be present for 2 - 4 weeks after symptoms begin.

Nerve conduction studies and electromyography are the electrodiagnostic tests most commonly performed.

Nerve Conduction Studies. To perform nerve conduction studies, surface electrodes are attached to the skin. Small electric shocks are then applied to measure the speed of nerve conduction.

Electromyography. To perform electromyography, a fine, sterile, wire electrode is inserted briefly into a muscle and the electrical activity is displayed on a viewing screen. Electromyography can be quite painful, and some experts question, in fact, whether it adds any valuable diagnostic information. They suggest it be limited to unusual cases or when other tests indicate that the condition is aggressive and may increase the risk for rapid, significant injury.

Blood and urine samples may be used to test for infections, arthritis, or other conditions.

Injecting a drug that blocks pain into the nerves in the back helps locate the level in the spine where problems occur.

A procedure called a facet block is also useful in locating areas of specific damage.

Provocative diskometry is a test that uses an injection of saline solution into the suspected disk to reproduce the pain, which is then followed by injection of an anesthetic to dull the pain.

Medications

The most commonly prescribed medications for the treatment of back pain are nonsteroidal anti-inflammatory drugs (NSAIDs). These drugs block prostaglandins, the substances that dilate blood vessels and cause inflammation and pain. Evidence suggests that short-term use of NSAIDs brings effective relief in patients with acute back pain. The benefits for chronic back pain are less certain.

There are dozens of NSAIDs. The most common are the following:

Over-the-counter NSAIDs include aspirin, ibuprofen (Advil, Nuprin, Motrin IB, Rufen), naproxen (Aleve), ketoprofen (Actron, Orudis KT).
Prescription NSAIDs include ibuprofen (Motrin), naproxen (Naprosyn, Anaprox), flurbiprofen (Ansaid), diclofenac (Voltaren), tolmetin (Tolectin), ketoprofen (Orudis, Oruvail), nabumetone (Relafen), dexibuprofen (Seractil), and indomethacin (Indocin).
Topical NSAIDs delivered in gels, creams, or patches do not appear to provide any long-term benefits in reducing arthritic pain.

Many experts now recommend that patients who take NSAIDs by mouth only do so for a short period of time. A 2004 review published in the British Medical Journal suggested that long-term use of NSAIDs does not actually reduce osteoarthritis pain and may increase patients’ risk of experiencing side effects. High dosages of NSAIDs can cause heart problems such as increased blood pressure, kidney problems, and stomach bleeding.

In April 2005, the FDA asked drug manufacturers of prescription NSAIDs to place an alert on their medicines warning people that the drugs have been linked to an increased risk for cardiovascular events and gastrointestinal bleeding. The FDA also requested manufacturers of OTC NSAIDs to revise their labels to include more specific language concerning potential cardiovascular and gastrointestinal risks. Aspirin does not contain such warning labels.

Long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) is the second most common cause of ulcers and the rate of NSAID-caused ulcers is increasing. Ulcers caused by nonsteroidal anti-inflammatory drugs (NSAIDs) are also more likely to bleed than those caused by the bacterium H. pylori.

Doctors cannot predict which patients taking these drugs will develop bleeding.

Among the groups at high risk for bleeding are elderly people, anyone with a history of ulcers of GI bleeding, patients with serious heart conditions, alcohol abusers, and those on certain medications, such anticoagulants ("blood thinners"), corticosteroids, or bisphosphonates (drugs used for osteoporosis).

Proton-pump inhibitors may help to prevent and heal ulcers caused by NSAIDs. Proton-pump inhibitors include omeprazole (Prilosec), esomeprazole (Nexium), and lansoprazole (Prevacid).

An ulcer is a crater-like lesion on the skin or mucous membrane that is caused by an inflammatory, infectious, or cancerous condition. To avoid irritating an ulcer, stop smoking and try to eliminate certain substances from your diet, including caffeine and alcohol. Prescription medicines are available to suppress the acid in the stomach that causes erosion of the stomach lining. Endoscopic therapy can be used to stop ulcer-related bleeding.

Coxibs block an inflammation-promoting enzyme called COX-2. This drug class was initially thought to work as well as NSAIDs, while causing less gastrointestinal distress. However, following numerous reports of cardiovascular events, gastrointestinal problems, and skin rashes, the FDA is currently re-evaluating the relative risks and benefits of this drug class. Rofecoxib (Vioxx) and valdecoxib (Bextra) have been withdrawn from the United States market. Celecoxib (Celebrex) is still available, but patients should ask their doctor if this drug is appropriate and safe for them.

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 the severe gastrointestinal problems that NSAIDs can. Some patients who take tramadol experience severe itching. A combination of tramadol and acetaminophen (Ultracet) is now available. It provides more rapid pain relief than tramadol alone.

Narcotics are pain-relieving and sleep-inducing drugs that act on the central nervous system. They are the most powerful medications available for the management of pain.

There are two types of narcotics:

Opiates are derived from natural opium such as morphine and codeine.
Opioids are synthetic drugs and include oxycodone (Percodan, Percocet, Oxycontin), hydrocodone (Vicodin), and oxymorphone (Numorphan).

Novel ways to deliver pain medicine have been developed. A skin patch containing an opioid called transdermal fentanyl (Duragesic) may relieve chronic back pain more effectively than oral opioids. For very severe pain, a small, patient-controlled pump called SynchroMed may be used. This device is implanted under the skin in the abdomen and delivers pulses of pain-relieving opioids to the spinal canal.

Common side effects of opioids include anxiety, constipation, nausea and vomiting, dizziness, drowsiness, paranoia, urinary retention, restlessness, and labored or slow breathing. Addiction is a risk, although less than is commonly believed when these medications are used for pain relief. In fact, when prescribed properly, use of opioids for chronic pain can be safer in some cases than on-going use of NSAIDs. Unfortunately, opioid abuse among young people is a major concern. Unless the pain is very severe, experts advise against routinely prescribing opioids.

Injections of different substances are sometimes used to treat low back pain caused by nerve impingement. The injection is usually an epidural, which is directed into the spaces between the outer membrane of the spine and the vertebrae. None of these substances cure the problem.

Corticosteroids. An injection of a corticosteroid (commonly called a steroid) is directed as close to the injured location as possible. Corticosteroids reduce inflammation. This approach may temporarily relieve sciatic pain until the body heals itself. Studies that measure the benefits of steroids on sciatica or low back pain are conflicting. There is some evidence that patients can experience rebound pain within a few months. Some experts have also raised concerns that even a single injection can cause serious and painful side effects, including meningitis and inflammation, although such risks are very low.
Hypertonic saline (salt water solution). Epidural injections of saline are being investigated for breaking up scar tissue. One 2001 study compared targeted injections of saline and steroids directed at the nerve root. Although steroid injections had more immediate benefits, both products offered improvement. By the third month, patients who had saline injections experienced less pain than the steroid group. A 2003 study found that epidural corticosteroid injections provided no greater benefit than saline injections for patients with sciatica.
Local anesthetics. Injections of anesthetics such as Xylocaine or bupivacaine may help some patients, although studies on their benefits are mixed.
Botulinum. Researchers are investigating whether injections of botulinum toxin (Botox) in the lower back can safely and effectively relieve pain. Very small amounts of Botox temporarily paralyzes muscle tissue. Botox is commonly used to smooth out wrinkles. Some studies have suggested that Botox may be very helpful in relieving chronic low back pain and sciatica caused by piriformis syndrome. In a 2001 study, the benefits of Botox injections for low back pain subsided within 6 months.

A 2002 review of studies concluded that antidepressants may lessen pain severity in some patients, although they had little effect on daily functioning. Antidepressants called tricyclics can be effective painkillers in non-depressed people with chronic back pain. Such antidepressants include amitriptyline (Elavil, Endep), desipramine (Norpramin), doxepin (Sinequan), imipramine (Tofranil), amoxapine (Asendin), nortriptyline (Pamelor, Aventyl), and maprotiline (Ludiomil). It should be noted that tricyclics can have severe side effects. Nonetheless, experts believe there is a useful role for these drugs that warrants further investigation.

A combination of nonsteroidal anti-inflammatory drugs (NSAIDs) and muscle relaxants such as cyclobenzaprine (Flexeril), diazepam (Valium), carisoprodol (Soma), or methocarbamol (Robaxin) are sometimes used for patients with acute low back pain. Medical evidence has found that they can help relieve non-specific low back pain, but some experts have warned that these drugs should be used cautiously, since they target the brain, not the muscles. Patients who take muscle relaxants may experience a number of central nervous system side effects such as drowsiness. The muscle relaxant Soma can be addictive and does little more than produce sleep.

Tumor-Necrosis Factor (TNF) Modifiers. TNF modifiers block the action of tumor necrosis factor, a protein involved in inflammatory response. Because of their anti-inflammatory properties, TNF modifier drugs are being investigated for the treatment of the nerve dysfunction and pain that occurs in sciatica. Some small studies indicate that infliximab (Remicade) may help reduce sciatica pain. Early studies suggest that another TNF modifier, etanercept (Enbrel), may be useful for treating sciatica and back pain. TNF modifiers are powerful drugs that can cause severe side effects.

Lidocaine Patch. A skin patch containing lidocaine, a local anesthetic, has been used specifically for herpes zoster pain. Early studies suggest that this patch, called Lidoderm, may provide significant relief for people who suffer from low back pain with very few adverse effects, even with continuous use of four patches a day. If further studies support its benefits, the patch could prove to be an important treatment

NO-NSAIDs. NO-NSAIDs are drugs that combine NSAIDs and nitric oxide (NO), a substance that enhances blood flow to the stomach and increases levels of protective mucus and bicarbonate. These agents show particular promise in providing pain relief and reducing the risk for GI problems.

Generally, 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 a number of 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.

Most herbal remedies used for back pain have both pain-relief and anti-inflammatory effects. Popular herbs for back pain relief include:

White willow bark (Salix alba) contains salicylates, the same chemicals found in aspirin.
Bromelain is an enzyme found in pineapple.
Boswellia (Boswellia serrata) is an herb commonly used in Indian Ayurvedic medicine.
Devil’s claw (Harpagophytum procumbens) is an African herb sometimes used to relieve arthritic pain.

White willow bark, bromelain, and Boswellia have blood-thinning properties and can interfere with anticoagulant medications such as warfarin (Coumadin).

Complementary and Alternative Medicine

A number of complementary and alternative treatments are used to relieve back pain. Complementary means it is used together with conventional medicine. Alternative means it is done in place of conventional medicine.

Acupuncture is now a common alternative treatment for certain kinds of pain. It involves inserting small needles or exerting pressure on certain "energy" points in the body. When the pins have been placed successfully, the patient is supposed to experience a sensation that brings a feeling of fullness, numbness, tingling, and warmth with some soreness around the acupuncture point. Unfortunately, rigorous studies of acupuncture are difficult to perform, and most evidence on its benefits is weak. In any case, it may be specifically helpful for certain patients with back pain, such as pregnant women, who must avoid medications. Anyone who undergoes acupuncture should be sure it is performed in a reputable location by experienced practitioners who use sterilized equipment.

Click the icon to see an image of acupuncture.

A number of well-conducted studies have supported the benefits of massage therapy for patients with chronic or acute back pain, especially when it is combined with exercise and patient education. In fact, one analysis in 2003 suggested it may reduce the costs of care. However, it is usually not covered by insurance.

According to a 2001 review of studies, only intensive programs that include both psychological and physical rehabilitation therapies were successful in reducing chronic low back pain and improving function. A number of effective approaches to low back pain -- collectively called mind-body techniques -- employ psychological, behavioral, or physical methods to promote relaxation and reduce stress. Although many may be helpful, evidence is lacking on the specific approaches that would be most successful and which patients would most likely benefit.

Stress Reduction. Stress reducing techniques, including relaxation methods and meditation, may be helpful. One study, for example, reported that meditation was beneficial in reducing pain and improving mood among chronic pain sufferers who had not responded to traditional care. Another found that after 3 weeks, patients who were in pain after back surgery had less discomfort and slept better after practicing relaxation imagery techniques while listening to music for 25 minutes a day.

Cognitive-Behavioral Therapy. Studies report that a course of cognitive-behavioral therapy helps reduce chronic back pain or at least enhances the patient's ability to deal with it. The primary goal of this form of therapy in such cases is to change the distorted perceptions that patients have of themselves and their approach to pain. Using specific tasks and self-observation, patients gradually shift their fixed ideas that they are helpless against the pain that dominates their lives to the perception that pain is only one negative and, to a degree, a manageable experience among many positive ones. In one study, therapists also taught relaxation techniques and methods to improve posture. The sessions lasted for 2.5 hours each week for 12 weeks. More research is needed.

Patient Education and Support Groups. A 2002 study reported that patients with chronic low back pain who participated in an expert-moderated e-mail support and discussion group had less pain and disability after 12 months. An Australian massive public-health campaign that educated patients and doctors about the importance of staying active and dispelled fears about long-term impairment from back pain dramatically reduced disability and worker compensation claims.

Spinal Manipulation for Uncomplicated Acute Low Back Pain. Spinal manipulation may be useful for acute back pain that persists beyond 2 - 3 weeks. There are a number of variations, but one example of a spinal manipulation technique is the following:

The patient first lies on their side.
The practitioner grasps the exposed shoulder and either the hip or knee and then presses the upper and lower portions of the body in opposite directions, so that the torso rotates.
The shifting vertebrae make a cracking or popping sound, indicating that they have exceeded the normal range of motion.
Often this results in a greater sense of ease and mobility. (The effect, however, may be temporary.)

Whether on-going manipulations relieve pain better that just one visit is a subject of debate. Some patients consider spinal manipulation to be highly effective for chronic low back pain. A major 2003 analysis, however, reported that current evidence did not support the benefits of spinal manipulation over general medical care or physical therapy for either acute or chronic back pain. [It was better than sham (fake) therapy, however.]

Spinal manipulations are typically performed by chiropractors, but osteopathic doctors also perform them.

One in three people with low back pain seek treatment from a chiropractor. Chiropractic was founded in the U.S. in the late 1800s. The specific goal of chiropractors is to perform spinal manipulations to improve nerve transmission. Many studies have now confirmed that patients feel more satisfied with their chiropractic care than with treatment from general practitioners.
Osteopathy was also founded in the 1800s. Its core approach to healing also involves physical manipulation. Osteopathy manipulates the bones, muscles, and tendons to optimize blood circulation. The general direction of osteopathy over the years has widened to employ a broader range of treatments that now approach those of standard medicine. One 1999 study reported that osteopathy was as effective as medical treatment in relieving low back pain and patients required far less medication and physical therapy. Osteopathic treatment was also far less expensive than traditional back pain treatments.

Both chiropractors and osteopaths offer verbal assurance and a precise treatment regimen. The direct physical connection through spinal manipulation reinforces the patient-practitioner relationship. The emotional effects of such connections may be as important for healing as the treatments themselves.

Mild and temporary side effects from spinal manipulation are common. The potential for serious adverse effects from low back manipulations is low. It should be strongly noted, however, that serious complications (including stroke or spinal cord or neck injury) have been reported with manipulations of the neck. Although little research has been done on such complications, an English survey indicated that they are more frequent than commonly thought.

Some chiropractors may take a lot of x-rays, particularly those of the full spine, which may have long-term harmful consequences. Patients should also be aware that some chiropractors use alternative treatments that have not been proven or rigorously studied. All patients should require objective evidence on the benefits of their treatments.

Vertebral Axial Decompression. Vertebral axial decompression (VAX-D) may reduce pain and improve function in patients with chronic low back pain, including sciatic pain that radiates down the leg. The patient lies face down on a special table, clutching hand grips and wearing a pelvic harness. The traction-like action alternately decompresses and relaxes the spine over 1-minute intervals. Each session lasts about 30 minutes. Ten to 20 sessions on successive days are often required. The procedure is thought to alleviate pain and enhance healing by relieving pressure within the disks, promoting the in-flow of oxygen, fluids, and nutrients to the spinal column. Some evidence supports its benefits, with reported success rates of around 70%. Because it is considered experimental, it is not yet covered by most insurers. More studies are needed to confirm its possible benefits.

Percutaneous Neuromodulation Therapy. A technique called percutaneous neuromodulation therapy (PNT) uses a small device delivers electrical stimulation to deep tissues and nerve pathways near the spine. It has shown some initial promise for relief of chronic back pain and may also improve mobility and sleep. Treatment sessions are conducted in the doctor's office and last about 30 minutes. A correct pattern of stimulation appears to be important for optimal relief and needs to be determined.

Electric Nerve Stimulation. Transcutaneous electric nerve stimulation (TENS) uses low-level electrical pulses to suppress back pain. A variant, percutaneous electrical nerve stimulation (PENS), applies these pulses through a small needle to acupuncture points. The standard procedure is to give 80 - 100 pulses per second for 45 minutes three times a day. The patients are barely aware of the sensation. Although a 2002 analysis of trials could find no direct evidence of benefit, small studies have reported some relief for chronic low back pain from either TENS or PENS. It is not known if these effects are long lasting. Neither approach is helpful for relief of acute low back pain in most patients.

Muscle Stimulation. Two investigative 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 then relax then the process is stopped. Discomfort is minimal. Small studies are reporting some help in relieving a number of condition the cause chronic pain, including low back pain.

Therapeutic ultrasound. Therapeutic ultrasound involves placing a small wand or probe directly onto the skin. The wand gives off sound waves, which gently vibration the area. Scientists in England are studying whether therapeutic ultrasound may help relieve pain and disability due to sciatica.

Intradiscal Electrothermal Treatment (IDET). Intradiscal electrothermal treatment (IDET) uses electricity to heat a painful disk. Heat is applied for about 15 minutes. Pain may temporarily feel worse, but after healing, the disk shrinks and becomes desensitized to pain. However, healing takes several weeks. The surgery may not work in obese patients.

Some studies have reported positive benefits to IDET; others say it does not significantly reduce pain. A randomized, blinded study published in the November 2005 journal Spine found that IDET was no better than a sham (fake) procedure in relieving chronic back pain due to disk disease. For the study, patients were randomly selected to receive either IDET or a sham procedure. After 6 months, there was no difference in pain symptoms between the two groups.

Exercise and Physical Therapy

Incorrect movements or long-term high-impact exercise is often a cause of back pain in the first place. People vulnerable to back pain should avoid activities that put undue stress on the lower back or require sudden twisting movements, such as football, golf, ballet, and weight lifting.

Exercise does not help acute back pain. In fact, overexertion may cause further harm.

An incremental aerobic exercise program (such as walking, stationary biking, swimming) may begin within 2 weeks of symptoms. Jogging is usually not recommended, at least not until the pain is gone and muscles are stronger.

Patients should avoid exercises that put the lower back under pressure until the back muscles are well toned. Such exercises include leg lifts done in a facedown position, straight leg sit-ups, and leg curls using exercise equipment.

In all cases, patients should never force themselves to exercise if, by doing so, the pain increases.

Exercise plays a very beneficial role in chronic back pain. Repetition is the key to increasing flexibility, building endurance, and strengthening the specific muscles needed to support and neutralize the spine. Exercise should be considered as part of a broader program to return to normal home, work, and social activities. In this way, the positive benefits of exercise not only affect strength and flexibility but they also alter and improve patients' attitudes toward their disability and pain. Exercise may also be effective when combined with a psychological and motivational program, such as cognitive-behavioral therapy.

There are different types of back pain exercises. A 2005 review in the Annals of Internal Medicine found that stretching exercises worked best for reducing pain, while strengthening exercises were best for improving function.

Back pain exercises include:

Low Impact Aerobic Exercises. Low-impact aerobic exercises, such as swimming, bicycling, and walking, can strengthen muscles in the abdomen and back without over-straining the back. Programs that use strengthening exercises while swimming may be a particularly beneficial approach for many patients with back pain. Medical research has shown that pregnant women who engaged in a water gymnastics program have less back pain and are able to continue working longer.
Lumbar Extension Strength Training. Exercises called lumbar extension strength training are proving to be effective. Generally, these exercises attempt to strengthen the abdomen, improve lower back mobility, strength, and endurance, and enhance flexibility in the hip and hamstring muscles and tendons at the back of the thigh.
Yoga, Tai Chi, Chi Kung. Practices originating in Asia that combine low-impact physical movements and meditation may be very helpful. They are designed to achieve a physical and mental balance and can be very helpful in preventing recurrences of low back pain.
Pilates, an exercise practice that uses yoga principles, may be specifically helpful.
Flexibility Exercises. Flexibility exercises may help reduce pain. A stretching program may work best when combined with strengthening exercises.
Retraining Deep Muscles. Some studies suggest a link between low back pain and impaired motor control of deep muscles of the back and trunk. According to these studies, contraction exercises specifically designed to retrain these muscles may be effective for patients with both acute and chronic pain.

Perform the following exercises at least three times a week:

Partial Sit-ups. Partial sit-ups or crunches strengthen the abdominal muscles.

Keep the knees bent and the lower back flat on the floor while raising the shoulders up 3- 6 inches.
Exhale on the way up and inhale on the way down.
Perform this exercise slowly 8 - 10 times with the arms across the chest.

Pelvic Tilt. The pelvic tilt alleviates tight or fatigued lower back muscles.

Lie on the back with the knees bent and feet flat on the floor.
Tighten the buttocks and abdomen so that they tip up slightly.
Press the lower back to the floor, hold for one second, and then relax.
Be sure to breathe evenly.

Over time increase this exercise until it is held for 5 seconds. Then, extend the legs a little more so that the feet are further away from the body and try it again.

Stretching Lower-Back Muscles. The following are three exercises for stretching the lower back:

Lie on the back with knees bent and legs together. Keeping arms at the sides, slowly roll the knees over to one side until totally relaxed. Hold this position for about 20 seconds (while breathing evenly) and then repeat on the other side.
Lying on the back, hold one knee and pull it gently toward the chest. Hold for 20 seconds. Repeat with the other knee.
While supported on hands and knees, lift and straighten right hand and left leg at the same time. Hold for 3 seconds while tightening the abdominal muscles. The back should be straight. Alternate with the other arm and leg and repeat on each side 8 - 20 times.

Note: No one with low back pain should perform exercises that require bending over right after getting up in the morning. At that time, the disks are more fluid-filled and more vulnerable to pressure from this movement.

Physical therapy with a trained professional may be useful if pain has not improved within the first 3 weeks. It is, in fact, important for any person who has chronic low back pain to have an exercise program guided by professionals who understand the limitations and special needs of back pain and who can address individual health conditions. One study indicated that patients who planned their own exercise did worse than those in physical therapy or doctor-directed programs.

Physical therapy typically includes the following:

The first stage involves patient education and training the patient in correct movement. Sometimes heat or electro-therapies (such as therapeutic ultrasound or low-energy lasers) are used, although their benefits are unproven.
If back pain persists beyond 5 weeks, physical therapy is used for rehabilitation. It uses exercises to help the patient keep the spine in neutral positions during all daily activities.

Surgery

Diskectomy is the surgical removal of the diseased disk. The procedure relieves pressure on the spine. It has been performed for 40 years with increasingly less invasive techniques being developed over time. However, few studies have been conducted to determine its real effectiveness. In appropriate candidates it provides faster immediate relief than medical treatment, but long-term benefits (over 5 years) are uncertain. A number of minimally invasive variations are now available.

When the soft, gelatinous central portion of an intervertebral disk is forced through a weakened part of a disk, it is called a slipped disk. Most slipped disks (herniated disks) take place in the lumbar area of the spine. Slipped disks are one of the most common causes of lower back pain. The mainstay of treatment is an initial period of rest with pain and anti-inflammatory medications followed by physical therapy. If pain and symptoms persist, surgery to remove the herniated portion of the intervertebral disk may be needed.

Microdiskectomy. Microdiskectomy is the current standard procedure. It is performed through a small incision (1 to 1-1/2 inch). The back muscles are lifted and moved away from the spine. After identifying and moving the nerve root, the surgeon removes the injured disk tissue under it. The procedure does not change any of the structural supports of the spine, including joints, ligaments, and muscles.

Other less invasive procedures that are available including the following:

Endoscopic Diskectomy. Endoscopy employs a catheter (a thin tube) that contains tiny cameras and surgical instruments that are inserted through small incisions. Various endoscopic approaches are proving to be useful for back surgery.
Percutaneous Diskectomy. Percutaneous diskectomy (PAD). This approach uses a tube with a device at the tip that cuts away some of the nucleus pulposus and a vacuum that then sucks this gelatinous matter out.
Laser Diskectomy. A number of investigative surgical procedures employ lasers. For example, endoscopic laser foraminoplasty (ELF) uses lasers to locate the likely source of pain and remove diseased tissue. The incision requires little more than a Band-Aid and complications are minimal. Long-term benefits are unknown, however.

It is not clear yet if any of these less-invasive procedures are any more effective than the standard microdiskectomy.

Complications and Outlook. Many patients still have back pain after diskectomy that delays discharge from the hospital. Narcotics are usually needed. Adding an injected NSAID may speed resolution of pain.

Scar tissue is a significant problem, since it can cause persistent low back pain afterward. Anti-scarring agents or certain devices may help reduce surgical scars and thereby postoperative pain. Other complications of spinal surgery can include nerve and muscle damage, infection, and the need for reoperation.

Patients now often remain in bed only 3 - 4 days after disk surgery. It may take 4 - 6 weeks for full recovery, however. Gentle exercise may be recommended at first. Starting intensive exercise 4 - 6 weeks after a first-time disk surgery appears to be very helpful for speeding up recovery.

Operations that remove a vertebra (laminectomy) or shave off part of one (laminotomy) may be used in certain cases of spinal stenosis or spondylolisthesis to decompress the nerve. They may also be used to remove benign tumors on the spine.

Click the icon to see an illustrated series detailing lumbar spinal surgery.

Although either procedure often brings immediate relief from pain, a 1999 statistical study suggested that it is inappropriately performed in 60% or more of sciatica cases. There are small risks to the operation, and it is not always successful. Some recurrence of back pain and sciatica occurs in half to two-thirds of postoperative patients. Minimally invasive variations are under investigation.

In cases where abnormal vertebrae position or movement is responsible for severe and chronic back pain, such as spinal stenosis or spondylolisthesis, surgeons may fuse vertebrae together. Fusion uses a bone graft or some other device to join the vertebrae together. In a 2001 study of patients with severe long-term back pain, 33% of patients who had spinal fusion had less back pain after 2 years, compared to 7% who received conservative treatment with physical therapy. Pain improved most in the 6 months following surgery. However, a 2005 clinical trial found that spinal fusion surgery worked no better than intensive rehabilitation in reducing disability. The intensive rehabilitation program included both physical and cognitive-behavioral therapy.

Many spinal fusion surgeries use a tiny hollow metal cage, which is implanted into the disk space. Bone is then removed from the patient's hip and packed inside the cage. Over time the bone grows through the holes and around the device, fusing the vertebrae. Alternatively, rather than performing a bone graft, the cage is filled with a sponge-like material containing a genetically-engineered protein called InFuse (rhBMP-2) that promotes bone to grow.

Click the icon to see an illustrated series detailing spinal fusion.

A number of video-assisted techniques have been developed. The new techniques are less invasive than standard "open" surgical approaches, which uses wide incisions. To date, however, the newer procedures have higher complication rates than the open approaches and some medical centers have abandoned them.

Percutaneous Vertebroplasty. Percutaneous vertebroplasty involves the injection of a cement-like bone substitute into vertebrae with compression fractures. It is done under endoscopic and x-ray guidance. The technique is proving useful for stabilizing the spine and relieving pain in patients with spinal compression fractures due to osteoporosis or cancer. A Mayo Clinic study found that patients who have the procedure have less back pain during rest and activity. A survey of records from more than 100 vertebroplasty patients revealed that most patients are more functional than before the procedure, and the benefits lasted for up to a year. Warning: The FDA has warned consumers that polymethylmethacrylate bone cement, used during vertebroplasty, could leak. Such leakage could cause damage to soft tissues and nerves. It is extremely important that the patient is sure that the health care provider has had significant experience performing the vertebroplasty procedure.

Percutaneous kyphoplasty. The health care provider injects bone cement into the space surrounding a fractured vertebra. (Vertebroplasty injects the cement directly into the vertebra.) Kyphoplasty is used to stabilize the spine and return spinal cord height to as normal as possible. However, a review published in 2006 by a nonprofit health services research agency found that the technique does not improve a person's back pain or quality of life. Kyphoplasty should only be done if bed rest, medicines, and physical therapy do not relieve back pain. Those with severe fractures or spinal infections should not have kyphoplasty.

Artificial Disk Replacement. Total disk replacement is an investigative procedure for some patients with severely damaged disks. The technique implants artificial disks (ProDisc, Link, SB Charite) consisting of two metal plates and a soft core. The surgery can be performed using a minimally invasive laparoscopic procedure, which is performed through tiny cuts using miniature tools and viewing devices. A study in 2003 was the first to suggest that it may eventually achieve results that are comparable to standard surgeries for disk herniation. An artificial cushioning device called the prosthetic disk nucleus (PDN) replaces only the inner gel-like core (nucleus pulposus) within the intervertebral space, rather than the entire disk. It is showing promise in early studies.

Nerve Blocks. A number of surgical techniques are available for relieving pain by impairing nerves that are causing pain due to impingement. Medical research has shown that 60% of the patients who received electrical stimulation to block the nerves reported at least 90% relief of pain after a year; 87% reported at least 60% relief.

Other Treatments

Radiofrequency Nerve Destruction. Radiofrequencies are being used to destroy nerves involved in the facet joints (or z-joints), which connect the vertebrae. Evidence is still weak on its benefits. A 2003 analysis suggested that it may be beneficial, however, for relief of neck pain and possibly for low back pain caused by problems in the facets joints. Serious infections have been reported.

Stem cell treatments. Researchers in England have pioneered a new technique to grow new spinal tissue using the patient's own stem cells. Stem cells are the building blocks of specific cells. Every cell in the human body starts (or "stems") from a stem cell. The new tissue will replace damaged spinal tissue and may relieve low back pain. Researchers expect the treatment to enter pre-clinical trials in about 1 year.

Specific Treatment for Acute Low Back Pain

Patients with short-term acute low back pain usually have the best results with the least aggressive treatments. The general approach is as follows:

Patients with no serious underlying cause should stay as active as possible within the limits of the back pain. (Bed rest is not recommended.)
Physical therapy or spinal manipulations may be helpful if pain continues for more than 2 - 3 weeks.
The patient should seek a specialist if pain continues for more than 1 month. (Some patients may need to see a specialist sooner if there is an underlying disorder, nerve damage, or injury.) Back pain due to medical conditions such as arthritis, osteoporosis, or pregnancy either goes away when the underlying condition disappears or is treated.

Home Care Tips for Relieving Pain

Resume normal activity as soon as possible. Bed rest is no longer recommended and may delay recovery. Activities should be done without strain or stretching.
Avoid intense exercise and physical activity, particularly heavy lifting and trunk twisting if there is acute back pain.
Try an over-the-counter nonsteroidal anti-inflammatory such as aspirin or ibuprofen. These medicines often provide significant benefits.
Apply heat (104°) to the painful area. Heat may work better than ibuprofen or acetaminophen. One group of researchers found that people with low back pain who wear low-level heat wraps for 8 hours a day have significant less pain and disability.
Try alternating between hot and cold packs. Some doctors recommend changing from hot to cold every 3 minutes and repeating this sequence three times. Others believe ice packs should be applied first. This routine should be done two or three times during the day. (Note: Heat or cold treatments do not have much effect on sciatica.)
Supportive back belts, braces, or corsets may help some people temporarily, but these products can reduce muscle tone over time and should be used only briefly.
Get plenty of sleep. Healthy sleep plays a vital role in recovery. Avoid caffeine in the afternoon and evening, and unwind before bed by taking a warm bath or practicing relaxation techniques. It is often difficult to get a good night's sleep when suffering from back pain, particularly because the pain can intensify at night. Some people may need medicine to help manage nighttime pain or treat sleeplessness. Lying curled up in a fetal position with a pillow between the knees or lying on the back with a pillow under the knees may help.

Prescription muscle relaxants may help some patients, although their benefits are uncertain. Once started, medications should be taken on a regular schedule in order to maintain consistent effectiveness.

Massage therapy may help relieve both acute and chronic low back pain. Several well-conducted studies have shown some benefit and suggest it may reduce the costs of care. Massage therapy may not be covered by health insurance.

Spinal manipulation may help, although it is not clear if it works any better than physical therapy or general care. Some experts recommend delaying this treatment until pain has persisted for 3 weeks, if possible, since the back pain will most likely have gone away on its own by then.

Acupuncture has not proven to have any value for acute low back pain in most patients, but may provide some help for patients with chronic low back pain.

Be aware of and avoid approaches that are not helpful. Certain approaches may even be harmful for acute low back pain. For example, permanent bipolar magnets (magnet therapies) can deactivate heart devices and must be kept at least six inches away from pacemakers or implantable cardioverter defibrillators. These magnets have gained some popularity as a non-invasive method of relieving pain, but no studies support the claims.

Specific Treatment for Chronic Low Back Pain

Evidence strongly suggests that only intensive treatment, involving both physical and psychological rehabilitation programs, can reduce pain and improve function in patients with chronic low back pain. Even with the best treatments, many patients with chronic back pain fail to have complete pain relief. They often must develop methods for coping with persistent pain.

Early treatments for severe or chronic low back pain are similar to those of acute uncomplicated low back pain.

Pain relievers, particularly non-steroidal anti-inflammatory drugs (NSAIDs), may help relieve symptoms, although they can have severe effects on the gastrointestinal tract over time. Some doctors have recommended long-term opioids for patients with severe chronic pain, but studies suggest they do not improve activity levels and can have significant side effects.

Corticosteroid injections and tricyclic antidepressants may be helpful for some patients.

Specific and regular exercise under the guidance of a trained professional is important for reducing pain and improving function, although patients often find it difficult to maintain therapy.

A new type of physical therapy, called Souchard's global postural re-education, helps relieve back pain symptoms due to degenerative disk disease, according to research presented at the 2005 American Academy of Neurology Annual Meeting. The method involves stretching weakened muscles around the spine and stomach. Researchers studied 102 people who had at least 7 months of severe back pain due to disk disease and who had received different types of treatment for more than 6 months. They attended the new physical therapy sessions two times the first week, then once a week for an average of 5 months. Ninety-two percent had significant pain relief and returned to their normal daily activities. The majority of those who had pain relief felt better after 3 weeks, and remained pain free for almost 2 years.

Alternative therapies may help. Transcutaneous electrical nerve stimulation (TENS) and massage may relieve pain. Mind-body techniques such as relaxation and meditation may be help reducing stress-related pain. Cognitive-behavioral therapy helps change behavior and attitudes toward pain.

Acupuncture may provide longer-lasting pain relief than physical therapy, according to a study in the British Medical Journal. For the study, 129 people were given either 6 acupuncture or physical therapy sessions. The study authors cautioned that the benefit of acupuncture greatly depended on the health care provider’s experience. Another study, published in the Archives of Internal Medicine, reported that acupuncture worked better than no treatment at all.

Yoga relieves low back pain better than conventional exercise or self-help books, according to a study published in the December 20, 2005, issue of Annals of Internal Medicine. For the study, 101 adults with low back pain who were randomly assigned to one of three groups. One group attended yoga classes and lessons; the second did aerobics, weight training, and stretching; and third group read a self-help book about back pain. After 12 weeks, those who took yoga could better perform daily activities requiring the back than those in the other two groups. After 26 weeks, those who took yoga had less pain and better back function, and used fewer pain relievers than the others.

Patients should always try all possible non-surgical treatments before opting for surgery. The most common reasons for surgery for low back pain are sciatica and spinal stenosis. Some experts believe that less than 1% of back pain patients need aggressive medical or surgical treatments.

Nevertheless, when it is appropriate, surgery can provide great relief. Many approaches and procedures are available or being investigated. However, there have been few well-conducted studies to determine if any type of back pain surgery works better than others, or if a single procedure is better than no surgery at all.

People who are obese and have low back pain may benefit from surgical weight loss surgery. A study in the journal Obesity Surgery found that bariatric (stomach stapling) surgery significantly improves the degree of disability in morbidly obese patients who have low back pain.

Before having any surgery, it is extremely important that the patient is sure that the surgeon has had significant experience with the procedure.

Nonsurgical Procedures. Patients with herniated disks should try nonsurgical treatments for at least 1 month before considering surgery. Nonsurgical procedures include spinal manipulation, massage therapy, and physical therapy. Patients should wait at least 2 - 3 weeks before using spinal manipulation.

Surgery. According to a 2001 review of studies, about 10% of patients have such bad back pain after 6 weeks that a diskectomy may be considered. Diskectomy is the standard procedure for herniated disks. For many of these patients, surgery may bring significant relief. In one study, 70% of patients with moderate-to-severe sciatica who had had surgery reported improvement. In most patients, the improvement was better than that achieved by 4 years of nonsurgical treatments. It is not clear if surgery maintains its advantage for longer periods of time.

Preventing Falls. Falling is a risk for patients with spinal stenosis. They should avoid alcohol and sedatives. Leg strengthening exercises such as walking and cycling may be helpful.

Nonsurgical Treatments. The use of common pain relievers such as NSAIDs, physical therapy, and spinal injections may be helpful for some patients.

Surgery. If pain is persistent, patients may require surgery, most often a procedure called decompressive laminectomy. Some patients may require spinal fusion as well. Studies suggest that surgery reduces back pain in many patients with spinal stenosis, at least for a few years. However, by 4 years after surgery, 30% of patients have severe pain again, and 10% have another operation. It should be noted that surgery does not always improve outcome and, in some cases, can even make it worse. Surgery can be an extremely effective approach, however, for certain patients whose severe back pain does not respond to conservative measures.

The general approach for patients with piriformis syndrome is corticosteroid injections and physical therapy. Botox injections are showing promise.

In carefully selected patients who do not respond to physical therapy and injections, some studies report dramatic pain relief with a surgical procedure that releases the piriformis muscle.

Prognosis

Most people with acute low back pain are back at work within a month and fully recover within a few months. According to one study, about a third of patients with uncomplicated low back pain significantly improved after a week; two-thirds recovered by 7 weeks.

However, studies now suggest that up to 75% of patients suffer at least one recurrence of back pain over the course of a year. In another study, after 4 years, less than half were symptom-free. Some doctors are approaching the problem as one that is not necessarily curable and which needs a consistent on-going approach.

Specific conditions can determine the rate of improvement:

In the majority of patients with herniated disks, the condition improves (although the actual physical improvement may be slower than the reduction in pain). Researchers attempted to identify factors most likely to predict an elevated risk for recurrent pain and found that only depression was a significant factor in the majority of those who had not recovered.
Spinal stenosis stabilizes in about 70% of cases and worsens in 15%.

Studies have found that when people stay home because of back injury, only 65% are back at work within a week. Nearly 14% are still absent at one month. If someone is on disability for more than 6 months, the chance of them returning to work is only 50%.

Low back pain accounts for significant losses in work days and dollars. In 1990, it cost the U.S. $23 billion in direct medical costs and possibly as much as $85 billion in total costs (such as lost productivity). Chronic back pain has become one of the most expensive causes of disability among workers under the age of 45. One study found that, although severe back pain comprised only 10% of workers compensation cases, it accounted for 86% of compensation costs.

Complications

Certain warning signs should alert a patient to see a doctor immediately for low back pain. Any very severe back pain warrants attention, particularly if any of the following conditions are present:

Being over 50
Recent injury
Severe pain
Pain awakens the person at night
Pain accompanied by fever (possible infection)
Pain increased by lying down
Pain unrelated to movement
Pain lasts for a month, and is accompanied by unexplained fever or weight loss
History or chronic use of corticosteroids
Intravenous drug use
History of urinary tract infection
In children, any severe neck or back pain or pain that persists for more than 3 days

Cauda equina syndrome is the impingement of the cauda equina (the four strands of nerves leading through the lowest part of the spine). It is an emergency condition that can cause severe complications of the bowel or bladder. Cauda equina syndrome is usually caused by massive extrusion of the disk material. It can cause permanent incontinence if not promptly treated with surgery. Symptoms of the cauda equina syndrome include:

Dull back pain
Weakness or numbness in the buttocks, in the area between the legs, or in the inner thigh, backs of legs, or feet. May cause difficulty in standing or stumbling.
An inability to control urination and defecation
Pain accompanied by fever (can indicate an infection)

Prevention

Exercise, diet, stress, and weight all have a significant influence on back pain. Changing certain lifestyle factors can help reduce and, possibly, prevent backaches.

Smokers are at higher risk for back problems, perhaps because smoking decreases blood circulation. The link may also be due to an unhealthy lifestyle in general. A British study found that young adults who were long-term smokers were nearly twice as likely to develop low back pain as nonsmokers.

Sedentary Lifestyle. People who do not exercise regularly face an increased risk for low back pain, especially when they perform sudden, stressful activities such as shoveling, digging, or moving heavy items. Although no definitive studies have been done to prove the relationship between lack of exercise and low back pain, some doctors believe that an inactive lifestyle may be to blame in some cases. Lack of exercise leads to the following conditions that may threaten the back:

Stiff muscles can make it hard to move, rotate, and bend the back.
Weak stomach muscles can increase the strain on the back and cause an abnormal tilt of the pelvis.
Weak back muscles may increase the risk for disk compression.
Obesity puts more weight on the spine and increase pressure on the vertebrae and disks. However, studies report only a weak association between obesity and low back pain.

Improper or Intense Exercise. Improper or excessive exercise may also increase one's chances for back pain.

Some research suggests that over time, high-impact exercise may increase the risk for degenerative disk disease. A survey of people who played tennis, however, found no increased risk for low back pain or sciatica.
Between 30 - 70% of cyclists experience low back pain. One 1999 study reported that 70% of cyclists reported improvement simply by adjusting the angle of the bicycle seat.
Improper exercise instruction and inattention to body movements can lead to back trouble. For example, a single jerky golf swing or incorrect use of exercise equipment (especially free weights, nautilus, and rowing machines) can cause serious back injuries.

The way a person moves, stands, or sleeps plays a major role in back pain.

Maintaining good posture is very important. This means keeping the ears, shoulders, and hips in a straight line with the head up and stomach pulled in. It is best not to stand for long periods of time. If it is necessary, walk as much as possible and wear shoes without heels, preferably with cushioned soles. Use a low foot stool and alternate resting each foot on top of it.
Sitting puts the most pressure on the back. Chairs should either have straight backs or low-back support. If possible, chairs should swivel to avoid twisting at the waist, have arm rests, and adjustable backs. While sitting, the knees should be a little higher than the hip, so a low stool or hassock is useful to put the feet on. A small pillow or rolled towel behind the lower back helps relieve pressure while either sitting or driving.
Riding in and driving a car for long periods of time increases stress. Move the car seat as far forward as possible to avoid bending forward. The back of the seat should not be reclined more than 30 degrees. If possible, the seat bottom should be tilted slightly upward in front. A traveler should stop and walk around about every hour. Avoid lifting or carrying objects immediately after the ride.

Anyone who engages in heavy lifting should take precautions when lifting and bending.

If an object is too heavy or awkward, get help.
Spread your feet apart to give a wide base of support.
Stand as close as possible to the object being lifted.
Bend at the knees, not at the waist. As you move up and down, tighten stomach muscles and tuck buttocks in so that the pelvis is rolled under and the spine remains in a natural "S' curve. (Even when not lifting an object, always try to use this posture when stooping down.)
Hold objects close to the body to reduce the load on the back.
Lift using the leg muscles, not those in the back.
Stand up without bending forward from the waist.
Never twist from the waist while bending or lifting any heavy object. If you need to move an object to one side, point your toes in that direction and pivot toward it.
If an object can be moved without lifting, pull it, don't push.

There are four natural curves in the spinal column: the cervical, thoracic, lumbar, and sacral curvature. The curves, along with the intervertebral disks, help to absorb and distribute stresses that occur from everyday activities such as walking or from more intense activities such as running and jumping.

Resources

www.niams.nih.gov -- National Institute of Arthritis and Musculoskeletal and Skin Diseases
www.aaos.org -- American Academy of Orthopaedic Surgeons
www.arthritis.org -- Arthritis Foundation
www.spine.org -- North American Spine Society
www.apta.org -- American Physical Therapy Association
www.ampainsoc.org -- American Pain Society
www.theacpa.org -- American Chronic Pain Association
www.iasp-pain.org -- International Association for the Study of Pain

References

Apkarian AV, Sosa Y, Sonty S, Levy RM, Harden RN, Parrish TB, et al. Chronic back pain is associated with decreased prefrontal and thalamic gray matter density. J Neurosci. 2004;24(46):10410-10415.

Fairbank J, Frost H, Wilson-MacDonald J, Yu LM, Barker K, Collins R; Spine Stabilisation Trial Group. Randomised controlled trial to compare surgical stabilisation of the lumbar spine with an intensive rehabilitation programme for patients with chronic low back pain: the MRC spine stabilisation trial. BMJ. 2005;330(7502):1233.

Filler AG, Haynes J, Jordan SE, Prager J, Villablanca JP, Farahani K, et al. Sciatica of nondisc origin and piriformis syndrome: diagnosis by magnetic resonance neurography and interventional magnetic resonance imaging with outcome study of resulting treatment. J Neurosurg Spine. 2005;2(2):99-115.

Freeman BJ, Fraser RD, Cain CM, Hall DJ, Chapple DC. A randomized, double-blind, controlled trial: intradiscal electrothermal therapy versus placebo for the treatment of chronic discogenic low back pain. Spine. 2005 Nov 1;30(21):2369-77; discussion 2378.

Friedrich M, Gittler G, Arendasy M, Friedrich KM. Long-term effect of a combined exercise and motivational program on the level of disability of patients with chronic low back pain. Spine. 2005;30(9):995-1000.

Frost H, Stewart-Brown S. Acupressure for low back pain. BMJ. 2006 Mar 25;332(7543):680-1.

Hayden JA, van Tulder MW, Malmivaara AV, Koes BW. Meta-analysis: exercise therapy for nonspecific low back pain. Ann Intern Med. 2005;142(9):765-775.

Hayden JA, van Tulder MW, Tomlinson G. Systematic review: strategies for using exercise therapy to improve outcomes in chronic low back pain. Ann Intern Med. 2005;142(9):776-785.

Mercado AC, Carroll LJ, Cassidy JD, Cote P. Passive coping is a risk factor for disabling neck or low back pain. Pain. 2005;117(1-2):51-57.

Melissas J, Kontakis G, Volakakis E, Tsepetis T, Alegakis A, Hadjipavlou A. The effect of surgical weight reduction on functional status in morbidly obese patients with low back pain. Obes Surg. 2005 Mar;15(3):378-81.

Pneumaticos SG, Chatziioannou SN, Hipp JA, Moore WH, Esses SI. Low back pain: prediction of short-term outcome of facet joint injection with bone scintigraphy. Radiology. 2006 Feb;238(2):693-8.

Ratcliffe J, Thomas KJ, MacPherson H, Brazier J. A randomised controlled trial of acupuncture care for persistent low back pain: cost effectiveness analysis. BMJ. 2006 Sep 23;333(7569):626.

Richardson SM, Curran JM, Chen R, et al. The differentiation of bone marrow mesenchymal stem cells into chondrocyte-like cells on poly-L-lactic acid (PLLA) scaffolds. Biomaterials. 2006 Aug;27(22):4069-78.

Sherman KJ, Cherkin DC, Erro J, Miglioretti DL, Deyo RA. Comparing Yoga, Exercise, and a Self-Care Book for Chronic Low Back Pain: A Randomized, Controlled Trial. Ann Intern Med. 2005; 143: 849 - 856.

Tao XG, Bernacki EJ. A randomized clinical trial of continuous low-level heat therapy for acute muscular low back pain in the workplace. J Occup Environ Med. 2005 Dec;47(12):1298-306.

Trout AT, Kallmes DF, Gray LA, Goodnature BA, Everson SL, Comstock BA, Jarvik JG. Evaluation of vertebroplasty with a validated outcome measure: the Roland-Morris Disability Questionnaire. Am J Neuroradiol. 2005 Nov-Dec;26(10):2652-7.

Review Date:
3/19/2007
Reviewed By:
Harvey Simon, MD, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital.

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adam.com

Menstrual disorders

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

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

Epilepsy

FitSugar — Wed, 08 Oct 2008 17:35:12 -0700

In This Report

Highlights
Introduction
Causes
Outlook and Effects
Diagnosis
Treatment
Treatment After The First S...
Medications
Surgery
Lifestyle Changes
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Drug Approval

In 2007, the Food and Drug Administration (FDA) approved levetiracetam (Keppra) for treatment of primary generalized tonic-clonic seizures in adults, and children ages 6 years and older, who have idiopathic generalized epilepsy. Levetiracetam was previously approved for partial-onset seizures and myoclonic seizures.

Carbamazepine and Genetic Testing

In 2007, the FDA recommended that patients of Asian ancestry get a genetic test prior to taking carbamazepine (Tegetrol, Equetro, Carbatrol). Rare, but serious, side effects of carbamazepine include life-threatening skin reactions such as Stevens-Johnson syndrome. The risk for these skin reactions is significantly higher for patients of Asian ancestry. A simple blood test can check for the presence of a genetic mutation that increases this risk. Patients who test positive for this gene should not take carbamazepine unless the benefits clearly outweigh the risks.

Epilepsy and Suicide Risk

People with epilepsy have a high risk for suicide, especially within 6 months of diagnosis, suggests a 2007 study in Lancet Neurology. The researchers found that suicide risk was especially high for people who have both epilepsy and another psychiatric condition (such as depression, anxiety, schizophrenia, or alcoholism). The researchers recommend that doctors carefully monitor newly diagnosed patients.

Ketogenic Diet

The ketogenic diet, which is characterized by high fat and low carbohydrate intake, is resurging in popularity for the treatment of children with difficult-to-control seizures, according to a 2007 review in Pediatrics. The ketogenic diet helps stop or reduce seizures in about a third of children. The diet is complex. Parents should seek supervision and guidance from a doctor or trained health professional.

Introduction

Epilepsy is characterized by unprovoked, recurring seizures that disrupt the nervous system and can cause mental and physical dysfunction. In the U.S., about 2.5 million people are affected by epilepsy and seizures. About 10% of the American population will experience at least one seizure during their lifetime.

The structures of the brain include: the brainstem, consisting of the spinal cord, the medulla oblongata, the pons and the midbrain; the cerebellum; the cerebrum (one half, or hemisphere shown); and the diencephalon.

Epilepsy affects all age groups. Males have a slightly higher risk than females. The incidence is highest in children, with another, but lesser, peak occurring after age 60. According to one estimate, 14% of epilepsy patients are under 15 years old, and about 25% are over age 64.

Every year, 25,000 - 40,000 American children have a first seizure that is unrelated to a fever. Epilepsy is decreasing in childhood but increasing in the elderly, probably because of mild strokes and cardiac arrest.

Epilepsy is not a single disorder but rather a wide spectrum of problems. What all types of epilepsy share are recurrent, unprovoked seizures caused by an uncontrolled electrical discharge from nerve cells in the cerebral cortex. This part of the brain controls higher mental functions, general movement, and the functions of the internal organs in the abdominal cavity, perception, and behavioral reactions.

Seizures are a symptom of epilepsy. Epilepsy types are generally put into two categories, which are based on the specific biologic mechanisms involved in the seizure and the anatomical location of the seizure. The two types are:

Partial (also called focal or localized) seizures. These seizures are more common than generalized seizures and occur in one or more specific locations in the brain. In some cases, partial seizures can spread to wide regions of the brain. They are likely to develop from specific injuries, but in most cases the exact origins are unknown.
Generalized seizures. These seizures typically occur in both sides of the brain. Many forms of these seizures are genetically based. There is usually normal neurologic function.

Experts are finding, however, that these categories do not actually reflect what is now known about the brain's anatomy. For example, the words "partial" and "generalized" suggest that seizures either involve only part of the brain or are widespread. However, a number of events in the brain occur with either type, muddying these distinctions. Researchers are now in the process of making clearer definitions and terms that reflect what actually is happening in the brain.

New classification systems better define specific epilepsies. Some professional groups now suggest that epilepsies be classified in the following five ways:

Type of seizure (partial or generalized)
Description of the seizure onset and evolution
Specific syndromes that are associated with one or more seizure types (however, not all seizures will be part of a syndrome)
Specific causes of the seizures, if known
Degree of impairment

These seizures are subcategorized as "simple" or "complex partial."

Simple Partial Seizures. A person with a simple partial seizure (sometimes known as Jacksonian epilepsy) does not lose consciousness, but may experience confusion, jerking movements, tingling, or odd mental and emotional events. Such events may include deja vu, mild hallucinations, or extreme responses to smell and taste. After the seizure, the patient usually has temporary weakness in certain muscles.
Complex Partial Seizures. Slightly over half of seizures in adults are complex partial type. About 80% of these seizures originate in the temporal lobe, the part of the brain located close to the ear. Disturbances there can result in loss of judgment, involuntary or uncontrolled behavior, or even loss of consciousness. They may lose consciousness briefly and appear to others as motionless with a vacant stare. Emotions can be exaggerated; some sufferers even appear to be drunk. After a few seconds, a patient may begin to perform repetitive movements, such as chewing or smacking of lips. Episodes usually last no more than 2 minutes. They may occur infrequently, or as often as every day. A throbbing headache may follow a complex partial seizure.

In some cases, simple or complex partial seizures evolve into what are known as secondarily generalized seizures. The progress may be so rapid that the partial stage is not even noticed.

While the term "partial" implies the seizures affect only small or specific brain locations, in reality, they almost always involve diffuse and even widespread areas. In the future, the term "focal seizures" will most likely replace the term "partial seizures," and its subcategories. Until new classifications are more widely in use, this report will continue to use the term "partial seizures" and its subcategories.

Generalized seizures are caused by nerve cell disturbances that occur in more widespread areas of the brain than do partial seizures. Therefore, they have a more serious effect on the patient. They are further subcategorized as tonic-clonic (or grand mal) or absence (petit mal) seizures.

Tonic-Clonic (Grand Mal) Seizures. The first stage of a grand mal seizure is called the tonic phase, in which the muscles suddenly contract, causing the patient to fall and lie stiffly for about 10 - 30 seconds. Some people experience a premonition or aura before a grand mal seizure. Most, however, lose consciousness without warning. If the throat or larynx is affected, there may be a high-pitched musical sound (stridor) when the patient inhales. Spasms occur for about 30 seconds to 1 minute. Then the seizure enters the second phase, called the clonic phase. The muscles begin to alternate between relaxation and rigidity. After this phase, the patient may lose bowel or urinary control. The seizure usually lasts a total of 2 - 3 minutes, after which the patient remains unconscious for a while and then awakens to confusion and extreme fatigue. A severe throbbing headache similar to migraine may also follow the tonic-clonic phases.
Absence (Petit Mal) Seizures. Absence or petit mal seizures are brief losses of consciousness that occur for 3 - 30 seconds. Physical movement and loss of attention may stop for only a moment. Such seizures may pass unnoticed by others. Small children may simply appear to be staring or walking distractedly. Petit mal may be confused with simple or complex partial seizures, or even with attention deficit disorder. [See In-Depth Report #30: Attention deficit hyperactivity disorder.] In petit mal, however, a person may experience attacks as often as 50 - 100 times a day. About 25% of patients with petit mal develop grand mal seizures. An electroencephalogram (EEG) test that shows a specific brain wave pattern can usually identify these patients.

Click the icon to see a depiction of a tonic-clonic seizure.

Atonic (Akinetic) Seizures. A person who has an atonic (or akinetic) seizure loses muscle tone. Sometimes it may affect only one part of the body so that, for instance, the jaw slackens and the head drops. At other times, the whole body may lose muscle tone, and the person can suddenly fall. A brief atonic episode is known as a drop attack.

Simply Tonic or Clonic Seizures. Seizures can also be simply tonic or clonic. In tonic seizures, the muscles contract and consciousness is altered for about 10 seconds, but the seizures do not progress to the clonic or jerking phase. Clonic seizures, which are very rare, occur primarily in young children, who experience spasms of the muscles but not tonic rigidity.

Myoclonic. Myoclonic seizures are a series of brief jerky contractions of specific muscle groups, such as the face or trunk.

Epilepsy is also grouped according to a set of common characteristics, including:

Patient age
Type of seizure or seizures
Whether a cause is known or not (idiopathic)

A few syndromes and inherited epilepsies are listed as follows. They do not represent all epilepsies.

West Syndrome (Infantile Spasms). West syndrome, also called infantile spasms, is a disorder that involves spasms and developmental delay in children within the first year, usually in infants ages 4 - 8 months.

Benign Familial Neonatal Convulsions. Benign familial neonatal convulsions (BFNC) are a rare, inherited form of generalized seizures that occur in infancy. BFNC appears to be caused by genetic defects that affect ion channels in nerve cells that carry potassium.

Juvenile Myoclonic Epilepsy (Impulsive Petit Mal). Juvenile myoclonic epilepsy, also called impulsive petit mal epilepsy, is characterized by generalized seizures, usually tonic-clonic marked by jerky movements (called myoclonic jerks), and sometimes absence seizures. This accounts for 7% of epilepsies, and usually occurs in individuals ages 8 - 20.

Adult Myoclonic Epilepsy. Some research suggests that adult myoclonic epilepsy may be a previously un-described and distinct syndrome. It involves the development of generalized epilepsy of unknown causes in middle-aged adults.

Lennox-Gastaut Syndrome. Lennox-Gastaut syndrome is a severe form of epilepsy in young children that causes multiple seizures and some developmental retardation. It usually involves absence, tonic, and partial seizures.

Myoclonic-Astatic Epilepsy. Myoclonic-astatic epilepsy (MAE) is a combination of myoclonic seizures and astasia (a decrease or loss of muscular coordination), often resulting in the inability to sit or stand without aid.

Progressive Myoclonic Epilepsy. Progressive myoclonic epilepsy is an inherited disorder occurring in children ages 6 - 15. It usually involves tonic-clonic seizures and marked sensitivity to light flashes. Although the disease was previously considered to be progressive throughout life, current therapies have significantly improved its outlook.

Autosomal Dominant Nocturnal Frontal Lobe Epilepsy. Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is a rare, inherited syndrome that usually occurs during childhood, typically around age 11. However, onset varies widely within families. Seizures can be dystonic (twisting contractions) or tonic (muscle contractions), or involve thrashing. They are brief, frequent, and occur in clusters during the night. The seizures often subside with age. ADNFLE appears to be caused by an alteration in the brain receptor neuronal nicotinic acetylcholine,

Landau-Kleffner Syndrome. Landau-Kleffner syndrome is an epileptic condition that results in the inability to communicate either with speech or by writing (aphasia).

Contactin-Associated Protein-Like 2 (CASPR2) Epilepsy. CASPR2 is associated with a childhood epilepsy and autism disorder found in closely related relatives in Amish communities.

Status epilepticus (SE) is a serious, potentially life-threatening, condition that can lead to chronic epilepsy. It occurs in 100,000 - 150,000 people in the U.S. each year, over half of whom are children. Permanent brain damage or death can result if the seizure is not treated effectively.

The condition is defined as recurrent convulsions that last for more than 20 minutes and are interrupted by only brief periods of partial relief. Although any type of seizure can be sustained or recurrent, the most serious form of status epilepticus is the generalized convulsive or tonic-clonic type. In more than a third of cases, status epilepticus occurs with the first seizure. The trigger is often unknown, but can include the following:

Failure to take anti-epileptic medications (accounts for about a third of status epilepticus events)
Abrupt withdrawal of certain anti-epileptic drugs, particularly barbiturates and benzodiazepines
High fever
Poisoning
Electrolyte imbalances (imbalance in calcium, sodium, and potassium)
Cardiac arrest
Stroke. In one study, about 9% of stroke patients with seizures had status epilepticus, which resulted in higher disability after the stroke, particularly if these severe seizures occurred within a week of the stroke
Low blood sugar in people with diabetes
Central nervous system infection
Brain tumor
Alcohol withdrawal

Causes

The cause of a seizure is determined in about 28% of partial epilepsy patients. In the rest, however, epilepsy is deemed idiopathic, which means that the cause is unknown. The age of seizure onset can sometimes offer a clue. Idiopathic epilepsy is rare in children and young adults.

Epileptic seizures are triggered by abnormalities in the brain that cause a group of nerve cells in the cerebral cortex to become activated simultaneously, emitting sudden and excessive bursts of electrical energy. A seizure's effect depends on the location in the brain where this electrical hyperactivity occurs. Effects range from brief moments of confusion to minor spasms to loss of consciousness.

Click the icon to see an animation about the nervous system.

Ion Channels. Sodium, potassium, and calcium act as ions in the brain. They produce electric charges that must fire regularly in order for a steady current to pass from one nerve cell in the brain to another. If the ion channels that carry them are genetically damaged, a chemical imbalance occurs. This can cause nerve signals to misfire, leading to seizures. Abnormalities in the ion channels are believed to be responsible for absence and many other generalized seizures.

Neurotransmitters. Abnormalities may occur in neurotransmitters, the chemicals that act as messengers between nerve cells. Three neurotransmitters are of particular interest:

Gamma aminobutyric acid (GABA), which helps prevent nerve cells from over-firing.
Serotonin's role in epilepsy is also being studied. Serotonin is a brain chemical that is important for well-being and associated behaviors (eating, relaxation, sleep). Imbalances in serotonin are also associated with depression.
Acetylcholine is a neurotransmitter that is important for learning and memory.

Dozens of genetic syndromes representing a variety of seizure patterns may account for the different forms epilepsy.

A genetic cause has been identified for at least some cases of juvenile myoclonic epilepsy, which represents 10% of all epilepsy cases. (Such research and other studies have pointed to the GABA signaling system as an important player in many cases of epilepsy.)

Febrile seizures are caused by high fever. They usually occur in children ages 3 months to 5 years. Between 10 - 15% of children with epilepsy have a history of febrile seizures before they develop epilepsy. However, febrile seizures are quite common and occur in about 3% of all children under 5 years old. Nearly all are brief and have no long-lasting effect.

In young children, high fever from a vaccination can, in rare instances, trigger seizures. These seizures are almost always temporary and have no serious consequences.

Some controversy arose a few years ago over the possibility that the DTP (diphtheria-tetanus-pertussis) vaccine might trigger epilepsy or other neurologic diseases. Some experts suggest that children who have neurologic events following their DTP shot already have a preexisting impairment such as epilepsy, which is revealed, but not caused by, the vaccine. Children with existing epilepsy may be at risk for seizures 2 or 3 days after the vaccination. Infants with suspected neurologic problems may have their vaccinations delayed until their neurologic situation is clarified, but not beyond their first birthday. Also, a newer version of the DTP vaccine does not contain a live virus and so reduces the risk of any seizure.

Brain Tumors. Both cancerous and noncancerous brain tumors can cause seizures in all patients.

Hydrocephalus and Shunts. Hydrocephalus occurs when cerebrospinal fluid (CSF) accumulates in the brain, leading to excessive swelling of the brain ventricles. The resulting pressure can damage the brain's tissue. Hydrocephalus itself is not commonly known to cause seizures, but its treatment, which involves insertion of a shunt, may cause them. The shunt is a device that drains the excess fluid from the brain. Up to half of children who receive shunts may experience epileptic seizures, particularly if the shunt is placed before 2 years of age. More research on its relationship to epileptic seizures is needed.

Focal Cortical Dysplasia. This is an abnormality in fetal development in which the normal migration of nerve cells is altered. It can cause very severe epilepsy that is difficult to treat.

Hippocampal Sclerosis. Hardened tissue (sclerosis) in the brain's hippocampus is the most commonly identified abnormality in patients with partial epilepsy. Such abnormal brain tissue leads to structural reorganization, and both the loss and regeneration of nerve cells.

Cavernous Angiomas. Cavernous angiomas are blood vessels that grow abnormally and, like a tumor, can put pressure on nerve tissue.

Other Causes of Seizures in Children. Seizures in infants and children may be due to birth defects, difficulties during delivery, or poisoning.

Alcohol Abuse. Alcohol abuse is one of the most common causes of adolescent- and adult-onset seizures. Seizures, nearly always generalized tonic-clonic, occur in about 10% of adults during withdrawal. Multiple seizures happen in about 60% of these patients. The first seizure occurs 7 hours to 2 days after the last drink, and the time between the first and last seizure is usually 6 hours or less. [For more information, see In-Depth Report #56: Alcoholism.]

Sudden withdrawal from certain antianxiety or antidepressant drugs such as benzodiazepines, barbiturates, and tricyclic antidepressants can also contribute to seizures.

Head Injuries in Adults. Head injuries to adults can cause seizures, with the risk highest in severe head trauma. A first seizure related to the injury can occur years later, but only very rarely. People with mild head injuries, which involve loss of consciousness for fewer than 30 minutes, have only a slight risk that lasts up to 5 years after the injury.

Head Injuries in Infants and Children. Infants are at high risk for head trauma, and the severity of injury may be difficult to determine. The risk of even one seizure is generally only a concern after severe head trauma. Most children who have had a minor or not very serious head injury do not need to have medications to prevent seizures, especially when an evaluation in the emergency department was unnecessary.

Stroke. Seizure is a symptom of a major stroke. Even injury to the brain from small strokes may cause seizures. Patients who have had a severe stroke are 5 times more likely to develop epilepsy than patients who have had a mild stroke.

Seizures in adults can also be caused by:

Low blood sugar (hypoglycemia), a complication of diabetes in both children and adults.
Medications such as theophylline, meperidine, tricyclic antidepressants, phenothiazines, lidocaine, quinolones, penicillins, selective serotonin re-uptake inhibitors, isoniazid, antihistamines, cyclosporine, interferons, cocaine, lithium, amphetamines, and alcohol (withdrawal).
Occupational exposure to environmental triggers. High exposure to certain chemicals has been linked with seizures.
Alzheimer's or other degenerative brain diseases in the elderly.
Infections of the brain and central nervous system such encephalitis and meningitis.

The organs of the central nervous system (brain and spinal cord) are covered by three connective tissue layers called the meninges. They consist of the pia mater (closest to the CNS structures), the arachnoid, and the dura mater (farthest from the CNS). The meninges help support blood vessels and contain cerebrospinal fluid. The structures are involved in meningitis, an inflammation of the meninges, which, if severe, may become encephalitis, an inflammation of the brain.

Between 20 - 45% of cases of untreatable seizures have a psychologic rather than physical origin. In this form of epilepsy, known as pseudoepilepsy or psychogenic epilepsy, the patient has no conscious intent of forcing a seizure and does not show unusual emotional behavior or signs of hysteria. It is very difficult to treat and can be very disabling. Pseudoepilepsy can usually be distinguished from true epilepsy using an electroencephalogram (EEG), which measures brain waves. The cause of pseudoepilepsy is unknown.

Outlook and Effects

Most patients can control their seizures with a single drug and stop drug treatment completely after 2 years without seizures. In fact, patients who respond well to an anti-epileptic drug (AED), have a better chance for remaining seizure-free in the future. In general, patients who do not have good control with medications are more likely to have difficulty with epilepsy treatment.

Injuries from Falls. Because many people with seizures fall, injuries are common. Although such injuries are usually minor, people with epilepsy have a higher incidence of fractures than those without the disorder. Epilepsy patients who take the drug phenytoin have an even higher risk, since the drug can cause osteoporosis.

Household Accidents. According to a 2006 study, the kitchen and bathroom are two of the most dangerous places for children with epilepsy. Parents should take precautions to prevent burning accidents from stoves and other heat sources. Children with epilepsy should never be left alone when bathing.

Driving and the Risk for Accidents. Being unable to drive is an extremely distressing and severe component of epilepsy. Drivers with well-controlled epilepsy are not at a high or unacceptable risk for automobile accidents. Uncontrolled epilepsy, however, poses a high risk. Needless to say, seizures can be very dangerous if they occur while a person is driving. Studies have reported that more than a fourth of drivers with uncontrolled epilepsy had a seizure-related accident at some time. Many of these accidents resulted in injuries to the patient or others.

Certain factors can help predict who may safely drive:

A long duration between seizures. In one study, being seizure-free for 6 months reduced the risk for accidents by 85%, and being seizure-free for 1 year lowered the risk by 93%. State laws restricting driving in people with seizures vary from requiring seizure-free periods of 3 months (which is too short for protection) to 18 months.
Having few seizure-related accidents.
Having a reliable pre-seizure warning sign, such as an aura.

Accidents while Swimming. Swimming poses another danger for people with epilepsy, particularly those with tonic seizures, which can cause the diaphragm to expel air quite suddenly. People with epilepsy who swim should avoid deep and cloudy water (a clear swimming pool is best), and always swim with a knowledgeable, competent, and experienced companion or have a supervisor on site.

Epileptic patients who are cured have a normal lifespan. Their long-term survival rates are lower than average if medications or surgery fail to stop the seizures. The lower survival rate is partly due to a higher-than-average risk for death due to accidents and suicide. The specific cause of the seizure may also contribute to fatalities.

There is a very low risk for sudden death in patients with epilepsy. Although the causes of such events are not fully known, experts suspect heart arrhythmias in many cases.

Long-Term General Effects. In general, the long-term effects of seizures vary widely depending on the seizure's cause. The long-term outlook for children with idiopathic epilepsy (epilepsy of unknown causes) is very favorable. One study reported that 68 - 92% of these patients were seizure-free after 20 years. Another study reported that they had a survival rate no different from children without these seizures.

Children whose epilepsy is a result of a specific condition (for example, a head injury or neurologic disorder) have higher mortality rates than the normal population, but their lower survival rates are most often due to the underlying condition, not the epilepsy itself.

Effect on Memory and Learning. The studies on the effects of seizures on memory and learning vary widely and depend on many factors. In general, the earlier a child has seizures and the more extensive the area of the brain affected, the poorer the outcome. Children with seizures that are not well-controlled are at higher risk for intellectual decline.

Social and Behavioral Consequences. Learning and language problems, and emotional and behavioral disorders, occur in a significant number of children with several of the partial epilepsy syndromes. These children perform worse on behavioral tests than do other children. Whether these problems are caused by the seizure disorder and anti-seizure medications or are simply part of the seizure disorder remains unclear.

Effect on Mental Functioning in Adults. The effects of adult epilepsy on mental functioning are not clear. More research is needed in this area, as results have been contradictory.

Psychological Health. About 25 - 75% of adults with epilepsy show signs of depression. People with epilepsy have a high risk for suicide, particularly in the first 6 months following diagnosis. The risk for suicide is highest among people who have epilepsy and an accompanying psychiatric condition such as depression, anxiety disorder, schizophrenia, or chronic alcohol use.

Overall Health. Many patients with epilepsy describe their overall health as "fair" or "poor," compared to those who do not have epilepsy. People with epilepsy also report a higher frequency of pain, depression, anxiety, and sleep problems. In fact, their overall health state is comparable to people with other chronic diseases, including arthritis, heart problems, diabetes, and cancer. Treatments can cause considerable physical effects, such as osteoporosis and weight changes.

Effects on Sexual Function. There have been studies suggesting that up to two-thirds of patients with epilepsy experience sexual disturbances, including impotence in men. Causes of these problems may be emotional, medication induced, or a result of changes in hormone levels:

Epilepsy in childhood may cause disturbances in hormones regulating puberty.
Persistent seizures in adults may be associated with other hormonal and neurologic changes that contribute to sexual dysfunction.
Negative emotions due to epilepsy can reduce sexual drive.
Medications may be responsible for many of these cases, although newer drugs may reduce this problem.

Studies have been conflicting on the effects of fertility from epilepsy, but most suggest that fertility rates among women with epilepsy are lower than among women in the general population. A number of factors, including anti-epileptic drugs (AEDs) or social factors such as marriage at an older age, may contribute to this lower rate. Certain AEDs, particularly valproate, disrupt ovulation and menstruation by increasing male hormone levels and weight and causing polycystic ovaries.

Preparing to Become Pregnant. A woman should visit her doctor at least 3 months before becoming pregnant to talk about risks of medications and the possibility of making any changes.

A woman who has been seizure-free for 2 or more years may attempt to discontinue drugs under her doctor’s supervision.
If she has not been seizure-free, she should continue medications but try to reduce them to a single drug, if possible. (Again, under a doctor’s supervision.)
If a woman taking antiseizure medications has an unplanned pregnancy, there may be no point in switching medications right away, since the effects of the drugs last for 10 weeks. However, she should notify her doctor immediately.
Folic acid is recommended for all pregnant women, and women with epilepsy should talk with their doctor about taking a supplement of folic acid (5 mg) at least 3 months before conception as well as during the first trimester.

Effect of Pregnancy on Seizure Frequency. The frequency and intensity of seizures vary widely in women with epilepsy. About 25% of pregnant women with epilepsy face an increase in events, and the risk is highest in those who have more than one seizure per month prior to becoming pregnant. In most cases, however, there is no change at all. Some pregnant women even have a decrease in seizures. The risk is lower in women who experience less than one seizure in the 9 months prior to becoming pregnant.

The following conditions may contribute to an increase in seizures during pregnancy:

Nausea and vomiting (vitamin B6 and antihistamines may help with nausea)
Fluid retention
Higher estrogen levels
Psychological and emotional stress
Medication noncompliance from fear of side effects
Problems with sleeping
Changes in absorption of anticonvulsants

Anti-epileptic drug levels are monitored at least three times during the pregnancy, more often if seizures are occurring or levels are not normal. Dosage levels should be adjusted accordingly.

Effects of Epilepsy on the Pregnant Patient and the Fetus. Women who become pregnant have a risk for uncontrolled seizures and birth defects from antiseizure medications. In studies of women who were carefully monitored, however, 95% of pregnancies (which is close to normal) had favorable outcomes.

Isolated seizures do not appear to pose any adverse effects to the mother or the unborn child, but repeated seizures and status epilepticus can lead to great dangers. In one study, the effect of epilepsy on complications during pregnancy was the same as in non-epileptic women except for a higher rate of premature deliveries (8.2% in the women with epilepsy).

Drugs Used During Pregnancy. Some types of anti-epileptic drugs (AEDs) can increase the risks for birth defects, especially when taken during the first trimester of pregnancy. Expert guidelines advise that pregnant women use the most effective medication for their type of epilepsy at the lowest dose possible to control seizures. They should also have their doctors take blood tests during pregnancy to monitor their drug levels.

The fetus should be carefully monitored with ultrasonic evaluation and sometimes amniocentesis (visual tests and examination of the fluid in the womb for birth defects and other fetal problems).

In general, research indicates that 90% of women who take AEDs will give birth to healthy children. Still, doctors recommend that women of child-bearing age use a drug other than valproate if possible.

The risk for malformation is higher when more medications are used. For example, there is a 3% risk of birth defects with women who use one anticonvulsant. The risk increases to 20% when four drugs are used.

Birth Defects Associated with Medication. The most common birth defects related to anti-epileptic drugs are:

Cleft lip or palate (risks from lamotrigine, phenobarbital, phenytoin, valproate especially when taken during the first trimester).
Genital or urinary abnormalities (risk from most standard drugs).
Neural tube defects (NTD) in the skull or spinal column (risk of 2% with valproate and 1% with carbamazepine). These complications are most often due to lower folic acid levels caused by both pregnancy itself and antiseizure drugs. Folic acid supplements can help prevent this problem.
Mental impairment (known risk with phenytoin and valproate; inconclusive in carbamazepine and phenobarbital).
Heart defects (risk from phenobarbital, phenytoin, valproate).

Many antiseizure drugs also cause a deficiency in vitamin K clotting factors that increases the risk for hemorrhage in the newborn. Treatment with vitamin K during the last month of pregnancy and a single dose given to the newborn is recommended.

Labor and Delivery. Seizures occur during labor and after delivery in a small percentage of women with epilepsy. The following labor complications are more common among pregnant women with epilepsy: Vaginal bleeding, anemia, and preeclampsia (extremely high blood pressure in the third trimester). If seizures occur during labor, they are generally treated intravenously with benzodiazepines or phenytoin. If tonic-clonic seizures, absence seizures, or status epilepticus occur, a cesarean section may be appropriate.

Postnatal Care

Monitoring the Infant. The infant should be thoroughly examined for any birth defects. Also, if the mother was given phenobarbital or primidone while pregnant, the infant should be monitored for up to 8 months to see if withdrawal symptoms develop. Drug dosages will also need to be adjusted for the mother after delivery.

Breast-feeding. Women on most AEDs typically can nurse their babies, since usually only a small amount of the drug enters the breast milk. The lowest levels are with phenytoin and valproate. (Ethosuximide and possibly levetiracetam are exceptions and should be avoided when a woman is breast-feeding. Women taking phenobarbital are also usually advised not to nurse.) A mother should watch for signs of lethargy or extreme sleepiness in her infant, which could be caused by her medication.

Diagnosis

An epilepsy diagnosis is often made during an emergency visit for a seizure. If a person seeks medical help for a previous or suspected seizure, the doctor will ask about the patient's medical history, including seizure events.

Conditions that cause similar symptoms to epilepsy include:

Syncope. Syncope, a brief lapse of consciousness in which blood flow is reduced to the brain, can mimic epilepsy. It often misdiagnosed as epilepsy. Patients with syncope do not have the rhythmic contracting and then relaxing of the body's muscles.
Migraines. Migraine headaches, particularly migraine with auras, may sometimes be confused with epilepsy. With epileptic seizure, the preceding aura is often seen as multiple, brightly colored, circular spots, while migraine sufferers tend to see black, white, or colorless lined or zigzag flickering patterns. Typically the migraine pain expands gradually over minutes toward one side.
Panic Attacks. In some patients, partial seizures may resemble a panic disorder. Symptoms of panic disorder include palpitations, sweating, trembling, sensation of breathlessness, chest pain, feeling of choking, nausea, faintness, chills or flushes, fear of losing control, and fear of dying.
Narcolepsy. Narcolepsy, a sleep disorder that causes a sudden loss of muscle tone and excessive daytime sleepiness, can be confused with epilepsy.

Electroencephalogram (EEG). The most important diagnostic tool for epilepsy is an EEG, which measures brain waves. Ideally, it should be performed within 24 hours of a seizure. An EEG recording session may last for less than an hour, but in some cases the doctor will want a day-long recording. Long-term monitoring may be necessary in some cases when patients do not respond to medications. Portable EEG units are available in some places, which can be used to monitor patients throughout normal activities. EEGs are not foolproof. Repeated EEGs are often needed to confirm a diagnosis, particularly for certain partial seizures that often produce an initially normal EEG reading.

Video Electroencephalography (Video EEG). For this task, patients are admitted to a special part of the hospital where they are monitored both by EEG and are also watched by a video camera. Patients may need this for a variety of reasons including withdrawal or addition of medications in a patient with difficult-to treat-epilepsy, before epilepsy surgery for some patients, and also when psychogenic nonepileptic seizures are suspected.

Computerized Tomography (CT) Scans. Usually, the first brain imaging test ordered for most adults and children with first-time seizures is a CT scan. This imaging technique is sensitive enough for most purposes. In children, even if the scan is normal, the doctor will follow up to be sure other problems are not present.

A CT (computed tomography) scan is a much more sensitive imaging technique than x-ray, allowing high definition of both the bony structures and the soft tissues. Clear images of organs such as the brain, muscles, joint structures, veins and arteries, as well as anomalies like tumors and hemorrhages may be obtained with or without the injection of contrasting dye.

Magnetic Resonance Imaging (MRI). Experts strongly recommend MRIs for children with first seizures in certain cases, such as children under 1 year old and those with seizures that are associated with any unexplained significant mental or motor problems. These images may help to determine if the disorder can be treated with surgery, and may be used as a guide for surgeons.

Other Advanced Imaging Techniques. More advanced scanning techniques are emerging as important tools for epilepsy researchers. By detecting abnormalities, such as changes in brain activity, positron emission tomography (PET) may help locate damaged or scarred locations in the brain where partial seizures are triggered. These findings may help determine which patients with severe epilepsy are good candidates for surgery. Single-photon emission computer tomography (SPECT) may also be used to decide if the surgery should be performed and what part of the brain needs to be removed. Both of these imaging techniques are generally only needed when an MRI of the brain has not been helpful.

Treatment

You cannot stop a seizure, but you can help the patient prevent serious injury.

Remain calm, and do not panic, then take the following actions:

Wipe away any excess saliva to prevent obstruction of the airway. Do not put anything in the patient's mouth. It is an old wives' tale that people having seizures will swallow their tongues.
Turn the victim gently on the side. Do not try to hold the patient down to prevent shaking.
Rest the patient's head on something flat and soft to protect it from banging on the floor and to support the neck.
Move sharp objects out of the way to prevent injury.

Do not leave the seizure victim alone. Anyone nearby should call 911. Patients should be taken to an emergency room when:

A first-time seizure occurs
Any seizure lasts beyond 2 - 3 minutes
The patient has been injured
The patient is pregnant
The patient is diabetic
Parents, caregivers, or bystanders are at all uncertain

Not all patients with chronic epilepsy need to go to the hospital after a seizure. Hospitalization may not be necessary in many patients whose seizure is not severe or repetitive, and who have no risk factors for complications. All patients or caregivers, however, should contact their doctor after a seizure occurs.

Initial Management. The earlier a patient is treated, the better the results. Initial management of status epilepticus consists of:

Administer any seizure medications
Support systems to maintain or attain normal breathing, blood pressure, electrolyte balances, body temperature, and heart functions
Oxygen for patients who may need it
Attention by medical personnel trained to determine any treatable cause of status epilepticus, such as drug withdrawal, low blood sugar, infection, substance abuse (particularly cocaine), or eclampsia (elevated blood pressure induced by pregnancy)

Medications for Status Epilepticus. Doctors will try one or more of the following medications initially:

Benzodiazepine. An intravenously (IV), intramuscularly, or rectally administered benzodiazepine such as lorazepam (Ativan), diazepam (Valium), clonazepam, or midazolam (Versed) is usually used.
Phenytoin or Fosphenytoin. Many doctors use phenytoin or fosphenytoin if seizures are not controlled by a benzodiazepine.
Phenobarbital. Although effective, barbiturates, such as phenobarbital (Barbita, Luminal), are generally used only when other drugs have failed.

All of these medications carry a risk for hypotension, an abrupt and possibly dangerous drop in blood pressure, which may require treatment.

Treatment After The First Seizure

Children with febrile seizures rarely have any long-term effects and generally do not require drug treatment. In very rare cases, children experience severe fever-related seizures known as complex febrile convulsions. In such cases, there is a risk for brain injury that may lead to temporal lobe epilepsy, but this is very small. Such seizures last over 15 minutes, occur more than once within 24 hours, and may affect only one side of the body.

Treatment with anti-epileptic drugs (AEDs) is usually initiated or strongly considered for the following patients:

Children and adults who have had two or three seizures, unless there is either a long separation between seizures or the seizure is provoked by an injury or other specific causes. (In children, risk for recurrence after a single unprovoked seizure is rare. The risk even after a second seizure is low, even when the seizure is prolonged.)
Children and adults after a single seizure if tests reveal any brain injury, or if specific syndromes put a person at special risk for recurrence, for instance, in cases of myoclonic epilepsy.

There is some debate about whether to treat every adult patient with an AED after a single initial seizure. Some experts do not recommend treating adult patients after a single seizure if they have a normal neurologic examination, EEG, and imaging studies. A 2005 study of patients with single or infrequent seizures found that while early AED treatment reduced the risk of seizure for a few years, it had no effect on long-term outcomes. This study also suggested that delaying AED treatment does not increase the risk of developing lifelong epilepsy.

Some doctors believe, however, that any adult who has a first seizure should begin on-going AED treatment, since 30 - 70% of these patients are likely to experience a subsequent event. According to one study, when young adults were given a single drug (usually carbamazepine) after a first generalized seizure, only 22% had a subsequent seizure compared to about 70% of those who were not given treatment.

Most epileptic seizures can be controlled using a single-drug regimen. First-line AED drugs include phenytoin (Dilantin), carbamazepine (Tegretol, Carbatrol), and divalproex sodium (Depakote). Patients generally begin with low doses and build up until the seizures are controlled or a toxic reaction occurs. If a single drug fails to control seizures, other drugs are added on. The specific drugs and whether more than one should be used are determined by various factors, including the patient's age and the seizure's type, frequency, and cause.

Drugs fail to control epilepsy in about 30% of patients. For patients who have little or no benefit from their initial drug regimen the likelihood of good or complete control from different medications or multidrug regimens is not very high.

Reasons for Failure. An AED may fail to reduce seizures due to such factors as:

The wrong dose level.
Improper timing.
Introducing the medication too rapidly.
Not managing conditions that triggered the seizure.
Instability of the drugs. Many of the tablet forms disintegrate easily with moisture, so pills should be stored in a dry place, not in the bathroom, and kept away from heat.
Patients not taking medication as prescribed. Over 40% of patients experience toxic or bothersome effects from older AEDs, which often causes them to withdraw. Among the most distressing are sleepiness, problems in coordination, and weight gain.
Some evidence suggests that about a quarter of patients who do not respond to AEDs actually have nonepileptic seizures that in many cases are caused by psychiatric conditions (such as panic attack or personality disorders).

The doctor should first address these issues. If the patient still does not respond, the doctor will usually try a different drug. If this fails, one or even two additional drugs at a time may be used. When seizures do not respond to the first two or three drugs, the odds of a fourth or fifth working diminish greatly, despite a number of new medications on the market. In such cases, the patient should ask about surgical alternatives.

Healthy Behaviors. In young people, a positive attitude, continued support from family and health care providers, emotional well-being, and good treatment results can increase patient compliance. Unhealthful behaviors, such as smoking and alcohol use, can have a negative effect.

During the first few months of therapy, the doctor will probably order blood tests once or twice to monitor drug levels and, if necessary, adjust dosages. Monitoring is used to check for AED complications, and to be sure the patient is complying with the regimen. Many experts feel, however, that these blood tests are a less reliable indicator of problems than the patient's own self-observations of his or her responses to the drug. For instance, blood tests may suggest that the dosage levels are insufficient according to general standards, yet the individual patient may be seizure-free and leading a normal life. It is very important that women have AED levels monitored during pregnancy.

An estimated 60% of all patients treated effectively can stop taking AEDs within 5 - 10 years. Evidence suggests that medications in children should not be halted for at least 2 years after the last seizure, particularly if they have partial seizures and abnormal EEGs. It is not clear whether children who have been free of generalized seizures need to wait more than 2 years or if they can withdraw earlier.

Children who tend to relapse after withdrawal from treatment usually have the following conditions or situations:

A family history of epilepsy
Require multiple medications to control seizures
Abnormal EEG readings after treatment has started
Partial seizures

There is also no clear evidence on whether adults who are free of any seizure type can safely withdraw from their medications within 2 years of their last seizure of if they should wait.

In any case, attempts to halt drugs should be done during periods when seizures will cause the least harm. For instance, the best time to test the effects of drug withdrawal in teenagers might be about a year before they are eligible to drive.

Anti-epileptic drugs interact with many other drugs, and may cause special problems in older patients who use multiple medications for other health problems. Elderly patients should have liver and kidney function tests performed before starting antiseizure medication. Standard drugs are usually effective, while safe, newer ones (including gabapentin, lamotrigine, oxcarbazepine, and gamma-vinyl-GABA) may sometimes prove to be useful as a sole therapy. These newer drugs also increase patient compliance because they tend to have fewer side effects than the older ones.

Hormonal fluctuations affect epilepsy in about a third to a half of female patients. Estrogen appears to increase activity, and progesterone reduces it. The effect of pregnancy on women with epilepsy is complex. The following treatments may help or affect women with epilepsy:

Hormonal Drugs that Suppress Ovulation. When seizures in women are worsened by hormonal changes, such as during the menstrual cycle, suppressing ovulation may be recommended using drugs called gonadotropin-releasing hormone agonists.
Oral contraceptives. Antiseizure medications affect many oral contraceptives (OCs). Carbamazepine, phenytoin, phenobarbital, primidone, oxcarbazepine, and topiramate reduce the effects of OCs. Valproate does not, and may even increase hormonal levels. Gabapentin, lamotrigine, tiagabine, and vigabatrin may also prove to be safe with OCs, but more research is needed. Progestins may be the best contraceptive drugs for women with epilepsy at this time. Injected progestins may actually help prevent seizures in some cases.

More information on epilepsy and pregnancy can be found in this report under Outlook and Effects.

Medications

Many newer anti-epilepsy drugs (AEDs) are now available and are usually better tolerated than the older, standard AEDs. They often cause less sedation and require less monitoring. Although they are generally approved for use as add-ons to standard drugs that fail to control seizures, many doctors are now prescribing them as single drugs. Specific choices usually depend on the individual's particular condition and the specific side effects of the AED. None has emerged as being superior to either standard or newer drugs. All appear to offer some benefits, but, as with standard antiseizure drugs, they also have troublesome side effects.

Valproate (Depakene, valproic acid) and its delayed release form, divalproex sodium (Depakote), are anticonvulsants. Valproate is the most widely prescribed anti-epileptic drug worldwide.

Uses. Valproate is the first choice for patients with generalized seizures and is used to prevent nearly all other major seizures as well.

General Side Effects. These drugs have a number of side effects that vary depending on dosage and duration. Most side effects occur early in therapy and then subside. General side effects include:

Stomach and intestinal problems, which are experienced by nearly half of patients after starting the drugs and may still occur after several years of use. Divalproex sodium (Depakote) has a lower risk for these side effects than valproate (Depakene).
Increased appetite with significant weight gain often becomes a problem and can be a major reason for noncompliance, particularly in young people.
Hand tremors, irritability, and hyperactivity in children are fairly common.
Temporary hair thinning and hair loss have occurred. Taking zinc and selenium supplements may help reduce the effect.
Young girls may develop secondary male characteristics, and premenopausal women are at increased risk for menstrual irregularities and polycystic ovaries, due to elevated male hormones. The effects are reversible. (These side effects also appear in women using other anti-epileptic drugs, but the risk from valproate appears to be higher.)
Studies have reported symptoms of Parkinson's disease preceded by hearing loss in people who have taken it for more than a year, but they were reversible when the drug was withdrawn.
Valproate poses a higher risk for serious birth defects than many other AEDs. These birth defects include skull and limb deformities, and brain, heart, and lung problems. Experts recommend that women of child-bearing age use a different type of anti-epilepsy drug than valproate. If valproate is used, it should be prescribed at the lowest possible dose.
Cases of pancreatitis, a serious and even life-threatening inflammation in the pancreas, have been reported in children and adults taking valproate. (It is still very rare, however.)
Valproate and divalproex sodium are not usually recommended for young children because of an unusual, but potentially fatal, toxic effect on the liver. This very rare effect is most likely to affect children under 2 years of age who have birth defects and are taking more than one antiseizure drug. Some doctors recommend monitoring blood levels for liver function once prior to administering valproate or divalproex sodium, monthly during the first 6 months, and then periodically after that.
Children with epilepsy who take valproic acid may eventually develop some problems in the kidney, although they are generally not significant.

Symptoms of Toxic Side Effects in Liver or Pancreas.

Abdominal pain
Nausea or vomiting
Loss of appetite
Lethargy
Acute confusion
Water retention
Easy bruising
Yellowish skin coloring

Carbamazepine (Tegretol, Equetro, Carbatrol) is an effective anticonvulsant and specific analgesic when used alone or with other drugs. Carbamazepine also has the added benefit of relieving depression and improving alertness. An extended release form is available that allows twice-daily dosing rather than 3 times a day. A chewable form makes it easier for children to take.

Uses. This drug is used to prevent the following seizures or epilepsy syndromes:

Partial seizures. Patients tend to tolerate this drug better than others, although responses differ among individuals
Grand mal seizures
Combinations of grand mal and partial seizures
Autosomal dominant nocturnal frontal lobe epilepsy (an inherited disorder).

Side Effects. Different side effects may develop or resolve at different points in the treatment duration. Initial side effects may include:

Double vision, headache, sleepiness, dizziness, and stomach upset. These usually subside after a week and can be greatly reduced by starting with a small dose and building up gradually.
Some people experience visual disturbances, ringing in the ears, agitation, or odd movements when drug levels are at their peak. The extended-release form of carbamazepine (Carbatrol) may help reduce these symptoms.

Serious side effects are less common but can include:

Carbamazepine may increase the risk for birth defects, especially if it is taken during the first trimester of pregnancy.
Skin reactions, including toxic epidermal necrolysis and Stevens-Johnson syndrome, so severe the drug has to be discontinued develop in about 6% of patients. These skin reactions cause skin lesions, blisters, fever, itching, and other symptoms. People of Asian ancestry have a 10 times greater risk for skin reactions than other ethnicities. The FDA recommends that patients of Asian ancestry get a blood test prior to starting the drug to determine if they have the gene variant that increases this risk.
Water retention can be a problem in older people.
Hormonal changes, particularly higher levels of male hormones in both men and women, pose some risk for sexual dysfunction over time.
A decrease in white blood cells occurs in about 10% of those taking the drug. This is generally not serious unless infection accompanies it.
Other blood conditions can arise that are also potentially serious. Patients should be sure to inform the doctor if they have any sign of irregular heartbeats, sore throat, fever, easy bruising, or unusual bleeding.
Long-term therapy can cause bone loss (osteoporosis) in women, who should take preventive calcium and vitamin D supplements.
Children are at higher risk for behavioral problems.

Note: Citrus fruit, especially grapefruit, can increase carbamazepine's adverse effects and should be avoided by those taking this drug.

Uses. Phenytoin (Dilantin) is effective for adults who have the following seizures or conditions:

Grand mal seizures
Partial seizures
Status epilepticus
Can be effective for people with head injuries who are at high risk for seizures

This drug is not useful for the following seizures:

Petit mal seizures
Myoclonic seizures
Atonic seizures

Side Effects. Side effects are sometimes difficult to control. Some people may develop a toxic response to normal doses, while others, such as those with alcoholism, may require higher doses to achieve benefits. As with any drug, side effects generally rely on dosage and duration. Using phenytoin in combination with newer add-on drugs can allow lower doses and may reduce some of the risks. Side effects may include:

Excess body hair, eruptions and coarsening of the skin, and weight loss
Gum disease
Staggering, lethargy, nausea, depression, eye-muscle problems, anemia, and an increase in seizures can occur as a result of high doses.
Liver damage may develop in rare cases.
Bone loss from long-term therapy. Patients should take preventive calcium and vitamin D supplements and exercise regularly to improve bone mass.
Severe and even rare life-threatening skin reactions (Stevens-Johnson syndrome)
An increased risk for birth defects

Phenobarbital (Luminal), also called phenobaritone, is a barbiturate anticonvulsant and is often the initial drug prescribed for newborns and young children. It is a relatively inexpensive drug. Primidone (Mysoline) is converted in the body to phenobarbital, and has the same benefits and adverse effects. It is reported that primidone is not as well-tolerated as phenobarbital. Some experts believe that primidone has no advantage over the other drug.

Uses. Barbiturates are used to also prevent grand mal (tonic-clonic) seizures or partial seizures. They are no longer typically used as a first-line drug.

Side Effects. Phenobarbital has fewer toxic effects on other parts of the body than most anti-epileptic drugs, and drug dependence is unusual, given the low doses used for patients with epilepsy. Nevertheless, withdrawal is common because of side effects, and therefore it is less likely to be used over time than other drugs, including phenytoin, another relatively inexpensive but effective drug.

Patients sometimes describe their state as "zombie-like." The most common and troublesome side effects are:

Drowsiness
Memory problems
Problems with tasks requiring sustained performance
Problems with motor skills
Hyperactivity in some patients, particularly in children and the elderly
Depression in some adults

Some controversy has arisen over studies indicating that children taking phenobarbital score lower on intelligence tests, even for some months after going off the drug.

Uses. Ethosuximide (Zarontin) is used for petit mal (absence) in children and adults when the patient has experienced no other type of seizures. Ethosuximide succeeds in abolishing petit mal seizures in 60% of patients and controls them in up to 90%. Methsuximide (Celontin), a drug similar to ethosuximide, may be suitable as an add-on treatment for intractable epilepsy in children without causing serious or permanent side effects.

Side Effects. Use of this drug can cause stomach problems, dizziness, loss of coordination, and lethargy. In rare cases, it has caused severe and even fatal blood abnormalities. Periodic blood counts are recommended for patients taking this drug.

Uses. Clonazepam (Klonopin) is recommended for myoclonic and atonic seizures that cannot be controlled by other drugs and for Lennox-Gastaut (absence variant). It may be useful in newborns when other drugs are ineffective. Although clonazepam can prevent generalized or partial seizures, patients generally develop tolerance to the drug, and then seizures recur.

Side Effects. People who have had liver disease or acute angle glaucoma should not take clonazepam, and people with lung problems should approach the drug with caution. Clonazepam can be addictive, and abrupt withdrawal has been known to trigger status epilepticus. Side effects include the following: drowsiness, imbalance and staggering, irritability, aggression, hyperactivity in children, weight gain, eye muscle problems, slurred speech, tremors, skin problems, and stomach problems.

Uses. Lamotrigine (Lamictal) is approved as add-on (adjunctive) therapy for partial seizures, and generalized seizures associated with Lennox-Gastaut syndrome, in children aged 2 years and older and in adults. Lamotrigine is also approved as add-on therapy for treatment of primary generalized tonic-clonic (PGTC) seizures, also known as “grand mal” seizures, in children aged 2 years and older and adults. Lamotrigine can be used as a single drug treatment (monotherapy) for adults with partial seizures who have not responded to monotherapy with carbamazepine, phenytoin, phenobarbital, primidone, or valproate. Birth control pills lower blood levels of lamotrigine.

Side Effects. Common side effects include dizziness, headache, blurred or double vision, lack of coordination, sleepiness, nausea, vomiting, insomnia, and rash. Although most cases of rash are mild, in rare cases the rash can become very severe. The risk of rash increases if the drug is started at too high a dose or if the patient is also taking valproate. (Serious rash is more common in young children who take the drug than it is in adults.) Rash is most likely to develop within the first 8 weeks of treatment. Be sure to immediately notify your doctor if you develop a rash, even if it is mild.

Studies suggest that lamotrigine may cause fewer problems with sexual function in men than other antiseizure drugs. A 2006 study indicated that lamotrigine may cause fewer cognitive problems (such as confusion and difficulty concentrating) than topiramate.

Gabapentin (Neurontin) is an effective add-on drug for controlling complex partial seizures and secondarily generalized partial seizures and is approved for adults and children with these seizures. It has achieved response rates in patients with resistant partial epilepsy. It is not at all useful for generalized petit mal seizures.

Side Effects. Its toxicity is low, and side effects include sleepiness, headache, fatigue, and dizziness. Some weight gain has been reported. Gabapentin has no significant interactive effects when taken with other drugs. Children may experience hyperactivity or aggressive behavior. Long-term adverse effects are still unknown.

Pregabalin (Lyrica) is similar to gabapentin.

Uses. Approved as add-on therapy to treat partial-onset seizures in adults with epilepsy. In clinical trials, half of the patients who received pregabalin experienced a 50% reduction in seizure frequency.

Side Effects. These may include dizziness, sleepiness, dry mouth, swelling in hands and feet, blurred vision, weight gain, and trouble concentrating

Uses. Topiramate (Topamax, generic) is similar to phenytoin and carbamazepine and is effective and safe for a wide variety of seizures in adults and children. It is approved as add-on therapy for patients 2 years and older with generalized tonic-clonic seizures, partial-onset seizures, or seizures associated with Lennox-Gastaut syndrome. It is also approved as single therapy for patients 10 years and older with tonic-clonic seizures or partial-onset seizures. Studies have shown a 34 - 87% reduction in seizure frequency with some patients becoming seizure-free.

Side Effects. Most side effects are mild to moderate and can be reduced or even prevented by beginning at low doses and increasing dosage gradually. Serious side effects may include glaucoma, decreased sweating, increased body temperature, kidney stones, sleepiness, dizziness, confusion, and trouble concentrating. Patients should immediately tell their doctor if they have blurred vision or eye pain. Topiramate may have fewer interactions with oral contraceptives than other AEDs.

Oxcarbazepine (Trileptal, generic) is similar to phenytoin and carbamazepine but generally has fewer side effects.

Uses. Approved as single therapy or add-on therapy for partial seizures in adults and for children ages 4 years and older.

Side Effects. Serious side effects, while rare, include Stevens-Johnson syndrome and toxic epidermal necrolysis. These skin reactions cause a severe rash that can be life threatening. Rash and fever may also be a sign of multi-organ hypersensitivity, another serious side effect associated with this drug. Oxcarbazepine can also reduce sodium levels (hyponatremia). Your doctor may want to monitor the sodium level in your blood. This drug can also reduce the effectiveness of birth control pills. Women who take oxcarbazepine may need to use a different type of contraceptive.

Zonisamide (Zonegran) is a unique drug that blocks sodium and calcium channels and may have nerve-protecting properties.

Uses. It is approved as add-on therapy for adults with partial seizures, and studies indicate it is often effective against infantile spasms (West syndrome) and myoclonic seizures.

Side Effects. Zonisamide increases the risk for kidney stones, which can be reduced with increased fluid intake and citrate. It has also been associated with reduced sweating and a sudden rise in body temperature, especially in hot weather. Children are especially at risk for this side effect, which can be serious. (The drug has not been approved for children.) Other side effects tend to decrease over time and include dizziness, forgetfulness, headache, weight loss, and nausea.

Levetiracetam (Keppra) is known as a nootropic drug.

Uses. This drug is approved both in oral and intravenous forms as add-on therapy for:

Partial onset seizures in adults and children ages 4 years and older
Myoclonic seizures in adults and adolescents ages 12 years and older who have juvenile myoclonic epilepsy
Primary generalized tonic-clonic seizures in adults and children ages 6 years and older who have idiopathic generalized epilepsy

Some experts believe that levetiracetam represents a significant advance and will prove to be an important first-line drug. Levetiracetam appears to have fewer drug interactions than other anti-epileptic drugs and may be particularly useful for older patients.

Side Effects. These tend to occur mostly in the first month. They include sleepiness and fatigue, muscle weakness and coordination difficulties, headache, flu symptoms, dizziness, behavioral abnormalities, possible risk of a reduced white blood cell count, and a higher rate of infections. Caution is advised for patients with kidney dysfunction. There have been some reports of adverse effects on mood (irritability, depression, and anxiety), but recent studies have found fewer such effects than with other AEDs. Epilepsy, rather than the drug, is likely to be the cause of these mood changes. About 1% of patients report considerable weight loss.

Tiagabine (Gabitril) has properties similar to phenytoin and carbamazepine, and is also showing promise.

Side Effects. Evidence has reported some significant side effects with its use, including dizziness, fatigue, agitation, and tremor. At least one study suggested that it has more adverse effects than lamotrigine and is not as well tolerated. In February 2005, the FDA issued a warning advising that tiagabine may cause seizures in patients without epilepsy. Tiagabine is only approved for use with other anti-epilepsy medicines to treat partial seizures in adults and children 12 years and older.

Felbamate. Felbamate (Felbatol) is an effective antiseizure drug. However, after reports of deaths from a serious blood condition known as aplastic anemia or from liver failure, felbamate is recommended only under certain circumstances. They include severe epilepsy, such as Lennox-Gastaut syndrome or as monotherapy for partial seizures in adults when other drugs fail.

Vigabatrin. Vigabatrin (Sabril) is a chemical called gamma-vinyl GABA. It was designed to increase the brain levels of gamma aminobutyric acid (GABA), the enzyme that inhibits seizure activity. It has serious side effects, however, and is generally prescribed in the U.S. only in certain cases, such as in low doses for patients with Lennox-Gastaut syndrome. Overseas it is also used for partial seizures and as first-line therapy in children with infantile spasms (West syndrome). Between 10 - 30% of people on long-term treatment have developed irreversible visual disturbances, including reductions in acuity and color vision. Men are at higher risk for this side effect than are women. Further studies are needed to determine the extent and severity of this complication, particularly in children. There is a slight risk for depression or psychosis when vigabatrin is used as add-on therapy, and particularly if the drug is administered too quickly. These risks are far lower if the drug is used as sole therapy.

Older Drugs. Some older but less effective drugs may still play a role against epilepsy:

Acetazolamide (Diamox) is sometimes used against common types of seizures, but patients quickly develop a tolerance for it. Some experts suggest it still may be useful when drug interactions are a problem, when a rapid effect is required, or when an additional drug is needed for a short time.
Trimethadione (Tridione) is effective for petit mal seizures, but has very serious side effects, and its use is severely limited.

Infantile spasms are treated with vigabatrin, adrenocorticotropic hormone (ACTH), or valproate. Some experts recommend that vigabatrin be given first and ACTH administered 10 - 14 days later. In one small study, no infants who were given this combination relapsed after 4 months. Newer drugs may also be effective for this problem, but their effects on small children are not yet wholly known.

New AEDs. Retigabine is an investigational GABA enhancer that works in a different way from existing AEDs. It is currently in phase III trials for treatment of partial-onset seizures in patients who are receiving other AEDs. Talampanel is another new type of drug, known as an AMAP receptor antagonist, that is currently in early trials. Other drugs under investigation are related to existing AEDs. For example, brivaracetam and seletracetam are similar to levetiraceptam, fluorofelbamate is similar to felbamate, and eslicarbazepine is similar to oxcarbazepine.

Cannabinoids. Cannabinoids are compounds in marijuana (cannabis) that may have properties that protect nerve cells. Some patients claim a reduction in seizures while other active users of marijuana report no effect on seizures. No one has reported worse seizures from the drug. Animal studies further support some protection from cannabinoids against seizures. Clinical studies using humans have not been conducted.

Melatonin. Melatonin is a hormone found in the brain that is best known for its role in sleep. Some researchers believe that it might have properties that could benefit patients with epilepsy. Melatonin is a powerful hormone that can have major effects on all parts of the body. No one with epilepsy should experiment with this supplement except as part of a clinical trial. In some studies, melatonin has been found to cause seizures in children who have existing neurologic problems.

Surgery

Surgical techniques to remove injured brain tissue may be appropriate for many patients with epilepsy. The surgeon's goal is to remove only the damaged tissue in order to prevent seizures and to avoid healthy brain tissue. Surgical techniques for reaching these goals have improved significantly over the past decades due to advances in imaging and monitoring, new surgical techniques, and a better understanding of the brain and epilepsy.

A number of tests using imaging and electroencephalography (EEG) can determine if surgery is an option:

The general approach is to first use long-term EEG monitoring to locate the brain tissue that triggers the epileptic event.
Advanced imaging techniques can provide valuable additional information. They include functional magnetic resonance imaging (fMRI), positron emission tomography (PET), or single-photon emission computer tomography (SPECT) scans.

If the imaging tests indicate that more than one site is involved or their results conflict, then more invasive monitoring of the brain may be required, although the newer imaging tests are proving to be very accurate tools. If such tests pinpoint a specific area in the brain as the location for seizures, surgery is possible. MEG, for example, is now approved for imaging parts of the brain involved with motor control, sensation, and language function, and may become important in evaluating patients who are likely candidates for surgery. The doctor will also examine the test results to determine if the offending nerve cells perform vital functions and try to predict surgical outcome in certain cases.

The major areas of the brain have one or more specific functions.

The most common surgical procedure for epilepsy is temporal lobectomy, which is performed when epilepsy occurs in the temporal lobe. (Surgery is not as successful in epilepsies that occur in the frontal lobe.) It involves removing small portions from the hippocampus. The hippocampus is a part of the brain that is involved in memory processing. It is part of the limbic system, which controls emotions.

Click the icon to see an image of the limbic system of the brain.

Candidates. Candidates for this surgery usually have a history of seizures. Anti-epileptic drugs have not helped them. Young children may be more difficult candidates because they often have injured areas outside the temporal lobes. Nevertheless, surgery can be very successful in many children, even if more than one area is involved.

Success Rates. New imaging techniques are dramatically improving the success rates of temporal lobe surgery. Studies have shown that many patients remain seizure-free after temporal lobectomy. In a randomized controlled trial, around 60% of patients became free of disabling seizures after surgery versus only 8% of patients treated with medications. In general, around 60 - 80% of patients are seizure free 1 - 2 years after surgery.

Patients may still need to take medications after surgery, even if seizures are very infrequent. Cure is not always possible, and some patients may still experience some seizures. Double vision is very common after the operation, but it is typically temporary and resolves within a few months.

Studies also suggest that temporal lobe surgery improves quality of life and can help relieve depression and anxiety. Other studies indicate that surgery may even prolong survival. Some experts theorize that surgery stabilizes parts of the brain that influence heart rate and may reduce the risk of sudden death, a rare complication of epilepsy.

Effects on Mental Functioning. Although surgery on the left temporal lobe does not impair intelligence to any significant degree, some studies suggest negative effects of mental functioning and behavior. A risk of impairment of verbal memory is also present.

In general, surgical effects on mental functioning and behavior depend on the extent and location of the surgical area.

Lesionectomy is a procedure that removes abnormal tissues in certain conditions, such as:

Cavernous angiomas (abnormal clusters of blood vessels)
Low-grade brain tumors
Cortical dysplasias (these are abnormalities in fetal development in which the normal migration of nerve cells is altered for some reason)

This local surgery, which can cure the patient's epilepsy, has become possible with the advent of advanced imaging techniques such as MRI.

Other surgical procedures called hemispherectomy and corpus callosotomy offer hope for specific patients. They include infants and young children with catastrophic seizures that occur in one, or part of, a hemisphere and for patients whose seizures are due to specific structural brain abnormalities or tumors.

Hemispherectomy. Hemispherectomy is the removal of half the brain, leaving the deep structures intact. Surgery can take 12 hours and there is always some paralysis on one side of the body. There is also a small risk for hydrocephalus, coma, or even death. Quality of life is almost always improved, however, and the surgery does not reduce intelligence.

Corpus Callosotomy. Corpus callosotomy involves cutting the nerve fibers that connect one side of the brain to another. It does not remove brain tissue. It may be done in two stages. In the first, there is a partial separation. If seizures continue, the surgeon may perform a complete separation. This surgery can reduce (although not entirely stop) uncontrolled tonic clonic seizures. It has been used in patients with specific syndromes, such as Lennox-Gastaut syndrome. The procedure can have very severe complications, however.

Electrical stimulation of areas in the brain that affect epilepsy is helping many patients with refractory epilepsy. Vagus nerve stimulation (VNS), an electrical stimulation of the vagus nerve, is now an accepted therapy for severe epilepsy that does not respond to AEDs. The two vagus nerves are the longest nerves in the body. They run along each side of the neck, then down the esophagus to the gastrointestinal tract. They affect swallowing, speech, and many other functions. They also appear to connect to parts of the brain that are involved with seizures. The procedure is as follows:

Click the icon to see a depiction of epilepsy treatment.

A battery-powered device similar to a pacemaker is implanted under the skin in the upper left of the chest.
A lead is then attached to the left vagus nerve in the lower part of the neck.
The neurologist programs the device to deliver mild electrical stimulation to the vagus nerve. (Patients may also pass a magnet over the device to give it an extra dose if they sense a seizure coming on. This appears to help about 25 - 30% of patients.)
The batteries wear out after 3 - 5 years and need to be removed and replaced by a simple surgical procedure.

An investigational approach called deep brain stimulation (DBS) targets the thalamus, the part of the brain that produces most epileptic seizures. Early results have been promising. Researchers are also studying other implanted brain and nerve stimulation devices such as the responsive neurostimulator system (RNS), which detects seizures and stops them by sending electrical stimulation to the brain. A third investigational approach, trigeminal nerve stimulation (TNS), stimulates a nerve involved in inhibiting seizures.

Candidates. The American Academy of Neurology recommends VNS for:

Patients who are over 12 years old, and
Have partial seizures that do not respond to medication, and
Are not appropriate candidates for surgery

Evidence is accumulating, however, to indicate that VNS is effective and safe for many patients of all ages and for refractory epilepsy of many types.

Success Rates. Studies are reporting that the procedure reduces seizures within 4 months by up to 50% and even more in many patients. Studies report that it has been effective for longer than 7 years. In one study that followed patients for a year, the benefits of VNS appeared to increase over time.

Complications. Vagus nerve stimulation does not eliminate seizures in most patients and is still somewhat invasive. VNS can cause shortness of breath, hoarseness, sore throat, coughing, ear and throat pain, or nausea and vomiting. These side effects can be reduced or eliminated by reducing the intensity of stimulation. Some studies suggest that the treatment causes adverse changes in breathing during sleep and may cause lung function deterioration in people with existing lung disease. People who have obstructive sleep apnea also should be cautious about this procedure. Turning off the VNS (for example before an MRI or surgery) may increase the risk for status epilepticus. (However, VNS may also be helpful for treating status epilepticus in some patients.)

Stereotactic Radio Surgery. Focused beams of radiation are able to destroy lesions deep in the brain without the need for open surgery. Typically used for brain tumors, stereotactic radio surgery is also under investigation for temporal lobe epilepsy and for seizures due to cavernous malformations. It may be used for patients when an open surgical approach is not possible.

Lifestyle Changes

The best preventive measure is to comply strictly with the drug regimen as prescribed. Seizures cannot be prevented by lifestyle changes alone, but people can make behavioral changes that improve their lives and give them a sense of control.

In most cases, there is no known cause for epileptic seizures, but specific events or conditions may trigger them and should be avoided.

Inadequate or Fragmented Sleep. Inadequate or fragmented sleep can set off seizures in many people. In one study, the lowest risk for seizures was during REM sleep (when dreams occur). The highest risk was during light non-REM stages of sleep. Using sleep hygiene or other methods to improve sleep may be helpful.

Food Allergies. Food allergies may provoke seizures in children who also have migraine headaches, hyperactive behavior, and abdominal pains. Parents should consult an allergist if they suspect foods or additives might be playing a role in such cases.

Alcohol and Smoking. Alcohol and smoking should be avoided, although light alcohol consumption does not appear to increase seizure activity in people who are not alcoholics or sensitive to alcohol.

Flashing Lights. Patients should avoid exposure to flashing or strobe lights. Video games have been known to trigger seizures in people with existing epilepsy, but apparently only if they are already sensitive to flashing lights. Seizures have been reported in Japan among people who watched cartoons with rapidly fluctuating colors and quick flashes. The frequency of flashes per second is measured in hertz (Hz). Screens that emit a lower hertz (such as 50 Hz screens sold in Europe) are more likely to cause seizures in people with epilepsy than a higher-hertz screen (such as 100 Hz screens sold in the U.S.).

Relaxation methods include diaphragmatic rhythmic breathing, biofeedback, and meditation techniques. No strong evidence supports their value on reducing actual attacks (although some people have reported that they have), but they may be helpful in reducing anxiety in people who have positive experiences with them. There have been some reports that deep breathing (a common relaxation technique) triggers seizures in certain people.

Exercise is important for many aspects of epilepsy, although it can be problematic. Weight-bearing exercise helps maintain bone density, which can be reduced by many of the medications, particularly the older ones. Exercise can also help to prevent weight gain, which is a problem with some drugs. There have been some reports that exercise may trigger seizures in some patients, but this is uncommon. A number of studies have found no significant association between physical activity and a higher incidence of seizures in patients with epilepsy. Nevertheless, if patients are concerned they should discuss this issue with their doctors.

Some small studies have reported significant benefits from the practice of yoga, which employs weight bearing and balancing postures. In one study, a system of meditation called Sahaja yoga changed EEG readings of brain waves and reduced seizures. Other studies report a 50% reduction in seizures and an overall decline in the number of attacks per month. Still, well-controlled studies are needed to confirm these benefits.

All patients should maintain a healthy diet, including plenty of whole grains, fresh vegetables, and fruits. In addition, dairy foods may be important to maintain calcium levels. Fasting has been used to prevent seizures since ancient times. In the 1920s, a high-fat, no-sugar, low protein diet, known as a ketogenic diet, was used to prevent seizures. It lost popularity after the introduction of anti-epileptic drugs but is now proving to be effective with many children. Researchers are investigating whether the Atkins diet (high protein, low carbohydrate) may help people with epilepsy. Both the ketogenic diet and the Atkins diet can interfere with some anti-epileptic medications such as topiramate. Talk to your doctor before beginning any special diet or a weight loss program.

The ketogenic diet, which is very high in fat (90%), very low in carbohydrates, and low in protein, has been studied and debated for decades. It has proven to be helpful for many children with severe epilepsy that does not respond to AEDs. It is not clear why it works. The standard theory is that burning fat instead of carbohydrates causes an increase in ketones. Excess ketones (called ketosis) appears to alter certain amino acids in the brain and to increase levels of the neurotransmitter gamma aminobutyric acid (GABA), which helps prevent nerve cells from over-firing.

Benefits of the Ketogenic Diet. Studies report that about 10 - 15% of children who use the diet are seizure free after 1 year, while 30% are nearly seizure free. Some parents report that the diet helps improve their children’s alertness, even if seizures continue. Many children who try the ketogenic diet are able to stop or at least reduce their medications.

Candidates of the Ketogenic Diet. The Ketogenic Diet seems to be most helpful for children who have difficult-to-control seizures, in particular:

Generalized and partial seizures (the diet does not appear to be as helpful for children with partial-onset seizures)
Myoclonic-atastic epilepsy
Infantile spasm

Typical Ketogenic Diet. (This diet must be professionally monitored! Parents can endanger their children if they try the program on their own without consulting a doctor or trained health expert.) The child fasts for the first 1 - 2 days, then the diet is gradually introduced. The regimen uses small amounts of carbohydrates and large amounts of fats (up to 90%), with very few proteins and no sugar. Children generally consume 75% of their usual daily calorie requirements.

A typical dinner may include a chicken cutlet or piece of fish, broccoli with cheese, lettuce with mayonnaise, and a whipped cream sundae. Vegetables may include celery, cucumbers, or asparagus, cauliflower, and spinach. Breakfast might consist of an omelet, bacon, and cocoa with cream. (Artificial sweeteners are used for any desserts.)

The diet is difficult, as a slight deviation from the diet can provoke a seizure. Children cannot take medications that contain sugar (which is common in many drugs produced for children). Some sunscreens and lotions contain sorbitol, a carbohydrate that can be absorbed through skin. About 40 - 50% of patients find the diet too difficult or ineffective and stop it after 6 months.

Researchers are also investigating the Atkins diet, a popular weight-loss diet that has similar effects but is less restrictive than the ketogenic diet. Early results indicate that it might be helpful for some young people. Another alternative is a low glycemic index diet, which contains even fewer carbohydrates than the Atkins diet. Still, parents should not put their children on these diets without support from a doctor.

Side Effects and Complications. To prevent serious side effects, children need regular monitoring by a doctor, especially when the diet is first initiated.

Side effects or complications that may occur at the start of the diet include:

Acidosis, a build-up of acid in the blood and body
Low blood sugar (hypoglycemia)
Stomach upset
Dehydration
Lethargy

Side effects that may occur later on include:

Unhealthy cholesterol and lipid levels
Kidney stones, which may be a complication of acidosis, occur in about 5% of children on the diet. Patients should drink plenty of fluids. Oral potassium citrate (Polycitra K) may be protective.
Slowing of growth (tends to occur more in younger children than older children
Decreased bone density

Because most patients remain on the diet for only 2 years, the risks for potential long-term damage appear minimal.

Many patients with epilepsy and parents whose children have epilepsy can benefit from support associations. These services are usually free and available in most cities.

Tips for Helping Children. Some of the following tips may help the child with epilepsy:

Children should be treated as normally as possible by parents and siblings.
Children should be assured that they will not die from epilepsy.
Often children can be given the hope that they will outgrow the disorder.
Most children will not have seizures triggered by sports or by any other ordinary activities that are enjoyable and healthy.
As soon as they are old enough, children should be active participants in maintaining their drug regimens, which should be presented in as positive a light as possible.

Therapies for Children and Adults. Because of the risks for serious emotional consequences, psychological therapy may be beneficial and even necessary for some adults and children. In one study, cognitive behavioral therapy was helpful in lowering seizure rates in young people with juvenile myoclonic epilepsy. This approach offers a structured counseling program that helps people change behaviors that can reduce seizure risk factors such as anxiety and insomnia.

Resources

www.epilepsyfoundation.org -- Epilepsy Foundation
www.aesnet.org -- American Epilepsy Society
www.aan.com -- American Academy of Neurology
www.ninds.nih.gov -- National Institute of Neurological Disorders and Stroke

References

Christensen J, Vestergaard M, Mortensen PB, Sidenius P, Agerbo E. Epilepsy and risk of suicide: a population-based case-control study. Lancet Neurol. 2007 Aug;6(:693-8.

Foldvary-Schaefer N, Wyllie E. Epilepsy. In: Goetz C, ed. Textbook of Clinical Neurology. 3rd edition. Saunders. 2007.

Freeman JM, Kossoff EH, Hartman AL. The ketogenic diet: one decade later. Pediatrics. 2007 Mar;119(3):535-43.

Johnson MV. Seizures in childhood. In: Behrman RE, ed. Nelson Textbook of Pediatrics. 17th edition. Saunders. 2004.

Krebs PP. Psychogenic nonepileptic seizures. Am J Electroneurodiagnostic Technol. 2007 Mar;47(1):20-8.

Krumholz A, Wiebe S, Gronseth G, et al. Practice Parameter: evaluating an apparent unprovoked first seizure in adults (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Neurology. 2007 Nov 20;69(21):1996-2007.

Kwan P, Brodie MJ. Emerging drugs for epilepsy. Expert Opin Emerg Drugs. 2007 Sep;12(3):407-22.

Leone MA, Solari A, Beghi E; FIRST Group. Treatment of the first tonic-clonic seizure does not affect long-term remission of epilepsy. Neurology. 2006 Dec 26;67(12):2227-9.

Salanova V, Worth R. Neurostimulators in epilepsy. Curr Neurol Neurosci Rep. 2007 Jul;7(4):315-9.

Spencer SS. Seizures and epilepsy. In: Goldman L, ed. Cecil Medicine. 23rd edition. Saunders. 2007.

Tomson T, Hiilesmaa V. Epilepsy in pregnancy. BMJ. 2007 Oct 13;335(7623):769-73.

Review Date:
12/31/2007
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

adam.com

Diabetes - type 2

FitSugar — Wed, 08 Oct 2008 17:34:58 -0700

In This Report

Highlights
Introduction
Causes
Risk Factors
Symptoms
Screening Tests
Treatment
Lifestyle Changes
Medications
Long-Term Complications
Emergency Complications
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Drug Approvals

Sitagliptin (Januvia), the first in a new class of diabetes drugs called DPP-4 inhibitors, was approved in 2006.
Janumet, a 2-in-1 pill that contains both sitagliptin and metformin, was approved in 2007.
These drugs are taken by mouth and may be more convenient for patients than exenatide (Byetta), a similar drug. DPP-4 inhibitors do not cause weight gain and may pose a lower risk for hypoglycemia than some other diabetes drugs.

Drug Safety Alert

Rosiglitazone (Avandia) may significantly increase the risk for heart attack, indicates a review published in the Journal of the American Medical Association. In 2007, a panel of experts from the Food and Drug Administration (FDA) agreed the drug increases the risk of heart attacks -- but concluded it should remain on the market. The panel did, however, recommend the FDA require rosiglitazone's maker to add warnings to the drug's label. Rosiglitazone and a similar drug, pioglitazone (Actos), are known to significantly increase the risks for heart failure. There is also evidence that these drugs increase the risk for bone fracture.

Anemia Drugs Warning

Patients with anemia associated with end-stage kidney disease, especially those on dialysis, should be aware of new warnings concerning dosing target levels of erythpoiesis-stimulating drugs. In 2007, the FDA warned that darbepoetin alfa (Aranesp) and epoetin alfa (Epogen and Procrit) can increase the risk for blood clots, stroke, and heart attacks when excessive doses are given. The FDA has defined target hemoglobin levels and recommends that patients who receive these drugs have frequent blood tests. Patients should also report to their doctors any unusual symptoms.

Genetics Research Breakthroughs

Scientists have now identified 10 genes that are associated with increased risk for type 2 diabetes. Six of these genes were discovered in 2006 and 2007.

Diabetes and Pre-Diabetes

About 20 million Americans have type 2 diabetes, and an additional 54 million have pre-diabetes. According to a 2007 study by the U.S. Centers for Disease Control, the prevalence of type 2 diabetes has been increasing by 5% each year since 1990. Rising rates of obesity may be one factor.
For people with pre-diabetes, lifestyle changes, such as losing weight, appear to work as well as drug treatment in delaying the progression to diabetes, according to a 2007 British Medical Journal study.

Introduction

The two major forms of diabetes are type 1 (previously called insulin-dependent diabetes mellitus, IDDM, or juvenile-onset diabetes) and type 2 (previously called noninsulin-dependent diabetes mellitus, NIDDM, or maturity-onset diabetes).

Both type 1 and type 2 diabetes share one central feature: elevated blood sugar (glucose) levels due to insufficiencies of insulin, a hormone produced by the pancreas. Insulin is a key regulator of the body's metabolism. It works in the following way:

During and immediately after a meal the process of digestion breaks down carbohydrates into sugar molecules (including glucose) and proteins into amino acids.
Right after the meal, glucose and amino acids are absorbed directly into the bloodstream, and blood glucose levels rise sharply.
The rise in blood glucose levels signals important cells in the pancreas, called beta cells, to secrete insulin, which pours into the bloodstream. Within 10 minutes after a meal, insulin rises to its peak level.
Insulin enables glucose and amino acids to enter cells in the body, particularly muscle and liver cells. Here, insulin and other hormones direct whether these nutrients will be burned for energy or stored for future use. (The brain and nervous system are not dependent on insulin; they regulate their glucose needs through other mechanisms.)
When insulin levels are high, the liver stops producing glucose and stores it in other forms until the body needs it again.
As blood glucose levels reach their peak, the pancreas reduces the production of insulin.
About 2 - 4 hours after a meal, both blood glucose and insulin are at low levels, with insulin being slightly higher. The blood glucose levels are then referred to as fasting blood glucose concentrations.

The pancreas is located behind the liver and is where the hormone insulin is produced. Insulin is used by the body to store and utilize glucose.

Type 2 diabetes is the most common form of diabetes, accounting for 90 - 95% of cases. The disease mechanisms in type 2 diabetes are not wholly known, but some experts suggest that it may involve the following three stages in most patients:

The first stage in type 2 diabetes is the condition called insulin resistance. Although insulin can attach normally to receptors on liver and muscle cells, certain mechanisms prevent insulin from moving glucose (blood sugar) into these cells where it can be used. Most patients with type 2 diabetes produce variable, even normal or high, amounts of insulin. In the beginning, this amount is usually sufficient to overcome such resistance.
Over time, the pancreas becomes unable to produce enough insulin to overcome resistance. In type 2 diabetes, the initial effect of this stage is usually an abnormal rise in blood sugar right after a meal (called postprandial hyperglycemia). This effect is now believed to be particularly damaging to the body.
Eventually, the cycle of elevated glucose further impairs and possibly destroys beta cells, thereby stopping insulin production completely and causing full-blown diabetes. This is made evident by fasting hyperglycemia, in which elevated glucose levels are present most of the time.

In type 1 diabetes, the disease process is more severe and onset is usually in childhood:

Beta cells in the pancreas that produce insulin are gradually destroyed. Eventually insulin deficiency is absolute.
Without insulin to move glucose into cells, blood glucose levels become excessively high, a condition known as hyperglycemia.
Because the body cannot utilize the sugar, it spills over into the urine and is lost.
Weakness, weight loss, and excessive hunger and thirst are among the consequences of this "starvation in the midst of plenty."
Patients become dependent on administered insulin for survival. [See In-Depth Report #9: Diabetes - type 1.]

Click the icon to see an image of the pancreas.

Conditions that damage or destroy the pancreas, such as pancreatitis, pancreatic surgery, or certain industrial chemicals can cause diabetes. Polycystic ovaries are highly associated with diabetes. Certain drugs can also cause temporary diabetes, including corticosteroids, beta-blockers, and phenytoin. Rare genetic disorders (Klinefelter's syndrome, Huntington's chorea, Wolfram's syndrome, leprechaunism, Rabson-Mendenhall syndrome, lipoatrophic diabetes) and hormonal disorders (acromegaly, Cushing syndrome, pheochromocytoma, hyperthyroidism, somatostatinoma, aldosteronoma) are associated with or increase the risk for diabetes.

Causes

Type 2 diabetes is caused by a complicated interplay of genes, environment, insulin abnormalities, increased glucose production in the liver, increased fat breakdown, and possibly defective hormonal secretions in the intestine. The recent dramatic increase indicates that lifestyle factors (obesity and sedentary lifestyle) may be particularly important in triggering the genetic elements that cause this type of diabetes.

The characteristic features of most patients with type 2 diabetes are:

Insulin resistance in muscle cells
Normal or even excessive levels of insulin (to compensate for this resistance), eventually followed by a drop in insulin production

In addition, researchers are trying to determine the factors that might promote insulin resistance:

Both obesity and insulin resistance at different phases are marked by elevated levels of free fatty acids and the hormones resistin and leptin. It is not known yet if elevated levels are simply a product of obesity or play some causal role in diabetes.
Insulin resistance is associated with a chronic low inflammatory response, which involves a number of immune factors, such as TGH-beta 1 and C-reactive protein. Such factors can cause damage over time and may be responsible for the association between insulin resistance and heart disease.

Type 2 diabetes has a genetic component. In 2006 and 2007, major breakthroughs in genetic research identified six new genes associated with type 2 diabetes. Ten genes have now been positively confirmed as increasing the risk for type 2 diabetes: TCF7L2, SLC30A8, HHEX, PPARG, KCNJ11, IGF2B2, CDKAL1, CDKN2A, CDKN2B, and FTO.

Most of these genes play a role in regulating insulin action, including the processes that occur in the pancreas’ insulin-producing beta cells. The FTO gene increases the risk for obesity, which itself is a risk factor for type 2 diabetes. These genes appear to cluster around three genetic regions that include a number of chromosomes. Scientists hope that future research will help uncover how genes influence the progression from pre-diabetes to diabetes, and how lifestyle and medical intervention may help delay or prevent this process.

Risk Factors

Nearly 21 million Americans have diabetes; up to 95% of these cases are type 2. In addition, 26% of Americans age 20 and older (and 40% of Americans age 65 and older) have impaired fasting glucose, a pre-diabetes condition that increases the risk for diabetes. According to the American Diabetes Association, 54 million people have pre-diabetes, bringing a total of 75 million Americans who either have diabetes or are at risk of developing it.

Historically, type 2 diabetes usually developed after the age of 40, but it is now also increasing in children. The prevalence of diabetes in the U.S. has increased by 5% each year since 1990, and experts believe that obesity is the major factor behind this dramatic growth rate. Given the current epidemic of obesity, experts estimate that over a third of all people born in 2002 will eventually develop diabetes. Furthermore, the dramatic increase in diabetes is occurring worldwide as American lifestyles become global. Evidence strongly suggests that healthy lifestyles can prevent most cases of type 2 diabetes. People with pre-diabetes can substantially lower their risk by losing weight through diet and exercise.

Healthy adults age 45 and older should get tested for diabetes. Patients who are younger than age 45 and who are overweight or have other risk factors should also ask their doctors about testing. According to the National Institutes of Health, the following are major risk factors for diabetes and pre-diabetes:

Age 45 or older
Family history of diabetes
Overweight
Inactive lifestyle (exercise less than 3 times a week)
African-American, Hispanic/Latin American, American Indian and Alaska Native, Asian-American, or Pacific Islander ethnicity
High blood pressure (140/90 mm/Hg or higher)
HDL (“good”) cholesterol less than 35 mg/dL or triglyceride level 250 mg/dL or higher
Have had diabetes during pregnancy (gestational diabetes) or have given birth to a baby that weighed more than 9 pounds
Polycystic ovary syndrome (metabolic disorder that affects female reproductive system
Acanthosis nigricans (dark, thickened skin around neck or armpits)
History of disease of blood vessels to the heart, brain, or legs
Diabetes test history of impaired fasting glucose (IFG) or impaired glucose tolerance (IGT)

Obesity is the number one risk factor for type 2 diabetes. It is estimated that 80 - 95% of the current dramatic increases in type 2 diabetes are due to obesity. Excess body fat appears to play a strong role in insulin resistance, but the way the fat is distributed is also significant. Weight concentrated around the abdomen and in the upper part of the body (apple-shaped) is associated with insulin resistance and diabetes, heart disease, high blood pressure, stroke, and unhealthy cholesterol levels. Waist circumferences greater than 35 inches in women and 40 inches in men have been specifically associated with a greater risk for heart disease and diabetes. (People with a "pear-shape" -- fat that settles around the hips and flank -- appear to have a lower risk for with these conditions.) However, obesity does not explain all cases of type 2 diabetes. It is also common among people in countries where weights tend to be low, such as Asia or India.

Metabolic Syndrome. A set of conditions referred to as metabolic syndrome (also called Syndrome X) is a pre-diabetic condition that is significantly associated with heart disease and higher mortality rates from all causes. The syndrome consists of obesity marked by abdominal fat, unhealthy cholesterol levels, high blood pressure, and insulin resistance. A 2002 study estimated that nearly a quarter of the U.S. population now has this condition. Even worse, according to a 2003 study, nearly a million American teenagers have this syndrome.

Between 25 - 33% of patients with type 2 diabetes have family members with diabetes. Having a first-degree relative with the disease poses a 40% risk of developing diabetes. One study reported that people with diabetic family histories have a higher risk for developing the disease at an earlier stage and with more severe features. Because families share many lifestyle features (eating and exercise habits) it is difficult to determine when genetics or environment play the major role. When clusters of type 1 and type 2 diabetes appear within families, genetic factors should be strongly suspected.

The risk for type 2 diabetes varies among population groups. Diabetes also seems to pose higher or lower risks for specific complications among ethnic groups. Genetic and socioeconomic factors, or both, seem to be involved in some ethnic differences, but in most cases the observed increase in ethnic groups in Americans is due to changes in traditional lifestyles.

African-Americans. African-American men have twice the risk of developing type 2 diabetes as Caucasian men. African-Americans with diabetes are also at higher risk for amputations than Caucasians. This is most likely due to a higher incidence of high blood pressure and smoking as well as poorer health care in African-Americans. Genetic factors may also play a role. For example, there is some evidence that African-Americans process insulin in the liver differently from Caucasians, which may make them more susceptible to diabetes when other risk factors are present.
Native Americans. The Pima tribe in Arizona has an incidence of type 2 diabetes that is 19 times higher than that of the white population. The risk for diabetic complications among young Pima adults is also very high. Other Native American tribes in North America are also at high risk for type 2 diabetes. The association between diet and diabetes among this population remains critical, however, in assessing the reason for their higher risk. For example, Pimas who live in Mexico exercise more and eat less fat (but consume more calories) than Pima tribes in Arizona. Mexican Pimas have a prevalence of diabetes of only 6%, while half of their Arizona Pima neighbors have diabetes.
Hispanic Americans. The rate of type 2 diabetes is also very high among Mexican-Americans, approximately double that for Caucasians. This group may also be at higher risk for heart problems than other ethnic groups with diabetes.
Asian-Americans. Overweight Asian-Americans and Pacific Islanders are at increased risk for developing type 2 diabetes. The risk for some Asian ethnic groups (such as Native Hawaiians and Filipinos) is twice that of Caucasians.

Smoking increases the risk for diabetes. According to a 2006 study, smokers are more than twice as likely to develop diabetes as people who have never smoked. Another 2006 study found that exposure to second-hand cigarette smoke also increases the risk for diabetes in non-smokers.

Low birth weight is now a recognized risk factor for type 2 diabetes and heart disease in adulthood. The reasons are unclear, although studies suggest it may represent a genetic factor. Studies have observed that babies of fathers with type 2 diabetes and of women who later developed type 2 diabetes tend to weigh less than babies of parents without diabetes. Such studies suggest that some parents may have some specific gene that affects insulin factors, putting both themselves and their children at risk for future diabetes. Theoretically, such a gene might also affect insulin factors in the developing fetus, causing low birth weight. (Of note, mothers of very high-weight babies are also at risk for diabetes -- although in these cases it is most often associated with gestational diabetes.)

Obesity-Related Type 2 Diabetes in Children. Until recent years, diabetes in children was almost always type 1 (an autoimmune disease). Between 1982 - 1994, however, the incidence of type 2 diabetes in children increased 10-fold. By 1996, a study reported that a third of all new diabetes cases in children were type 2. This increase parallels the rising epidemic in childhood obesity that has occurred both in the U.S. and worldwide, notably Europe and Japan. In some areas of Japan, type 2 diabetes has now become the dominant form of diabetes in children and adolescents. Obesity in children is also related to abnormalities in cholesterol, blood pressure, and insulin levels in adults. Administering glucose tolerance tests in overweight children may be helpful in identifying those at high risk for diabetes.

Maturity-Onset Diabetes in Caucasian Youth. Maturity-onset diabetes in youth (MODY) is a rare genetic form of type 2 diabetes that develops only in Caucasian teenagers. It accounts for 2 - 5% of type 2 cases. (This form of type 2 diabetes is not associated with obesity.)

An estimated 5% of pregnant women develop a form of type 2 diabetes, usually temporary, in their third trimester called gestational diabetes.

Gestational diabetes is diabetes that first appears during pregnancy. It usually develops during the third trimester of pregnancy. After delivery, blood sugar (glucose) levels generally return to normal, although 25% of these women develop type 2 diabetes within 15 years.

Who Gets Gestational Diabetes? Estimates for the prevalence of gestational diabetes are generally about 4%. Some studies, however, have suggested significantly higher rates. In one German study, 13% of pregnant women were diagnosed with this form of diabetes, including many who did not have any risk factors.

A pregnant woman's risk factors include:

Family history of diabetes
African-American, Hispanic, Asian, or Pacific Islander ethnicity
Overweight
Older than 25 years
Gestational diabetes with past pregnancy
Having given birth to a child weighing over 9 pounds
Diagnosis of pre-diabetes

Who Should Be Tested for Gestational Diabetes? A number of expert groups recommend that all pregnant women be tested for gestational diabetes between their 24th - 28th week. Pregnant women at high risk for diabetes should be tested earlier. The only women who do not need to be tested are those at very low risk. Generally they have the following characteristics:

Under 25 years old
Normal weight
No first-degree relatives with diabetes
Not belonging to high-risk ethnic groups

Effect of Diabetes on the Fetus. Because glucose crosses the placenta, a woman with diabetes can pass high levels of blood glucose to the fetus. In response, the fetus secretes high level of insulin. Studies indicate that such conditions may affect the developing fetus as soon as it is conceived, placing the unborn child at risk for:

Excessive fetal weight gain, which can lead to complications during delivery
Birth defects
Breathing problems and delayed lung development
Low blood sugar
Higher future risk for obesity and diabetes

Effect of Diabetes on the Pregnant Woman. In addition to endangering the fetus, diabetes also presents risks to the pregnant woman.

The most serious potential complications from gestational diabetes are high blood pressure during pregnancy, a condition called preeclampsia that is potentially dangerous. Because gestational diabetes increases the size of the fetus, it is also increases the likelihood that a woman will require a Cesarean delivery. Gestational diabetes also increases the risk that a woman will later develop type 2 diabetes.

How Is Gestational Diabetes Managed? Some suggestions for preventing complications include:

In most cases, increases in glucose levels can be managed with diet and exercise. Aerobic exercise before and during pregnancy may lower glucose levels and help protect women at risk or those who have gestational diabetes. (Any pregnant woman should check with her doctor before embarking on a vigorous exercise regimen.)
If a woman with gestational diabetes cannot control her glucose with lifestyle measures, she is usually given insulin.

The placenta provides the fetus with oxygen and nutrients and takes away waste, such as carbon dioxide, via the umbilical cord.

Polycystic Ovary Syndrome. Polycystic ovary syndrome (PCOS) is a condition that affects about 6% of women and results in the ovarian production of high amounts of androgens (male hormones), particularly testosterone. It appears to be an important cause of many menstrual disorders. Women with PCOS are at higher risk for insulin resistance, and about half of PCOS patients also have diabetes.

Click the icon to see an image of polycystic ovary syndrome.

Schizophrenia. While no definitive association has been established, research has suggested an increased background risk of diabetes among people with schizophrenia. In addition, many of the new generation of antipsychotic medications may elevate blood glucose levels. Patients taking antipsychotic medications (such as clozapine, olanzapine, risperidone, aripiprazole, quetiapine fumarate, ziprasidone) should receive a baseline blood glucose level test and be monitored for any increases during therapy.

Depression. According to a 2007 study, adults who have severe clinical depression may have a greater risk of developing type 2 diabetes than those who have never experienced depressive symptoms.

Hepatitis C. Patients with hepatitis C have a higher incidence of type 2 diabetes. The reasons for this are unclear.

Symptoms

Type 2 diabetes usually begins gradually and progresses slowly. Symptoms in adults include:

Excessive thirst
Increased urination
Fatigue
Blurred vision
Weight loss
In women, vaginal yeast infections or fungal infections under the breasts or in the groin
Severe gum problems
Itching
Erectile dysfunction in men
Unusual sensations, such as tingling or burning, in the extremities

Symptoms in children are often different:

Most children are obese or overweight
Increased urination is mild or even absent
Many children develop a skin problem called acanthosis, which is characterized by velvety, dark colored patches of skin

Screening Tests

There are no clear-cut guidelines for when to screen for diabetes. Some experts recommend that everyone over age 45 be tested regularly for diabetes, although others do not feel this necessary in people without symptoms or risk factors. In fact, early screening may identify some people with impaired glucose levels that would eventually normalize. Such people might be treated unnecessarily with medications that pose a risk for high blood sugar (hypoglycemia).

Still, given the risk for serious complications with diabetes and the potential value of early treatments, most experts recommend that all adults over 45 be screened and that younger adults be screened if they have one or more of the following conditions:

A weight that is 20% more than ideal body weight
Risk factors for heart disease (high blood pressure, unhealthy cholesterol levels -- especially for patients with low HDL cholesterol and high triglyceride levels
A close relative with diabetes
A high-risk ethnic group background
In women, having delivered a baby weighing over 9 pounds or having a history of gestational diabetes

Some experts recommend that children over age 10 should be tested for type 2 diabetes (even if they have no symptoms), if they are overweight and have at least two of the above mentioned risk factors.

Fasting Plasma Glucose. The fasting plasma glucose (FPG) test is the standard test for diabetes. It is a simple blood test taken after 8 hours of fasting. Results indicate:

FPG levels are considered normal up to 100 mg/dL (or 5.5 mmol/L).
Levels between 100 - 125 mg/dL (5.5 - 7.0 mmol/L) are referred to as impaired fasting glucose or pre-diabetes. These levels are considered to be risk factors for type 2 diabetes and its complications.
Diabetes is diagnosed when FPG levels are 126 mg/dL (7.0 mmol/L) or higher.

The FPG test is not always reliable, so a repeat test is recommended if the initial test suggests the presence of diabetes, or if the test is normal in people who have symptoms or risk factors for diabetes. For example, people who take the test in the afternoon and show normal results may actually have abnormal levels that would be revealed if they were tested in the morning.

A 2005 study suggested that even people with FPG levels in the high end of the normal range (high 90s) may be at increased risk for developing type 2 diabetes. Obesity further increases this risk. Patients with FPG levels in the upper 90s should strive to exercise and lose weight to help lower their FPG levels.

Glucose Tolerance Test. The oral glucose tolerance test (OGTT) is more complex than the FPG and may overdiagnose diabetes in people who do not have it. Some experts recommend it as a follow-up after FPG, if the latter test results are normal but the patient has symptoms or risk factors of diabetes. The test uses the following procedures:

It first uses an FPG test.
A blood test is then taken 2 hours later after drinking a special glucose solution.

The following results suggest different conditions:

OGTT levels are considered normal up to 140 mg/dL.
Levels between 140 - 199 mg/dL are referred to as impaired glucose tolerance or pre-diabetes.
Diabetes is diagnosed when OGTT levels are 200 mg/dL or higher.

Both the FPG and OGTT require that the patient not eat for at least 8 hours prior to the test.

Test for Glycated Hemoglobin. Tests for blood levels of glycated hemoglobin, also known as hemoglobin A1c (HbA1c), are not currently used for an initial diagnosis, but they are useful for determining the severity of diabetes. Some experts think this test can help predict complications in people who have FPG levels between 110 - 139, which are above normal but do not indicate full-blown diabetes.

The basis for its use as a diagnostic measurement in diabetes is as follows:

Hemoglobin is a protein molecule found in red blood cells. When glucose binds to it, the hemoglobin becomes modified, a process called glycosylation.
Glycosylation affects a number of proteins, and elevated levels of glycolated hemoglobin are strongly associated with complications of diabetes.
A glycated hemoglobin level of 1% above normal range identifies diabetes in 98% of patients. Normal HbA1c levels do not necessarily rule out diabetes, but if diabetes is present and levels are normal, the risk for complications is low.

The test is not affected by food intake so it can be taken at any time. A home test has been developed that might make it easier to measure HbA1c. In general, measurements suggest the following:

Normal HbA1c levels should be below 7%.
Levels of 11 - 12% glycolated hemoglobin indicate poor control of carbohydrates. High levels are also markers for kidney trouble.

Screening for Heart Disease. All patients with diabetes should be tested for hypertension and unhealthy cholesterol and lipid levels and given an electrocardiogram. For cholesterol, people with diabetes should aim for LDL levels below 100 mg/dL, HDL levels over 50 mg/dL, and triglyceride levels below 150 mg/dL. Blood pressure goals should be 130/80 mmHg or lower. Other tests may be needed in patients with signs of heart disease.

The electrocardiogram (ECG, EKG) is used extensively in the diagnosis of heart disease, from congenital heart disease in infants to myocardial infarction and myocarditis in adults. Several different types of electrocardiogram exist.

Screening for Kidney Damage. The earliest manifestation of kidney damage is microalbuminuria, in which tiny amounts (30 - 300 mg per day) of protein called albumin are found in the urine. About 20% of type 2 patients show evidence of microalbuminuria upon diagnosis of diabetes. (However, not all people with type 2 diabetes eventually develop kidney disease.) Microalbuminuria typically shows up in patients with type 2 diabetes who have high blood pressure.

The American Diabetes Association recommends that people with diabetes receive an annual microalbuminuria urine test. Patients should also have their blood creatinine tested at least once a year. Creatinine is a waste product that is removed from the blood by the kidneys. High levels of creatinine may indicate kidney damage. A doctor uses the results from a creatinine blood test to calculate the glomerular filtration rate (GFR). The GFR is an indicator of kidney function; it estimates how well the kidneys are cleansing the blood.

Screening for Retinopathy. The American Diabetes Association recommends that patients with type 2 diabetes get an initial comprehensive eye exam by an ophthalmologist or optometrist shortly after they are diagnosed with diabetes, and once a year thereafter. (People at low risk may need follow-up exams only every 2 - 3 years.) The eye exam should include dilation to check for signs of retinal disease (retinopathy).

Screening for Neuropathy. All patients should be screened for nerve damage (neuropathy), including a comprehensive foot exam. Patients who have loss of sensation in their feet should be sure to have a foot exam every 3 - 6 months to check for ulcers or infections.

Screening for Thyroid Abnormalities. Thyroid function tests should be administered.

Treatment

Pre-diabetes precedes the onset of type 2 diabetes. People who have pre-diabetes have fasting blood glucose levels that are 100 - 125 mg/dL -- higher than normal, but not yet high enough to be classified as diabetes. (Pre-diabetes used to be referred to as “impaired glucose tolerance.”) Pre-diabetes greatly increases the risk for diabetes.

Treatment of pre-diabetes is very important. Research shows that lifestyle and medical interventions can help prevent, or at least delay, the progression to diabetes. While insulin-regulating drugs such as metformin (Glucophage) and acarbose (Precose) are sometimes prescribed, evidence indicates that lifestyle changes can be at least as effective as drug therapy. The most important lifestyle treatment for people with pre-diabetes is to lose weight through diet and regular exercise. Even a modest weight loss of 10 - 15 pounds can significantly reduce the risk of progressing to diabetes.

Because people with pre-diabetes have a higher risk for heart disease and stroke, diet and exercise are also very important for heart health, as is quitting smoking. It is also important to have your doctor check your cholesterol and blood pressure levels on a regular basis. Your doctor should also check your fasting blood glucose levels every 1 - 2 years.

The major treatment goals for people with type 2 diabetes are:

Treat all conditions that place the patients at risk for heart disease and stroke, which are the major killers of people with type 2 diabetes.
Control blood glucose levels. The goal is to achieve fasting blood glucose levels of less than 110 mg/dL and glycolated hemoglobin (HbA1c) levels of less than 7%. The objective is to reduce complications in small blood vessels and the nerve damage associated with diabetes.

An intensive multi-pronged approach is critical for reducing complications and improving survival rates in patients with diabetes. Intensive therapy includes:

Healthy lifestyle changes: Regular exercise; heart-healthy diet; quitting smoking.
Controlling blood sugar levels. Monitor blood sugar and hemoglobin HbA1C levels. Oral anti-hyperglycemic drugs such as metformin are first-line drug treatments. Insulin may eventually be needed.
Heart-protective drugs. These medications include various drugs to control high blood pressure (ACE inhibitors, diuretics, others) and cholesterol (statins, fibrates). Controlling high blood pressure is a proven factor in reducing mortality rates. Aspirin may help prevent blood clots and heart attack.

Different goals may be required for specific individuals, including pregnant women, very old and very young people, and those with accompanying serious medical conditions. Treating children with type 2 diabetes depends on the severity of the condition at diagnosis. Metformin is approved for children. Formerly, only insulin was approved for treating children with diabetes.

Lifestyle Changes

A simple heart-healthy diet with weight control and exercise is important for people with pre-diabetes and may be sufficient for some people with type 2 diabetes. Some patients may be able to control their blood sugar with lifestyle measures and not need medication. Even for patients who do need to take drugs, lifestyle plays an essential role in controlling diabetes. Lifestyle changes can be difficult to initiate and sustain, however. Patients should surround themselves with a solid network of doctors, dietitians, family, and friends who understand both their condition and their needs.

Although there are many major dietary approaches for protecting health, experts generally agree on the following recommendations for heart protection:

Choose fiber-rich food (whole grains, legumes, nuts) as the main source of carbohydrates, along with a high intake of fresh fruits and vegetables. High fiber foods help improve blood glucose levels. Whole grain cereals, which are rich in both fiber and magnesium, may also help reduce the risk for diabetes.
Limit saturated fats (found mostly in animal products) to less than 7% of total daily calories and avoid trans fatty acids (found in hydrogenated fats and many commercial products and fast foods). Choose unsaturated fats (particularly omega-3 fatty acids found in vegetable and fish oils).
In selecting proteins, choose soy protein, poultry, and fish over meat. A 2006 study found that soy does not help improve cholesterol. However, experts still recommend it as a heart-healthy food choice.
Weight control, quitting smoking, and exercise are essential components of any diet program.

[See In-Depth Report #43: Heart-healthy diet.]

There is no such thing as a single diabetes diet. Patients should meet with a professional dietitian to plan an individualized diet within the general guidelines that takes into consideration their own health needs.

Healthy eating habits along with good control of blood glucose are the basic goals, and several good dietary methods are available to meet them. General dietary guidelines for diabetes recommend:

Carbohydrates should provide 45 - 65% of total daily calories. The type and amount of carbohydrate are both important. Best choices are vegetables, fruits, beans, and whole grains. These foods are also high in fiber. Patients with diabetes should monitor their carbohydrate intake either through carbohydrate counting or meal planning exchange lists.
Fats should provide 25 - 35% of daily calories. Monounsaturated (olive, peanut, canola oils; avocados; nuts) and omega-3 polyunsaturated (fish, flaxseed oil, walnuts) fats are the best types. Limit saturated fat (red meat, butter) to less than 7% of daily calories. Choose nonfat or low-fat dairy instead of whole milk products. Limit trans-fats (hydrogenated fat found in snack foods, fried foods, commercially baked goods) to less than 1% of total calories.
Protein should provide 12 - 20% of daily calories, although this may vary depending on a patient’s individual health requirements. Patients with kidney disease should limit protein intake to less than 10% of calories. Fish, soy, and poultry are better protein choices than red meat.

[For detailed information, including diabetic exchange lists and carbohydrate counting, see In-Depth Report #42: Diabetes diet.]

Being overweight is the number one risk factor for type 2 diabetes. Even modest weight loss can help prevent type 2 diabetes from developing. It can also help control or even stop progression of type 2 diabetes in people with the condition and reduce risk factors for heart disease. Patients should aim to lose weight if their body mass index (BMI) is 25 - 29 (overweight) or higher (obese).

The American Diabetes Association recommends that patients aim for a small but consistent weight loss of ½ - 1 pound per week. Most patients should follow a diet that supplies at least 1,000 - 1,200 kcal/day for women and 1,200 - 1,600 kcal/day for men.

Unfortunately, not only is weight loss difficult to sustain, but many of the oral medications used in type 2 diabetes cause weight gain as a side effect. For obese patients who cannot control weight using dietary measures alone, weight-loss drugs, such as orlistat (Xenical) or sibutramine (Meridia), may be helpful. Orlistat may have specific benefits for people with diabetes. It may not only help achieve weight but also improve glucose, cholesterol, and lipid levels. In 2007, the FDA approved a non-prescription form of orlistat (alli). [See In-Depth Report #53: Obesity.]

Sedentary habits, especially TV watching, are associated with significantly higher risks for obesity and type 2 diabetes. Regular exercise, even of moderate intensity (such as brisk walking), improves insulin sensitivity and may play a significant role in preventing type 2 diabetes -- regardless of weight loss. An important study reported a 58% lower risk for type 2 diabetes in adults who performed moderate exercise for as little as 2.5 hours a week.

Aerobic Exercise. Aerobic exercise has significant and particular benefits for people with diabetes. Regular aerobic exercise, even of moderate intensity, improves insulin sensitivity. People with diabetes are at particular risk for heart disease, so the heart-protective effects of aerobic exercise are especially important. Moderate exercise protects the heart in people with type 2 diabetes, even if they have no risk factors for heart disease other than diabetes itself.

For improving glycemic control, the American Diabetes Association recommends at least 150 minutes per week of moderate-intensity physical activity (50 - 70% of maximum heart rate) or at least 90 minutes per week of vigorous aerobic exercise (more than 70% of maximum heart rate). Exercise at least 3 days a week, and do not go more than 2 consecutive days without physical activity.

Strength Training. Strength training, which increases muscle and reduces fat, is also helpful for people with diabetes who are able to do this type of exercise. The American Diabetes Association recommends performing resistance exercise three times a week. Build up to three sets of 8 - 10 repetitions using weight that you cannot lift more than 8 - 10 times without developing fatigue. Be sure that your strength training targets all of the major muscle groups.

Exercise Precautions. The following are precautions for all people with diabetes, both type 1 and type 2:

Because people with diabetes are at higher than average risk for heart disease, they should always check with their doctors before undertaking vigorous exercise. For fastest results, frequent high-intensity (not high-impact) exercises are best for people who are cleared by their doctors. For people who have been sedentary or have other medical problems, lower-intensity exercises are recommended.
Strenuous strength training or high-impact exercise is not recommended for people with uncontrolled diabetes. Such exercises can strain weakened blood vessels in the eyes of patients with retinopathy. High-impact exercise may also injure blood vessels in the feet.

Patients who are taking medications that lower blood glucose, particularly insulin, should take special precautions before embarking on a workout program:

Monitor glucose levels before, during, and after workouts (glucose levels swing dramatically during exercise).
Avoid exercise if glucose levels are above 300 mg/dL or under 100 mg/dL.
Inject insulin in sites away from the muscles used during exercise; this can help avoid hypoglycemia.
Drink plenty of fluids before and during exercise; avoid alcohol, which increases the risk of hypoglycemia.
Insulin-dependent athletes may need to decrease insulin doses or take in more carbohydrates prior to exercise, but may need to take an extra dose of insulin after exercise (stress hormones released during exercise may increase blood glucose levels).
Wear good, protective footwear to help avoid injuries and wounds to the feet.
Some blood pressure drugs can interfere with exercise capacity. Patients who use blood pressure medication should consult their doctors on how to balance medications and exercise. Patients with high blood pressure should also aim to breathe as normally as possible during exercise. Holding the breath can increase blood pressure.

[See In-Depth Report #29: Exercise.]

According to the American Diabetes Association, people with diabetes should aim for preprandial (before eating) plasma glucose levels of 90 - 130 mg/dL and postprandial (after eating) plasma glucose levels less than 180 mg/dL. Hemoglobin A1C levels should be less than 7%.

Measuring Blood Glucose. In patients being treated with insulin or insulin-producing or sensitizing drugs, it is important to monitor blood glucose levels carefully to avoid hypoglycemia. Different goals may be required for specific individuals, including pregnant women, very old and very young people, and those with accompanying serious medical conditions.

Blood glucose levels are generally more stable in type 2 diabetes than in type 1, so experts usually recommend measuring blood levels only once or twice a day. For patients who have become insulin-dependent, more intensive monitoring is necessary. Usually, a drop of blood obtained by pricking the finger is applied to a chemically treated strip. The glucose level is read on a standard meter or a small, portable digital display device. For patients who have trouble controlling hypoglycemia (low blood sugar) or fluctuating blood sugar levels, continuous glucose sensor monitors are also available. In 2007, the FDA approved the STS-7 System, which continuously measures glucose levels for up to 7 days through a sensor inserted beneath the skin of the abdomen. Continuous glucose sensor monitors do not replace fingerstick glucose meters and test strips, but are used in combination with them. [See In-Depth Report #9: Diabetes - type 1.]

Measuring Hemoglobin A1C. Hemoglobin A1c (also called HbA1c , HA1c, or A1C) is measured periodically every 2 - 3 months to determine the average blood-sugar level over the lifespan of the red blood cell. Normal A1C levels should be below 7%. Home tests are also available for measuring A1C.

To monitor the amount of glucose within the blood a person with diabetes should test their blood regularly. The procedure is quite simple and can often be done at home.

Some research suggests that not getting enough sleep may impair insulin use and increase the risk for obesity. More research is needed, but it is always wise to improve sleep habits.

Medications

The American Heart Association now recommends that patients should aim for the following test results for intensive control of glucose levels:

Fasting plasma glucose concentrations below 110 mg/dL.
Glycolated hemoglobin (HbA1c) levels of less than 7%. Controlling HbA1c is the most important factor for reducing the risk of complications in patients with diabetes. According to one 2000 study, a 1% reduction in people with elevated glycolated hemoglobin levels lowers the risk for complications by 21%.

Evidence clearly supports strict glycemic control for reducing complications in the nervous system and blood vessels that occur in both type 1 and type 2 diabetes. Research shows that tight glucose control can help prevent heart disease and complications.

Managing risk factors for heart disease and stroke, particularly strict control of blood pressure, may be more important for improving survival than strict control of blood glucose levels for some patients. Such goals also seem to be more attainable for many patients with type 2 diabetes.

Oral Anti-Hyperglycemic Drugs. Many oral anti-hyperglycemic drugs are available to help patients with type 2 diabetes control their blood sugar levels. Most of these drugs are aimed at using or increasing sensitivity to the patient's own natural stores of insulin. Metformin is the only drug to date that achieves lower mortality rates. Oral type 2 diabetes drugs include:

Biguanides (metformin). Metformin increases tissue sensitivity to available insulin. Metformin also has beneficial effects on cholesterol, blood pressure, and clotting factors. It does not cause weight gain or hypoglycemia. Diarrhea and digestive problems are the most common side effects. Metformin produces lower mortality rates than other drugs, including insulin, and should be considered as first-line therapy for most patients with type 2 diabetes.
Sulfonylureas (glyburide, glipizide, glimepiride, repaglinide). Stimulate insulin secretion but can cause hypoglycemia more than other drugs.
DPP-4 inhibitors (sitagliptin). Also called gliptins, DPP-4 inhibitors were first approved in 2006 and are the newest class of oral diabetes drugs. Like metformin, they do not cause weight gain and have low risks for hypoglycemia.
Meglitinides (repaglinide, nateglinide). Stimulate insulin secretion. These newer drugs are better than sulfonylureas in controlling glucose spikes after meals.
Thiazolidinediones (pioglitazone and rosiglitazone). Reduce insulin resistance. These drugs improve cholesterol levels and may reduce the risk for blood clots. However, they can cause swelling from fluid build-up, which can worsen heart failure or even precipitate it. They may also injure the liver.
Alpha-glucosidase inhibitors (acarbose and miglitol). Slow intestinal absorption of carbohydrates. Have only modest effects on diabetes and have gastrointestinal side effects. Can slightly raise HDL (“good”) cholesterol levels.
Combinations of these drugs, particularly with metformin, are often used to increase effectiveness.

A 2007 review in the Annals of Internal Medicine compared these various classes of medications. The review found that older drugs -- such as metformin and sulfonylureas -- are less expensive than and work as well as newer diabetes drugs. In particular, the review cited metformin as a safe and effective drug because it does not cause weight gain or too-low blood sugar. Metformin can also help lower LDL (“bad”) cholesterol.

Injectable Anti-Hyperglycemic Drugs. In 2005, the FDA approved two new injectable drugs to help patients improve blood sugar control:

Exenatide (Byetta). Exenatide is the first drug in a new class of drugs called incretin mimetics. It lowers blood glucose levels by increasing insulin secretion. Exenatide is used in combination with oral antihyperglycemics, such as metformin or a sulfonylurea drug.
Pramlintide (Symlin). Pramlintide is a first-in-class drug that is a synthetic form of the hormone amylin. The drug is meant for patients who take insulin but still have difficulty controlling their glucose levels.

Insulin Replacement. Insulin replacement may be required when natural insulin reserves are depleted. It is typically started in combination with an oral drug. Eventually, some patients may need to go on full insulin replacement. In addition to injectable forms of insulin, an inhaled insulin product (Exubera) is now available.

Metformin (Glucophage) is a biguanide, which works by reducing glucose production in the liver and by making tissues more sensitive to insulin. Many experts recommend it as a first choice for most patients with type 2 diabetes who are insulin resistant, particularly if they are overweight. Metformin achieves lower mortality rates from diabetes and all causes than other drugs. In one comparison study, it achieved the lowest mortality rates (8%) compared to insulin (28%), a sulfonylurea (16%), and a thiazolidinedione (14%). Combinations with insulin-secreting drugs, other insulin-sensitizing drugs, or insulin itself are particularly effective.

Metformin does not cause hypoglycemia or add weight, so it is particularly well-suited for obese patients with type 2 diabetes. (In some studies, in fact, patients lost weight.) Metformin also appears to have beneficial effects on cholesterol and lipid levels and may help protect the heart. Some research has suggested that it significantly reduces the risk for heart attack. It is also the first choice for children who need oral drugs and is proving to be very effective for women with polycystic ovary syndrome and insulin resistance.

Side Effects. Side effects include:

A metallic taste
Gastrointestinal problems, including nausea, and diarrhea
Interference with absorption of vitamin B12 and folic acid, (which are important for protection against heart disease)
Rare reports of lactic acidosis, a potentially life-threatening condition, particularly in people with risk factors for it. Major studies, however, found no greater risk with metformin than with any of the other drugs used for type 2 diabetes.

Certain people should not use this drug, including anyone with heart failure or kidney or liver disease. It is rarely suitable for adults over age 80.

Sulfonylureas are oral drugs that stimulate the pancreas to release insulin. They are also first-line oral drugs. For adequate control of blood glucose levels, the drugs should be taken only 20 - 30 minutes before a meal. A number of brands are available, including chlorpropamide (Diabinese), tolazamide (Tolinase), acetohexamide (Dymelor), glipizide (Glucotrol), tolbutamide (Orinase), glyburide (Micronase), glimepiride (Amaryl), and repaglinide (Prandin).

Most patients can take sulfonylureas for 7 - 10 years before they lose effectiveness. Combinations with small amounts of insulin or with other oral anti-hyperglycemic drugs (such as metformin or a thiazolidinedione) may extend their benefits. A combination of glyburide and metformin in one pill (Glucovance) is available. Glucovance may be particularly beneficial for patients with unhealthy cholesterol levels and poor control of their blood sugar levels. Some doctors recommend the combination as first-line treatment.

An encouraging 2000 study of patients with severe type 2 diabetes reporting that combinations of insulin with either chlorpropamide or glipizide achieved better glucose control over the long term than insulin alone.

Side Effects and Complications. In general, sulfonylureas should not be used by women who are pregnant or nursing or by individuals who are allergic to sulfa drugs. Side effects may include:

Weight gain (some sulfonylureas, such as glimepiride, may produce less weight gain than others)
Water retention
Although sulfonylureas pose a lower risk for hypoglycemia than insulin does, the hypoglycemia produced by sulfonylureas may be especially prolonged and dangerous. The newer sulfonylureas, such as glimipiride, have much less risk of hypoglycemia than older sulfonylureas.
Some sulfonylureas may pose a slight risk for cardiac events.

Sulfonylureas interact with many other drugs, and patients should be sure to inform their doctor of any medications they are taking, including alternative or over-the-counter drugs.

Meglitinides stimulate beta cells to produce insulin. They include repaglinide (Prandin), nateglinide (Starlix), and mitiglinide. These drugs are rapidly metabolized and short-acting. If taken before every meal, they actually mimic the normal effects of insulin after eating. Patients, then, can vary their meal times with this drug. (Nateglinide appears to work more quickly and is shorter-acting than repaglinide). These drugs may be particularly helpful in combination with metformin or other drugs. They may also be a good choice for people with potential kidney problems.

Side Effects. Side effects include diarrhea and headache. As with the sulfonylureas, repaglinide poses a slightly increased risk for cardiac events. (Newer drugs, such as nateglinide, may pose less of a risk.) People with heart failure or liver disease should use them with caution and be monitored.

Thiazolidinediones, also known as peroxisome proliferator-activated receptor (PPAR) agonists, include rosiglitazone (Avandia) and pioglitazone (Actos). They improve insulin sensitivity by activating certain genes involved in fat synthesis and carbohydrate metabolism. These drugs are usually taken once or twice per day; however, it may take several days before the patient notices any results from them and several weeks before they take full effect. Thiazolidinediones are usually taken in combination with other oral drugs or insulin.

Side Effects. Thiazolidinediones can have serious side effects. They tend to increase fluid-build up, which can cause or worsen heart failure in some patients. Combinations with insulin increase the risk. They should not be used by patients with existing heart failure and should be used cautiously in those with risk factors for heart failure.

In 2007, a study published in the New England Journal of Medicine (NEJM) raised serious concerns that rosiglitazone may increase the risk of heart attack. The study reviewed 42 clinical trials of rosiglitazone. Results suggested that patients who took rosiglitazone were 43% more likely to have a heart attack, and 64% more likely to die from overall heart causes, than patients with diabetes who did not take the drug. A subsequent interim analysis in the NEJM found that while rosiglitazone was definitely associated with increased risk of heart failure, the data were insufficient to determine if the drug increases heart attack risk. The FDA has concluded that rosiglitazone may increase the risk of heart attack and will likely restrict its use. In 2007, a panel of experts from the Food and Drug Administration (FDA) agreed the drug increases the risk of heart attacks -- but concluded it should remain on the market. The panel did, however, recommend the FDA require rosiglitazone's maker to add warnings to the drug's label. Patients who take rosiglitazone, especially those who have heart disease or who are at high risk for heart attack, should discuss their treatment options with their doctors.

Thiazolidinediones may cause more weight gain than other diabetes medications or insulin. Any patient who experiences sudden weight gain, water retention, or shortness of breath should immediately call their doctor. These drugs have also been linked to increased risks for bone fracture.

There have been rare reports of rosiglitazone causing or worsening diabetic macular edema. This is an eye condition associated with diabetic retinopathy that causes swelling in the macular area of the retina. Symptoms include blurred vision and decreased color sensitivity. Most patients who had this side effect also had swelling in the feet and legs (peripheral edema). The condition resolved or improved when patients stopped taking the drug.

Thiazolidinediones can also cause liver damage. Patients who take these drugs should have their liver enzymes checked regularly.

Alpha-glucosidase inhibitors, including acarbose (Precose, Glucobay) and miglitol (Glyset), reduce glucose levels by interfering with the absorption of starch in the small intestine. Acarbose tends to lower insulin levels after meals, a particular advantage, since higher levels of insulin after meals are associated with an increased risk for heart disease. Some evidence suggests that early use of these drugs may reduce heart risk factors, including high blood pressure. A 2002 study of acarbose suggested that these drugs may possibly delay the development of type 2 diabetes in high-risk individuals. Alpha-glucosidase inhibitors are not as effective alone as other single oral drugs, but combinations, such as with metformin, insulin, or a sulfonylurea, increase their effectiveness.

Side Effects. These medications need to be taken with meals. Unfortunately, about a third of patients stop taking the drug because of flatulence and diarrhea, particularly after high-carbohydrate meals. The drug may also interfere with iron absorption.

Alpha-glucosidase inhibitors do not cause hypoglycemia when used alone, but combinations with other drugs do. In such cases, it is important that the patient receive a solution that contains glucose or lactose, not table sugar. This is because acarbose inhibits the breakdown of complex sugar and starches, which includes table sugar.

Incretin mimetics belong to a new class of drugs that help improve blood sugar control. Incretins include glucagon-like peptide-1 (GLP-1) inhibitors and DDP-4 inhibitors.

In 2005, the FDA approved exenatide (Byetta), the first GLP-1 inhibitor drug. Exenatide is an injectable drug that is a synthetic version of the hormone found in the saliva of the Gila monster, a venomous desert lizard. Exenatide is injected twice a day, 1 hour before morning and evening meals. It is prescribed for patients with type 2 diabetes who have not been able to control their glucose with metformin or a sulfonylurea drug. It can be taken in combination with these drugs or alone.

Side Effects. Exenatide stimulates insulin secretion only when blood sugar levels are high and so has less risk for causing low blood sugar (hypoglycemia) when it is taken alone. However, the risk for hypoglycemia increases when exenatide is taken along with a sulfonylurea drug. There does not appear to be a risk for hypoglycemia when exenatide is used along with metformin. Other side effects may include nausea, vomiting, and diarrhea.

A 2005 study compared exenatide to insulin for improving glucose control in patients taking metformin and a sulfonylurea. Both insulin and exenatide worked well for glucose control. Patients lost weight with exenatide and gained weight with insulin. However, patients who received exenatide had significantly more problems with nausea, vomiting, and diarrhea than those who received insulin.

Dipeptidyl peptidase-4 (DPP-4) inhibitors, also called gliptins, are the second class of incretin drugs. In October 2006, the FDA approved the first DPP-4 inhibitor -- sitagliptin (Januvia). It can be used alone or in combination with metformin or a thiazolidinedione drug. In April 2007, the FDA approved Janumet, which combines sitagliptin with metformin in one pill. Other DPP-4 drugs being studied include vildagliptin (Galvus) and saxagliptin.

DPP-4 inhibitors work in a similar way to GLP-1 inhibitors. However, unlike exenatide, which is given by injection, DPP-4 inhibitor drugs are taken as pills by mouth.

Like exenatide, DPP-4 inhibitors do not cause weight gain, have low risks for hypoglycemia, and have few severe side effects. The most common side effects include upper respiratory tract infection, sore throat, and diarrhea.

Insulin replacement is the best treatment for strict control of blood glucose and is required once natural insulin reserves are depleted. Because type 2 diabetes is progressive, most patients eventually require insulin, typically starting it in combination with an oral anti-hyperglycemic drug. However, when a single oral drug fails to control blood sugar it is not clear whether it is better to add insulin replacement or to add a second or third oral drug.

Some experts advocate using insulin as early as possible for optimal control. However, in patients who still have insulin reserves, there is concern that extra natural insulin will have adverse effects. Low blood sugar (hypoglycemia) and weight gain are the main side effects of insulin therapy. Some research suggests that insulin may also cause heart complications. A 2006 study reported that insulin therapy increases the risk of developing high blood pressure (hypertension). It is still not clear if insulin replacement improves survival rates compared to oral drugs, notably metformin.

One approach is to combine insulin with metformin, which achieves blood glucose control without added weight gain. Newer forms of insulin analogues, such as glargine, may be especially helpful for people with type 2 diabetes and reduce the risk for hypoglycemia.

Fortunately, studies to date have not reported any adverse cardiac effects in patients with type 2 diabetes who take insulin. In fact, insulin has been associated, in some cases, with improvement in heart risk factors. More research is needed to clarify these important issues.

Forms of Insulin. Experts are working toward administering insulin so that it closely mimics the daily pattern of insulin, which responds to blood sugar levels by surging after meals and then falling to a steady base level afterward. To achieve this, doctors may use two insulin types:

Fast-Acting Insulins for Surges. Insulin lispro and aspart are fast-acting insulins. They mimic insulin's response to food intake. They are taken before meals, and their short action reduces the risk for hypoglycemia afterward.
Slower Insulins for Base Levels. Intermediate forms (including NPH and lente) and long-acting forms (glargine, ultralente) were developed to provide a steady level of insulin throughout the day. To date, glargine (Lantus) seems to be the most successful in achieving this goal in type 2 diabetes.

In 2006, the FDA approved the first non-injected form of insulin. Exubera is an inhaled form of insulin. It is approved for adults but should not be used by patients who smoke or have quit smoking within the past 6 months. Patients with asthma, bronchitis, or emphysema should also not use inhaled insulin. Clinical trials indicate that Exubera can provide sustained blood sugar control over a 2-year period. Patients in the trials who took Exubera experienced half as much weight gain as those who took injected insulin. Scientists are also developing other types of non-injected insulin, including spray formulas.

In a 2005 trial, Exubera improved blood sugar control when it was added to or substituted for combination oral drug therapy (sulphonylurea and thiazolidenedione). However, as with other forms of insulin, Exubera caused more hypoglycemia and weight gain than the oral anti-hyperglycemic drugs.

Pramlintide (Symlin) is a new type of injectable drug that may help patients who take insulin but still need better blood sugar control. The FDA approved this drug in 2005. Pramlintide is a synthetic form of amylin, a hormone that is related to insulin. Pramlintide is used in combination with insulin to lower blood sugar levels in the 3 hours after meals.

[See In-Depth Report #9: Diabetes - type 1.]

Sodium Glucose Uptake Transporter 2 (SGLT-2) Inhibitors. SGLT-2 inhibitors are a new class of drug being investigated for treatment of type 2 diabetes. Preliminary trials for two of these drugs, dapagliflozin and serglifozin, have shown promising results in helping improve blood glucose control. The drugs are being tested in combination with metformin.

Various fraudulent products are often sold on the Internet as “cures” or treatments for diabetes. These dietary supplements have not been studied or approved. In 2006, the FDA and Federal Trade Commission (FTC) launched a crackdown on these scams. The FDA and FTC warn patients with diabetes not to be duped by bogus and unproven remedies.

Long-Term Complications

Patients with diabetes have higher mortality rates than people who do not have diabetes regardless of sex, age, or other factors. Heart disease and stroke are the leading causes of death in these patients. All lifestyle and medical efforts should be made to reduce the risk for these conditions.

People with type 2 diabetes are also at risk for nerve damage (neuropathy) and abnormalities in both small and large blood vessels (vascular injuries) that occur as part of the diabetic disease process. Such abnormalities produce complications over time in many organs and structures in the body. Although these complications tend to be more serious in type 1 diabetes, they still are of concern in type 2 diabetes. All people with diabetes should aim for fasting blood glucose levels of less than 110 mg/dL and hemoglobin HbA1C of less than 7%.

There are two important approaches to preventing complications from diabetes:

Intensive control of blood glucose and keeping glycosylated hemoglobin (HbA1c) levels below 7%. Tight blood glucose and HbA1c control can prevent complications due to vascular (blood vessel) abnormalities and nerve damage (neuropathy) that can cause major damage to organs, including the eyes, kidneys, and heart.
Managing risk factors for heart disease. Control of blood glucose also helps the heart, but its benefits occur over time. It is very important that people with diabetes control blood pressure, cholesterol levels, and other factors associated with heart disease.

Heart attacks account for 60% and strokes for 25% of deaths in patients with diabetes. Diabetes affects the heart in many ways:

Both type 1 and 2 diabetes speed the progression of atherosclerosis (hardening of the arteries). Diabetes can adversely affect blood lipid levels by lowering HDL ("good cholesterol") and increasing triglycerides. This can lead to coronary artery disease, heart attack, or stroke. According to a 2007 study, the risk of stroke doubles within 5 years of type 2 diabetes diagnosis.
Impaired nerve function (neuropathy) associated with diabetes also causes heart abnormalities. Some experts estimate that the mortality rates from neuropathy-related heart conditions range between 15 - 53%.
Women with diabetes are at particularly high risk for heart problems. A 2007 study indicated that while progress has been made in reducing mortality rates among men with diabetes, women with diabetes continue to face a high risk of death from heart disease and overall causes.

Tight blood sugar control may help protect blood vessels and reduce the risk for blood clotting. It is still not known whether intensive control will have a major protective effect on the heart, however. People with diabetes must be sure to use other measures as well to protect the heart.

Aspirin for Reducing the Risk for Blood Clots. Taking a daily aspirin (75 - 162 mg/day) reduces the risk for blood clotting and may help protect against heart attacks and heart disease. In a 2000 study, low-dose aspirin was associated with a 30% lower risk for death from heart disease in adults with type 2 diabetes.

Controlling Blood Pressure. Strict control of blood pressure is critical for preventing complications of diabetes and has proven to improve survival rates. Patients should strive for blood pressure levels of less than 130/80 mm Hg (systolic/diastolic). (Controlling systolic pressure may be especially important for reducing the risk for kidney complications.)

Dozens of anti-hypertensive drugs are available. Most fall into the following categories:

Diuretics rid the body of extra sodium (salt) and water. There are three main types of diuretics: Potassium-sparing, thiazide, and loop.
Angiotensin-converting enzyme (ACE) inhibitors reduce the production of angiotensin, a chemical that causes arteries to narrow.
Angiotensin-receptor blockers (ARBs) block angiotensin.
Beta-blockers block the effects of adrenaline and ease the heart’s pumping action.
Calcium-channel blockers (CCBs) decrease the contractions of the heart and widen blood vessels.

The American Diabetes Association (ADA) recommends any of these classes of drugs as first-line treatment for hypertension. New research suggests, however, that beta-blockers are less effective at preventing strokes and heart attacks than other types of blood pressure medications. Many patients require more than one type of drug to control blood pressure. For patients with diabetes who have microalbuminuria, the ADA strongly recommends ACE inhibitors or ARBs. Microalbuminuria is an accumulation of protein in the blood, which can signal the onset of kidney disease (nephropathy).

Anti-hypertensive drugs that block or reduce angiotensin are the first option for many people with diabetes. Angiotensin is a natural chemical that influences all aspects of blood pressure control and also interferes with insulin's normal metabolic signaling. In fact, angiotensin may be the common factor linking diabetes and high blood pressure.

The 2005 landmark Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) indicated that a thiazide-type diuretic works as well as an ACE inhibitor or CCB for patients with diabetes and high blood pressure. Compared with ACE inhibitors or CCBs, diuretics appeared to be better at lowering systolic blood pressure and preventing heart failure. In addition, the trial suggested that diuretics are especially helpful for African-Americans, by offering greater protection than ACE inhibitors or CCBS in preventing strokes.

Several 2006 studies suggested that anti-hypertensive drugs may increase the risk of developing diabetes. One study found more risk for thiazide diuretics and beta-blockers than ACE inhibitors and CCBs. Another study indicated that the ACE inhibitor ramipril had a lower risk of causing diabetes in African-Americans than a CCB or beta-blocker. A 2007 review in the Lancet also found a higher risk for new-onset diabetes with beta-blockers and diuretics, a medium risk with CCBs, and the lowest risk with ARBs and ACE inhibitors.

Research in this subject is important for patients with pre-diabetes who have high blood pressure. Results of future research may help doctors decide which treatment is most appropriate for patients with high blood pressure who are at high risk for diabetes. [See In-Depth Report #14: High blood pressure.]

Improving Cholesterol and Lipid Levels. Abnormal cholesterol and lipid levels are common in diabetes. High LDL (“bad”) cholesterol should always be lowered, but people with diabetes also often have additional harmful imbalances including low HDL (“good”) cholesterol and high triglycerides. Patients should aim for LDL levels below 100 mg/dL, HDL levels over 50 mg/dL and triglyceride levels below 150 mg/dL. Patients with diabetes and existing heart disease should strive for even lower LDL levels; the American Diabetes Association recommends LDL levels below 70 mg/dL for these patients.

Statins are the best cholesterol-lowering drugs. They include atorvastatin (Lipitor), lovastatin (Mevacor, generics), pravastatin (Pravachol), simvastatin (Zocor, generics), fluvastatin (Lescol), and rosuvastatin (Crestor). These drugs are very effective for lowering LDL cholesterol levels. Recent studies indicate that aggressive high-dose statin therapy may be an important treatment approach for high-risk patients who need to substantially lower their LDL levels. A 2006 study found that patients with diabetes and heart disease who were treated with 80 mg daily of atorvastatin had a 25% lower risk of heart attack and stroke than patients who received the standard 10 mg daily dose.

The primary safety concern with statins has involved myopathy, an uncommon condition that can cause muscle damage and, in some cases, muscle and joint pain. A specific myopathy called rhabdomyolysis can lead to kidney failure. People with diabetes and risk factors for myopathy should be monitored for muscle symptoms

Although lowering LDL is beneficial, statins are not as effective as other medications -- such as fibrates, niacin, ezetimbe, or bile acid sequesters -- in addressing HDL and triglyceride imbalances. This is a common problem in type 2 diabetes. Combinations of statins with one of these drugs may be helpful for people with diabetes who have heart disease, low HDL, and near-normal LDL levels. Although combinations of statins and fibrates or niacin increase the risk of myopathy, both combinations are considered safe if used with extra care. Research presented at the 2007 annual meeting of the American Diabetes Association suggested that statins and fibrates may also help reduce the risk of developing peripheral neuropathy, the diabetes-associated nerve damage that can lead to loss of sensation in the feet.

Gemfibrozil (Lopid) and fenofibrate (Tricor) are usually the first choice for fibrate drugs. Niacin has the most favorable effect on raising HDL and lowering triglycerides of all the cholesterol drugs. However, about 30% of patients who take high-dose niacin experience increased blood glucose levels. Moderate doses of niacin can achieve lipid control without causing serious blood glucose problems. [See In-Depth Report #23: Cholesterol.]

Kidney disease (nephropathy) is a very serious complication of diabetes. With this condition, the tiny filters in the kidney (called glomeruli) become damaged and leak protein into the urine. Over time this can lead to kidney failure. Urine tests showing microalbuminuria (small amounts of protein in the urine) are important markers for kidney damage.

Prevention and Treatment of Nephropathy. Tight control of blood sugar and blood pressure is essential for preventing the onset of kidney disease. Long-term studies report that strict control of these two conditions produces a 60% reduction in new cases of nephropathy and a delay in progression of the disease. ACE inhibitors and ARBs, two classes of blood pressure medications, are very helpful for preventing or slowing the progression of diabetic kidney disease.

A doctor may recommend a low-protein diet for patients whose kidney disease is progressing despite tight blood sugar and blood pressure control. Protein-restricted diets can help slow disease progression and delay the onset of end-stage renal disease (kidney failure). However, patients with end-stage renal disease who are on dialysis generally require higher amounts of protein. [See In-Depth Report #42: Diabetes diet.]

Diabetic nephropathy occurs in about 20 - 40% of patients with diabetes and is the leading cause of end-stage renal disease. If the kidneys fail, dialysis is required. Symptoms of kidney failure may include swelling in the feet and ankles, itching, fatigue, and pale skin color.

Anemia is a common complication of end-stage kidney disease. Patients on dialysis usually require injections of erythropoiesis-stimulating drugs to increase red blood cell counts and control anemia. Dosing target levels of erythropoiesis-stimulating drugs are controversial, especially for patients with chronic kidney disease. In 2006, two important New England Journal of Medicine studies indicated that aggressive dosing to completely normalize hemoglobin levels does not work better than standard dosing that only partially corrects anemia.

In 2007, the FDA issued new warnings on darbepoetin alfa (Aranesp) and epoetin alfa (Epogen and Procrit). The warnings describe an increased risk with blood clots, strokes, and heart attacks in patients with end-stage kidney disease when these drugs were given at higher than recommended doses. The FDA has set new dosing and hemoglobin target levels for these drugs.

Another controversy surrounding erythropoiesis-stimulating drugs concerns their overuse at dialysis centers. A 2007 study in the Journal of the American Medical Association suggested that large, for-profit dialysis centers tend to administer higher-than-appropriate doses of these drugs compared to nonprofit facilities. The study suggested that for-profit centers are giving higher doses for financial, not medical, reasons.

The FDA recommends that patients with end-stage kidney disease who receive erythropoiesis-stimulating drugs should:

Maintain hemoglobin levels that do not exceed 12 g/dL
Receive frequent blood tests to monitor hemoglobin levels
Contact their doctors if they experience such symptoms as shortness of breath, pain, swelling in the legs, or increases in blood pressure

[See In-Depth Report #57: Anemia.]

Click the icon to see an image of the pancreas and kidneys.

Diabetes reduces or distorts nerve function, causing a condition called neuropathy. Neuropathy refers to a group of disorders that affect nerves. The two main types of neuropathy are:

Peripheral (affects nerves in the toes, feet, legs, hand, and arms)
Autonomic (affects nerves that help regulate digestive, bowel, bladder, heart, and sexual function)

Peripheral neuropathy particularly affects sensation. It is a common complication that affects nearly half of people with type 1 or type 2 diabetes after 25 years. The most serious consequences of neuropathy occur in the legs and feet and pose a risk for ulcers and, in very severe cases, amputation. Peripheral neuropathy usually starts in the fingers and toes and moves up to the arms and legs (called a stocking-glove distribution). Symptoms include:

Tingling
Weakness
Burning sensations
Loss of the sense of warm or cold
Numbness (if the nerves are severely damaged, the patient may be unaware that a blister or minor wound has become infected)
Deep pain

Autonomic neuropathy can cause digestive problems (constipation, diarrhea, nausea, vomiting), bladder infections, and erectile dysfunction. In some cases, neuropathy may mask angina, the chest pain warning for heart disease and heart attack. Patients with diabetes should be aware of other warning signs of a heart attack, including sudden fatigue, sweating, shortness of breath, nausea, and vomiting.

Blood sugar control is the only treatment for neuropathy. Studies show that tight control of blood glucose levels delays the onset and slows progression of neuropathy. A 2005 study also suggested that heart disease risk factors can increase the likelihood of developing neuropathy. Lowering triglycerides, losing weight, reducing blood pressure, and quitting smoking may help prevent the onset of neuropathy.

Prevention of Neuropathy. Patients with type 2 diabetes should receive regular screenings for loss of sensation in feet and other signs of neuropathy. A 2007 study suggested that statin and fibrate drugs, which are used to control cholesterol, may help protect against diabetic peripheral neuropathy.

Pain Relief for Peripheral Neuropathy. A number of different drugs are used for peripheral neuropathy pain relief. They include:

Nonprescription analgesics such as aspirin, acetaminophen, and non-steroidal anti-inflammatory drugs (NSAIDs). (Patients with stomach or kidney problems should check with their doctors before using these drugs.)
Prescription painkillers, such as tramadol (Ultram). Tramadol is a drug that is similar to opioids. It can help relieve pain but has significant side effects, including nausea, constipation, and headache.
Topical medications, particularly capsaicin (the active ingredient in hot peppers), are applied to the skin to relieve minor local pain. A 5% lidocaine patch has also shown good results in clinical trials.
Tricyclic antidepressants, such as amitriptyline (Elavil) or doxepin (Sinequan), are effective in reducing pain from neuropathy in up to 75% of patients. A combination of doxepin and capsaicin (applied to the skin) may be particularly beneficial. Unfortunately, tricyclics may cause heart rhythm problems.
Duloxetine (Cymbalta) is a serotonin and norepinephrine reuptake inhibitor, a newer type of antidepressant, which was approved in 2004 for treatment of pain associated with diabetic peripheral neuropathy.
The anti-convulsant drug pregabalin (Lyrica) was approved in 2004 for neuropathic pain management. It is classified as a controlled substance (like narcotics), which indicates a potential risk for abuse. Other anti-seizure drugs used for peripheral neuropathy pain relief include gabapentin (Neurontin) and valproate (Depakote).

Treatments under investigation include acetyl-l-carnitine and intravenous alpha-lipoic acid. Patients may also benefit from transcutaneous electrostimulation (TENS), a treatment that involves administering mild electrical pulses to painful areas. Alternative treatments such as hypnosis, biofeedback, relaxation techniques, and acupuncture have helped some patients manage pain. Doctors also recommend lifestyle measures such as walking and wearing elastic stockings.

Treatments for Other Complications of Neuropathy. Neuropathy also impacts other functions, and treatments are needed to reduce their effects. If diabetes affects the nerves in the autonomic nervous system, then abnormalities of blood pressure control and bowel and bladder function may occur. Erythromycin, domperidone (Motilium), or metoclopramide (Reglan) may be used to relieve delayed stomach emptying caused by neuropathy.

Erectile dysfunction is also associated with neuropathy. Evidence shows that phosphodiesterase type 5 (PDE-5) drugs, such as sildenafil (Viagra), vardenafil (Levitra), and tadalafil (Cialis), are safe and effective, at least in the short term, for patients with diabetes. Typical side effects are minimal but may include headache, flushing, and upper respiratory tract and flu-like symptoms.

Perhaps the most serious consequences of diabetic neuropathy occur in the lower limbs. An estimated 15% of patients with diabetes experience serious foot problems. They are the leading cause of hospitalizations for these patients.

Diabetes is responsible for more than half of all lower limb amputations performed in the U.S. Each year there are about 88,000 non-injury amputations, 50 - 75% of them due to diabetes. The number is increasing as the prevalence in diabetes type 2 rises. According to a 2005 study in the Lancet, every 30 seconds someone in the world receives a lower limb amputation due to diabetes. About 85% of amputations start with foot ulcers, which develop in about 12% of people with diabetes.

In general, foot ulcers develop from infections, such as those resulting from blood vessel injury. A 2006 study reported that people with diabetes who develop foot infections are 155 times more likely to have an amputation than people who did not develop infections. Foot infections often develop from injuries. Even minor infections can develop into severe complications. Numbness from nerve damage, which is common in diabetes, compounds the danger since the patient may not be aware of injuries. About one-third of foot ulcers occur on the big toe.

A 2003 government survey found that those at higher risk for foot ulcers tend to be people with diabetes who are overweight, smokers, and those with a long history of diabetes. People who have the disease for more than 20 years and are insulin-dependent are at the highest risk. Related conditions that put people at risk include peripheral neuropathy, peripheral artery disease, foot deformities, and a history of ulcers. [See In-Depth Report #102: Peripheral artery disease and intermittent claudication.]

Charcot Foot. Charcot foot or Charcot joint (medically referred to as neuropathic arthropathy) occurs in about 2.5% of people with diabetes. Early changes appear like an infection, with the foot becoming swollen, red, and warm. A seriously affected foot can become deformed. The bones may crack, splinter, and erode, and the joints may shift, change shape, and become unstable. It typically develops in people who have neuropathy to the extent that they cannot feel sensation in the foot and are not aware of an existing injury. Instead of resting an injured foot or seeking medical help, the patient often continues normal activity, causing further damage.

Charcot foot is initially treated with strict immobilization of the foot and ankle; some centers use a cast that allows the patient to move and still protects the foot. A 2001 study in the U.K. concluded that a single dose of pamidronate, a bisphosphonate, reduces bone turnover, symptoms, and disease activity. When the acute phase has passed, patients usually need lifelong protection of the foot using a brace initially and custom footwear.

Measures to Prevent Foot Ulcers. Preventive foot care can significantly reduce the risk of ulcers and amputation. Some tips for preventing problems include:

Patients should inspect their feet daily and watch for changes in color or texture, odor, and firm or hardened areas, which may indicate infection and potential ulcers.
When washing the feet, the water should be warm (not hot), and the feet and areas between the toes should be thoroughly dried afterward. Check water temperature with the hand or a thermometer before stepping in.
Moisturizers should be applied, but not between the toes.
Corns and calluses should be gently pumiced and toenails trimmed short and the edges filed to avoid cutting adjacent toes.
Patients should not use medicated pads or try to shave the corns or calluses themselves.
Well-fitting footwear is very important. People should be sure the shoe is wide enough; according to a 2001 study, 30% of patients with diabetes wear shoes that are too narrow. Patients should also avoid high heels, sandals, thongs, and going barefoot. Shoes with a rocker sole reduce pressure under the heel and front of the foot by 35 - 65% and may be particularly helpful. Custom-molded boots increase the surface area over which foot pressure is distributed. This reduces stress on the ulcers and allows them to heal.
Shoes should be changed often during the day.
Wear socks, particularly with extra padding (which can be specially purchased).
Patients should avoid tight stockings or any clothing that constricts the legs and feet.
Foot pain, numbness, or tingling is worse at night; diphenhydramine (Benadryl) may help.
A specialist in foot care should be consulted for any problems.

People with diabetes are prone to foot problems because the disease can cause damage to the blood vessels and nerves, which may result in decreased ability to sense trauma to the foot. The immune system is also altered, so that the patient cannot efficiently fight infection.

Treating Foot Ulcers in Diabetes. About one-third of foot ulcers will heal within 20 weeks with good wound care treatments. Treatments include:

Antibiotics are generally given. In some cases, hospitalization and intravenous antibiotics for up to 28 days may be needed for severe foot ulcers.
In virtually all cases, wound care requires debridement, which is the removal of injured tissue until only healthy tissue remains. Debridement may be accomplished using chemical (enzymes), surgical, or mechanical (irrigation) means.
Hydrogels (Nu-Gel, Intrasite Gel, Scherisorb, Clearsite, Duoderm, Geliperm) are helpful in healing ulcers and are noninvasive and soothing.
Felted foam may be helpful in healing ulcers on the sole of the foot. Felted foam uses a multi-layered foam pad over the bottom of the foot with an opening over the ulcer.

Other Treatments for Foot Ulcers. Doctors are also using or investigating other treatments to heal ulcers. These include:

Administering hyperbaric oxygen (oxygen given at high pressure) is showing promise in promoting healing. In one study, patients who had had ulcers that had not responded to treatment for over 3 months received daily treatments that lasted 90 minutes for 2 weeks. About 15 days after completion, patients who received oxygen had significant reduction in ulcers, sometimes with complete healing. Other studies are also demonstrating good results.
Monochromatic near-infrared photo energy (MIRE) uses light therapy to improve sensation in the feet of patients with peripheral neuropathy.
Total-contact casting (TCC) uses a cast that is designed to match the exact contour of the foot and to distribute weight along the entire length of the foot. It is usually changed weekly. It may be helpful for ulcer healing and for Charcot foot. Although it is very effective in healing ulcers, recurrence is common.

Diabetes accounts for 12,000 - 24,000 of new cases of blindness annually and is the leading cause of new cases of blindness in adults age 20 - 74. The most common eye disorder in diabetes is retinopathy. People with diabetes are also at higher risk for developing cataracts and certain types of glaucoma, such as primary-open angle glaucoma (POAG). The risk for POAG is especially high for women with type 2 diabetes. [See In-Depth Report #26: Cataracts and In-Depth Report #25: Glaucoma.]

Description of Retinopathy. Retinopathy is a condition in which the retina in the eye becomes damaged. The two primary abnormalities that occur are a weakening of the blood vessels in the retina and the obstruction in the capillaries -- probably from very tiny blood clots. Retinopathy generally occurs in one or two phases:

Click the icon to see an image of diabetic retinopathy.

The early and more common type of this disorder is called nonproliferative or background retinopathy. The blood vessels in the retina are abnormally weakened. They rupture and leak, and waxy areas may form. If these processes affect the central portion of the retina, swelling may occur, causing reduced or blurred vision.
If the capillaries become blocked and blood flow is cut off, soft, "woolly" areas may develop in the retina's nerve layer. These woolly areas may signal the development of proliferative retinopathy. Often there are no symptoms of progressing retinopathy. In this more severe condition, new abnormal blood vessels form and grow on the surface of the retina. They may spread into the cavity of the eye or bleed into the back of the eye. Major hemorrhage or retinal detachment can result, causing severe visual loss or blindness. The sensation of seeing flashing lights may indicate retinal detachment.

Click the icon to see an animation on diabetic retinopathy.

According to a 2003 study, about 40% of young adults with type 1 diabetes had developed retinopathy within 10 years of diagnosis. (Although this rate is high, it is significantly lower than in previous years when blood glucose control was not as strict.) The risk is lower in patients with type 2 diabetes, although in one study over 20% had signs of retinopathy 6 years after diagnosis. Patients who are newly diagnosed with type 2 diabetes should get a comprehensive eye examination, including dilation. In general, all patients with diabetes should have a yearly eye examination. Patients with no signs of retinal damage or low risk factors for retinopathy may only require screening every 2 - 3 years.

Prevention of Retinopathy. Fortunately, severe and even moderate vision loss is largely preventable with tight control of blood glucose levels. (Intense glucose control can cause early worsening of retinopathy, although this is nearly always counterbalanced by long-term benefits.) Tight control of blood pressure can also help protect against retinopathy. Aspirin therapy does not help prevent retinopathy.

Treatment of Retinopathy. Patients with severe diabetic retinopathy or macular edema (swelling of the retina) should be sure to see an eye specialist who is experienced in the management and treatment of diabetic retinopathy. Once damage to the eye develops, laser eye surgery may be needed. Laser surgery can help reduce vision loss in high-risk patients.

Studies indicate that patients with type 2 diabetes face a higher than average risk of developing dementia caused either by Alzheimer's disease or problems in blood vessels in the brain. Problems in attention and memory can occur even in people under age 55 who have had diabetes for a number of years. In one study of people with type 1 diabetes, high glucose levels (hyperglycemia) were associated with slower brain function, including less verbal fluency and slower ability to do mental arithmetic.

Respiratory Infections. People with diabetes face a higher risk for influenza and its complications, including pneumonia, possibly because the disorder neutralizes the effects of protective proteins on the surface of the lungs. In fact, deaths among people with diabetes increase by 5 - 15% during flu epidemics, and they are six times more likely to be hospitalized with complications from flu than nondiabetic patients who have flu. Everyone with diabetes should have annual influenza vaccinations and a vaccination against pneumococcal pneumonia.

Urinary Tract Infections. Women with diabetes face a significantly higher risk for urinary tract infections, which are likely to be more complicated and difficult to treat than in the general population.

Diabetes doubles the risk for depression. Furthermore, according to one study, depression, in turn, increases the risk for hyperglycemia and complications of diabetes. Restoring mental health, both through medication and psychotherapy, not only improves quality of life but may help patients control their blood sugar levels.

Diabetes changes bone quality and density, but the effects differ, depending on type:

Type 1 diabetes is associated with a slightly reduced bone density, putting patients at risk for osteoporosis and possibly fractures. The best medications for bone loss in patients with diabetes are bisphosphonates, such as alendronate (Fosamax) and risedronate (Actonel). They not only help prevent bone loss but may even reduce daily insulin requirements in patients taking insulin. [See In-Depth Report #18: Osteoporosis.]
Type 2 diabetes, on the other hand, is associated with an increased bone density but is also associated with fractures. In such cases, the bone quality itself may be impaired.

Older patients with either type of diabetes are at risk for falling, which compounds the risk for fracture.

Diabetes increases the risk for other conditions, including:

Hearing loss
Periodontal disease
Carpal tunnel syndrome
Nonalcoholic fatty liver disease, also called nonalcoholic steatohepatitis (NASH), a particular danger for people who are obese
Colorectal cancer
Uterine cancer

Emergency Complications

People with diabetes who need to intensively control glucose levels are at risk for low blood sugar (hypoglycemia). Hypoglycemia, also called insulin shock, develops if blood sugar levels fall below normal. It may also be caused by insufficient intake of food, excess exercise, or alcohol intake. The condition is usually manageable, but occasionally it can be severe or even life threatening, particularly if the patient fails to recognize the symptoms. Mild hypoglycemia is common among people with type 2 diabetes, but severe episodes are rare, even among those who are taking insulin. Still, all patients who intensively control blood sugar (glucose) levels should be aware of warning symptoms.

Risk Factors for Severe Hypoglycemia. People at highest risk for severe hypoglycemia are those who intensively control blood glucose and also have one or more of the following conditions:

Long-term diabetes
Less education on their condition
A previous history of severe hypoglycemia
Hypoglycemia unawareness

Hypoglycemia unawareness is a condition in which people become insensitive to hypoglycemic symptoms. It affects about 25% of patients who use insulin, nearly always people with type 1 diabetes. In such cases, hypoglycemia appears suddenly, without warning, and can escalate to a severe level. Even a single recent episode of hypoglycemia may make it more difficult to detect the next episode. With vigilant monitoring and by rigorously avoiding low blood glucose levels, patients can often regain the ability to sense the symptoms. However, even very careful testing may fail to detect a problem, particularly one that occurs during sleep.

Symptoms. Mild hypoglycemia symptoms usually occur at moderately low and easily correctable levels of blood glucose. They include:

Sweating
Trembling
Hunger
Rapid heartbeat

Severely low blood glucose levels can cause neurologic symptoms, such as:

Confusion
Weakness
Disorientation
Combativeness
In rare and worst cases, coma, seizure, and death

Preventive Measures. The following tips may help avoid hypoglycemia or prepare for attacks:

Patients are at highest risk for hypoglycemia at night. Bedtime snacks may be helpful.
Patients who intensively control their blood sugar should monitor blood levels as often as possible, four times or more per day. This is particularly important for patients with hypoglycemia unawareness.
In adults, it is also particularly critical to monitor blood glucose levels before driving, when hypoglycemia can be very hazardous.
Patients who use medications that put them at risk for hypoglycemia should always carry hard candy, juice, sugar packets, or commercially available glucose substitutes designed for individuals with diabetes.

Family and friends should be aware of the symptoms and be prepared:

If the patient is helpless (but not unconscious), family or friends should administer three to five pieces of hard candy, two to three packets of sugar, half a cup (four ounces) of fruit juice, or a commercially available glucose solution.
If there is inadequate response within 15 minutes, additional oral sugar should be provided or the patient should receive emergency medical treatment, including intravenous administration of glucose.
Family members and friends can learn to inject glucagon, a hormone, which, in contrast to insulin, raises blood glucose.

Click the icon to see a glucagon kit.

Diabetic ketoacidosis (DKA) is a life-threatening complication caused by insulin depletion. Until recently, it was a complication almost exclusively of type 1 diabetes. In such cases, it is nearly always due to noncompliance with insulin treatments. However, DKA is being reported increasingly in type 2 diabetes, especially among Hispanic- and African-Americans. It is not clear what causes total insulin depletion in these patients. Researchers are trying to learn which individuals are at particular risk.

Diabetic ketoacidosis often develop as follows:

The process is usually triggered in insulin-deficient patients by a stressful event, most often pneumonia or urinary tract infections. Other triggers include alcohol abuse, physical injury, pulmonary embolism, heart attacks, or other illnesses.
Severely low insulin levels cause excessive amounts of glucose in the bloodstream (hyperglycemia).
Fat breakdown then accelerates and increases the production of fatty acids.
These fatty acids are converted into chemicals called ketone bodies, which are toxic at high levels.

Symptoms and complications may include:

Nausea and vomiting
Abnormally deep and rapid breathing with frequent sighing
Rapid heartbeat
If the condition persists, coma and, eventually, death, may occur; however, over the past 20 years, death from DKA has decreased to about 2% of all cases.
Other serious complications from DKA include aspiration pneumonia and adult respiratory distress syndrome.

Life-saving treatment uses rapid rehydration with a saline solution followed by low-dose insulin and potassium replacement.

Resources

www.diabetes.org -- American Diabetes Association
www.niddk.nih.gov -- National Institute of Diabetes and Digestive and Kidney Diseases
www.americanheart.org -- American Heart Association
www.kidney.org -- National Kidney Foundation
www.nei.nih.gov -- National Eye Institute
www.medicalert.org -- Medic Alert
www.eatright.org -- American Dietetic Association
http://limaye.ecri.org -- Limaye Center

References

American Diabetes Association (ADA). Standards of medical care in diabetes. IV. Prevention/delay of type 2 diabetes. Diabetes Care. 2007 Jan;30(Suppl 1):S7-8.

American Diabetes Association (ADA). Standards of medical care in diabetes. V. Diabetes care. Diabetes Care. 2007 Jan;30(Suppl 1):S8-15.

American Diabetes Association (ADA). Standards of medical care in diabetes. VI. Prevention and management of diabetes complications. Diabetes Care. 2007 Jan;30(Suppl 1):S15-24.

Amori RE, Lau J, Pittas AG. Efficacy and safety of incretin therapy in type 2 diabetes: systematic review and meta-analysis. JAMA. 2007 July 11;298:194-206.

Aschner P, Kipnes MS, Lunceford JK, Sanchez M, Mickel C, Williams-Herman DE, et al. Effect of the dipeptidyl peptidase-4 inhibitor sitagliptin as monotherapy on glycemic control in patients with type 2 diabetes. Diabetes Care. 2006 Dec;29(12):2632-7.

Bolen S, Feldman L, Vassy J, Wilson L, Yeh H-C, Marinopoulos S, et al. Systematic review: comparative effectiveness and safety of oral medications for type 2 diabetes mellitus. Ann Intern Med. 2007 Jul 17; 147(6). [Epub ahead of print]

Carnethon MR, Biggs ML, Barzilay JI, Smith NL, Vaccarino V, Bertoni AG, et al. Longitudinal association between depressive symptoms and incident type 2 diabetes mellitus in older adults: the cardiovascular health study. Arch Intern Med. 2007 Apr 23;167(:802-7.

Charbonnel B, Karasik A, Liu J, Wu M, Meininger G; Sitagliptin Study 020 Group. Efficacy and safety of the dipeptidyl peptidase-4 inhibitor sitagliptin added to ongoing metformin therapy in patients with type 2 diabetes inadequately controlled with metformin alone. Diabetes Care. 2006 Dec;29(12):2638-43.

Drueke TB, Locatelli F, Clyne N, Eckardt KU, Macdougall IC, Tsakiris D, et al. Normalization of hemoglobin level in patients with chronic kidney disease and anemia. N Engl J Med. 2006 Nov 16;355(20):2071-84.

Elliott WJ, Meyer PM. Incident diabetes in clinical trials of antihypertensive drugs: a network meta-analysis. Lancet. 2007 Jan 20;369(9557):201-7.

Florez JC, Jablonski KA, Bayley N, Pollin TI, de Bakker PI, Shuldiner AR, et al. TCF7L2 polymorphisms and progression to diabetes in the Diabetes Prevention Program. N Engl J Med. 2006 Jul 20;355(3):241-50.

Frayling TM, Timpson NJ, Weedon MN, Zeggini E, Freathy RM, Lindgren CM, et al. A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity. Science. 2007 May 11;316(5826):889-94. Epub 2007 Apr 12.

Gillies CL, Abrams KR, Lambert PC, Cooper NJ, Sutton AJ, Hsu RT, et al. Pharmacological and lifestyle interventions to prevent or delay type 2 diabetes in people with impaired glucose tolerance: systematic review and meta-analysis. BMJ. 2007 Feb 10;334(7588):299. Epub 2007 Jan 19.

Grant SF, Thorleifsson G, Reynisdottir I, Benediktsson R, Manolescu A, Sainz J, et al. Variant of transcription factor 7-like 2 (TCF7L2) gene confers risk of type 2 diabetes. Nat Genet. 2006 Mar;38(3):320-3. Epub 2006 Jan 15.

Gregg EW, Gu Q, Cheng YJ, Narayan KM, Cowie CC. Mortality trends in men and women with diabetes, 1971-2000. Ann Intern Med. 2007 Jun 18; [Epub ahead of print]

Home PD, Pocock SJ, Beck-Nielsen H, Gomis R, Hanefeld M, Jones NP, et al. Rosiglitazone evaluated for cardiovascular outcomes--an interim analysis. N Engl J Med. 2007 Jul 5;357(1):28-38. Epub 2007 Jun 5.

Jeerakathil T, Johnson JA, Simpson SH, Majumdar SR. Short-term risk for stroke is doubled in persons with newly treated type 2 diabetes compared with persons without diabetes: a population-based cohort study. Stroke. 2007 Jun;38(6):1739-43. Epub 2007 May 3.

Lee AJ, Hiscock RJ, Wein P, Walker SP, Permezel M. Gestational diabetes mellitus: clinical predictors and long-term risk of developing type 2 diabetes: a retrospective cohort study using survival analysis. Diabetes Care. 2007 Apr;30(4):878-83.

Pasquale LR, Kang JH, Manson JE, Willett WC, Rosner BA, Hankinson SE. Prospective study of type 2 diabetes mellitus and risk of primary open-angle glaucoma in women. Ophthalmology. 2006 Jul;113(7):1081-6. Epub 2006 Jun 6.

Nissen SE, Wolski K. Effect of rosiglitazone on the risk of myocardial infarction and death from cardiovascular causes. N Engl J Med. 2007 Jun 14;356(24):2457-71. Epub 2007 May 21.

Psaty BM, Furberg CD. Rosiglitazone and cardiovascular risk. N Engl J Med. 2007 Jun 14;356(24):2522-4. Epub 2007 May 21.

Schulze MB, Schulz M, Heidemann C, Schienkiewitz A, Hoffmann K, Boeing H. Fiber and magnesium intake and incidence of type 2 diabetes: a prospective study and meta-analysis. Arch Intern Med. 2007 May 14;167(9):956-65.

Scott LJ, Mohlke KL, Bonnycastle LL, Willer CJ, Li Y, Duren WL, et al. A genome-wide association study of type 2 diabetes in Finns detects multiple susceptibility variants. Science. 2007 Jun 1;316(5829):1341-5. Epub 2007 Apr 26.

Singh AK, Szczech L, Tang KL, Barnhart H, Sapp S, Wolfson M, et al. Correction of anemia with epoetin alfa in chronic kidney disease. N Engl J Med. 2006 Nov 16;355(20):2085-98.

Thamer M, Zhang Y, Kaufman J, Cotter D, Dong F, Hernen MA. Dialysis facility ownership and epoetin dosing in patients receiving hemodialysis. JAMA. 2007 Apr 18;297(15):1667-74.

Vardi M, Nini A. Phosphodiesterase inhibitors for erectile dysfunction in patients with diabetes mellitus. Cochrane Database Syst Rev. 2007 Jan 24(1):CD002187.

Zeggini E, Weedon MN, Lindgren CM, Frayling TM, Elliott KS, Lango H, et al. Replication of genome-wide association signals in UK samples reveals risk loci for type 2 diabetes. Science. 2007 Jun 1;316(5829):1336-41. Epub 2007 Apr 26.

Review Date:
7/31/2007
Reviewed By:
Harvey Simon, MD, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital.

A.D.A.M. Copyright

adam.com

Fibromyalgia

FitSugar — Wed, 08 Oct 2008 17:35:02 -0700

In This Report

Highlights
Introduction
Causes
Risk Factors
Diagnosis
Conditions with Similar Sym...
Prognosis
Treatment
Lifestyle Changes
Behavioral Therapy
Medications
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Causes

People with fibromyalgia have decreased activity in opioid receptors in parts of the brain that affect mood and the emotional aspect of pain, researchers have found. This might explain why fibromyalgia patients are likely to experience depression, and are not very responsive to opioid painkillers.
Researchers have identified a conflict between sensory perception and nervous system processing in people with fibromyalgia. One study suggests that people with the condition might have greater awareness of, or less tolerance for, movement problems (such as tremor) that don't match with their expected sensory feedback. This mismatch in sensory signals might enhance the perception of pain.

Treatment

New research adds to the evidence that exercise relieves some of the symptoms of fibromyalgia. Women with fibromyalgia who took part in a program that combined aerobic, strength training, and flexibility exercises had better physical and emotional function, as well as reduced symptoms. Another study found that an at-home exercise program improved upper body pain and function, especially in women who were having functional difficulties at the beginning of the study.
An anti-convulsant medication, gabapentin (Neurontin), significantly improved pain in fibromyalgia patients compared to placebo. Patients who took gabapentin also reported that they slept better and felt less tired.
The selective serotonin-reuptake inhibitor paroxetine (Paxil) significantly lowered patient scores on a fibromyalgia symptom questionnaire, and was well-tolerated, although the drug do much for their pain.

Introduction

Fibromyalgia is a syndrome of unknown causes that results in lasting, sometimes debilitating, muscle pain and fatigue. Fibromyalgia is also known as fibrositis or fibromyositis.

Pain. The primary symptom of fibromyalgia is pain. The pain can be in one place or all over. The exact locations of the pain are called tender points. The pain of fibromyalgia is often is described as follows:

Tender point pain occurs in local sites, usually in the neck and shoulders. The pain then spreads out from these areas. The actual pain starts at the muscles. The joints are not affected. There are no lumps or nodes associated with these points of pain, and no signs of inflammation (swelling). People diagnosed with fibromyalgia feel pain in at least 11 of 18 specific tender points.
Widespread pain described as stiffness, burning, and aching. The pain also "radiates," or spreads, to nearby areas. Most patients report feeling some pain all the time. Many describe it as "exhausting." The pain can vary depending on the time of day, weather changes, physical activity, and the presence of stressful situations. The pain is often more intense after disturbed sleep.

Fatigue and Sleep Disturbances. Another major complaint is fatigue. Some patients report that fatigue is more unbearable than their pain. Sleep disturbances, particularly restless legs syndrome, are also very common. Fatigue and sleep disturbances are almost universal in patients with fibromyalgia. Some experts believe that if these symptoms are not present, doctors should seek a diagnosis other than fibromyalgia.

Depression and Mood. Up to a third of patients have depression. Disturbances in mood and concentration are also very common. These conditions often go undiagnosed in patients with fibromyalgia.

Other Symptoms. The following symptoms may also be present:

Digestive problems, including irritable bowel syndrome with gas, and alternating diarrhea and constipation
Dizziness
Painful menstrual periods
Tension or migraine headaches
Tingling or numbness in the hands and feet
Urinary frequency caused by bladder spasms

Symptoms in Children. In general, children with fibromyalgia most often have sleep disorders and widespread pain.

Causes

The most common type is primary fibromyalgia, in which the causes are not known. Many experts believe that fibromyalgia is not a disease, but rather a chronic pain condition brought on by several abnormal body responses to stress. Physical injuries, emotional trauma, or viral infections such as Epstein-Barr may be triggers of the disorder, but none have proven to be a cause of primary fibromyalgia.

Research published in the December 2006 issue of Current Pain and Headache Reports found that the areas in the brain that are responsible for the sensation of pain are different in fibromyalgia patients from the same areas in healthy people.

People with fibromyalgia have been found to have decreased activity in opioid receptors in parts of the brain that affect mood and the emotional aspect of pain. This reduced response might explain why fibromyalgia patients are likely to havedepression, and are less responsive to opioid painkillers, researchers say.

Sleep disturbances are common in fibromyalgia. Both adult and young patients with fibromyalgia have a higher-than-average rate of a sleep disorder called periodic limb movement disorder (PLMD). PLMD used to be called nocturnal myoclonus. Patients with PLMD involuntarily contract their leg muscles every 20 - 40 seconds during sleep. This may occasionally wake up the patient.

Some researchers believe that fibromyalgia does not lead to poor sleeping patterns, but that sleep disturbances come first. Researchers continue to investigate the link between fibromyalgia and sleep.

In one study, healthy volunteers reported fibromyalgia-like pain after they had been subjected to disrupted deep sleep. Disturbed sleep appears to trigger factors in the immune system that cause inflammation, pain, fatigue, and lower tolerance to pain. A 2004 study found that patients with fibromyalgia have increased rates of cyclic alternating sleep pattern (CAP). Increased CAP produced serious sleep problems, which were strongly linked to symptom severity. Previous studies have also suggested that CAP may be related to PLMD.
A 2004 report found that sleep disorders that cause breathing problems are common in women with fibromyalgia.
Other biological measures of troubled sleep, however, such as levels of the hormone melatonin, which helps regulate circadian rhythms and the sleep-wake cycle, appear to be normal in most people with fibromyalgia.

Many abnormalities of hormonal, metabolic, and brain chemical activity have been described in studies of fibromyalgia patients. Changes appear to occur in several brain chemicals, although no regular pattern has emerged that fits most patients. Since there has been no clear cause-and-effect relationship established, this may be a result of the effects of pain and stress on the central nervous system, and not a cause of fibromyalgia.

Serotonin. Of particular interest to researchers is serotonin, an important nervous system chemical messenger found in the brain, gut, and other areas of the body. Serotonin plays important roles in feelings of well-being, adjusting pain levels, and promoting deep sleep. Serotonin abnormalities have been linked to many disorders, including depression, migraines, and irritable bowel syndrome. Lower serotonin levels have also been noted in some patients with fibromyalgia.

Stress Hormones. Researchers have also found abnormalities in the hormone system known as the hypothalamus-pituitary-adrenal gland (HAP) axis. The HAP axis controls important functions, including sleep, response to stress, and depression. Changes in the HAP axis appear to produce lower levels of the stress hormones norepinephrine and cortisol. (By contrast, levels of stress hormones in depression are higher than normal.) Deficiencies in the levels of stress hormones produce impaired and weaker responses to psychological or physical stresses. (Examples of physical stress include infection or exercise.)

The hypothalamus is a highly complex structure in the brain that regulates many important brain chemicals.

Click the icon to see an image of the adrenal glands.

Low Growth Hormone Levels. Some studies have reported low levels of insulin-like growth factor-1 (IGF-1) in about a third of fibromyalgia patients. IGF-1 is a hormone that is controlled by the adult growth hormone, and promotes bone and muscle growth. Low levels of growth hormone are related to impaired thinking, lack of energy, muscle weakness, and intolerance to cold. Studies suggest that changes in growth hormone likely stem from the hypothalamus in the brain. While researchers did not find a link between IGF-1 levels and fibromyalgia, a 2005 study indicated that serum growth hormone levels may be a marker of the disorder.

Abnormal Pain Perception and Substance P. Some studies have suggested that fibromyalgia may involve too much activity in the parts of the central nervous system that process pain (the nociceptive system). Brain scans of fibromyalgia patients have suggested abnormalities in pain processing centers. For example, researchers have detected up to three times the normal level of substance P in the cerebrospinal fluid of fibromyalgia patients. Substance P, a chemical messenger of the nervous system, is associated with increased pain perception.

Some fibromyalgia patients may also be oversensitive to external stimulation, and overly anxious about the sensation of pain. This increase in awareness is called generalized hypervigilance. One study compared patients with fibromyalgia or rheumatoid arthritis to those without chronic pain. Researchers then measured the different groups' responses to pain and noise. Of the three groups, the fibromyalgia patients were least tolerant, and most aware, of such stimuli. However, one analysis of studies on fibromyalgia found no strong support for the hypervigilance theory.

A conflict between sensory perception and nervous system processing might occur in people with fibromyalgia. Fibromyalgia patients have been found to have greater awareness of, or less tolerance for, movement problems (such as tremor) that don't match with their expected sensory feedback. This mismatch in sensory signals might enhance the perception of pain.

Fibromyalgia has symptoms that resemble those of some rheumatic illnesses, including rheumatoid arthritis and lupus (systemic lupus erythematosus). These are autoimmune diseases in which a defective immune system mistakenly attacks the body's own healthy tissue, producing inflammation and damage. The pain in fibromyalgia, however, does not appear to be due to autoimmune factors, and there is little evidence to support a role for an inflammatory response in fibromyalgia.

Although not primary causes, psychological and social factors may contribute to fibromyalgia in three ways:

They could make individuals susceptible to fibromyalgia.
They may play some role in triggering the onset of the condition.
They may perpetuate, or be responsible for, the condition.

Studies have reported a greater number of severe experiences of emotional and physical abuse in patients with fibromyalgia, compared with the general population. Most often, the abuse came from family members or partners. This suggests that post-traumatic stress disorder (PTSD) or chronic stress may play a strong role in the development of fibromyalgia in some patients. PTSD, an anxiety disorder, is a reaction to a specific traumatic event. Symptoms of this condition, which can last for years after the traumatic event, include emotional withdrawal, hopelessness, irritability, mood swings, sleep problems, inability to concentrate, and an excessive startle response to noise. Some evidence indicates that PTSD actually results in changes in the brain, possibly from long-term over-exposure to stress hormones.

Some research found muscle abnormalities in fibromyalgia patients. These problems can be classified as the following:

Biochemical abnormalities: For example, one study reported that fibromyalgia patients had lower levels of the muscle-cell chemicals phosphocreatine and adenosine triphosphate (ATP). Such chemicals regulate the level of calcium in muscle cells. Calcium is an important component in the muscles' ability to contract and relax. If ATP levels are low, calcium is not "pushed back" into the cells, and the muscle remains contracted.
Functional abnormalities: The pain and stress of the disease itself may harm muscle function.
Structural and blood flow abnormalities: Some researchers saw overly thickened capillaries (tiny blood vessels) in the muscles of fibromyalgia patients. The abnormal capillaries could produce lower levels of compounds essential for muscle function, as well as reduce the flow of oxygen-rich blood to the muscles.

To date, none of these abnormalities have a clearly defined relationship with fibromyalgia.

Risk Factors

About 3.7 million Americans have fibromyalgia. The condition affects 2% of Americans, including 3.4% of women and 0.5% of men.

Some evidence suggests that several factors may make people more susceptible to fibromyalgia. These risk factors include:

Being female
Coming from a very stressful culture or environment
Having a psychological vulnerability to stress
Having had difficult experiences in childhood

Nine out of 10 fibromyalgia patients are women. Women may be more prone to develop fibromyalgia during menopause.

The disorder usually occurs in people ages 20 - 60 years, though it can occur at any time. Some studies have noted peaks around age 35. Others note that fibromyalgia is most common in middle-aged women. In one study, cases of fibromyalgia increased with age, and reached a frequency of more than 7% among people in their 60s and 70s.

Juvenile Primary Fibromyalgia. This type of fibromyalgia appears in adolescents, typically after age 13, with a peak incidence at age 14. It is uncommon, but studies indicate that its incidence may be increasing. One study found that 1.2% of school children, all girls, met the criteria for fibromyalgia. Other studies have found an even higher frequency of fibromyalgia in children. Symptoms are similar to adult fibromyalgia, but outcomes may be better in young people.

Studies report a higher incidence of fibromyalgia among family members. It is not clear if genetic or psychological factors, or both, are involved.

One study reported that 28% of the children of mothers with fibromyalgia also develop the disorder. Offspring who developed fibromyalgia were no more likely to have psychological disorders than those who did not.
Another study noted that 66% of parents of children with fibromyalgia reported some sort of chronic pain. About 10% of them had fibromyalgia.

Diagnosis

There is no obvious, objective method for diagnosing fibromyalgia. The criteria used for studying fibromyalgia are very helpful, particularly if the patient does not have any accompanying disorder, such as depression or arthritis, which could complicate the diagnosis. Failure to meet the criteria, however, does not rule out fibromyalgia. Fibromyalgia should be suspected in any person with muscle and joint pain with no identifiable cause.

In 1990, the American College of Rheumatology (ACR) set the following criteria for the classification of fibromyalgia:

A. Widespread pain must be present for at least 3 months. This pain must appear in all of the following locations:

Both sides of the body
Above and below the waist
Along the length of the spine

B. Pain in at least 11 of 18 specific areas called tender points on the body. The pain experienced when pressing on a tender point is very localized and intensely painful (not just tender). Tender points are located in the following areas:

The left or right side of the back of the neck, directly below the hairline
The left or right side of the front of the neck, above the collar bone (clavicle)
The left or right side of the chest, right below the collar bone
The left or right side of the upper back, near where the neck and shoulder join
The left or right side of the spine in the upper back between the shoulder blades (scapula)
The inside of either arm, where it bends at the elbow
The left or right side of the lower back, right below the waist
Either side of the buttocks below the hip bones
Either kneecap

Other Factors. The ACR classification provides a guideline, but doctors will also use a patient's medical history and other symptoms to reach a diagnosis. Fibromyalgia is often diagnosed when other diseases have been excluded. Long-term symptoms that may indicate fibromyalgia include:

Fatigue
Headache
Morning stiffness
Numbness or tingling in the hands and feet
Sleep disturbance

The 18 fibromyalgia tender points are located throughout the body. According to the American College of Rheumatology, a diagnosis of fibromyalgia requires widespread body pain plus localized pain in 11 of these 18 specific points.

A doctor should always take a careful personal and family medical history, which would include a psychological profile and a history of any factors that might indicate disorders other than fibromyalgia. Such factors might include:

Infectious diseases
Muscle weakness
Physical injuries
Rashes
Recent weight change
Sexual, physical, or substance or alcohol abuse

Patients should report any drugs they take, including vitamins and over-the-counter or herbal medications.

Pressure on Tender Spots. Any physical examination for fibromyalgia requires that the doctor press firmly on all potential tender spots. They must be painful when pressed, not simply tender. In addition, for a doctor to reach a diagnosis of fibromyalgia, these tender sites should normally not show signs of inflammation (redness, swelling, or heat in the joints and soft tissue). The tender points may also change in location and sensitivity over time. A doctor, then, may recheck tender points that do not respond the first time, in patients who have other significant symptoms.

Detection of Other Causes of Symptoms. A health care provider will also examine nails, skin, mucous membranes, joints, spine, muscles, and bones to help rule out arthritis, thyroid disease, and other disorders.

No blood, urine, or other laboratory tests can provide a definitive diagnosis of fibromyalgia. If such tests show abnormal results, the doctor should look for other disorders. Tests for specific diseases depend on family histories and other symptoms. They may include:

Blood count
Sedimentation rate
Tests of certain antibodies
Thyroid and liver function tests

The doctor may suggest follow-up psychological profile testing, if laboratory results do not indicate a specific disease.

Conditions with Similar Symptoms

Between 10 - 30% of all doctor office visits are due to symptoms that resemble those of fibromyalgia, including fatigue, malaise, and widespread muscle pain. Since no laboratory test can confirm a diagnosis of fibromyalgia, doctors will usually first test for similar conditions. It should be noted that a diagnosis of many of the disorders below may not always rule out fibromyalgia, since it can accompany other common and similar conditions.

Several conditions overlap or often coexist with fibromyalgia, and have similar symptoms. It is not clear if these conditions cause fibromyalgia, are risk factors for the disorder, have causes in common with fibromyalgia, or have no relationship at all with it.

Chronic Fatigue Syndrome. There is a significant overlap between fibromyalgia and chronic fatigue syndrome (CFS). In a 2003 study, for example, 43% of CFS patients also had a diagnosis of fibromyalgia. As with fibromyalgia, the cause of CFS is unknown. A doctor can diagnose either disorder based only on symptoms reported by the patient. The two disorders share most of the same symptoms. They are also treated almost identically. The differences are primarily the following:

Pain with tender points is the primary symptom in fibromyalgia. Some patients with CFS exhibit similar tender pressure points. However, muscle pain is less prominent in patients with CFS.
Fatigue is the dominant symptom in CFS. It is severe and not relieved by rest or sleep, and it is not the result of excessive work or exercise.

Some doctors believe that fibromyalgia is simply an extreme type of chronic fatigue syndrome. There Some physical evidence, however, indicates that the two disorders are distinct, with treatments that are specific to each.

Myofascial Pain Syndrome. Myofascial pain syndrome can be confused with fibromyalgia and may also accompany it. Unlike fibromyalgia, myofascial pain tends to occur in trigger points, as opposed to tender points, and typically there is no widespread, generalized pain. Trigger-point pain occurs in tight muscles, and when the doctor presses on these points, the patient may experience a muscle twitch. Unlike tender points, trigger points are often small lumps, about the size of a pencil eraser.

Major Depression. The link between psychological disorders and fibromyalgia is very strong and problematic. Certain studies report that 50 - 70% of fibromyalgia patients have a lifetime history of depression. Only 18 - 36% of fibromyalgia patients, however, also have major depression, a severe form of depression.

Some studies found that people who have both psychological disorders and fibromyalgia are more likely to seek medical help, compared with patients who simply have symptoms of fibromyalgia. If this is the case, study results may be biased, favoring a higher-than-actual association between depression and fibromyalgia.

Depression most likely does not cause fibromyalgia, but it may increase susceptibility. Depressed feelings in people with fibromyalgia can certainly be normal responses to the pain and fatigue caused by this syndrome. Such emotions, however, are temporary and related to the situation a person is in. They are not considered to be a depression disorder. Unlike ordinary periods of sadness, an episode of major depression disorder can last many months.

Symptoms of major depression include the following:

Depressed mood every day
Feeling worthless or inappropriately guilty
Inability to concentrate or make decisions
Insomnia or excessive sleeping
Low energy every day
Restlessness or a sense of being slowed down
Significant weight gain or loss (of 10% or more of an individual's typical body weight)
Suicidal thoughts

If several of the above symptoms are present, and none of the physical symptoms (particularly the tender points) of fibromyalgia exist, the condition is most likely major depression.

Chronic Headache. Chronic primary headaches such as migraines are common in fibromyalgia patients. Some experts believe that migraine headaches and fibromyalgia may even share common defects in the systems that regulate certain chemical messengers in the brain, including serotonin and epinephrine (adrenaline). Low levels of magnesium have also been noted in patients with both fibromyalgia and migraines. In fact, chronic migraine sufferers who fail to benefit from usual therapies may also have fibromyalgia.

Symptoms of a migraine attack may include heightened sensitivity to light and sound, nausea, vision problems (auras), speech difficulty, and intense pain predominating on one side of the head.

Multiple Chemical Sensitivity. Multiple chemical sensitivity (MCS) is a term that describes conditions in which certain chemicals can cause symptoms similar to CFS or fibromyalgia in some people. Still, as with CFS and fibromyalgia, some experts are uncertain whether MCS is a medical condition or if it is psychologically based.

In one study, for example, CFS patients who believed their problem was chemically triggered were exposed to either an active chemical or a placebo (an inactive substance). Both groups reported symptoms, including those only exposed to a placebo. Because everyone is exposed to many chemicals on a daily basis, it is very difficult to determine whether chemicals are responsible for specific symptoms.

Experts have come up with criteria to help recognize MCS:

Symptoms can be produced by exposure to the chemical at levels lower than previously or usually tolerated.
Symptoms can be triggered by multiple substances that are chemically unrelated.
Symptoms involve multiple organ systems.
The condition is chronic.
The symptoms always happen with repeated exposure to a chemical. (These are often common chemicals found in popular products, such as perfumes, fabric softeners, and air fresheners.)
The symptoms improve when the chemical is removed.

Restless Legs Syndrome. About 15% of people with fibromyalgia have restless legs syndrome. Restless legs syndrome is an unsettling and poorly understood movement disorder that is sometimes described as a sense of unease and weariness in the lower leg that is aggravated by rest and relieved by movement.

Disorders Affected by the Sympathetic (also called Autonomic) Nervous System. Other conditions that commonly accompany fibromyalgia include:

Chest pain and heart palpitations
Mitral valve prolapse
Sudden drop in blood pressure

Certain stress-related disorders commonly occur with fibromyalgia, and have overlapping symptoms. In fact, some experts believe these disorders so often interact that they may all be part of one general condition.

Chemicals and environmental toxins -- exposure to various chemicals and environmental toxins such as solvents, pesticides, or heavy metals (cadmium, mercury, or lead) can cause fatigue, chronic pain, and other symptoms of fibromyalgia.
Irritable bowel syndrome
Osteoarthritis -- a common form of arthritis than can coexist with fibromyalgia. The two conditions may be confused, particularly in elderly people. Osteoarthritis, however, causes joint pain, not widespread or generalized pain.

Osteoarthritis is a chronic disease of the joint cartilage and bone. It is often thought to result from "wear and tear" on a joint, although there are other causes, such as congenital defects, trauma, and metabolic disorders. Joints appear larger, are stiff and painful, and usually feel worse the more they are used throughout the day.

Temporomandibular joint disorders

Some tests may be positive for one or more of these diseases. However, if the results are uncertain or weak, or if these conditions have been treated successfully, fibromyalgia should not be ruled out if the patient still meets the criteria for it.

Multiple sclerosis. This condition may have symptoms similar to those of fibromyalgia. Magnetic resonance imaging (MRI) scans often detect patches of tissue in the brain that confirm the presence of multiple sclerosis (MS). MRI findings combined with other tests and clinical findings usually make this diagnosis fairly certain. However, some patients may have symptoms that suggest MS, but diagnostic tests cannot confirm the diagnosis. Some of these patients may have symptoms similar to those of fibromyalgia.

Click the icon to see an image of multiple sclerosis.

Sjogren syndrome. This condition, characterized by dry eyes and mouth, is sometimes mistaken for fibromyalgia.

Autoimmune diseases. Rheumatoid arthritis, systemic lupus erythrometosis, and Sjogren syndrome are usually easy to diagnose but may develop slowly and be difficult to diagnose at first. Even if a doctor determines that a patient is most likely to have fibromyalgia, the doctor should keep track of any changes in symptoms over time in case one of these other illnesses is actually present.

Lyme Disease. Lyme disease is a bacterial disease transmitted by ticks. Health care providers can usually diagnose early Lyme disease correctly, but a delayed response or recurrence of this disorder may be mistaken for fibromyalgia. Some experts believe that 15 - 50% of patients referred to clinics for Lyme disease actually have fibromyalgia. Late Lyme disease can usually (but not always) be ruled out using blood tests that identify the organism that causes this disease. If fibromyalgia patients are incorrectly diagnosed and treated for Lyme disease with prolonged courses of antibiotics, the drugs may have serious side effects.

Drugs and Alcohol. Fatigue is a side effect of many prescription and over-the-counter medications, such as antihistamines. In addition, symptoms of dependency on, or abuse of, alcohol or drugs appear as constant fatigue. Health care providers should consider medications as a possible cause of fatigue if an individual has recently started, stopped, or changed medications. Withdrawal from caffeine can produce depression, fatigue, and headache.

Polymyalgia Rheumatica. Polymyalgia rheumatica is a condition that causes pain and stiffness, and generally occurs in older women. Tender points are also present with this disorder, although they almost always occur in the hip and shoulder area. Morning stiffness is common, and patients may also experience fever, weight loss, and fatigue. A higher-than-normal erythrocyte sedimentation rate (ESR) can suggest polymyalgia rheumatica. Elevated ESR, however, also occurs with other conditions. Polymyalgia rheumatica often gets better in about a year, but there is a risk of persistent disease. Worse, it is sometimes associated with a rare condition called temporal arteritis, which may cause blindness if not treated, so an accurate diagnosis of polymyalgia rheumatica is important.

Prognosis

Fibromyalgia can be mild or disabling, and the emotional toll can be substantial. About half of all patients have difficulty with routine daily activities, or are unable to perform them. An estimated 30 - 40% of patients have had to quit work or change jobs. In a 2003 study, patients with either CFS or fibromyalgia were more likely to suffer losses of jobs, possessions, and support from friends and family than were people suffering from other conditions that caused fatigue.

The pain, emotional consequences, or sleep disturbances that come with fibromyalgia may lead to self-medication and overuse of sleeping pills, alcohol, drugs, or caffeine.

Outlook in Adults. Some studies show that fibromyalgia symptoms remain stable over the long term, while others report a better outlook, with 25 - 35% of patients reporting improvement in pain symptoms over time. Studies suggest that regular exercise specifically improves the outlook. Those with a significant life crisis, or who were on disability, had a poorer outcome than others. Outcome was determined by improvements in the patients' ability to work, their own feelings about their condition, pain sensation, and levels of disturbed sleep, fatigue, and depression. Although the disease is life-long, it does not get worse and is not fatal.

Outlook in Children. Children with fibromyalgia tend to have a better outlook than adults with the disorder. Several studies reported that more than half of children with fibromyalgia recover in 2 - 3 years.

Treatment

Many patients with fibromyalgia are treated first with medication; however, the American Pain Society Fibromyalgia Panel recommends a combined approach using cognitive-behavioral therapy, education, medication, and exercise.

Fibromyalgia is a mysterious condition. Its causes are still largely unknown, as is how it inflicts damage. No strong evidence indicates that any single treatment (or combination of treatments) has any significant effect for most patients. However, in 2007 the U.S. Food and Drug Administration approved pregabalin (Lyrica) as the first drug treatment for fibromyalgia after a study showed the medicine reduced fibromyalgia pain by at least 50% in 63% of patients.

Treatment usually involves not only relieving symptoms but also changing a pateint's attitude about their disease. Treatment should also teach patients behaviors that help them cope.

Treatments usually involve trial and error:

Patients may start with physical therapy, exercise, stress reduction techniques, and cognitive-behavioral therapy.
If these methods fail to improve symptoms, an antidepressant or muscle relaxant may be added to the treatment. Doctors usually prescribe these drugs because they can may improve pain tolerance.
Patient education and programs that encourage coping skills are an important part of any treatment plan.

According to a 2005 study published in the Clinical Journal of Pain, a combination of non-drug therapies works just as well as drug therapy in improving pain, depression, and disability. This combination includes exercise, stress management, massage, and diet.

Patients must have realistic expectations about the long-term outlook of their condition, and their own individual abilities. It is important to understand that fibromyalgia can be managed, and patients can live a full life. The following tips may be helpful when starting a treatment program for fibromyalgia:

The goal of therapy is to relieve symptoms, not cure them.
Treatment must be tailored to each patient, and a combination approach is often needed.
Patients must begin all treatments with the attitude that these treatments are trial-and-error. There is no clear treatment solution. Patients and doctors need to work together to make the best choices for individual symptoms and concerns.
Treatments are long-lasting, in some cases life-long, and patients should not be discouraged by the return of symptoms (relapses).
Enlisting family members, partners, and close friends, particularly to help with exercise and stretching programs, can be helpful.
Becoming involved with support groups of fellow patients also benefits many patients. Support groups may also benefit family members, particularly parents of children with fibromyalgia. One study noted that the severity of the disorder increased in children whose parents were less able to cope with their child's pain.

The definition of improvement is personal. For example, some patients are pleased with only a 10% reduction in pain and other symptoms.

Lifestyle Changes

Many studies have shown that exercise is the most effective component in managing fibromyalgia, and patients must expect to take part in a long-term exercise program. Physical activity prevents muscle wasting, increases well-being, and, over time, reduces fatigue and pain. Many studies have also demonstrated the exercise can improve physical and emotional function, as well as reduce symptoms, including pain.

Programs often combine aerobic, strength-training, and flexibility exercises with self-management education. Some studies have shown improvements lasting for up to 9 months after the exercise program.

Graded Exercise. The basic approach used for fibromyalgia is called graded exercise. Graded exercise means you slowly increase the amount of your physical activity.

In general, graded exercise involves:

A very gradual program of activity, beginning with mild exercise and building in intensity over time.
Stretching exercises before exercising. A daily stretching routine can help relax tense muscles and prevent muscle soreness.
Walking, swimming, and using equipment such as treadmills or stationary bikes. Swimming and water therapy are good because they don't require putting weight on the joints.

Patients who try hard exercises too early actually experience an increase in pain, and are likely to become discouraged and quit.

Every patient must be prepared for relapses and setbacks, but should not get discouraged. Patients who do not respond to one type of exercise might consider experimenting with another form.

Physical therapy can be very helpful. Studies suggest that physical therapy may reduce muscle overload, lessen fatigue from poor posture and positioning, and help condition weak muscles.

Sleep is essential, particularly since sleep disruptions worsen pain. Many patients with fibromyalgia have trouble getting a restful and healing night's sleep. Those who are unable to sleep consistently have low improvement. Swing shift work, for example, is extremely hard on fibromyalgia patients. Poor sleep habits can add to sleep problems. Tips for good sleep habits include:

Avoid caffeine or alcohol 4 - 6 hours before bedtime.
Avoid drinking fluids right before bedtime so that needing to uriniate does not disturb your sleep.
Avoid exercising 6 hours before bedtime.
Avoid large meals before bedtime. A light snack, however, may help you sleep.
Avoid naps, especially in the evening or late afternoon.
Establish a regular time for going to bed and getting up in the morning. Maintain this schedule even on weekends and during vacation.
If you are unable to fall asleep after 15 or 20 minutes, go into another room and start a quiet activity. Return to bed when you feel sleepy.
Minimize light and maintain a comfortable, moderate temperature in the bedroom. Keep the bedroom well ventilated.
Use the bed only for sleep and sexual relations.

[For more information see In-Depth Report #27: Insomnia.]

Fibromyalgia patients should maintain a healthy diet low in animal fat and high in fiber, with plenty of whole grains, fresh fruits, and vegetables. Although everyone should be careful about calories from fats, some are healthy.

Omega-3 Fatty Acids. Oils containing omega-3 fatty acids are of particular interest for arthritic pain. Such oils are found in cold-water fish. You can also purchase these oils as supplements called EPA-DHA or omega 3.

Omega-3 fatty acids are a form of polyunsaturated fat that the body gets from food. Omega-3s are known as essential fatty acids (EFAs) because they are important for good health. These healthy fatty acids can be found in certain fish, dark green leafy vegetables, and some oils. Omega-3 fatty acids have anti-inflammatory properties, which help prevent blood clots, lower cholesterol and triglyceride levels, and reduce blood pressure. Omega-3s may also reduce the risks and symptoms of diabetes, stroke, rheumatoid arthritis, asthma, inflammatory bowel disease, ulcerative colitis, some cancers, and mental decline.

Vegetarian Diet. A vegan diet has no meat, dairy, or eggs and includes uncooked fruits, vegetables, nuts, and germinated seeds. The actual benefit of various vegetarian diets remains unproven.

Relaxation and stress-reduction techniques are proving to be helpful in managing chronic pain. Evidence shows that people with fibromyalgia have a more stressful response to daily conflicts and encounters than those without the disorder. Several relaxation and stress-reduction techniques may be helpful in managing chronic pain:

Biofeedback
Deep breathing exercises
Hypnosis
Massage therapy
Meditation
Muscle relaxation techniques

Biofeedback. Evidence from controlled trials does not suggest that biofeedback techniques may be very helpful for fibromyalgia patients. During a biofeedback session, electric leads are taped to a subject's head. The person is encouraged to relax using any method that works. Brain waves are measured and an audio signal sounds when alpha waves are detected. Alpha waves are brain waves that occur with a state of deep relaxation. By repeating the process, people using biofeedback connect the sound with the relaxed state, and learn to achieve relaxation on their own.

Meditation. Meditation, used for many years in Eastern cultures, is now widely accepted in this country as an effective relaxation technique. A number of studies are reporting its benefits for fibromyalgia patients who practice on a continued and regular basis. The practiced meditator can achieve the following physical benefits:

Reduced heart rate, blood pressure, adrenaline levels, and skin temperature while meditating.
Improved well-being.
Better sleep -- some research has reported an increase in melatonin levels in experienced meditators. Melatonin is important in regulating the sleep-wake cycle.
Less pain, possibly from reductions in levels of cortisol, a stress hormone.

An important goal for both religious and therapeutic meditation practices is to quiet the mind, essentially to relax thought. This redirection of brain activity from thoughts and worries to the senses disrupts the stress response and prompts relaxation and renewed energy. Several meditation techniques are available. Some may be more useful for fibromyalgia than others.

Breath meditation. Other meditative forms involve focusing on the present moment and observing (but not examining or judging) one's thoughts. During breath meditation, one sits upright with the spine straight and the eyes closed. The subject begins to breathe regularly and continues to observe the outward exhalation of the breath. As the mind wanders, one simply notes the thoughts as a fact and returns to the breath. A variant of this technique called mindfulness meditation has been helpful for fibromyalgia patients. It involves focusing on the present moment and letting thoughts pass without the accompanying breathing exercises.
Fixed point meditation involves focusing on a stationary object, mental image (such as a candle flame), or internal sound (such as a mantra). When the mind begins to wander, the meditator gently brings concentration back to the central image or sound. This exercise promotes focus, but it is often experienced as a thinking exercise. A popular variety of this type of meditation is known as transcendental meditation, or TM.
Mini-meditation. This method involves heightening awareness of the immediate surrounding environment. One should first choose a simple routine activity when alone. For example, while washing dishes concentrate on the feel of the water and dishes. Allow the mind to wander to any immediate sensory experience, such as sounds outside the window, smells from the stove, or colors in the room. If the mind begins to think about the past or future, abstractions, or worries, redirect it gently back.

People who try meditation for the first time should understand that it can be difficult to quiet the mind, and should not be discouraged by lack of immediate results. Some recommend meditating for no longer than 20 minutes in the morning after awakening and then again in the early evening before dinner. Even once a day is helpful. A person should probably not meditate before going to bed, because it causes some people to wake up in the middle of the night, alert and unable to return to sleep.

Hypnosis. In one small, short-term controlled study, hypnosis was more effective than physical therapy in improving function and reducing pain.

Massage Therapy. Massage therapy is thought to stimulate the parasympathetic nervous system, which slows down the heart and relaxes the body. In one study, patients who were given 30-minute massage sessions twice a week experienced lower stress and anxiety and less pain after 5 weeks compared to a group receiving an alternative therapy called transcutaneous electrical stimulation (TENS).

Because of the difficulties in treating fibromyalgia, many patients seek alternative therapies. Everyone should be wary of those who promise a quick cure or urge the purchase of expensive but potentially dangerous treatments.

Although some studies have reported benefit from these treatments, there is not enough evidence to recommend them. In one analysis, evidence was weakest on the advantages of so-called manipulative ("hands-on") approaches, such as chiropractic treatments.

Acupuncture. Studies continue to report conflicting results on acupuncture's ability to relieve pain. Several small studies suggest that it offers some benefit, especially to those who cannot take medicines because of their side effects. A larger controlled study found that inserting needles at fibromyalgia-related pressure points was no better at relieving pain for fibromyalgia than randomly inserting needles ("sham acupuncture"). A 2006 review of five randomized, controlled trials did not find enough evidence to support the use of acupuncture for fibromyalgia.

Click the icon to see an image of acupuncture.

Chiropractic or Osteopathic Manipulation. Chiropractic or osteopathic manipulation may also help some patients. While some studies have reported pain relief and improved sleep with osteopathic manipulation, larger controlled studies are needed to clearly identify whether manipulation is an effective treatment. Osteopathic techniques may include manipulation of the spine or muscle tissue release. Note that there is always some very small risk for adverse effects from any of these techniques. For example, in rare cases manipulation of the neck has caused stroke or damage to the large blood vessels in the neck.

Hydrotherapy and Similar Treatments. Hydrotherapy, also called balneotherapy, involves soaking in water, such as hot tubs, pools, or baths, to help relieve pain.

Herbal or Natural Remedies. Some alternative agents are being investigated for fibromyalgia:

Melatonin, a natural hormone associated with the sleep-wake cycle, may have benefits for some patients with fibromyalgia.
S-adenosylmethionine (SAMe) is a natural substance that has antidepressant, anti-inflammatory, and analgesic properties. It has shown some benefit in controlled studies.

It is extremely important for patients to realize that any herbal remedy or natural medicine that has positive effects most likely has negative side effects and toxic reactions, just as any conventional drug does. You should consult a doctor before using any untested products or dietary supplements. You should also discuss with your doctor any potential interactions between the supplements and any medications you take.

Generally, manufacturers of herbal remedies and dietary supplements do not need approval from the U.S. Food and Drug Administration 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 a number of reported cases of serious and even deadly side effects from herbal products. Always check with your doctor before using any herbal remedies or dietary supplements.

Behavioral Therapy

Studies continue to show that fibromyalgia patients feel better when they deal with the specific conditions of their disorder and their lives. Cognitive-behavioral therapy (CBT) enhances a patient's belief in their own abilities and helps them develop methods for dealing with stressful situations. CBT, also called cognitive therapy, is a known, effective method for dealing with chronic pain from arthritic conditions. Some evidence also suggests that cognitive-behavioral therapy can help some patients with fibromyalgia.

Although the effects of CBT and other non-medication treatments for fibromyalgia do not always last over the long-term, they may help certain groups of people, particularly those with a high level of psychological stress.

CBT may be particularly useful for addressing insomnia, one of the hallmark symptoms of fibromyalgia. Patients who received CBT for insomnia woke up 50% less at night, and had fewer symptoms of insomnia and improved mood.

The Goals of CBT. The primary goals of CBT are to change any unclear or mistaken ideas and self-defeating behaviors. Using specific tasks and self-observation, patients learn to think of pain as something other than a negative factor that controls their life. Over time, the idea that they are helpless against the pain goes away and, instead, they learn that they can manage the pain.

Cognitive therapy is particularly helpful in defining and setting limits -- a behavior that is extremely important for these patients. Many fibromyalgia patients live their lives in extremes. They first become heroes or martyrs, pushing themselves too far until they collapse. This collapse reverses the way they view themselves, and they then think of themselves as complete failures, unable to cope with the simplest task. One important aim of cognitive therapy is to help such patients discover a middle route. Patients learn to prioritize their responsibilities and drop some of the less important tasks or delegate them to others. Learning these coping skills can eventually lead to a more manageable life. Patients learn to view themselves and others with a more flexible attitude.

The Procedure. Cognitive therapy usually does not last long, typically 6 - 20 one hour sessions. Patients also receive homework, which usually includes keeping a diary and trying tasks they have avoided because of negative attitudes.

A typical cognitive therapy program may involve the following measures:

Keep a Diary. Patients are usually asked to keep a diary, a key part of cognitive therapy. The diary serves as a general guide for setting limits and planning activities. Patients use the diary to track any stress factors, such as a job or a relationship that may be making the pain worse or better.
Confront Negative or Discouraging Thoughts. Patients are taught to challenge and reverse negative beliefs. For example, "I'm not good enough to control this disease, so I'm a total failure" becomes the coping statement, "Where is the evidence that I can control this disease?"
Set Limits. Limits are designed to keep both mental and physical stress within manageable levels, so that patients do not become discouraged by getting "in over their heads." For example, tasks are broken down into incremental steps, and patients focus on one at a time.
Seek out Pleasurable Activities. Patients list a number of enjoyable low-energy activities that they can conveniently schedule.
Prioritize. Patients learn to drop some of the less critical tasks or delegate them to others.

Patients should learn to accept that relapses occur, and that over-coping and accomplishing too much too soon can often cause a relapse of symptoms. Patients should respect these relapses and back off. They should not consider them a sign of failure.

Research also shows that patient education can be effective in treating fibromyalgia, especially when combined with CBT, exercise, and other therapies. Educational programs can take the form of group discussions, lectures, or printed materials, although there isn't any clear evidence on which type of education works best.

Cognitive therapy may be expensive and not covered by insurance. Alternative and effective approaches that are free or less costly include strong, intelligently managed support groups or group psychotherapy. In one center, educational discussion groups were as effective, or even more so, than a cognitive therapy program. Such results are not typical in all centers, of course. Therapeutic success varies widely depending on the skill of the therapist.

Medications

Typically the first choice in drug treatment of fibromyalgia has consisted of an antidepressant or a muscle relaxant. The goal has been to improve sleep and pain tolerance. Medications from other drug classes (such as sleeping aids and pain relievers) may also be prescribed. Patients receive drug treatments in combination with exercise, patient education, and behavioral therapies. In 2007 the Food and Drug Administration approved Pregabalin (Lyrica) as the first drug for the treatment of fibromyalgia.

Pregabalin is an anti-epileptic. Also called anti-seizure drugs and anti-convulsants, these medicines affect the chemical messenger gamma aminobutyric acid (GABA), which helps prevent nerve cells from over-firing.

Pregabalin was previously approved in 2004 to treat nerve pain and diabetic peripheral neuropathy. A 2005 study of 529 patients with fibromyalgia reported that 450 mg per day of pregabalin reduced pain and improved sleep quality and fatigue symptoms. Study results presented in November 2006 showed pregabalin cut fibromyalgia pain by at least 50% in 63% of patients, and the effect was long-lasting. The study, lasting 6 months, was one of the longest controlled studies of pregabalin in fibromyalgia to date. The most common side effects include mild-to-moderate dizziness and sleepiness. Pregabalin can impair motor function and cause problems with concentration and attention. Patients should talk to their doctor about whether pregabalin may impair their ability to drive.

Studies have shown that another anti-convulsant, gabapentin (Neurontin), which is approved for treatment of postherpetic neuralgia, affects pain transmission pathways and may relieve pain associated with fibromyalgia when compared with placebo. Patients who took gabapentin also reported that they slept better and were less tired.

The main classes of antidepressants used for treating fibromyalgia are tricyclics, selective serotonin-reuptake inhibitors (SSRIs), and serotonin-norepinephrine reuptake inhibitors (SNRIs). Although these drugs are antidepressants, doctors prescribe them to improve sleep and relieve pain in non-depressed patients with fibromyalgia. The dosages used for managing fibromyalgia are generally lower than dosages prescribed for treating depression. If a patient has depression in addition to fibromyalgia, higher doses may be required.

Tricyclics. Tricyclic antidepressants cause drowsiness and can be helpful for improving sleep. The tricyclic drug most commonly used for fibromyalgia is amitriptyline (Elavil, Endep), which produces modest benefits with pain, but which can lose effectiveness over time. Other tricyclics include desipramine (Norpramin), doxepin (Sinequan), imipramine (Tofranil), amoxapine (Asendin), and nortriptyline (Pamelor, Aventyl).

Generally, only small doses of tricyclic antidepressants are needed to relieve fibromyalgia. Therefore, although tricyclics have several side effects, these side effects may be less frequent in fibromyalgia patients than in those taking tricyclics for depression. Side effects most often reported include:

Blurred vision
Difficulty urinating
Dizziness
Drowsiness
Dry mouth
Heart rhythm disturbances
Sexual dysfunction
Weight gain

As with all medications, tricyclics must be taken as directed. An overdose can be life-threatening.

Unfortunately, not all patients respond to tricyclics, and their effects wear off in some patients, sometimes after only a month.

Selective Serotonin-Reuptake Inhibitors. Selective serotonin-reuptake inhibitors (SSRIs) increase serotonin levels in the brain, which may have specific benefits for fibromyalgia patients. Commonly prescribed SSRIs include fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil), and fluvoxamine (Luvox). Studies suggest they may improve sleep, fatigue, and well-being in many patients. Studies are mixed on whether they improve pain. SSRIs should be taken in the morning, since they may cause insomnia. Common side effects are agitation, nausea, and sexual dysfunction, including delay or loss of orgasm and low sex drive.

Serotonin-Norepinephrine Reuptake Inhibitors. Serotonin-norepinephrine reuptake inhibitors (SNRIs) are also known as dual inhibitors because they act directly on two chemical messengers in the brain -- norepinephrine and serotonin. These drugs include:

Duloxetine (Cymbalta) is gaining attention as a treatment for fibromyalgia. In a 2004 study, 207 patients with fibromyalgia were randomized to receive either 60 mg of duloxetine twice a day or placebo for 12 weeks. Duloxetine significantly improved pain and tenderness and was effective for both depressed and non-depressed patients. Duloxetine was most effective for women, but very few men were enrolled in this trial.
Venlafaxine (Effexor) is similar to fluoxetine (Prozac) in effectiveness and tolerability for most patients. As with SSRIs, and unlike other newer antidepressants, venlafaxine impairs sexual function. Although clinical trials have shown that the drug is safe and effective in most people, there have been reports of changes in blood pressure. There have also been reports of problems with the electrical system of the heart when taking this drug. These side effects may cause serious problems in elderly patients. Some patients report severe withdrawal symptoms, including dizziness and nausea.
Milnacipran (Ixel) is under investigation and is not yet approved in the United States. It is specifically being researched for helping people with fibromyalgia and similar pain syndromes. In a 2004 study of 125 patients, milnacipran improved fibromyalgia pain and other symptoms, including fatigue, sleep, and depression.

Cyclobenzaprine (Flexeril) relaxes muscle spasms in specific locations without affecting overall muscle function. Cyclobenzaprine is related to the tricyclic antidepressants and has similar side effects, including drowsiness, dry mouth, and dizziness. A 2004 review of five randomized controlled trials found that patients who received cyclobenzaprine were three times more likely to report improvement in fibromyalgia symptoms than patients who received placebo.

Zolpidem (Ambien) or other newer sleep medications such as zaleplon (Sonata) and eszopiclone (Lunesta) may improve sleep for patients who suffer from insomnia.

Pain relief is of major concern for patients with fibromyalgia. Pain relievers for fibromyalgia include:

Tramadol (Ultram), used alone or in combination with acetaminophen (Tylenol), is commonly prescribed for relief of fibromyalgia pain. Its most common side effects are drowsiness, dizziness, constipation, and nausea. Tramadol should not be used in combination with tricyclic antidepressants.
For relief of mild pain, acetaminophen is most often recommended. Anti-inflammatory drugs, which are commonly used for arthritic conditions, are less useful for the pain of fibromyalgia, since the pain is not caused by muscle or joint inflammation. Anti-inflammatory drugs include corticosteroids and nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin and ibuprofen (Advil).
Capsaicin (Zostrix) is an ointment prepared from the active ingredient in hot chili peppers. Capsaicin is helpful in relieving painful areas in other disorders. It may have some value for fibromyalgia patients.
Opioids, or narcotics, may be used occasionally by certain patients with moderate-to-severe pain, or those with significant problems performing everyday tasks. Such patients should use narcotics only if they cannot find relief with other, less potent treatments. Some patients may get combinations of narcotic pain relievers and acetaminophen for periodic pain. Some physicians prescribe opioids, such as oxycodone (Roxicodone) or morphine sulfate (Duramorph), for patients who need ongoing relief. However, the benefit of opioids in fibromyalgia treatment is highly controversial. Physicians should take a careful medical and psychological profile of the patient before prescribing opioids. The patients should be evaluated periodically for continuing pain relief, side effects, and indications of dependence.
Pramipexole, a drug used to treat Parkinson’s disease and restless legs syndrome, may help relieve pain and fatigue in people with fibromyalgia, according to one study. Pramipexole stimulates production of dopamine, a chemical messenger in the brain. Researchers compared pramipexole with a dummy pill (placebo). After 3.5 months, 36% of those who took pramipexole said they felt much better, compared to 9% of those who received a dummy pill. Overall, patients had a 50% or greater decrease in pain.
One small 2005 study conducted in Spain suggests that the atypical antipsychotic olanzapine (Zyprexa) may be a beneficial add-on therapy for patients with fibromyalgia. Although proven effective for some chronic pain conditions, olanzapine and other antipsychotics cause unpleasant and potentially serious side effects.

Tropisetron. Tropisetron (Navoban) is a drug used to reduce vomiting during chemotherapy. European studies suggest that it may also help patients with fibromyalgia by reducing pain, dizziness, and depression, and by improving sleep. Fatigue and dizziness are the most common side effects.

Much of the pain patients experience occurs where muscles join tendons or bones, particularly when the muscles are stretched. Stretching or flexibility exercises are part of the warm-up and cool-down routines of any regular exercise program. Stretching techniques may also use injections or cooling agents to inactivate the pressure points so that muscles can be more effectively stretched. These techniques must be performed by a person other than the patient, usually a family member or close friend. With either injections or the spray, the benefits may last from a few days to weeks. Neither the spray nor the injection is useful without muscle stretching.

Spray and Stretch. One technique is known as "spray and stretch." This method uses the following approach:

The patient must be in a comfortable position.
The partner presses on suspected tender points and the patient reports any pain.
The points, when targeted, are sprayed with either ethyl chloride (Chloroethane) or Fluori-Methane. These chemicals are not numbing medicines. They cool the blood vessels in the skin to inactivate the tender points. Numbing skin creams do not appear to be effective for this treatment.
The spray bottle is held upside-down about 12 - 18 inches from the targeted area. The patient's face should be covered if the spray is being used near the head.
The patient's partner then slowly stretches the affected muscle.

After the procedure, the muscle should feel looser, and the patient should have a greater range of motion with that muscle.

Trigger-Point Injections. In some cases, "trigger-point injections" of a numbing drug, such as lidocaine, may be used for particularly painful tender points as an aid to stretching.

The injection causes intense, but brief, pain in the trigger point. After the medication has taken effect, however, the muscle's ability to stretch is much greater.
There is some soreness afterward, which can be severe. After an injection, spraying the whole muscle with cooling agents may inactivate less severe tender points.
In some cases, injections may be needed several times over 6 - 8 weeks.

Resources

www.rheumatology.org -- American College of Rheumatology
www.niams.nih.gov -- National Institute of Arthritis and Musculoskeletal and Skin Diseases
www.arthritis.org -- Arthritis Foundation
www.fmaware.org -- National Fibromyalgia Foundation
www.fmpartnership.org -- National Fibromyalgia Partnership
www.fmnetnews.com -- Fibromyalgia Network
www.aapainmanage.org -- American Academy of Pain Management
www.ampainsoc.org -- American Pain Society
www.medicalacupuncture.org -- American Association of Medical Acupuncture
www.asch.net -- American Society of Clinical Hypnosis
www.aabt.org -- Association for Advancement of Behavior Therapy
www.clinicaltrials.gov -- Find a clinical trial

References

Arnold LM, Goldenberg DL, Stanford SB, Lalonde JK, Sandhu HS, Keck PE, et al. Gabapentin in the treatment of fibromyalgia: a randomized, double-blind, placebo-controlled multicenter trial. Arthritis & Rheumatism. 2007;56:1336-1344.

Assefi NP, Sherman KJ, Jacobsen C, Goldberg J, Smith WR, Buchwald D. A randomized clinical trial of acupuncture compared with sham acupuncture in fibromyalgia. Ann Intern Med. 2005; 143(1): 10-9.

Da Costa D, Abrahamowicz M, Lowensteyn I, Bernatsky S, Dritsa M, Fitzcharles MA, Dobkin PL. A randomized clinical trial of an individualized home-based exercise programme for women with fibromyalgia. Rheumatology. 2005;44:1422-1427.

Harris RE, Clauw DJ. How Do We Know That the Pain in Fibromyalgia Is "Real"? Current Pain and Headache Reports. 2006;10:403-7.

Harris RE, Clauw DJ, Scott DJ, McLean SA, Gracely RH, Zubieta JK. Decreased central u-opioid receptor availability in fibromyalgia. J Neurosci. 2007;27:10000-10006.

Holman AJ, Myers RR. A Randomized, Double-Blind, Placebo-Controlled Trial of Pramipexole, a Dopamine Agonist, in Patients With Fibromyalgia Receiving Concomitant Medications. Arthr Rheum. 2005; 52(: 2495-2505.

Mannerkorpi K, Henriksson C. Non-pharmacological treatment of chronic widespread musculoskeletal pain. Best Pract Res Clin Rheumatol. 2007;21:513-534.

McCabe CS, Cohen H, Blake DR. Somaesthetic disturbances in fibromyalgia are exaggerated by sensory-motor conflict: implications for chronicity of the disease? Rheumatology. 2007;46:1587-1592.

Mease P. Fibromyalgia syndrome: review of clinical presentation, pathogenesis, outcome measures, and treatment. J Rheumatol Suppl. 2005;32(10):2063.

Rico-Villademoros F, Hidalgo J, Dominguez I, García-Leiva JM, Calandre EP. Atypical antipsychotics in the treatment of fibromyalgia: a case series with olanzapine. Prog Neuropsychopharmacol Biol Psychiatry. 2005; 29(1): 161-4.

Rooks DS, Gautam S, Romeling M, Cross ML, Stratigakis D, Evans B, et al. Group exercise, education, and combination self-management in women with fibromyalgia. Arch Intern Med. 2007;167;2192-2200.

Van Koulil S, Effting M, Kraaimaat FW, van Lankveld W, van Helmond T, Cats H, et al. Cognitive-behavioural therapies and exercise programmes for patients with fibromyalgia; state of the art and future directions. Ann Rheum Dis. 2007;66:571-581.

Zheng L, Faber K. Review of the Chinese medical approach to the management of fibromyalgia. Curr Pain Headache Rep. 2005;9(5): 307-12.

Review Date:
12/17/2007
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

adam.com

Allergic rhinitis

FitSugar — Wed, 08 Oct 2008 17:35:27 -0700

In This Report

Highlights
Introduction
Causes
Symptoms
Risk Factors
Prognosis
Diagnosis
Treatment
Other Treatments
Decongestants
Antihistamines
Corticosteroids
Immunotherapy
Prevention
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Drug Approval

Ciclesonide (Omanaris), a corticosteroid nasal spray, has been approved for treatment of seasonal and perennial allergic rhinitis (hay fever) in adults and children age 12 years and older.

FDA Drug Warnings

The antihistamine promethazine (Phenergan) should not be given to children younger than age 2 because it may cause serious breathing problems.
Omalizumab (Xolair) may cause a life-threatening allergic reaction (anaphylaxis). This drug is used to treat allergy-related asthma, but is also being investigated as an allergy treatment.

Cough and Cold Medicines for Children

In 2007, the FDA began reviewing the safety and effectiveness of cough and cold medicines for children. These medicines contain antihistamines, decongestants, expectorants, and cough suppressants. The FDA is particularly concerned about the use of these medicines in children younger than 2 years of age. Overdoses can cause serious heart problems and death. However, many experts are concerned that the currently recommended dosages are themselves not safe.

Immunotherapy (Allergy Shots)

Immunotherapy is safe and effective for patients with allergic rhinitis, particularly those who have not been helped by other treatments, indicates a 2007 review in the Cochrane Database.
An experimental DNA-based ragweed vaccine is showing promise in early clinical trials. In a 2006 pilot study published in the New England Journal of Medicine, six weekly injections of the vaccine helped improve symptoms with benefits lasting into the following ragweed season.

Allergic Rhinitis and Sleep

Allergic rhinitis can cause sleep disorders and interfere with sleep quality, indicates a 2006 study in the Archives of Internal Medicine. In the study of nearly 600 patients with allergic rhinitis, patients with severe allergic rhinitis experienced worse sleep problems than those with mild allergic rhinitis.

Allergic Rhinitis and Parkinson’s Disease

Allergic rhinitis may be associated with the later development of the neurological disorder Parkinson’s disease, suggests a 2006 study in Neurology. Both conditions are associated with an inflammatory response.

Introduction

The nose is separated into two passages by a wall of cartilage called the septum. The nasal passages are lined with a membrane that produces a clear liquid called mucus. Mucus is a one of the body's defense systems:

The mucus traps small particles and bacteria, which may enter the nose as a person breathes.
The trapped bacteria usually do not cause harm in healthy individuals.
However, the bacteria can lead to a daily cycle of congestion and decongestion.
When one side of the nose is congested, air passes through the open (decongested) side. The sides alternate between being wide-open and partly or completely blocked.

If the congestion becomes severe or other changes occur that irritate the nasal passage, rhinitis develops. To be diagnosed with rhinitis, the patient must experience at least two of the following symptoms for an hour or more on most days:

Runny nose
Obstruction in the nasal passage
Nasal itching
Sneezing

Click the icon to see an image showing symptoms of allergic rhinitis.

These symptoms may occur as a result of colds or environmental irritants, such as allergens, cigarette smoke, chemicals, changes in temperature, stress, exercise, or other factors.

Infectious Rhinitis. If symptoms last less than 6 weeks, the condition is referred to as acute rhinitis and is usually caused by a cold or infection, or temporary overexposure to environmental chemicals or pollutants. [See In-Depth Report #94: Colds and the flu.]

Chronic Rhinitis. When rhinitis lasts for a longer period, the condition is called chronic rhinitis. Allergies are often the cause, but structural problems or chronic infections could also be to blame.

Aging Process. The elderly are at risk for chronic rhinitis as the mucous membranes become dry with age. In addition, the cartilage supporting the nasal passages weakens, causing changes in airflow. In such cases, therapy involves avoiding possible allergens and airborne irritants as well as measures to keep the nasal passages moist. Decongestants are not helpful.

Irritative Rhinitis. Irritative rhinitis is caused by an overreaction to irritants, such as cigarette smoke, dozens of other air pollutants, strong odors, alcoholic beverages, and exposure to cold. The nasal passages become red and engorged. This reaction is not the same as an allergic reaction, although both are associated with increased numbers of white blood cells called eosinophils.

Vasomotor Rhinitis. Vasomotor rhinitis, also sometimes called idiopathic or irritant rhinitis, is congestion and stuffy nose that is produced by the changes in blood vessels and nerve cells in the nasal passages. It occurs in response to irritants, including smoke, environmental toxins, changes in temperature and humidity, stress, and even sexual arousal. This over-reaction is not associated with any immune response. The biologic causes are unknown. Some research has found an association between vasomotor rhinitis and gastroesophageal reflux disorder (GERD, a common cause of heartburn), which some experts think may be due to a common defect in the nervous system that controls muscle action. Symptoms of vasomotor rhinitis are similar to most of those caused by allergies. Usually, however, they are more severe and occur predominantly on one side of the nose.

Foreign Objects. Blockage in young children is very often caused by foreign objects that they have pushed up their nose. If they are left in place, they may eventually cause infection and nasal discharge, (usually in one side of the nose), which may be yellow or green and foul smelling.

Blockage in the Nose from Polyps or Structural Abnormalities. A number of conditions may block the nasal passages. Surgery may be helpful for certain cases.

Polyps. These are soft, gray, fluid-filled sacs that develop off stalk-like structures on the mucus membrane. They impede mucus drainage and restrict airflow. Polyps usually develop from sinus infections that cause overgrowth of the mucus membrane in the nose. They do not regress on their own and may multiply and cause considerable obstruction.
Deviated Septum. A common structural abnormality that causes rhinitis is a deviated septum. The septum is the inner wall of cartilage and bone that separates the two sides of the nose. When deviated, it is not straight but shifted to one side, usually the left.
Other Causes of Blockage. Rarely, cleft palates, overgrowth of bones in the nose, or tumors cause rhinitis.

Nonallergic Rhinitis in Children. Chronic nasal congestion in children often accompanies a susceptibility to ear, sinus, or adenoid infections. Adenoids are spongy tissue masses located between ends of the nasal passages and the soft tissue in the back of the throat. Enlarged adenoids may also cause ear problems. The bacteria that cause these other infections, however, are not usually the cause of this chronic rhinitis.

Medications and Illegal Drugs. A number of drugs can cause rhinitis or worsen it in people with conditions such as deviated septum, allergies, or vasomotor rhinitis:

Overuse of decongestant sprays used to treat nasal congestion can, over time (3 - 5 days) cause inflammation in the nasal passages and worsen rhinitis.
Many people with allergies and asthma are sensitive to common painkillers known as nonsteroidal anti-inflammatory drugs (NSAIDs). These include aspirin, ibuprofen (Motrin, Advil, Nuprin, Rufen), and naproxen (Aleve), among many others. Aspirin and products containing aspirin can even cause life-threatening asthma attacks in some highly susceptible individuals. NSAIDs vary, however, and some patients may not have a reaction to all of them. For minor pain, acetaminophen (Tylenol), which is not an NSAID, is usually recommended for patients with intolerance to NSAIDs. A pharmacist should be consulted if the ingredients of any over-the-counter preparations are not known.
Other medications that may cause rhinitis include oral contraceptives, hormone replacement therapy, anti-anxiety drugs (particularly alprazolam), some antidepressants, and some blood pressure medications, including beta-blockers and vasodilators.
Sniffing cocaine damages nasal passages and can cause chronic rhinitis.

Estrogen in Women. Elevated levels of estrogen appear to increase mucus production and swelling in the nasal passages and can cause congestion. This effect is most apparent in women during pregnancy. In such cases the condition usually clears up after delivery. Oral contraceptives and hormone replacement therapies that contain estrogen have also been associated with nasal congestion in some women.

Medical Conditions. Hypothyroidism is associated with chronic rhinitis. People with certain genetic or other medical conditions that specifically affect the mucous membranes are at also risk, although rhinitis in such people is apt to be only one of many more serious conditions, including chronic sinusitis and respiratory problems. Wegener's granulomatosis, for example, is a serious but very rare illness that causes long-term swelling and tumor-like masses in air passages.

Rare genetic disorders that cause chronic rhinitis include the following:

Cystic fibrosis, in which the mucus is very thick.
Kartagener's syndrome. With this condition the body's major internal organs are located in the mirror-image position of their normal location. In addition, the body's cilia (hair-like-projections on many body tissues that help to move mucus and other fluids) are impaired or motionless.

In both disorders, mucus build-up also produces an environment favorable to infection-causing organisms.

Click the icon to see an image of a deviated septum.

Click the icon to see an image of the adenoids.

Causes

The allergic process, called atopy, and its connection to asthma is not completely understood. It involves various airborne allergens or other triggers that set off a cascade of events in the immune system leading to inflammation and hyperreactivity in the airways.

The conductor in an orchestra of immune factors that contribute to allergies and asthma appears to be a category of white blood cells known as helper T cells, in particular a subgroup called Th2 cells.
Th2 cells overproduce interleukins (ILs), immune factors that are molecular members of a family called cytokines, which are involved in the inflammatory process.

Interleukins 4, 9, and 13 may be responsible for a first-phase asthma attack. These interleukins stimulate the production and release of antibody groups known as immunoglobulin E (IgE). People with both asthma and allergies appear to have a genetic predisposition for overproducing IgE.
During an allergic attack, these IgE antibodies bind to special cells in the immune system called mast cells, which are generally concentrated in the lungs, skin, and mucous membranes. This bond triggers the release of a number of active chemicals, importantly potent molecules known as leukotrienes. These chemicals cause airway spasms, overproduce mucus, and activate nerve endings in the airway lining.
Another cytokine, interleukin 5, appears to contribute to a late-phase inflammatory response. This interleukin attracts white blood cells known as eosinophils. These cells accumulate and remain in the airways after the first attack. They persist for weeks and mediate the release of other damaging particles that remain in the airways.

One theory blames the dramatic increase in asthma and allergies on the reductions in childhood infections that have occurred with modern hygiene and antibiotic use. The basic theory rests on the idea that infections stimulate production of specific immune factors called Th1 cells. As these cells build up, they replace other immune factors called Th2 cells, which react to allergens -- a less serious threat to the body. Without infections to stimulate the production of the Th1 infection fighters, the Th2 allergen fighters are not replaced, and they persist at high levels, making the growing child more susceptible to allergies and asthma.

A number of different studies support this theory:

Some studies suggest that being part of a large family or attending day care increases the risk for early respiratory infections but reduces the risk of childhood asthma. The occasional cold, then, may be protective.
In a 2002 study, researchers measured levels of bacterial byproducts called endotoxins in the mattress dust of 812 children. Those with the highest levels had an 80% lower rate in allergies and asthma.
Another study further found a strong association between allergy development and the absence of certain beneficial bacteria (called probiotics) in infants' intestines. Infants who were born in more hygienic environments tended to lack these bacteria. Antibiotic overuse and modern hygiene may reduce these helpful organisms. (Probiotics are available in active yogurt cultures and in supplements, which are being studied for protection.)

According to many studies, the standard vaccinations against serious childhood infections pose no risk for developing asthma or hay fever. Some studies have even reported lower risk for asthma and allergies in the second and third years after vaccinations.

Some evidence suggests that the increase in allergies and asthma may be due to overexposure to indoor allergens. These may include wall-to-wall carpeting, cats, and mold produced by dampness in homes. Children who spend hours indoor each day may become overexposed to indoor allergens. This exposure is intensified by the recent trend of making homes more energy-efficient, which may result in more dust mites being trapped inside. However, other studies suggest that early exposure to allergens may actually prevent the development of allergies in children.

Seasonal allergic rhinitis occurs only during periods of intense airborne pollen or spores. It is commonly, although inaccurately, called hay fever or rose fever, depending on whether it occurs in the late summer or spring. No fever accompanies this condition, and the allergic response is not dependent on either hay or roses. In general, triggers of seasonal allergy in the U.S. include:

Ragweed. Ragweed is the most dominant cause of allergic rhinitis in the U.S., affecting about 75% of allergy sufferers. One plant can release 1 million pollen grains a day. Ragweed occurs everywhere in the U.S., although it is less common in western coastal states, southern Florida, northern Maine, Alaska, and Hawaii. The effects of ragweed in the northern states are first felt in middle to late August and last until the first frost. Ragweed allergies tend to be most severe before midday.
Grasses. Grasses affect people in mid-May to late June. Grass allergies are experienced more in the late afternoon.
Tree Pollen. Small pollen grains from certain trees usually produce symptoms in late March and early April.
Mold Spores. Mold spores that grow on dead leaves and release spores into the air are common allergens throughout the spring, summer and fall. Mold spores may peak on dry windy afternoons or on damp or rainy days in the early morning.

Click the icon to see an animation about allergies.

Major weather changes, such as El Nino, can affect the timing of allergy seasons. For example, in 1998, when the effects of El Nino were very strong, allergy attacks were markedly increased, and maximum tree pollen counts occurred 2 - 4 weeks earlier and mold counts 2 - 3 months earlier than the previous year.

Allergens in the House. Allergens in the house can trigger attacks in people with year-long allergic rhinitis, called perennial rhinitis. Household allergens may include the following:

House dust and mites. Dust mites, specifically mite feces, are coated with enzymes that contain a powerful allergen.
Cockroaches
Pet dander
Molds growing on wallpaper, house plants, carpeting, and upholstery

However, some studies are suggest that early exposure to some of these allergens, including dust mites and pets, may prevent allergies from developing in the first place in children.

Fossil Fuels. There may be an association between traffic-related air pollution and allergic rhinitis. Some experts believe that refined fossil fuels, such as diesel fuel and particularly kerosene, are important triggers for allergic rhinitis. In people who already have allergies or asthma, exposure to such fossil fuels may worsen symptoms.

Symptoms

The general symptoms of rhinitis are congestion, runny nose, and postnasal drip, in which mucous drips into the throat from the back of the nasal passage, especially when lying on the back. Symptoms may vary depending on the cause of rhinitis. Symptoms of influenza and sinusitis must also be differentiated from allergies and colds.

Symptoms of allergic rhinitis occur in two phases, early and late.

Early Phase Symptoms. The early phase occurs within minutes of exposure to the allergens and includes:

Runny nose
Frequent or repetitive sneezing
Itching in the nose, eyes, throat, or roof of the mouth

Late-Phase Symptoms. The late phase occurs 4 - 8 hours later and may include one or more of these symptoms:

Nasal congestion and possibly plugged ears. Children may push their nose upward with the palm of their hand or twitch their nose rabbit-like to clear the obstruction.
Fatigue.
Mental changes can include irritability, a slight decrease in attention span, worsened memory, and slower thinking.
Other common physical symptoms include a decreased sense of smell, plugged ears, sinus headache, postnasal drip or some combination. In severe allergies, dark circles may develop under the eye. The lower eyelid may be puffy and lined with creases.

Risk Factors

Allergic rhinitis affects between 20 - 40 million Americans of all ages. As with asthma and many upper respiratory infections, the incidence in allergic rhinitis is increasing. Allergies most often appear first in childhood, and allergic rhinitis is the most common chronic condition in childhood, although it can develop at any age. About 20% of allergic rhinitis cases are due to seasonal allergies, 40% to perennial (chronic) rhinitis, and the rest are mixed.

Genetic factors are the major determinants of allergies.

If both parents have an allergy, the child's risk is 75%.
If one parent is allergic, the child's risk is 50%.

Having other allergies increases the risk for allergic rhinitis. Here are some examples:

Young children who have eczema (an allergic skin reaction) have a later risk for allergic rhinitis and asthma. In fact, a family history of eczema increases the risk.
Food allergies are associated with allergic rhinitis and asthma. (Early feeding patterns, time of weaning, and introduction of solid food do not appear to affect this risk.)
Asthma, especially in patients who develop it as adults, may increase allergic sensitivity to ragweed and other allergens. Patients who have asthma and a genetic tendency towards allergies (atopy) are also at risk for rhinitis.

Birth Month. Some studies report a higher risk of allergies and asthma in children born in winter months and lower risk in those born during the summer.

Breastfeeding. Some researchers suggest that the dramatic increase in asthma and allergies may be due to fewer women breastfeeding their infants. In a number of studies, breastfeeding has been associated with a lower risk for allergies and asthma -- at least until age 2. Breastfeeding can also help prevent other upper respiratory infections. The American Academy of Pediatrics recommends feeding infants exclusively breast milk for the first 6 months of life.

Prognosis

Seasonal allergic rhinitis tends to diminish as a person ages. The earlier the symptoms start, the greater the chances for improvement. People who develop hay fever in early childhood tend not to have the allergy in adulthood. In one study, over half of allergic subjects reported that by 40 years of age their symptoms had decreased, and a quarter were symptom-free. In some cases, allergies go into remission for years and then return later in life. People who develop allergies after age 20, however, tend to continue to have hay fever at least into middle age.

People with allergic rhinitis may be at higher risk for other allergies, including potentially serious food or latex allergies.

Although allergic rhinitis is not considered a serious condition, it nonetheless can interfere with many important aspects of life. A 2006 survey of nasal allergy sufferers reported that symptoms made patients feel tired (80%), miserable (65%), irritable (62%), and interfered with work performance (52%).

People with allergic rhinitis, particularly those with perennial allergic rhinitis, may experience sleep disorders and daytime fatigue. Often they attribute this to medication, but studies suggest congestion may be the culprit in these symptoms. In addition, a 2002 study indicated that patients with seasonal allergies experience hundreds of brief, subtle awakenings, called "microarousals," each night. In such cases, people are not aware that they wake up, but such events can cause fatigue the next day. A 2006 study of nearly 600 patients with allergic rhinitis found that sleep disorders and poor sleep quality were prevalent. Patients who had severe allergic rhinitis had worse sleep problems than those with mild allergic rhinitis.

Asthma and allergies often coexist, and the allergic response plays a strong role in childhood asthma. About 70 - 85% of children with asthma have allergies. Aggressive treatment of allergies in children with asthma can lower the risk for asthma attacks. Treating allergies in children may also help prevent the onset of asthma.

Any chronic rhinitis, whether allergic or nonallergic, can cause swelling in the turbinate, which may become persistent (turbinate hypertrophy). The turbinate is a tiny shelf-like bony structure that protrudes in the nasal passageways. It helps warm, humidify, and clean the air that passes over it. If turbinate hypertrophy develops, it causes persistent nasal congestion and, sometimes, pressure and headache in the middle of the face and forehead. This condition requires surgery.

Children with severe allergies may have a higher risk for behavioral problems than those without allergies. Some research suggests that allergic rhinitis is responsible for 2 million missed school days each year.
There have been reports that 30 - 45% of people with allergic rhinitis also suffer from ear infections (otitis media).
Chronic nasal obstruction from year-round allergies can affect a child's appearance. If a child can only breathe through the mouth, the continual force of air passing through the oral cavity can change facial development. Such changes may include an elongated face and an overbite from teeth coming in at an abnormal angle.
Chronic rhinitis can cause headaches and also affect a child's sleep, concentration, hearing, appetite, and growth.

Depression. Some evidence has linked depression with allergies. A 2002 study, for example, found that people with depression reported a higher rate of allergic disorders (71%) compared to nondepressed individuals (43%). During allergy season, patients with allergies were more likely to experience mood changes, including sadness, lethargy, and mental fatigue, than at other times. Some evidence suggests that specific immune factors in the allergic response can cause depressive symptoms. Other research indicates that both may have a common cause.

Parkinson’s Disease. A 2006 study suggested that allergic rhinitis may be associated with the later development of the neurological disorder Parkinson’s disease. The researchers think that the inflammatory response may be the link between the two conditions. However, there is not yet any evidence that treating allergic rhinitis can prevent Parkinson’s disease.

Chronic Fatigue Syndrome (CFS). Some, although not all, studies have reported that a majority of patients with CFS also have allergies to foods, pollen, metals (such as nickel or mercury), or other substances. One theory is that allergens, like viral infections, may trigger a harmful overreaction of the immune system that can cause fatigue, joint aches, and fever as well as hormone and brain chemical disturbances. (However, most people with allergies do not have CFS.)

Diagnosis

To determine the cause of allergic rhinitis, the doctor will ask a number of questions about:

Time of day and year of rhinitis episodes. Rhinitis that appears seasonally is typically due to pollens and outdoor allergens. If symptoms occur throughout the year, the doctor will suspect perennial allergic or non-allergic rhinitis.
Family history of allergies.
History of medical problems.
In women, if they are pregnant or taking drugs that contain estrogen (oral contraceptives, hormone replacement therapy).
Use of other medications including decongestants, which can cause a rebound effect.
Pets.
Any additional unusual symptoms. As examples, bloody nasal discharge and obstruction in only one nasal passage could suggest a tumor. Fatigue, sensitivity to cold, weight gain, and depression may be signs of hypothyroidism.

The doctor will examine the inside of the nose with an instrument called a speculum. This is a painless examination allowing the doctor to check for redness and other signs of inflammation. The doctor will also usually check the eyes, ears, and chest.

A skin test is a simple method for detecting common allergens. Patients are usually tested for a panel of common allergens. Skin tests are rarely needed to diagnose mild seasonal allergic rhinitis, since the cause is usually obvious. The skin test is not appropriate for children younger than age 3.

The procedure is as follows:

Patients should not take antihistamines for at least 12 - 72 hours before the test. Otherwise an allergic reaction may not show up.
Small amounts of suspected allergens are applied to the skin with a needle prick or scratch or are injected a few cells deep into the skin. The injection test may be more sensitive than the standard prick test.
If an allergy is present, a hive (a swollen reddened area) forms within about 20 minutes.

The test is not completely accurate. For instance, a 2001 study reported that testing detected allergies in less than half of children with rhinitis. Furthermore, about 15 - 20% of people may have a skin reaction without actually having an allergy.

Nasal Smear. The doctor may take a nasal smear. The nasal secretion is examined microscopically for factors that might indicate a cause, such as increased numbers of white blood cells, indicating infection, or high counts of eosinophils. High eosinophil counts indicate an allergic condition, but low counts do not rule out allergic rhinitis.

Tests for IgE. Blood tests for IgE immunoglobulin production may also be performed. One test is called the radioallergosorbent Test (RAST), used to detect increased levels of allergen-specific IgE in response to particular allergens. Blood tests for IgE may be less accurate than skin tests. They should be performed only on patients who cannot undergo skin testing or when skin test results are uncertain.

In people with chronic rhinitis, the doctor may also check for sinusitis. Imaging tests may be useful if other tests are ambiguous.

A test called transillumination, in which a doctor shines a bright light against the patient's cheek or forehead, is an inexpensive method for checking for abnormalities in the sinus cavities, although it is not highly accurate.
CT scans may be useful for some cases of sinusitis.

Click the icon to see an image of a CT scan.

In certain cases of chronic or unresponsive seasonal rhinitis, a doctor may use endoscopy to examine for any irregularities in the nose structure. Endoscopy uses a tube inserted through the nose that contains a miniature camera to view the passageways.

Treatment

If rhinitis is caused by non-allergic conditions, particularly if there are accompanying symptoms indicating a serious problem, the doctor should treat any underlying disorders. If rhinitis is caused by medications, such as decongestants, the patient may need to stop taking them or find alternatives.

Patients with chronic allergic rhinitis may require daily medications. Patients with severe seasonal allergies should start medications a few weeks before the pollen season and continue taking them until the season is over. Effective medications include:

Drugs that reduce the inflammatory response are important for preventing severe allergic rhinitis. Nasal corticosteroids (commonly called steroids) are now considered to be the most effective measure for preventing allergy attacks. Other anti-inflammatory drugs include leukotriene-antagonists and nasal cromolyn.
Antihistamine tablets relieve sneezing and itching and can prevent nasal congestion before an allergy attack. Many brands are available by prescription and over-the-counter.
Immunotherapy ("allergy shots") may be considered for patients with severe seasonal allergies that do not respond to treatment. It may also prevent asthma and the development of new allergies in children. Many experts now recommend immunotherapy for people with both asthma and allergies. Newer immunotherapeutic approaches using specially designed antibodies and vaccines are also showing promise.

All drug treatments have side effects, some very unpleasant and, in rare cases, serious. Patients may need to try different drugs until they find one that relieves symptoms without producing excessively distressing side effects.

Because seasonal allergies generally last only a few weeks, most doctors do not recommend the more potent prescription treatments for children. It is important for parents to determine if the child is actually under severe distress and that the parent is not simply responding to their own anxiety when they hear the child snorting or snoring. Prescription drugs are required only in severe cases. However, in children with both asthma and allergies, treatments for allergic rhinitis may also improve asthmatic symptoms.

Treating Mild Allergy Attacks. Mild allergy attacks usually require little more than reducing exposure to allergens and using a nasal wash. Dozens of treatments are available for allergic rhinitis. Many are available over-the-counter, but some require a prescription. They include the following:

Nasal washes
Decongestants that relieve nasal congestion and itchy eyes
Decongestant/antihistamine combinations

Due to side effects, decongestants should not be used in children ages 14 years or younger. Also, overuse of nasal decongestions can actually worsen sinus congestion.

Treating Severe Allergic Rhinitis. Patients with chronic allergic rhinitis, particularly if they also have asthma, may require daily medications. These drugs include:

Antihistamines. The newer non-sedating antihistamines -- such as cetirizine (Zyrtec), loratadine (Claritin), fexofenadine (Allegra), or desloratadine (Clarinex) -- cause less drowsiness than older antihistamines, such as Benadryl. Some of the newer drugs, such as Zyrtec and Clarinex, may also relieve nasal congestion.
Anti-inflammatory drugs. Nasal corticosteroids are now considered to be the most effective measure for preventing allergy attacks. They are recommended for patients with very severe allergies that do not respond to antihistamines.
Leukotriene-antagonists and nasal cromolyn may be beneficial in specific cases of allergies
Immunotherapy ("allergy shots") works well for many patients with severe allergies. It is also proving to reduce asthma symptoms and the use of asthma medications in patients with known allergies.

Itching and redness in the eyes sometimes respond to oral antihistamines. Eye drops, however, provide faster relief, and a combination of the two may be best. The following are eye drops for itchy eyes. Others are also available. Individual responses vary, and patients need to find which specific treatment works best for them.

Antihistamine eye drops: azelastine (Optivar), olopatadine (Patanol), ketotifen (Zaditor), levocabastine (Livostin) for relief of both nasal symptoms and itchy red eyes
Decongestant eye drops: phenylephrine (Allergan Relief), naphazoline (Naphcon, Opcon-A, VasoClear), tetrahydrozoline (Murine Plus, Visine)
Combination decongestant/antihistamine: Visine A.
Corticosteroids: loteprednol (Lotemax, Alrex), pemirolast (Alamast).

General Side Effects and Warning.

All eye drops can cause stinging, and some may result in headache and congestion.
No one should continue taking eye drops if they experience pain, changes in vision, worsened redness, or irritation, or if the condition lasts more than 3 days.
Do not touch the tip of the device to the eye or touch other surfaces with it. Replace the cap after using. Discard any solution that changes color or becomes cloudy.
People who have heart disease, high blood pressure, an enlarged prostate gland, or glaucoma should talk to their doctor before taking these types of eye drops.

Other Treatments

For mild allergic rhinitis, a nasal wash can be helpful for removing mucus from the nose. You can purchase a saline solution at a drug store or make one at home (one cup of warm water, half teaspoon salt, pinch of baking soda). Over-the-counter saline nasal sprays that contain benzalkonium chloride as a preservative may actually worsen symptoms and infection.

Simple method for administering a nasal wash:

Lean over the sink head down.
Pour some solution into the palm of the hand and inhale it through the nose, one nostril at a time.
Spit the remaining solution out.
Gently blow the nose.

The solution may also be inserted into the nose using a large rubber ear syringe, available at a pharmacy. In this case the process is:

Lean over the sink head down.
Insert only the tip of the syringe into one nostril.
Gently squeeze the bulb several times to wash the nasal passage.
Then press the bulb firmly enough so that the solution passes into the mouth.
Repeat the process in the other nostril.

Nearly half of asthma or allergy sufferers resort to alternative treatments. To date, however, little evidence supports treatments such as high-dose vitamins, homeopathic remedies, and most herbal remedies. Some relaxation methods, such as massage therapy, may be beneficial in reducing stress related to allergy symptoms. According to research presented at a 2004 allergy conference, acupuncture is now the most popular alternative treatment among allergy sufferers. The following are examples of recent areas of research:

Acupuncture may provide symptom relief for persistent allergic rhinitis in children, according to results published in a 2004 pediatrics journal. The study compared the effects of active versus sham acupuncture. Larger trials are needed to confirm these results.
Butterbur (also known as Petasites hybridus, butter dock, blatterdock, bog rhubarb, and exwort) is a plant found in Europe, North American, and parts of Asia. It is a traditional herbal remedy used for seasonal allergies and asthma. In a 2002 study, it was as effective and less sedating than a commonly prescribed antihistamine for treating seasonal allergies over a 2-week period.
Probiotics are beneficial bacteria that may help protect against allergies and asthma. Probiotics are available in active yogurt cultures and in supplements, which are being studied for protection.

The following are special concerns for people with allergic rhinitis:

Grapeseed extract is sometimes touted as a natural antihistamine. A 2002 study, however, reported no benefits from it.
A 2002 study found no benefits with homeopathy immunotherapy for asthmatic patients allergic to dust mites.
Some patients have reported worse symptoms after drinking herbal teas, which may contain leaves or pollens the patient is sensitive to. Herbal remedies themselves can trigger an allergic reaction. For example, echinacea is of special concern. This herbal remedy actually boosts the immune system. People with nasal congestion may mistakenly take it because it is often used to treat colds. In the case of allergies, however, echinacea may worsen symptoms or even trigger them in people who haven't experienced them. People with autoimmune diseases or who have plant allergies should particularly avoid it.
A Chinese herbal cold and allergy remedy sold as Aller Relief contains trace amounts of aristolochic acid, a chemical that is toxic to the kidneys and a carcinogen. Products containing aristolochic acid have been associated with several reports of kidney failure in Europe. Of specific concern are studies suggesting that up to 30% of herbal patent remedies imported from China have been laced with potent pharmaceuticals such as phenacetin and steroids. Asian herbal remedies may also contain toxic metals.
Aromatherapy is often used for relaxation. Some of the exotic plant extracts in these formulas have been associated with a wide range of skin allergies.

Decongestants

For mild allergic rhinitis, a nasal wash can be helpful for removing mucus from the nose. Decongestants may help dry nasal congestion. They work by shrinking vessels in the nose. By reducing blockage, they decrease the risk of developing sinusitis caused by viruses or bacteria. Many over-the-counter decongestants are available, either in tablet form or as nasal or inhaled decongestants that are applied directly into the airways as sprays, drops, or vapors.

Nasal-delivery decongestants are applied directly into the nasal passages with a spray, gel, drops, or vapors. Nasal decongestants come in long-acting or short-acting forms. The effects of short-acting decongestants last about 4 hours; long-acting decongestants last 6 - 12 hours. The active ingredients in nasal decongestants include oxymetazoline, xylometazoline, and phenylephrine. Nasal forms work faster than oral decongestants and may not cause as much drowsiness. However, they can cause dependency and rebound.

Dependency and Rebound. The major hazard with nasal-delivery decongestants, particularly long-acting forms, is a cycle of dependency and rebound effects. The 12-hour brands pose a particular risk for this effect.

With prolonged use (more than 3 - 5 days), nasal decongestants lose effectiveness and can cause swelling in the nasal passages.
The patient then increases the frequency of the dose. As the congestion worsens, the patient may respond with even more frequent doses.
This causes dependency and increased nasal congestion.

Tips for Use. The following precautions are important for people taking nasal decongestants:

When using a nasal spray, spray each nostril once. Wait a minute to allow absorption into the mucosal tissues, and then spray again.
Do not share droppers and inhalators with other people.
Discard sprayers, inhalators, or other decongestant delivery devices when the medication is no longer needed. Over time, these devices can become reservoirs for bacteria.
Discard the medicine if it becomes cloudy or unclear.

Oral decongestants also come in many brands, which have similar ingredients. The most common active ingredient is pseudoephedrine (Sudafed, Actifed, Drixoral), sometimes in combination with an antihistamine. [The alternative decongestant, phenylpropanolamine (PPA) was taken off the market.] A small 2006 study reported that over-the-counter pseudoephedrine works just as well as the prescription drug montelukast (Singulair) in controlling allergic rhinitis symptoms. Patients in the study received a once-daily morning dose (240 mg) of ephedrine. Researchers suggest that taking pseudoephedrine in the morning, as opposed to later in the day or before bedtime, can help patients avoid side effects such as insomnia and nervousness.

Decongestants have certain adverse effects, which are more apt to occur in oral than nasal decongestants. These side effects include:

Agitation and nervousness
Drowsiness (particularly with oral decongestants and in combination with alcohol)
Changes in heart rate and blood pressure
Avoid combinations of oral decongestants with alcohol or certain drugs, including monoamine oxidase inhibitors (MAOI) and sedatives.

Individuals at Risk for Complications from Decongestants. People who may be at higher risk for complications are those with certain medical conditions, including disorders that make blood vessels highly susceptible to contraction. Such conditions include:

Heart disease
High blood pressure
Thyroid disease
Diabetes
Prostate problems that cause urinary difficulties
Migraines
Raynaud's phenomenon
High sensitivity to cold
Emphysema or chronic bronchitis. (Individuals with these conditions should particularly avoid high-potency, short-acting nasal decongestant.)
Medications that increase serotonin levels, such as certain antidepressants, anti-migraine drugs, diet pills, St. John's wort, and methamphetamine. The combination of these medicines and decongestants can cause blood vessels in the brain to narrow suddenly, causing severe headaches and even stroke.

Anyone with these conditions should not use oral or nasal decongestants without a doctor's guidance. Other people who should not use decongestants without first consulting a doctor include:

Pregnant women
Children. The American College of Chest Physicians advises against the use of over-the-counter decongestants and other cold medications in children ages 14 years or younger. Children are at particular risk for side effects that depress the central nervous system. Such symptoms cause changes in blood pressure, drowsiness, deep sleep, and, rarely, coma. In 2007, the FDA began reviewing the safety and effectiveness of cough and cold remedies for children.

In 2000, the Food and Drug Administration (FDA) took action to ban oral decongestants containing phenylpropanolamine (PPA) from the U.S. market. This action was in response to reports of an increased risk of stroke in young women who took products containing this ingredient. All major brands that previously contained PPA have now substituted other active ingredients (usually pseudoephedrine) and are safe to use.

Anyone with old forms of decongestant should check the labels and discard them if they contain phenylpropanolamine.

Antihistamines

Histamine is one of the chemicals released when antibodies overreact to allergens. It is the cause of many symptoms of allergic rhinitis. Antihistamines can help relieve:

Itching, sneezing, and nasal discharge
Other allergy symptoms unrelated to rhinitis, including hives and some rashes
Nasal congestion, for some of the newer antihistamines, such as cetirizine (Zyrtec) and desloratadine (Clarinex)

If possible, patients should take antihistamines before an anticipated allergy attack.

Many antihistamines are available. They include short-acting and long-acting forms and are available as tablets, nasal-inhalers, eye drops, and syrups. Antihistamines are generally categorized as first- and second-generation. First-generation antihistamines may cause more side effects than newer second-generation ones.

There are some notes of caution when taking any antihistamine:

Antihistamines may thicken mucus secretions and can worsen bacterial rhinitis or sinusitis.
Antihistamines can lose their effectiveness over time, and a different one may need to be tried.

First-Generation Antihistamines Ingredients and Brand Names. The older, so-called first generation antihistamines include:

Diphenhydramine (Benadryl)
Carbinoxamine (Clistin)
Clemastine (Tavist)
Chlorpheniramine (Chlor-Trimeton). Some health professionals recommend this drug if antihistamines are required during pregnancy. It may be as effective as the second generation antihistamines and much less expensive.
Brompheniramine (Dimetane)
Promethazine (Phenergan). This antihistamine should never be used for children younger than age 2 because it may cause life-threatening breathing problems.

First-generation antihistamines contain compounds called anticholinergics, which tend to produce more side effects than second-generation antihistamines.

Side Effects

Drowsiness and impaired thinking
Dry mouth
Dizziness
Agitation
Insomnia or nightmares
Sore throat
Rapid heart beat and chest tightness (uncommon and should be reported)
Men with enlarged prostate glands may experience difficulty urinating

Drowsiness and First-Generation Antihistamines. Drowsiness is the most distressing side effect reported from first-generation antihistamines, and is potentially serious. It may pose a higher than average risk for work-related and automobile accidents than alcohol, narcotics, or prescription sedatives. However, some studies have not found any strong differences in sedation between the first- and second-generation antihistamines. Still, experts caution against the first-generation antihistamines for people most at risk from sedative effects, particularly elderly individuals. To reduce risks, take the antihistamine at home a few hours before bedtime, and do not combine it with alcohol or tranquilizers. Do not drive or operate heavy machinery.

The newer second-generation antihistamines do not contain anticholinergics, so they do not usually cause drowsiness to the extent that the first generation antihistamines do. They are sometimes referred to collectively as nonsedating antihistamines.

A major 2003 analysis reported that although Benadryl, the most common first-generation antihistamine, had a more negative effect on daily activities than the newer antihistamines, the differences were modest. Researchers in the study concluded that no clear distinction exists between the first- and second-generation antihistamines.

Brand Names. The second-generation drugs include:

Loratadine (Claritin). Claritin is available over-the-counter and is approved for children ages 2 and older. Desloratadine (Clarinex) is similar to Claritin but stronger and longer-lasting. It is available only by prescription.
Cetirizine (Zyrtec). Zyrtec is approved for both indoor and outdoor allergies. It is the only antihistamine to date approved for infants as young as 6 months. It is available over-the-counter.
Fexofenadine (Allegra) is also available over-the-counter.
Acrivastine (Semprex)
Ebastine, norastemizole, levocetirizine, and mizolastine are other second-generation antihistamines under investigation in the U.S. and Europe. Some may prove to be useful for specific populations.

For nonprescription antihistamines, some studies suggest that cetirizine (Zyrtec) is more effective than Allegra or Claritin in improving symptoms, including those in children. However, cetirizine can cause drowsiness when taken at high doses.

Zyrtec and Claritin are approved for children younger than 5 years, although most antihistamines appear to be safe in children. Zyrtec is the only antihistamine approved for both indoor and outdoor allergies and for infants as young as 6 months. Both are available in syrup form. Studies with Zyrtec have reported fewer symptoms in children allergic to dust mites, and one study reported that infants with allergies who were given Zyrtec were much less likely to develop asthma later on than untreated infants. Claritin, at this time, is generally the preferred drug for young people, however, because it has the least negative effect on concentration and learning. Women who are pregnant or nursing should avoid these medications unless recommended by a doctor.

Side Effects and Precautions

Common side effects include headache, dry mouth, and dry nose. (These are often only temporary and go away during treatment.)
Drowsiness occurs in about 10% of adults and between 2 - 4% of children.
Uncommon side effects include rapid heart beat and chest tightness. Tell your doctor if these effects occur.
Extended-release forms of Claritin and Zyrtec have other ingredients that can cause other symptoms, including nervousness, restlessness, and insomnia. Some patients taking Claritin-D 24 Hour Extended Release tablets have reported obstruction in the upper gastrointestinal tract, including difficulty swallowing.

Drug and Food Interactions. Two earlier second generation drugs, terfenadine (Seldane) and astemizole (Hismanal), in rare cases, caused dangerous heart rhythm abnormalities, particularly in high doses or in people who had liver disease. They also caused interactions with certain other medications and grapefruit juice. Both Seldane and Hismanal have been taken off the market. Allegra, Zyrtec, and Claritin do not appear to pose any of the dangers associated with Seldane.

Until more is known, however, anyone who takes a second-generation antihistamine should probably avoid or use with caution combinations with grapefruit juice or the drugs that caused problems with Seldane and Hismanal. Such medications include:

The antibiotics clarithromycin (Biaxin) and troleandomycin
Certain HIV protease inhibitors
Antidepressant serotonin-reuptake inhibitors (Prozac, Paxil, and Serzone)

Azelastine (Astelin) and levocabastine (Livostin) are available in nasal spray form. They can reduce nasal congestion as well as allergy symptoms. Both reduce symptoms, although azelastine may be more effective in some patients. Their disadvantages are a bitter taste, drowsiness, and expense. They are not as effective as steroid nasal sprays.

Many prescription and non-prescription products that combine antihistamines and decongestants are available. Combinations sold over-the-counter include Allerest, Sudafed Severe Cold Formula, Vicks DayQuil, Benadryl Allergy/Sinus, Contac Day/Night Allergy & Sinus. Prescription combinations include Claritin-D, Allegra D, and Zyrtec-D. Symptoms may improve within 60 minutes, with congestion clearing up first.

Corticosteroids

A number of drugs are available for reducing the inflammatory response in allergies. These drugs can help prevent an allergy attack from occurring.

Nasal-spray corticosteroids (commonly called steroids) are considered the most effective drugs for treating severe allergic rhinitis. Corticosteroids suppress important stress and other hormones in a region of the brain called the HPA axis. The suppression of these hormones blocks the inflammatory response that triggers an allergic attack. Steroids do not relieve symptoms immediately. It may take several hours before their effects are felt. Nasal spray steroids benefits include:

Reducing inflammation and mucus production
Improving night sleep and daytime alertness in patients with perennial allergic rhinitis
Treating polyps in the nasal passages

Comparison studies report that nasal steroid sprays work better than second generation antihistamines, such as loratadine (Claritin) and cetirizine (Zyrtec), and are possibly even more effective than allergy shots. They have no effect on itchy eyes, however.

Nasal-Spray Brands. Corticosteroids available in nasal spray form include:

Triamcinolone (Nasacort). Approved for children over age 6.
Mometasone furoate (Nasonex). Approved for use in patients age 3 and older.
Fluticasone (Flonase, Flounce, generic). Approved for children over age 4.
Beclomethasone (Beconase, Vancenase), flunisolide (Nasalide), and budesonide (Rhinocort). Approved for children over age 6.
Ciclesonide (Omnaris). Approved for patients age 12 and older.

Side Effects. Corticosteroids are powerful anti-inflammatory drugs. Although oral steroids can have many side effects, the nasal-spray form affects only local areas and has less risk for widespread side effects unless the drug is used excessively. Side effects of nasal steroids may include:

Dryness, burning, stinging in the nasal passage
Sneezing
Headaches and nosebleed (uncommon but should be reported to your doctor immediately)

Possible Long-Term Complications. All corticosteroids suppress stress hormones. This effect is known to produce some serious long-term complications in people who take oral steroids. Researchers have found far fewer concerns with nasal administration or inhaled forms, but there may be certain problems:

Effect on growth. The major concern for children is whether nasal steroids, like other forms of steroids, will adversely affect growth. Studies report either a temporary and slight (about half an inch) early effect on growth or no effect at all.
Effect on eyes. Glaucoma is a known side effect of oral steroids. Some ophthalmologists have observed higher pressure in the eye (a sign of glaucoma) in some patients taking nasal steroid sprays. (Studies have found no increased risk for cataracts in young people who have taken intranasal steroids). The eye pressure appears to return to normal after stopping the steroid, but periodic eye examinations are advised.
Use during pregnancy. Steroids appear to be safe during pregnancy, but pregnant women should talk to their doctor about other options before taking them.
Nasal passage injury. Steroid sprays may injure the nasal septum (the bony area that separates the nasal passage) if the spray is directed onto it. This complication is very rare.
Lower resistance to infection. People with any infectious disease or injury in the nose should not take these drugs until the disease or wound has been treated and cured.

Cromolyn serves as both an anti-inflammatory drug and a specific blocker for allergens. The standard cromolyn nasal spray (Nasalcrom) is not as effective as steroid nasal sprays but does work well for many people with mild allergies. It is one of the preferred first-line therapies for pregnant women with mild allergic rhinitis. It may take up to 3 weeks to experience full benefit.

Side Effects. Cromolyn has no major side effects, but minor ones include nasal congestion, coughing, sneezing, wheezing, nausea, nosebleeds, and dry throat. The spray can cause burning or irritation.

Leukotriene-antagonists are oral drugs that block leukotrienes, powerful immune system factors that are important in causing airway constriction and mucus production in allergy-related asthma. Leukotriene-antagonists include zafirlukast (Accolate), montelukast (Singulair), zileuton (Ziflo), and pranlukast (Ultair, Onon). These drugs are mainly used to treat asthma. Montelukast was approved in 2003 to treat seasonal allergies, and in 2005 to treat indoor allergies.

Immunotherapy

Immunotherapy (commonly referred to as "allergy shots") is a safe and effective treatment for patients with allergies. It is based on the premise that people who receive injections of a specific allergen will lose sensitivity to that allergen. The most common allergens for which shots are given are house dust, cat dander, grass pollen, and mold.

Immunotherapy benefits include:

Targeting the specific allergen.
Reducing sensitivity in airways in the lungs as well as in the upper airways.
Preventing the development of new allergies in children.
Reducing asthma symptoms and the use of asthma medications in patients with known allergies. Research suggests it may also help prevent the development of asthma in children with allergies.

Candidates for Immunotherapy. Immunotherapy may be given to anyone over age 7 whose allergies are severe and who do not respond to medication. Many experts agree that immunotherapy should be considered as soon as possible for children with asthma and allergies. Immunotherapy is safe for pregnant women who are already receiving it, although half-strength doses are generally recommended, and it should not be started during pregnancy.

Individuals at Risk for Complications. People who should probably avoid immunotherapy include those who have:

An extreme response to skin tests (this may predict an allergic reaction).
Wheezing.
Uncontrolled severe asthma or lung disease.
Patients taking certain medications (such as beta-blockers).
The health status of anyone should be determined before starting treatment.

The major downside to immunotherapy is that it requires a prolonged course of weekly injections. The process generally includes:

Injections of diluted extracts of the allergen are given on a regular schedule, usually twice a week to weekly at first, then in increasing doses until a maintenance dose has been reached. It usually takes several months and may take up to 3 years to reach a maintenance dose.
At that time, intervals between shots can be 2 - 4 weeks, and the treatment is continued for another 3 - 5 years.
Patients can experience some relief within 3 - 6 months. If there is no benefit within 12 - 18 months, discontinue the shots.

After stopping immunotherapy, about a third of allergy sufferers no longer have any symptoms, a third have improved symptoms, and a third relapse.

The use of an injection series is effective, but patients often fail to comply with the regimens. Some other schedules and delivery methods are being investigated that might make the program easier and less distressing.

Rush Immunotherapy. Investigators are studying "rush immunotherapy," in which patients achieve the full maintenance dose with several shots a day over a period of 3 - 5 days. Rush therapy uses modifications that reduce the risk of severe reactions to excessive doses. Studies suggest that it is effective and safe, with few side effects other than itching. Patients must be monitored closely during this period, however, for severe reactions.

Oral Forms. Trials are underway to test oral forms of immunotherapy as an alternative to allergy shots. These methods include using a pill taken by mouth or a sublingual (under-the-tongue) tablet. Although oral and sublingual immunotherapy is prescribed in many countries in Europe and South America, it is not approved in the United States and is not considered accepted therapy at this time.

Injections for ragweed and, sometimes, dust mites have higher risks for side effects than other allergy shots. If complications or allergic reactions develop, they usually occur within 20 minutes, although some can develop up to 2 hours after the shot is given.

Side effects of immunotherapy include:

General itching, swelling, red eyes, hives, soreness at the injection site.
Less common side effects are low blood pressure, asthma worsening, or difficulty breathing. This is due to an extreme hypersensitivity response called anaphylaxis. It can also occur if excessive doses are given.
In rare cases, particularly because of excessive doses or if a patient has a serious lung problem, severe reactions can occur, which can be life threatening.
Premedicating patients with antihistamines and corticosteroids may help reduce the risk of reactions to immunotherapy, although this could mask early warning signs.

In a 10-year study, the incidence of any adverse effect was less than two-tenths of 1%, and the great majority of events were mild. The risk for a fatal response is estimated to be 1 in 63 million injections. (As a comparison, the risk for a fatal reaction to penicillin is much higher, 1 in 7.5 million injections.)

Vaccines. Of particular interest is the development of immunotherapeutic vaccines that use more specific targets to produce an insensitivity to allergens. One such vaccine uses a small protein from the allergen, which is injected into the patient. Other vaccines under investigation are those that use the allergen's genetic material (its DNA) to promote tolerance to the allergen. In a promising 2006 pilot study, patients who received 6 weekly injections of a DNA-based experimental ragweed vaccine had symptom reductions that lasted a year later into a second ragweed season. Researchers will be testing this vaccine in further clinical trials.

Monoclonal Antibodies. Monoclonal antibodies (MAb) are genetically-developed antibodies that are designed to target and attack very specific factors. A MAb known as omalizumab (Xolair) prevents the antibody immunoglobulin E (IgE) from triggering the inflammatory events that lead to allergies. Studies in recent years have suggested that omalizumab may help reduce symptoms and improve quality of life for patients with non-seasonal allergic rhinitis. A 2006 study suggested that treatment with omalizumab before and during ragweed allergy shots may help reduce immunotherapy side effects. The drug is currently approved for asthma. In 2007, the FDA warned that omalizumab may cause a life-threatening allergic reaction (anaphylaxis) in some patients.

Prevention

People with existing allergies should avoid irritants or allergens. These triggers include:

Pollen. This is the primary cause of allergic rhinitis.
Dust mites, specifically mite feces, which are coated with enzymes that contain a powerful allergen. These are the primary allergens inside the home.
Animal dander (flakes of skin) and hair from cats, house mice, and dogs. House mice are proving to be significant sources of allergens, particularly in urban children.
Molds.
Fungi.
Cockroaches are major asthma triggers and may reduce lung function even in people without a history of asthma.
Some research suggests that alcohol intake may influence allergy severity. One study found that as little as one drink a day is enough to worsen dust mite allergies.
Some studies suggest that early exposure to some of these allergens, including dust mites and pets, may actually prevent allergies from developing in children.

Controlling Pets. People who already have pets and are not allergic to them are probably at low risk for developing such allergies later on. When children are exposed to more than one dog or cat during their first year, they have a much lower risk for not only pet allergies but also seasonal allergies and asthma. (Pet exposure does not protect them from other allergens, notably dust mites and cockroaches).

In children who have an existing allergy to pets, however, the pets should be given away or kept outside. If this isn't possible, they should at least be confined to carpet-free areas outside the bedroom. Cats harbor significant allergens, which can even be carried on clothing. Dogs usually present fewer problems. Washing animals once a week can reduce allergens. Dry shampoos, such as Allerpet, that remove allergens from skin and fur and are now available for both cats and dogs and are easier to use than wet shampoos.

For small children, stuffed animals might serve as a comforting replacement, although they might harbor dust mites. Putting stuffed animals in the freezer for 24 hours before washing them kills the dust mites. For best effect, this process should be done weekly.

Preventing Exposure to Cigarette and Cooking Smoke. Parents who smoke should quit. Studies show that exposure to second-hand smoke in the home increases the risk for asthma and asthma-related emergency room visits in children. [For help in quitting, see In-Depth Report # 41: Smoking.]

Controlling Dust. Spray furniture polish is very effective for reducing both dust and allergens. Air cleaners, filters for air conditioners, and vacuum cleaners with High Efficiency Particulate Air (HEPA) filters can help remove particles and small allergens found indoors. Neither vacuuming nor the use of anti-mite carpet shampoo, however, is effective in removing mites in house dust. Vacuuming actually stirs up both mites and cat allergens. People with these types of allergies should avoid having carpets or rugs in their homes.

Bedding and Curtains. Many experts recommend reducing exposure to dust mites by enclosing mattresses and pillows in semipermeable coverings. (Vinyl mattress covers limit airflow and may worsen, or even cause, asthma in children.) However, several 2005 studies suggested that such covers do not prevent allergies or asthma. Curtains should be replaced with shades or blinds and bedding washed using the highest water temperature setting.

Reducing Humidity in the House. Dust mites thrive in humidity, and damp houses increase the risk for mold. On-going humidifiers can worsen the problem. If they are used, humidity levels should not exceed 40%, and humidifiers should be cleaned daily with a vinegar solution.

Exterminating Pests (Cockroaches and Mice). Use professional exterminators to eliminate cockroaches. (One study reported that ridding a home of cockroaches and cleaning the house using standard housecleaning techniques failed to eliminate the cockroach allergens themselves.) Exterminate mice and attempt to remove all dust, which might contain mouse urine and dander.

Avoiding Outdoor Allergens. The following are some recommendations for avoiding allergens outside:

Start taking allergy medications 1 - 2 weeks before ragweed season begins. Be sure to take allergy medications before going outside. If regular medications do not work, ask your doctor about allergy shots.
Camping and hiking trips should not be scheduled during times of high pollen count (May and June for grass pollen and September to October for ragweed).
Patients who are allergic should avoid barns, hay, raking leaves, and mowing grass. (A mask can be worn during outdoor chores to help reduce pollen exposure.)
Sunglasses can help prevent pollen from getting into eyes.
After being outdoors, clean off pollen residue by bathing, washing hair and clothes, and using a nasal salt water rinse.

Some evidence suggests that people with allergic rhinitis and asthma may benefit from a diet rich in omega-3 fatty acids (found in fish, almonds, walnuts, pumpkin, and flax seeds) and fruits and vegetables (at least five servings a day). Some studies also suggest reducing sodium, trans fatty acids (hydrogenated fats found in commercial products and baked goods), and omega-6 fatty acids (found in most vegetable oils). Investigators are also studying probiotics -- so-called good bacteria, such as lactobacillus and bifidobacterium, which can be obtained in supplements.

Resources

www.aaaai.org -- American Academy of Allergy, Asthma & Immunology
www.acaai.org -- American College of Allergy, Asthma & Immunology
www.niaid.nih.gov -- National Institute of Allergy and Infectious Diseases
www.njc.org -- National Jewish Medical and Research Center
www.lungusa.org -- The American Lung Association

References

Bower JH, Maraganore DM, Peterson BJ, Ahlskog JE, Rocca WA. Immunologic diseases, anti-inflammatory drugs, and Parkinson disease: a case-control study. Neurology. 2006 Aug 8;67(3):494-6.

Calderon M, Alves B, Jacobson M, Hurwitz B, Sheikh A, Durham S. Allergen injection immunotherapy for seasonal allergic rhinitis. Cochrane Database Syst Rev. 2007 Jan 24;(1):CD001936.

Creticos PS, Schroeder JT, Hamilton RG, Balcer-Whaley SL, Khattignavong AP, Lindblad R, et al. Immunotherapy with a ragweed-toll-like receptor 9 agonist vaccine for allergic rhinitis. N Engl J Med. 2006 Oct 5;355(14):1445-55.

Leger D, Annesi-Maesano I, Carat F, Rugina M, Chanal I, Pribil C, et al. Allergic rhinitis and its consequences on quality of sleep: An unexplored area. Arch Intern Med. 2006 Sep 18;166(16):1744-8.

Review Date:
3/22/2007
Reviewed By:
Harvey Simon, MD, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital.

A.D.A.M. Copyright

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

Attention deficit hyperactivity disorder

FitSugar — Wed, 08 Oct 2008 17:35:28 -0700

In This Report

Highlights
Introduction
Risk Factors
Causes
Diagnosis
Other Disorders Associated ...
Complications
Treatment
Medications
Behavioral Management
Other Treatments
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Drug Approval

In 2007, the Food and Drug Administration (FDA) approved lisdexamfetamine (Vysvanse), a new stimulant drug for the treatment of attention-deficit/hyperactivity disorder (ADHD). The active ingredient in lisdexamfetamine is similar to dextroamphetamine, the drug used in Dexedrine and Adderall.

Drug Warning

In 2007, the FDA instructed the manufacturers of all ADHD drugs to include drug warning labels describing the risks for heart and psychiatric side effects. Doctors should carefully evaluate patients for any risk factors. Reports have linked ADHD drugs to sudden death in patients with serious heart problems. There is also a slightly increased risk for auditory hallucinations, paranoia, and manic behavior even in patients with no history of psychiatric problems. The FDA warning applies to all stimulant ADHD drugs and to the non-stimulant drug atomoxetine (Strattera).

Ritalin Can Stunt Growth

After 3 years of methylphenidate (Ritalin) treatment, children are about an inch shorter and 6 pounds lighter than their peers who do not take this drug, according to a 2007 study in the Journal of the American Academy of Child and Adolescent Psychiatry.

ADHD Improves Over Time

ADHD symptoms may improve over time regardless of the treatment approach, indicates a 2007 study in the Journal of the American Academy of Child and Adolescent Psychiatry. Researchers found that medication, behavioral therapy, or a combination of the two all helped produce improvement after 3 years. There appeared to be no significant difference between children who took medication and those who did not.

Neurofeedback May Help ADHD

Neurofeedback (also known as biofeedback) is a non-drug treatment that may help improve attention and behavior problems associated with ADHD. This treatment approach involves teaching children to control their brain wave activity.

Introduction

According to the U.S. National Institute of Mental Health, attention deficit hyperactivity disorder (ADHD) is a legitimate psychologic condition.

ADHD is a syndrome generally characterized by the following symptoms:

Inattention
Distractibility
Impulsivity
Hyperactivity

Some experts categorize ADHD into three subtypes:

Behavior marked by hyperactivity and impulsivity, but not inattentiveness
Behavior marked by inattentiveness, but not hyperactivity and impulsivity
A combination of the above two

There is some debate over these criteria. Some argue the condition is over-diagnosed. Others say it's underdiagnosed. (See Difficulties in Identifying Children with ADHD later in this article.) One-third of cases are accompanied by learning disabilities and other neurologic or emotional problems, making an ADHD diagnosis particularly difficult. It is likely that the term attention-deficit hyperactivity disorder will eventually give way to subgroups of problems that include some of these general symptoms.

In the United States, about 4.7 million children ages 3 - 17 have been diagnosed at some point with ADHD. This accounts for 7.4% of all American children in this age range.

ADHD is a genuine disorder, but it is telling that the U.S. accounts for 90% of worldwide prescriptions for stimulants for ADHD. It is not known whether this reflects a real increase in ADHD, or a better ability to recognize it. Some say it may be an indication of a culture that places excessive value on normalcy and academic achievement at the expense of more frequent diagnoses.

Symptoms of ADHD usually occur before the age of 7. Studies indicate that ADHD symptoms in preschool children with ADHD do not differ significantly from older children.

The classic ADHD symptoms do not always adequately describe the child's behavior, nor do they describe what is actually happening in the child's mind. Some experts are focusing on deficits in "executive functions" of the brain to understand and describe all ADHD behaviors. Such impaired executive functions in ADHD children can cause the following problems:

Inability to hold information in short-term memory
Impaired organization and planning skills
Difficulty in establishing and using goals to guide behavior, such as selecting strategies and monitoring tasks
Inability to keep emotions from becoming overpowering
Inability to shift efficiently from one mental activity to another

Hyperactivity. The term hyperactive is often confusing since, for some, it suggests a child racing around non-stop. A boy with ADHD playing a game, for instance, may have the same level of activity as another child without the syndrome. But when a high demand is placed on the ADHD child's attention, his brain motor activity intensifies beyond the levels of the other children. In a busy environment, such as a classroom or a crowded store, ADHD children often become distracted and react by pulling items off the shelves, hitting people, or spinning out of control into erratic, silly, or strange behavior.

Impulsivity and Temper Explosions. Even before the "terrible twos," impulsive behavior is often apparent. The toddler may gleefully make erratic and aggressive gestures, such as hair pulling, pinching, and hitting. Temper tantrums, normal in children after age 2, are usually exaggerated and not necessarily linked to a specific negative event in the life of an ADHD child. One of the most painful events a parent may experience is an abrupt and aggressive attack that may occur after cuddling a young ADHD child. Often this reaction seems to be caused not by anger, but by the child's apparent inability to endure overstimulation or displays of physical affection.

Attention and Concentration. ADHD children are usually distracted and made inattentive by an overstimulating environment (such as a large classroom). They are also inattentive when a situation is low-key or dull. Some experts believe that certain parts of the brain in ADHD children may be underactive, so the children fail to be aroused by nonstimulating activities. In contrast, they may exhibit a kind of "super concentration" to a highly stimulating activity (such as a video game or a highly specific interest). Such children may even become over-attentive -- so absorbed in a project that they cannot modify or change the direction of their attention.

Impaired Short-Term Memory. Many experts now believe that an essential feature in ADHD, as well as in learning disabilities, is an impaired working (also called short-term) memory. People with ADHD can't hold groups of sentences and images in their mind long enough to extract organized thoughts. They are not necessarily inattentive. Instead, a patient with ADHD may be unable to remember a full explanation (such as a homework assignment), or unable to complete processes that require remembering sequences, such as model building. In general, children with ADHD are often attracted to activities (television, computer games, or active individual sports) that do not tax the working memory, or produce distractions. Children with ADHD have no differences in long-term memory compared with other children.

Inability to Manage Time. Studies suggest that children with ADHD have difficulties being on time and planning the correct amount of time to complete tasks. (This may coincide with short-term memory problems.) In one study, although children with probable ADHD were able to self-report many ADHD symptoms, they tended to believe they used their time wisely, in contrast to reports by their teacher.

Lack of Adaptability. ADHD children have a very difficult time adapting to even minor changes in routines, such as getting up in the morning, putting on shoes, eating new foods, or going to bed. Any shift in a situation can precipitate a strong and noisy negative response. Even when they are in a good mood, they may suddenly shift into a tantrum if met with an unexpected change or frustration. In one experiment, ADHD children could closely focus their attention when directly cued to a specific location, but they had difficulty shifting their attention to an alternative location.

Hypersensitivity and Sleep Problems. ADHD children are often hypersensitive to sights, sounds, and touch. They usually complain excessively about stimuli that seem low key or bland to others. Sleeping problems usually occur well after the point when most small children sleep through the night. In one study, 63% of children with ADHD had trouble sleeping.

A. Either 1 or 2 should be present:

1. Should have 6 or more of the following symptoms of inattention, persisting for at least 6 months to a degree that is maladaptive and inconsistent with developmental level:

Often fails to give close attention to detail, makes careless mistakes

Often has difficulty sustaining attention in tasks or play

Often does not seem to listen when spoken to directly

Often does not follow through and fails to finish tasks

Has difficulty organizing tasks and activities

Avoids or dislikes tasks requiring sustained mental effort

Often loses things necessary for tasks or activities

Is often easily distracted by extraneous stimuli

Is often forgetful in daily activities

2. Should have 6 or more of the following symptoms of hyperactivity-impulsivity that lasts for at least 6 months to a degree that is maladaptive and inconsistent with developmental level:

Often fidgets or squirms when sitting

Has difficulty remaining seated when required to do so

Often runs about or climbs excessively in inappropriate situations

Has difficulty playing quietly

Is often "on the go"

Often talks excessively

Often blurts out answers to questions before they have been completed

Has difficulty waiting for his or her turn

Often interrupts or intrudes on others

Note: Patients with A1 symptoms are diagnosed with ADHD, predominantly inattentive type. Those with A2 are diagnosed with ADHD, predominantly hyperactive-impulsive type. Those with both A1 and A2 are diagnosed as ADHD, combined-type.

B. Onset of some symptoms before the age of 7. However, children with the inattentive subtype are not often diagnosed until they are above 7 years of age.

C. Symptoms occur in two or more settings. For example, at home and at school.

D. Clear evidence of significant impairment in social or academic functioning.

E. Not caused by a pervasive developmental disorder, schizophrenia, or any other psychotic disorder, and is not better accounted for by another mental disorder, including anxiety or depression.

Source: American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th Ed. (Text Revision). Washington, DC: 2000.

Risk Factors

ADHD is most often diagnosed in boys. However, there is some evidence that it is underdiagnosed in girls. Until recently, all major studies were conducted using boys as subjects. Important studies on girls with ADHD are now underway. A major study reported that girls with the condition experience the same multiple impairments as boys do.

Although ADHD is primarily thought of as a childhood disorder, diagnoses of attention-deficit disorder in adults are on the rise. Methylphenidate (Ritalin) was prescribed for nearly 800,000 adults in the U.S. in 1997, nearly three times the number in 1992. As of 2005, experts estimated that ADHD affects about 4.1% of adults ages 18 - 44 years in a given year.

How Is ADHD Identified in Adults?

Research suggests that ADHD affects 2 - 6% of the adult population, assuming that one- to two-thirds of cases persist into adulthood. ADHD in adults always occurs as a continuum of the childhood condition. Adult-onset symptoms are likely due to other factors. Diagnosing adult ADHD can be a difficult problem since hyperactivity typically wanes as children get older, while attention and organizational problems may develop in older people. Some experts believe, then, that the number of adults with ADHD is underestimated.

A rating scale using four factors may be useful in identifying adults with ADHD:

Inattention and memory problems. (Examples: losing or forgetting things, being absent-minded, not finishing things, misjudging time, depending on others for order, having trouble getting started, changing jobs or projects in the middle.)
Hyperactivity and restlessness. (Examples: always being on the go, fidgety, easily bored, taking risks, liking active and fast paced jobs and activities, such as being a sales representative or stockbroker.)
Impulsivity and emotional instability. (Examples: saying things without thinking first, interrupting others, being annoying to others, easily frustrated, easily angered, having unpredictable moods, driving recklessly, having high relationship and job turnover.)
Problems with self worth. (Examples: Avoids new challenges, appears confident to others but not to oneself.)

Doctors use adult reports of their childhood behaviors and experiences when searching for clues for a diagnosis. Interestingly, the disorder seems to be distributed equally between adult women and men.

How Serious Is Attention Deficit Disorder in Adults?

Accompanying Emotional, Personality, and Learning Disorders. Between 19 - 37% of adults with ADHD have depression or bipolar disorder. Between 25 - 50% have an anxiety disorder. Bipolar disorder plus ADHD, in fact, may be very difficult to differentiate from ADHD alone in adults.

Accompanying Learning Disorders. About 20% of adults with ADHD have learning disorders, usually dyslexia and auditory processing problems. These problems should be considered in any treatment plan.

Effect on Work. Compared to adults without ADHD, those with the condition tend to reach lower educational levels, earn less money, and be fired more often. In fact, one article reported that by the time they are in their 30s, about 35% of ADHD adults are self-employed.

Substance Abuse. About 1 in 5 adults with ADHD also contend with substance abuse. Studies indicate that adolescents with ADHD are twice as likely to smoke cigarettes as their peers who do not have ADHD. Cigarette smoking during adolescence is a risk factor for the development of substance abuse in adulthood.

Sleep Disorders. Sleep disorders, especially restless legs syndrome and sleep apnea, are common in adults and children with ADHD. Sleep apnea is a disorder in which a person temporarily stops breathing during sleep, perhaps hundreds of times. In most cases the person is unaware of it, although sometimes they awaken and gasp for breath. It is usually accompanied by snoring. One report suggested that treating sleep apnea in adults with both conditions may help reduce ADHD symptoms. [For more information, see In-Depth Report #65: Sleep apnea.]

Causes

Brain Structures. Research using advanced imaging techniques shows there is a difference in the size of certain parts of the brain in children with ADHD compared to children who do not have ADHD. The areas showing change include the prefrontal cortex, the caudate nucleus and globus pallidus, and the cerebellum:

The prefrontal cortex is located in the front of the brain. It is thought to be the brain's command center. It regulates the brain’s ability to block certain responses. Numerous imaging studies have indicated that the prefrontal cortex of the brain in people with ADHD may be less active than in those without the disorder.
The caudate nucleus and globus pallidus, located near the center of the brain, speed up or stop orders coming from the prefrontal cortex. In some reports, these areas have been smaller than average in young children with ADHD, but tended to become normal as the children got older. Abnormalities in these areas may impair a person's ability to stop certain actions, resulting in the impulsivity typical of people with ADHD.
The cerebellum is the area above the brain stem. This area helps control muscle tone and balance, and synchronizes muscle activity. This has been found to be smaller in children with ADHD compared to those without the condition.

Brain Chemicals. Abnormal activity of certain brain chemicals in the prefrontal cortex may contribute to ADHD. The chemicals dopamine and norepinephrine are of special interest. Dopamine and norepinephrine are neurotransmitters, or chemical messengers, that affect both mental and emotional functioning. They also play a role in the "reward response." This response occurs when a person experiences pleasure in response to certain stimuli (such as food or love). Studies suggest that increased levels of the brain chemicals glutamate, glutamine, and GABA -- collectively called Glx -- interact with the pathways that transport dopamine and norepinephrine.

Nerve Pathways. Another area of interest is a network of nerves called the basal-ganglia thalamocortical pathways. Abnormalities along this neural route have been associated with ADHD, Tourette syndrome, and obsessive-compulsive disorders, all of which share certain symptoms.

Genetic factors may play the most important role in ADHD. The relatives of ADHD children (both boys and girls) have much higher rates of ADHD, antisocial, mood, anxiety, and substance abuse disorders than the families of non-ADHD children. A study reported that 90% of children with a diagnosis of ADHD shared it with their twin.

Genetic Factors Regulating Dopamine and Advantages in Early Man. Most of the research on the underlying genetic mechanisms targets the neurotransmitter dopamine. Variations in genes that regulate specific dopamine receptors have been identified in a high proportion of people with addictions and ADHD. Such genes have been associated with novelty seeking and extroversion. Some experts theorize that the genetic variants may have first appeared thousands of years ago, and affect as many as half of ADHD children. Furthermore, the genetic variations may have offered some benefits to their early carriers. In such people, a genetic predilection for novelty-seeking and risk-taking may have supplied an advantage in reproduction, mating, hunting, and achieving dominance.

Genetic Resistance to Thyroid Hormone. About 50% of adults and 70% of children with a genetic resistance to thyroid hormone, essential for normal brain development, have ADHD. People who have this condition appear to have a more severe form of ADHD. The thyroid disorder is not a common cause of ADHD. Only those with a family history of thyroid disease are at risk.

Infant malnutrition is a strong risk indicator of ADHD. Even if children receive enough food later on, infants who suffer from malnutrition may develop behavior problems, the most prevalent being attention-deficit disorder.

Deficiencies in Zinc and Essential Fatty Acids. Several dietary factors have been researched in association with ADHD, including sensitivities to certain food chemicals, deficiencies in fatty acids (compounds that make up fats and oils) and zinc, and sensitivity to sugar.

Some studies have found an association between deficiencies in certain fatty acids and ADHD. Other research reports an association between zinc deficiencies and ADHD. Zinc aids in the breakdown of fatty acids, which affects dopamine, the neurotransmitter likely to be involved with ADHD.

No clear evidence has emerged, however, that implicates any of these nutritional factors in ADHD.

Research suggests that prenatal exposure to tobacco, alcohol, environmental lead, and other toxins may increase the risk for ADHD and conduct disorders.

Diagnosis

Important factors for making a diagnosis of attention-deficit hyperactivity disorder (ADHD) include:

Children between ages 6 - 12 should first be evaluated for ADHD if they show symptoms of inattention, hyperactivity, impulsivity, academic underachievement, or behavior problems in at least two settings. Such behaviors should have been harmful for the child academically or socially for at least 6 months.
The child should meet the official symptom guidelines.
A diagnosis requires detailed reports by parents or caregivers. It should be noted that a mother's description of her child's behavior is a very accurate and reliable guide for diagnosing ADHD. Parents should not be shy about insisting on further evaluation if their experience does not match a doctor's single observation of their child.
Guidelines for primary care doctors emphasize the importance of obtaining direct evidence from the classroom teacher or other school-based professionals about the child's symptoms and their duration, and evidence of functional impairment in the school setting.
The child should be assessed for accompanying conditions (such as learning difficulties).

No laboratory or imaging tests exist to reliably diagnose ADHD. A diagnosis relies only on behavioral symptoms and ruling out other disorders. Many experts believe that the disorder is both over- and underdiagnosed. Diagnosis of attention-deficit hyperactivity disorder is difficult for some of the following reasons:

Factors Leading to the Over-Diagnosis of ADHD:

The popularity methylphenidate (Ritalin) has encouraged some parents and teachers to pressure doctors into prescribing this standard ADHD drug for children who are aggressive or who have poor grades. Often with careful testing many of these children do not meet the criteria for the illness. Children may have other diagnoses, other behavioral or emotional problems, or no problems at all.
Other factors that may contribute to misdiagnosis include children who are young for their grade and therefore socially and intellectually immature, and social and economic problems such as single parent households.

Factors Leading to the Under-Diagnosis of ADHD:

Some evidence suggests that many girls with ADHD may go underdiagnosed. Research indicates that girls with ADHD are often inattentive but not hyperactive or impulsive. In fact, older girls with ADHD tend to have social problems due to withdrawal and internalized emotions, showing symptoms of anxiety and depression. The inattentive subtype, in any case, may first show up in older children and adolescents.
Doctors may fail to diagnose children with ADHD because they often behave normally in the quiet doctor's office where there are no distractions to trigger symptoms. In addition, doctors may be unfamiliar with how to diagnose the condition.
In spite of the fact that there seems to be no differences in response to treatment among population groups, African-American, Hispanic, and Asian children with ADHD are half as likely to be diagnosed and treated as Caucasian children. By high school, the racial disparity increases to the level that the medication rate for blacks is one-fifth of that for whites.

The doctor will first require a detailed history of the child's behavior. Doctors will match this against a standardized checklist to define the disorder.

The parents should describe the following:

Specific problems, beginning as early as possible, they have encountered during the child's development -- school reports are very helpful
Sibling relationships
Recent life changes
A family history of ADHD
Eating habits
Sleep patterns
Speech and language development
Any problems during the mother's pregnancy or during delivery
Any history of medical or physical problems, particularly allergies, chronic ear infections, and hearing difficulties

The health professional will want to know how the parents handle different situations, and may want to observe them interacting with the child.

The child should also be given a general physical examination to determine if any medical conditions are present. The child should be given a hearing test to rule out hearing abnormalities as a source of behavioral problems.

Various tests are available to test neurologic, intellectual, and emotional development problems. Most involve learning and problem solving tasks that help define the particular areas that are most disabling. Blood or other laboratory tests are currently recommended only if the doctor suspects lead toxicity or other medical problems.

Although some doctors use a trial of a psychostimulant (usually Ritalin) to facilitate diagnosis, most experts strongly recommend against this method of diagnosis, because it is not always accurate. An improvement in symptoms is considered suggestive of ADHD, while in non-ADHD children the stimulant often increases agitation and hyperactivity. Many children and adults without the disorder have a similar response, and such a diagnostic trial may lead to unnecessary prescriptions of this drug.

Other Disorders Associated with ADHD

Several disorders may mimic or accompany attention-deficit disorder. ADHD exists alone in only about one-third of children. Many professionals object to the use of the single term "attention-deficit hyperactivity disorder" to encompass such a wide spectrum of behaviors, which they believe should be categorized into subgroups. Many of these problems require other modes of treatment and should be diagnosed separately, even if they accompany ADHD.

Attention-deficit disorder can appear without hyperactivity, in which case the child's primary symptoms are distractibility and an inability to persist in tasks.

About 14% of children diagnosed with ADHD also have oppositional-defiant disorder (ODD). The most common symptom for this disorder is a pattern of negative, defiant, and hostile behavior toward authority figures that lasts more than 6 months. In addition to displaying inattentive and impulsive behavior, these children demonstrate aggression, have frequent temper tantrums, and display antisocial behavior. A significant number of children with ODD also have anxiety disorders and depression, which should be treated separately. Many children who develop ODD at an early age go on to develop conduct disorder.

Some children with ADHD also have conduct disorder, which describes a complex group of behavioral and emotional disturbances seen in children. It includes aggression towards people and animals, destruction of property, deceitfulness, lying, or stealing, and general violation of rules.

Pervasive developmental disorder (PDD) is rare and usually marked by autistic-type behavior, hand-flapping, repetitive statements, slow social development, and speech and motor problems. If a child who has been diagnosed with ADHD does not respond to treatment, the parents might inquire about PDD, which often responds to antidepressants. Some children with PDD may also benefit from stimulants.

Children with ADHD often have difficulties with tasks that involve listening or hearing. Research is indicating that symptoms of the two disorders often overlap but may actually be two distinct disorders. Hearing problems themselves may cause ADHD symptoms.

Children diagnosed with attention-deficit disorder may also have bipolar disorder, commonly called manic depression. Indications of this problem include episodes of depression and mania (with symptoms of irritability, rapid speech, and disconnected thoughts), sometimes occurring at the same time. [For more information, see In-Depth Report #66: Bipolar disorder.] Both disorders often cause inattention and distractibility and may be difficult to distinguish, particularly in children. Children with mania and ADHD may have more aggression, behavioral problems, and emotional disorders than those with ADHD alone. In some cases, ADHD in children or adolescents can even be a marker for an emerging bipolar disorder. The primary way to differentiate bipolar disorder from ADHD is by the presence of a manic or hypomanic episode, which occurs in patients with bipolar disorder but not with ADHD. Most children with bipolar will also respond to the drug valproate, which does not typically work for ADHD in children.

Anxiety disorders commonly accompany ADHD. Obsessive-compulsive disorder is a specific anxiety disorder that shares many characteristics with ADHD and may share a genetic component. Young children who have experienced traumatic events, including sexual or physical abuse or neglect, exhibit characteristics of ADHD, including impulsivity, emotional outbursts, and oppositional behavior.

Sleep disorders or disturbances are very common with ADHD patients. Insomnia is common. In addition, specific sleep disorders -- restless legs syndrome and sleep-disordered breathing -- have been identified with hyperactivity and conduct disorder.

Restless Legs Syndrome (RLS). Some experts believe RLS and periodic limb movement disorder are strongly associated with ADHD in some children. One theory is that the two are linked by a common mechanism. The disorders have much in common, including poor sleep habits, twitching, and the need to get up suddenly and walk about frequently. They may even be genetically linked. For example, both have been associated with lower levels of dopamine in the brain, which is associated with faulty motor control, a common problem in both disorders.

Sleep-Disorder Breathing and Sleep Apnea. Some research has shown an association between mild symptoms of ADHD and sleep-disordered breathing, including snoring and obstructive sleep apnea in children and adults. Treating the sleep-related breathing disorders may improve the attention disorder in some children. (One study indicated that such problems are unlikely to be associated with children with moderate to severe ADHD.) [For more information, see In-Depth Report #65: Sleep apnea.]

Tourette Syndrome and Other Genetic Disorders. Several genetic disorders cause symptoms resembling ADHD, including fragile X and Tourette syndrome. About 50% of those with Tourette syndrome also have ADHD, and some of the treatments are similar.

Other Medical Conditions. A number of medical conditions, including hyperthyroidism and vision problems, can produce ADHD-like symptoms.

Lead. Children who ingest even low amounts of lead may manifest symptoms similar to those of ADHD. A child may be easily distractible, disorganized, and have trouble thinking logically. The major cause of lead toxicity is exposure to leaded paint, particularly in homes that are old and in poor repair.

Complications

More than half of children with attention-deficit disorder have accompanying disorders, including anxiety, depression, and conduct disorders. Children with ADHD who experience anxiety or depression are also more likely to suffer from low self-esteem.

Anti-Social Behavior. Even if these emotional disorders are absent in childhood, the ADHD child's relationship with others is volatile, and they are often unhappy from a very young age. Research indicates that any boy or girl with ADHD, particularly an aggressive child, has trouble getting along with others, and is less liked by his or her peers.

Children with the inattentive subtype of ADHD are more likely to be picked on and to spend time alone.
Children with the combined subtypes tend to have different problems. Boys with ADHD are less likely than others to empathize with people in difficult circumstances. A best friend can turn into an enemy overnight when, for example, a boy with ADHD does not perceive his friend's fearful response to over-aggressive roughhousing and fails to let up. The next day the child with ADHD has forgotten the event; the ex-friend hasn't. When a child with ADHD hurts someone, the child either may go into a state of denial or blame himself excessively. As ostracism, fear, and ridicule from peers persist from year to year, the unstable behavior, originally neurologic, becomes emotionally based. Unless this cycle is broken, serious adult problems can evolve.

Substance Abuse in Young People. Studies consistently report that young people with ADHD -- in particular those with conduct or mood disorders -- have a higher than average risk for substance abuse and that it starts in younger ages. In one study, for example, by age 11 nearly 20% of children with ADHD had tried smoking cigarettes, drinking alcohol, or both. Biologic factors associated with ADHD may make these individuals susceptible to substance abuse. Many of these young people are self-medicating their condition. In fact, according to a major analysis, Ritalin or other stimulants used to treat ADHD may help protect such patients against substance abuse. (Boys with ADHD and conduct disorder, however, still face a high risk for substance abuse. Girls with ADHD and emotional disorders may also still have a higher risk.)

High-Risk Behavior. Impulsivity in young people with ADHD can certainly cause them to take chances before thinking them through, putting them in situations where the consequences become clear only after the action has been taken. Children with ADHD and high levels of aggression are at higher risk for delinquent behavior in adolescents and criminal activity in adulthood. However, children with ADHD who are not aggressive have a lower and even normal risk for dangerous activities. Even in aggressive children with ADHD, close parental attention and early treatment can limit the risk considerably.

Although speech and learning disorders are common in children with ADHD, the disorder does not affect intelligence. People with ADHD span the same IQ range as the general population.

Many children with ADHD are underachievers, and half are held back in school at least once. Some evidence suggests that inattention may be a major factor in low academic performance in these children. About 20% also have reading difficulties, and 60% have serious handwriting problems. Adults with ADHD are also at very high risk for these conditions.

Some research suggests that ADHD persists in one- to two-thirds of those diagnosed with the condition in childhood. Many researchers describe the pattern of ADHD as they would a chronic illness, with remission and periods of worsening.

The time and attention needed to deal with a child with ADHD can change internal family relationships and have devastating effects on parents and siblings.

Effect on Parents. Studies indicate that any intervention for the child must include the parents. Parents who are responsive to their child in a positive way can help reduce the chances for oppositional behaviors. But it can be very difficult. A child with ADHD is wonderful one day and terrible the next, for no apparent reason. The parent can feel betrayed and hurt, and believe they have no control over their child. Parents must protect themselves and their child by establishing tough but kind rules about where their space ends and the child's begins. The are many effects on parents:

Mothers generally get the brunt of the emotional and physical abuse that a child with ADHD can produce.
Parents may have to give up on the idea of an immaculate house and a hot meal every night. Parents must learn that striving for perfection is among the most counterproductive goals to pursue in raising a child with ADHD, or any child.
Parents must face the hostility and anger of other parents and see their own child rejected. It is very easy to fall into an emotional black hole, and feel alone, inadequate, and helpless.
Marriages are often stressed to the breaking point because of exhaustion and disagreements between the husband and wife on how to respond to the child.

Effect on Siblings. Siblings of children with ADHD have particular difficulties, and are also at risk for psychologic impairment, depression, drug abuse, and language disorders. The non-ADHD sibling does not have the control a parent does in the management of the ADHD child's behavior and is very likely to feel alienated and alone. Children without ADHD are often victimized by siblings with ADHD who may be demanding or bullying.

A sibling who does not receive attention in their own right may begin to imitate undesirable behaviors or to act out negatively in other ways. It is very important to make the brothers and sisters equally vital to the family's functioning. However, they should never be made to feel that their value in the family is as caregivers of the ADHD sibling.

Treatment

A combination of a psychostimulant, most commonly methylphenidate (Ritalin), and cognitive-behavioral therapy is proving to be the best option for treatment of children with ADHD. Although medication can be helpful during the initial years of treatment, some research indicates that the benefits of medication eventually wear off. It appears that for ADHD symptoms may improve naturally over time, regardless of the treatment approach.

Signs that ADHD may be easing include not having to adjust medication dosages during growth spurts, no deterioration when a drug dose is missed, or new abilities to concentrate during “drug holidays.” (School vacation times are a good period to test the effectiveness of temporarily stopping medication.) The American Academy of Child and Adolescent Psychiatry suggests that parents evaluate whether medication can safely be withdrawn when children with ADHD have been free of symptoms for at least 1 year. If a child’s condition worsens after medication withdrawal, the drug should be resumed.

Developing a Treatment Approach. The following guidelines may be useful in determining a treatment approach for children with ADHD:

Behavioral techniques, possibly including dietary changes, should be tried first, if possible.
If the symptoms are severe or do not respond, a trial using medication (usually psychostimulants), in conjunction with behavior modification therapy, is advisable.

Cognitive behavioral therapy (CBT) is often administered by mental health providers, with both primary care physicians and psychiatrists prescribing medications. Unfortunately, many children do not have access to behavioral therapies, either because of lack of time or available resources.

Specific Patient Populations. Unfortunately, such guidelines do not address the following specific patient groups:

There are no definite guidelines for treating preschool children with severe ADHD. Some parents have reported very good long-term results with behavioral interventions at this age.
There are no reliable guidelines on how to treat the inattentive subtype of ADHD, which might be more common in girls.
There are no defined treatments for ADHD patients with accompanying conditions, including impaired working memory and deficits in language processing.
There are no defined treatments for children with ADHD and accompanying emotional problems, such as bipolar or anxiety disorders. (There is some evidence, for example, that children with ADHD plus anxiety disorders do worse on psychostimulants.)

Determining a Medication Regimen. Doctors still have a difficult time predicting which medications will produce beneficial results, so treatment is individualized and performed on a trial and error basis, which requires close observation and cooperation between all participants. In developing an effective medication plan, the following steps may be helpful:

Before any drug is administered, a child should be given a thorough examination for any medical problems to be sure there are no medical conditions that interfere with the medication.
Both the doctor and the parents should be very clear about the specific behaviors they hope the medication will target.
The goal is to use the lowest possible dosage that produces improved behavior.
If an initial regimen doesn't work, changing the dosage, or changing to a different medication often brings improvement.
Frequent follow-up visits should be scheduled to assess the response and to detect possible side effects.

Arguments For and Against Psychostimulants. Many parents are very disturbed by the idea of putting their children on intensive stimulant drug regimens, possibly for years, particularly given the uncertainties in diagnosis and the negative publicity surrounding the use of these drugs. Although the decision to use these drugs should not be made lightly, the negative social and emotional effects of the disorder itself for many children with ADHD are far more severe and long-lasting than the use of these drugs. For some parents and children, medication seems like a miracle and can provide desperate families with a quality of life for which they had almost given up hope. Whether or not psychostimulants are used, children and families should understand that ongoing efforts around behavior control will be necessary.

Of great concern is the dramatic increase in prescriptions for psychostimulants among preschool children. Although low doses of methylphenidate (Ritalin) may help preschoolers (ages 3 - 5 years) with ADHD, the drug can cause considerable side effects in many children. These side effects include insomnia, nervousness, anxiety, loss of appetite and weight, and slowed growth. Children in one large study grew about an inch less and weighed about 6 pounds less than normal after 3 years of methylphenidate treatment. Doctors must carefully consider the risks versus benefits when prescribing ADHD drugs to preschoolers. Children who do receive these drugs need to be carefully monitored by their doctors.

Treatment for Adult ADHD. As with children, adults with ADHD are treated with a combination of medication and psychotherapy. For medication, stimulant drugs or the non-stimulant drug atomoxetine (Strattera) are usually first-line treatments, with antidepressants a secondary option. Atomoxetine is approved specifically for adults with ADHD. Adults who have heart problems or heart condition risk factors should be aware of the cardiovascular risks associated with ADHD medication. There have been ADHD medication-associated incidents of sudden death in patients with underlying serious heart problems, and reports of stroke and heart attack in adults with cardiac risk factors.

Research increasingly supports the view that interventions for the ADHD child must also include the parents if they are to be successful. Teachers and school officials should also be educated and involved in the process.

Parents who feel they have the most control over their child's situation experience the least psychological stress and depression. Parents who are responsive in a positive way also help reduce the chances for their child developing oppositional behaviors. But it can be very difficult, particularly for parents who have ADHD themselves. In fact, parents who have severe ADHD symptoms are less likely to respond to parent training programs unless they get help for themselves.

In addition to behavioral therapy for the child, family therapy may help ADHD children and their parents and siblings cope with the emotional conflicts that nearly always arise in the lifelong process of managing the condition. Separate psychological therapies for specific family members might be needed, particularly in light of the high incidence of psychiatric and other emotional problems in families with ADHD children.

Medications

Several types of medication are available to treat ADHD.

Psychostimulants are the primary drugs used to treat ADHD. Although these drugs stimulate the central nervous system, they have a calming effect on people with ADHD.

These drugs include:

Methylphenidate (Ritalin, Concerta, Metadate, Daytrana)
Dexmethylphenidate (Focalin)
Amphetamine-Dextroamphetamine (Adderall)
Dextroamphetamine (Dexedrine, Dextrostat)
Lisdexamfetamine (Vyvanse)

Pemoline (Cylert), another stimulant drug, was withdrawn from the U.S. market in 2005 after several reports of liver failure.

Methylphenidate and Dexmethylphenidate. Methylphenidate drugs (Ritalin, Metadate, Concerta, Daytrana) are the most commonly used psychostimulants for treating ADHD in both children and adults. Dexmethylphenidate (Focalin) is a similar drug. These drugs increase dopamine, a neurotransmitter important for cognitive functions such as attention and focus.

With the exception of Daytrana, all of these drugs are pills taken by mouth. Daytrana, approved in 2006, is the first skin patch drug for ADHD. A patch is applied to the hip each day and delivers a 9-hour dose of methylphenidate.

These drugs are available in short-acting and long-acting dosage forms. The short-acting forms need to be taken several times a day, including during school hours. As the drug wears off, a rebound effect can occur, and ADHD symptoms can intensify. For this reason, the long-acting dosage forms have become popular.

Amphetamine, Dextroamphetamine, and Lisdexamfetamine. Amphetamine-dextroamphetamine (Adderall), dextroamphetamine (Dexedrine, Dextrostat), and lisdexamfetamine (Vyvanse) work by blocking the reabsorption of the brain chemicals dopamine and norepinephrine. Side effects can include stomach problems and mood changes, including sadness, anxiety, and irritability.

Psychostimulant medications are associated with some significant risks. All ADHD stimulant drugs carry warnings that they should not be used by patients with structural heart problems or pre-existing heart conditions (high blood pressure, heart failure, or heart rhythm disturbances). These drugs have been associated with sudden death in children with heart problems. They have also been associated with sudden death, stroke, and heart attack in adults with a history of heart disease. In addition, these drugs may slightly increase the risk for auditory hallucinations, paranoia, and manic behavior even in patients who do not have a history of psychiatric problems. The FDA has directed manufacturers of ADHD medications to warn all patients taking these medicines of their potential cardiovascular and psychiatric risks.

Stimulant drugs may also:

Worsen behavior and thought disturbance in patients with a pre-existing psychotic disorder.
Cause a mixed or manic episode in patients who have both ADHD and bipolar disorder.
Increase aggressive behavior or hostility. Patients beginning stimulant drug treatment should be monitored for worsening of these behaviors.
Slow growth and weight gain in children. Children who take stimulant drugs should have their growth monitored. If they do not gain height or weight at a normal rate, they may need to stop taking the drug.

Side Effects. All stimulants have a number of side effects:

The most common side effects of any stimulant are nervousness and sleeplessness, although some parents have reported improved sleep patterns in their children after taking stimulants.
Tics or jerky, disordered movements occur in about 9% of children.
Other side effects include irritability, stomach pain, headache, depression, hair loss, and lack of spontaneity.

Symptoms of Overdose. Symptoms of overdose include changes in heart rhythm and rate, hypertension, confusion, breathing difficulties, sweating, vomiting, and muscle twitches. If they occur, parents should call the doctor immediately. Even among young people who abuse Ritalin, however, less than 1% experience severe side effects (rapid heart rate, hypertension), and outcomes are generally good. Side effects may be very severe, however, if Ritalin is overused and taken with other drugs. A 2006 study reported that over 3,000 people are treated in hospital emergency rooms due to side effects from ADHD drugs. Sixty-one percent of these visits involved accidental ingestion or overdose.

Concerns for Abuse. Studies on both animals and humans suggest that Ritalin lacks the properties that create addiction, particularly in doses used for treating ADHD. Although methylphenidates have properties similar to amphetamines, their drug levels rise very slowly in the brain at the oral doses given for ADHD. This slow rise prevents a so-called "high" and subsequent addiction to the drug. Some stimulant drugs, such as lisdexamfetamine, may pose a lower risk for abuse than others.

The primary danger for drug abuse from stimulants appears to occur in non-ADHD young people who purchase these drugs illegally. In one study, for instance, 16% of children with ADHD reported pressure from their fellow students to sell or give them their medication. While people ages 18 - 25 are more likely to use ADHD drugs for non-medical uses, children ages 12 - 17 are more likely to suffer adverse effects from medication misuse and to require treatment at an emergency room. If a child abuses another drug (alcohol, prescription medication) along with the ADHD medication, the chance for serious side effects is even greater.

Atomoxetine (Strattera) was the first non-stimulant approved for ADHD in children and the first treatment approved for adult ADHD. The drug works by increasing levels of both norepinephrine and dopamine, which are generally lower than normal in ADHD. The most common side effect is decreased appetite. A few cases of atomoxetine-associated liver injury have been reported, and the FDA has warned doctors that the drug should be discontinued at the first signs of jaundice or liver problems. Long-term effects, such as any impact on growth, are still unknown. Atomoxetine may cause suicidal thinking in children and adolescents, especially during the first few months of treatment. Parents should monitor children taking atomoxetine for any changes in mood or behavior, and immediately contact their doctor if changes occur.

Antidepressants are not FDA-approved for ADHD treatment, but may be helpful in certain circumstances. Because antidepressants appear to work about as well as behavioral therapy, doctors recommend that patients first try psychotherapy before using antidepressants.

Bupropion (Wellbutrin) and tricyclics are the types of antidepressants used for ADHD. Bupropion affects the reuptake of the serotonin, norepinephrine, and dopamine neurotransmitters. Side effects include restlessness, agitation, sleeplessness, headache, and stomach problems. Bupropion should not be used by patients who have a seizure disorder.

Tricyclics are an older type of antidepressant that are effective but have many side effects. Imipramine (Tofranil) and nortriptyline (Pamelor, Aventil) are the tricyclics most commonly prescribed for ADHD. A third tricyclic, desipramine (Norpramin) should only be used if patients are not helped by other tricyclics. (Desipramine has caused sudden death in some children and adolescents.)

Tricyclic antidepressants can cause disturbances in heart rhythm. Children should have an electrocardiogram when they first begin to take this drug, and after any dose increase.

[For more information, see In-Depth Report #8: Depression ].

Alpha-2 agonists stimulate the neurotransmitter norepinephrine, which appears to be important for concentration. They include clonidine (Catapres) and guanfacine (Tenex). They are used for Tourette syndrome and may be beneficial when other drugs have failed for ADHD children with tics or those whose primary symptoms are severe impulsivity and aggression. These drugs are mainly prescribed in combination with a stimulant.

These drugs have a number of side effects. Sedation is the most common. A clonidine skin patch, which gradually releases the medication, helps reduce the sedative effect. Because clonidine slows the heart down, it can have adverse effects in some children. Going off too quickly or missing doses can cause rapid heartbeats and other symptoms that may lead to severe problems. Doctors strongly recommend that no child be given this medication without a preliminary examination for heart problems, and no child with existing heart, kidney, or circulatory problems should take it.

Behavioral Management

Behavioral techniques for managing the child with ADHD are not intuitive for most parents and teachers. To learn them, caregivers may need help from qualified health care professionals or from ADHD support groups. At first, the idea of changing the behavior of a highly energetic, obstinate child is daunting. It is futile and damaging to try to force a child with ADHD to be like most children. It is possible, however, to limit destructive behavior and to instill a sense of self-worth that will help overcome negativity toward life, which is one of the great dangers of the disorder.

Bringing up a child with ADHD, like bringing up any child, is a process. No single point is ever reached where the parent can sit back and say, "That's it. My child is now OK, and I don't have to do anything more." The child's self worth will evolve with an increasing ability to step back and consider the consequences of an action and then to control that action before taking it. But this does not happen overnight. A growing child with ADHD is different from other children in very specific ways, presenting challenges at every age.

Setting Priorities for the Parent. Parents must first establish their own levels of tolerance. Some parents are easygoing and can accept a wide range of behaviors, while others cannot. To help a child achieve self-discipline requires empathy, patience, affection, energy, and toughness. Some tips to help the parents include:

Parents should prepare a list giving priority to those behaviors they think are the most negative, such as fighting with other children or refusing to get up in the morning. The least negative behaviors on the bottom of the list should be ignored temporarily or even permanently (refusing to wear anything but red T-shirts).
Certain odd behaviors that are not hurtful to the child or to others may be an indication of creative or humorous attempts to adapt (making up silly songs or drawing violent pictures). These should be accepted as part of the child's unique and positive development, even if they seem peculiar to the parent.
It is important to keep in mind that no one is a saint. Loving parents who occasionally lose their tempers will not damage their children forever. In fact, non-abusive open disapproval or dismay is far less destructive to both parent and child than harboring resentment beneath a false calm.

Establishing Consistent Rules for the Child. Parents must be as consistent as possible in their approach to the child, which should reward good behavior and discourage destructive behavior. Rules should be well-defined but flexible enough to incorporate harmless idiosyncrasies. It is very important to understand that children with ADHD have much more difficulty adapting to change than do children without the condition. (For example, the child should do homework every day but might choose to start it after a TV show or computer game.)

Managing Aggression. Some useful tips for managing aggression include:

Parents should try to give little attention to mildly disruptive behaviors that allow this energetic child to let off some harmless steam. The parent will also be wasting energy that will be needed when the negative behavior becomes destructive, abusive, or intentional.
The use of "time-out," isolating the child immediately for a short period of time, is an effective measure for allowing both the caregiver and the child to cool down. The child should immediately (and without emotion) be removed from a situation in which they are endangered or endangering others. The child should view time out as a way of cooling off and getting a distance on their behavior, not as isolation from others.
To channel physical aggression and impulsivity in the ADHD toddler, the parents must teach them to use verbal responses. (A parent may need to allow verbal responses that would be unacceptable in another child.)
When the ADHD child becomes older and if the verbal responses become intentionally abusive and socially undesirable, the parent must redirect this form of aggression into more acceptable activities, such as competitive one-on-one sports, energetic music, video games, or big colorful paintings. Competitive video games, such as sports games, may also be an option.
Sometimes a parent can anticipate situations when an ADHD child is likely to misbehave, but all too often the child explodes for no apparent reason. If the blow-up occurs in public, the parents should complete their activities and leave as quickly as possible.

Establishing a Reward System. Children with ADHD respond particularly well to reward systems. One study reported that they performed equally well when encouraged either by a direct reward for a correct response or with the use of a system called response-cost. With this system, the child is given the reward first and allowed to keep it if their behavior remains appropriate.

Some suggested tips for rewarding the ADHD child are:

Create charts with points or stars for good behavior or for completed tasks. It is important to give points for even simple positive behaviors, which may be taken for granted in other children (responding happily to a change in plans, changing an obscenity to a more acceptable expletive).
Rewards for any child can include playing a favorite game with the child, extending bedtime by an hour, or allowing an extra half-hour of TV.
Rewards of food or gifts should be used infrequently, if at all. They can create other problems, such as being overweight, having a bad diet, or making continuous demands for objects.
A reward system should rotate different types of rewards, because such children are easily bored.
Children with ADHD respond better with small rewards promised in the short-term than large rewards offered in the future. One approach that employs both short- and long-term rewards uses a system that gives the child points for specific positive behaviors. As the children accumulate points, they can use them for larger tangible rewards, such as a favorite video game or CD.
Rewards should be promised only when caregivers are fairly certain they can follow through. ADHD children respond with much greater frustration than non-ADHD children to disappointment, and are likely to have a strong (and noisy) negative reaction. A parent must remember that this response is part of the ADHD child's make-up and not necessarily in their control.

Improving Concentration and Attention. Research indicates that ADHD children perform significantly better when their interest is engaged. Parents should be on the lookout for activities that hold the child's concentration. Some options that may help an ADHD child to focus include:

Many ADHD children are particularly lured by the computer, which is a very promising tool. A number of non-violent computer games are available that offer problem-solving techniques using characters, narrative, and humor.
Swimming, tennis, and other sports that focus attention and limit peripheral stimuli are often appealing. ADHD children often do not do well with team sports, although they are interested. Children with ADHD are less likely to become distracted in sports that require constant alertness, such as football or basketball. In baseball, positions such as pitching or catching are preferable to the outfield, where attention easily wanders. Finding a coach that understands the child’s difficulties is very helpful.
Some experts are enthusiastic about martial arts, such as Tae Kwon Do, which can offer an appropriate and controlled emotional outlet, help to focus attention, and teach self-restraint, self-discipline, and tolerance. Care should be taken to select an instructor who makes such goals a priority.
Learning an instrument may be one of the best ways for an ADHD child to develop a more rhythmic and balanced sense of self. Music, even simply listening to it, is often very important for these children. (Parents may have to tolerate music that does not please them.)

Even if a parent is successful in managing the child at home, difficulties often arise at school. The ultimate goal for any educational process should be the happy and healthy social integration of the ADHD child with their peers.

Preparing the Teacher. Although teachers can expect at least one student in every classroom to have ADHD, there is currently little training that prepares them for managing these children. The teacher should be prepared for the certain behaviors in the child with ADHD:

Students with ADHD are often demanding, talkative, and highly visible.
Inattention is a major factor in low academic performance. It causes them to frequently forget homework or miss assignments. Children with ADHD often require frequent reminders or visual cues (such as posters) for rules and regulations. Having the child sit in the front of the classroom may be helpful for both increasing attention and reducing noisy activity.
Lack of fine motor control makes taking notes very difficult, and handwriting is often poor. Using a typewriter or computer can compensate for this. One useful skill that has helped some children is learning to type at an early age, around the third or fourth grade.
Rote memorization and math computation, which require following a set of ordered steps, are often difficult. (Children with ADHD may do better with math concepts.)
Many children with ADHD respond well to school tasks that are rapid, intense, novel, or of short duration (such as spelling bees or competitive educational games), but they almost always have problems with long-term projects where there is no direct supervision.

The Role of the Parent in the School Setting. The parent can help the child by talking to the teacher before the school year starts about their child's situation:

The first priority for the parent is to develop a positive, not adversarial, relationship with the child's teacher.
The parent must acknowledge the teacher's situation, for the teacher must deal not only with the ADHD child's behavior but also with the needs of all the other children.
Frequent brief and sympathetic conversations with the teacher can be helpful and can lead to coordination of efforts, particularly if they provide reciprocal information about progress or setbacks.
Finding a tutor to help after school may be helpful. It is not clear, however, if tutoring offers significant benefits for children whose academic problems stem from inattention unless it is structured specifically to address this problem.

Special Education Programs. The Individuals with Disabilities Education Act (IDEA) requires the school to identify and evaluate children who may need help and to provide special services. However, parents sometimes report pressure by the school to put their children on medication or force them into special classrooms without clear educational justification. The schools, in these cases, may be acting illegally.

High-quality special education can be extremely helpful in improving learning and developing a child's sense of self worth. Many families, however, may not have appropriate programs available for them. Programs vary widely in their ability to provide quality education. Parents must be aware of certain limitations and problems with special education:

Special education programs within the normal school setting often increase the child's feelings of social alienation.
If the educational strategy focuses only on abnormal behavior, it will fail to take advantage of the creative, competitive, and dynamic energy that often accompanies ADHD behavior.
There is no federally funded special education category specifically targeted to ADHD.

If, in fact, ADHD is as common as studies are indicating, the best approach may be to treat the syndrome as a variant of the norm and train teachers to manage these children within the context of a normal classroom.

Special programs are also required under the Rehabilitation Act and by the Americans with Disabilities Act (ADA) for students at institutions of higher learning. It is the student's responsibility, however, to inform the administration at their college or university that they need such services. Unfortunately, many college students are reluctant to do this, although such programs can provide important and beneficial assistance in improving their academic performance.

Other Treatments

A number of diets have been suggested for people with ADHD. Several well-conducted studies have failed to support dietary effects of sugar and food additives on behavior, except possibly in a very small percentage of children. Still various studies have reported behavioral improvement with diets that restrict possible allergens in the diet. Parents may want to discuss with their doctor implementing an elimination diet of certain foods that would not be harmful and that might help.

Food Allergies. Evidence suggests that children with behavioral difficulties may be sensitive to certain chemicals in foods. Studies vary widely, however, on how many cases of ADHD may be associated with sensitivities or allergies to food chemicals or additives, with results ranging widely from 5 - 62%. Among the suspected additives and foods that parents and studies report as inciting behavioral changes are the following:

Any artificial colorings (particularly yellow, red, or green)
Other chemical additives -- for example, BHT or BHA
Milk
Chocolate
Eggs
Wheat
Foods containing salicylates, including all berries, chili powder, apples and cider, cloves, grapes, oranges, peaches, peppers (bell & chili), plums, prunes, tomatoes

In one small study, 62% of children who were given only rice, turkey, pears, and lettuce to eat for 2 weeks experienced at least a 50% improvement in symptoms. Nevertheless, about a quarter of the children pulled out because they could not stick with the diet or they became ill.

Feingold Diet. The most well-known diet for ADHD is the Feingold diet, a salicylate- and additive-free diet, which requires rigorous vigilance over a child's eating habits. This diet also prohibits aspirin, which contains salicylates. Some parents report great success with this diet, although it may be difficult to impose. One study that reported the diets efficacy suggested that it might not provide enough nutritive value, although the diet provides a wide range of healthy foods to select from. It is certainly wise, in any case, to avoid food with artificial colors and flavors and to provide a healthy balance of fresh, natural foods.

Essential Fatty Acids. Omega-3 fatty acids, found in fatty fish and certain vegetable oils, are important for normal brain function and may have some benefits for people with ADHD. It is not clear if supplements of fatty acid compounds, such as docosahexaenoic acid (DHA) and eicosapentaneoic acid (EPA), provide any advantages.

Zinc. Zinc is important for the metabolism of certain neurotransmitters that play a role in ADHD, and deficiencies have been associated with some cases of ADHD. Long-term use of zinc, however, can cause anemia and other side effects in people without deficiencies and it has no effect on ADHD in these patients. In any case, testing for trace minerals, such as zinc, is not standard procedure when evaluating children suspected to have ADHD.

Sugar. Although parents often blame sugar for causing children to become impulsive or hyperactive, a number of studies strongly indicate that sugar plays no role in hyperactivity. One study reported, in fact, that ADHD children had fewer problems after a high-carbohydrate breakfast than after a high-protein one. Another reported that children actually moved more slowly after a high-sugar meal, suggesting the carbohydrates may have a sedative effect. (Still, it's probably always wise for any child to cut down on sugar.)

Techniques that use biologic or auditory feedback are proving to be effective tools for increasing children's attention -- a primary factor in low academic performance.

Neurofeedback. Neurofeedback is an approach that uses electronic devices to help the child control their own brain wave activity. Electrodes are pasted to the child's head and pick up signals from the brain. The child watches images, such as moving graphs, on a computer monitor that reflect the child's brain wave activity. Children are then taught certain high-level mental activities at the point when feedback information on the screen indicates that they are fully concentrating. Children usually attend forty 50-minute sessions, usually twice a week. Small studies have reported significant improvement in inattention, impulsivity, and response time.

Interactive Metronome and Musical Therapy. Interactive metronome uses feedback from sound to improve attention, motor control, and certain academic skills. In this technique study, children wear headphones and sensors on their hands and feet. They perform a number of exercises to a rhythmic computer-beat. Training sessions are completed in 3 - 5 weeks. Some small studies have reported improvement in attention, motor control, language processing, and behavior. (In support of this, some parents report that learning a musical instrument helped their children significantly.)

Procedures and Non-Drug Therapies. A number of alternative approaches are used for children and adults with mild ADHD symptoms. For example, daily massage therapy may help people with ADHD feel happier, fidget less, be less hyperactive, and focus on tasks. Other alternative approaches that may be helpful include relaxation training, meditation, and music therapy. Based on existing evidence, these treatments may be helpful for symptom management but are not proven to benefit the underlying disorder.

Natural Remedies. A number of parents resort to alternative remedies as an alternative to psychostimulants and other drugs. Small trials have found some herbs and supplements -- such as oral flower essence, ginkgo biloba, panax ginseng, melatonin, and pine bark extract (Pycnogenol) --may possibly have benefits for ADHD. Based on existing evidence, however, none can be recommended, particularly for children.

The following are special concerns for people taking natural remedies for attention-deficit disorders:

Melatonin. High doses of melatonin have been associated with an increased risk for seizures in children with existing neurologic disorders.
Gingko. The risk for side effects from gingko appear to be low, but there is an increased risk for bleeding and interaction with anti-clotting medications at high doses.
Ginseng. There have been contaminated forms of imported ginseng. Ginseng also has been associated with low blood sugar and a higher risk for bleeding. In addition, a great number of ginseng products have been found to contain little or no ginseng.

Resources

www.aap.org -- American Academy of Pediatrics
www.nimh.nih.gov -- National Institute of Mental Health
www.chadd.org -- Children and Adults with Attention-Deficit Disorder
www.add.org -- Attention Deficit Disorder Association
www.aabt.org -- Association for Behavioral and Cognitive Therapies
www.psych.org -- American Psychiatric Association
www.parentsmedguide.org -- Medication Guide for Treating ADHD
www.aacap.org -- American Academy of Child and Adolescent Psychiatry
www.nichcy.org -- National Dissemination Center for Children with Disabilities
www.ncld.org -- National Center for Learning Disabilities
www.ldaamerica.org -- Learning Disabilities Association of America

References

Braun JM, Kahn RS, Froehlich T, Auinger P, Lanphear BP. Exposures to environmental toxicants and attention deficit hyperactivity disorder in U.S. children. Environ Health Perspect. 2006 Dec;114(12):1904-9.

Heinrich H, Gevensleben H, Strehl U. Annotation: neurofeedback - train your brain to train behaviour. J Child Psychol Psychiatry. 2007 Jan;48(1):3-16.

Jensen PS, Arnold LE, Swanson JM, et al. 3-year follow-up of the NIMH MTA study. J Am Acad Child Adolesc Psychiatry. 2007 Aug;46(:989-1002.

Nigg JT, Breslau N. Prenatal smoking exposure, low birth weight, and disruptive behavior disorders. J Am Acad Child Adolesc Psychiatry. 2007 Mar;46(3):362-9.

Pliszka S; AACAP Work Group on Quality Issues. Practice parameter for the assessment and treatment of children and adolescents with attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry. 2007 Jul;46(7):894-921.

Steiner H, Remsing L; Work Group on Quality Issues. Practice parameter for the assessment and treatment of children and adolescents with oppositional defiant disorder. J Am Acad Child Adolesc Psychiatry. 2007 Jan;46(1):126-41.

Swanson JM, Elliott GR, Greenhill LL, et al. Effects of stimulant medication on growth rates across 3 years in the MTA follow-up. J Am Acad Child Adolesc Psychiatry. 2007 Aug;46(:1015-27.

Valera EM, Faraone SV, Murray KE, Seidman LJ. Meta-analysis of structural imaging findings in attention-deficit/hyperactivity disorder. Psychiatry. 2007 Jun 15;61(12):1361-9. Epub 2006 Sep 1.

Wilens TE, Upadhyaya HP. Impact of substance use disorder on ADHD and its treatment. J Clin Psychiatry. 2007 Aug;68(:e20.

Williams JH, Ross L. Consequences of prenatal toxin exposure for mental health in children and adolescents: a systematic review. Eur Child Adolesc Psychiatry. 2007 Jun;16(4):243-53. Epub 2007 Jan 2.

Review Date:
12/27/2007
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

adam.com

Eating disorders

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

In This Report

Highlights
Introduction
Risk Factors
Causes
Complications of Bulimia...
Complications of Anorexia...
Symptoms
Diagnosis
Treatment
Treatment for Bulimia
Treatment for Anorexia
Therapy
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Eating Disorders Overview

Eating disorders typically occur among young women.
Bulimia nervosa involves a pattern of bingeing and purging. Many people with bulimia nervosa also suffer from depression.
Anorexia nervosa involves a pattern of self-starvation. Patients often have an accompanying anxiety disorder (such as obsessive compulsive disorder) or depression. Patients who have anorexia and depression have a high risk for suicide. Some studies estimate that anorexia nervosa has the highest death rate of any psychiatric disorder.

Treatment of Bulimia Nervosa

Bulimia nervosa is treated with a combination of psychotherapy and medication. Cognitive behavioral therapy, which is given along with nutritional counseling, is the preferred psychotherapeutic approach. Selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine (Prozac), are the first choice for drug therapy.

Treatment of Anorexia Nervosa

Unlike bulimia nervosa, anorexia nervosa does not respond as well to drug treatment, although SSRIs are sometimes used as an adjunct to psychotherapy. Therapy that includes the entire family -- not just the patient -- is an important part of the treatment process, as is nutritional education. Patients who are severely underweight and who have other physical risks may need to be hospitalized while weight is restored. Recovery is a long process that can take 5 - 6 years to achieve.

Introduction

Eating disorders are behavioral issues brought on by a complex interplay of factors, which may include emotional and personality disorders, family pressures, a possible genetic or biologic susceptibility, and a culture in which there is an overabundance of food and an obsession with thinness. There are four general categories of eating disorders:

Bulimia nervosa
Anorexia nervosa
Binge eating
Eating disorders not otherwise specified

These are not new disorders. Although anorexia nervosa was first defined as a medical problem in the late 1800s, descriptions of self-starvation have been found even in medieval writings.

Bulimia nervosa is more common than anorexia, and it usually begins early in adolescence. It is characterized by cycles of bingeing and purging, and typically takes the following pattern:

Bulimia is often triggered when young women attempt restrictive diets, fail, and react by binge eating. (Binge eating involves consuming larger than normal amounts of food within a 2-hour period.)
In response to the binges, patients compensate, usually by purging, vomiting, using enemas, or taking laxatives, diet pills, or drugs to reduce fluids.
Patients then revert to severe dieting, excessive exercise, or both. (Some patients with bulimia follow bingeing only with fasting and exercise. They are then considered to have non-purging bulimia.)
The cycle then swings back to bingeing and then to purging again.
Some studies have reported that patients with bulimia average about 14 episodes of binge-purging per week. To be diagnosed with bulimia, however, a patient must binge and purge at least twice a week for 3 months. (Some experts believe that going through the cycle only once a week is sufficient for a diagnosis.)
In some cases, the condition progresses to anorexia. Most people with bulimia, however, have a normal to high-normal body weight, although it may fluctuate by more than 10 pounds because of the binge-purge cycle.

Young people who occasionally force vomiting after eating too much are not considered bulimic, and most of the time this occasional unhealthy behavior does not continue beyond youth.

The term "anorexia" literally means absence of appetite. Anorexia nervosa involves an aversion to food that leads to a state of starvation and emaciation. It is a very serious illness that some experts believe is an entirely different condition from bulimia and should be not be diagnosed as a simple eating disorder.

Facts associated with anorexia nervosa:

At least 15% to as much as 60% of normal body weight is lost.
The patient with anorexia nervosa has an intense fear of gaining weight, even when severely underweight.
Individuals with anorexia nervosa have a distorted image of their own weight or shape and deny the serious health consequences of their low weight.
Women with anorexia nervosa miss at least three consecutive menstrual periods. (Some experts believe women can be anorexic without this occurrence.)

Patients with this condition are often characterized as anorexia restrictors or anorexic bulimic patients. Each type is equally prevalent.

Anorexia restrictors reduce their weight by severe dieting.
Anorexic bulimic patients maintain emaciation by purging. Although both types are serious, the bulimic type, which imposes additional stress on an undernourished body, is the more damaging.

Severe anorexia is common in the elderly, who may experience weight loss because of social isolation, impaired gastrointestinal function, or loss of certain chemicals related to the feeding drive. Such age-related anorexia, however, is not synonymous with anorexia nervosa, a psychologic disorder.

Bingeing without purging is characterized as compulsive overeating (binge eating) with the absence of bulimic behaviors, such as vomiting or laxative abuse (used to eliminate calories). Binge eating usually leads to becoming overweight.

To be diagnosed as a binge eater, a person typically has the following characteristics:

Bingeing at least twice a week for 6 months
Consuming 5,000 - 15,000 calories in one sitting
Eating three meals a day plus frequent snacks
Overeating continually throughout the day, rather than consuming large amounts of food during binges

Since binge eating disorder is generally associated with weight gain, it will not be further discussed in this report. [For more information, see In-Depth Report #53: Weight control and diet.]

A fourth category called eating disorders not otherwise specified (NOS) has been established to define eating disorders not specifically defined as anorexia or bulimia. This category includes:

Infrequent binge-purge episodes (occurring less than twice a week or having such behavior for less than months)
Repeated chewing and spitting without swallowing large amounts of food
Normal weight and anorexic behavior

Such patients tend to be older at diagnosis. Although less serious than other eating disorders, these patients still face similar health problems, including a higher risk for fractures and other conditions.

Risk Factors

Many factors contribute to the risk of developing an eating disorder. In the United States, about 7 million women and 1 million men suffer from eating disorders.

Eating disorders occur most often in adolescents and young adults. However, new research finds that they are increasingly prevalent among young children. Eating disorders are more difficult to identify in young children because they are rarely suspected.

Studies indicate that eating disorders occur predominantly among girls and women. About 90 - 95% of patients with anorexia nervosa, and about 80% of patients with bulimia nervosa, are female.

Most studies of individuals with eating disorders have been conducted using Caucasian middle-class females. Studies now indicate, however, that minority populations (including Hispanic Americans and African-Americans) are increasingly affected.

Living in any economically developed nation on any continent appears to pose a risk for eating disorders. Within nations, eating disorders can affect people of all socioeconomic levels.

People with eating disorders tend to share similar personality and behavioral traits, including low self-esteem, dependency, and problems with self-direction. Specific psychiatric personality disorders may put people at higher risk for eating disorders.

Avoidant Personalities. Some studies indicate that many patients with anorexia nervosa have avoidant personalities. This personality disorder is characterized by:

Being a perfectionist
Being emotionally and sexually inhibited
Having less of a fantasy life than people with bulimia or those without an eating disorder
Being perceived as always being "good," not being rebellious
Being terrified of being ridiculed or criticized or of feeling humiliated

People with anorexia are extremely sensitive to failure, and any criticism, no matter how slight, reinforces their own belief that they are "no good".

Obsessive-Compulsive Personality. Obsessive-compulsive personality defines certain character traits (being a perfectionist, morally rigid, or preoccupied with rules and order). This personality disorder has been strongly associated with a higher risk for anorexia. These traits should not be confused with the anxiety disorder called obsessive-compulsive disorder (OCD), although they may increase the risk for this disorder.

Borderline Personalities. Borderline Personality Disorder (BPD) is associated with self-destructive and impulsive behaviors. People with BPD tend to have other co-existing mental health problems, including eating disorders.

Narcissistic Personalities. Studies have also found that people with bulimia or anorexia are often highly narcissistic and tend to:

Have an inability to soothe oneself
Have an inability to empathize with others
Have a need for admiration
Be hypersensitive to criticism or defeat

Many patients with eating disorders experience depression and anxiety disorders. Depression, anxiety, or both is also common in families of patients with eating disorders. It is not clear if emotional disorders, particularly obsessive-compulsive disorder (OCD), cause the eating disorders, increase susceptibility to them, or share common biologic cause.

Obsessive-Compulsive Disorder (OCD). Obsessive-compulsive disorder is an anxiety disorder that occurs in up to two thirds of patients with anorexia and up to one third of patients with bulimia. In fact, some experts believe that eating disorders are variants of OCD. Obsessions are recurrent or persistent mental images, thoughts, or ideas, which may result in compulsive behaviors (repetitive, rigid, and self-prescribed routines) that are intended to prevent the manifestation of the obsession. Women with anorexia and OCD may become obsessed with exercise, dieting, and food. They often develop compulsive rituals (weighing every bit of food, cutting it into tiny pieces, or putting it into tiny containers). The presence of OCD with either anorexia or bulimia does not, however, appear to have any influence on whether a patient improves or not.

Obsessive-compulsive disorder is an anxiety disorder characterized by an inability to resist or stop continuous, abnormal thoughts or fears combined with ritualistic, repetitive, and involuntary defense behavior.

Other Anxiety Disorders. A number of other anxiety disorders have been associated with both bulimia and anorexia, including:

Phobias. Phobias often precede the onset of the eating disorder. Social phobias, in which a person is fearful about being humiliated in public, are common in both types of eating disorders.
Panic Disorder. Panic disorder often follows the onset of an eating disorder. It is characterized by periodic attacks of anxiety or terror (panic attacks).
Post-Traumatic Stress Disorder. Many women with serious eating disorders report a past traumatic event, and many exhibit symptoms of post-traumatic stress disorder (PTSD) -- an anxiety disorder that occurs in response to life-threatening circumstances.

Depression. Depression is common in people with eating disorders, for both anorexia and bulimia. Major depression is unlikely to be a cause of eating disorders, however, because treating and relieving depression rarely cures an eating disorder. In addition, depression often improves after anorexic patients begin to gain weight.

Extreme eating disorder behaviors, including use of diet pills, laxatives, diuretics, and vomiting, are reported more often in overweight teenagers. Researchers are working on strategies for preventing the development of eating disorders among overweight adolescents. A 2006 study that targeted overweight college-age women reported success with an Internet-based cognitive behavioral therapy program that helped these women become more comfortable with their body weight and shape. The program also included information on the risks of eating disorders, and education on healthy eating and weight maintenance.

Body Dysmorphic Disorder. Body dysmorphic disorder (BDD) involves a distorted view of one's body that is caused by social, psychologic, or possibly biologic factors. It is often associated with anorexia or bulimia, but it can also occur without any eating disorder. People with this disorder commonly suffer from emotional disorders, including obsessive-compulsive disorder and depression. As part of obsessive thinking, some people with BDD may obsess about a perceived deformity in one area of their body, and may repeatedly seek cosmetic surgery to "correct" it. People with BDD are also at higher risk for suicidal thinking and attempts. Some evidence suggests that treatment with fluoxetine (Prozac), a common antidepressant known as an SSRI helps reduce this problem, even in people without an eating disorder.

Muscle Dysmorphia. Experts are also increasingly reporting a disorder in which people have distorted body images involving their muscles. It tends to occur in men who perceive themselves as being "puny," which results in excessive body building, preoccupation with diet, and social problems. Such individuals are prone to eating disorders and other unhealthy behaviors, including the use of anabolic steroids.

Highly competitive athletes are often perfectionists, a trait common among people with eating disorders.

Female Athletes. Excessive exercise is associated with many cases of anorexia (and, to a lesser degree, bulimia). In young female athletes, anorexia postpones puberty, allowing them to retain a muscular boyish shape without the normal accumulation of fatty tissues in breasts and hips that may blunt their competitive edge. Many coaches and teachers compound the problem by overstressing calorie counting and loss of body fat.

In response, people who are vulnerable to such criticism may lose excessive weight, which has been known to be deadly even for famous athletes. The term "female athlete triad" in fact, is now a common and serious disorder facing young female athletes and dancers and describes the combined presence of the following problems:

Eating disorders, including anorexia
Amenorrhea (absence or irregular menstruation)
Osteoporosis (bone loss, which appears to be related to low weight)

Male Athletes. Male wrestlers and lightweight rowers are also at risk for excessive dieting. One-third of high school wrestlers use a method called weight-cutting for rapid weight loss. This process involves food restriction and fluid depletion by using steam rooms, saunas, laxatives, and diuretics. Although male athletes are more apt to resume normal eating patterns once competition ends, studies show that the body fat levels of many wrestlers are still well below their peers during off-season and are often as low as 3% during wrestling season.

Men and Women in the Military. Studies also show a higher-than-average risk for eating disorders in men and women in the military. A study of eating behavior on one Army base reported that 8% of the women had an eating disorder, compared to 1 - 3% in the civilian female population.

In general, vegetarianism, with careful planning, is a healthy practice for both adults and adolescents. Studies report, however, that vegetarianism in adolescence may be a risk factor for eating disorders in both males and females. Vegetarian teens have been found to be twice as likely to diet frequently, four times as likely to intensively diet, and eight times as likely to use laxatives as their non-vegetarian peers.

These studies do not mean that being a vegetarian equates with having an eating disorder. They do suggest, however, that parents with children who suddenly become vegetarians should be sure that their children are eating a balanced meal with sufficient protein, calories, and important minerals, such as calcium. Parents also might suspect anorexic behavior in their child under certain conditions:

If the child has stopped eating meat only to avoid fat rather than from other motives, such as love of animals or to improve health.
If the vegetarian diet coincides with rapid weight loss.
If the child avoids important vegetable products because of calories (such as whole grains) or because of fats and oils (such as tofu, nuts, and dairy products).

Eating disorders may be more common in teenagers with chronic illness, such as diabetes or asthma. Some recent research suggests an endocrinological link between obesity, diabetes, and eating disorders.

Diabetes. Eating disorders are particularly serious problems for people with either type 1 or type 2 diabetes.

Binge eating (without purging) is most common in type 2 diabetes and, in fact, the obesity it causes may even trigger this diabetes in some people.
Both bulimia and anorexia are common in type 1 diabetes. A 2005 study indicated that as many as 25% of young women with type 1 diabetes may develop abnormal eating habits, and that the combination of diabetes and an eating disorder can have serious health consequences in the women's future. Diabetic women often omit or underuse insulin in order to control weight. If such patients develop anorexia, their extremely low weight may appear to control the diabetes for a while. Eventually, however, if they fail to take insulin and continue to lose weight, these patients develop life-threatening complications.

Click the icon to see an image of type 1 diabetes.

There is a greater risk for eating disorders and other emotional problems for girls who undergo early puberty, when the pressures experienced by all adolescents are intensified by experiencing, possibly alone, these early physical changes, including normal increased body fat. One interesting study reported that:

Before puberty, girls ate quantities of food appropriate to their body weight, were satisfied with their bodies, and noted their depression increased with lower food intake.
After puberty, girls ate about three-quarters of the recommended calorie intake, had a worse body self-image, and noted their depression increased with higher food intake.

This study reported on girls without eating disorders, but it certainly suggests patterns that can lead to eating problems, particularly in girls who go through puberty early. Other studies also indicate that girls who start menstruating at a younger age are more likely to develop eating disorders.

Causes

There is no single cause for eating disorders. Although concerns about weight and body shape play a role in all eating disorders, the actual cause of these disorders appear to result from many factors, including cultural and family pressures and emotional and personality disorders. Genetics and biologic factors may also play a role.

Negative influences within the family may play a major role in triggering and perpetuating eating disorders. Some studies have produced the following observations and theories regarding family influence.

Insecure Infancy. Some experts theorize that parents who fail to provide a safe and secure foundation in infancy may foster eating disorders. In such cases, children experience so-called insecure attachments. They are more likely to have greater weight concerns and lower self-esteem than are those with secure attachments.
Parental Behaviors. Poor parenting by both mothers and fathers has been implicated in eating disorders. One study found that 40% of 9- and 10-year-old girls trying to lose weight generally with the urging of their mothers. Some studies have found that mothers of anorexics tend to be over-involved in their child's life, while mothers of people with bulimia are critical and detached. Overly critical fathers, brothers, or both may play a factor in the development of anorexia in both girls and boys.
Family Meals. How often a family eats together may influence whether a child develops an eating disorder. A study published in the Journal of Adolescent Health found that young girls who ate 3 - 4 meals per week with their families were about half as likely to engage in extreme weight control behaviors as girls who ate family meals less often.
Family History of Addictions or Emotional Disorders. Studies report that people with either anorexia or bulimia are more likely to have parents with alcoholism or substance abuse than are those in the general population. Parents of people with bulimia appear to be more likely to have psychiatric disorders than parents of patients with anorexia.
History of Abuse. Women with eating disorders, particularly bulimia, appear to have a higher incidence of sexual abuse. Studies have reported sexual abuse rates as high as 35% in women with bulimia.
Family History of Obesity. People with bulimia are more likely than average to have an obese parent or to have been overweight themselves during childhood.

At least one study has reported that the most positive way for parents to influence their children's eating habits and to prevent weight problems and eating disorders is to have healthy eating habits themselves.

Anorexia is eight times more common in people who have relatives with the disorder, and some experts estimate that genetic factors are the root cause of many cases of eating disorders. Twins had a tendency to share specific eating disorders (anorexia nervosa, bulimia nervosa, and obesity). Researchers have identified specific chromosomes that may be associated with bulimia and anorexia. In particular, regions on chromosome 10 have been linked to bulimia as well as obesity. Some evidence has also reported an association with genetic factors responsible for serotonin, the brain chemical involved with both well-being and appetite. Researchers have also pinpointed certain proteins such as brain-derived neurotrophic factor (BDNF). This protein may influence an individual's susceptibility to developing an eating disorder.

The approach to food in Western countries is extremely problematic. Enough food is produced in the U.S. to supply 3,800 calories every day to each man, woman, and child, far more than any single person needs to sustain life. Obesity is a global epidemic, and few people living in this over-fed and sedentary culture eat a meal guiltlessly.

One interesting anthropologic study reported the following observations:

During historical periods or in cultures where women are financially dependent and marital ties are stronger, the standard is toward being curvaceous, possibly reflecting a cultural or economic need for greater reproduction.
During periods or in cultures where female independence has been possible, the standard of female attractiveness tends toward thinness.

The response of the media to the cultural drive for thinness and the overproduction of food both likely play major roles in triggering obesity and eating disorders.

On the one hand, advertisers heavily market weight-reduction programs and present anorexic young models as the paradigm of sexual desirability.
Clothes are designed and displayed for thin bodies in spite of the fact that few women could wear them successfully.
On the other hand, the media floods the public with attractive ads for consuming foods, especially "junk" foods.

Hormonal abnormalities are common in eating disorders and include chemical abnormalities in the thyroid, the reproductive regions, and areas related to stress, well-being, and appetite. Many of these chemical changes are certainly a result of malnutrition or other aspects of eating disorders, but they also may play a role in perpetuating or even creating susceptibility to the disorders.

The primary setting of many of these abnormalities originate in a small area of the brain called the limbic system. A specific system called hypothalamic-pituitary-adrenal axis (HPA) may be particularly important in eating disorders. It originates in the following regions in the brain:

Hypothalamus. The hypothalamus is a small structure that plays a role in controlling our behavior, such as eating, sexual behavior and sleeping, and regulates body temperature, emotions, secretion of hormones, and movement.

Click the icon to see an image of the hypothalamus.

The pituitary gland. The pituitary gland is involved in controlling thyroid functions, the adrenal glands, growth, and sexual maturation.
Amygdala. This small almond-like structure lies deep in the brain and is associated with regulation and control of major emotional activities, including anxiety, depression, aggression, and affection.

Click the icon to see an image of the brain-thyroid link.

Stress Hormones. The HPA systems trigger the production and release of stress hormones called glucocorticoids, including the primary stress hormone cortisol. Chronically elevated levels of stress chemicals have been observed in patients with anorexia and bulimia. Cortisol is very important in marshaling systems throughout the body (including the heart, lungs, circulation, metabolism, immune systems, and skin) to deal quickly with any threat.

Release of Neurotransmitters. The HPA system also releases certain neurotransmitters (chemical messengers) that regulate stress, mood, and appetite and are being heavily investigated for a possible role in eating disorders. Abnormalities in the activities of three of them, serotonin, norepinephrine, and dopamine, are of particular interest. Serotonin is involved with well-being, anxiety, and appetite (among other traits), and norepinephrine is a stress hormone. Dopamine is involved in reward-seeking behavior. Recent research suggests that people with anorexia have increased activity in the brain's dopamine receptors. This overactivity may explain why people with anorexia do not experience a sense of pleasure from food and other typical comforts.

Ghrelin. High levels of ghrelin, a hormone that increases the feeling of hunger and slows metabolism, have been noted in patients with anorexia and bulimia.

Low-Leptin Levels. Leptin is a hormone that appears to trigger the hypothalamus to stimulate appetite, and low levels have been observed in people with anorexia and bulimia.

Low Reproductive Hormones. The hypothalamic-pituitary system is also responsible for the production of important reproductive hormones that are severely depleted in anorexics. Although most experts believe that these reproductive abnormalities are a result of anorexia, others have reported that in 30 - 50% of people with anorexia, menstrual disturbances occurred before severe malnutrition set in and remained a problem long after weight gain, indicating that hypothalamic-pituitary abnormalities precede the eating disorder itself.

In some cases, infection has been associated with anorexia. In such cases, immune factors released to fight these infections may cause inflammation and injury in the areas of the brain that affect appetite and behavior.

Streptococcal Infection. The bacteria responsible for strep throat and rheumatic fever -- called group A beta-hemolytic streptococcal (GABHS) -- is now a suspect in some cases of anorexia. Some children who have been infected with these bacteria develop a syndrome that includes obsessive-compulsive disorder (OCD), tics, and anorexia nervosa. The syndrome is called PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus). More research is needed to confirm this as an actual cause of anorexia and to determine if it may be treatable with antibiotics.

Epstein Barr Virus. Epstein Barr, the virus that causes mononucleosis, has also been associated with the development of anorexia.

Click the icon to see an image of infectious mononucleosis.

Complications of Bulimia

Most studies report that patients who have bulimia without severe weight loss have a much better outlook than patients with anorexia. Some studies have suggested that 60 - 80% of bulimic patients are in remission within 3 months of treatment. However, relapse is common, and over half of women with bulimia continue to battle disordered eating habits for years. In one study, bulimia itself persisted in 10 - 25% of patients after treatment.

Many medical problems are directly associated with bulimic behavior, including:

Tooth erosion, cavities, and gum problems
Water retention, swelling, and abdominal bloating
Acute stomach distress
Fluid loss with low potassium levels (due to excessive vomiting or laxative use; can lead to extreme weakness, near paralysis, or lethal heart rhythms)
Irregular periods
Swallowing problems and esophagus damage

Forced vomiting causes repetitive assaults on the esophagus (the food pipe) from forced vomiting. It is not clear, however, if swallowing problems are common.

The esophagus connects the nose and mouth with the stomach. The epiglottis folds over the trachea when a swallow occurs, to prevent the swallowed substance from being inhaled into the lungs. When a person is unable to swallow because of illness or coma, a tube may be inserted either through the mouth or nose, past the epiglottis, through the esophagus and into the stomach. Nutrients pass directly through the tube into the stomach.

Rupture of the esophagus, or food pipe
Weakened rectal walls (rare, but serious condition that requires surgery)

Click the icon to see an image of the rectum.

A number of self-destructive behaviors occur with bulimia:

Smoking. Many teenage girls with eating disorders smoke because it is thought to help prevent weight gain.
Impulsive Behaviors. Women with bulimia are at higher-than-average risk for dangerous impulsive behaviors, such as sexual promiscuity, self-cutting, and kleptomania. Some studies have reported such behaviors in half of those with bulimia.
Alcohol and Substance Abuse. An estimated 30 - 70% of patients with bulimia abuse alcohol, drugs, or both. This rate is higher than that of the general population and for people with anorexia. However, this higher rate of substance abuse may be a distortion because studies are conducted only on diagnosed patients. Bulimia tends not to get diagnosed. And reports of bulimia in the community (where the incidence of the eating disorder is higher than statistics suggest) indicate that substance abuse is actually lower than in people with anorexia.

Women with bulimia frequently abuse over-the-counter medications, such as laxatives, appetite suppressants, diuretics, and drugs that induce vomiting (ipecac). None of these drugs is without risk. For example, ipecac poisonings have been reported, and some people become dependent on laxatives for normal bowel functioning. Diet pills, even herbal and over-the-counter medications, can be hazardous, particularly if they are abused.

Complications of Anorexia

Anorexia nervosa is a very serious illness that has a wide range of effects on the body and mind. It is also associated with other problems, ranging from frequent flus and general poor health to life-threatening conditions. Some experts believe that it should not be approached as a simple eating disorder but as a serious condition requiring staging according to severity.

At this time, no treatment program for anorexia nervosa is completely effective. Recovery rates vary between 23 - 50%, and relapses range from 4 - 27%. Recovery takes an average of 5 - 6 years from the time of diagnosis. Up to 30% of patients do not recover.

Even after treatment and weight gain, many patients continue to display characteristics of the disorder, including perfectionism and a drive for thinness, which could keep them at risk for recurrence.

Some research suggests that anorexia nervosa has the highest death rate of any psychiatric disorder. According to different studies, the risk for early death is higher for people with the following conditions or characteristics:

Being younger
Having bulimia anorexia (twice as high in this group than in the anorexic-restrictor types)
Being severely low in weight at the time of treatment
Being sick for more than 6 years
Having been previously obese
Having an accompanying severe psychological disorder including personality disorders

One of the most serious effects of anorexia is hormonal changes, which can have severe health consequences.

Reproductive hormones, including estrogen and dehydroepiandrosterone (DHEA), are lower. Estrogen is important for healthy hearts and bones. DHEA, a weak male hormone, may also be important for bone health and for other functions.
Thyroid hormones are lower.
Stress hormones are higher.
Growth hormones are lower. Children and adolescents with anorexia may experience retarded growth.

The result of many of these hormonal abnormalities in women is long-term, irregular or absent menstruation (amenorrhea). This can occur early on in anorexia, even before severe weight loss. Over time this causes infertility, bone loss, and other problems. Low weight alone may not be sufficient to cause amenorrhea. Extreme fasting and purging behaviors may play an even stronger role in hormonal disturbance.

Adolescents with eating behaviors associated with anorexia (fasting, frequent exercise to lose weight, and self-induced vomiting) are at high risk for anxiety and depression in young adulthood. Alcohol and drug abuse are more common in patients with anorexia. Suicide has been estimated to account for as many as half the deaths in anorexia with studies showing up to a fifth of anorexic patients attempting suicide.

Heart disease is the most common medical cause of death in people with severe anorexia. The effects of anorexia on the heart are:

Dangerous heart rhythms, including slow rhythms known as bradycardia, may develop. Such abnormalities can show up even in teenagers with anorexia.

Bradycardia is a slowness of the heartbeat, usually at a rate under 60 beats per minute (normal resting rate is 60 - 100 beats per minute).

Blood flow is reduced
Blood pressure may drop
The heart muscles starve, losing size
Cholesterol levels tend to rise

Click the icon to see an image of cholesterol.

A primary danger to the heart is from abnormalities in the balance of minerals, such as potassium, calcium, magnesium, and phosphate, which are normally dissolved in the body's fluid. The dehydration and starvation that occurs with anorexia can reduce fluid and mineral levels and produce a condition known as electrolyte imbalance. Electrolytes (calcium and potassium) are critical for maintaining the electric currents necessary for a normal heartbeat. An imbalance in these electrolytes can be very serious and even life threatening unless fluids and minerals are replaced. Heart problems are a particular risk when anorexia is compounded by bulimia and the use of ipecac, a drug that causes vomiting.

After treatment and an increase in weight, estrogen levels are usually restored and periods resume. In severe anorexia, however, even after treatment, normal menstruation never returns in 25% of such patients.

If a woman with anorexia becomes pregnant before regaining normal weight, she faces a higher risk for miscarriage, cesarean section, and for having an infant with low birth weight or birth defects. She is also at higher risk for postpartum depression.
Women with anorexia who seek fertility treatments have lower chances for success.

Most pregnant women with a history of eating disorders have healthy pregnancies. However, some studies suggest that they may face higher risks for a number of complications, including cesarean sections, postpartum depression, miscarriages, complicated deliveries, and premature birth. Many studies indicate that babies born to mothers with eating disorders have a higher risk for low birth weight. However, an encouraging 2006 study reported that mothers with a history of anorexia nervosa do not have a higher risk for pregnancy complications or poor birth outcomes.

Almost 90% of women with anorexia experience osteopenia (loss of bone minerals), and 40% have osteoporosis (more advanced loss of bone density). Up to two-thirds of children and adolescent girls with anorexia fail to develop strong bones during their critical growing period. Boys with anorexia also suffer from stunted growth. The less the patient weighs, the more severe the bone loss. Women with anorexia who also binge-purge face an even higher risk for bone loss.

Bone loss in women is mainly due to low estrogen levels that occur with anorexia. Other biologic factors in anorexia also may contribute to bone loss, including high levels of stress hormones (which impair bone growth) and low levels of calcium, certain growth factors, and DHEA (a weak male hormone). Weight gain, unfortunately, does not completely restore bone. Only achieving regular menstruation as soon as possible can protect against permanent bone loss. The longer the eating disorder persists the more likely the bone loss will be permanent.

Testosterone levels decline in boys as they lose weight, which also can affect their bone density. In young boys with anorexia, weight restoration produces some catch-up growth, but it may not produce full growth.

People with severe anorexia may suffer nerve damage that affects the brain and other parts of the body. The following nerve-related conditions have been reported:

Seizures
Disordered thinking
Numbness or odd nerve sensations in the hands or feet (peripheral neuropathy)

Brain scans indicate that parts of the brain undergo structural changes and abnormal activity during anorexic states. Some of these changes return to normal after weight gain, but there is evidence that some damage may be permanent. Still, the extent of the neurologic problems is unclear.

Anemia is a common result of anorexia and starvation. In one study, 38% of anorexic participants had anemia. A particularly serious blood problem is pernicious anemia, which can be caused by severely low levels of vitamin B12. If anorexia becomes extreme, the bone marrow dramatically reduces its production of blood cells, a life-threatening condition called pancytopenia.

Bloating and constipation are both very common problems in people with anorexia.

In very late anorexia, the organs simply fail. The main warning sign is high blood levels of liver enzymes, which require immediate administration of calories.

Eating disorders are very serious for young people with type 1 diabetes. A study of over 2,000 women found that bulimia, or a combination of bulimia and anorexia, was more common among women with type 1 diabetes.

The complications of eating disorders that affect all patients are even more dangerous in this group of patients. Low blood sugar, for example, is a danger for anyone with anorexia, but it is a particularly dangerous risk for those with diabetes. If patients do not take their insulin, high blood sugar, which is also very dangerous, can occur. Unfortunately, patients with eating disorders may skip or reduce their daily insulin in order to decrease their intake of calories. Extremely high blood sugar levels can cause diabetic ketoacidosis, a condition in which acidic chemicals (ketones) accumulate in the body. This condition can lead to coma and death.

Symptoms

Possibly the most bewildering symptom of eating disorders is the distorted body image (body dysmorphia ). Although people typically associate distorted body image with severe anorexia, one study indicated that distortion may be more prevalent in people with bulimia. People with bulimia were more likely than those with anorexia to overestimate their size. There was also a greater disparity between what they wanted to look like and what they believed they looked like.

People with bulimia nearly always practice it in secret, and, although they may be underweight, they are not always anorexic. Symptoms or signs of bulimia may, therefore, be very subtle and go unnoticed. They may include:

Evidence of discarded packaging for laxatives, diet pills, emetics (drugs that induce vomiting), or diuretics (medications that reduce fluids)
Regularly going to the bathroom right after meals
Suddenly eating large amounts of food or buying large quantities that disappear right away
Compulsive exercising
Broken blood vessels in the eyes (from the strain of vomiting)
Pouch-like appearance to the corners of the mouth due to swollen salivary glands (occurs within days of vomiting in about 8% of people with bulimia)
Dry mouth
Tooth cavities, diseased gums, and irreversible enamel erosion from excessive acid
Rashes and pimples
Small cuts and calluses across the tops of finger joints due to self-induced vomiting

Weight Loss. The primary symptom of anorexia is major weight loss from excessive and continuous dieting, which may either be restrictive dieting or binge-eating and purging.

Other symptoms of anorexia may include:

Infrequent or absent menstrual periods
Compulsive exercising coupled with excessive thinness
Refusal to eat in front of others
Ritualistic eating, including cutting food into small pieces
Hypersensitivity to cold -- some women wear several layers of clothing to both keep warm and hide their thinness
Yellowish skin, especially on the palms of the hands and soles of the feet -- from eating too many vitamin A-rich vegetables such as carrots
Dry skin covered with fine hair
Thin scalp hair
Cold or swollen feet and hands
Stomach problems, including bloating after eating
Confused or slowed thinking
Poor memory or judgment

Diagnosis

The first step towards a diagnosis is to admit the existence of an eating disorder. Often, the patient needs to be compelled by a parent or others to see a doctor because the patient may deny and resist the problem. Some patients may even self-diagnose their condition as an allergy to carbohydrates, because after being on a restricted diet, eating carbohydrates can produce gastrointestinal problems, dizziness, weakness, and palpitations. This may lead such people to restrict carbohydrates even more severely.

It is often extremely difficult for parents as well as the patient to admit that a problem is present. For example, because food is such an intrinsic part of the mother-child relationship, a child's eating disorder might seem like a terrible parental failure. Parents may have their own emotional issues with weight gain and loss and perceive no problem with having a "thin" child.

It is recommended that a supportive companion be present during part of the initial medical interview to offer additional information on the patient's eating history and to help offset any resistance or denial the patient may express.

Various questionnaires are available for assessing patients. The Eating Disorders Examination (EDE), which is an interview of the patient by the doctor, and the self-reported Eating Disorders Examination-Questionnaire (EDE-Q) are both considered valid tests for assessing eating disorder diagnosis and determining specific features of the individual’s condition (such as vomiting or laxative use).

Another test is called the SCOFF questionnaire. It is proving to be very reliable in accurately identifying both very young and adult patients who meet the full criteria for anorexia or bulimia nervosa. (It may not be as accurate in people who do not meet the full criteria.)

SCOFF Questionnaire

Do you make yourself Sick because you feel uncomfortably full?

Do you worry you have lost Control over how much you eat?

Have you recently lost more than One stone 's worth of weight (14 pounds) in a 3-month period?

Do you believe yourself to be Fat when others say you are too thin?

Would you say that Food dominates your life?

Answering yes to two of these questions is a strong indicator of an eating disorder.

In spite of the prevalence of bulimia, a majority of doctors have never diagnosed bulimia in a patient. Younger and female doctors are more likely to detect bulimia. A doctor should make a diagnosis of bulimia if there are at least two bulimic episodes per week for 3 months. Because people with bulimia tend to have complications with their teeth and gums, dentists could play a crucial role in identifying and diagnosing bulimia.

Generally, an observation of physical symptoms and a personal history will quickly confirm the diagnosis of anorexia. The standard criteria for diagnosing anorexia nervosa are:

The patient's refusal to maintain a body weight normal for age and height
Intense fear of becoming fat even though underweight
A distorted self-image that results in diminished self-confidence
Denial of the seriousness of emaciation and starvation
The loss of menstrual function for at least 3 months

The doctor then categorizes the anorexia further:

Restricting (severe dieting only)
Anorexia bulimia (binge-purge behavior)

Because the disorder rarely shows up in men, doctors may not be on the lookout for it in male patients, even if they show classic symptoms of anorexia. Doctors should be very aware of these symptoms in anyone, particularly in athletes and dancers.

Once a diagnosis is made, doctors should immediately check for any serious complications of starvation. They should also rule out other medical disorders that might be causing the anorexia. Tests should include:

A complete blood count
Tests for electrolyte imbalances (low potassium levels mean the disorder is more likely to be accompanied by the binge-purge syndrome)
Test for protein levels
An electrocardiogram and a chest x-ray
Tests for liver, kidney, and thyroid problems
A bone density test

Treatment

Treatment goals for eating disorders include:

Restore normal weight for anorexia nervosa
Reduce, and hopefully stop, binge eating and purging for bulimia nervosa
Treat physical complications and any associated psychiatric disorders
Teach patients proper nutritional habits and how to develop healthy eating patterns and meal plans
Change patients’ dysfunctional thoughts about the eating disorder
Improve self-control, self-esteem, and behavior
Provide family counseling
Prevent relapse

The first major difficulty in treating eating disorders is resistance by everyone involved:

The anorexic patient often believes that the emaciation is normal and even attractive.
The bulimic patient may feel that purging is the only way to prevent obesity.
Even worse, the anorexic condition may be encouraged by friends who envy thinness or by dance or athletic coaches who encourage low body fat.
The family itself may deny the problem and be obstructive or manipulative, adding to the difficulties of treatment.

It is very important that the patient and any close friends and relatives be informed about the serious potential of these conditions and the importance of receiving immediate help.

A multidisciplinary team approach with consistent support and counseling is essential for long-term recovery from all severe eating disorders. Depending on the severity and type of disorder, team members may include:

Doctors specializing in relevant medical complications
Dietitians
Cognitive-behavioral therapists
Psychotherapists
Nurses

All should be skilled in treating eating disorders. Studies have found that people treated by such specialists have a lower mortality rate than those treated only as psychiatric patients.

Patients may drop out of programs if they have unrealistic expectations of being "cured" simply through the therapists' insights. Before a program begins, the following possibilities should be made clear:

The process is painful and requires hard work on the part of the patient and family.
A number of therapeutic methods are likely to be tried until the patient succeeds in overcoming these difficult disorders.
Relapse is common but should not be greeted with despair. (In one study, about 90% of bulimic patients responded to treatments after 6 years.)

Although the outcome for bulimics is generally more favorable than for anorexics, long-term studies are showing recovery in most people treated for anorexia.

Psychotherapies. Eating disorders are nearly always treated with some form of psychiatric or psychologic treatment. Depending on the problem, certain psychologic approaches may work better than others.

Medications. Various medications may be helpful for patients depending on the type of eating disorder, psychiatric state, and severity of the condition.

Nutritional Rehabilitation. Nutritional counseling can help patients regain weight and learn normal expectations concerning hunger and eating patterns.

The patient’s condition, social circumstances, and health insurance coverage determine the type of treatment facility -- inpatient hospitalization, residential hospitalization, partial hospitalization, or outpatient care. Weight is not the sole determining factor. The patient’s overall physical condition, psychological state, behavior patterns, and family support are all factors. Patients and their families should discuss with their doctors the various options available and how structured and intense the treatment should be.

Treatment for Bulimia

Some experts recommend a stepped approach for patients with bulimia, which follow specific stages depending on the severity and response to initial treatments:

Support groups. This is the least expensive approach and may be helpful for patients who have mild conditions with no health consequences.
Cognitive-behavioral therapy (CBT) along with nutritional therapy is the preferred first treatment for bulimia that does not respond to support groups.
Drugs. The drugs used for bulimia are typically antidepressants known as selective serotonin-reuptake inhibitors (SSRIs). A combination of CBT and SSRIs is very effective if CBT alone is not helpful.

Patients with bulimia rarely need hospitalization except under the following circumstances:

Binge-purge cycles have led to anorexia
Drugs are needed for withdrawal from purging
Major depression is present

Psychologic Therapy. Cognitive-behavioral therapy (CBT) is the first-line of therapy for most patients with bulimia and is successful in about 60% of cases. Patients who do not respond to CBT tend to be less committed to the treatment, are more preoccupied with their symptoms, and have ritualized eating behaviors. Interpersonal therapy may be tried if CBT fails. Some studies have found that bulimic patients respond well to self-help CBT with a CD-ROM or manual. These methods, the research found, reduced the incidence of both binging and vomiting. Patients who do not respond to CBT may wish to try interpersonal therapy (also known as “talk therapy’), where therapists help patients explore how social and family relationships may affect their eating disorder.

Antidepressants. The most common antidepressants prescribed for bulimia are selective serotonin reuptake inhibitors (SSRIs) such as:

Fluoxetine (Prozac)
Sertraline (Zoloft)
Paroxetine (Paxil)
Fluvoxamine (Luvox)

Studies are mixed, however, on whether SSRIs offer an additional advantage in reducing binge-eating compared to CBT. Fluoxetine has been approved for bulimia and is considered the drug of choice, although some studies suggest that other SSRIs work just as well.

Antidepressants may increase the risks for suicidal thoughts and actions during the first few months of treatment. In particular, adolescents and young adults should be carefully monitored during this time period for any changes in behavior.

Topiramate. The antiepileptic drug topiramate (Topamax) has been shown in studies to reduce bingeing and purging episodes in patients with bulimia. However, due to this drug’s risk for serious side effects, topiramate should be used only if other medication has failed. In addition, because people tend to lose weight while taking topiramate, it should not be used by patients who have low or even normal body weight.

Treatment for Anorexia

Treatment goals for patients with anorexia require a team approach. Doctors should immediately check and treat any medical problems related to the condition, such as bone loss, imbalances in important electrolytes, and any hormonal deficiencies, including thyroid and reproductive hormones. Nutrition rehabilitation and psychotherapy also plays an important part in anorexia therapy.

Many moderately to severely ill anorexic patients require hospitalization when:

Weight loss continues even with outpatient treatment
Weight is 30% below ideal body weight
Depression is severe or the patient is suicidal
There are symptoms of medical complications (disturbed heart rate, low potassium levels, altered mental status, low blood pressure, severe sensations of cold)

When severe metabolic or medical problems occur, patients with anorexia may need to be hospitalized either voluntarily or involuntarily. A variety of partial hospitalization or day care programs are also available.

Duration of Inpatient Treatment. For people with severe anorexia, many experts believe that 10 - 12 weeks of hospitalization with full nutritional support are required to reach ideal body weight. Check to see how many days your insurance company allows for inpatient treatment. Many rarely cover more than 15 days in the hospital. It is particularly important for women with both diabetes and anorexia to achieve 100% of ideal weight before being released.

The body mass index (BMI) is the measurement of body fat. It is derived by multiplying a person's weight in pounds by 703 and then dividing it twice by the height in inches.

A healthy BMI for women over age 20 is 19 - 24.
Those over 24 are considered to be at risk for health problems related to obesity.
Those under 17.5 are considered to be at risk for health problems related to anorexia. (However, young teenagers can have lower BMIs without necessarily being anorexic.)

For example, a woman who is 5'5" and weighs 125 pounds has a healthy BMI of 21. A woman at the same height who weighs 90 pounds would have a dangerously low BMI of 15.

Nutritional intervention is essential. Weight gain is associated with fewer symptoms of anorexia and with improvements in both physical and mental function. Restoring good nutrition can help reduce bone loss, and raising the level of energy available to the body by balancing food intake and exercise can normalize hormonal function. Restoring weight is also essential before the patient can fully benefit from additional psychotherapeutic treatments.

Goals for Weight Gain and Good Nutrition. A weight-gain goal of 2 - 3 pounds a week for hospitalized patients, and 0.5 - 1 pound a week for outpatients, is strongly encouraged. Patients typically begin with a calorie count as low as 1,000 - 1,600 calories a day, which is then gradually increased to 2,000 - 3,500 calories a day. Patients may initially experience intensified anxiety and depressive symptoms, as well as fluid retention, in response to weight gain. These symptoms decrease as the weight is maintained.

Tubal Feedings. Feeding tubes that pass through the nose to the stomach are not commonly used, since many experts believe they discourage a return to normal eating habits and because many patients interpret their use as punishing forced feeding. However, for patients who are at significant risk or for those who refuse to eat, tube feeding through the nose or through a tube inserted through the abdomen into the stomach can help with weight gain and improve the nutritional status of the patient. One method is to administer such feedings only at nighttime, with the patient eating normally during the day.

Intravenous Feedings. Intravenous feedings may be needed in life-threatening situations. This involves inserting a needle into the vein and infusing fluids containing nutrients directly into the bloodstream. Intravenous feedings must be administered carefully. When given at home, no more than the prescribed amount should be used. Overzealous administration of glucose solutions can trigger the so-called refeeding syndrome, in which phosphate levels drop severely and cause a condition called hypophosphatemia. Emergency symptoms include irritability, muscle weakness, bleeding from the mouth, disturbed heart rhythms, seizures, and coma.

The role of exercise in recovery is complex, since, for those with anorexia, excessive exercise is often a component of the original disorder. However, very controlled exercise regimens may be used as both a reward for developing good eating habits and as a way to reduce the stomach and intestinal distress that accompanies recovery. Exercise should not be performed if severe medical problems still exist and if the patient has not gained significant weight. The goal of exercise should be on improving physical fitness and health, not on burning off calories.

Psychologic Therapies Used in Anorexia. Family therapy is an important component of anorexia treatment, especially for children and adolescents. Adults usually begin with motivational psychotherapy that provides an empathetic setting and rewards positive efforts towards weight gain. After weight is restored, cognitive behavioral therapy techniques are helpful.

Antidepressants. Studies have not reported many benefits for treating anorexia nervosa with selective serotonin reuptake inhibitors (SSRIs), the antidepressants that are often useful for patients with bulimia. A few studies suggest that these drugs could be useful for people with anorexia nervosa who also have obsessive-compulsive disorder (OCD).

Doctors hoped that SSRIs could help prevent relapse in patients who have successfully restored their body weight. However, in a well-designed study in the Journal of the American Medical Association there was no difference in the time to relapse between patients who received fluoxetine (Prozac) and those who received placebo.

Nutritional Supplements. Calcium and vitamin D supplements are often recommended. Some studies have reported that zinc supplements may help patients gain weight.

Therapy

Eating disorders are nearly always treated with some form of psychiatric or psychologic treatment. Depending on the problem, different psychologic approaches may work better than others.

Cognitive-behavioral therapy (CBT) works on the principle that a pattern of false thinking and belief about one's body can be recognized objectively and altered, thereby changing the response and eliminating the unhealthy reaction to food. One approach for bulimia is the following:

Over a period of 4 - 6 months the patient builds up to eating 3 meals a day, including foods that the patient has previously avoided.
During this period, the patient monitors and records the daily dietary intake along with any habitual unhealthy reactions and negative thoughts toward eating while they are occurring.
The patient also records any relapses (binges or purging). Such lapses are reported objectively and without self-criticism and judgment.
The patient discusses the responses with a cognitive therapist at regular sessions. Eventually the patient is able to discover the false attitudes about body image and the unattainable perfectionism that underlies the opposition to food and health.
Once these habits are recognized, food choices are broadened, and the patient begins to challenge any entrenched and automatic ideas and responses. The patient then replaces them with a set of realistic beliefs along with actions based on reasonable self-expectations.

Interpersonal therapy deals with depression or anxiety that might underlie the eating disorders along with social factors that influence eating behavior. This therapy does not deal with weight, food, or body image at all.

The goals are the following:

To express feelings
To discover how to tolerate uncertainty and change
To develop a strong sense of individuality and independence
To address any relevant sexual issues or traumatic or abusive event in the past that might be a contributor of the eating disorder

Studies generally report that interpersonal therapy is not as effective as cognitive therapy for bulimia and binge eating, but may be useful for some patients with anorexia. The skill of the therapist plays a strong role in its success.

Because of the major role family attitudes play in eating disorders, one of the first steps in treating the patient with early-onset anorexia is to also treat the family. Family therapy can be useful for both younger and older patients.

If the patient is hospitalized, experts recommend that family therapy start after the patient has gained weight, but before discharge. It should usually continue after the patient has left the hospital.

The feelings of intense guilt and anxiety that caregivers experience are probably similar to those produced by living with a person who is suicidal. An over-involved parent may even support the patient's eating disorder for various reasons:

Some parents may be afraid of releasing some underlying anger or grief directed at the patient.
Other parents may identify with the goal of thinness and not even perceive that their child is unhealthily underweight.

In such cases, it is extremely important that the family members fully understand the danger of this disorder and that they are collaborating in their child's illness, or even death, by encouraging this state.

Resources

www.nimh.nih.gov -- National Institute of Mental Health
www.anad.org -- National Association of Anorexia Nervosa and Associated Disorders
www.aedweb.org -- Academy for Eating Disorders
www.nationaleatingdisorders.org -- Eating Disorders Awareness and Prevention
www.eatright.org -- American Dietetic Association
www.aabt.org -- Association for Behaviorial and Cognitive Therapies
www.psych.org -- The American Psychiatric Association
www.aacap.org -- American Academy of Child and Adolescent Psychiatry

References

American Psychiatric Association. Treatment of patients with eating disorders, third edition. American Psychiatric Association. Am J Psychiatry. 2006 Jul;163(7 Suppl):4-54.

Berkman ND, Lohr KN, Bulik CM. Outcomes of eating disorders: a systematic review of the literature. Int J Eat Disord. 2007 May;40(4):293-309.

Bulik CM, Berkman ND, Brownley KA, Sedway JA, Lohr KN. Anorexia nervosa treatment: a systematic review of randomized controlled trials. Int J Eat Disord. 2007 May;40(4):310-20.

Morris J, Twaddle S. Anorexia nervosa. BMJ. 2007 Apr 28;334(7599):894-8.

Signorini A, De Filippo E, Panico S, De Caprio C, Pasanisi F, Contaldo F. Long-term mortality in anorexia nervosa: a report after an 8-year follow-up and a review of the most recent literature. Eur J Clin Nutr. 2007 Jan;61(1):119-22. Epub 2006 Aug 2.

Schmidt U, Lee S, Beecham J, et al. A randomized controlled trial of family therapy and cognitive behavior therapy guided self-care for adolescents with bulimia nervosa and related disorders. Am J Psychiatry. 2007 Apr;164(4):591-8.

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