FitSugar

Move It: Full Sit Up with Bridge

FitSugar — Tue, 05 Jun 2007 09:30:00 -0700

In a recent poll, I asked you all if your summer fitness goal is to have flat abs or a toned tush. Now, while the majority voted for flat abs I thought I'd share this exercise with you all that works both areas of concern. It's a full sit-up/bridge combo and it works your backs side and your torso splendidly.

Start with a basic bridge.
On an exhale, push your pelvis up. Keep your back straight and in neutral spine - imagine your abs and back muscles sandwiching your spine.

You will feel your hamstrings and glutes work.
If you want to work your inner thighs a bit, place something between your knees (like a pillow) and hold it there for the duration of the series.
Lower your pelvis down to the ground as you inhale. As your pelvis lowers, bring your arms up.

Next, do a full sit up.

Exhale and roll all the way up to sitting with your hands behind your head. You put your hands behind so you can't jerk yourself up by swinging your arms up.

Keep your feet firmly planted on the ground.
Focus on pulling your deep abs to your spine as your roll up. Work the abs not the hip flexors.

Roll down and onto your back.
Inhale generously into your back as you roll down, keeping the navel pulled to the spine.

Focus on hollowing out your abs even though you are moving quickly, move with control.
Get ready to bring your hands to your sides as bridge up again.

That completes one set.

Aim to to do 20 reps, but remember quality is more important than quality and speed. Do not fling your self up and down, use your abs and focus on control.

Fit's tip: If I were my trainer, I would definitely stick a small pillow between my knees. Work to keep your legs truly parallel through out this exercise, it is much better form.

Sometimes Smaller Is Better

OnSugar Blog — Wed, 16 Dec 2009 03:47:49 -0800

Here's a healthy eating tip from the OnSugar blog Coach Lark Says.

I am continually amazed at how great I feel when I stick to eating small portions instead of stuffing myself until I'm full. Every day I can pull it off, I feel energized and light on my feet.

"Small portions" generally means eating food that is roughly the size of your own fist . . . Like a half a sandwich, a half a cup of oatmeal, or a piece of fruit.

To see what Coach Lark ate today, read more.

Today, for instance, this is how I ate:

a tangerine at 5:30am
a half a fist-sized portion of oatmeal at 8:00am
a bacon, egg and cheese sandwich (on an English muffin) at 9:30am
a romaine lettuce salad at 12:30pm with carrots, red cabbage, onions, celery, radishes and a little bit of blue cheese dressing
a half an apple and a half a banana at 3:00pm
I worked out at 5:00pm and then had a spicy crab sushi roll right afterward

Now, obviously I'm not on a diet. I allow myself to splurge on goodies like bacon and blue cheese dressing - within reason. I balance it out with a lot of fresh fruits and veggies and fibers. In addition, I drink water all day. Today I had the energy of a super hero! And I can guarantee that I burned off any calories I took in with a balance of activity and allowing my body to properly digest with this "grazing" technique.

There are a lot of gimmicky diets out there, but limiting how much food I put in my belly at any one sitting is the best and healthiest way I know how to manage my weight. I attempt to eat this way every day. It's an ongoing battle to stick to healthy eating habits, but with this tactic, I don't feel deprived and starved . . . ever.

I am not always perfect in my eating habits. Sometimes I do pig out. But I keep trying, and I do the best I can.

My advice is this: If you can pull the small-portions eating plan off for just one day, you'll have created an experiential template going forward. Try it and see how you feel. You'll be inspired, you'll see!

As a dear friend and client said to me this morning, "It seems like we are always fattening ourselves up for the famine that never arrives."

It's time to relax. There is always more food in our future!

Want to see more? Start following Coach Lark Says or start your own OnSugar blog. We'd love to post your inspiring stories and helpful advice here on FitSugar too!

5 Symptoms You Shouldn't Ignore

FitSugar — Mon, 09 Nov 2009 05:50:35 -0800

We don't always feel 100 percent all the time, and it's normal to feel a little nauseous, tired, or sniffly every once in a while. These are minor symptoms though, and usually go away on their own. But there are a few red flag signals our bodies flash to warn us of serious medical conditions, and they're symptoms you shouldn't pass off as nothing. WebMD spoke to the authors of Your Body's Red Light Warning Signals, and here are some symptoms that require a doctor's visit or emergency care.

Difficulty breathing. Tightness in the chest, wheezing, shallow breathing, or constantly coughing are all symptoms of asthma. If a person has these symptoms or full-on asthma attacks, and they're left untreated, the muscles used for breathing can get tired. That means the amount of oxygen getting into the lungs will decrease, while the levels of carbon dioxide increase. This has a drowsing effect on the brain, and the person may stop breathing, which could result in death.
Blood in your urine. When you go to the bathroom, you shouldn't see blood, and if you do, it could be a sign of kidney stones, bladder infections, or cancer of the kidney, urethra, or bladder. Even if you don't feel pain, call your doctor.

To see the other red flags keep reading

Smarter Eats: Use Smaller Plates and Grab It to Go

FitSugar — Thu, 29 Oct 2009 13:30:34 -0700

I grew up in a house where I was told to clean my plate. Not always a bad thing but it stuck with me for many years, even after serving sizes kept growing. I'm also a fast eater, something I've been working on, but I sometimes overeat before realizing I am full. A few things I've done to help kick my habits are using smaller plates and always taking food to go.

After inheriting some dishware from my grandmother I noticed that the dinner plates used during her era are much smaller than the ones we use today. I now use these dishes at home, which has reduced my portion size - yet I'm just as satisfied after every meal. Scientists confirmed that the brain takes visual cues when it comes to eating. If we see it, we somehow believe that we have to eat it and will end up feeling unsatiated even if we're physically full.

Portion sizes are out of control in restaurants. To remedy this I usually have half of my meal packed up to enjoy as lunch the next day. I don't go out of my way to starve myself, but it's always pretty obvious when you're given too much food at one sitting. If it's a restaurant I frequent a lot and know that the portion is going to be big, I ask my server ahead of time to make me a doggie bag before the plate even gets to my table.

Assess Your Ab Work

FitSugar — Fri, 25 Sep 2009 03:47:59 -0700

Countless crunches and multiple sets of Russian twists might tone your abs, but they're not so great for your back. Not only that, but they aren't functional movement, meaning the strength gained in these exercises won't really help you outside the gym. Repeatedly rounding the spine in a crunch or full sit-up sets the stage for a disk injury. Repeatedly twisting, especially if your abs are weak, also puts stress on the spine.

The safest and most effective way to work your abs is to use them to stabilize your torso against motions. The elbow plank is the perfect beginner ab exercise, since it works the extensor muscles, which line and stabilize the spine, in combination with the abs. Adding leg lifts to your plank, while keeping the pelvis and ribs stable, will take the plank to the next level. Working with free weights, moving from a squat into an overhead press, will work your abs too. Work one-armed to force your obliques to kick into action.

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

Restless legs syndrome and related disorders

FitSugar — Wed, 08 Oct 2008 17:35:14 -0700

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Treatment

The American Academy of Sleep Medicine recommends medications for restless legs syndrome (RLS) or periodic limb movement disorder (PLMD) only for persons who fulfill strict diagnostic criteria and experience too much daytime sleepiness as a result of these conditions. (Excessive daytime sleepiness results from nighttime sleeplessness due to RLS or PLMD symptoms).
The U.S. Food and Drug Administration (FDA) announced in March 2007 that the dopamine agonist drug pergolide (Permax) has been voluntarily withdrawn from the market. This drug can cause serious damage to the heart valves of patients who take it.
The FDA approved pramipexole (Mirapex) for use in moderate-to-severe restless legs syndrome (RLS) in November 2006.
Bupropion (Wellbutrin), a newer antidepressant, may also be helpful for RLS. Bupropion, a weak dopamine reuptake inhibitor, causes a slight increase in the availability of dopamine in the brain. It is not addictive and does not have the severe side effects of other RLS drugs, but more research is needed to determine its usefulness. It is not FDA approved for RLS.

Research

Results from a large study show that RLS is more common in children and teens than epilepsy and diabetes. The study also found that more than 70% of affected children had at least one biological parent with RLS.
Two recently-published studies found an abnormal gene on chromosome 6 makes some people susceptible to RLS and PLMD.
People with type 2 diabetes have higher rates of secondary RLS. Nerve pain (neuropathy) related to their diabetes cannot fully explain this increased rate in RLS.

Introduction

Restless legs syndrome (RLS) is an unsettling and poorly understood movement disorder affecting 3 - 15% of the general population. RLS can affect both children and adults. Although effective treatments are available, the condition often remains undiagnosed.

Symptoms of RLS. The core symptom of RLS is an irresistible urge to move the legs (medically known as akathisia). Some people describe this symptom as a sense of unease and weariness in the lower leg, which is aggravated by rest and relieved by movement. Specific characteristics of RLS include:

"Pulling, searing, drawing, tingling, bubbling, or crawling" beneath the skin, usually in the calf area, causing an irresistible urge to move the legs. These sensations can occur not only in the lower legs, but they can also affect the thighs, feet, and even the upper body. RLS-type symptoms may also occur in the arms. This may be the first symptom of RLS in some people.
About 80% of patients with RLS also experience semi-rhythmic movements called periodic limb movement disorder (PLMD).
Itching and pain, particularly aching pain, may be present.
Patients experience symptoms when they feel most relaxed and their legs are at rest. (Movement, however, brings relief.) Symptoms usually occur at night when lying down, or sometimes during the day while sitting.
Episodes of RLS usually develop between 10 p.m. and 4 a.m. Symptoms are often most severe shortly after midnight. They typically occur for 30 - 60 seconds, and they usually resolve by morning. If the condition becomes more severe, people may begin to have symptoms during the day. These symptoms are always worse at night, however.
At night, the unpleasant sensations and the resulting uncontrollable urge to move the legs can often disturb sleep. Ignoring the need to move the legs usually only builds up tension until they jerk uncontrollably. If patients experience symptoms during the day, they usually feel compelled to move their legs in order to relieve the symptoms, making it difficult to sit during air or car travel or through classes or meetings.

Late-onset and Early-onset Forms. There appear to be two forms of RLS, early-onset and late-onset. Each form may have different characteristics:

People with early-onset RLS (occurring in the teenage years or earlier) tend to have a family history of the disorder. They also usually have RLS without accompanying pain.
Those with late-onset RLS usually do not have a family history of RLS. Their condition is more likely the result of a problem with the nervous system, and symptoms may include pain in the lower legs.

The medical term for periodic limb movement disorder (PLMD) is nocturnal myoclonus. PLMD symptoms include:

Episodes that usually occur during the night, peaking near midnight, as they do in restless legs syndrome (RLS).
Leg muscles contract and jerk every 20 - 40 seconds during sleep. Such movements may last less than 1 second, or as long as 10 seconds.
Unlike RLS, contractions in PLMD usually do not wake patients. PLMD is distinct from the brief and sudden movements that occur just as people are falling asleep, jolting them awake.

Although 80% of RLS sufferers have PLMD, only about 30% of people with PLMD also have RLS. While treatments for the two conditions are similar, PLMD is a separate syndrome. PLMD is also very common in narcolepsy, a sleep disorder that causes people to fall asleep suddenly and uncontrollably.

Cramps that awaken people during sleep are very common, and they are not part of restless legs syndrome or periodic limb movement disorder. They can be very painful and may cause a person jump out of bed in the middle of the night. They typically affect a specific area of the calf or the sole of the foot.

Circadian Rhythm. In sleep studies, subjects spend about one-third of their time asleep, suggesting that most people need about 8 hours of sleep each day. However, individual adults differ in the amount of sleep they need to feel well rested. Infants may sleep as many as 16 hours a day.

The daily cycle of life, which includes sleeping and waking, is called a circadian rhythm (circadian means "about a day"), or the biological clock. Hundreds of bodily functions follow biologic clocks, but sleeping and waking comprise the most prominent circadian rhythm. The sleeping and waking cycle is about 24 hours long. If confined to windowless apartments, with no clocks or other time cues, sleeping and waking only as their bodies dictate, humans typically live on slightly longer than 24-hour cycles.

The circadian rhythm usually takes the following daily patterns:

Humans prefer daytime activity and nighttime rest.
A natural peak in sleepiness occurs at mid-day, the traditional siesta time.
Daily rhythms interact with other factors that may interfere or change individual patterns:
- The fraction-of-a-second-firing of nerve cells in the brain may be faster or slower in different individuals.
- The monthly menstrual cycle in women can shift the pattern.

Light signals coming through the eyes reset the circadian cycles each day, so changes in season, or changes in exposures to light and dark, can unsettle the pattern.

The Response in the Brain to Light Signals. The brain's response to light signals is an important key factor in sleep:

Light signals travel to a tiny cluster of nerves in the hypothalamus (in the center of the brain). This cluster is the body's master clock, which is called the supra chiasmatic nucleus (SCN). The SCN is named for its location, which is just above (supra) the optic chiasm, a major junction where nerves transmit information about light from the eyes.
The approach of dusk each day prompts the SCN to signal the nearby pineal gland (named so because it resembles a pinecone) to produce the hormone melatonin.
Researchers think that melatonin acts as the body's time-setting hormone. It also appears to trigger the need to sleep. The longer a person is in darkness, the longer the duration of melatonin secretion. Staying in bright light can decrease the secretion of melatonin.

Sleep consists of two distinct states that alternate in cycles, and reflect differing levels of brain nerve cell activity:

Non-Rapid Eye Movement Sleep. Non-rapid eye movement (NREM) sleep is also called quiet sleep. NREM is further subdivided into three stages of progression:

Stage 1: Light sleep
Stage 2: "True" sleep
Stage 3 to 4: Deep "slow-wave" or delta sleep

With each ascending stage, awakening becomes more difficult. It is not clear what governs NREM sleep in the brain. A balance between certain hormones, particularly growth and stress hormones, may be important for deep sleep.

Rapid Eye-Movement Sleep. Rapid eye-movement (REM) sleep is also called active sleep. Most vivid dreams occur in REM sleep. Brain activity in REM sleep is comparable to that in waking, but the muscles are virtually paralyzed, possibly preventing people from acting out their dreams. Except for vital organs like the lungs and heart, the only muscles not paralyzed during REM sleep are the eye muscles. REM sleep may be critical for learning and for day-to-day mood regulation. When people are sleep-deprived, their brains must work harder than when they are well rested.

The REM/NREM Cycle. The cycle between quiet and active sleep generally follows this pattern:

After about 90 minutes of NREM sleep, eyes move rapidly behind closed lids, giving rise to REM sleep.
As sleep progresses the NREM/REM cycle repeats.
With each cycle, NREM sleep becomes progressively lighter, and REM sleep becomes progressively longer, lasting from a few minutes early in sleep to perhaps an hour at the end of the sleep cycle.

The hypothalamus is a highly complex structure in the brain that regulates many important brain chemicals. Malfunction of this area of the brain may give rise to cluster headaches.

Causes

The main cause of restless legs syndrome (RLS) is unknown. Researchers are investigating neurologic (nervous system) problems that may arise either in the spinal cord or the brain. One current theory suggests that a deficiency in a brain chemical called dopamine causes restless legs syndrome.

RLS may often have a genetic basis, particularly in those who develop it before age 40. When the condition occurs in older adults, it is most likely due to a neurological problem.

The central nervous system is comprised of the brain and spinal cord. The peripheral nervous system includes all peripheral nerves.

People with restless legs syndrome (RLS) often have a family history of the disorder. Researchers have detected specific genetic locations or factors that might be responsible for this condition. Much of the research comes from studies of families with a strong history of RLS-related conditions. In 2005, researchers linked a location on chromosome 12 to RLS. They named this genetic marker RLS1. Locations on chromosomes 14 and 9 may also be associated with hereditary forms of RLS.

Dopamine and Neurologic Abnormalities in the Brain. Some research suggests that neurologic abnormalities involved with restless legs syndrome (RLS) and periodic limb movement disorder (PLMD) start in the brain. A variety of studies support the theory that an imbalance in neurotransmitters (chemical messengers in the brain), notably dopamine and serotonin, may play a part in RLS. Dopamine and serotonin cause numerous nerve impulses that affect muscle movement. The effect is similar to what happens in Parkinson's disease. Moreover, drugs that increase dopamine levels treat both disorders. However, Parkinson's disease itself does not seem to increase the risk for RLS. Nor does RLS early in life predispose to Parkinson's later on.

Neurologic Abnormalities in the Spine. Other research suggests that restless legs syndrome may be due to nerve impairment in the spinal cord. Researchers considered that such abnormalities were likely to start in nerve pathways in the lower spine. However, some patients with RLS have symptoms in the arms, indicating that the upper spine may also be involved.

Neuropathy. Some experts suggest that RLS, particularly if it occurs in older adults, may be a form of neuropathy, which is an abnormality in the nervous system outside the spine and brain. Nevertheless, there is no evidence of a causal relationship.

Iron deficiency, even at a level too mild to cause anemia, has been linked to restless legs syndrome (RLS) in some people. Studies suggest, in fact, that RLS in some people may be due to a problem with getting iron into cells that regulate dopamine in the brain. Some studies have reported RLS in 25 - 30% of people with low iron levels. The common connection between RLS and Parkinson's disease, in turn, may be not having enough iron in these patients.

The cause or causes of periodic limb movement disorder (PLMD) are not clear. Some research suggests that it may be due to abnormalities in the autonomic nervous system, which regulates the involuntary actions of the smooth muscles, heart, and glands.

Risk Factors

Restless legs syndrome (RLS) may affect 2.5 - 15% of the general population. It is more common in women than in men, and its frequency increases with age. The disorder affects an estimated 10 - 28% of adults older than age 65. In about 40% of patients, RLS begins in adolescence.

RLS may be more common than epilepsy and diabetes in children and teens. More than 70% of affected children in one study had at least one biological parent with RLS.

As many as two-thirds of people with restless legs syndrome (RLS) have a family history of the disorder. If so, RLS is more likely to occur before they turn 40. (A family history of RLS is less likely in people who develop it as older adults.) RLS is also more common in people from northern and western Europe, giving added support for a genetic basis for some cases.

Restless legs syndrome (RLS) and periodic leg movement disorder (PLMD) in children are strongly associated with inattention and hyperactivity. One study suggested that a quarter of children diagnosed with attention-deficit hyperactivity disorder (ADHD) also have RLS or PLMD, and this may actually contribute to inattentiveness and hyperactivity. The disorders have much in common, including poor sleep habits, twitching, and the need to get up suddenly and walk about frequently. Some evidence suggests that the link between the diseases may be a deficiency in the brain chemical dopamine.

About 20% of pregnant women report having restless legs syndrome (RLS). The condition usually goes away about a month after delivery. RLS in this population has been strongly associated with deficiencies in iron and the B vitamin folate.

Between 20 - 62% of people undergoing dialysis report restless legs syndrome. Symptoms often disappear after a kidney transplant.

Anxiety can cause restlessness and agitation at night. These symptoms can cause (or strongly resemble) restless legs syndrome.

The following medical conditions are also associated with restless legs syndrome (RLS), although the relationships are not clear. In some cases, these conditions may contribute to RLS, or they may have a common cause. In some cases, they may coexist due to other risk factors:

Osteoarthritis (degenerative joint disease). About 72% of patients with RLS also have osteoarthritis, a common type of arthritis affecting mostly older adults.
Varicose veins. Varicose veins occur in 14% of patients with RLS. Sclerotherapy treatments, in which doctors inject medications into affected veins, may relieve symptoms in such cases.
Obesity
Diabetes -- people with type 2 diabetes may have higher rates of secondary RLS. Nerve pain (neuropathy) related to their diabetes cannot fully explain this increased rate in RLS.
Hypertension
Hypothyroidism (a condition in which the thyroid gland does not make enough hormones)
Fibromyalgia (chronic pain of unknown cause)
Rheumatoid arthritis
Emphysema (a lung disease usually caused by smoking)
Chronic alcoholism
Sleep apnea (pauses in breathing during sleep) and snoring
Chronic headaches
Brain or spinal injuries

Many muscle and nerve disorders. Hereditary ataxia, a group of genetic diseases that affects the central nervous system and causes loss of motor control, is of particular interest. Researchers believe that hereditary ataxia may supply clues to the genetic causes of RLS.

Osteoarthritis is a chronic disease of the joint cartilage and bone, 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.

Click the icon to see an image of hypothyroidism.

Click the icon to see an image of fibromyalgia.

Click the icon to see an image of rheumatoid arthritis.

Click the icon to see an image of emphysema.

Several environmental and dietary factors can worsen or provoke restless legs syndrome (RLS):

Iron deficiencies. People who are deficient in iron are at risk for restless legs syndrome, even if they do not have anemia
Folic acid or magnesium deficiencies
Smoking
Alcohol abuse
Caffeine (coffee drinking is specifically associated with PLMD)
Stress
Fatigue
Prolonged exposure to cold

Drugs that worsen or provoke the condition include:

Antidepressants
Antipsychotic drugs
Anti-nausea drugs
Beta-blockers (a type of heart medication)
Antihistamines
Oral decongestants
Diuretics
Asthma drugs
Spinal anesthesia (anesthesia-induced restless legs syndrome typically disappears on its own within several months)

About 6% of the general population has periodic limb movement disorder (PLMD). Among the elderly, the prevalence increases to 25 - 58%. Studies suggest that PLMD may be especially common in elderly women. As with RLS, numerous conditions are associated with PLMD. They include sleep apnea, spinal cord injuries, stroke, narcolepsy, and diseases that destroy nerves or the brain over time. Certain medications, including some antidepressants and anti-seizure medications, may also contribute to PLMD.

Complications

Restless legs syndrome rarely results in any serious consequences. But in some cases, severe and persistent symptoms can cause considerable mental distress, chronic insomnia, and daytime sleepiness.

Sleep deprivation, and the daytime sleepiness that follows, is increasingly recognized as a cause of mood disruption and a contributor to industrial errors and motor vehicle crashes.

Effect on Daily Performance and Activities. Studies suggest that sleeplessness worsens many waking behaviors. These include:

Reduced concentration. Deep sleep deprivation appears to impair the brain's ability to process information.
Impaired task performance. Missing several hours of nightly sleep over the course of a week can negatively affect performance levels and mood. In fact, sleep deprivation can cause impaired performance levels comparable to those of intoxicated people.
Effect on learning. Whether sleeplessness significantly impairs learning is unclear. Some studies have reported problems in memorization, although others have found no differences in test scores between people with temporary sleep loss and those with full sleep.

In addition, since restless legs syndrome (RLS) is worse when resting, people with severe RLS may avoid daily activities that involve long periods of sitting, such as going to movies or traveling long distances.

Studies in Swedish working-aged men and women reported that those with restless legs syndrome (RLS) were more apt to be socially isolated, to have frequent daytime headaches or depression, and to complain of reduced libido or problems related to sleepiness.

RLS can contribute to insomnia. Insomnia itself can increase the activity of hormones and pathways in the brain that produce emotional problems. Even modest alterations in waking and sleeping patterns can have significant effects on a person's mood. Persistent insomnia may even predict the future development of mood disorders in some cases.

It is not clear if RLS is responsible for negative mood states or if anxiety or depression contributes to RLS. Anxiety can cause agitation and leg restlessness that resemble RLS, and depression and RLS symptoms also overlap. In addition, certain types of antidepressant drugs -- such as serotonin reuptake inhibitors -- can increase periodic limb movements during sleep.

Diagnosis

A diagnosis of restless legs syndrome or nocturnal leg cramps often relies solely on the patient's description of symptoms. In general, the recommended approach is first to take a sleep and personal history. The doctor may conduct an interview that includes the following questions:

How would you describe your sleep problem?
How long have you had this sleep problem?
How long does it take you to fall asleep?
How many times a week does the problem occur?
How restful is your sleep?
What are the leg problems like (cramps, twitching, crawling feelings)?
What is your sleep environment like? Noisy? Not dark enough?
What medications are you taking (including the use of antidepressants and self-medications -- such as herbs, alcohol, and over-the-counter or prescription drugs)?
Are you taking or withdrawing from stimulants, such as coffee or tobacco?
How much alcohol do you drink per day?
What stresses or emotional factors may be present in your life?
Have you experienced any significant life changes?
Do you snore or gasp during sleep? (This may be an indication of sleep apnea. Sleep apnea is a condition in which breathing stops for short periods many times during the night. It may worsen symptoms of restless legs syndrome or insomnia.)
If you have a bed partner, does he or she notice that you have jerking legs, interrupted breathing, or thrashing while you sleep?
Are you a shift worker?

Keeping a Record of Sleep. To help answer these questions, the patient may need to keep a sleep diary. Every day for 2 weeks, the patient should record all sleep-related information, including responses to questions listed above described on a daily basis. Recording sleep behavior using an extended-play audio or videotape can be very helpful in diagnosing sleep apnea.

A bed partner can help by adding their observations of the patient's sleep behavior.

Some high-risk patients may need to consult a sleep specialist or go to a sleep disorders center before their sleep problem can be diagnosed. At most centers, patients undergo an in-depth analysis, usually supervised by a team of consultants from various specialties, who can provide both physical and psychiatric evaluations. Centers should be accredited by the American Academy of Sleep Medicine.

Among the signs that may indicate a need for a sleep disorders center are:

Insomnia due to psychological disorders
Sleeping problems due to substance abuse
Snoring and sudden awakening with gasping for breath (possible sleep apnea)
Severe restless legs syndrome
Persistent daytime sleepiness
Sudden episodes of falling asleep during the day (possible narcolepsy)

Overnight polysomnography involves several tests to measure different functions during sleep. It is typically performed in a sleep center and may help rule out sleep apnea or confirm the effectiveness of restless legs syndrome (RLS) treatments.

The patient arrives about 2 hours before bedtime without having made any changes in daily habits. Polysomnography electronically monitors the patient as he or she passes, or fails to pass, through the various sleep stages. Polysomnography tracks the following:

Brain waves
Body movements
Breathing
Heart rate
Eye movements
Changes in breathing and blood levels of oxygen

Actigraphy uses a small wristwatch-like device (such as Actiwatch) to monitor sleep quality in people with suspected restless legs syndrome (RLS), periodic leg movement disorder (PLMD), insomnia, sleep apnea, and other sleep-related conditions. Patients can wear the device on their wrists or ankles. It measures and records muscle movements during sleep. For example, with PLMD, actigraphy can provide information on the total duration of movements, the number of occurrences, whether PLMD occurs simultaneously in both legs, and its effects on sleep.

Actigraphy is not as accurate as polygraphy because it cannot measure all the biological effects of sleep. It is more accurate than a sleep log, however, and very helpful for recording long periods of sleep.

The Epworth sleepiness scale uses a simple questionnaire to measure excessive sleepiness during eight situations.


Situation	Chance of Dosing
Sitting and reading	(Indicate a score of 0 to 3) 0 = no chance of dozing 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing
Watching TV	(Indicate a score of 0 to 3) 0 = no chance of dozing 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing
Sitting inactive in a public place	(Indicate a score of 0 to 3) 0 = no chance of dozing 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing
Riding as a passenger in a car for an hour without a break	(Indicate a score of 0 to 3) 0 = no chance of dozing 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing
Lying down to rest in the afternoon when circumstances permit	(Indicate a score of 0 to 3) 0 = no chance of dozing 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing
Sitting and talking to someone	(Indicate a score of 0 to 3) 0 = no chance of dozing 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing
Sitting quietly after a lunch without alcohol	(Indicate a score of 0 to 3) 0 = no chance of dozing 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing
Sitting in a car while stopped for a few minutes in traffic	(Indicate a score of 0 to 3) 0 = no chance of dozing 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing
Score Results 1-6: Getting enough sleep. 4-8: Tends to be sleepy but is average. 9 and over: Very sleepy and suggestive of sleep-disordered breathing. Patient should seek medical advice.

Because of the high association between restless legs syndrome and iron deficiency, a test for low iron stores should be part of the diagnostic workup in restless legs syndrome (RLS). There are two steps in making this diagnosis:

The first step is to determine if a person is actually deficient in iron.
If iron stores are low, the second step is to diagnose the cause of the iron deficiencies, which will help determine treatment.

Determining if Iron Stores are Low: The following findings are important in determining that a person is iron deficient:

Blood cells viewed under the microscope are pale (hypochromic) and abnormally small (microcytic). They are also mostly uneven in shape. These findings suggest iron deficiency, but they can also appear in anemia resulting from chronic disease and in thalassemia.
Hemoglobin and iron levels are low. These findings further suggest iron deficiency, but they can also occur in cases of anemia due to chronic disease.
Ferritin levels are low. Ferritin is a protein that binds to iron, and low levels typically mean the patient does not have enough iron in their body. However, high levels of ferritin in the blood do not always mean a patient has enough iron. For example, pregnant women may have high ferritin levels even in their third trimester, yet still be iron deficient. Ferritin levels may also be normal, or even elevated, in patients with inflammation resulting from anemia due to chronic disease, even if these patients also so not have enough iron in their body.
A test that measures a factor called serum transferrin receptor (TfR) is proving to be very sensitive in identifying iron deficiency in some patients, including the elderly with chronic diseases and possibly pregnant women.

Determining Causes of Iron Deficiency. When iron deficiency anemia is diagnosed, the next step is to determine what causes the iron deficiency itself.

Dietary iron deficiency is most common in children and infants. It is rare in adults.
Heavy menstrual or abnormal uterine bleeding is usually the cause of iron deficiencies in young women. Increased need for iron during pregnancy is also a common cause of iron deficiency in pregnant women.
If doctors suspect internal bleeding as the cause of iron deficiency, they look first to the digestive tract as the possible source. A diagnosis in such cases can often be made if the patient has noticed blood in their stools, (the stool would be black and tarry or red-streaked). Often, however, bleeding may be present but not visible. In such cases, stool tests for this hidden (occult) blood are required. The patient may need additional tests to diagnose the cause of bleeding. One common test is endoscopy, in which a fiberoptic tube is used to look into the gastrointestinal tract. Doctors recommend it particularly when the source of bleeding is unclear.

If the patient's diet suggests low iron intake and doctors cannot find other causes of iron deficiency, they may recommend a month-long trial of iron supplements. If the patient fails to respond, they will need further evaluation.

Certain laboratory tests may be helpful in determining causes of restless legs syndrome (RLS) or conditions that rule it out. They include:

Blood glucose tests for diabetes
Tests for kidney problems
In certain cases, tests for thyroid hormone, magnesium, and folate levels

In addition to other sleep-related leg disorders, a number of other medical conditions may have features that resemble restless legs syndrome (RLS). The doctor will need to consider these disorders in making a diagnosis.

Peripheral Neuropathies. Peripheral neuropathies are nerve disorders in the hands or feet. Several conditions can cause these disorders, and they can produce pain, burning, tingling, or shooting sensations in the arms and legs. Diabetes is a very common cause of painful peripheral neuropathies. Other causes include alcoholism, rheumatoid arthritis, systemic lupus erythematosus, amyloidosis, HIV infection, kidney failure, and certain vitamin deficiencies. Symptoms of peripheral neuropathies may mimic RLS. However, unlike RLS, they are not usually associated with restlessness, movement does not relieve the discomfort, and they do not worsen at bedtime.

Deep Vein Thrombosis. Deep vein thrombosis (DVT) is a blood clot in a deep vein in the body, usually in the leg. It may cause pain, swelling, and aching in the leg where the clot has developed. It can occur in people with heart disease, with varicose veins, during pregnancy, in women from hormonal treatments, from injury to the leg, or from inactivity (such as after surgery or during long flights). In women, it can also result from hormonal treatments. Left untreated, DVT can be a very serious and even life-threatening condition.

This picture shows a red and swollen thigh and leg caused by a blood clot (thrombus) in the deep veins in the groin (iliofemoral veins), which prevents normal return of blood from the leg to the heart.

Intermittent Claudication and Peripheral Artery Disease. Peripheral artery disease (PAD) occurs when atherosclerosis (commonly called hardening of the arteries) affects the feet and legs. In such cases, blocked arteries reduce the flow of oxygen-rich blood to the legs or feet. Intermittent claudication is an important symptom of PAD and occurs in between one-third and one-half of these patients. The word claudication describes the pain that occurs in PAD patients when they exercise, particularly when they walk. In intermittent claudication, blood flows only enough to meet the needs of the person at rest. The result is leg pain during exercise, which disappears during rest.

Click the icon to see an image of peripheral artery disease.

Akathisia. Akathisia is a state of restlessness or agitation, and feelings of muscle quivering. A condition called hypotensive akathisia is caused by failure in the autonomic nervous system. Unlike RLS, it occurs at any time of the day and usually only when the patient is sitting -- not lying down. Drugs used to treat schizophrenia and other psychoses can cause akathisia, as can anti-nausea drugs. The condition also occurs when drugs to treat Parkinson's disease are withdrawn.

Painful Legs and Moving Toes Syndrome. A rare disorder affecting one or both legs, painful legs and moving toes syndrome is marked by a constant, deep, throbbing ache in the limbs and involuntary toe movements. The discomfort may be mild or severe. It gets worse with activity and usually stops during sleep. Usually, the cause is unknown, though it may arise from spinal injuries or herpes zoster infection. The condition is difficult to treat, although the drug baclofen, combined with either clonazepam or carbamazepine, has shown some success. Other treatments that may help include orthotics for the shoes and transcutaneous electrical nerve stimulation (TENS).

Meralgia Paresthetica. An uncommon nerve condition, meralgia paresthetica causes numbness, pain, tingling, or burning on the front and side of the thigh. It usually occurs on one side of the body, and the cause may be compression of the thigh nerve as it passes through the pelvis. It typically occurs in people aged 30 - 60 years, but it can affect people of all ages. It often goes away on its own.

Treatment

The first step in treating a patient who complains of sleeplessness and restless legs syndrome is to try to improve sleep and eliminate possible causes of restless legs syndrome (RLS). Doctors normally try to achieve these goals without the use of drugs, initially. A non-drug approach is a particularly important first step for elderly patients.

The doctor should first try to treat any underlying medical conditions that may be causing restless legs.
If medications may be causing RLS, the doctor should try to prescribe alternatives, if possible.

If the cause cannot be determined, it is best to first try better sleep habits and relaxation methods. These approaches may help, even if the patient needs drug therapy later on.

Some people report help or relief from restless legs syndrome (RLS) with the following behaviors or devices:

Hot baths or cold compresses help some patients.
Ergonomic measures -- for example, patients might find it useful to work at a high stool, where they can dangle their legs. In meetings or during air travel, it is helpful to have an aisle seat.
Changing sleep patterns -- some patients report that symptoms do not occur if they sleep late in the morning. Therefore, if feasible, patients can try changing sleep patterns.
Avoiding caffeine, alcohol, and nicotine also improves some cases of RLS.

Some patients recommend alternative treatments for RLS, such as acupuncture and massage. To date, however, there is not enough data on the effectiveness of these treatments.

Some people have reported benefits from:

Vitamin E (800 - 1,200 IU per day)
Calcium, magnesium, or potassium supplements
Folic acid supplements for people with folate deficiencies

Folate (folic acid) is necessary for the production of red blood cells and for the synthesis of DNA (which controls heredity and is used to guide the cell in its daily activities). Folic acid also helps with tissue growth and cell function. In addition, it helps to increase appetite when needed and stimulates the formation of digestive acids.

Because restless legs syndrome (RLS) is associated with iron insufficiency, people with the condition should get enough iron from their diet. [See In-Depth Report #57: Anemia.] Iron is found in foods either in the form of heme or non-heme iron:

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

The Effects of Food on Iron Absorption. 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.
Eating more vitamin C-rich foods can enhance absorption of non-heme iron during a single meal. In any case, vitamin C-rich foods are healthy. They include broccoli, cabbage, citrus fruits, melon, tomatoes, and strawberries. One orange or 6 ounces of orange juice can double the amount of iron your body absorbs from plant foods. (Taking vitamin C supplements does not appear to have any significant effect on how much iron your body stores.)
Foods containing riboflavin (vitamin B2) may help enhance the formation of hemoglobin from iron. Sources include liver, dried fortified cereals, and yogurt.

Certain nutrients impede the body's absorption of dietary iron. They include:

Polyphenols (found in tea, coffee, red wine, berries, and apples)
Phytates (found in foods such as seeds, dried beans, soy, and bran). Such foods are typically high in fiber. It is often believed that fiber itself impedes iron absorption, but researchers report that it has little or no effect.
Calcium. Calcium impairs the absorption of heme and non-heme iron. However, calcium intake must be quite high to cause any significant problems.

The Effects of Cooking Methods on Iron. Cooking methods can enhance the amount of iron in your body. Cooking in cast iron pans and skillets is a well-known way to increase the iron content of food. According to one study, boiling, steaming, or stir-frying in utensils composed of any material significantly increased the release of non-heme iron stored in vegetables.

Iron supplements can significantly reduce symptoms in people with restless legs syndrome (RLS) who are also iron deficient. Patients should use them only when dietary measures have failed. Iron supplements do not appear to be useful for RLS patients with normal or above normal iron levels.

Supplement Forms. To replace iron, the preferred forms of iron tablets are ferrous salts, usually ferrous sulfate (Feosol, Fer-In-Sol, Mol-Iron). Other forms include ferrous fumarate (Femiron, FerroSequels, Feostat, Fumerin, Hemocyte, Ircon), ferrous gluconate (Fergon, Ferralet, Simron), polysaccharide-iron complex (Niferex, Nu-Iron), and carbonyl iron (Elemental Iron, Feosol Caplet, Ferra-Cap). Specific brands and forms may have certain advantages. The following are some examples:

Prolonged-release ferrous sulfate (Slow Fe) may enhance iron absorption with fewer side effects than standard ferrous sulfate pills.
FerroSequels contains a stool softener, which helps prevent constipation.
Polysaccharide-iron complex has fewer side effects and equal absorption rates compared to ferrous salts. It is very expensive, however.
Carbonyl iron is composed of very fine tiny uniform spheres of iron powder and may prove to be less toxic than ferrous iron.
Coated or combination pills do not appear to offer any additional advantages and may hinder absorption of the iron.

Regimen. A reasonable approach for patients with RLS is to take 65 mg of iron (or 325 mg of ferrous sulfate) along with 100 mg of vitamin C on an empty stomach, 3 times a day.

IMPORTANT: As few as 3 adult iron tablets can poison, and even kill, children. This includes any form of iron pill. No one, not even adults, should take a double dose of iron if they miss one dose.

Tips for taking iron are:

For best absorption, take iron between meals. (Iron may cause stomach and intestinal disturbances, however. Some experts believe that you can take low doses of ferrous sulfate with food and avoid the side effects.)
Always drink a full 8 ounces of fluid with an iron pill.
Keep tablets in a cool place. Bathroom medicine cabinets may be too warm and humid, which may cause the pills to disintegrate.

Side Effects. Common side effects of iron supplements include the following:

Constipation and diarrhea -- these are rarely severe, although iron tablets can aggravate existing digestive problems such as ulcers and ulcerative colitis.
Nausea and vomiting may occur with high doses, but you can control this by taking smaller amounts. Switching to ferrous gluconate may help some people with severe digestive problems.
Black stools are normal when taking iron tablets. In fact, if they do not turn black, the tablets may not be working effectively. This tends to be a more common problem with coated or long-acting iron tablets.
If the stools are tarry looking as well as black, if they have red streaks, or if cramps, sharp pains, or soreness in the stomach occurs, bleeding in the digestive tract may be causing the iron deficiency, and the patient should call the doctor immediately.
Acute iron poisoning is rare in adults, but can be fatal in children who take adult-strength tablets.

Interactions With Other Drugs. Certain medications, including antacids, can reduce iron absorption.

Iron tablets may also reduce the effectiveness of other drugs, including:

Antibiotics: tetracycline, penicillamine, and ciprofloxacin
Anti-Parkinson's disease drugs: methyldopa, levodopa, and carbidopa

At least 2 hours should elapse between doses of these drugs and doses of iron supplements.

Supplementary Treatments. The following supplements may improve iron absorption:

Adding either ascorbic acid (vitamin C) or succinic acid to ferrous sulfate treatment will improve absorption of iron stores. Ascorbic acid added to iron treatment, however, may worsen some of the side effects. Succinic acid added to ferrous sulfate does not appear to increase side effects.
Some studies have found that the addition of zinc to iron supplements increases hemoglobin levels more than iron alone. Some evidence suggests that zinc affects a hormone called insulin-like growth factor-I (IGF-I), which plays a role in the regulation of red blood cell production.

Exercise earlier in the day may be one of the best ways to achieve healthy sleep. However, vigorous exercise and stimulation (including sexual activity) within 1 - 2 hours of bed time may worsen restless legs syndrome (RLS). A study found that people who walked briskly for 30 minutes, four times a week, improved minor sleep disturbances after 4 months. Regular, moderate exercise, healthful in any case, may help prevent RLS. Patients report that either bursts of excessive energy or long sedentary periods worsen symptoms.

Benign nocturnal leg cramps, sometimes known as a charley horse, are muscle spasms in the calf that can occur one or many times during the night. Cramping may also occur in the soles of the feet. They typically last from a few seconds to a few minutes. Some people experience them regularly, others only on isolated occurrences.

Causes of Nocturnal Leg Cramps. In most cases, the cause of nocturnal leg cramps remains unknown. Among the conditions that might cause leg cramps are:

Calcium and phosphorus imbalances, particularly during pregnancy
Low potassium or sodium (salt) levels
Overexertion, standing on concrete for long periods, or prolonged sitting (especially with the legs contorted)
Having structural disorders in the legs or feet (such as flat feet)
Medical causes of muscle cramping include hypothyroidism, Addison's disease, uremia, hypoglycemia, anemia, and certain medications. Various diseases that affect nerves and muscles, such as Parkinson's, cause leg cramps. Peripheral neuropathy, a complication of diabetes, can cause cramp-like pain, numbness, or tingling in the legs. Patients with kidney disease undergoing dialysis are also prone to leg cramps.

Individuals at Higher Risk for Nocturnal Leg Cramps. Nocturnal leg cramps occur at all ages but peak at different times. They are particularly common in adolescence, during pregnancy, and in older age, affecting up to 70% of adults over age 50 at some point.

Pregnant women and those taking diuretics are also at risk for leg cramps because of low calcium levels and an imbalance in calcium and phosphorus.

Consequences of Nocturnal Leg Cramps. Nocturnal leg cramps, like restless legs syndrome, rarely have any serious consequences. However, they can be extremely painful and long lasting. In some cases, severe and persistent symptoms can cause chronic insomnia and considerable mental distress.

Managing Nocturnal Leg Cramps. Once a cramp begins, straighten the leg, flex the foot upward toward the knee, or grab the toes and pull them toward the knee.

Walking or shaking the affected leg, then elevating it, may also help.

If soreness persists, a warm bath or shower or an ice pack may bring relief.

Lifestyle Tips for Preventing Nocturnal Leg Cramps. Nighttime leg cramps are generally treated with lifestyle changes.

Everyone with leg cramps should drink plenty of water (at least 6 - 8 glasses daily) to maintain adequate fluid levels.
Pregnant women and others who get legs cramps due to low calcium levels should reduce milk intake, because drinking milk does not correct the underlying imbalances in calcium and phosphorus. Instead, they should boost calcium levels by taking nonphosphate calcium supplements.
To prevent cramps from occurring, nightly stretching exercises may be the best preventive measure. Patients should stand about 30 inches from a wall and, keeping the heels flat on the floor, lean forward and slowly move the hands up the wall to achieve a comfortable stretch. A few minutes on a stationary bicycle at bedtime may also help.
While in bed, loose covers should be used to prevent the toes and feet from pointing, which causes calf muscles to contract and cramp. Propping the feet up higher than the torso may also help.
During the week, swimming and water exercises are a good way to keep muscles stretched, and wearing supportive footwear is also important.

Quinine. Quinine had been widely used to prevent leg cramping. The U.S. Food and Drug Administration (FDA) banned its sale over the counter because it reportedly caused some serious, although rare, side effects. These side effects include bleeding problems and heart irregularities. Other, less serious side effects include headaches, vision problems, and rash.

The FDA has since banned the marketing of most quinine drugs, cautioning against the off-label (non-approved) use of the drug to treat RLS. Only one form of the drug, Qualaquin, is approved for sale, for the treatment of some types of malaria. Pregnant women and those with liver problems should avoid quinine in any form.

Supplements. Some small studies indicate that the mineral magnesium, taken as magnesium citrate or magnesium lactate, may provide some benefit to people with leg cramps, including pregnant women.

In one small study, taking vitamin B complex was helpful. Other supplements tried for leg cramps include vitamin E, calcium, and potassium or sodium chloride, but these do not appear to be very effective. Sodium chloride (salt) may be helpful, but Western diets already contain too much sodium.

Medications

The American Academy of Sleep Medicine recommends medications for restless legs syndrome (RLS) or periodic limb movement disorder (PLMD) only for persons who fit strict diagnostic criteria, and who experience excessive daytime sleepiness as a result of these conditions. (Excessive daytime sleepiness results from nighttime sleeplessness due to RLS or PLMD symptoms). Little is known about the best way to treat RLS, but some experts suggest the following:

Over-the-counter pain relievers and possibly mineral and vitamin supplements (particularly folic acid in people who might be deficient) should be the first form of treatment.
People with RLS should have a test for iron deficiency. If they are iron deficient, they should start treatment with iron supplements.
Dopaminergic drugs (drugs that increase levels of dopamine) are the standard medicines for treating severe RLS, PLMD, or both.
Other drugs may be helpful if dopaminergic drugs fail, or for patients who have frequent -- but not nightly -- symptoms. These include opiates (pain relievers), benzodiazepines (sedative hypnotic drugs), or anticonvulsants. However, benzodiazepines and opiates can become habit forming and addictive.

Before taking stronger medications, people should try over-the-counter pain relievers, such as acetaminophen (Tylenol) or non-steroidal anti-inflammatory drugs (NSAIDs), which include ibuprofen (Advil, Motrin, Rufen), naproxen (Anaprox, Naprosyn, Aleve), and ketoprofen (Orudis KT, Aktron).

Although NSAIDs work well, long-term use can cause stomach problems, such as ulcers and bleeding, and possible heart problems. In April 2005, the Food and Drug Administration asked drug manufacturers of NSAIDs to include a warning label on their product that alerts users of an increased risk for heart-related problems and digestive tract bleeding.

Dopaminergic drugs increase the availability of the chemical messenger dopamine in the brain, and are the first-line treatment for severe restless legs syndrome (RLS) and periodic leg movement disorder (PLMD). These drugs significantly reduce the number of limb movements per hour, and improve the subjective quality of sleep. Patients with either condition who take these drugs have experienced up to 100% reduction in symptoms.

Dopaminergic drugs, however, can have severe side effects (they are ordinarily used for Parkinson's disease). They do not appear to be as helpful for RLS related to dialysis as they do for RLS from other causes.

Dopaminergic drugs include dopamine precursors and dopamine receptor agonists.

Dopamine Precursors. The dopamine precursor levodopa (L-dopa) was once a popular drug for severe RLS. The standard preparations (Sinemet, Atamet) combine levodopa with carbidopa, which improves the action of levodopa and reduces some of its side effects, particularly nausea. Levodopa can also be combined with benserazide (Madopar) with similar results, but Sinemet is almost always used in America. (Levodopa combinations are well tolerated and safe.)

Patients typically start with a very low dose taken 1 hour before bedtime. The dosage is increased until the patient finds relief. Patients sometimes need to take an extended form or to take it again during the night.

Levodopa acts fast, and the treatment is usually effective within the first few days of therapy. One study reported that a combination therapy of regular-release L-dopa plus sustained release L-dopa was effective in improving sleep.

Serious common side effects of L-dopa treatment (and, to lesser extent, of dopamine receptor agonists) are augmentation and rebound. Many studies report that augmentation (worsening of symptoms that occur earlier in the day) occurs in up to 70% of patients who take L-dopa. The risk is highest for patients who take daily doses, especially doses at high levels (greater than 200 mg/day). For this reason, patients should use L-dopa only intermittently (fewer than 3 times per week). The drug should be immediately discontinued if augmentation does occur. Following withdrawal from L-dopa, patients can switch to a dopamine receptor agonist.

The rebound effect causes increased leg movements at night or in the morning as the dose wears off, or as tolerance to the drug builds up.

Dopamine Receptor Agonists. Dopamine receptor agonists (also called dopamine agonists) mimic the effects of dopamine by acting on dopamine receptors in the brain. They are now generally preferred to L-dopa. Because they have fewer side effects than L-dopa, including rebound effect and augmentation, these drugs may be used on a daily basis. (Rebound effect is the worsening of symptoms over time; augmentation means the appearance of symptoms earlier in the day. About 30% of patients who take dopamine receptor agonists have reported augmentations symptoms. As the newer drugs are taken for longer periods and at higher doses, however, their augmentation rates may become closer to those of L-dopa.)

Dopamine agonists have been shown to relieve symptoms in 70 - 90% of patients. Dopamine agonists can be ergot-derived (such as cabergoline) or non-ergot derived (such as pramipexole and ropinirole). The newer non-ergotamine derivatives may induce fewer side effects than ergot-derived drugs. Studies on these medications report the following:

Ropinirole (Requip) is a non-ergotamine dopamine agonist. Approved in 2005, ropinirole is the first drug approved specifically for treatment of moderate-to-severe RLS (more than 15 RLS episodes a month). Side effects are generally mild but may include nausea, vomiting, drowsiness, and dizziness.
The Food and Drug Administration (FDA) approved pramipexole (Mirapex) for use in moderate-to-severe RLS in November 2006. However, patients may fall asleep, without warning, while taking this drug, even while performing activities such as driving.

Cabergoline (Dostinex) is also showing promise in clinical trials. In one study, cabergoline was used for RLS after levodopa had either failed or resulted in increased symptoms. Patients in the study reported relief or freedom from symptoms after 4 weeks of use. A 2006 study indicated that a single evening dose of cabergoline improved both day and nighttime limb movements, and sleep disturbances.The FDA announced in March 2007 that the dopamine agonist pergolide (Permax) was voluntarily withdrawn from the market. Studies confirmed that this drug could cause serious damage to the heart valves of patients who take it. These problems have not been reported with ropinirole or pramipexole, which are chemically different then pergolide.

Other Dopamine Agonists. Rotigotine is a unique dopamine agonist that is being developed in patch form for RLS. In May 2007, the FDA approved this patch for treatment of early Parkinson's disease. Other dopamine agonists that have shown some promise in small studies include alpha-dihydroergocryptine, or DHEC (Almirid), and piribedil (Trivastal).

Regimens. The effects of L-dopa are apparent in 15 - 30 minutes. Dopamine receptor agonists, meanwhile, take at least 2 hours to start working. Some doctors recommend regular use of dopamine receptor agonists for patients who experience nightly symptoms, and L-dopa for those whose symptoms occur only occasionally.

Side Effects. Common side effects of dopaminergic drugs vary but may include feeling faint or dizzy (especially when standing up), headaches, abnormal muscle movements, rapid heartbeat, insomnia, bloating, chest pain, and dry mouth. Nausea may be especially common. Adding the drug domperidone may help to relieve this side effect. In rare cases, dopaminergic drugs can cause hallucinations or lung disease.

Because these drugs may cause daytime drowsiness, patients should be extremely careful while driving or performing tasks that require concentration.

Long-term use of dopaminergic drugs can lead to loss of effectiveness (tolerance). Adding a drug called entacapone (Comtan) may prolong the duration of action of carbidopa-levodopa therapy (Sinemet), but it can cause nausea.

Rebound effect, augmentation, and tolerance can reduce the value of dopaminergic drugs in the treatment of RLS. Using the lowest dose possible can minimize these effects.

Withdrawal Symptoms. Patients who withdraw from these drugs typically experience very severe RLS symptoms for the first 2 days after stopping. RLS eventually returns to pre-treatment levels after about a week. The longer a patient uses these drugs, the worse their withdrawal symptoms.

Benzodiazepines, such as clonazepam (Klonopin), are known as sedative hypnotics. Doctors prescribe them for insomnia and anxiety. They may be helpful for some patients with restless legs syndrome (RLS) that disrupts sleep. Clonazepam may be particularly helpful for children with both periodic limb movement disorder and symptoms of attention deficit hyperactivity disorder. The medicine also may be helpful for patients with RLS who are undergoing dialysis.

Side Effects. Elderly people are more susceptible to side effects. They should usually start at half the dose prescribed for younger people, and should not take long-acting forms. Side effects may differ depending on whether the benzodiazepine is long-acting or short-acting.

The drugs may increase depression, a common condition in many people with insomnia.
Breathing problems may occur with overuse or in people with pre-existing respiratory illness.
Long-acting drugs have a very high rate of residual daytime drowsiness compared to others. They have been associated with a significantly increased risk for automobile accidents and falls in the elderly, particularly in the first week after taking them. Shorter-acting benzodiazepines do not appear to pose as high a risk.
There are reports of memory loss (so-called traveler's amnesia), sleepwalking, and odd mood states after taking triazolam (Halcion) and other short-acting benzodiazepines. These effects are rare and probably enhanced by alcohol.
Because benzodiazepines cross the placenta and enter breast milk, pregnant and nursing women should not use them. There are some reports of an association between the use of benzodiazepines in the first trimester of pregnancy and the development of cleft lip in newborns. Studies are conflicting at this point, but, due to other known side effects of benzodiazepines, pregnant women should not use these drugs, if possible.
In rare cases, overdoses have been fatal.

Interactions. Benzodiazepines are potentially dangerous when used in combination with alcohol. Some drugs, such as the ulcer medication cimetidine, can slow the breakdown of benzodiazepine.

Withdrawal Symptoms. Withdrawal symptoms usually occur after prolonged use and indicate dependence. They can last 1 - 3 weeks after stopping the drug and may include:

Gastrointestinal distress
Sweating
Disturbed heart rhythm
In severe cases, patients might hallucinate or experience seizures, even a week or more after they stop taking the drug.

Rebound Insomnia. Rebound insomnia, which often occurs after withdrawal, typically includes 1 - 2 nights of sleep disturbance, daytime sleepiness, and anxiety. The chances of rebound are higher with the short-acting benzodiazepines than with the longer-acting ones.

Narcotics are pain-relieving drugs that act on the central nervous system. They are sometimes prescribed for severe cases of restless legs syndrome (RLS). They may be a good choice if pain is a prominent feature. Some evidence also suggests that narcotics reduce the frequency of periodic leg movements.

There are two types of narcotics, both of which have been used for severe RLS:

Opiates (such as morphine and codeine) come from natural opium. Some patients report relief with the use of the opiate fentanyl (Duragesic), available in skin patch form. An implanted pump that uses morphine and an anesthetic called bupivacaine is showing promise for patients with severe RLS. The pump delivers the drugs to the fluid surrounding the spinal cord (cerebrospinal fluid).
Opioids are synthetic drugs. The most common example is oxycodone (Percodan, Percocet, Roxicodone, Oxycontin). Apomorphine is a morphine derivative. In one study, when injected under the skin at night, it reduced nocturnal discomfort and leg movements in some patients.

Although the use of narcotics for severe RLS is controversial, some studies have suggested that even when the treatments are long-term, they are rarely addictive for pain sufferers except among patients with a history of substance abuse.

The use of such drugs may be beneficial when included as part of a comprehensive pain management program. Such a program involves screening prospective patients for possible drug abuse, and regularly monitoring those who are taking narcotics. Doses should be adjusted as necessary to achieve an acceptable balance between pain relief and side effects. Patients on long-term opiate therapy should also be monitored periodically for sleep apnea, a condition that causes breathing to stop for short periods many times during the night. Sleep apnea may worsen symptoms of RLS, insomnia, and other complaints.

Tramadol. Tramadol (Ultram) is a pain reliever that has been used as an alternative to opioids. In one study, tramadol was very effective for RLS and produced few or no side effects. It has opioid-like properties, but is not as addictive. (However, there are reports of dependence and abuse with this drug as well.) Withdrawal after long-term use (longer than a year) can cause intense symptoms, including diarrhea, insomnia, and even restless legs syndrome itself.

Antiseizure drugs -- such as gabapentin (Neurontin), valproic acid (valproate, divalproex, Depakote, Depakene), and carbamazepine (Tegretol) -- relax blood vessels and are being tested for restless legs syndrome (RLS). Gabapentin, a newer antiseizure drug, is showing particular promise for mild-to-moderate RLS. One study reported that it improved RLS symptoms and sleep, particularly in patients who also experienced pain. It was also effective for periodic leg movement disorder. A new gabapentin product is in phase III clinical trials for the treatment of RLS. The new drug, known as XP13512, converts to gabapentin in the intestines, and therefore may reduce some of the side effects experienced by patients taking antiseizure medications.

Side Effects. All antiseizure drugs have potentially severe side effects. Therefore, patients should try these medications only after non-drug methods have failed. Side effects of many anti-seizure drugs include nausea, vomiting, heartburn, increased appetite with weight gain, hand tremors, irritability, and temporary hair thinning and hair loss (taking zinc and selenium supplements may help reduce this last effect). Some antiseizure drugs can also cause birth defects and, in rare cases, liver toxicity. Gabapentin may have fewer of these side effects than valproic acid or carbamazepine.

Antidepressants. Bupropion (Wellbutrin), a newer antidepressant, may be helpful for restless legs syndrome (RLS). Bupropion is a weak dopamine reuptake inhibitor -- it causes a slight increase in the availability of dopamine in the brain. The drug is not addictive and does not have the severe side effects of other RLS drugs, but more research is needed to determine if it is useful.

Clonidine. Clonidine (Catapres), a drug used for high blood pressure, is helpful for some patients and may be an appropriate choice for patients who have RLS accompanied by hypertension. It also may help patients with RLS who are undergoing hemodialysis.

Baclofen. The anti-spasm drug baclofen (Lioresal) appears to reduce intensity of RLS (although not frequency of movements).

Resources

www.aasmnet.org -- American Academy of Sleep Medicine
www.sleepfoundation.org -- National Sleep Foundation
www.ninds.nih.gov -- National Institute of Neurological Disorders and Stroke
www.nhlbi.nih.gov/about/ncsdr/ -- National Center on Sleep Disorders Research
www.rls.org -- Restless Legs Syndrome Foundation
www.wemove.org -- Worldwide Education and Awareness for Movement Disorders

References

Bogan RK, Fry JM, Schmidt MH, Carson SW, Ritchie SY. Ropinirole in the treatment of patients with restless legs syndrome: a US-based randomized, double-blind, placebo-controlled clinical trial. Mayo Clin Proc. 2006 Jan;81(1):17-27.

Claman DM; Redline S; Blackwell T, Ancoli-Israel S, Surovec S, Scott N, et al. Prevalence and correlates of periodic limb movements in older women. J Clin Sleep Med. 2006 Oct;2(4):438-445.

Merlino G, Fratticci L, Valente M, et al. Association of restless legs syndrome in type 2 diabetes: a case-control study. Sleep. 2007; 30(7): 866-71.

Oertel WH, Benes H, Bodenschatz R, Peglau I, Warmuth R, Happe S, et al. Efficacy of cabergoline in restless legs syndrome: a placebo-controlled study with polysomnography (CATOR). Neurology. 2006 Sep 26;67(6):1040-6.

Partinen M, Hirvonen K, Jama L, Alakuijala A, Hublin C, Tamminen I, et al. Efficacy and safety of pramipexole in idiopathic restless legs syndrome: a polysomnographic dose-finding study--the PRELUDE study. Sleep Med. 2006 Aug;7(5):407-17.

Picchietti D, Winkelman JW. Restless legs syndrome, periodic limb movements in sleep, and depression. Sleep. 2005 Jul 1;28(7):891-8.

Picchietti D. Restless legs syndrome: prevalence and impact in children and adolescents--the Peds REST study. Pediatrics. 2007; 120(2): 253-66.

Stefansson H, Rye DB, Hicks A, et al. A Genetic Risk Factor for Periodic Limb Movements in Sleep. N Engl J Med. 2007;357:639-47.

Winkelman JW, Sethi KD, Kushida CA, Becker PM, Koester J, Cappola JJ, et al. Efficacy and safety of pramipexole in restless legs syndrome. Neurology. 2006 Sep 26;67(6):1034-9.

Winkelmann J, Schormair B, Lichtner P, et al. Genome-wide association study of restless legs syndrome identifies common variants in three genomic regions. Nat Genet (in press). [cited in: Winkelmann J. Periodic Limb Movements in Sleep - Endophenotype for Restless Legs Syndrome? N Engl J Med. 2007; 357:703-05.]

Review Date:
10/22/2007
Reviewed By:
Harvey Simon, MD, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital.

A.D.A.M. Copyright

adam.com

Insomnia

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

In This Report

Highlights
Introduction
Causes of Short-Term or Tra...
Causes of Chronic Insomnia...
Risk Factors
Prognosis
Diagnosis
Treatment
Medications
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Sedative Hypnotic Drug Warnings

In March 2007, the FDA ordered stronger warning labels on sedative hypnotic drugs. These medications include benzodiazepine and non-benzodiazepine drugs, such as zolpidem (Ambien), eszopiclone (Lunesta), ramelteon (Rozerem), and triazolam (Halcion). The FDA warned that these drugs may be associated with:

Severe allergic reactions (anaphylaxis) and severe facial swelling (angioedema), which can occur even the first time a drug is taken
Complex sleep-related behaviors, such as sleep driving, making phone calls, and preparing and eating food while asleep

Patients who take sleeping pills should be sure to follow the directions. These include not combining sleeping pills with alcohol or other drugs and not taking more than the prescribed dose. All patients prescribed sedative hypnotic drugs should receive a patient medication guide that describes the potential risks, and precautions to reduce these risks.

Behavioral and Psychological Therapies

Behavioral and psychological treatments, such as cognitive behavioral therapy and relaxation techniques, are effective approaches for insomnia and can produce long-lasting benefits, according to a 2006 study in Sleep.
Behavioral interventions help over 80% of children who try them, indicates another 2006 Sleep study.

Complementary and Alternative Medicine

More than 1.6 million adults use complementary and alternative medicine to treat their insomnia, according to results of a national survey published in the Archives of Internal Medicine. About half of patients who tried herbal medicine or relaxation techniques found that these approaches helped improve their sleep.
In 2006, the American Academy of Sleep Medicine issued a position statement advising that there is only limited scientific evidence that herbal remedies are effective sleep aids.

Insomnia and Mood Disorders

Chronic insomnia can increase the risk of developing depression and anxiety, according to a 2007 study in Sleep. Research also indicates that insomnia and daytime sleepiness can cause and worsen depression and anxiety in children as well as adults.

Introduction

Insomnia comes from the Latin words for “no sleep.” Insomnia is characterized by:

Difficulty falling asleep
Difficulty staying asleep
Waking up too early in the morning

Some experts believe that poor quality (“non-restorative”) sleep is also related to insomnia. Insomnia can cause daytime fatigue, irritability, and impaired performance. About 60 million Americans each year suffer from insomnia.

Insomnia may be primary or secondary:

Primary insomnia means that the inability to sleep is not caused by other health problems.
Secondary insomnia is due to other health conditions that interfere with sleep. Some experts prefer the term “co-morbid insomnia.”

Insomnia, usually temporary, is often categorized by how long it lasts:

Transient insomnia lasts for a few days.
Short-term insomnia lasts for no more than 3 weeks.
Chronic insomnia occurs at least 3 nights per week for 1 month or longer.

Insomnia may also be defined in terms of inability to sleep at conventional times. The following examples are referred to as circadian rhythm disorders:

Delayed Sleep-Phase Syndrome. Delayed sleep-phase syndrome is the term for a circadian clock that runs late but reliably. People who have this condition (usually adolescents) fall asleep very late at night or in early morning hours, but then sleep normally.
Advanced Sleep-Phase Syndrome. This syndrome tends to develop in older people. It produces excessive sleepiness in the morning and undesired awakening early (3 - 5 a.m.) in the morning.

In sleep studies, subjects spend about one-third of their time asleep, suggesting that most people need about 8 hours of sleep each day. Individual adults differ in the amount of sleep they need to feel well rested, however. (Infants may sleep as many as 16 hours a day.)

The daily cycle of life, which includes sleeping and waking, is called a circadian (meaning "about a day") rhythm, commonly referred to as the biologic clock. Hundreds of bodily functions follow biologic clocks, but sleeping and waking comprise the most prominent circadian rhythm. The sleeping and waking cycle is approximately 24 hours. (If confined to windowless apartments, with no clocks or other time cues, sleeping and waking as their bodies dictate, humans typically live on slightly longer than 24-hour cycles.) It usually takes the following daily patterns:

Humans are designed for daytime activity and nighttime rest.
Additionally, there is a natural peak in sleepiness at mid-day, the traditional siesta time.

In addition, daily rhythms intermesh with other factors that may interfere or change individual patterns:

The fraction-of-a-second-firing of nerve cells in the brain may be faster or slower in different individuals.
The monthly menstrual cycle in women can shift the pattern.
Light signals coming through the eyes reset the circadian cycles each day, so changes in season or various exposures to light and dark can unsettle the pattern. The importance of sunlight as a cue for circadian rhythms is dramatized by the problems experienced by people who are totally blind. They commonly suffer trouble sleeping and other rhythm disruptions.

The response to light signals in the brain is an important key factor in sleep:

Light signals travel to a tiny cluster of nerves in the hypothalamus in the center of the brain, the body's master clock, which is called the supra chiasmatic nucleus (SCN).
This nerve cluster takes its name from its location, which is just above (supra) the optic chiasm, which is a major junction for nerves transmitting information about light from the eyes.
The approach of dusk each day prompts the SCN to signal the nearby pineal gland (named so because it resembles a pine-cone) to produce the hormone melatonin.
Melatonin is thought to act as the body's time-setting hormone. The longer a person is in darkness the longer the duration of melatonin secretion. Secretion can be diminished by staying in bright light. Melatonin also appears to trigger the need to sleep.

Sleep consists of two distinct states that alternate in cycles and reflect differing levels of brain nerve cell activity:

Non-Rapid Eye Movement Sleep (NonREM). NonREM sleep is also termed quiet sleep. NonREM is further subdivided into three stages of progression:

Stage 1 (light sleep)
Stage 2 (so-called true sleep)
Stage 3 to 4 (deep "slow-wave" or delta sleep)

With each descending stage, awakening becomes more difficult. It is not known what governs NonREM sleep in the brain. A balance between certain hormones, particularly growth and stress hormones, may be important for deep sleep.

Rapid Eye-Movement Sleep (REM). REM sleep is termed active sleep. Most vivid dreams occur in REM sleep. REM-sleep brain activity is comparable to that in waking, but the muscles are virtually paralyzed, possibly preventing people from acting out their dreams. In fact, except for vital organs like lungs and heart, the only muscles not paralyzed during REM are the eye muscles. REM sleep may be critical for learning and for day-to-day mood regulation. When people are sleep-deprived, their brains must work harder than when they are well rested.

The REM/NREM Cycle. The cycle between quiet (nonREM) and active (REM) sleep generally follows this pattern:

After about 90 minutes of nonREM sleep, eyes move rapidly behind closed lids, giving rise to REM sleep.
As sleep progresses the nonREM/REM cycle repeats.
With each cycle, nonREM sleep becomes progressively lighter, and REM sleep becomes progressively longer, lasting from a few minutes early in sleep to perhaps an hour at the end of the sleep episode.

Causes of Short-Term or Transient Insomnia

A reaction to change or stress is one of the most common causes of short-term and transient insomnia. This condition is sometimes referred to as adjustment sleep disorder.

The trigger could be a major or traumatic event such as:

An acute illness
Injury or surgery
The loss of a loved one
Job loss

Temporary insomnia could also develop after a relatively minor event, including:

Extremes in weather
An exam
Traveling
Trouble at work

In most cases, normal sleep almost always returns when the condition resolves, the individual recovers from the event, or the person becomes used to the new situation. Treatment is needed if sleepiness interferes with functioning or if it continues for more than a few weeks. Individual responses to stress vary and some people may not experience insomnia at all, even during very stressful situations while others may suffer from insomnia in response to very mild stressors.

Fluctuations in female hormones play a major role in insomnia in women over their lifetimes. This insomnia is usually temporary.

During Menstruation. Progesterone promotes sleep, and levels of this hormone plunge during menstruation, causing insomnia. (When they rise during ovulation, women may become sleepier than usual.)
During Pregnancy. The effects of changes in progesterone levels in the first and last trimester can disrupt normal sleep patterns.
Menopause. Insomnia can be a major problem in the first phases of menopause, when hormones are fluctuating intensely. Insomnia during this period may be due to different factors that occur. In some women, hot flashes, sweating, and a sense of anxiety can awaken women suddenly and frequently at night. Insomnia may also be caused by psychologic distress provoked by this life passage. In many cases, insomnia is temporary. However, a 2006 study found that hot flashes in perimenopausal and postmenopausal women are strongly associated with chronic insomnia (sleep problems lasting more than 1 month). Treating hot flashes may help resolve chronic insomnia.

Air travel across time zones often causes insomnia. After long plane trips, 1 day of adjustment is usually needed for each time zone crossed. Traveling west to earlier times seems to be less traumatic than going east to a later time because it is easier to lengthen a circadian phase than to shorten it.

In one study, 20% of adults reported that light, noise, and uncomfortable temperatures caused their sleeplessness. Depending on the time of day, too much or too little light can disrupt sleep.

Excessive Light at Night. A person's biologic circadian clock is triggered by sunlight, and very bright artificial light maintains wakefulness. One study indicated that even dim artificial light might disrupt sleep.
Insufficient Light During the Day. Insufficient exposure to light during the day, as occurs in some disabled elderly patients who rarely venture outside, may also be linked with sleep disturbances. One study suggested that when a person is exposed to bright daylight, melatonin levels increase in response to darkness at night, which aids sleep.

Caffeine. Caffeine is a stimulant, which can interfere with falling asleep.

Nicotine. Nicotine is also a stimulant, but quitting smoking itself can lead to transient insomnia. In fact, it has been suggested that if sleeping could be improved during withdrawal from smoking, perhaps it would be easier to quit smoking.

Partner's Sleep Habits. In one survey, 17% of women and 5% of men reported that their partner's sleep habits impaired their own sleep. Snoring can certainly be a factor in a partner's insomnia.

Medications. Insomnia is a side effect of many common medications, including over-the-counter preparations that contain caffeine. People who suspect their medications are causing them to lose sleep should check with their doctors or pharmacists.

Causes of Chronic Insomnia

Sleep problems seem to run in families. About 35% of people with insomnia have a family history of insomnia, with the mother being the most commonly affected family member. Still, because so many factors are involved in insomnia, a genetic component is difficult to define.

Abnormal levels of certain brain chemicals have been observed in some people with chronic insomnia.

Melatonin. Low levels of melatonin, the hormone secreted by the pineal gland, have sometimes been observed in chronic insomnia.
Stress Hormones. Some studies have reported persistently high levels of stress hormones, particularly cortisol, in people with chronic insomnia, particularly insomnia related to aging and psychiatric disorders. High levels of cortisol reduce REM sleep. However, a 2003 study of people with chronic insomnia reported that cortisol levels were high only when their sleep was of poor quality. When they slept well, levels were lower. This study and other research suggests that high levels of stress hormones are caused by poor sleep, rather than being the cause.
Growth Hormone. Normal aging is associated with a blunting of regular, cyclical surges of growth hormone, which may affect sleep as one gets older. This hormone, which is normally secreted in the late night, is associated not only with growth but with deep, slow-wave sleep. (Older people generally have less slow-wave sleep.)

Chronic insomnia occurs in people who have persistently high levels of stress hormones and a shift in the levels of certain immune factors. Studies indicate that people with chronic insomnia have higher levels of interleukin-6 and tumor necrosis factor during the day, but lower levels at night. These immune factors, called cytokines, cause symptoms of fatigue. Levels are usually higher at night in people with healthy sleep. The implications of these immune changes in people with insomnia are not known.

Many cases of chronic insomnia cases have a psychologic or psychiatric basis. The disorders that most often cause insomnia are:

Anxiety.
Depression. Sleep abnormalities are an integral part of depressive disorders, with more than 90% of depressed patients experiencing insomnia.
Bipolar disorder.

Insomnia may also cause emotional problems. It is often unclear which condition has triggered the other, or if the two conditions, in fact, have a common source.

In many cases, it is unclear if chronic insomnia is a symptom of some physical or psychological condition or if it is a primary disorder of its own. In most instances, a mix of psychological and physical conditions causes the insomnia.

Psychophysiologic insomnia occurs when:

An episode of transient insomnia disrupts the person's circadian rhythm.
The patient begins to associate the bed not with rest and relaxation but with a struggle to sleep. A pattern of sleep failure emerges.
Over time, this event repeats, and bedtime becomes a source of anxiety. Once in bed, the patient broods over the inability to sleep, the consequences of sleep loss, and the lack of mental control. All attempts to sleep fail.
Eventually excessive worry about sleep loss becomes persistent and provides an automatic nightly trigger for anxiety and arousal. Unsuccessful attempts to control thoughts, images, and emotions only worsen the situation. After such a cycle is established, insomnia becomes a self-fulfilling prophecy that can persist indefinitely.

Sometimes anxiety and the inability to sleep dates back to childhood when parents used various threats to force their children into sleep for which they may not have been ready.

In one survey, 22% of adults reported that health conditions, pain, or discomfort impaired their sleep. These conditions can include:

Nightly Leg Problems. Leg disorders that occur at night, such as restless legs syndrome or leg cramps, are of special note. They are very common and an important cause of insomnia, particularly in older people.

Medical Problems. Among the many medical problems that can cause chronic insomnia are allergies, arthritis, cancer, fibromyalgia, heart disease, gastroesophageal reflux disease (GERD), hypertension, asthma, emphysema, rheumatologic conditions, Alzheimer's disease, Parkinson's disease, hyperthyroidism, and attention deficit hyperactivity disorder.

Medications. Among the many medications that can cause insomnia are antidepressants (fluoxetine, bupropion), theophylline, lamotrigine, felbamate, beta-blockers, and beta-agonists.

An estimated 10 -15% of chronic insomnia cases result from substance abuse, especially alcohol, cocaine, and sedatives. One or two alcoholic drinks at dinner, for most people, pose little danger of alcoholism and may help reduce stress and initiate sleep. Excess alcohol or alcohol used to promote sleep, however, tends to fragment sleep and cause wakefulness a few hours later. It also increases the risk for other sleep disorders, including sleep apnea and restless legs. Alcoholics often suffer insomnia during withdrawal and, in some cases, for several years during recovery.

Shift work throws off the body's circadian rhythm and may lead to chronic insomnia.

Risk Factors

Studies estimate that between 25 - 33% of adults experience some insomnia each year. In spite of this widespread problem, however, studies suggest that only about 30% of American adults who visit their doctor ever discuss sleep problems. And, doctors seem rarely to ask patients about their sleep habits or problems.

A 2003 study suggested that there were seven significant factors that predicted high risk for insomnia:

Being older
Having conflicts with relatives
Being overworked on the job
Being overworked at home
Having a sick relative
Having low social status
Having a psychiatric or psychologic problem

Stressful events do not cause insomnia in everyone. However, negative thoughts and attitudes toward events can be significant factors in insomnia. In one study, for example, the number of stressful events did not differ between good and poor sleepers. Those with insomnia, however, tended to experience these stressful events more intensively than the healthy sleepers.

In another study, patients with insomnia and good sleepers were asked to record their pre-sleep images using a handheld counter. People with insomnia not only reported fewer images, but their images also tended to be more unpleasant than those of good sleepers. More of the images in people with insomnia were related to intimate relationships and to sleep itself. The images of sleepers were more likely to be random and disconnected.

Studies report that the strongest risk factors for insomnia are psychiatric problems (particularly depression) and physical complaints (such as headaches and chronic pain) that have no identifiable cause (called somatic symptoms). About 90% of people with depression have insomnia. A study presented at the 2005 Associated Professional Sleep Societies meeting indicated that insomnia may contribute to, and prolong, depression. Researchers analyzed data from over 1,800 adults age 65 years and older. Compared with depressed patients who did not have sleep problems, depressed patients with insomnia were 11 times more likely to remain depressed after 6 months and 17 times more likely to still be depressed after a year. The researchers suggested that treating insomnia may help patients recover from depression more quickly.

Overall, insomnia is more common in women than men, although men are not immune from insomnia. Sleep efficiency deteriorates equally in men and women as they get older.

Men. One major study suggested that as men age from 16 - 50, they lose about 80% of their deep sleep. During that period, light sleep increases and REM sleep remains unchanged. (The study did not use women as subjects, and there is some evidence to suggest they are not as affected.) After age 44, REM and total sleep diminish and awakenings increase.

Women. It is not clear why women suffer more from insomnia than men. Some theories include:

In women, a number of hormonal events can disturb sleep, including premenstrual syndrome, menstruation, pregnancy, and menopause. All these conditions are short-term, however, and in most cases the wakefulness associated with them is temporary and can be eliminated with sleep hygiene and time.
After childbirth, most women develop a high sensitivity to the sounds of their children, which causes them to wake easily. Women who have had children sleep less efficiently than women who have not had children. It is possible that many women never unlearn this sensitivity and continue to wake easily long after the children have grown.
Women are at higher risk than men are for depression and anxiety, which are known risk factors for insomnia. In fact, some researchers believe that this is a main reason for the gender differences in insomnia.

After menopause, women are susceptible to the same environmental and biologic causes of insomnia as men. In fact, older women who are not bothered by sleeplessness tend to have longer and better sleep than noninsomniac men their own age.

As people grow older, sleep patterns change. In a major 2003 survey, a third of older adults reported that they woke up frequently during the night. About a quarter of participants reported waking up too early and being unable to go back to sleep. In the same study, 33% of adults age 55 - 64 reported waking up feeling unrefreshed.

Although age itself does not appear to be a risk factor for insomnia, a number of factors may interfere with sleep as one gets older:

Elderly people are more likely to be sedentary than younger adults.
Medical conditions that cause pain or nighttime distress are common in the elderly and pose a high risk for insomnia. They include arthritis, gastrointestinal distress, frequent urination, lung disease, and heart conditions.
Neurologic diseases in the elderly, such as restless legs syndrome, Parkinson's, Alzheimer's, and other forms of dementia can cause nighttime disorientation, confused wandering, and delirium.
Older people often take a number of prescription drugs whose side effects include insomnia.
The elderly are prone to grief, depression, and anxiety, emotional factors that can cause sleeplessness. One study of healthy older adults found that psychologic factors, such as anxiety and depression, were more likely to cause insomnia than illness, medications, or living conditions.
Melatonin levels are generally lower in older people. Some research suggests, however, that elderly people have lower levels simply because they stay mostly indoors and do not receive adequate sunlight.

Lack of sleep at night can lead to excessive sleepiness during the day. A 2006 study reported the following risk factors for excessive daytime sleepiness among the elderly:

Male gender
Sleep apnea or other sleep breathing disorders
Nighttime chest wheezing
Poor sleep quality
Longer time spent in REM sleep
More than 3 episodes of nighttime pain within a week
Medications that cause sleepiness

Sleep loss among the elderly is not inevitable. While older people are more susceptible to many conditions that can cause insomnia, treatments and a healthy lifestyle, particularly regular exercises, are as useful in providing relief to the elderly as to the young. And, a number of studies have found no significant increase in insomnia in older healthy adults.

Shift workers are at considerable risk for insomnia. In a major survey, 65% of shift workers reported one or more symptoms of insomnia at least a few nights a week. Workers over age 50 and those whose shifts are always changing are particularly susceptible to insomnia, although night-shift workers also have a high rate of sleeplessness. One study found that 53% of night-shift workers fall asleep on the job at least once a week, implying that their internal clocks do not adjust to unusual work times. (They are also at much higher risk than other workers for automobile accidents due to their drowsiness and may also have a higher risk for health problems in general.) A Japanese study reporting on different aspects of insomnia found that excessive computer work was associated with all forms of insomnia. People who were over-involved with their work tended to have trouble falling asleep, and they tended to awaken earlier than average.

Among the many conditions that pose a high risk for insomnia are:

Frequent travel, particularly crossing time lines
Post-traumatic stress syndrome
Brain injuries
Many chronic medical conditions ranging from seemingly minor ones, such as tinnitus (ringing in the ears) to major conditions, such as respiratory problems, heart disease, or being on dialysis

Prognosis

A 2002 study of sleeping habits in over 1 million people reported that people who slept 7 hours a night lived the longest. People who slept more than 8 hours or less than 6 hours, or who took sleeping pills, had lower survival rates.

Insomnia is not life-threatening, except in very rare cases, such as in those who have the genetic disorder called fatal familial insomnia. This rare degenerative brain disease develops in late adulthood.

Sleepiness causes as many as 200,000 automobile accidents in the U.S. and 1,500 deaths from such accidents. Studies indicate that drowsy driving is as risky as drunk driving. In a major 2003 survey, 60% of young adults reported driving while drowsy, and 20% dosed off while driving. In the study, 1% of adults who dozed off reported having an accident because of it. (One study strongly suggested that it is habitual sleepiness, however, and not just being sleepy at the time of an accident that places people at higher risk.)

Surveys show that people with severe insomnia have a quality of life that is almost as poor as those who have chronic conditions, such as heart failure. In addition to more daytime sleepiness, people with insomnia complain of more attention and memory problems compared to good sleepers.

Insomnia can also lead to irritability, mistakes at work, and poorer relationships.

Effect on Thinking and Performance. Studies suggest that insomnia makes it harder to concentrate and perform tasks.

Reduced concentration. Deep sleep deprivation impairs the brain's ability to process information.
Impaired task performance. One study reported that missing only 2 - 3 hours of sleep every night for a week significantly impaired performance and mood. An Australian study reported that 17 hours of sleep deprivation causes impaired performance levels comparable to those found in people who have blood alcohol levels indicating intoxication.
Memory problems. Whether insomnia significantly impairs learning is unclear. Some studies have reported problems in memorization, although others have found no differences in test scores between people with temporary sleep loss and those with full sleep.

Insomnia and Depression. Although stress and depression are major causes of insomnia, insomnia may also increase the activity of the hormones and pathways in the brain that can produce emotional problems. Research indicates that chronic insomnia can increase the risk of developing depression and anxiety. Some investigators are exploring the possibility of preventing psychiatric disorders by early recognition and treatment of insomnia.

Even modest alterations in waking and sleeping patterns can have significant effects on a person's mood. In both children and adults, the combination of insomnia and daytime sleepiness can produce more severe depression than either condition alone.

Effects on the Heart. Although there has been some concern that insomnia may increase the risk for heart problems, little evidence has supported any significant dangers. One study reported signs of heart and nervous system activity in people with chronic insomnia that might place such individuals at risk for coronary heart disease. If it exists, however, this increased danger is very modest compared with other risk factors for heart disease. Yet another report suggested that sleep complaints in elderly people without coronary artery disease predicted a first heart attack. Sleep disorders in such cases may have been a marker for depression, however, which is a risk factor for heart attacks in elderly people.

Effects on Weight. Lack of sleep can cause weight gain and obesity. In a 16-year study of over 68,000 women, those who slept no more than 5 hours a night were 32% more likely to gain at least 33 pounds, and those who slept 6 hours had a 12% increased risk of weight gain compared to women who slept at least 7 hours a night.

Effects on the Immune System. A 2003 study reported significant differences in immune factors among sleepers, with higher levels of certain infection-fighters observed in good sleepers than in people with chronic insomnia. The significance of these findings is still unknown, however.

Diagnosis

Diagnosing sleep disturbance and its cause is the most important step in restoring healthy sleep. However, there is little agreement, even among experts, on the best methods for effectively assessing a patient's insomnia.

A major difficulty in diagnosing this problem is its subjective nature. One study showed that there was no difference in sleep behaviors between people who said they were insomniacs and people who said they weren't. People who believe they have insomnia may have actually had frequent brief awakenings during sleep that they perceive as being continuously awake.

A number of questionnaires are available for determining whether a patient has insomnia or other sleep disorders. For example, the doctor may ask:

How would you describe your sleep problem?
How long have you had the sleep problem?
How long does it take to fall asleep?
How many times a week does it occur?
How restful is sleep?
Do you have trouble falling asleep or do you wake up too early?
What is the sleep environment like (Noisy? Not dark enough?)?
How does insomnia affect daytime functioning?
What medications do you take? (Include herbs, alcohol, and over-the-counter or prescription drugs.)
Are you taking or withdrawing from stimulants, such as coffee or tobacco?
How much alcohol is consumed per day?
What stresses or emotional factors may be present?
Have you experienced any significant life changes?
Do you snore or gasp during sleep (an indication of sleep apnea)?
Do you have leg problems (cramps, twitching, crawling feelings)?
If there is a bed partner? Is this person's behavior distressing or disturbing?
Are you a shift worker?

Sleep Diary. If the patient cannot answer these questions, keeping a sleep diary is a helpful diagnostic tool. Every day for 2 weeks, the patient should record all sleep-related information, including responses to questions listed above described on a daily basis. A bed partner can help by adding their observations of the patient's sleep behavior.

The Epworth Sleepiness Scale. The Epworth Sleepiness Scale (ESS) uses a simple questionnaire to measure excessive sleepiness during eight situations.


Situation	Chance of Dozing 0 = no chance of dozing 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing
Sitting and reading.	(Indicate a score of 0 to 3)
Watching TV.	(Indicate a score of 0 to 3)
Sitting inactive in a public place (e.g., a theater or a meeting).	(Indicate a score of 0 to 3)
As a passenger in a car for an hour without a break.	(Indicate a score of 0 to 3)
Lying down to rest in the afternoon when circumstances permit.	(Indicate a score of 0 to 3)
Sitting and talking to someone.	(Indicate a score of 0 to 3)
Sitting quietly after a lunch without alcohol.	(Indicate a score of 0 to 3)
In a car, while stopped for a few minutes in traffic.	(Indicate a score of 0 to 3)
Score Results	1-6: Getting enough sleep 4-8: Tends to be sleepy but is average. 9-15: Very sleepy and should seek medical advice. Over 16: Dangerously sleepy

Multiple Sleep Latency Test. The multiple sleep latency test (MSLT) uses a machine to measure the time it takes to fall asleep while lying in a quiet room during the day:

The patient takes four or five scheduled naps 2 hours apart.
People with healthy sleep habits fall asleep in about 10 - 20 minutes.
The test can detect changes in sleepiness associated with sleep deprivation in patients with insomnia.

It has limitations, however, and does not take into consideration any situations that may affect the patients' mental state and the actual home situation. The test is used mainly after other sleep disorders have been ruled out and the doctor is uncertain whether or not insomnia is a correct diagnosis.

If unexplained insomnia persists after treatment or there is evidence of a primary sleep disorder, such as sleep apnea or narcolepsy, the doctor may recommend a sleep specialist or a sleep disorders center. Centers are accredited by the American Academy of Sleep Medicine. Patients should investigate centers carefully, to be sure that they offer full sleep studies.

Among the signs that may indicate a need for a sleep disorders center are:

Insomnia due to psychologic disorders
Sleeping problems due to substance abuse
Snoring and sudden awakening with gasping for breath (possible sleep apnea)
Severe restless legs syndrome
Persistent daytime sleepiness
Sudden episodes of falling asleep during the day (possible narcolepsy)

At most sleep disorders centers, patients undergo an in-depth analysis, usually supervised by a multidisciplinary team of consultants who can provide both physical and psychiatric evaluations.

Treatment

The American Academy of Sleep Medicine (AASM) recommends cognitive behavioral therapy (CBT) and prescription medications as the main treatments for insomnia. According to the AASM, these treatment options can improve both quality and quantity of sleep for people with insomnia.

Experts agree that behavioral therapies should be the first-line treatment for insomnia. For children in particular, medications should rarely be used as initial treatment. A 2006 study reported that behavioral interventions can provide sustained improvement in over 80% of children with insomnia.

Prevention of sleeplessness depends upon the patient's ability to learn how to relax and sleep well. A number of behavioral methods are aimed at achieving these goals. Behavioral techniques can actually cure chronic insomnia in many cases and studies report that they help nearly all patients with primary chronic insomnia. The benefits of psychological and behavioral therapy in managing insomnia are long-lasting.

Although medications are equally effective for helping people with insomnia to sleep, they cannot cure the condition. In addition, behavioral methods act faster. Behavioral methods work in all age groups, including children and elderly patients.

Behavioral methods include:

Stimulus control
Cognitive behavioral therapy
Progressive muscle relaxation
Paradoxical intention
Biofeedback
Sleep restriction
Imagery tasks

Studies have reported that between 70 - 80% of patients who are treated with non-drug methods experience improved sleep with an average treatment duration of only 5 hours over a 4-week period. Furthermore, studies report that 75% of those who have been taking drugs are able to stop or reduce their use.

Proper sleep hygiene is the first step and should accompany any behavioral method. A number of behavioral approaches are available, but all have the same basic goals:

To reduce the time it takes to go to sleep to below 30 minutes
Reduce wake-up periods during the night

Stimulus Control. Stimulus control is now considered the standard treatment for primary chronic insomnia and may be helpful for some patients with secondary insomnia as well. The primary goal of stimulus control is to regain the idea that the bed is for sleeping. It involves the following:

Go to bed only when ready to sleep or for sex.
If unable to sleep within 15 - 20 minutes, get up and go into another room. (People who find it physically difficult to get out of bed should sit up and do something relatively arousing, like reading a book.)
Maintain a regular wake-up time no matter how few hours you actually sleep.
Avoid naps.

Cognitive-Behavioral Therapy. Cognitive behavioral therapy (CBT) is a form of therapy that emphasizes observing and changing negative thoughts about sleep such as, "I'll never fall asleep." It uses actions intended to change behavior. A 2004 study of young and middle-aged adults suggested that CBT is more effective than medication in treating chronic insomnia, and should be considered as a first-line intervention. Adding medication to CBT did not provide additional benefit. In a 2006 study of older adults, CBT worked better than zopiclone (Imovane) in managing chronic insomnia. [Zopiclone is a European sleep medication that is similar to the American drug eszopiclone (Lunesta).] Compared to zopiclone or placebo, CBT helped patients spend less time awake at night. The benefits of 6 weeks of weekly CBT sessions lasted for 6 months.

Progressive Muscle Relaxation. Progressive muscle relaxation is another technique for inducing sleep that works well for many people. It takes about 10 minutes to perform:

Focus on one specific muscle group at a time. Most people start with the muscles in one foot. Inhale and tense the foot muscles for about 8 seconds. (Do this gently. It is not intended to cause severe pain or muscle contractions.)
Relax the foot, and let it become loose and limp. Stay relaxed for 15 seconds, then repeat with the other foot.
Move up to the next muscle group and repeat the sequence, doing one side of the body at a time. Move progressively from each foot and leg up through the abdomen and chest, to each hand and arm, then to the neck, shoulders, and face.

Paradoxical Intention. Paradoxical intention is a psychological approach that is based on doing the opposite of what one wants or fears and takes it to the extreme. The first step is to make a plan to take such a paradoxical approach to insomnia.

Instead of going through activities leading to sleep, the patient prepares for staying awake and doing something energetic.
In some cases, people may take specific psychological barriers to sleep to an extreme limit. For example, if worry is a factor in insomnia, the patient intensifies the worries.

Biofeedback. Biofeedback is also effective, but requires being monitored with an electroencephalogram (EEG), a device that measures brain waves. Patients are given feedback to recognize certain states of tension or sleep stages so that they can either avoid or repeat them voluntarily.

Sleep Restriction Therapy. Sleep restriction therapy may be effective, although evidence is inconclusive. In a 2001 study, patients practiced sleep hygiene and sleep restriction. Sleep hygiene was very helpful during the first 2 months while sleep restriction led to sustained benefits and deeper sleep. The approach is a systematic method for achieving sleep and restricting the time spent in bed.

The first step is to calculate a person's sleep efficiency number:

Keep a sleep diary for 14 days. Calculate the average hours of actual sleep and hours in bed. Then divide the average hours slept by the hours spent in bed. The result, given as a percentage, is the sleep efficiency number. (For example, if a patient sleeps an average of 5 hours out of 7 hours spent in bed then the result is .714, and the sleep efficiency percentage is 71%.)
The patient's goal is to achieve sleep efficiencies of between 85 - 90%, which means only 10 - 15% of the time is spent staying awake in bed. (Sleep efficiency in older people normally falls between 75 - 85%.)

To achieve this goal, the patient takes the following actions:

Begin by going to bed 15 minutes later than usual the first week.
If 85% sleep efficiency isn't reached by the end of the week, add another 15 minutes before going to bed. Refrain from going to bed even if tired, although bedtime should not be reduced below 5 hours.
Once efficiency reaches 90% or more, begin to go to bed 15 minutes earlier each week.

Other parts of the program include stopping any sleep medications and following good sleep hygiene. People using this treatment have reported lasting improvements after just 8 weeks, and studies suggest that it is significantly more successful than relaxation techniques.

Imagery Tasks. A 2002 study enrolled people whose chronic insomnia was associated with unwanted thoughts and worries. They were given specific positive mental tasks that gave them a sense of positive control (as opposed to their real life concerns, which felt out of their control). These images distracted them and allowed them to fall asleep faster. In support of this approach, another study evaluated patients with insomnia who were given a problem before sleep. One group was asked to think of the problem in images and the other in words. The group who used imagery fell asleep more quickly and woke up with less anxiety.

Sleep Hygiene. The term sleep hygiene is used to describe simple behaviors that may help everyone improve their sleep.

Establish a regular time for going to bed and getting up in the morning. Stick to this schedule even on weekends and during vacations.
Use the bed for sleep and sexual relations only, not for reading, watching television, or working. Excessive time in bed disrupts sleep.
Avoid naps, especially in the evening.
Exercise before dinner. A low point in energy occurs a few hours after exercise; sleep will then come more easily. Exercising close to bedtime, however, may increase alertness.
Take a hot bath about 1.5 - 2 hours before bedtime. This alters the body's core temperature rhythm and helps people fall asleep more easily and more continuously. (Taking a bath shortly before bed increases alertness.)
Do something relaxing in the 30 minutes before bedtime. Reading, meditation, and a leisurely walk are all appropriate activities.
Keep the bedroom relatively cool and well ventilated.
Do not look at the clock. Obsessing over time will just make it more difficult to sleep.
Eat light meals, and schedule dinner 4 - 5 hours before bedtime. A light snack before bedtime can help sleep, but a large meal may have the opposite effect.
Spend a half hour in the sun each day. The best time is early in the day. (Take precautions against overexposure to sunlight by wearing protective clothing and sunscreen.)
Avoid fluids just before bedtime so that sleep is not disturbed by the need to urinate.
Avoid caffeine in the hours before sleep.
If one is still awake after 15 - 20 minutes, go into another room, read or do a quiet activity using dim lighting until feeling very sleepy. (Don't watch television or use bright lights.)
If distracted by a sleeping bed partner, moving to the couch or a spare bed for a couple of nights might be helpful.
If a specific worry is keeping one awake, thinking of the problem in terms of images rather than in words may allow a person to fall asleep more quickly and to wake up with less anxiety.

Exercise may be one of the best ways to promote healthy sleep. One study found that exercise is as good for inducing sleep as the use of benzodiazepines, a prescription sleep aid. Some research has found that yoga practice may have specific benefits on sleep health. Yoga uses meditation, deep breathing techniques, and movements that emphasize stretching and balance.

The circadian rhythm is more a function of darkness and light rather than actual time of day. Bright light can discourage drowsiness, and darkness can cause sleepiness, day or night. The use of a special box that gives off very bright fluorescent light (over 4,000 lux) for about 30 minutes each day may be helpful.

The following people might benefit from light therapy:

Shift workers. Light therapy should be maximized during hours they are at work and minimized when they need to sleep.
Frequent travelers. Light therapy may be useful for adjusting to new time zones and reducing jet lag.
Nursing home patients.
People with delayed sleep-phase syndrome. These people have a natural tendency to fall asleep very late at night or in early morning hours, but then sleep normally.

Patients should check with their doctors before using light therapy. The following people should avoid light therapy or use it only under a doctor's direction:

Anyone with eyes or skin that are highly sensitive to light
Anyone taking medications that increase the risk for photosensitivity
People with bipolar disorder

Timing of the therapy depends on the type of insomnia or sleep schedule of the individual. For example, in people who cannot get to sleep at night, light therapy in the morning and restricting bright light at night may be helpful. People who wake up early in the morning may benefit from light therapy performed in the evening, although a 2002 study reported that it had no effect in this group. Some light boxes have dawn/dusk simulators that help determine the correct brightness.

Medications

According to a major 2003 survey, about 20% of American older adults use some form of sleep aid, including prescription or over-the-counter drugs or alcohol. Furthermore, 15% use such aids every night.

However, while behavioral or psychologic techniques can actually cure insomnia, prolonged use of sleeping pills can only result in dependency.

In general, the following precautions are important:

Start with non-prescription medication.
Drugs used specifically for improving sleeping are called sedative hypnotics. These drugs include benzodiazepines and non-benzodiazepines. Until recently benzodiazepines were most commonly prescribed, but newer non-benzodiazepines may be better tolerated and have less risk of dependency. These medicines, however, may be associated with potentially severe allergic reactions, such as anaphylaxis and facial swelling (angioedema). These medicines may also cause hazardous behaviors, such as driving, making phone calls, or eating while asleep. If you need to take one of these prescription drugs, start with as low a dose as possible.
For adults over age 60 years, studies suggest that the risks of sedative hypnotics may far outweigh their benefits.
As a general rule, do not take either prescription nor non-prescription sleeping pills on consecutive days or for more than 2 - 4 days a week.
If insomnia is still a problem after stopping the drug and continuing with good sleep hygiene, this pattern can be repeated again, but for only up to 4 weeks.
Medication should be withdrawn gradually, and the patient should be aware of the possibility of rebound insomnia after stopping medication.
Alcohol intensifies the side effects of all sleeping medication and should be avoided.
If chronic insomnia is a companion to depression or anxiety, treating these problems first may be the best approach.

Brands with Antihistamines. Many over-the-counter sleeping medications use antihistamines, which cause drowsiness. Diphenhydramine is the most common antihistamine used non-prescription sleep aids. Some drugs contain diphenhydramine alone (Nytol, Sleep-Eez, Sominex), while others contain combinations of diphenhydramine with pain relievers (Anacin P.M., Excedrin P.M., Tylenol P.M.). Doxylamine (Unison) is another antihistamine used in sleep medications. Certain antihistamines indicated only for allergies, such as chlorpheniramine (Chlor-Trimeton), diphenhydramine (Benadryl), or hydroxyzine (Atarax or Vistaril) may also be used as mild sleep-inducers.

Unfortunately, most of these drugs leave patients feeling drowsy the next day and may not be very effective in providing restful sleep. Side effects include:

Daytime sleepiness
Dizziness
Drunken movements
Blurred vision
Dry mouth and throat

In general, these drugs should be avoided by people with angina, heart arrhythmias, glaucoma, or problems urinating. They should not be used at the same time as medications that prevent nausea or motion sickness. Some non-prescription sleeping aids, such as those containing doxylamine, should also be avoided by patients with chronic lung disease.

Common Pain Relievers. When sleeplessness is caused by minor pain, simply taking acetaminophen (Tylenol) or a non-steroidal anti-inflammatory drug (NSAID) such as ibuprofen (Advil, Motrin), can be very helpful without causing any daytime sleepiness. The extra "P.M." antihistamine found in combination products is simply an extra, needless chemical in these situations.

Benzodiazepines, also referred to as benzodiazepine receptor agonists (BzRAs), were once the most commonly prescribed sedative hypnotics. Originally developed in the 1960s to treat anxiety, these drugs nonselectively target receptor sites in the brain that modulate the effects of the neurotransmitter gamma-aminobutyric acid (GABA).

Brands. Commonly prescribed benzodiazepines:

Long-acting benzodiazepines include flurazepam (Dalmane) and clonazepam (Klonopin), quazepam (Doral).
Medium- to short-acting benzodiazepines include triazolam (Halcion), lorazepam (Ativan), alprazolam (Xanax), temazepam (Restoril), oxazepam (Serax), prazepam (Centrax), estazolam (ProSom), and flunitrazepam (Rohypnol). Short-acting benzodiazepines may be useful for air travelers who want to reduce the effects of jet lag.

Side Effects. Elderly people are more susceptible to side effects and should usually start at half the dose prescribed for younger people. They should not take long-acting forms.

Side effects may differ depending on whether the benzodiazepine is long- or shorting acting. They include:

Severe allergic reactions, including facial swelling, can occur even with the first use of a benzodiazepine drug.
Respiratory problems may occur with overuse or in people with pre-existing respiratory illness
The drugs may increase depression, a common co-condition in many people with insomnia.
Respiratory depression may occur with overuse or with people with pre-existing respiratory illness.
Long-acting drugs have a very high rate of residual daytime drowsiness compared to other types of sleeping pills. They have been associated with a significantly increased risk for automobile accidents and falls in the elderly, particularly in the first week after taking them. Shorter-acting benzodiazepines do not appear to pose as high a risk.
Memory loss (so-called traveler's amnesia), sleepwalking, sleep driving, eating while asleep and other odd mood states may occur. These effects are enhanced by alcohol.
Incontinence. In one study, 33% of patients experienced incontinence at least twice a week. The risk is highest in the elderly and with older, long-acting drugs.
Because these drugs cross the placenta and enter breast milk, pregnant women or nursing mothers should not use them. Benzodiazepine use in the first trimester of pregnancy may be associated with the development of cleft lip in newborns.
In rare cases, overdoses have been fatal.

Interactions. Benzodiazepines are potentially dangerous when combined with alcohol. Some medications, like the ulcer medication cimetidine, can slow the metabolism of the benzodiazepine.

Withdrawal Symptoms. Withdrawal symptoms usually occur after prolonged use and indicate dependence. They can last 1 - 3 weeks after stopping the drug and may include:

Gastrointestinal distress
Sweating
Disturbed heart rhythm
In severe cases, patients might hallucinate or experience seizures, even a week or more after the drug has been stopped.

Rebound Insomnia. Rebound insomnia, which often occurs after withdrawal, typically includes 1 - 2 nights of sleep disturbance, daytime sleepiness, and anxiety. In some cases, patients may experience the return of the original severe insomnia. The chances for rebound are higher with the short-acting benzodiazepines than with the longer-acting ones.

Newer short-acting non-benzodiazepines can induce sleep with fewer side effects than the benzodiazepines. Both benzodiazepine and non-benzodiazepine sedative hypnotics act on GABA-A receptor sites in the brain, but non-benzodiazepines are more specific in the subunits they target. Developed in the late 1980s, these drugs are increasingly prescribed and are becoming the hypnotics of choice for many doctors.

Brands and Benefits. Non-benzodiazepine hypnotics currently approved in the United States are zolpidem (Ambien, Ambien CR), zaleplon (Sonata), eszopiclone (Lunesta), and ramelteon (Rozerem).

Zolpidem (Ambien, generic) is one of the most commonly prescribed drugs for insomnia. It lasts longer than zaleplon. Patients should not take it unless they plan on getting at least 7 - 8 hours of sleep. The recommended dose is 10 mg/day for adults, although elderly patients may be prescribed half that dose. A 2002 study suggested that the drug might be used on an as-needed basis, with up to 5 tablets taken a week. After 3 weeks, two-thirds of the patients taking zolpidem this way were able to reduce their tablet intake by more than 25% without losing improvements in sleep. Ambien CR, an extended-release form, received approval from the Food and Drug Administration (FDA) in late 2005. It is the first extended-release prescription medicine for insomnia. The medicine is delivered in two steps. The first layer dissolves quickly, allowing the patient to fall asleep. The second layer helps the patient stay asleep.
Zaleplon (Sonata) is the shortest-acting hypnotic available. Because it is rapidly eliminated from the body it may be best for people who have difficulty falling asleep, not those who wake up often throughout the night. The drug takes effect within 30 minutes and may be taken at bedtime or later as long as the patient can sleep for at least 4 hours. The recommended dose is 5 - 10 mg/day. The drug is usually taken for 7 - 10 days.
Eszopiclone (Lunesta) is a newer, non-benzodiazepine hypnotic approved by the FDA in 2004. It may help improve both sleep maintenance and daytime alertness. Eszopiclone is related to zopiclone (Imovane), which has been used for many years in Europe. Unlike other sleep medications, eszopiclone can be taken on a long-term basis. In clinical trials, patients used eszopiclone for up to 6 months. Recommended doses are 2 - 3 mg/day for adults and 2 mg/day for elderly patients. Patients whose main problem is falling asleep may need only 1 mg/day.
Ramelteon (Rozerem) was approved by the FDA in 2005. Ramelteon is a novel non-benzodiazepine hypnotic. Unlike most sleep drugs, which target the gamma-aminobutyric acid (GABA) receptors, ramelteon targets the MT1 and MT2 receptors. Ramelteon does not cause dependence and is the first sleep drug not designated as a controlled substance.

These drugs can be particularly helpful for preventing jet lag (but zolpidem should not be used on flights less than 7 - 8 hours). They also may be helpful for people who also have accompanying mood disorders, such as depression or post-traumatic stress disorder. Because they are short-acting, zaleplon and zolpidem may pose fewer risks for falls and memory loss in elderly patients. In general, these drugs are recommended for short-term use (7 - 10 days) and treatment should not exceed 4 weeks. No studies have yet confirmed safety for longer-term use.

Side Effects. All of these drugs have fewer morning side effects than the benzodiazepines, including morning sedation and memory loss (although they can occur to some degree). Zolpidem’s (Ambien) record of adverse effects is similar to that of triazolam (Halcion), the short-acting benzodiazepine. Zaleplon (Sonata) and Ramelteon (Rozerem) appear to have less severe morning side effects. When patients first start taking any of these drugs, they should use caution during morning activities until they are sure how the drug affects them.

General side effects are mild but may include:

Drowsiness
Dizziness
Fatigue
Headache
Unpleasant taste
Diarrhea

Rarer side effects may include sleepwalking and hallucinations. In 2006, reports emerged of zolpidem (Ambien) causing sleepwalking and, even more bizarrely, sleep-driving. Most of these cases likely were due to patients using zolpidem along with alcohol or other drugs or taking more than the recommended dose. However, in March 2007, the FDA ordered stronger warning labels for zolpidem and all other non-benzodiazepine drugs. The new labels warn that that these drugs can cause sleep-related behavior, including sleep-driving, making phone calls, and preparing and eating food while asleep. In addition, severe allergic reactions (anaphylaxis) and facial swelling (angioedema) can occur even the first time one of these drugs is taken.

Anyone who receives a prescription for these medicines will also get a patient medication guide explaining the risks of the drugs and the precautions to take. Talk to your doctor if you have any questions concerning these drugs or their potential side effects.

Patients should carefully read the information labels for all drugs and follow the directions. Some sleeping pills take 30 - 60 minutes to take effect, while others (such as zolpidem) are fast-acting. For zolpidem, patients should:

Take zolpidem immediately before going to sleep
Take zolpidem only when able to get a full night’s sleep (7 – 8 hours)
Not drink alcohol the same evening
Not take more than the prescribed dose
Use caution in the morning when getting out of bed, driving, or operating heavy machinery

Interactions. As with any hypnotics, alcohol increases the sedative effects of these drugs. These hypnotics also interact with other drugs, including rifampin, ketoconazole, erythromycin, and cimetidine. They may also interfere or be interfered by other drugs. Patients should report all medications to their doctors.

Dependency, Withdrawal Symptoms, and Rebound Insomnia. The risk for rebound insomnia, dependence, and tolerance is lower with non-benzodiazepine hypnotics than with benzodiazepine drugs. These drugs are still subject to abuse. In any case, no hypnotic should be taken for more than 7 - 10 days or at higher than the recommended dose without a doctor's approval.

Antidepressants are sometimes used to treat insomnia that may be caused by depression (secondary insomnia). In addition, some antidepressants with sedating properties are prescribed for the treatment of primary insomnia. For example, trazodone has been frequently prescribed in low doses as a hypnotic to help induce sleep. However, there are few studies that address its safety and efficacy as a drug for treating insomnia in non-depressed patients. Several studies have warned against trazodone's use in elderly patients, due to its risk for side effects (daytime sleepiness, dizziness, priapism) and drug interactions. In fact, all hypnotics can have serious side effects in the elderly, and all must be used with caution.

Chloral Hydrate. Chloral hydrate has been in use since 1832. It has significant adverse effects, however, and most experts believe it no longer has a role in the treatment of insomnia. In any case, it does not appear to be effective in the elderly. Chloral hydrate poses a risk for addiction, and it can be fatal in overdose. It also has cancer-causing properties. Side effects include irritation of the skin, mucous membranes, and stomach. People with stomach, heart, kidney, or liver disorders should not take this drug at all. If a child is given it (usually for minor surgery), that child should never be given chloral hydrate again in their lifetime.

Barbiturates. Barbiturates (Seconal, Nembutal) were the standard sleeping medications before the introduction of benzodiazepines. Overdose is dangerous and frequent; addiction and abuse are common. These drugs should rarely or never be prescribed for insomnia.

Indiplon. The FDA is reviewing indiplon, a new non-benzodiazepine hypnotic.

According to results from a national survey published in 2006 in the Archives of Internal Medicine, more than 1.6 million Americans use complementary and alternative therapies to treat insomnia. Many people choose herbal and dietary supplement remedies. Some, such as chamomile tea or lemon balm, are generally harmless for most people. Others have more serious side effects and interactions. [See Box.] According to a 2007 study, valerian and melatonin are among the most popular alternative remedies for insomnia.

Although about half of people who use herbal medicine report that these products help their sleep, experts are not sure whether these remedies really work or whether a placebo effect is the main reason for the improvement. The American Academy of Sleep Medicine (AASM) states that there is only limited scientific evidence to show that herbal and dietary supplements are effective sleep aids. The AASM recommends that these products should be taken only if approved by a doctor. Be sure to talk to your doctor if you are considering taking any herbal or dietary supplement. Some of these products can interact with prescription medications.

Melatonin is the most studied natural remedy for insomnia. A 2005 analysis of 17 melatonin studies found that melatonin significantly reduced the time to fall asleep (sleep onset) and the time spent asleep (sleep duration). However, there are no consistent standards on melatonin doses. Some research suggests that 0.3 mg may be the most effective dosage in many people with insomnia. However, higher doses may keep some people awake.

Although melatonin may not have many benefits for most people with chronic insomnia, studies suggest that it may help the following individuals:

Elderly people. It may help certain older people with insomnia, such as those with evidence of low melatonin levels and those dependent on prescription sleeping medications. It is not clear, however, how significant the benefits are.
People without sight. A 2000 study reported that melatonin can help people without sight retrain their circadian cycle so that they can sleep at regular hours. The best dosages and timing, however, need to be clarified.
Travelers suffering jet lag. Some studies have reported that melatonin may help prevent jet lag in some travelers.
Those in withdrawal from prescription sleep medication. Melatonin may help people who are dependent on sleeping medications withdraw from these drugs and maintain good quality sleep.
People with delayed sleep syndrome. It might be somewhat helpful for people who fall asleep very late at night or in early morning hours but then sleep normally.
Children. Melatonin may help some children with chronic insomnia. In one small study, or example, melatonin was specifically helpful for children with Asperger syndrome, who are at risk for sleep disturbances. More research is warranted, however. At this time, no one should give their child melatonin without a doctor's recommendation.

Melatonin is a powerful hormone that can have major effects on all parts of the body. Doses of melatonin over 0.3 mg can disrupt the circadian system in the brain. Long-term consequences are unknown. High doses have been associated with the following adverse events:

Mental impairment
Severe headaches
Nightmares

Interactions with other drugs are not completely known. Melatonin is classified as a dietary supplement and not as a drug, so its quality is not regulated in the U.S.

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. Patients should always check with their doctors before using any herbal remedies or dietary supplements.

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

Chamomile. Many people drink chamomile tea for its sedative properties. Although it is generally safe, it may cause allergic reactions in people who have plant or pollen allergies.

Valerian root. Valerian is an herb that has sedative qualities and has been helpful in people with insomnia. One study reported that it was also useful for helping patients withdraw from benzodiazepines -- the standard prescription sleeping pills. In another study, 83% of patients rated the effects of valerian on sleep as being very good. In the same study, valerian was as effective as oxazepam, a standard prescription sleeping medication. Valerian's side effects may include vivid dreams. High doses of valerian can cause blurred vision, excitability, and changes in heart rhythm. Valerian's effects can be dangerously increased if it is used with standard sedatives.

Chinese Herbal Remedies. Studies suggest that up to 30% of herbal patent remedies imported from China are laced with potent pharmaceuticals such as phenacetin and steroids. They may also contain toxic metals. The herbal remedy Sleeping Buddha was recalled in 1998 because it contained a benzodiazepine, the major ingredient in many prescription sleeping pills, and also appeared to increase the risk for birth defects in pregnant women. Reports of a few cases of acute hepatitis have occurred from Jin Bu Huan, a Chinese herbal remedy sold as treatment for pain and insomnia.

Kava. Kava has been used to relieve anxiety and improve sleep. It is not considered safe. There have been reports of liver failure and death from this herb, with highest risk in those with liver disease. Other side effects include itchy, scaly skin, muscle weakness, and problems with coordination. It also interacts dangerously with certain medications, including alprazolam, an anti-anxiety drug. Kava also increases the strength of certain other drugs, including other sleep medications, alcohol, and antidepressants.

Tryptophan and 5-L-5-hydroxytryptophan (HTP). Tryptophan is an amino acid used in the formation of the neurotransmitter serotonin, which is known to promote well-being and has been associated with healthy sleep. L-tryptophan was marked for insomnia and other disorders but was withdrawn from the market after contaminated batches caused a rare and even fatal disorder called eosinophilia myalgia syndrome. 5-HTP, a byproduct of tryptophan, is still available as a supplement. There have been reports that some brands contain a substance called Peak X, which may be harmful. There is little evidence that 5-HTP relieves insomnia.

Resources

www.aasmnet.org -- American Academy of Sleep Medicine
www.nhlbi.nih.gov/about/ncsdr -- National Center for Sleep Disorders Research
www.sleepfoundation.org -- National Sleep Foundation
www.sleepeducation.com -- Sleep Education from the American Academy of Sleep Medicine
www.wfsrs.org -- World Federation of Sleep Research Societies
www.clinicaltrials.gov -- Find clinical trials

References

Bliwise DL, Ansari FP. Insomnia associated with valerian and melatonin usage in the 2002 National Health Interview Survey. Sleep. 2007 July 1;30(7):881-884.

Liu X, Buysse DJ, Gentzler AL, Kiss E, Mayer L, Kapornai K, et al. Insomnia and hypersomnia associated with depressive phenomenology and comorbidity in childhood depression. Sleep. 2007 Jan 1;30(1):83-90.

Mindell JA, Emslie G, Blumer J, Genel M, Glaze D, Ivanenko A, et al. Pharmacologic management of insomnia in children and adolescents: consensus statement. Pediatrics. 2006 Jun;117(6):e1223-32.

Mindell JA, Kuhn B, Lewin DS, Meltzer LJ, Sadeh A; American Academy of Sleep Medicine. Behavioral treatment of bedtime problems and night wakings in infants and young children. Sleep. 2006 Oct 1;29(10):1263-76.

Morin CM, Bootzin RR, Buysse DJ, Edinger JD, Espie CA, Lichstein KL. Psychological and behavioral treatment of insomnia: update of the recent evidence (1998-2004). Sleep. 2006 Nov 1;29(11):1398-414.

Neckelmann D, Mykletun A, Dahl AA. Chronic insomnia as a risk factor for developing anxiety and depression. Sleep. 2007 July 1;30(7):873-880.

Pearson NJ, Johnson LL, Nahin RL. Insomnia, trouble sleeping, and complementary and alternative medicine: Analysis of the 2002 National Health Interview Survey data. Arch Intern Med. 2006 Sep 18;166(16):1775-82.

Review Date:
7/18/2007
Reviewed By:
Harvey Simon, MD, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital.

A.D.A.M. Copyright

adam.com

Gastroesophageal reflux disease and heartburn

FitSugar — Wed, 08 Oct 2008 17:35:29 -0700

In This Report

Highlights
Introduction
Causes
Risk Factors
Symptoms
Complications
Barrett's Esophagus
Diagnosis
Treatment
Prevention
Medications
Surgery
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

New Research

Obesity and GERD. Increased weight in women is linked to more frequent GERD symptoms, according to the Nurses' Health Study, which included 10,545 female participants. Overweight and obese women were two to three times more likely to have frequent symptoms than women of normal weight. GERD symptoms decreased nearly 40% in women whose body mass index (BMI) dropped by more than 3.5, compared to women whose BMI remained the same.
Proton-Pump Inhibitors and Bone Fracture. Long-term use of PPIs may increase the risk of hip fractures in older adults, according to a study in the Journal of the American Medical Association. People taking high doses of PPIs for more than a year were 2.6 times as likely to fracture a hip as those who were not taking the drug. The authors suggested that the stomach acids blocked by PPIs may be needed to absorb calcium, or the drugs may interfere with the body's natural process of breaking down and rebuilding bones.
PPIs and H2 Blockers in Children. Otherwise healthy children who take PPI inhibitors or H2 blockers may be at increased risk for intestinal and respiratory infections, according to a study of 186 children with GERD. The rate of gastroenteritis and community-acquired pneumonia significantly increased in children who were taking these medications when researchers compared the 4 months before and after enrollment in the study.

New Approval

Proton-Pump Inhibitor Approved for Adolescents. Esomeprazole (Nexium) delayed-release capsules have been approved for use in children ages 12 - 17 for the short-term treatment of GERD. Research shows that this medication reduces heartburn symptoms in adolescents.

Introduction

Gastroesophageal reflux disease (GERD) is a condition in which acids from the stomach move backward into the esophagus (an action called reflux). Reflux occurs if the muscular actions in the esophagus or other protective mechanisms fail.

Click the icon to see an animation about heartburn.

The hallmark symptoms of GERD are:

Heartburn: a burning sensation in the chest and throat.
Regurgitation: a sensation of acid backed up in the esophagus.

Although acid is a primary factor in damage caused by GERD, other products of the digestive tract, including pepsin and bile, can also be harmful.

Heartburn is a condition in which the acidic stomach contents back up into the esophagus, causing pain in the chest area. This reflux usually occurs because the sphincter muscle between the esophagus and stomach is weakened. Standing or sitting after a meal can help reduce the reflux that causes heartburn. Continuous irritation of the esophagus lining as in gastroesophageal reflux disease is a risk factor for the development of adenocarcinoma.

The esophagus, commonly called the food pipe, is a narrow muscular tube about nine-and-a-half inches long. It begins below the tongue and ends at the stomach. The esophagus is narrowest at the top and bottom; it also narrows slightly in the middle. The esophagus consists of three basic layers:

An outer layer of fibrous tissue.
A middle layer containing smoother muscle.
An inner membrane, which contains numerous tiny glands.

Click the icon to see an image of the esophagus.

When a person swallows food, the esophagus moves it into the stomach through the action of peristalsis, wave-like muscle contractions. In the stomach, the starch, fat, and protein in food are broken down by acid and various enzymes, notably hydrochloric acid and pepsin. The lining of the stomach has a thin layer of mucous that protects it from these fluids.

If acid and enzymes back up into the esophagus, however, its lining offers only a weak defense. The esophagus is protected using specific muscles and other factors.

The most important structure protecting the esophagus may be the lower esophageal sphincter (LES). The LES is a band of muscle around the bottom of the esophagus where it meets the stomach.

The LES opens after a person swallows to let food enter the stomach and then immediately closes to prevent regurgitation of the stomach contents, including gastric acid.
The LES maintains this pressure barrier until food is swallowed again.

Click the icon to see an image of the stomach.

If the pressure barrier is not sufficient to prevent regurgitation and acid backs-up (reflux), then peristaltic action of the esophagus serves as an additional defense mechanism and pushes the contents back down into the stomach.

Esophagitis. In most people, GERD symptoms are short-lived and occur infrequently. In about 20% of cases, however, the condition becomes chronic. When the acid causes irritation or inflammation, the condition is called esophagitis. If the damage becomes extensive and injures the esophagus, the disorder is known as erosive esophagitis.

Non-Erosive Esophageal Reflux Disease. Symptoms of gastroesophageal reflux disease can occur without any signs of inflammation or injury to the esophagus. This condition is also referred to as non-erosive esophageal reflux disease (NERD). NERD rarely progresses to full-blown GERD. Patients with NERD have no signs of inflammation or erosion in the esophagus, but they experience certain symptoms of GERD, such as burning sensations behind the breastbone for at least 3 months. Researchers suggest that nerves lying near the surface of the lining become exposed to acid that has penetrated the layers. The nerves then trigger prolonged and painful symptoms in response.

Barrett's Esophagus. A small percentage of patients with GERD may eventually develop Barrett's esophagus, a serious complication of GERD that results in precancerous changes in the tissue lining the esophagus.

Eosinophilic Esophagitis. This is a distinct disorder characterized by difficult or painful swallowing. It can occur along with GERD. The lining of the esophagus develops furrows and rings. This condition can be treated with swallowed fluticasone propionate, the active ingredient in some asthma medications.

Causes

Anyone who eats a large amount of acidic foods can have mild and temporary heartburn. This is especially true when lifting, bending over, or taking a nap after eating a large meal high in fatty, acidic foods. Persistent GERD, however, may be due to various conditions, including abnormal biologic or structural factors.

The band of muscle tissue called the LES is responsible for closing and opening the lower end of the esophagus and is essential for maintaining a pressure barrier against contents from the stomach. It is a complex area of smooth muscles and various hormones. If it weakens and loses tone, the LES cannot close up completely after food empties into the stomach. In such cases, acid from the stomach backs up into the esophagus. Dietary substances, drugs, and nervous system factors can weaken the LES and impair its function.

A study showed that more than half of GERD patients had abnormal nerve or muscle function in the stomach. These abnormalities cause impaired motility, which is the inability of muscles to act spontaneously. The stomach muscles do not contract normally, which causes delays in stomach emptying, increasing the risk for acid back-up.

Some studies suggest that most people with atypical GERD symptoms (such as hoarseness, chronic cough, or the feeling of having a lump in the throat) may have specific abnormalities in the esophagus. (In one study, such abnormalities appeared in 73% of patients who had atypical symptoms.)

Motility Abnormalities. Problems in spontaneous muscle action (peristalsis) in the esophagus commonly occur in GERD, although it is not clear if such occurrences are a cause or result of long-term effects of GERD.

Adult-Ringed Esophagus. This condition is characterized by an esophagus with multiple rings and persistent trouble with swallowing (including getting food stuck in the esophagus). It occurs mostly in men.

The hiatus is a small hole in the diaphragm through which the esophagus passes into the stomach. It normally fits very snugly, but it may weaken and enlarge. When this happens, part of the stomach muscles may protrude into it, producing a condition called hiatal hernia. It is very common, occurring in over half of people over 60 years old, and is rarely serious. Until recent years, it was believed that most cases of persistent heartburn were caused by a hiatal hernia. Hiatal hernia may impair LES muscle function. Studies have failed to confirm evidence, however, that it is a common cause of GERD, although its presence may increase GERD symptoms in patients with both conditions.

A hiatal hernia occurs when part of the stomach protrudes up into the chest through the sheet of muscle called the diaphragm. This may result from a weakening of the surrounding tissues and may be aggravated by obesity or smoking.

Studies indicate that 31 - 43% of reflux may be hereditary. An inherited risk exists in many cases of GERD, possibly because of inherited muscular or structural problems in the stomach or esophagus. Genetic factors may play an especially strong role in susceptibility to Barrett's esophagus, a precancerous condition caused by very severe GERD.

At least half of people with asthma also have GERD. Some experts speculate that the coughing and sneezing accompanying asthmatic attacks cause changes in pressure in the chest that can trigger reflux. Certain asthma drugs that dilate the airways may relax the LES and contribute to GERD. On the other hand, GERD has been associated with a number of other upper respiratory problems and may be a cause of asthma, rather than a result.

Crohn's disease is a chronic ailment that causes inflammation and injury in the colon and other parts of the gastrointestinal tract, including the esophagus. Other disorders that may affect areas that can contribute to GERD include diabetes, any gastrointestinal disorder, peptic ulcers, lymphomas, and cancer.

Click the icon to see an image of inflammatory bowel disease.

Helicobacter Pylori, also called H. pylori, is a bacterium found in the mucous membranes and is now known to be a major cause of peptic ulcers. Antibiotics used to eradicate H. pylori are now accepted treatment for curing ulcers. Of some concern, however, are studies indicating that H. Pylori may actually protect against GERD by reducing stomach acid. Furthermore, curing ulcers by eliminating the bacteria might actually trigger GERD in some people. Studies are mixed, however, on whether patients with cured H. Pylori infections are at risk for GERD. An analysis of 8 studies reported no higher risk for GERD after antibiotic treatments, nor was GERD any worse in patients who already had it. Seven of the 8 studies, however, were conducted only 2 months after antibiotic treatment. Longer follow-up studies are needed to determine long-term consequences, if any.

In any case, the bacteria should be eradicated in infected patients with existing GERD who are taking ongoing acid suppressing agents. There is some evidence that the combination of H. pylori and chronic acid suppression in these patients can lead to atrophic gastritis, a precancerous condition in the stomach.

In some cases, the esophagus appears normal, but GERD symptoms are present. This may indicate an over-reaction of the immune system to irritants that are introduced into the esophagus. In such cases, the immune system reacts with an exaggerated (or hyper-reactive) response, triggering the release of certain factors that end up causing inflammation and possibly injury. (This event is similar to the asthmatic response in the airways.)

NSAIDs. Nonsteroidal anti-inflammatory drugs (NSAIDs), common causes of peptic ulcers, may also cause GERD and increase severity in people who already have GERD. In a 3-year study of 25,000 people, NSAID users were twice as likely to have GERD symptoms as non-users. Symptoms did not become evident until after about 6 months of regular use. There are dozens of NSAIDs, including over-the-counter aspirin, ibuprofen (Motrin, Advil, Nuprin), and naproxen (Aleve), as well as prescription anti-inflammatory medicines. A person with GERD who takes the occasional aspirin or other NSAID will not necessarily experience adverse effects. This is especially true if there are no risk factors or indications of ulcers. Acetaminophen (Tylenol), which is NOT an NSAID, is a good alternative for those who want to relieve mild pain. It does not, however, relieve inflammation.

Other Drugs. Many other drugs can cause GERD, including but not limited to the following: calcium channel blockers (used to treat high blood pressure and angina), anticholinergics (used in drugs that treat urinary tract disorders, allergies, and glaucoma), beta adrenergic agonists (used for asthma and obstructive lung diseases), dopamine (used in Parkinson's disease), bisphosphonates (used to treat osteoporosis), sedatives, antibiotics, potassium, or iron pills.

Weakened peristaltic movement in the esophagus may contribute to GERD. If the mucous membrane is impaired, even a normal amount of acid can harm the esophagus. Pressure on the abdomen caused by obesity and also wearing tight clothing can contribute to acid backing up into the esophagus.

Click the icon to see an image of peristalsis.

Risk Factors

GERD occurs monthly in about half of American adults. People of all ages are susceptible to GERD. Elderly people with GERD tend to have a more serious condition than younger people.

Eating Pattern. Anyone who eats a heavy meal and subsequently lies on the back or bends over from the waist is at risk for an attack of heartburn. Anyone who snacks at bedtime is at high risk for heartburn.

Pregnancy. Pregnant women are particularly vulnerable to heartburn in their third trimester as the growing uterus puts increasing pressure on the stomach. Heartburn in such cases is often resistant to dietary interventions and even antacids.

Obesity. A number of studies suggest that obesity contributes to GERD and may increase the risk for erosive esophagitis in GERD patients. The Nurses' Health Study found that being overweight or obese significantly increased GERD symptoms in women. The higher a woman's body mass index (BMI), the study found, the more frequent were her symptoms. Women who lost weight in the study saw a decrease in their symptoms. Research suggests that the prevalence of GERD symptoms among obese patients has been underreported. Other researchers have reported that increased BMI is associated with a higher risk for cancer of the esophagus (esophageal adenocarcinoma).

Respiratory Diseases. People with asthma are at very high risk for GERD. One study indicated that patients with chronic obstructive pulmonary diseases (e.g., emphysema or chronic bronchitis) were more likely to have GERD.

Chronic obstructive pulmonary disease (COPD) refers to chronic lung disorders that result in blocked air flow in the lungs. The two main COPD disorders are emphysema and chronic bronchitis, the most common causes of respiratory failure. Emphysema occurs when the walls between the lung's air sacs become weakened and the sacs get enlarged and filled with too much air. Damage from COPD is usually permanent and irreversible.

Smoking. Increasing evidence indicates that smoking raises the risk for GERD. Studies suggest that smoking reduces LES muscle function, increases acid secretion, impairs muscle reflexes in the throat, and damages protective mucous membranes. Smoking reduces salivation, which helps neutralize acid. Whether it is the smoke, nicotine, or both that triggers GERD is unknown. Some people who use nicotine patches to quit smoking, for example, experience heartburn, but it is not clear if it's the nicotine or stress that produces acid back-up.

Alcohol Use. Alcohol has mixed effects on GERD. It relaxes the LES muscles and, in high amounts, may irritate the mucous membrane of the esophagus. All alcoholic beverages increase stomach acid levels. A combination of heavy alcohol use and smoking increases the risk for esophageal cancer. (Small amounts of alcohol, however, may actually protect the mucosal layer.)

In general, overweight Caucasian males over 40 are at highest risk for complications, notably Barrett's esophagus. Others at high risk for severe symptoms, inflammation, or both include:

People who use nonsteroidal anti-inflammatory drugs (NSAIDs). Studies suggest that certain NSAID users are at higher risk for GERD, including older adults, women, alcohol and tobacco users, and patients with asthma, hiatal hernia, or obesity. One study reported that NSAIDs put people at risk for ulcers but not for erosive esophagitis or strictures. Interestingly, NSAIDs are being studied for protection against Barrett's esophagus.
People with hiatal hernia

GERD is very common in children of all ages, but it is usually mild. Heartburn has been reported in 1.8% of 3-year-olds and in 5.2% of young people 10 - 17 years old. Children with the following conditions are at higher risk for severe GERD:

Neurologic impairments
Food allergies
Scoliosis
Cyclic vomiting
Cystic fibrosis
Problems in the lungs, ear, nose, or throat
Any medical condition affecting the digestive tract

Symptoms in Children. A physician should examine any child who has the following symptoms as soon as possible, because they may indicate complications such as anemia, failure to gain weight, or respiratory problems. Symptoms of severe GERD in infants and small children may include:

Chronic coughing
Frequent infections
Wheezing
Gasping or frequent cessation in breathing while asleep (called sleep apnea). However, one study found no association between GERD and apneas in premature infants.
Frequent vomiting in infants. About half of all infants up to 3 months old regurgitate milk at least once a day. Some simply spit up; others vomit large amounts after feedings. Vomiting in infants and older children is rarely a sign of GERD. In infants it usually resolves by age one. Severe vomiting -- particularly if it is bilious (green colored) -- always requires a doctor's visit, since it could be a symptom of severe obstruction.
Having to burp babies very frequently during and after feeding.

Babies and children may experience these symptoms without having GERD. An Australian study suggested that many infants who have normal irritability may be treated inappropriately for reflux disorders.

Feeding Problems. Feeding problems may be more severe than previously thought in children with GERD. In one study, children who had GERD and problems swallowing tended to refuse food and were late in eating solids. They also cried more and reacted more negatively in general than non-GERD babies. Such behaviors negatively affected the mothers as well. These findings were supported in an earlier study which reported that children at 1 year who had GERD in infancy were no longer spitting up, but still tended to have negative dining experiences ("too slow," "upsetting"). However, these children were at no greater risk for respiratory illnesses than other 1-year-old children.

Associations with Asthma and Infections in the Upper Airways. In addition to asthma, GERD is associated with other upper airway problems, including ear infections and sinusitis. Some experts argue that the association with common childhood infections and asthma is unfounded, since GERD is normal in most children.

Dental Erosion. GERD can cause irreversible loss of tooth enamel. Based on a 2002 study, some experts suggest checking for GERD in children with dental erosions. In the study, no child without GERD experienced loss of tooth enamel.

Rare Complications in Infants. Although GERD is very common, the following complications are very rare and only occur in certain cases:

Failure to thrive
Feeding problems and severe vomiting may cause anemia
Acid back-up may be inhaled into the airways and cause pneumonia

The infant's life may be in danger if acid reflux causes spasms in the larynx severe enough to block the airways. In fact, some experts believe this action may contribute to sudden infant death syndrome (SIDS). More research is needed to determine whether this association is valid.

Managing GERD in Infancy. Here are some hints on managing GERD in infants:

During and after feeding, infants should be positioned vertically and burped frequently.
If a baby with GERD is fed formula, the mother should ask the doctor how to thicken it in order to prevent splashing up from the stomach.
Parents of infants with GERD should discuss the baby's sleeping position with their pediatrician. Experts strongly recommend that all healthy infants sleep on their backs to help prevent sudden infant death syndrome (SIDS). For babies with GERD, however, lying on the back may obstruct the airways. In one study, infants with gastroesophageal reflux who spent prolonged periods of time in infant seats, including car seats, had more reflux than those who spent waking time on their stomachs. If the physician recommends that babies with GERD sleep on their stomachs, parents should be sure that their infant's mattress is very firm, possibly tilted up at the head, and that there are no pillows. The baby's head should be turned so that the mouth and nose are completely unobstructed.
Because food allergies may trigger GERD in children, parents may want to discuss a dietary plan with their physician that starts the child on formulas using non-allergenic proteins, and then incrementally adds other foods until symptoms are triggered.

Managing GERD in Children. The same drugs used in adults may be tried in children with chronic GERD. While some drugs are available over the counter, they should not be given to children without physician supervision.

Milder medications, such as antacids, are used first.
H2 blockers may be tried next. They are available over the counter and include famotidine (Pepcid AC), cimetidine (Tagamet HB), ranitidine (Zantac 75), and nizatidine (Axid AR). The FDA has issued a warning on Pepcid AC for adults with kidney problems.
Proton-pump inhibitors (PPIs), such as omeprazole (Prilosec) and lansoprazole (Prevacid), are even more powerful agents that suppress the production of stomach acid. Delayed-release esomeprazole (Nexium) capsules have been approved for use in children ages 12 - 17 for the short-term treatment of GERD. One study found that esomeprazole (Nexium) in either a 20 or 40 mg dose once a day significantly reduced heartburn symptoms in adolescents. PPIs appear to be safe and effective even for children as young as 1 year old who fail the less intensive therapies. However, a 2006 study found that otherwise healthy children who were treated with H2 blockers and PPIs had an increased risk of developing respiratory and intestinal infections.

Surgical fundoplication involves wrapping the upper curve of the stomach (fundus) around the esophagus. The goal of this surgical technique is to strengthen the LES. Until recently, surgery was the primary treatment for children with severe complications from GERD because older drug therapies had severe side effects, were ineffective, or had not been designed for children. However, with the introduction of proton-pump inhibitor drugs, some children may be able to avoid surgery. Surgical fundoplication can be performed laparoscopically through small incisions. In one study, of 238 children from 5 months to 16 years of age who underwent laparoscopic fundoplication, all but 9 were symptom free at least 5 years after the surgery. A 2006 study found that children who underwent antireflux surgery before age 4 were less likely to be hospitalized again, or to have reflux-related events such as pneumonia and esophagitis after the surgery.

Symptoms

Heartburn. Heartburn is the primary symptom of GERD. It is a burning sensation that radiates up from the stomach to the chest and throat. Heartburn is most likely to occur in connection with the following activities:

After a heavy meal
Bending over
Lifting
Lying down, particularly on the back

According to one study, nearly three-quarters of patients with frequent GERD symptoms experience them at night. Patients with nighttime GERD also tend to experience more severe pain than those whose symptoms occur at other times. One study found that patients with nighttime pain reported levels of severity that were similar to those reported in angina and heart failure.

The severity of heartburn does not necessarily indicate actual injury in the esophagus. For example, Barrett's esophagus, which causes precancerous changes in the esophagus, may trigger few symptoms, especially in elderly people. On the other hand, people can suffer severe heartburn without the presence of damage to the esophagus.

Dyspepsia. Up to half of GERD patients have dyspepsia, a syndrome consisting of the following:

Pain and discomfort in the upper abdomen
Fullness in the stomach
Nausea after eating

People can have dyspepsia without having GERD.

Regurgitation. Regurgitation is the feeling of acid backing up in the throat. Sometimes acid regurgitates as far as the mouth and can be experienced as a "wet burp." Uncommonly, it may come out forcefully as vomit.

Many patients with GERD do not experience heartburn or regurgitation. Elderly patients with GERD often have less typical symptoms than do younger people. Instead symptoms may appear in other locations.

Chest Sensations or Pain. Patients may have the sensation that food is trapped behind the breastbone. Chest pain is a common symptom of GERD. It is very important to differentiate it from chest pain caused by heart conditions, such as angina and heart attack.

Symptoms in the Throat. Less commonly, GERD may produce symptoms that occur in the throat:

Acid laryngitis. A condition that includes hoarseness, dry cough, the sensation of having a lump in the throat, and the need to repeatedly clear the throat.
Trouble swallowing (dysphagia). In severe cases, patients may even choke or food may become trapped in the esophagus, causing severe chest pain. This may indicate a temporary spasm that narrows the tube, or it could also be an indication of serious esophageal damage or abnormalities.
Chronic sore throat
Persistent hiccups

Coughing and Respiratory Symptoms. Asthmatic symptoms, such as coughing and wheezing, may occur. In fact, in one study, GERD alone accounted for 41.1% of cases of chronic cough in nonsmoking patients. The incidence was even higher when GERD and asthma were combined.

Chronic Nausea and Vomiting. Nausea that persists for weeks or even months and is not attributable to a common cause of stomach upset may be a symptom of acid reflux. In rare cases, vomiting can occur as often as once a day. All other causes of chronic nausea and vomiting should be ruled out, including ulcers, stomach cancer, obstruction, and pancreas or gallbladder disorders.

Complications

Nearly everyone has an attack of heartburn at some point in their lives. In the vast majority of cases the condition is temporary and mild, causing only transient discomfort. If patients develop persistent gastroesophageal reflux disease with frequent relapses, however, and it remains untreated, serious complications may develop over time. They can include the following:

Erosive esophagitis (severe inflammation in the esophagus)
Severe narrowing (stricture) of the esophagus
Barrett's esophagus
Problems in other areas, including the teeth, throat, and airways leading to the lungs

Older people are at higher risk for complications from persistent GERD. The following conditions also put individuals at risk for recurrent and serious GERD:

The esophagus is very inflamed.
Initial symptoms are severe.
Symptoms persist in spite of treatments that successfully heal the esophagus.
There are severe underlying muscular abnormalities.

Erosive esophagitis develops in chronic GERD patients when acid causes enough irritation and inflammation to produce extensive injuries in the esophagus. Some studies have suggested that overweight Caucasian males with GERD are at highest risk for this condition. In anyone, however, the longer and more severe the GERD condition, the higher the risk for erosive esophagitis.

Bleeding. In one study, bleeding occurred in more than 8% of patients with erosive esophagitis (severe inflammation of the esophagus), which is associated with GERD. In very severe cases, the patient may detect dark-colored, tarry stools (indicating the presence of blood) or may vomit blood, particularly if ulcers have developed in the esophagus. This is a sign of severe damage and requires immediate attention.

Sometimes long-term bleeding can result in iron-deficiency anemia and may even require emergency transfusions. This condition can occur without heartburn or other warning symptoms, or even obvious blood in the stools.

Barrett's Esophagus (BE) and Esophageal Cancer. In some cases, BE develops as an advanced stage of erosive esophagitis. BE results in abnormal cellular changes in the esophagus that, in turn, put a patient at risk for esophageal cancer. There are many issues involved with BE, however, including its prevalence and true severity, that are unresolved.

Of note, GERD itself poses no significant risk for esophageal cancer. One study reported an annual incidence of 6.5 cancer cases per 10,000 people with regular GERD symptoms.

If the esophagus becomes severely injured over time, narrowed regions called strictures can develop, which may impair swallowing (dysphagia). Food may even become blocked in some cases. Stretching procedures or surgery may be required to restore normal swallowing. Paradoxically, strictures may actually prevent other GERD symptoms by helping to keep acid from traveling up the esophagus.

Asthma. Asthma and GERD often occur together. Studies report that reflux disorder coincides with 32 - 80% of asthma cases. Some theories for the causal connection between GERD and asthma are as follows:

Acid leaking from the lower esophagus in GERD stimulates the vagus nerves, which run through the gastrointestinal tract. These stimulated nerves trigger the nearby airways in the lung to constrict, which causes asthma symptoms.
Acid back-up that reaches the mouth may be inhaled into the airways (aspirated). Here, the acid triggers a reaction in the airways that causes asthma symptoms.

There is some evidence that asthma causes GERD. In contrast, some evidence suggests that GERD causes asthma. Some clinical trials report that treating GERD in patients who also have asthma reduces symptoms of both conditions. Not all such patients report improved asthma symptoms with GERD treatments, and these treatments do not appear to have much effect on actual lung function. One study suggested that this approach works in asthmatic individuals who tended to be overweight and to have severe GERD in the lower part of the esophagus.

Other Respiratory and Airway Conditions. Current studies indicate an association between GERD and various upper respiratory problems that occur in the sinuses, ear and nasal passages, and airways of the lung. People with GERD appear to have an above-average risk for chronic bronchitis, chronic sinusitis, emphysema, pulmonary fibrosis (lung scarring), and recurrent pneumonia. If a person inhales fluid from the esophagus (aspirates) into the lungs, serious pneumonia can occur. It is not yet known whether treatment of GERD would also reduce the risk for these respiratory conditions.

Dental erosion (the loss of the tooth's enamel coating) is a very common problem among GERD patients, including children. It results from the acid backing up into the mouth and eroding the enamel.

An estimated 20 - 60% of patients with GERD have atypical symptoms in the throat (hoarseness, sore throat) without any significant heartburn. A failure to diagnose and treat GERD may lead to persistent throat conditions such as chronic laryngitis, hoarseness, difficulty in speaking, sore throat, cough, constant throat clearing, and granulomas (soft, pink bumps) on the vocal cords.

GERD commonly occurs with obstructive sleep apnea, a condition in which breathing stops temporarily but repeatedly during sleep. It is not clear which condition is responsible for the other, but GERD is particularly severe when both conditions occur together. One study reported that spasms in the vocal cords caused by acid reflux may block the flow of air and cause sleep apnea in adults. On the other hand, other research suggests that the disordered breathing in sleep apnea alters pressure in the chest area and causes GERD. Both conditions may also have risk factors in common, such as sleeping on the back. Studies suggest that in such patients GERD can be markedly improved with a continuous positive airway pressure (CPAP) device, which opens the airways and is the standard treatment for severe sleep apnea.

Barrett's Esophagus

Barrett's esophagus (BE) is a serious condition in which changes occur in the cells that line the lower esophagus and cause the cells to become abnormal and precancerous. Barrett's esophagus is categorized as either long-segment or short-segment disease:

Long-segment BE occurs when abnormal cells affect 3 cm or more of the esophagus. This condition occurs in about 3 - 7% of GERD patients. It is associated with a more severe condition.
Short-segment BE affects less than 3 cm of the esophagus and is found in about 10 - 17% of GERD patients.

About 10% of patients with symptomatic GERD have BE. In some cases, BE develops as an advanced stage of erosive esophagitis. Some studies suggest that individuals at highest risk for BE are obese white males over the age of 50 with persistent GERD who drink alcohol. However, a number of studies have reported no relationship between alcohol use or being male and overweight with BE. Such studies have also reported no higher risk in smokers or relatives of BE patients. Only the persistence of symptoms suggested a higher risk. Nevertheless, not all patients with BE have either esophagitis or symptoms of GERD.

The true prevalence of BE, in fact, is not entirely clear, since studies suggest that significantly more than half of people with BE have no GERD symptoms at all. BE, then, is likely to be much more prevalent and probably less harmful than is currently believed. (BE that occurs without symptoms can only be identified in clinical trials or in autopsies, so it is difficult to determine the true extent.) Some evidence suggests that the presence of specific immune factors may be involved in determining the development of BE.

The rate of esophageal cancer has been rising steadily at about 2% a year in white men. The American Cancer Society estimates that there will be 15,560 new cases of esophageal cancer and 13,940 deaths from the disease in 2007. Esophageal cancer is also very difficult to cure. The 5-year survival rate for all stages of esophageal cancer is 17% in white patients, and 12% in African-American patients. Most cases of esophageal cancer start with BE, with less than half of the cases developing with any symptoms. Of note, only a minority of BE patients develop cancer. Some evidence suggests that acid reflux may contribute to the development of cancer in BE. Researchers have speculated that exposure to extra acid in people with Barrett's esophagus produces more of an enzyme called NOX5-S, which may put stress on cells, leading to DNA damage.

Evidence suggests that asymptomatic BE is quite common in the general population, and if true, BE would pose far less of a threat than is now believed. (GERD itself poses no significant risk for esophageal cancer. One study reported an annual incidence of 6.5 cancer cases per 10,000 people with regular GERD symptoms.)

Barrett's esophagus is diagnosed using endoscopy, a procedure that involves inserting a tube down the throat so that the physician can view the esophagus.

Monitoring High-Risk GERD Patients. Some experts recommend a one-time screening test for BE using endoscopy in high-risk patients (such as Caucasian overweight men) with chronic GERD.

Monitoring Patients with Barrett's Esophagus for Cancer. Periodic endoscopy is recommended for detecting early cancer in patients who have been diagnosed with Barrett's esophagus. In an important 2002 study, 5-year survival was 73% in BE patients whose cancer was detected with endoscopy screening and was 0% in patients who were not regularly screened.

To date, no treatments can reverse the cellular damage done after Barrett's esophagus has developed, although some procedures are showing promise.

Medications. Some evidence suggests that a combination of proton-pump inhibitors to suppress acid, coupled with anti-inflammatory COX-2 inhibitors, might be a promising approach.

Proton-Pump Inhibitors. Some experts recommend very aggressive treatments to reduce acid reflux using high-dose proton-pump inhibitors. The standard agent has been omeprazole (Prilosec). Newer oral PPIs include lansoprazole (Prevacid), esomeprazole (Nexium), and rabeprazole (Aciphex). Even when drugs relieve symptoms completely, the condition usually recurs within months after the drugs are discontinued. In chronic cases, drugs may need to be taken throughout a patient's life. These agents provide no protection against Barrett's esophagus. Still, there is some evidence that acid reflux may contribute to the development of cancer in BE, although it is not yet known if acid blockers have any protective effects against cancer in these patients.
COX-2 (cyclooxygenase-2) inhibitors reduce inflammation and pain, as do well-known agents such as aspirin and ibuprofen, but COX-2 inhibitors may pose less of a risk for peptic ulcers and bleeding. Some early evidence suggests they may be protective against cancerous changes in patients with Barrett's esophagus. However, Vioxx and Bextra have been withdrawn from the market due to their association with an increased risk of heart attack. Celebrex remains available, but must be used with caution, especially by patients with cardiovascular risk factors. Also, research is mixed on the benefits of NSAIDs for esophageal cancer. Some studies have found that they may decrease the risk of developing or dying from esophageal cancer. However, a 2007 study indicated that a small dose of Celebrex did not prevent the progression of cancer in Barrett's esophagus patients.

Peptic ulcers may lead to emergency situations. Severe abdominal pain with or without evidence of bleeding may indicate a perforation of the ulcer through the stomach or duodenum. Vomiting of a substance that resembles coffee grounds, or the presence of black tarry stools, may indicate serious bleeding.

Procedures to Remove the Mucous Lining. Various techniques or devices have been developed to remove (ablate) the mucous lining of the esophagus. The intention is to remove early cancerous or precancerous tissue and allow regrowth of new and hopefully healthy tissue in the esophagus. Such techniques include photodynamic therapy (PDT) or laser, electrical, or heat probes.

Studies on the use of these ablation techniques combined with aggressive use of proton-pump inhibitors or surgical treatments are very encouraging. Some of these techniques may eventually even offer potential cures. At this time, they can be very effective in removing harmful tissue, although the benefits do not last in all patients. In one study, an average of 5.6 years after anti-GERD surgery and laser treatment, only a third of patients showed no evidence of renewed precancerous cell growth. These procedures also have complications, such as possible problems swallowing, that patients should discuss with their physician.

Esophagectomy. Esophagectomy is the surgical removal of all or part of the esophagus. Patients with Barrett's esophagus, who are otherwise healthy, are candidates for this procedure if endoscopy shows developing cancer. After esophageal removal, in total or in part, a new conduit for foods and fluids must be established to replace the absent esophagus. Alternatives include the stomach, colon, and part of the small intestine called the jejunum. The stomach is the optimal choice.

Diagnosis

If a patient suffers from chronic heartburn, chances are good the patient also has GERD. (Occasional heartburn does not necessarily indicate the presence of GERD.) The following is the general diagnostic approach:

A physician can usually make an easy diagnosis of GERD if the patient finds relief from persistent heartburn and acid regurgitation after taking antacids for short periods.
If the diagnosis is uncertain but the physician still suspects GERD, a drug trial using a proton-pump inhibitor medication, such as omeprazole (Prilosec) identifies 80 - 90% of people with the conditions. This class of medication blocks stomach acid secretion.

Laboratory or more invasive tests, including endoscopy, may be required if the diagnosis is still uncertain, if atypical symptoms are present, if Barrett's esophagus is suspected, or if complications, such as signs of bleeding or difficulty in swallowing, are present. Some of these tests are described below.

A barium swallow radiograph (x-ray) is useful for identifying structural abnormalities and erosive esophagitis (severe inflammation). When taking this test, the patient drinks a solution containing barium, then x-rays are taken. This test can show stricture, active ulcer craters, hiatal hernia, erosion, or other abnormalities. The test cannot reveal mild irritation.

Upper endoscopy, also called esophagogastroduodenoscopy or panendoscopy, is more accurate than a barium-swallow radiograph. It is also more invasive and expensive. It is widely used in GERD, including for identifying and grading severe esophagitis, for periodic monitoring of patients with Barrett's esophagus or for screening people at high risk, or when other complications are suspected. It is also now employed as part of various surgical techniques.

Endoscopy to Diagnose GERD. Endoscopy may be performed either in a hospital or in a doctor's office:

First, the patient should eat nothing for at least 6 hours before the procedure.
The doctor administers a local anesthetic using an oral spray and an intravenous sedative to suppress the gag reflex and to relax the patient.
Next, the physician places an endoscope (a thin flexible plastic tube containing a tiny camera) into the patient's mouth and down the esophagus. The procedure does not interfere with breathing. It may be slightly uncomfortable for some patients; others are able to sleep through it.
Once the endoscope is in place, the tiny camera allows the physician to see the surface of the esophagus and to search for abnormalities, including hiatal hernia and damage to the mucous lining.
The physician performs a biopsy (the removal and microscopic examination of small tissue sections). The biopsy may detect tissue injury indicative of GERD. It may also be used to detect cancer or other conditions, such as yeast (Candida albicans) or viral infections (e.g., herpes simplex and cytomegalovirus). Such infections are more likely to occur in people with impaired immune systems.
Complications from the procedure are uncommon. If they occur, complications are almost always mild and typically include minor bleeding from the biopsy site or irritation where medications were injected.

If a patient has moderate-to-severe GERD symptoms and the procedure reveals injury in the esophagus, usually no further tests are needed to confirm a diagnosis. The test is not foolproof, however. A visual view misses about half of esophageal abnormalities.

Capsule Endoscopy. Capsule endoscopy was first approved for use in 2001. A new version of this pill-sized camera, renamed PillCam, was approved by the FDA in 2004. PillCam reduces the imaging time previously required by the original capsule endoscopy technique. The PillCam capsule contains tiny video cameras on both ends. After the patient swallows the capsule, a series of 2600 color pictures are transmitted to a recording device where they can be downloaded and interpreted by a doctor. A newer version of the PillCam takes 14 frames per second as opposed to the 4 frames per second of the original device. The newer PillCam is superior in visualizing the entire esophagus and in identifying GERD. The entire procedure takes 20 minutes. The capsule is naturally passed through the digestive system within 24 hours. Capsule endoscopy may provide a more attractive and less invasive alternative for patients than traditional endoscopy. However, while capsule endoscopy is useful as a screening device for diagnosing esophageal conditions such as GERD and Barrett's esophagus, traditional endoscopy is still required for gathering tissue samples or removing polyps.

The (ambulatory) pH monitor examination may be employed to determine acid back-up. It is useful when endoscopy has not detected damage to the mucous lining in the esophagus, but GERD symptoms are present. pH monitoring may be used when patients have not found relief from medicine or surgery. The traditional trans-nasal catheter diagnostic procedure involved inserting a tubular probe through the nose and down to the esophagus. The tube was left in place for 24 hours. This test was irritating to the throat, and uncomfortable and awkward for most patients.

A new method, known as the Bravo pH test, uses a small capsule-sized data transmitter that is temporarily attached to the wall of the esophagus during endoscopy. The capsule records pH levels and transmits these data to a pager-sized receiver worn by the patient. Patients can continue their usual diet and activity schedule during the 24 - 48-hour monitoring period. After a few days, the capsule detaches from the esophagus, passes through the digestive tract, and is eliminated through a bowel movement.

Manometry is a technique that measures muscular pressure. It employs a tube containing various openings, which is placed through the esophagus. As the muscular action of the esophagus exerts pressure on the tube in various locations, a computer connected to the tube measures it. It is useful for the following situations:

To determine if a GERD patient would benefit from surgery by measuring pressure exerted by the lower esophageal sphincter muscles (LES).
To detect impaired stomach motility (an inability of the muscles to contract normally), which cannot be surgically corrected with standard procedures.
To determine if impaired peristalsis or other motor abnormalities are causing chest pain in people with GERD who have these symptoms.

Blood and Stool Tests. Stool tests may show traces of blood that are not visible. Blood tests for anemia should be performed if bleeding is suspected.

Bernstein Test. For patients with chest pain in which the diagnosis is uncertain, a procedure called the Bernstein test may be useful, although it is rarely used. A tube is inserted through the patient's nasal passage. Then solutions of hydrochloric acid and saline are administered separately into the esophagus. If the acid infusion causes symptoms and the saline solution does not, then a diagnosis of GERD is established.

Because many illnesses share similar symptoms, careful analysis and consideration of the patient's history is key to an accurate diagnosis. The following are only a few of the conditions that could accompany or resemble GERD.

Dyspepsia. The most common disorder confused with GERD is dyspepsia, which is defined as pain or discomfort in the upper abdomen without heartburn. Specific symptoms may include a feeling of fullness (particularly early in the meal), bloating, and nausea. Dyspepsia can be a symptom of GERD, but does not always occur with GERD. The drug metoclopramide (Reglan) helps stomach emptying and may be helpful for this condition.

Angina and Chest Pain. About 600,000 people come to emergency rooms each year with chest pains. More than 100,000 of these people are believed to actually have GERD. Chest pain from both GERD and from severe angina can occur after a heavy meal. In general, a heart problem is probably not responsible for the pain if it is worse at night and does not occur after exercise. It should be noted that the two conditions often coexist. In fact, there is some theory that in patients with coronary artery disease, acid reflux may actually trigger angina. In such cases, experts believe that acid in the esophagus may activate nerves that temporarily impair blood flow to the heart.

Asthma. Because asthma and GERD commonly occur together, physicians must be sure that each disorder is diagnosed accurately.

Other Diseases. Many gastrointestinal diseases (e.g., inflammatory bowel disease, ulcers, intestinal cancers) can cause GERD, but they are often easily identified, since they have other symptoms and affect other areas of the intestinal tract.

Treatment

Acid suppression continues to be the mainstay for treating GERD. The aim of drug therapy is to reduce the amount of acid present and improve any abnormalities in muscle function of the lower esophageal sphincter (LES), the esophagus, or the stomach.

Most cases of gastroesophageal reflux are mild and can be managed with lifestyle changes and over-the-counter medications and antacids.

Patients with moderate-to-severe symptoms that do not respond to lifestyle measures, or who are diagnosed at a late stage may be started on more or less potent agents depending on their complications at diagnosis. Experts argue, however, about the best way to initiate drug treatment for GERD in most of these patients. The two major treatment options are known as the step-up and step-down approaches:

Step-up. With a step-up drug approach the patient first tries an H2 blocker drug, which is available over the counter. These drugs include famotidine (Pepcid AC), cimetidine (Tagamet HB), ranitidine (Zantac 75), and nizatidine (Axid AR). If the condition fails to improve, therapy is "stepped up" to the more powerful proton-pump inhibitors, usually omeprazole (Prilosec).
Step-down. A step-down approach first uses a more potent agent, most often a proton-pump inhibitor (PPI), such as omeprazole (Prilosec). When patients have been symptom-free for 2 months or longer, they are then "stepped down" to a half-dose. If symptoms do not recur, the drug is withdrawn. If symptoms recur, the patient is put on high-dose H2 blockers. In one study using this step-down approach, 58% of patients remained symptom-free after a year, with 27% not using any medications at all. Some physicians argue that the step-down approach should be used for most patients with moderate-to-severe GERD.

Recent guidelines indicate that PPIs should be the first drug treatment, and that these drugs should be given once a day for approximately 8 weeks. Even when symptoms are completely relieved by medication, they usually return within a few months after drug treatment has stopped. Long-term maintenance may be necessary.

If neither approach relieves symptoms, the physician should look for other conditions. Endoscopy and other tests might be used to confirm GERD and rule out other disorders. In some cases, bile, not acid, may be responsible for symptoms, so that acid-reducing or blocking agents would not be helpful. (Bile is a fluid that is present in the small intestine and gallbladder.)

Surgery may be indicated under certain circumstances:

If lifestyle changes and drug treatments have failed
In patients with other medical complications
In younger people with chronic GERD, who face a lifetime of expense and inconvenience with maintenance drug treatment

Some physicians are recommending surgery as the treatment of choice for many more patients with chronic GERD, particularly since minimally invasive surgical procedures are becoming more widely available, and since only surgery improves regurgitation. Furthermore, persistent GERD appears to be much more serious than was previously believed, and the long-term safety of acid suppression using medication is still uncertain.

Nevertheless, anti-GERD procedures have many complications and high failure rates (ranging from 30% at 5 years to 63% at 10 years) and, as with medications, current surgical procedures cannot cure GERD. About 15% of patients still require anti-GERD medications after surgery. Furthermore, about 40% of surgical patients are at risk for new symptoms after surgery (e.g., gas, bloating, trouble swallowing), with most occurring more than a year after surgery. Finally, evidence -- notably an important 2002 Swedish study -- now strongly suggests that the procedure does not reduce the risk for esophageal cancer in high-risk patients, such as those with Barrett's esophagus. New procedures may improve current results, but at this time patients should consider surgical options very carefully with both a surgeon and their primary doctor.

Prevention

People with heartburn should first try lifestyle and dietary changes. In one study, 44% of patients who experienced symptoms of gastroesophageal reflux disease (GERD) reported improvement after changing their diet. Some suggestions are the following:

Avoid or reduce consumption of foods and beverages that contain caffeine, chocolate, peppermint, spearmint, and alcohol. Both caffeinated and decaffeinated coffees increase acid secretion.
Avoid all carbonated drinks, because they increase the risk for GERD.
Although physicians often advise patients with GERD to cut down on fatty foods, many studies have found no evidence that a low-fat or high-fat meal makes any difference in symptom exacerbation. One small study, however, found that the frequency of GERD symptoms increased with a high-fat compared to a low-fat diet. Better studies are needed to confirm this. In any case, as a rule, it is always wise to avoid saturated fats (which are from animal products), and cut down on all fats if one is overweight.
Choose low-fat or skim dairy products, poultry, or fish. Increasing protein may help strengthen muscles in the muscle valve.
Consume whole-grain products rich in selenium, which may have some protective role against dangerous cell changes in Barrett's esophagus.
Eat a diet rich in fruits and vegetables, although it's best to avoid acidic vegetables and fruits (e.g., oranges, lemons, grapefruit, pineapple, tomatoes).

Patients who have trouble swallowing should avoid tough meats, vegetables with skins, doughy bread, and pasta.

Nearly three-quarters of patients with frequent GERD symptoms have them at night. Patients with nighttime GERD also tend to experience severe pain. It is very important to take preventive measures before going to sleep. Some suggestions for preventing acid reflux at night are as follows:

After meals, take a walk or, at the very least, remain upright.
Avoid bedtime snacks. In general, avoid eating for at least 2 hours prior to bedtime.
When going to bed, try lying on the left side rather than on the right. The stomach is located higher than the esophagus when a person sleeps on the right side, which can put pressure on the lower esophageal sphincter (LES), increasing the risk for fluid back-up.
Sleep in a tilted position to help keep acid in the stomach at night. To do this, raise the bed at an angle using 4- to 6-inch blocks at the head of the bed and use a wedge-support to elevate the top half of the body. (Extra pillows that only raise the head actually increase the risk for reflux.)

A reflux board is prescribed for use in children who have gastroesophageal reflux. A board tilts the child upward while he is lying in bed to prevent the stomach contents from going back into the esophagus and mouth, and possibly into the lungs.

Quitting smoking is essential.
People who are overweight should try to reduce food intake and exercise to lose weight.
People with GERD should avoid tight clothing, particularly around the abdomen.
If possible, GERD patients should avoid nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin, ibuprofen (Motrin, Advil), or naproxen (Aleve), among others. Tylenol (acetaminophen) is a good alternative pain reliever.

Although gum chewing is commonly believed to increase the risk for GERD symptoms, one study reported it might be helpful. Because saliva helps neutralize acid and contains a number of other factors that protect the esophagus, chewing gum 30 minutes after a meal has been found to help relieve heartburn and even protect against damage caused by GERD. Chewing on anything at all can help since it stimulates saliva production.

Medications

Antacids neutralize digestive acids and are the primary drugs for mild symptoms. They are best used alone for relief of occasional and unpredictable episodes of heartburn. They all work by neutralizing the acid in the stomach. They may also stimulate the defensive systems in the stomach by increasing bicarbonate and mucous secretion. Many antacids are available without a prescription and are the first drugs recommended to relieve heartburn and mild symptoms. Despite the many brands, they all rely on various combinations of three basic ingredients: magnesium, calcium, or aluminum.

Magnesium. Magnesium salts are available in the form of magnesium carbonate, magnesium trisilicate, and most commonly, magnesium hydroxide (Milk of Magnesia). The major side effect of magnesium salts is diarrhea. Magnesium salts offered in combination products with aluminum (Mylanta and Maalox) balance the side effects of diarrhea and constipation.

Calcium. Calcium carbonate (Tums, Titralac, and Alka-2) is a potent and rapid acting antacid that can cause constipation. These antacids are actually sources of calcium. There have been rare cases of hypercalcemia (elevated levels of calcium in the blood) in people taking calcium carbonate for long periods of time. This can lead to kidney failure and is very dangerous. None of the other antacids has this side effect.

Aluminum. Aluminum salts (Amphogel, Alternagel) are also available. The most common side effect of antacids containing aluminum salts is constipation. People who take large amounts of antacids that contain aluminum may also be at risk for calcium loss, which can lead to 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.

It is generally believed that liquid antacids work faster and are more potent than tablets, although evidence suggests that they all work equally well. Antacids can interact with a number of drugs in the intestines by reducing their absorption. These drugs include tetracycline, ciprofloxacin (Cipro), propranolol (Inderal), captopril (Capoten), and H2 blockers. Interactions can be avoided by taking the drugs 1 hour before or 3 hours after taking the antacid. Long-term use of nearly any antacid increases the risk for kidney stones.

H2 blockers impede acid production by blocking or antagonizing the actions of histamine, a chemical found in the body that encourages acid secretion in the stomach. They are available over the counter and provide symptom relief in about half of GERD patients. It takes 30 - 90 minutes for them to work, but the benefits last for hours. The drugs are usually taken at bedtime. Some people may need to take them twice a day.

H2 blockers inhibit acid secretion for 6 - 24 hours and are very useful for people who need persistent acid suppression. They may also prevent heartburn episodes in people who are able to predict its occurrence. In some studies, H2 blockers improved asthmatic symptoms in people who have both conditions. A 2001 study suggested, however, that they rarely provide complete symptom relief for chronic heartburn and dyspepsia and they have done little to reduce office visits to physicians for GERD.

Brands. Four H2 blockers are currently available in the U.S.:

Famotidine (Pepcid AC). Famotidine (Pepcid AC, Pepcid Oral) is the most potent H2 blocker. The most common side effect of famotidine is headache, which occurs in 4.7% of people who take it. Famotidine is virtually free of drug interactions, but the FDA has issued a warning on its use in patients with kidney problems.
Cimetidine (Tagamet, Tagamet HB). Cimetidine (Tagamet) is the oldest H2 blocker. It has few side effects; approximately 1% of people taking it will experience mild temporary diarrhea, dizziness, rash, or headache. Cimetidine interacts with a number of commonly used medications, such as phenytoin, theophylline, and warfarin. Long-term use of excessive doses (more than 3 grams a day) may cause impotence or breast enlargement in men. These problems resolve after the drug is discontinued.
Ranitidine (Zantac, Zantac 75, Zantac Efferdose, Zantac injection, Zantac Syrup). Ranitidine (Zantac) interacts with very few drugs. In a recent study, ranitidine provided more pain relief and healed ulcers more quickly than cimetidine in people less than 60 years old, but there was no difference in older patients. A common side effect associated with ranitidine is headache, which occurs in about 3% of the people who take it.
Nizatidine Capsules (Axid AR, Axid Capsules, Nizatidine Capsules). Nizatidine (Axid) is nearly free of side effects and drug interactions. A controlled-release form is proving to help alleviate nighttime GERD symptoms.

Famotidine is excreted primarily by the kidney. This can pose a danger to people with kidney problems. Physicians are now being advised by the U.S. Food and Drug Administration (FDA) and Health Canada to reduce the dose and increase the time between doses in patients with kidney failure. Use of the drug in those with impaired kidney function can affect the central nervous system and may result in anxiety, depression, insomnia or drowsiness, and mental disturbances.

Drug Combinations.

Over-the-counter antacids and H2 blockers: This combination may be the best approach for many people who experience heartburn after eating. Both classes of drugs are effective in relieving GERD, but have different timing. Antacids work within a few minutes but are short-acting, while H2 blockers take longer but have long-lasting benefits. Pepcid AC combined with an antacid (calcium carbonate and magnesium) is now available as Pepcid Complete.
Proton-pump inhibitors and H2 blockers: Physicians sometimes recommend a nighttime dose of an H2 blocker for people who are taking proton-pump inhibitors twice a day. This is based on the belief that adding the H2 blocker will prevent a rise in acid reflux at night. An important 2002 study, however, reported no additional benefits from the nighttime H2 blocker. Some experts recommended an H2 blocker in patients who are on proton-pump inhibitors only to prevent breakthrough symptoms, such as before a heavy meal.

Long Term Complications. In most cases, these agents have good safety profiles and few side effects. H2 blockers can interact with other drugs, although some less so than others. In all cases, however, the physician should be made aware of any other drugs a patient is taking. More research is needed. Anyone with kidney problems should use famotidine only under the direction of a physician.

Concerns and Limitations. Some experts are concerned that the use of acid-blocking drugs in people with peptic ulcers may mask ulcer symptoms and increase the risk for serious complications.

These agents provide no protection against Barrett's esophagus. In fact, of concern are reports that long-term acid suppression with these drugs may cause cancerous changes in the stomach in patients who are infected with H. pylori. Research on this question is still ongoing.

Proton-pump inhibitors (PPIs) suppress the production of stomach acid and work by inhibiting the molecule in the stomach glands that is responsible for acid secretion, which is called the gastric acid pump. According to recent guidelines, initial drug treatment should be with PPIs once daily for about 8 weeks.

The standard agent has been omeprazole (Prilosec), which is now available over the counter without a prescription. Newer prescription oral PPIs include esomeprazole (Nexium), lansoprazole (Prevacid), rabeprazole (Aciphex), and pantoprazole (Protonix).

Studies report significant relief from PPIs in most patients with heartburn. PPIs are effective for healing erosive esophagitis and may also be helpful in patients with chronic laryngitis that is suspected to be caused by GERD. The newer agents provide quicker symptom relief compared to omeprazole. However, a comparison study suggested that, to date, esomeprazole (Nexium) is the only newer oral PPI to show any significant advantage over omeprazole (Prilosec). All PPIs are more effective than the H2 blockers.

In addition to relieving most common symptoms, including heartburn, proton-pump inhibitors also have the following advantages:

They are effective in relieving chest pain and laryngitis caused by GERD.
They may also reduce acid reflux that typically occurs during strenuous exercise.

Patients with impaired esophageal muscular action are still likely to experience acid breakthrough and reflux at night. Proton-pump inhibitors also may have little or no effect on regurgitation or asthmatic symptoms. Some experts believe, however, that they should be the first drugs of choice, even for patients with milder symptoms. At this time, these drugs are recommended for the following patients:

Those with moderate symptoms that do not respond to H2 blockers
Those with severe symptoms
Those who have respiratory complications
Those who have persistent nausea
Those who have esophageal injury

These agents have no affect against non-acid reflux, such as bile back-up.

Adverse Effects. Proton-pump inhibitors may pose the following concerns:

Side effects are uncommon but may include headache, diarrhea, constipation, nausea, and itching.
Proton-pump inhibitors should be avoided by pregnant women and nursing mothers, although recent studies suggest that they do not pose an increased risk of birth defects.
They may interact with certain drugs, such as anti-seizure agents (such as phenytoin), anti-anxiety drugs (such as diazepam), and blood thinners (such as warfarin).
Long-term use of high-dose PPIs may produce vitamin B12 deficiencies, but studies are needed to confirm whether there is any significant risk. High-dose PPIs used over the long-term also may increase the risk of hip fracture in older adults, according to one study.

There is some evidence that acid reflux may contribute to the higher risk of cancer in BE, but it is not yet confirmed whether acid-blockers have any protective effects against cancer in these patients. In fact, the long-term use of proton-pump inhibitors by people with H. pylori may, in theory at least, reduce acid secretion enough to cause atrophic gastritis (chronic inflammation of the stomach). This condition is a risk factor for stomach cancer. To compound concerns, long-term use of PPIs may mask symptoms of stomach cancer and so delay a diagnosis. To date, however, there have been no reports of an increased risk of stomach cancer with the long-term use of these drugs.

Sucralfate (Carafate) protects the mucous lining in the gastrointestinal tract. It seems to work by sticking to an ulcer crater and protecting it from damage due to stomach acid and pepsin. It may be helpful for maintenance therapy in people with mild-to-moderate GERD. Other than constipation, which occurs in 2.2% of patients, the drug has few side effects. Sucralfate interacts with a wide variety of drugs, however, including warfarin, phenytoin, and tetracycline.

Most drugs used for GERD have no effect on non-acid reflux, such as back-up of bile. Baclofen, known as a gamma-amino butyric acid agonist, is commonly used to reduce muscle spasms. Investigators are now showing that it can reduce both acid and non-acid reflux episodes (as much as 70% in one study) and increase LES pressure, an important factor for preventing back-up.

Surgery

The standard surgical treatment for GERD is fundoplication. The goal of this procedure is twofold:

To increase LES pressure and, therefore, prevent acid back-up (reflux)
To repair any present hiatal hernia

There are two primary approaches:

Open Nissen fundoplication (the more invasive technique)
Laparoscopic fundoplication

In general, the overall long-term benefits of these procedures are similar. Some studies report that more than 90% of patients are free of heartburn after the operation and satisfied with their choice, even after 5 years. Fundoplication relieves GERD-induced coughs and some other respiratory symptoms in up to 85% of patients. (Its effect on asthma associated with GERD, however, is unclear.) It may enhance stomach emptying and improve peristalsis in about half of patients. (It may actually cause abnormal peristalsis in about 14% of patients, although in such cases the problem does not appear to be very significant.)

Still, it has other significant limitations and postoperative problems. For example, the results of one 2003 survey suggested that 18% of surgical patients still required anti-GERD medications and 38% had new symptoms (e.g., gas, bloating, trouble swallowing), with most occurring more than a year after surgery. Other studies have reported similar results. Also, fundoplication does not cure GERD. Finally, evidence from a 2002 Swedish study strongly suggests that the procedure does not reduce the risk for esophageal cancer in high-risk patients, such as those with Barrett's esophagus.

Candidates. Fundoplication is recommended for patients whose condition includes one or more of the following:

Esophagitis (inflamed esophagus)
Symptoms that persist or are recurrent in spite of anti-reflux drug treatment
Strictures
Failure to gain or maintain weight (children)

Fundoplication has little benefit for patients with impaired stomach motility (an inability of the muscles to move spontaneously).

The Open Nissen Fundoplication Procedure. Until recently, most fundoplication procedures for GERD have been the 360° Nissen fundoplication. This is called an open procedure because it requires wide surgical incisions.

With this procedure, the physician wraps the upper part of the stomach (fundus) completely around the esophagus to form a collar-like structure.
The collar places pressure on the LES and prevents stomach fluids from backing up into the esophagus.
Open fundoplication requires a 6- to 10-day hospital stay.

Click the icon to see an illustrated series detailing gastroesophageal reflux surgery.

Laparoscopic Fundoplication. The standard invasive fundoplication procedure has been replaced in many cases by a less invasive fundoplication procedure that uses laparoscopy. In the operation:

Tiny incisions are made in the abdomen.
Small instruments and a tiny camera are inserted into tubes, through which the surgeon can view the region.
The surgeon creates a collar using the fundus, although the area is smaller to work with.

When performed by experienced surgeons, the procedure shows results that are equal to those of standard open fundoplication, but with faster recovery time.

Overall, laparoscopic fundoplication appears to be safe and effective in people of all ages, even babies. Laparoscopy is more difficult to perform in certain patients, including those who are obese, who have a short esophagus, or who have a history of previous surgery in the upper abdominal area. It may also be less successful in relieving atypical symptoms of GERD, including cough, abnormal chest pain, and choking. In about 8% of laparoscopies, it is necessary to convert to open surgery during the procedure because of unforeseen complications.

Other Variations. There are now a number of variants of fundoplication procedures. Examples include the following:

Toupet fundoplication employs only a partial wrap, as does a Thal fundoplication. Partial fundoplication procedures may be more effective in patients with poor or no esophageal motility (spontaneous muscle contraction). Those with normal motility may do better with the full-circle wrap.
Others use a very short and "floppy" Nissen full wrap.

Many surgeons report that such limited fundoplications result in earlier feeding and discharge from the hospital and a lower incidence of complications (trouble swallowing, gas bloating, gagging) than the full Nissan fundoplication. A British study, however, reported no significant differences in swallowing problems.

Postoperative Problems and Complications after Fundoplication. Postoperative problems can include a delay in intestinal functioning causing bloating, gagging, and vomiting. These side effects usually resolve in a few weeks. A 2003 study suggested, however, that 38% of patients develop such symptoms, and most occur more than a year after the procedures. If symptoms persist or if they start weeks or months after surgery, particularly if vomiting is present, then surgical complications are likely. Complications include the following:

An excessively wrapped fundus. This is fairly common and can cause difficulty swallowing (dysphagia), as well as gagging, gas, bloating, or an inability to burp. (A follow-up procedure that dilates the esophagus using an inflated balloon may help correct dysphagia, although it cannot treat other symptoms.)
Bowel obstruction
Wound infection
Injury to nearby organs
Respiratory complications, such as a collapsed lung. These are uncommon, particularly with laparoscopic fundoplication.
Muscle spasms after swallowing food. This can cause intense pain, and patients may require a liquid diet, sometimes for weeks. This is a rare complication in most patients, but it can be very high in children with neurologic abnormalities. Such children are already at very high risk for GERD.

Reasons for Treatment Failure. Long-term failure rates after fundoplication are 30% after 5 years and 63% after 10 years. Hiatal herniation is the most common reason for surgical failure and the need for a repeat fundoplication. Other common reasons for reoperation include breakdown, slippage, and excessive tightness of the wrap. Surgeon experience can lessen complication risks. Some studies have reported that repeat operations after open procedures occur in 9 - 30% of cases and 13% after laparoscopy. (Repeat surgery usually has good results.)

A number of treatments that make use of endoscopy are being used or investigated for increasing LES pressure and preventing reflux, as well as for treating severe GERD and its complications.

Transoral Flexible Endoscopic Suturing. Transoral flexible endoscopic suturing (sometimes referred to as Bard's procedure) uses a tiny device at the end of the endoscope that acts like a miniature sewing machine. It places stitches in two locations near the LES, which are then tied to tighten the valve and increase pressure. There is no incision and no need for general anesthesia.

Radiofrequency. Radiofrequency energy generated from the tip of a needle (sometimes called the Stretta procedure) heats and destroys tissue in the problem spots in the LES. Either the resulting scar tissue strengthens the muscle, or the heat kills the nerves that caused the malfunction. Patients may experience some chest or stomach pain afterwards. Few serious side effects have been reported, although there have been reports of perforation, hemorrhage, and even death. A recent study reported that 81% of patients remained symptom-free for up to 3 years following the Stretta procedure.

Implants. In 2003, the FDA approved the Enteryx procedure as a treatment option for people who have persistent symptoms of GERD and who regularly take and respond to PPIs. In 2005, however, the manufacturer of Enteryx (Boston Scientific), voluntarily removed Enteryx from clinical use due to problems related to the difficult injection technique.

Techniques to Stop Bleeding. Endoscopic ablation treatment of bleeding involves using a probe passed through the endoscopic tube, which applies electricity or heat to coagulate blood and stop the bleeding.

Dilation Procedures. Strictures (abnormally narrowed regions) may need to be dilated (opened) with endoscopy. Dilation may be performed by inflating a balloon in the passageway. About 30% of patients who need this procedure require a series of dilation treatments over a long duration in order to fully open the passageway. Long-term use of proton-pump inhibitors may reduce the duration of treatments.

One study also suggested that dilation may help correct swallowing problems that can occur after fundoplication. In the study dilation improved dysphagia in 67% of the surgical patients who had experienced it.

A recent advance is the development of small-caliber upper endoscopy, which does not require sedation and can be performed in the physician's office.

Resources

http://digestive.niddk.nih.gov -- National Digestive Diseases Information Clearinghouse
www.gastro.org -- American Gastroenterological Association
www.acg.gi.org -- American College of Gastroenterology
www.asge.org -- American Society for Gastrointestinal Endoscopy
www.ssat.com -- Society for Surgery of the Alimentary Tract
www.naspgn.org -- North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition
www.reflux.org -- Pediatric/Adolescent Gastroesophageal Reflux Association
www.iffgd.org -- International Foundation for Functional Gastrointestinal Disorders

References

DeVault KR, Castell DO. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. Am J Gastroenterol. 2005;100(1):190-200.

Deviere J, Costamagna G, Neuhause H, Voderholzer W, Louis H, Tringali A, et al. Nonresorbable copolymer implantation for gastroesophageal reflux disease: a randomized sham-controlled multicenter trial. Gastroenterology. 2005;128(3):532-540.

Esposito C, Montupet P, van Der Zee D, Settimi A, Paye-Jaouen A, Centonze A, Bax NK. Long-term outcome of laparoscopic Nissen, Toupet, and Thal antireflux procedures for neurologically normal children with gastroesophageal reflux disease. Surg Endosc. 2006 Jun;20(6):855-8. Epub 2006 May 12. Accessed June 2, 2006.

Gilger MA, Yeh C, Chiang J, Dietrich C, Brandt ML, El-Serag HB. Outcomes of surgical fundoplication in children. Clin Gastroenterol Hepatol. 2004;2(11):978-984.

Gold BD, Schelman JM, Sabesin SM, Vitat P. Updates on the management of upper gastrointestinal disorders in primary care setting:NSAID-related gastropathies and pediatric reflux disease. The Journal of Family Practice. March 2007;56(3):S1-S11.

Hirano I, Richter JE, and the Practice Parameters Committee of the American College of Gastroenterology. ACG practice guidelines: esophageal reflux testing. American Journal of Gastroenterology. 2007;102:668-685.

Kim CY, O'Rourke RW, Chang EY, Jobe BA. Unsedated small-caliber upper endoscopy: an emerging diagnostic and therapeutic technology. Surg Innov. 2006 Mar;13(1):31-9.

Koslowsky B, Jacob H, Eliakim R, Adler SN. PillCam ESO in esophageal studies: improved diagnostic yield of 14 frames per second (fps) compared with 4 fps. Endoscopy. 2006 Jan;38(1):27-30.

Remedios M, Campbell C, Jones DM, Kerlin P. Eosinophilic esophagitis in adults: clinical, endoscopic, histologic findings,and response to treatment with fluticasone propionate. Gastrointest Endosc. 2006 Jan;63(1):3-12.

Rudolph CD, Mazur LJ, Liptak GS, Baker RD, Boyle JT, Colletti RB, et al. Guidelines for evaluation and treatment of gastroesophageal reflux in infants and children: recommendations of the North American Society for Pediatric Gastroenterology and Nutrition. J Pediatr Gastroenterol Nutr. 2001;32 Suppl 2: S1-S31.

Review Date:
5/22/2007
Reviewed By:
Harvey Simon, MD, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital.

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

A.D.A.M. Copyright

The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 for all medical emergencies. Links to other sites are provided for information only -- they do not constitute endorsements of those other sites. © 1997-2010 A.D.A.M., Inc. Any duplication or distribution of the information contained herein is strictly prohibited.

adam.com

Heart attack and acute coronary syndrome

FitSugar — Wed, 08 Oct 2008 17:34:57 -0700

In This Report

Highlights

Introduction

Symptoms

Prognosis

Risk Factors

Diagnosis

Treatment

Medications

Surgery

Rehabilitation

Resources

References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Drug Approval

In 2006, the FDA approved the use of clopidogrel (Plavix) for patients who have had a STEMI heart attack and who will not be having angioplasty. A STEMI is a very severe type of heart attack caused by sudden and total artery blockage.

Angioplasty and Stents

Surgery with angioplasty and stents that is performed more than 3 days after a heart attack offers no advantage over standard drug therapy for clinically stable patients, indicates an important 2006 New England Journal of Medicine study. Experts recommend that this procedure be performed to open blocked arteries within 12 hours of a heart attack.

Drug-Coated Stents

Drug-coated stents may be better than bare metal stents for patients who have had a STEMI heart attack, suggest several New England Journal of Medicine studies. However, recent research has raised concern that these types of stents increase the risk for blood clots.

Patients who have a drug-coated stent must take aspirin and clopidogrel (Plavix) for at least 1 year after the stent is inserted, according to an important 2007 advisory from the American Heart Association (AHA). The combination of these drugs can help prevent blood clots.

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

NSAIDs such as acetaminophen (Tylenol), ibuprofen (Advil) should be used with caution by patients who have had a heart attack:

In 2007, the AHA warned that NSAIDs (with the exception of aspirin) and COX-2 inhibitors increase the risk of heart attack and stroke. The AHA is recommending that doctors change the way they prescribe these pain relievers for patients who have or are at risk for heart disease.

A 2006 Journal of the American Medical Association study suggested that the prescription NSAID diclofenac (Cataflam) carries a higher risk for heart attack than other NSAIDs.

Introduction

The heart is the human body's hardest working organ. Throughout life it continuously pumps blood enriched with oxygen and vital nutrients through a network of arteries to all parts of the body's tissues. In order to perform the arduous task of pumping blood to the rest of the body, the heart muscle itself needs a plentiful supply of oxygen-rich blood, which is provided through a network of coronary arteries. These arteries carry oxygen-rich blood to the heart's muscular walls (the myocardium).

Coronary artery disease is the most common cause of heart attacks. Coronary artery disease is the end result of a complex process called atherosclerosis (commonly called "hardening of the arteries"). This causes blockage of arteries (ischemia) and prevents oxygen-rich blood from reaching the heart. A full-blown heart attack occurs when blood flow to the myocardium is blocked and tissue death occurs from loss of oxygen, severely damaging the heart. The medical term for heart attack is myocardial infarction. [See In-Depth Report #3: Coronary artery disease.]

Click the icon to see an image of atherosclerosis.

Heart attack (or myocardial infarction) is the most serious outcome of atherosclerosis. It can occur as a result of one or two effects of atherosclerosis:

(1) If the artery becomes completely blocked and ischemia becomes so extensive that oxygen-bearing tissues around the heart die.

(2) If the plaque itself develops fissures or tears. Blood platelets adhere to the site to seal off the plaque, and a blood clot (thrombus) forms. A heart attack can then occur if the formed blood clot completely blocks the passage of oxygen-rich blood to the heart.

Click the icon to see an image of an acute myocardial infarction.

Angina is the primary symptom of coronary artery disease and is typically experienced as chest pain. There are two kinds of angina:

Stable Angina is predictable chest pain that can usually be managed with lifestyle measures and medications, such as low-dose aspirin.

Unstable angina is a much more serious situation than stable angina that is often an intermediate stage between stable angina and a heart attack. Unstable angina is part of a condition called acute coronary syndrome.

Acute coronary syndrome (ACS) is a severe and sudden heart condition that requires aggressive treatment, but has not developed into a full blown heart attack. Acute coronary syndrome includes:

Unstable angina. Unstable angina is a much more serious situation than stable angina. It is often an intermediate stage between stable angina and a heart attack.

NSTEMI (non ST-segment elevation myocardial infarction). This condition, also called non Q-wave myocardial infarction, is diagnosed when blood tests and ECGs suggest a developing heart attack. The injury in the arteries is less severe than with a full-blown heart attack.

Symptoms

ANYONE WHO BELIEVES THEY ARE HAVING A HEART ATTACK SHOULD IMMEDIATELY CALL THE EMERGENCY MEDICAL SYSTEM (911 IN THE UNITED STATES).

In people with known heart disease, any unusual chest pain or other symptoms of heart attack that do not clear up with medications are signals to go to the hospital. The degree of pain and the specific symptoms before a heart attack vary greatly among individuals. Onset can be abrupt, gradual, or intermittent.

Chest Pain. People with heart disease or risk factors should be concerned about any chest pain, usually precipitated by exercise or stress, that interrupts normal activities and does not clear up after resting or taking angina medications. Chest symptoms might be experienced as follows:

Pain is typically felt as a crushing weight against the chest, accompanied by profuse sweating. The pain may radiate to the left shoulder and arm, the neck or jaw, and even infrequently to the right arm. The arm may be tingling or numb.

Some people may have only a tingling sensation or a sense of fullness, squeezing, or pressure in the chest.

In some patients with a history of heart disease, chest pain is mild. Such patients may have experienced unexplained fatigue, depression, and ill health within a month of a heart attack.

Although chest pain is the classic symptom, it occurs in only about half of patients with a heart attack.

Other Common Symptoms. Other common symptoms of a heart attack include:

Nausea, vomiting, and cold sweats

A feeling of indigestion or heartburn

Fainting

A great fear of impending death, a phenomena known as angor animi

Uncommon Symptoms. Some studies suggest that nearly half of patients with heart attack do not have chest pain as the primary symptom. Common atypical symptoms of a heart attack include:

Shortness of breath

Cardiac arrest

Dizziness, weakness, and fainting

Abdominal pain

Patients most likely to have atypical symptoms are women and the very elderly (although they can certainly have classic heart attack symptoms as well.)

In one study, 52% of elderly people with acute coronary syndrome had atypical symptoms that included shortness of breath, nausea, profuse sweating, pain in the arms, and fainting. Such symptoms were more likely to occur in people with personal or family history of heart disease.

Before a heart attack, women are more likely than men to be nauseous and experience pain high in the abdomen or chest. Their first symptom may be extreme fatigue after physical activity rather than chest pain. Chest pain in women is also more likely to be caused by non-heart problems than in men.

Symptoms That Are Less Likely to Indicate a Heart Attack. The following are symptoms that are more likely to be due to causes other than a heart event:

Sharp pain brought on by lung movements or coughing

Pain that is mainly or only in the middle or lower abdomen

Pain that can be pinpointed with the top of one finger

Pain that can be reproduced by moving or pressing on the chest wall or arms

Pain that is constant and lasts for hours (although no one should wait hours if they suspect they are having a heart attack)

Pain that is very brief and lasts for a few seconds

Pain that spreads to the legs

The presence of these symptoms, however, does not always rule out a serious heart event.

Chest pain is a very common symptom in the emergency room, but heart problems account for only 10% to a third of all episodes. High on the list of other causes of chest pain are the following:

The most common causes of chest pain are muscular and bone problems. Problems affecting the ribs and chest muscles include injured muscles, fractures, arthritis, spasms, and infections.

Anxiety attacks

Gastrointestinal disorders (gallstone attacks, peptic ulcer disease, hiatal hernia, heartburn)

Asthma

Spasm in the coronary artery

Abnormalities of the heart muscle itself

Rupture of the aorta, collapsed lung, acute inflammation of the heart, or a blood clot in the lung

Hyperthyroidism

Anemia

Vasculitis (a group of disorders that cause inflammation of the blood vessels)

Exposure to high altitudes (rare)

Immediately call 911 or the local emergency number.

If patients have been previously diagnosed with angina, they should take one nitroglycerin dose either as an under-the-tongue tablet or in spray form at the onset of symptoms. They should take another dose every 5 minutes up to three doses or when the pain is relieved, whichever comes first.

It should be noted, however, that only 20% of heart attacks occur in patients with long-standing angina.

Anyone who has heart disease or risk factors for it and experiences heart attack symptoms should immediately contact emergency services.

The patient should chew an aspirin (250 - 500 mg) and be sure that emergency health providers are informed of this so an additional dose is not given.

Patients who experience chest pain should go immediately to the nearest emergency room, preferably traveling by ambulance. They should not drive themselves.

Prognosis

Each year, an estimated 650,000 Americans will suffer a first heart attack, and 450,000 will have a recurrent episode. Currently, half of the men and 63% of the women who died of heart disease had no warning prior to their fatal attacks.

Heart attacks may be rapidly fatal, evolve into a chronic disabling condition, or lead to full recovery. The long-term prognosis for both length and quality of life after a heart attack depends on its severity and the preventive measures taken afterward.

About 88% of patients under age 65 who experience a heart attack can expect to return to work. About 12,600,000 Americans who have had heart attacks, angina, or both are alive today. However, within 6 years of a heart attack, 18% of men and 35% of women have a recurrent attack. And, about 22% of men and 46% of women develop heart failure.

Although no tests can absolutely predict whether another heart attack will occur, experts estimate that up to 30% of fatal attacks, and many follow-up surgeries, could be avoided with healthy lifestyle changes and adherence to medical treatments. Two-thirds of patients who have suffered a heart attack, however, do not take the necessary steps to prevent another.

Higher Risk Individuals. A heart attack is always more serious in certain people:

Elderly (particularly those who are thinner)

People with a history of heart disease or risk factors for heart disease

People with heart failure

People with diabetes

People on long-term dialysis

Women are more likely to die after a heart attack than men. The risk is highest in younger women (although in the younger population, the risk for having a first heart attack and then dying from it is very low). It is still unclear why heart attacks are more severe in this group.

Factors Occurring at the Time of a Heart Attack That Increase Severity. The presence of other conditions during a heart attack can contribute to a poorer outlook:

Arrhythmias (disturbed heart rhythms). A dangerous arrhythmia called ventricular fibrillation is a major cause of short-term death from heart attack. Such arrhythmias are more likely to occur within the first 4 hours and are associated with a high mortality rate. Patients who are successfully treated, however, have the same long-term prognosis as those who do not experience such arrhythmias.

Signs of severe physical damage to the heart may indicate a poorer outlook.

Shock. This very dangerous condition is associated with very low blood pressure, reduced urine levels, and cellular abnormalities. Shock occurs in about 7% of heart attacks. The incidence has not declined over recent years, although its survival rates have improved.

Heart block, also called atrioventricular (AV) block, is a condition in which the electric conduction of nerve impulses to specialized muscles in the heart is slowed or interrupted. Although heart block is dangerous, it can be treated effectively with a pacemaker, and it rarely causes any long-term complications in patients who survive it.

Heart attacks and acute coronary syndrome pose a high risk for stroke. According to a major 2002 study, the risk for stroke after heart attack is 2.5% in the first 6 months and 5% per year thereafter. In the study, patients with a higher risk (about 4%) for stroke within 6 months of a heart attack were older (over age 75), African-American, had a history of stroke, atrial fibrillation, hypertension, diabetes, or peripheral artery disease. Most people who fall into these categories have more than one of these risk factors.

Risk Factors

About 25% of all Americans have one or more risk factors for heart disease, increasing their risk for heart attack. Most risk factors for heart disease are related to lifestyle. Some risk factors, (such as age, gender, and ethnicity) cannot be changed. Nevertheless, overall risks can be reduced with healthy lifestyle changes. [See In-Depth Report #3: Coronary artery disease.]

The American Heart Association's guidelines for preventing heart disease recommend:

Improve Cholesterol. People with at least two risk factors and a 10-year risk for heart disease or stroke of more than 20% should aim for LDL levels of less than 100 mg/dl. Statins are now used in more cases.

Keep Blood Pressure Low. People in normal health should have a blood pressure reading of 120/80 mm Hg or less. According to new guidelines, blood pressure readings of 120/80 are considered normal, readings of 140/90 or higher indicate hypertension, and readings in between the two are called pre-hypertension. Patients with diabetes or chronic kidney disease should maintain blood pressure readings of 130/80 mm Hg or less, while others should be no higher than 140/90 mm Hg.

Exercise. Everyone in normal health should engage in at least moderate physical activity for a minimum of 30 minutes on most -- if not all -- days of the week.

Healthy Diet. Everyone should aim for a diet that contains a healthy balance of fruits, vegetables, grains, fish, nuts, legumes, poultry, lean meat, and low-fat dairy items. Avoid saturated fats and trans-fatty acids.

Quit Smoking. Also avoid exposure to second-hand smoke.

Maintain Weight. People should aim for a BMI index of 18.5 - 24.9.

Take Aspirin. People at high risk for heart disease should take a low-dose aspirin every day, unless they have medical reasons to avoid aspirin.

Control Diabetes. People with diabetes should aim for fast blood glucose levels of less than 110 mg/dl and hemoglobin A1C of less than 7%.

Control Atrial Fibrillation. People with atrial fibrillation should use anticoagulants to reduce the risk for blood clots.

The approach for managing acute coronary syndrome involves lifestyle changes and medications. Experts have come up with a mnemonic device (ABCDE) for remembering the factors that are fundamental for management of acute coronary syndrome:

A. Antiplatelets, anticoagulants, and ACE inhibitors

B. Blood pressure and beta-blockers

C. Cholesterol-lowering drugs (typically statins) and cigarettes (stopping)

D. Diet and diabetes control

E. Exercise and education

Age. About 85% of people who die from heart disease are over the age of 65.

Gender. Coronary artery disease and heart attacks are much more common in middle-aged men. Women have, on average, 10 - 15 more years of heart disease-free life than do men, but as women age, they catch up to men. Women are more likely to have angina than men are. Younger women with heart disease often do not have the same symptoms as their male counterparts and may be less likely to be diagnosed correctly. They are also more likely than men are to die after a heart attack. Evidence suggests that this is because women tend to be older and sicker than men at the time of a first attack. A 2002 study indicated, however, that with early aggressive treatment women with acute coronary syndrome do as well or better than men with the same condition and treatments.

Ethnicity. Of all major ethnic groups, African-American women face the highest risk for death from heart disease, and their rate of heart attacks is increasing. (Mortality rates in men do not differ much by race.) Native American men have a lower risk for heart disease than Caucasian men, and Hispanics have the lowest risk for heart disease of all major American population groups.

Timing of Heart Attack. A 2007 study suggested that patients who are admitted to a hospital on a weekend are less likely to receive aggressive heart attack treatment and less likely to survive than patients who are treated on a weekday. However, no one can predict when a heart attack will occur. The most important point is to get treatment quickly, regardless of the day of the week. And, if you think you having a heart attack, call an ambulance -- or have someone call for you -- to ensure prompt treatment. Do not drive yourself.

Cholesterol. Cholesterol is a white, powdery substance that is found in all animal cells and in animal-based foods (not in plants). In spite of its bad press, cholesterol is an essential nutrient necessary for many functions. However, when certain cholesterol levels rise in the blood, they can have dangerous consequences, depending on the type of cholesterol.

Low-density lipoprotein (LDL) cholesterol is the "bad" cholesterol responsible for many heart problems. Triglycerides are another type of lipid (fat molecule) that can be bad for the heart. High-density lipoprotein (HDL) cholesterol is the "good" cholesterol that helps protect against heart disease. Doctors test for a "total cholesterol" profile that includes measurements for LDL, HDL, and triglycerides. The ratio of these lipids can affect heart disease risk. [See In-Depth Report #23: Cholesterol.]

Cholesterol Goals. In 2004, the National Cholesterol Education Program updated its clinical practice guidelines. The new recommendations set lower treatment goals for LDL levels based on a patient's risk factors for heart disease.

These risk factors include:

Having a first-degree female relative diagnosed with heart disease before age 65 or a first-degree male relative diagnosed before age 55

Being male and over age 45 or female and over age 55

Cigarette smoking

Diabetes

High blood pressure

Metabolic syndrome (risk factors associated with obesity such as low HDL levels and high triglycerides)

Having two or more of these risk factors indicates a greater than 20% chance of having a heart attack within 10 years.

Risk Level
Goal (d/L)

OptimalGoal(d/L)

Very High Risk
70

70

High Risk
100

70

Moderate Risk
130

100

Low Risk
160

130

LDL cholesterol, together with other risk factors for heart disease, is the best determinant for whether cholesterol therapy is needed and whether it is working properly. In particular, the new guidelines emphasize lower LDL levels and earlier treatment for people with coronary artery disease, or other forms of atherosclerosis, and diabetes.

Total Cholesterol Goals

LDL Goals

HDL Goals

Triglyceride Goals

Less than 200 mg/dL is desirable.

Between 200 and 239 is borderline.

Over 240 is high.

70 mg/dL or less is the new goal for very high-risk patients (recent heart attack; current active or unstable cardiovascular or cerebrovascular disease; or two multiple risk factors as defined above.)

Below 100 mg/dl is optimal for everyone. It should be the goal for high-risk people including those with existing heart disease, diabetes, or two or more risk factors for heart disease; 70 mg/dL is an optimal goal for these individuals.

130 mg/dl or below for people with two or more risk factors; 100 mg/dL is the optimal goal.

160 mg/dl or less for people at less risk (one or zero risk factors); 130 mg/dL is an optimal goal.

Anything over 160 is high, with levels over 190 being very high. LDL levels over 190 require medication even with no other cardiac risk factors present.

Levels above 40 mg/dL are desirable; levels above 60 mg/dL are optimal.

Below 150 mg/dL is normal.

150-199 is borderline high.

200-499 is high.

Over 500 is very high.

*Risk factors for heart disease include a family history of early heart problems before age 55 for men (before age 65 for women), smoking, high blood pressure, diabetes, being older (over 45 for men and 55 for women), and having HDL levels below 35 mg/dl. People with two or more of these risk factors may have a 10-year risk of heart attack that exceeds 20%, and may therefore need to aim for LDL levels of 100 mg/dL or below.

Other Lipids. Elevated levels of other fatty molecules (lipids) are also now thought to be important indicators of heart disease risk. Studies are finding an elevated risk for angina and first heart attacks in people with elevated levels of lipoprotein(a), or lp(a). This lipoprotein falls somewhere in density between HDL and LDL and may have some properties that increase the risk for blood clots. Some experts suggest, however, that high levels of lp(a) may merely be markers of late-stage atherosclerosis, not a cause.

High blood pressure, or hypertension, has long been a proven cause of coronary artery disease. Blood pressure is categorized as normal, prehypertensive, and hypertensive (which is further divided as Stage 1 or 2 according to severity). High blood pressure is generally considered to be a blood pressure reading greater than or equal to 140 mm Hg (systolic) or greater than or equal to 90 mm Hg (diastolic). Blood pressure readings in the prehypertension category (120 - 139 systolic or 80 - 89 diastolic) indicate an increased risk for developing hypertension. [See Blood Pressure Ranges table.]

A normal blood pressure reading is 120/80 mm Hg or lower. Most people with high blood pressure should aim for a goal of below 140/90 mm Hg. Patients with certain health problems should aim lower (blood pressure in patients with kidney disease, heart failure, or diabetes should be equal to or lower than 130/80 mm Hg.) [See In-Depth Report #14: High blood pressure.]

Blood Pressure Category

Ranges for Most Adults (systolic/diastolic)

Normal Blood Pressure (systolic/diastolic)

Systolic below 120 mm Hg

Diastolic below 80 mm Hg

Prehypertension (Formerly Classified as Normal to High-Normal Blood Pressure)

Systolic 120 to 139 mm Hg

Diastolic 80 to 89 mm Hg

(NOTE: 139/89 or below should be the minimum goal for everyone. People with diabetes or chronic kidney disease should strive for 130/80 or less.)

Mild Hypertension (Stage 1)

Systolic 140 to 159 mm Hg

Diastolic 90 to 99 mm Hg

Moderate-to-Severe Hypertension (Stage 2)

Systolic over 160 mm Hg and/or

Diastolic over 100 mm Hg

Note: If one of the measurements is in a higher category than the other, the higher measurement is usually used to determine the stage. For example, if systolic pressure is 165 (Stage 2) and diastolic is 92 (Stage 1), the patient would still be diagnosed with Stage 2 hypertension. It should be strongly noted that a high systolic pressure should be a major focus of concern in most adults.

American obesity is at epidemic levels in all age groups. The effect of obesity on cholesterol levels is complex. Although obesity does not appear to be strongly associated with overall cholesterol levels, among obese individuals triglyceride levels are usually high while HDL (beneficial cholesterol) levels tend to be low, both risk factors for heart disease. Obesity, in any case, has other effects (hypertension, increase in inflammation) that pose major risks to the heart.

Obesity is particularly hazardous when it is one of the components of the metabolic syndrome. This syndrome is diagnosed when three of the following are present: abdominal obesity, low HDL cholesterol, high triglyceride levels, high blood pressure, and insulin resistance. Metabolic syndrome is a pre-diabetic condition that is significantly associated with heart disease and higher mortality rates from all causes. A 2002 study estimated that 24% of the population now has this condition. Obesity is highly linked with type 2 diabetes, in any case. And diabetes itself poses a significant risk for high cholesterol levels and heart disease. [See In-Depth Report #53: Weight control and diet.]

People who are sedentary are almost twice as likely to suffer heart attacks as are people who exercise regularly. Exercise has several effects that benefit the heart and circulation, including improving cholesterol and lipid levels, reducing inflammation in the arteries, assisting weight loss programs, and helping to keep blood vessels flexible and open. Studies continue to show that physical activity and avoiding high-fat foods are the two most successful means of reaching and maintaining heart healthy levels of fitness and weight.

Experts have been attempting to define how much exercise is needed to produce heart benefits. In 2002, a well-conducted study on overweight adults confirmed previous research that reported beneficial changes in cholesterol and lipid levels even when people performed low amounts of moderate or high intensity exercise (walking or jogging 12 miles a week). However, more intense exercise is required to significantly change cholesterol levels, notably by increasing HDL (the so-called good cholesterol). Overweight people who have trouble losing pounds can still achieve considerable heart benefits by exercising. Resistance (weight) training has also been associated with heart protection. Exercises that train and strengthen the chest muscles may prove to be very important for patients with angina.

Some studies suggest that people may gain the greatest heart protection benefit from the total daily amount of energy they expend, rather than from the length of a single exercise session. Therefore, the best way to exercise may be in multiple short bouts of intense exercise, which can be particularly helpful for older people.

Sudden strenuous exercise (such as snow shoveling and mowing lawns) can put people at risk for angina and heart attack. Activities that involve raising the arms above the head may also be risky. Patients with angina should never exercise shortly after eating. People with risk factors for heart disease should seek medical clearance and a detailed exercise prescription. And all people, including healthy individuals, should listen carefully to their bodies for signs of distress as they exercise. [See In-Depth Report #29: Exercise.]

Heart disease and stroke are the leading causes of death in people with diabetes. People with diabetes are at risk for the following heart-risk conditions, and the more of these conditions they have, the worse the outlook:

High blood pressure (hypertension) --up to 75% of cardiovascular problems in people with diabetes may be due to hypertension.

Very unhealthy cholesterol and lipid balances (high triglyceride levels and lower high density lipoprotein).

Blood clotting problems.

Impaired nerve function (neuropathy), which can also damage the heart. In fact, some experts estimate that the mortality rates from neuropathy-related heart conditions ranges from 15 - 53%.

Patients with both diabetes and heart disease may have a higher risk for silent ischemia, a condition in which people have blocked arteries but do not experience the angina, the chest pain that signals heart disease [See In-Depth Report #9: Diabetes - type 1 ; or In-Depth Report #60: Diabetes - type 2.]

Smokers in their 30s and 40s have a heart-attack rate that is five times higher than their nonsmoking peers. Cigarette smoking may be directly responsible for at least 20% of all deaths from heart disease, or about 120,000 deaths annually. Smoking cigars may increase the risk of early death from heart disease, although evidence is much stronger for cigarette smoking. Although heavy cigarette smokers are at greatest risk, a 2002 study suggested that people who smoke as few as three cigarettes a day are at higher risk for blood vessel abnormalities that endanger the heart. Regular exposure to passive smoke also increases the risk of heart disease in nonsmokers. [See In-Depth Report #41: Smoking.]

Eating habits can either protect or hurt the heart. Experts generally agree on the following heart-smart recommendations:

Choose fiber-rich food (whole grains, legumes, nuts) as the main source of carbohydrates, along with a high intake of fresh fruits and vegetables.

Avoid saturated fats (found mostly in animal products) and 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, legumes, poultry, and fish over meat. Fat free and low fat dairy products (skimmed milk, yogurt) are also healthy choices.

Controlling weight, quitting smoking, and exercising are essential companions of any diet program.

After starting any heart healthy diet, it generally takes an average of 3 - 6 months before any noticeable reduction in cholesterol occurs, although some people have reported better levels in as few as 4 weeks. An intensive program may be necessary to achieve significant improvements in cholesterol levels and to reduce other heart risk factors. [See In-Depth Report #43: Heart-healthy diet.]

Stress. The effects of mental stress on heart disease are controversial. Stress can affect the heart when it activates the sympathetic nervous system (the automatic part of the nervous system that affects many organs, including the heart). Some studies suggest an association between acute stress and a higher risk for serious cardiac events, such as heart rhythm abnormalities and heart attacks, in people with heart disease. However, not all studies report strong evidence that stress has any effect on the heart, particularly in people without any history of heart disease. [See In-Depth Report #31: Stress.]

Depression. Depression increases the severity of heart attack and may even impair a patient's response to medication for heart disease. Although people with heart disease may certainly become depressed, this does not explain entirely the link between the two problems. The data now suggest that depression itself may be a true risk factor for heart disease as well as its increased severity. Several studies have suggested that depression has biologic effects on the heart, including blood clotting and heart rate. A study in 2001, for example, reported an association between depression and a greater risk for death from heart problems even in people without a history of heart disease. A 2002 study reported a higher risk for heart failure in women -- although not in men -- with depression. The more severe the depression, the more dangerous to the health, although even mild depression, including feelings of hopelessness, experienced over many years, may harm the heart, even in people with no early signs of heart disease. [See In-Depth Report #8: Depression.]

Benefits of Moderate Drinking. Several studies have found heart protection from moderate intake of alcohol (one or two glasses a day). Moderate alcohol consumption can help boost HDL levels. Alcohol may also prevent blood clots and inflammation. Although red wine is most often cited for healthful properties, any type of alcoholic beverage appears to have similar benefit.

Adverse Effects of Heavy Drinking on the Heart. By contrast, heavy drinking harms the heart; heart disease is the leading cause of death in alcoholics. Evidence suggests that people who consume more than three drinks a day have abnormal blood clotting factors. Heavy alcohol consumption can raise blood pressure, and binge drinking may increase the risk for hemorrhagic stroke (caused by bleeding in the brain). Large doses of alcohol can trigger irregular heartbeats, which can be dangerous in people with existing heart disease.

Pregnant women and people who can't drink moderately should not drink at all.

In 2005, the FDA warned that all nonsteroidal anti-inflammatory drugs (NSAIDs) -- with the exception of aspirin -- carry heart risks. NSAIDs and COX-2 inhibitors may increase the risk for death in patients who have experienced a heart attack. The risk is greatest at higher dosages, but not necessarily for length of time. According to a 2006 Danish study of heart attack survivors, patients do not need to take NSAIDs for long periods of time to be at risk.

NSAIDs include nonprescription drugs like ibuprofen (Advil, Motrin) and prescription drugs like diclofenac (Cataflam, Voltaren). Celecoxib (Celebrex) is currently the only COX-2 inhibitor that is available in the U.S. It has been linked to cardiovascular risks such as heart attack and stroke. Patients who have had heart attacks should talk to their doctors before taking any of these drugs.

A 2006 comprehensive report from the U.S. Agency for Healthcare Quality and Research indicated that both NSAIDs and COX-2 inhibitors pose similar risks for heart attacks. The report found that one particular NSAID, naproxen (Aleve, Naprosyn), may present less risk of heart attack for some patients, but other studies have contradicted this finding. A 2006 Journal of the American Medical Association study suggested that diclofenac (Voltaren, Cataflam) poses a higher risk for heart attack than other NSAIDs.

In 2007, the American Heart Association issued a scientific statement encouraging doctors to change the way they prescribe pain relief medication for patients with or who are at risk for heart disease. The AHA recommends that patients first try non-drug methods of pain relief (physical therapy, exercise, weight loss to reduce stress on joints, and heat or cold therapy). If these methods don’t work, patients should take the lowest possible dose of acetaminophen (Tylenol) or aspirin. COX-2 inhibitors, such as celecoxib (Celebrex), should be the last resort.

Anemia. Anemia has adverse effects on the heart and increases the severity of cardiac conditions, including heart failure and heart attacks.

Iron Overload. An inherited disease called hemochromatosis, in which the intestinal tract absorbs too much iron from food, has been associated with atherosclerosis and heart attack. About 10% of Caucasians carry the gene. There is no strong evidence that excess iron levels in people without hemochromatosis can contribute to heart disease.

Sleep Apnea. Obstructive sleep apnea is a condition in which tissues in the upper throat collapse at intervals during sleep, thereby blocking the passage of air. It has been strongly associated with high blood pressure and obesity, but is also associated with heart disease and heart attacks, regardless of these risk factors. Some evidence suggests that obstructive apneas cause an increase in stiffness and inflammation in the arteries.

Pregnancy Complications. Although women of child-bearing age are generally at low risk of heart attack, pregnancy can increase the risk for women with certain health conditions. Pregnant women who have diabetes, high blood pressure, or coronary artery disease are at greater risk of having a heart attack than healthy pregnant women. Smoking can increase the risk of heart attack during pregnancy by eight times. Pregnant women who are over 40 years old are at much greater risk than younger women.

Diagnosis

When a patient comes to the hospital with chest pain, the following diagnostic steps are usually taken to determine any heart problems, and, if present, their severity.

The patient will report all symptoms so that a health professional can rule out either a non-heart problem or possible other serious accompany conditions.

An electrocardiogram (ECG) reading is taken, which records the waves made the heart. It is the key tool for determining if heart problems are causing chest pain and, if so, how severe they are.

Blood tests showing elevated levels of certain factors (troponins and CK-MB) indicate heart damage. (The doctor will not wait for results, however, before administering treatment if a heart attack is strongly suspected.)

Imaging tests, including echocardiogram and perfusion scintigraphy, help rule out a heart attack if there is any question.

An electrocardiogram (ECG or EKG) measures and records the electrical activity of the heart. The waves measured by the ECG correspond to the contraction and relaxation pattern of the different parts of the heart. Specific waves seen on an ECG are named with letters:

P. The P wave is associated with the contractions of the atria (the two chambers in the heart that receive blood from outside).

QRS. The QRS is a series of waves associated with ventricular contractions. (The ventricles are two major pumping chambers in the heart.)

T and U. These waves follow the ventricular contractions.

Click the icon to see an image of a normal sinus rhythm.

Doctors use a term called the P-Q or P-R interval, which is the time taken for an electrical impulse to travel from the atria to the ventricle.

The most important wave patterns in diagnosing and determining treatment for a heart attack are called ST elevations and Q waves.

Elevated ST Segments: Heart Attack. Elevated ST segments are strong indicators of a heart attack in patients with symptoms and other indicators. They suggest that an artery to the heart is blocked and that the full thickness of the heart muscle is damaged. When this finding coincides with a heart attack, the condition is sometimes referred to as either as a Q-wave myocardial infarction or a STEMI (ST-segment elevation myocardial infarction). STEMI heart attacks are very severe and usually have complete artery blockage. ST-elevations are strong indicators for aggressive treatments (thrombolytic drugs or angioplasty) to reopen blood vessels. (ST segment elevations do not always mean the patient has a heart attack. Also, some patients do not have elevated ST segments. Other factors are important in making a diagnosis.)

Non-Elevated ST Segments: Angina and Acute Coronary Syndrome. A depressed or horizontal ST wave suggests some blockage and the presence of a heart disease, even if there is no angina present. It occurs in about half of patients with other signs of a heart event. This finding, however, is not very accurate, particularly in women, and can occur without heart problems. In such cases, laboratory tests are needed to determine the extent, if any, of heart damage. In general, one of the following conditions may be present:

Stable Angina (blood test results or other tests show no serious problems and chest pain resolves). Most patients with angina can go home. (Between 25 - 50% of people who have angina or silent ischemia have normal ECG readings.)

Acute Coronary Syndrome (ACS). This includes severe and sudden heart conditions that require aggressive treatment but have not developed into a full-blown heart attack. ACS, refers to either unstable angina or NSTEMI (non ST-segment elevation myocardial infarction) -- also referred to as non Q-wave myocardial infarction. Unstable angina is potentially serious, and chest pain is persistent, but blood tests do not show markers for heart attack. With NSTEMI, the blood tests suggest a developing heart attack, but most likely, injury in the arteries is less serious than with a full-blown heart attack.

An echocardiogram is a noninvasive test that uses ultrasound images of the heart. This test is more expensive than an ECG, but it can be very valuable, particularly when used with an exercise stress test, to detect the location and extent of heart muscle damage.

Nuclear ventriculography (also known as a radionuclide test) uses radioactive materials called tracers to make heart chambers and blood vessels visible. The procedure is noninvasive. It is a reliable measure of severe heart events and can help identify if damage has occurred from a heart attack. A radioactive isotope such as thallium (or technetium) is injected into the patient's vein. The radioactive isotope attaches to red blood cells and passes through the heart in the circulating blood. The isotope can then be traced through the heart using special cameras or scanners. The images may be combined with an electrocardiogram. The patient is tested while resting, then tested again during an exercise stress test. If the scan detects damage, more images are taken 3 or 4 hours later. Damage due to a prior heart attack will persist when the heart scan is repeated. Injury caused by angina, however, will have resolved by that time.

Angiography is an invasive test. It is used for patients who show strong evidence for severe obstruction on stress and other tests and for patients with acute coronary syndrome.

A narrow tube is inserted into an artery, usually in the leg or arm, and then threaded up through the body to the coronary arteries.

A dye is injected into the tube, and an x-ray records the flow of dye through the arteries.

This process provides a map of the coronary circulation, revealing any blocked areas.

Click the icon to see an image of cardiac catheterization.

Click the icon to see an image of dye injected into the coronary arteries.

Major complications include stroke, heart attacks, and kidney damage. These risks are very low (about 0.1%), however, if the procedure is done in an experienced medical center (one that performs at least 300 of these operations every year). Allergic reactions can also occur. The procedure is expensive, and between 10 - 30% of patients who have this procedure have normal results.

Magnetic Resonance Angiography (MRA). MRA is a very promising noninvasive imaging technique that can provide three-dimensional images of the major arteries to the heart and identify disease with high accuracy. Experts believe this approach will eventually be a good alternative to angiography.

Tests that measure kidney function can help predict which patients are at greatest risk of heart attack, stroke, or death from heart disease. Kidney tests measure proteins in the blood that are filtered through the kidneys. These proteins include creatinine and blood urea nitrogen (BUN). A more recent type of kidney test measures the protein cystatin C. Recent research suggests that the cystatin C kidney test may be better at predicting cardiovascular risks in elderly patients.

When heart cells become damaged, they release different enzymes and other molecules into the blood stream. Elevated levels of such markers of heart damage in the blood or urine may help predict a heart attack in patients with severe chest pain and help determine treatment. Some markers include:

Troponins. The proteins cardiac troponin T and I are released when the heart muscle is damaged. Both are proving to be among the best diagnostic indications of heart attacks. They help to identify many individuals with ACS who might otherwise be misdiagnosed.

Creatine kinase myocardial band (CK-MB). CK-MB has been a standard marker, but the MB fraction is not as accurate as troponin levels, since elevated levels can appear in people without heart injury.

Myoglobin. Myoglobin is a protein found in heart muscles. It is released early in the injured heart and may be useful in combination with CK-MB and the troponins.

Newer biomarkers, including C-reactive protein (CRP), homocysteine, B-type natriuretic peptide (BNP), urinary albumin, and fibrinogen.

Several 2006 studies that evaluated how well biomarkers predict the risk of heart events concluded that they do not provide much more useful information than standard risk factors (high blood pressure, unhealthy cholesterol levels, diabetes). At this time, most experts feel that these standard disease risk factors provide the best predictors of the likelihood of developing coronary artery disease, heart attack, or stroke.

Treatment

Treatment options will depend on whether the patient has angina, acute coronary syndrome, or a full-blown heart attack.

Patients who are diagnosed with acute coronary syndrome (ACS) may be at risk for a heart attack. ACS refers to either unstable angina or NSTEMI (non ST-segment elevation myocardial infarction). Unstable angina is potentially serious and chest pain is persistent, but blood tests do not show markers for heart attack. With NSTEMI, the blood tests suggest a developing heart attack, but most likely, injury in the arteries is less serious than with a full-blown heart attack.

Doctors use a patient's medical history, various tests, and the presence of certain factors to help predict which ACS patients are most at risk for developing a more serious condition. The degree of chest pain itself is not necessarily useful for determining the actual damage in the heart.

Depending on how severe the condition is, the patient is then given either medical treatments or more invasive approaches, such as angioplasty. Some experts believe that even if patients with ACS are only given drug therapy, they should still be transferred to centers equipped for angioplasty.

Early supportive treatments are similar for patients who have ACS or those who have had a heart attack.

Oxygen. Oxygen is almost always administered right away, usually through a tube that enters through the nose. The patient is given aspirin if one was not taken at home.

Medications for Relieving Symptoms.

Nitroglycerin. Most patients will receive nitroglycerin after a heart attack, usually under the tongue. Nitroglycerin decreases blood pressure and dilates the blood vessels around the heart, increasing blood flow. Nitroglycerin may be given intravenously in certain cases (recurrent angina, congestive heart failure, or high blood pressure). Some evidence suggests that intravenous administration may help reduce long-term heart muscle changes that can occur after a heart attack. (Patients with very low blood pressure or severely slow heart rate will not receive nitroglycerin.)

Morphine. Morphine not only relieves pain and reduces anxiety but also dilates blood vessels, aiding the circulation of blood and oxygen to the heart. Morphine can decrease blood pressure and slow down the heart. In patients in which such effects may worsen their heart attacks, other drugs such as meperidine (Demerol) or nalbuphine (Nubain) may be used.

Anticlotting Medications. Appropriate anticlotting medications are started immediately in all patients.

Aspirin (antiplatelet drug) should be taken immediately after a heart attack. It can be either swallowed or chewed, but chewing provides more rapid benefit. If the patient has not taken an aspirin at home, it will be given at the hospital.

Clopidogrel (a stronger antiplatelet drug) is usually given along with other anticlotting drugs. It is sometimes used in place of aspirin.

Heparin (an anticoagulant) is usually given to moderate- to high-risk patients. Low-molecular weight heparin (LMWH), such as enoxaparin, is now recommended over standard heparin. Fondaparinux (Arixtra) is another type of blood thinner that is showing promise for treating patients with STEMI (ST-elevation myocardial infarction), a severe type of heart attack. Fondaparinux may also be better than enoxaparin for patients with acute coronary syndrome (ACS).

Glycoprotein IIb/IIIa inhibitors (antiplatelet drugs), most often tirofiban, are added for patients undergoing angioplasty. These drugs include tirofiban (Aggrastat) and abciximab (ReoPro). They are also beneficial for nonsurgical patients with ACS, notably NSTEMI (non ST-segment elevation myocardial infarction).

After a heart attack, clots form in the injured artery within 4 - 6 hours in 90% of patients. Opening a clotted artery as quickly as possible is the best approach to improving survival.

The standard medical and surgical solutions for opening arteries are:

Angioplasty, also called percutaneous coronary intervention (PCI), is standard procedure for opening the arteries. Coronary artery bypass graft (CABG) is sometimes used as an alternative to angioplasty. Angioplasty should be performed no later than 12 hours after a heart attack.

Thrombolytics are known as blood-clot-busting drugs and are the standard medications used to open the arteries. They are administered as soon as possible in centers where angioplasty is not available or in patients who are not good candidates for angioplasty.

The best candidates for either thrombolytic therapy or angioplasty are:

Adults younger than 75 years old with elevated ST segments or indications of bundle branch block (an ECG reading showing an interruption in the electrical pathway within the heart).

Patients whose symptoms occur within 12 hours of treatment.

Specific Candidates for Emergency Angioplasty. Most patients who meet the criteria for either thrombolytic drugs or angioplasty do better with angioplasty (although only in centers equipped to do this procedure).

Good candidates for angioplasty include:

Elderly patients (including those over age 75) who meet the criteria for both approaches tend to do better with angioplasty than thrombolytic therapy

Patients with diabetes who meet the criteria for both approaches

Patients under age 75 who go into shock, provided that angioplasty can be performed within 18 hours of shock (There is no advantage for patients over 75 who are in shock.)

As with thrombolytic treatments, angioplasty is most effective when performed within 12 hours of symptoms, and the sooner the better. Unfortunately not all communities have centers experienced in the procedure. The experience of the medical center's staff is critical for optimal benefits, and not all surgeons are experienced in angioplasty. However, the procedure is becoming increasingly available, and overall mortality rates are improving over time with angioplasty. Patients or their families should be sure their surgeon has performed at least 75 of these procedures and that the medical center has performed at least 200.

Specific Candidates or Non-Candidates for Thrombolytics. People who meet the criteria for either thrombolytics or angioplasty may benefit from thrombolytic drugs even if they have high-risk conditions such as diabetes, high systolic blood pressure less than 180 mm Hg, or a history of heart attack.

Several studies report that women do worse after thrombolytic therapy. Evidence indicates, however, that they are generally older and have more serious medical conditions when they seek treatment. One study also reported that women were given these drugs an average of 14 minutes later than men were. Women on thrombolytic therapy still do better than those not given these drugs. The bottom line is that thrombolytic therapy is life-saving, and appropriate candidates, regardless of age or gender, should not be denied this therapy.

Thrombolytics should be avoided or used with great caution in the following patients:

People older than age 75 -- a 2000 study suggested that their risk of death was 38% higher than patients in their age group who were not given therapy; a higher risk exists in such older patients even if they are otherwise healthy.

Patients with elevated ST segments whose symptoms have continued beyond 12 hours

Pregnant women

People who have experienced recent trauma (especially head injury) or invasive surgery

People with active peptic ulcers

Patients who have been given prolonged CPR

Current users of anticoagulants

Thrombolytics should not be used in the following patients:

Patients who have experienced any recent major bleeding

Patients with low ST segments

Patients with a history of stroke

Patients with uncontrolled high blood pressure

After a heart attack, the patient may need a number of different medications, depending on their risk factors for a future heart attack:

Beta-blockers reduce the oxygen demand of the heart by slowing the heart rate and lowering arterial pressure. They have been proven to help improve survival in patients who have had a heart attack.

Angiotensin converting enzyme (ACE) inhibitors should be given on the first day to all patients, unless there are medical reasons for not taking them.

Calcium channel blockers may provide relief in patients with unstable angina whose symptoms do not respond to nitrates and beta blockers. They are also useful for patients with Prinzmetal's angina.

Statins. Statins are important cholesterol lowering drugs that are beneficial for patients who have experienced a heart attack. They may also have heart-protective properties that go beyond lowering cholesterol.

Atropine. Atropine may be given for a very low heart rate (bradycardia) or signs of atrioventricular (AV) block, in which electric conduction of nerve impulses to specialized muscles in the heart is slowed or interrupted.

Severely ill patients, particularly those in cardiogenic shock (a dangerous condition that includes a drop in blood pressure and other abnormalities) or with heart failure, will be monitored closely and stabilized. Oxygen is administered, and fluids are given or replaced when it is appropriate to either increase or reduce blood pressure. Such patients may be given dopamine, dobutamine, or both. Other treatments depend on the specific condition.

Heart failure. Intravenous furosemide may be administered. Patients may also be given nitrates, and ACE inhibitors, unless they have a severe drop in blood pressure or other conditions that preclude them. Clot-busting drugs or angioplasty may be appropriate and life-saving in many of these patients, although heart failure patients are less likely to be given these treatments.

Cardiogenic Shock. A procedure called intra-aortic balloon counterpulsation (IABP) is proving to help these patients when used in combination with thrombolytic therapy. IABP involves inserting a catheter containing a balloon, which is inflated and deflated within the artery to boost blood pressure. Left ventricular assist devices and early angioplasty might be considered.

An important study published in 2006 in the Journal of the American Medical Association indicated that early surgical intervention is important for patients who have cardiogenic shock. The study found that patients who had angioplasty or bypass surgery within 6 hours of a heart attack complicated by shock had greatly improved odds for long-term survival compared to patients who received intensive medical therapy with clot-busting drugs.

An arrhythmia is a deviation from the heart's normal beating pattern caused when the heart muscle is deprived of oxygen and is a dangerous side effect of a heart attack. A very fast or slow rhythmic heart rate often occurs in patients who have had a heart attack, and is not usually a dangerous sign.

Premature beats or very fast arrhythmias called tachycardia, however, may be predictors of ventricular fibrillation. This is a lethal rhythm abnormality, in which the ventricles of the heart beat so rapidly that they do not actually contract but quiver ineffectually. The pumping action necessary to keep blood circulating is lost.

Preventing Ventricular Fibrillation. People who develop ventricular fibrillation do not always experience warning arrhythmias, and to date, there are no effective drugs for preventing arrhythmias during a heart attack.

Potassium and magnesium levels should be monitored and maintained.

Intravenous beta-blockers followed by oral administration of the drugs may help prevent arrhythmias in certain patients.

Treating Ventricular Fibrillation.

Defibrillators. Patients who develop ventricular arrhythmias are given electrical shocks with defibrillators to restore normal rhythms. Some studies suggest that implantable cardioverter-defibrillators (ICDs) may prevent further arrhythmias in heart attack survivors of these events who are at risk for further arrhythmias. Patients with ICDs should not take fish oil supplements, as they may increase the risk of ventricular fibrillation.

Antiarrhythmic Drugs. Antiarrhythmic drugs include lidocaine, procainamide, or amiodarone. Amiodarone or another antiarrhythmic drug may be used afterward to prevent future events.

Managing Other Arrhythmias. People with an arrhythmia called atrial fibrillation have a higher risk for stroke after a heart attack and should be treated with anticoagulants such as warfarin (Coumadin). Other rhythm disturbances called bradyarrhythmias (very slow rhythm disturbances) frequently develop in association with a heart attack and may be treated with atropine or pacemakers.

[For more information on atrial fibrillation, ICDs, and pacemakers see In-Depth Report #45: Stroke.]

Medications

Thrombolytic, also called clot-busting or fibrinolytic, drugs are now mainstays in the early treatment of many patients with heart attacks. These drugs dissolve the clot, or thrombus, responsible for causing artery blockage and heart-muscle tissue death.

The standard thrombolytic drugs are recombinant tissue plasminogen activators or rt-PAs. They include alteplase (Activase) and reteplase (Retavase). Both are similar in effectiveness, although reteplase is easier to administer. Tenecteplase (TNKase), a newer drug, can be delivered more rapidly than alteplase, and to date, survival rates are similar. Streptokinase (Kabikinase, Streptase) is sometimes used but is somewhat less effective that the others.

The sooner that thrombolytic drugs are given after a heart attack, the better. The benefits of thrombolytics are highest within the first 3 hours. They can still help if given within 12 hours of a heart attack.

A thrombolytic drug, such as alteplase or tenecteplase, is typically given by IV along with heparin, an anticoagulant drug. (Heparin, like aspirin, cannot destroy existing blood clots but can prevent clots from reforming after they are broken up.) Enoproxin, a form of heparin called low-molecular weight heparin, may be more beneficial than standard heparin.

Other anticlotting drugs are being tested in combination with thrombolytic drugs for emergency treatment following a severe heart attack. Several 2005 studies have indicated that the antiplatelet drug clopidogrel (Plavix) can help prevent arteries from reclosing, and a second heart attack, when given along with aspirin and thrombolytic drugs. The studies evaluated patients who received thrombolytic drugs for treatment of STEMI (severe heart attacks with complete artery blockage).

Hemorrhagic stroke, usually occurring during the first day, is the most serious complication of thrombolytic therapy, but fortunately it is rare. Streptokinase given without heparin poses the lowest risk (although it is also less effective than other regimens in restoring blood flow). In general, the mortality rate from bleeding is only 3 in 1,000 patients treated with thrombolytics, whereas 39 patients in 1,000 would die without these clot-busting drugs. Recent evidence suggests that the survival benefits of thrombolytic therapy, particularly in combination with aspirin, last for years.

Anti-clotting drugs that inhibit or break up blood clots are used at every stage of heart disease. They are generally classified as either antiplatelets or anticoagulants. All anti-clotting therapies carry the risk of bleeding, which can lead to dangerous situations, including stroke.

Anti-platelet Drugs. These drugs prevent formation of blood platelets. Platelets are very small disc-shaped blood cells that are important for blood-clotting.

Aspirin. Aspirin is an antiplatelet drug. It is the most common anti-clotting drug and nearly anyone with heart disease is advised to take it daily in low dose.

Thienopyridines. Clopidogrel (Plavix) and ticlopidine (Ticlid) are thienopyridines, another type of anti-platelet drug.

Glycoprotein IIb/IIIa Inhibitors. These powerful blood-thinning drugs include abciximab (ReoPro), eptifibatide (Integrilin), tirofiban (Aggrastat), and lamifiban. They are administered intravenously in the hospital and are used with angioplasty and stent placement. They are proving to be helpful for ACS patients with NSTEMI (non ST-segment elevation myocardial infarction).

Anticoagulants. Anticoagulants thin blood. They include:

Heparin

Fondaparinux (Arixtra)

Warfarin (Coumadin)

Direct thrombin inhibitors such as argatroban (Novastan), danaparoid (Orgaran), and lepirudin (Refludan)

How Anti-Clotting Drugs Are Used For Heart Attacks. Unlike the thrombolytic (clot-busting) drugs, which are used to break up blood clots during a heart attack, anti-clotting drugs are used to prevent blood clots from forming in the first place. Such drugs are sometimes used along with thrombolytics, immediately after a heart attack, and also as on-going maintenance to prevent a heart attack.

Aspirin is given immediately, and heparin is usually started during or at the end of the thrombolytic infusion.

Clopidogrel (Plavix) is given along with aspirin, heparin, and thrombolytic (“clot busting”) drugs as emergency treatment following a heart attack and to prepare for angioplasty surgery. In 2006, the FDA approved clopidogrel for patients who have had a STEMI heart attack and who are not going to have angioplasty. Clopidogrel is also helpful for patients with acute coronary syndrome. A 2006 study suggested that clopidogrel plus aspirin may not work better than aspirin alone in preventing a first heart attack. However, many studies show that clopidogrel is an important treatment for patients who have already had a heart attack. Clopidogrel and aspirin may reduce the risk of a second heart attack by 30%. The combination of clopidogrel (or ticlopidine) and aspirin is essential for patients who have a drug-eluting stent. In 2007, the American Heart Association recommended that patients with drug-eluting stents take this drug combination for at least 1 year after the stent is inserted to reduce the risks of blood clots.

All of these drugs pose a risk for bleeding. [See In-Depth Report #03: Coronary artery disease.]

Beta-blockers reduce the oxygen demand of the heart by slowing the heart rate and lowering pressure in the arteries. They are effective for reducing deaths from heart disease. These drugs include propranolol (Inderal), carvedilol (Coreg), bisoprolol (Zebeta), acebutolol (Sectral), atenolol (Tenormin), labetalol (Normodyne, Trandate), metoprolol (Lopressor, Toprol-XL), and esmolol (Brevibloc).

Administration During a Heart Attack. The beta-blocker metoprolol is given through an IV within the first few hours of a heart attack to reduce the destruction of heart tissue. However, a study suggests that emergency intravenous use of metoprolol may increase the risk of cardiac shock.

Prevention After a Heart Attack. Beta-blockers taken by mouth are also used on a long-term basis (“maintenance therapy”) after a first heart attack to help prevent future heart attacks.

Side Effects. Beta-blocker side effects include fatigue, lethargy, vivid dreams and nightmares, depression, memory loss, and dizziness. They can lower HDL (“good”) cholesterol. Beta-blockers are categorized as non-selective or selective. Non-selective beta-blockers such as carvedilol and propranolol can narrow bronchial airways. These beta-blockers should not be used by patients with asthma, emphysema, or chronic bronchitis.

Patients should not abruptly stop taking these drugs. The sudden withdrawal of beta-blockers can rapidly increase heart rate and blood pressure. The doctor may want the patient to slowly decrease the dose before stopping completely.

In 2004, the National Cholesterol Education Program issued updated recommendations on how to control cholesterol levels. These guidelines emphasize that patients should lower their LDL (“bad”) cholesterol and recommend that more people take LDL-lowering medication. Lowering LDL cholesterol and raising HDL (“good”) cholesterol can significantly reduce the risk of heart disease. Several different types of drugs (statins, bile-acid binding resins, niacin, and fibrates) are used to treat cholesterol. [See In-Depth Report #23: Cholesterol.]

Statins are the most important of these drugs. Brands include lovastatin (Mevacor), pravastatin (Pravachol), simvastatin (Zocor), fluvastatin (Lescol), atorvastatin (Lipitor), and rosuvastatin (Crestor). A major analysis of over 200 studies found that statins reduced the risk for heart problems by 60% and stroke by 17%. A 2005 review found that the more that statins lower LDL, the more they reduce CAD and other heart disease risks.

An important 2006 study found that aggressive treatment with statins may have the potential to reverse coronary artery disease. In the study, rosuvastatin reduced fatty plaque in the arteries in addition to improving LDL and HDL cholesterol levels. However, a follow-up 2007 study of rosuvastatin indicated that while the drug slowed the rate of atherosclerotic progression, it did not reverse heart disease. Future studies will continue to investigate this issue.

A 2006 review of studies indicated that early, intensive therapy with statins can help reduce the risk of death, unstable angina, and revascularization (surgery to restore blood flow) for patients with acute coronary syndrome. The review indicated that statins work best when they are prescribed within 14 days of hospitalization for acute coronary syndrome. The researchers found that the effect of statins began about 4 months after starting drug therapy and that benefits lasted up to 2 years.

Side effects of statins may include stomach upset, headaches, skin rashes, muscle aches, sexual dysfunction, drowsiness, dizziness, nausea, constipation, and peripheral neuropathy (numbness or tingling in the hands and feet).

The main safety concern with statins is an uncommon condition called myopathy, which can cause muscle and joint pain and possible muscle damage. Doctors will immediately stop statin therapy if myopathy occurs. Patients should talk to their doctor about any unusual muscle discomfort or weakness or if their urine becomes brown-colored. Statins can also affect the liver, particularly at higher doses, so patients taking these drugs should receive regular liver function tests.

Angiotensin converting enzyme (ACE) inhibitors are important drugs for treating patients who have had a heart attack, particularly for patients at risk for heart failure. These drugs are commonly used to treat hypertension and are recommended as first-line treatment for people with diabetes and kidney damage.

ACE inhibitors include captopril (Capoten), ramipril (Altace), enalapril (Vasotec), quinapril (Accupril), benazepril (Lotensin), perindopril (Aceon), and lisinopril (Prinivil, Zestril).

Side Effects. Side effects of ACE inhibitors are uncommon but may include an irritating cough, excessive drops in blood pressure, and allergic reactions. In the past, doctors sometimes avoided giving aspirin to patients who were taking ACE inhibitors because the combination was believed to cause kidney problems. But, a 2005 study of patients with both coronary artery disease and heart failure found that taking aspirin and ACE inhibitor together is safe.

Magnesium has blood-thinning properties and may help open blood vessels. It is important to correct any magnesium deficiencies in patients (such as those who are taking diuretics).

Flu Shots. Influenza vaccinations may help protect patients against another heart attack during flu season.

Antibiotics. Researchers have investigated antibiotics for treating patients with heart disease and past infection of the bacteria Chlamydia pneumoniae. Results from several large-scale clinical trials, published in 2003 in the Journal of the American Medical Association (JAMA) and presented in 2004 at the European Society of Cardiology annual meeting, suggest that antibiotic treatment provides no benefit in preventing heart attack or other cardiac events in patients with coronary artery disease. While it is still possible that C. pneumoniae may play a role in triggering inflammatory responses associated with ACS, antibiotic therapy is no longer considered appropriate for treatment or prevention of heart disease.

Stem Cell Therapy. Researchers are investigating whether infusions of adult stem cells can help improve outcomes in patients who have a heart attack. Results from three small trials, published in 2006 in the New England Journal of Medicine, suggested that stem cell therapy may have some benefits in improving heart function. None of the studies reported treatment complications. Research presented at the 2007 American College of Cardiology annual meeting discussed intravenous stem cell therapy with Provacel (a commercial stem cell preparation). In the small study, patients who received Provacel had fewer adverse events (such as arrhythmia) and improved heart, lung, and overall function compared to patients who received placebo. Patients in the study received a Provacel infusion within 10 days of having a heart attack.

Surgery

Percutaneous coronary intervention (PCI), also called angioplasty, and coronary artery bypass graft surgery are the standard operations for opening narrowed or blocked arteries. They are known as revascularization procedures.

Emergency angioplasty is the standard procedure for heart attacks. It should be performed within 12 hours of a heart attack. Clot-buster drugs can help prevent damage, but must be given with 1 hour of a heart attack.

Coronary bypass surgery is typically used as elective surgery for patients with blocked arteries. It may be used after a heart attack if angioplasty or thrombolytics fail or are not appropriate. It is usually not performed for a few days to allow recovery of the heart muscles.

Click the icon to see an illustrated series detailing a heart bypass surgery.

Percutaneous coronary intervention (PCI), also called angioplasty, involves procedures such as percutaneous transluminal coronary angioplasty (PTCA) that help open the blocked artery. A typical angioplasty procedure involves the following steps:

Click the icon to see an image of an angioplasty.

The cardiologist threads a narrow catheter (a tube) containing a fiber into the blocked vessel.

The cardiologist opens the blocked vessel using balloon angioplasty, in which a tiny deflated balloon is passed through the catheter to the vessel.

The balloon is inflated to compress the plaque against the walls of the artery, flattening it out so that blood can once again flow through the blood vessel freely.

The balloon is inflated to compress the plaque against the walls of the artery, flattening it out so that blood can once again flow through the blood vessel freely.

To keep the artery open afterwards, doctors use a device called a coronary stent, an expandable metal mesh tube that is implanted during angioplasty at the site of the blockage.

Once in place, the stent pushes against the wall of the artery to keep it open. Stenting is improving results in patients with heart attack who have emergency angioplasty. It also significantly prevents reclosure and reduces heart attack rates in patients with ACS.

Experts recommend that appropriate patients receive angioplasty and stenting within 90 minutes after having a heart attack and no later than 12 hours following an attack. Although some hospitals have been performing angioplasty and stenting for up to a month following a heart attack, a landmark 2006 study found that delayed surgical intervention is not helpful for most patients. The Occluded Artery Trial (OAT), published in the New England Journal of Medicine, reported that balloon angioplasty and stenting failed to prevent heart complications in patients who received the procedure 3 – 28 days after a heart attack. The trial compared angioplasty to medications (aspirin, ACE inhibitors, beta-blockers, statins, clopidogrel).

Experts are now recommending delayed angioplasty and stenting only for patients who are unstable or who continue to have chest pain following a heart attack. This procedure may also be appropriate for patients who cannot tolerate beta-blocker drugs, which are commonly prescribed to help improve survival after a heart attack.

Complications occur in about 10% of patients (about 80% within the first day). Serious side effects include heart attack and the need for additional surgery. Best results occur in hospital settings with experienced teams and backup. Women who have angioplasty after a heart attack have a higher risk of death than men.

Reclosure and Blockage During or Shortly after Angioplasty. Reclosure of the artery often occurs during or shortly after angioplasty. A number of anticlotting drugs are used to reduce this risk. Clopidogrel (Plavix) is often given along with aspirin and thrombolytic drugs (such as abciximab) in the days before angioplasty surgery, to help prevent heart attack or stroke following surgery. Research suggests that abciximab (ReoPro) is especially helpful for patients with acute coronary syndrome.

Prevention of Restenosis. Narrowing or reclosing of the artery (restenosis) occurs within a year of angioplasty in many angioplasty patients, often requiring a repeat operation. In restenosis, the narrowing of the artery is usually due to scarring, not blood clots. Drug-eluting stents, which are coated with sirolimus (Rapamune) or paclitaxel (Taxol), can help prevent restenosis. Several 2006 studies indicated that this type of stent may be better than a bare metal stent for patients who have experienced a STEMI heart attack. However, because drug-eluting stents reduce arterial tissue growth, they can increase the risks of blood clots.

In February 2007, the American Heart Association and other professional organization issued an extremely important joint advisory statement. The statement advises that all patients who have drug-eluting stents must continue to take aspirin and clopidogrel (or, rarely,) ticlopidine for at least 1 year after the stent is inserted to reduce the risk of blood clots. Clopidogrel and ticlopidine are thienopyridine drugs that, like aspirin, help prevent blood platelets from clumping together. It is very important that patients who have drug-eluting stents take both aspirin and a thienopyridine drug. If for some reason patients cannot take a thienopyridine drug, they should receive a bare metal stent instead of a drug-eluting stent. [See In-Depth Report #03: Coronary artery disease.]

Click the icon to see an illustrated series detailing balloon angioplasty.

Coronary artery bypass graft surgery (CABG) is the alternative elective procedure to angioplasty for opening blocked arteries in patients with severe angina, particularly those who have two or more blocked arteries. It is a very invasive procedure, however:

The chest is opened, and the blood is rerouted through a lung-heart machine.

The heart is stopped during the procedure.

Segments of veins or arteries taken from elsewhere in the patient's body are fashioned into grafts, which are used to reroute the blood. The blood vessel grafts are placed in front of and beyond the blocked arteries, so the blood flows through the new vessels around the blockage.

Mortality rates with this procedure after a heart attack are much higher (6%) than when it is used electively (1 - 2%). How or when it should be used after a heart attack, then, is controversial. A 2002 study attempted to determine which patients are at highest risk for poor results from CABG after a heart attack. The study found higher risks for women, patients over age 75, and those with heart failure or other severe heart problems.

Rehabilitation

Lifestyle measures, particularly dietary factors, are equally important in preventing heart attacks and must be strenuously adhered to.

Physical rehabilitation is extremely important after a heart attack. It has been associated with a 25% reduction in mortality rates at 3 years. Rehabilitation may include:

Leg exercises may start as early as the first day. The patient usually sits in a chair on the second day, and begins to walk on the second or third day.

Most patients undergo low-level exercise tolerance tests early in their recovery. One study suggests that exercise testing within 3 days after a relatively minor attack may allow patients to go home earlier.

After 8 - 12 weeks, many patients, even those with heart failure, benefit from supervised exercise programs. Health professionals should provide the patient with schedules for low-level aerobic home-activity. Strength (resistance) training is also important. Tai Chi, a Chinese martial art, appears to be very beneficial and safe for people after a heart attack. It should be noted that the risk for serious heart events during rehabilitation is very low.

Patients generally return to work in about 2 months, although timing can vary depending on the severity of the condition.

Sexual activity after a heart attack carries a very low risk and is believed to be safe, particularly in people who had exercised regularly before the attack. In any case, the feelings of intimacy and love that accompany healthy sex can help offset depression, a far greater risk for a future attack.

Major depression affects between 15 - 23% of patients with ACS or heart attacks. Many studies suggest that depression is a major predictor for increased mortality in both women and men. (One reason may be that depressed patients are less likely to comply with their heart medications.)

Psychotherapeutic techniques, especially cognitive behavioral therapies, are very helpful. Doctors have been reluctant to prescribe antidepressant drugs after ACS or a heart attack because older antidepressants tended to have adverse effects on the heart. Newer antidepressants may be safer. Studies on sertraline (Zoloft), one of the selective serotonin reuptake inhibitor (SSRI) antidepressants, have not reported harmful effects for patients who have had a heart attack. It is not yet clear if other SSRIs are equally safe and effective.

Resources

www.nhlbi.nih.gov -- National Heart, Lung, and Blood Institute

www.acc.org -- American College of Cardiology

www.americanheart.org -- American Heart Association

References

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Assmus B, Honold J, Schachinger V, Britten MB, Fischer-Rasokat U, et al. Transcoronary transplantation of progenitor cells after myocardial infarction. N Engl J Med. 2006 Sep 21;355(12):1222-32.

Chou R, Helfland M, Peterson K, Dana T, Roberts C. Comparative Effectiveness and Safety of Analgesics for Osteoarthritis. Comparative Effectiveness Review No. 4. (Prepared by the Oregon Evidence-based Practice Center under Contract No. 290-02-0024.) Rockville, MD: Agency for Healthcare Quality and Research. September 2006.

Crouse JR 3rd, Raichlen JS, Riley WA, Evans GW, Palmer MK, O'Leary DH, et al. Effect of rosuvastatin on progression of carotid intima-media thickness in low-risk individuals with subclinical atherosclerosis: the METEOR Trial. JAMA. 2007 Mar 28;297(12):1344-53. Epub 2007 Mar 25.

Eisenstein EL, Anstrom KJ, Kong DF, Shaw LK, Tuttle RH, Mark DB, et al. Clopidogrel use and long-term clinical outcomes after drug-eluting stent implantation. JAMA. 2007 Jan 10;297(2):159-68. Epub 2006 Dec 5.

Folsom AR, Chambless LE, Ballantyne CM, Coresh J, Heiss G, Wu KK, et al. An assessment of incremental coronary risk prediction using C-reactive protein and other novel risk markers: the atherosclerosis risk in communities study. Arch Intern Med. 2006 Jul 10;166(13):1368-73.

Gislason GH, Jacobsen S, Rasmussen JN, Rasmussen S, Buch P, Friberg J, et al. Risk of death or reinfarction associated with the use of selectivecyclooxygenase-2 inhibitors and nonselective nonsteroidal antiinflammatory drugs after acute myocardial infarction. Circulation. 2006 Jun 27;113(25):2906-13. Epub 2006 Jun 19.

Grines CL, Bonow RO, Casey DE Jr, Gardner TJ, Lockhart PB, Moliterno DJ, et al. Prevention of premature discontinuation of dual antiplatelet therapy in patients with coronary artery stents: a science advisory from the American Heart Association, American College of Cardiology, Society for Cardiovascular Angiography and Interventions, American College of Surgeons, and American Dental Association, with representation from the American College of Physicians. Circulation. 2007 Feb 13;115(6):813-8. Epub 2007 Jan 15.

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Review Date:
4/16/2007
Reviewed By:
Harvey Simon, MD, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital.

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Risk Level	Goal (d/L)	OptimalGoal(d/L)
Very High Risk	70	70
High Risk	100	70
Moderate Risk	130	100
Low Risk	160	130


Total Cholesterol Goals	LDL Goals	HDL Goals	Triglyceride Goals
Less than 200 mg/dL is desirable. Between 200 and 239 is borderline. Over 240 is high.	70 mg/dL or less is the new goal for very high-risk patients (recent heart attack; current active or unstable cardiovascular or cerebrovascular disease; or two multiple risk factors as defined above.) Below 100 mg/dl is optimal for everyone. It should be the goal for high-risk people including those with existing heart disease, diabetes, or two or more risk factors for heart disease; 70 mg/dL is an optimal goal for these individuals. 130 mg/dl or below for people with two or more risk factors; 100 mg/dL is the optimal goal. 160 mg/dl or less for people at less risk (one or zero risk factors); 130 mg/dL is an optimal goal. Anything over 160 is high, with levels over 190 being very high. LDL levels over 190 require medication even with no other cardiac risk factors present.	Levels above 40 mg/dL are desirable; levels above 60 mg/dL are optimal.	Below 150 mg/dL is normal. 150-199 is borderline high. 200-499 is high. Over 500 is very high.
*Risk factors for heart disease include a family history of early heart problems before age 55 for men (before age 65 for women), smoking, high blood pressure, diabetes, being older (over 45 for men and 55 for women), and having HDL levels below 35 mg/dl. People with two or more of these risk factors may have a 10-year risk of heart attack that exceeds 20%, and may therefore need to aim for LDL levels of 100 mg/dL or below.


Blood Pressure Category	Ranges for Most Adults (systolic/diastolic)
Normal Blood Pressure (systolic/diastolic)	Systolic below 120 mm Hg Diastolic below 80 mm Hg
Prehypertension (Formerly Classified as Normal to High-Normal Blood Pressure)	Systolic 120 to 139 mm Hg Diastolic 80 to 89 mm Hg (NOTE: 139/89 or below should be the minimum goal for everyone. People with diabetes or chronic kidney disease should strive for 130/80 or less.)
Mild Hypertension (Stage 1)	Systolic 140 to 159 mm Hg Diastolic 90 to 99 mm Hg
Moderate-to-Severe Hypertension (Stage 2)	Systolic over 160 mm Hg and/or Diastolic over 100 mm Hg
Note: If one of the measurements is in a higher category than the other, the higher measurement is usually used to determine the stage. For example, if systolic pressure is 165 (Stage 2) and diastolic is 92 (Stage 1), the patient would still be diagnosed with Stage 2 hypertension. It should be strongly noted that a high systolic pressure should be a major focus of concern in most adults.