ANKYLOSING SPONDYLITIS

Report #7209; 8/23/97

When a person has severe lower back pain, doctors often order blood tests for arthritis and a genetic marker called HLAB27. Positive tests often lead to a diagnosis of ankylosing spondylitis, an arthritis of the spine.

Most doctors think that ankylosing spondylitis is an autoimmune disease in which a person's immunity is so stupid that it attacks and destroys the joints in his back, rather than just doing its job of protecting a person from infection. However, several recent papers show that ankylosing spondylitis may actually be caused by infection. One recent paper shows that people who have this condition are more likely to have genital infections with mycoplasma, chlamydia and ureaplasma (1). Virtually all patients have changes in their gut similar to those seen in another so-called autoimmune disease called Crohn's disease (2). Other evidence of infection is that sufferers often have high blood levels of IGG and IGA antibodies that the body produces to kill Klebsiella bacteria that normally live in the intestines of healthy people (3,4,5,5A) and that the disease appears to be transmissible (6). The surface structure of Klebsiella contains 2 molecules similar to that of a genetic marker for ankylosing spondylitis called HLA-B27. When the pain is severe, large amounts of Klebsiella are found in stool samples, and those with ankylosing spondylitis often have intestinal ulcers in the end of the small intestine. A low starch diet that reduces the concentration of klebsiella has been reported to alleviate the back pain (7). Another recent study shows that ankylosing spondylitis may be spread from person to person. The next step is to see if long-term treatment with antibiotics, such as doxycycline, azithromycin, metronidazole or a quinolone can be effective in treating ankylosing spondylitis. The disease rarely goes away by itself (12). Please check with your doctor.

By Gabe Mirkin, M.D., for CBS Radio News

1) U Lange, M Berliner, W Weidner, HG Schiefer, KL Schmidt, K Federlin. Ankylosing spondylitis and infections of the male urogenital tract: Exploration of urinary tract infection in correlation to rheumatologic parameters. Zeitschrift Fur Rheumatologie 55: 4 (JUL-AUG 1996):249-255.

2) H Mielants, M Devos, C Cuvelier, EM Veys. The role of GUT inflammation in the pathogenesis of spondyloarthropathies. Acta Clinica Belgica 51: 5 (OCT 1996):340-349.

3) O Makiikola, K Lehtinen, K Granfors. Similarly increased serum IgA1 and IgA2 subclass antibody levels against Klebsiella pneumoniae bacteria in ankylosing spondylitis patients with/without extra-articular features. British Journal of Rheumatology 35: 2 (FEB,1996):125-128.

4) O Ardicoglu, MB Atay, H Ataoglu, N Etiz, H Ozenci. Ig A antibodies to Klebsiella in ankylosing spondylitis. Clinical Rheumatology 15: 6 (NOV1996):573-576.

5) Y Tani, H Tiwana, S Hukuda, J Nishioka, M Fielder, C Wilson, S Bansal, A Ebringer. Antibodies to Klebsiella, Proteus, and HLA-B27 peptides in Japanese patients with ankylosing spondylitis and rheumatoid arthritis. Journal of Rheumatology 24: 1 (JAN 1997):109-114. 5A) O Makiikola, R Hallgren, L Kanerud, N Feltelius, L Knutsson, K Granfors. Enhanced jejunal production of antibodies to Klebsiella and other Enterobacteria in patients with ankylosing spondylitis and rheumatoid arthritis. Annals of the Rheumatic Diseases 56: 7 (JUL 1997):421-425.

6) S Weinreich, J Capkova, B Hoebehewryk, C Boog, P Ivanyi. Grouped caging predisposes male mice to ankylosing enthesopathy. Annals of the Rheumatic Diseases 55: 9 (SEP 1996):645-647.

7) A Ebringer, C Wilson. The use of a low-starch diet in the treatment of patients suffering from ankylosing spondylitis. Clinical Rheumatology 15: Suppl. 1 (JAN 1996):62-66.

8) SGM Meuwissen, JBA Crusius, AS Pena, AJ Dekkersaeys, BAC Dijkmans. Spondyloarthropathy and idiopathic inflammatory bowel diseases. Inflammatory Bowel Diseases 3: 1 (SPR 1997):25-37.

9) K Granfors. Host-microbe interaction in HLA-B27-associated diseases. Annals of Medicine 29: 2 (APR 1997):153-157.

10) H Tiwana, C Wilson, RS Walmsley, AJ Wakefield, MSN Smith, NL Cox, MJ Hudson, A Ebringer. Antibody responses to gut bacteria in ankylosing spondylitis, rheumatoid arthritis, Crohn's disease and ulcerative colitis. Rheumatology International 17: 1 (MAY 1997):11-16. Klebsiella in the pathogenesis of AS and Proteus in RA. The role of Klebsiella in inflammatory bowel disease requires further study.

11) W Kuon, R Lauster, U Bottcher, A Koroknay, M Ulbrecht, M Hartmann, M Grolms, S Ugrinovic, J Braun, EH Weiss, J Sieper. Recognition of chlamydial antigen by HLA-B27-restricted cytotoxic T cells in HLA-B*2705 transgenic CBA (H-2(k)) mice. Arthritis and Rheumatism 40: 5 (MAY 1997):945-954.

12) Y Tani, H Sato, N Tanaka, S Hukuda. Antibodies against bacterial lipopolysaccharides in Japanese patients with ankylosing spondylitis. British Journal of Rheumatology 36: 4 (APR 1997):491-493.

13) KC Mounzer, MJ Dinubile. Prophylactic use of antibiotics and vaccines in patients with rheumatologic disorders. Rheumatic Disease Clinics of North America 23: 2(MAY 1997):259.

14) JT Gran, JF Skomsvoll. The outcome of ankylosing spondylitis: A study of 100 patients. British Journal of Rheumatology 36: 7 (JUL 1997):766-771.

Drug Treatment for Ankylosing Spondylitis

The primary objective of drug therapy for ankylosing spondylitis is to reduce pain, stiffness, and discomfort. Drugs play an important role in the therapeutic process. Currently, there are three major groups of drugs taken as treatment for AS. The first group of drugs is thought to slow the disease process itself and are also known as antirheumatic drugs. Included in this group is sulfasalazine, which has been shown to suppress the activity of the ankylosing spondylitis. However, a drug has not yet been found to improve both systemic disease activity and arrest the development and progression of radiological erosions and ankylosis of the joints (Gran, 1992). The second group of drugs include the non-steroidal anti-inflammatory drugs (NSAIDs), which do not necessarily influence the progression of the disease, but do suppress inflammation. Because reducing the inflammatory process alone does not always change the course of the disease, researchers are led to believe that there are other factors involved in the progression of the disease. This also leads to serious questioning about the role of inflammatory activity in AS. The last group of drugs consists primarily of analgesics and muscle relaxants. These drugs are needed so patients can do required exercises that are necessary to prevent further deformities and disability as well as relieve major discomforts.

Currently, there are many "disease-modifying antirheumatic" drugs under study. There has been much research done on the effects of sulfasalazine treatment in AS patients. Many studies show that treatment of AS with sulfasalazine when compared to placebo treated controls have shown significant improvement in disease management and suppression of disease activity. However, more studies are needed in order to confirm that this drug does in fact have this kind of effect. Because a long term study has not yet been done, the influence of sulfasalazine on the development of erosion and eventual bony ankylosis of the spine and sacroiliac joints is not known (Gran, 1992). Sulfasalazine is widely used because of its ability to reduce the activity of peripheral arthritis in AS patients. Some of the major side effects of sulfasalazine therapy include gastrointestinal discomfort and central nervous system toxicity. Also, there may be fever, skin rash, hepatotoxicity, and leucopenia (an abnormal decrease in white blood cell count) (Gran, 589). These effects usually appear within the first three months of therapy. Other antirheumatic drugs under study include penicillamine and methotrexate. Because penicillamine was only found to be effective in producing marked improvement in the disease course in one patient to date, it is not a recommended drug for AS. Methotrexate is also used in management of the disease. Furthermore, it has been discovered that taking calcium folinate in conjunction with methotrexate significantly decreases the adverse effects of methotrexate therapy (Gran, 1992).

Because drug therapy currently does not have a remedy for bony ankylosis, it is necessary to employ nonsteroidal anti-inflammatory drugs (NSAIDs) for the management of ankylosis spondylitis. Administration of NSAIDs does not change the course of bony ankylosis. NSAIDs only serve to reduce inflammation in affected areas and thus decrease the rate of some disease activity. However, disease activity is not always suppressed and bony ankylosis, nevertheless, occurs. Because of this phenomena, the role of inflammation in the disease process is under question. The primary use of NSAIDs is to reduce musculoskeletal pain and stiffness and swelling in peripheral joints. Some of the primary NSAIDs used for treating AS include: phenylbutazone, indomethacin, naproxen, piroxicam, sulindac, ibuprofen, diclofenac, etodolac, and flurbiprofen. The most significant harmful side effect of treatment of AS by NSAIDs is gastrointestinal toxicity. The most frequent side effects are indigestion, dyspepsia, and gastric ulcers. NSAIDs inhibit prostaglandin synthesis, leading to an increase in production of gastric acids, which in turn leads to gastric ulceration. Thus, it is necessary in many cases to take a prostaglandin analogue (misoprostol or omeprazole) in combination with a NSAID.

In order to make drug treatment in AS patients most effective, it is necessary to administer drugs at strategic times. For instance, since pain and stiffness is usually most severe during the night and early morning, it is wise to take the drug treatment at night before bedtime and once again in the morning (Gran, 1992).

The last group of drugs administered for management of AS include analgesics and muscle relaxants. Because of its toxicity, analgesics should only be employed as an alternative when NSAIDs cannot be tolerated. Analgesics should be used to help relieve pain and allow patients to perform necessary physical exercises. Such analgesics include paracetamol (acetaminophen) and dextropropoxyphene. Paracetamol is the standard drug for reoccurring back pain. It does not have anti-inflammatory properties, but does not cause gastric irritation which is so often associated with use of NSAIDs. These drugs are useful for short term treatment of moderate pain. Because painful muscle spasm is often associated with acute low back pain, using a muscle relaxant in combination with analgesic can help to relieve back pain (Porter, 194).  

Ankylosing Spondylitis has been a disorder that affects men for years. This page is meant to provide basic information and should not be used as a diagnostic tool. Anyone experiencing symptoms should be seen by a licensed medical professional.

What is ankylosing spondylitis?

Ankylosing spondylitis is a form of chronic inflammation of the spine and the sacroiliac joints. The sacroiliac joints are located in the low back where the sacrum (the bone directly above the tailbone) meets the iliac bones (bones on either side of the upper buttocks). Chronic inflammation in these areas causes pain and stiffness in and around the spine. Over time, chronic spinal inflammation (spondylitis) can lead to a complete cementing together (fusion) of the vertebrae, a process called ankylosis. Ankylosis causes total loss of mobility of the spine.
Ankylosing spondylitis is also a systemic rheumatic disease. Therefore, it can cause inflammation in other joints away from the spine, as well as other organs, such as the eyes, heart, lungs, and kidneys. Ankylosing spondylitis shares many features with several other arthritis conditions, such as psoriatic arthritis, reactive arthritis, and arthritis associated with Crohn's disease and ulcerative colitis. Each of these arthritic conditions can cause disease and inflammation in the spine, other joints, eyes, skin, mouth, and various organs. In view of their similarities and tendency to cause inflammation of the spine, these conditions are collectively referred to as "spondyloarthropathies." For more information, please read the following articles; Psoriatic Arthritis, Reactive Arthritis, Crohn's Disease and Ulcerative Colitis.

Ankylosing spondylitis is 2-3 times more common in males than in females. In women, joints away from the spine are more frequently affected than in men. Ankylosing spondylitis affects all age groups, including children. The most common age of onset of symptoms is in the second and third decades of life.

What causes ankylosing spondylitis?

The tendency for developing ankylosing spondylitis is believed to be genetically inherited, and the majority (nearly 90%) of patients with ankylosing spondylitis is born with the HLA-B27 gene. Blood tests have been developed to detect the HLA-B27 gene marker, and have furthered our understanding of the relationship between HLA-B27 and ankylosing spondylitis. The HLA-B27 gene appears only to increase the tendency of developing ankylosing spondylitis, while some additional factor(s), perhaps environmental, are necessary for the disease to appear or become expressed. For example, while 7% of the United States population has the HLA-B27 gene, only 1% of the population actually has the disease ankylosing spondylitis. In Northern Scandinavia (Lapland), 1.8% of the population has ankylosing spondylitis while 24% of the general population has the HLA-B27 gene. Even among HLA-B27 positive individuals, the risk of developing ankylosing spondylitis appears to be further related to heredity. In HLA-B27 positive individuals who have relatives with the disease, their risk of developing ankylosing spondylitis is 12% (6 times greater than for those whose relatives do not have ankylosing spondylitis). How inflammation occurs and persists in different organs in ankylosing spondylitis is a subject of active research. The initial inflammation may be a result of an activation of body's immune system by a bacterial infection. Once activated, the body's immune system becomes unable to turn itself off, even though the initial bacterial infection may have long subsided. Chronic tissue inflammation resulting from the continued activation of the body's own immune system in the absence of active infection is the hallmark of an autoimmune disease.



What are the symptoms of ankylosing spondylitis?

The symptoms of ankylosing spondylitis are related to inflammation of the spine, joints, and other organs. Inflammation of the spine causes pain and stiffness in the low back, upper buttock area, neck, and the remainder of the spine. The onset of pain and stiffness is usually gradual and progressively worsens over months. Occasionally, the onset is rapid and intense. The symptoms of pain and stiffness are often worse in the morning, or after prolonged periods of inactivity. The pain and stiffness are often eased by motion, heat and a warm shower in the morning. Because ankylosing spondylitis often affects patients in adolescence, the onset of low back pain is sometimes incorrectly attributed to athletic injuries in younger patients.
Patients who have chronic, severe inflammation of the spine can develop a complete bony fusion of the spine (ankylosis). Once fused, the pain in the spine disappears, but the patient has a complete loss of spine mobility. These fused spines are particularly brittle and vulnerable to breakage (fracture) when involved in trauma, such as motor vehicle accidents. A sudden onset of pain and mobility in the spinal area of these patients can indicate bone fracture. The lower neck (cervical spine) is the most common area for such fractures.

Chronic spondylitis and ankylosis cause forward curvature of the upper torso (thoracic spine), limiting breathing capacity. Spondylitis can also affect areas where ribs attach to the upper spine, further limiting lung capacity. Ankylosing spondylitis can cause inflammation and scarring of the lungs, causing coughing and shortness of breath, especially with exercise and infections. Therefore, breathing difficulty can be a serious complication of ankylosing spondylitis.
Patients with ankylosing spondylitis can also have arthritis in joints other than the spine. Patients may notice pain, stiffness, heat, swelling, warmth, and/or redness in joints such as the hips, knees, and ankles. Occasionally, the small joints of the toes can become inflamed, or "sausage" shaped. Inflammation can occur in the cartilage around the breast bone (costochondritis) as well as in the tendons where the muscles attach to the bone (tendinitis) and ligament attachments to bone. Some patients with this disease develop Achilles tendinitis, causing pain and stiffness in the back of the heel, especially when pushing off with the foot while walking up stairs.

Ankylosing Spondylitis
Other areas of the body affected by ankylosing spondylitis include the eyes, heart, and kidneys. Patients with ankylosing spondylitis can develop inflammation of the iris, called "iritis." Iritis is characterized by redness and pain in the eye, especially when looking at bright lights. Recurrent attacks of iritis can affect either eye. In addition to the iris, the ciliary body and choroid of the eye can become inflamed and this is referred to as uveitis. Iritis and uveitis can be serious complications of ankylosing spondylitis that can damage the eye and impair vision, and may require an eye specialist's (ophthalmologist) urgent care. Special treatments for serious eye inflammation are discussed in the treatment section below. [It should be noted that iritis and inflammation of the spine can occur in other forms of arthritis such as reactive arthritis (formerly Reiter syndrome), psoriatic arthritis, and the arthritis of inflammatory bowel disease.]

A rare complication of ankylosing spondylitis involves scarring of the heart's electrical system, causing an abnormally slow heart rate. A heart pacemaker may be necessary in these patients to maintain adequate heart rate and output. The part of the aorta closest to the heart can become inflamed, resulting in leakage of the aortic valve. These patients can develop shortness of breath, dizziness, and heart failure.
Advanced spondylitis can lead to deposits of protein material called amyloid into the kidneys and result in kidney failure. Progressive kidney disease can lead to chronic fatigue and nausea and can require removal of accumulated blood poisons by a filtering machine (dialysis).

How is ankylosing spondylitis diagnosed?

The diagnosis of ankylosing spondylitis is based on evaluating the patient's symptoms, a physical examination, x-ray findings, and blood tests. Symptoms include pain and morning stiffness of the spine and sacral areas with or without accompanying inflammation in other joints, tendons, and organs. Early symptoms of ankylosing spondylitis can be very deceptive, as stiffness and pain in the low back can be seen in many other conditions. It can be particularly subtle in women, who tend to (though not always) have more mild spine involvement. Years can pass before the diagnosis of ankylosing spondylitis is even considered.
The examination can demonstrate signs of inflammation and decreased range of motion of joints. This can be particularly apparent in the spine. Flexibility of the low back and/or neck can be decreased. There may be tenderness of the sacroiliac joints of the upper buttocks. The expansion of the chest with full breathing can be limited because of rigidity of the chest wall. Severely affected persons can have a stooped posture. Inflammation of eyes can be further evaluated with an ophthalmoscope.
Further clues to the diagnosis are suggested by x-ray abnormalities of the spine and the presence of the blood test genetic marker, the HLA-B27 gene. Other blood tests may provide evidence of inflammation in the body. For example, a blood test called the sedimentation rate is a nonspecific marker for inflammation throughout the body, and is often elevated in conditions such as ankylosing spondylitis. Urinalysis is often done to look for accompanying abnormalities of the kidney as well as to exclude kidney conditions that may produce back pain that mimics ankylosing spondylitis. Patients are further evaluated for symptoms and signs of other related spondyloarthropathies, such as psoriasis, venereal disease or dysentery (reactive arthritis or Reiter's disease), and inflammatory bowel disease (ulcerative colitis or Crohn's disease).

What are treatment options for ankylosing spondylitis?

The treatment of ankylosing spondylitis involves the use of medications to reduce inflammation or suppress immunity, physical therapy, and exercise. Medications decrease inflammation in the spine, and other joints and organs. Physical therapy and exercise help improve posture, spine mobility and lung capacity.

Aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs) are commonly used to decrease pain and stiffness of the spine and other joints. Commonly used NSAIDs include indomethacin (Indocin), tolmetin (Tolectin), sulindac (Clinoril), naproxen (Naprosyn), and diclofenac (Voltaren). Their common side effects include stomach upset, nausea, abdominal pain, diarrhea, and even bleeding ulcers. These medicines are frequently taken with food in order to minimize side effects.

In some patients with ankylosing spondylitis, inflammation of the spine and other joints may not respond to NSAIDs alone. In these patients, the addition of sulfasalazine (Azulfidine) may bring about long-term reduction of inflammation.

Oral or injectable corticosteroids (cortisone) are potent anti-inflammatory agents and can effectively control spondylitis and other inflammations in the body. Unfortunately, corticosteroids can have serious side effects when used on a long-term basis. These side effects include cataracts, thinning of the skin and bones, easy bruising, infections, diabetes, and destruction of large joints, such as the hips.

For persistent ankylosing spondylitis which is unresponsive to antiinflammatory medications, agents that suppress body immunity are considered. Methotrexate (Rheumatrex, Trexall) can be administered orally or by injection. Frequent blood tests are performed during methotrexate treatment because of its potential for toxicity to the liver, which can even lead to cirrhosis, and toxicity to bone marrow, which can lead to severe anemia. Recently, medications that block a messenger protein of inflammation (called TNF) have been shown to be very effective for treating ankylosing spondylitis. Examples of TNF-blockers include etanercept (Enbrel) and infliximab (Remicade).

Physical therapy for ankylosing spondylitis includes instructions and exercises to maintain proper posture. This includes deep breathing for lung expansion, and stretching exercises to improve spine and joint mobility. Since ankylosis of the spine tends to cause forward curvature, patients are instructed to maintain erect posture as much as possible and to perform back extension exercises. Patients are also advised to sleep on a firm mattress and avoid the use of a pillow in order to prevent spine curvature. Ankylosing spondylitis can involve the areas where the ribs attach to the upper spine as well as the vertebral joints, thus limiting lung breathing capacity. Patients are instructed to maximally expand their chest frequently throughout each day to minimize this limitation.

Ankylosing Spondylitis
Exercise programs are customized for the individual patient. Swimming is preferred, as it avoids jarring impact of the spine. Ankylosing spondylitis need not limit a patient's involvement in athletics. Patients can participate in carefully chosen aerobic sports when their disease is inactive. Aerobic exercise is generally encouraged as it promotes full expansion of the breathing muscles and opens the airways of the lungs.
Inflammation and diseases in other organs are treated separately. For example, inflammation of the iris of the eyes (iritis or uveitis) may require cortisone eye drops (pred forte) and high doses of cortisone by mouth. Additionally, atropine eye drops are often given to relax the muscles of the iris. Sometimes injections of cortisone into the affected eye are necessary when the inflammation is severe. Heart disease in patients with ankylosing spondylitis may require a pacemaker placement or medications for congestive heart failure.
Cigarette smoking is strongly discouraged in patients with ankylosing spondylitis, as it can accelerate lung scarring and seriously aggravate breathing difficulties. Occasionally, patients with severe lung disease related to ankylosing spondylitis may require oxygen supplementation and medications to improve breathing.

Patients may need to modify their activities of daily living and adjust features of the work-place. For example, workers can adjust chairs and desks for proper postures. Drivers can use wide rear-view mirrors and prism glasses to compensate for the limited motion in the spine.
Finally, patients who have severe disease of the hip joints and spine may require orthopedic surgery.
What is in the future for patients with ankylosing spondylitis?

Ankylosing spondylitis and each of the spondyloarthropathies are areas of active research. The relationship between infectious agents and the triggering of chronic inflammation is vigorously being pursued. Factors that perpetuate "auto-immunity" are being identified. The characteristics of the gene marker HLA-B27 are being further defined. In fact, there are now known to be seven different subtypes of HLA-B27. Results of ongoing research will lead to a better understanding and treatment of the group of diseases collectively known as spondyloarthropathies.

Ankylosing Spondylitis

PATIENT INFORMATION

The word ANKYLOSING means stiffening and SPONDYLITIS means inflammation of the spine. As the name implies ANKYLOSING SPONDYLITIS is a condition that results in progressive stiffening of the spine due to inflammation in the joints between the vertebrae. The inflammation also affects the sacroiliac joints situated on either side of the sacrum. It affects males more than females and occurs most commonly between the ages of 15 and 35 years. The initial symptoms are those of stiffness and low grade back pain which is worst first thing in the morning. it could affect any part of the spine, i.e. the lumbar, the thoracic, and the cervical spine. Apart from the spine the thoracic cage is also frequently affected by the inflammation and consequent pain and stiffness.

The pain results from the inflammation and is a feature early in the illness. The stiffness results from fibrosis which occurs when inflammation has gone on for some time, a stage called fibrous ankylosis. Such stiffening could be prevented and relieved by regular movement of the areas involved. If this is not done, the fibrous tissue contracts increasing the stiffness, leading to deformity with stooping posture in the spine and eventually gives way to calcification and bone formation called bony ankylosis. At this stage, the stiffness and deformity are fixed and cannot be mobilised.

The most important aspect of management is regular mobilising exercises to all parts of the spine and the thoracic cage, in order to prevent fibrous ankylosis and most of all bony ankylosis. If started early and continued regularly, i.e. every day, the result is excellent with little restriction of movement or deformity. These exercises have to be done irrespective of the patient's lifestyle as they make sure that every part of the spine is mobilised.

Sometimes we also include exercises to the shoulders and the hips which are the most frequently involved joints outside the spine.

Swimming is a good sport for patients with spondylitis as it moves the shoulders and hips. On the other hand, prolonged periods of immobilisation such as sitting continuously for long periods, or being confined to bed for a number of days are things that one should, as far as possible, refrain from if one has spondylitis.

The anti-inflammatory medication that may be prescribed contributes to relieving the pain and inflammation but is not a substitute for the regular exercise programme.

Further information can be obtained from the UK National Ankylosing Spondylitis Association

Please send your comments or questions to: Penny J. Gilmer, Ph.D. Professor, Department of Chemistry, Florida State University, Tallahassee, FL 32306-4390 gilmer@sb.fsu.edu.
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