Inclusion Body Myositis


Site presented by Bill Tillier.


■ 1. Overview.  

■ 2. Complications/Comorbidities

■ 3. Diagnosis and Treatment.

■ 4. Causes and Research.

4.2.5 Current IBM Research.  

■ 5. Physical adaptation.  

■ 6. Psychological aspects.  

■ 7. Further resources.  

■ Website Miscellaneous:

Search the site.

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■ 1. Overview.

▣ 1.1 Introduction.

⧈ 1.1.1 The disease.

 Inclusion Body Myositis (IBM) is a rare disease that comes on very slowly, attacking muscles, damaging and weakening them; primarily focused on the muscles in the arms and legs. It is poorly understood, very complicated, and hard to diagnose. It has no known cause and is chronic and progressive. It appears that IBM may be a type of autoimmune disorder. No effective treatment has been developed. It is a disease associated with aging—it is usually seen after the age of 50. In the past it has been commonly known as sporadic inclusion body myositis (sIBM). This disease occurs spontaneously—it just strikes "out of the blue" and is not inherited: it is not passed on to subsequent generations.

⧈ 1.1.2 This web page.

⚀ This webpage begins with section 1, giving a broad overview of what IBM is. Section 2 presents the common complications seen as IBM progresses and some other diseases that commonly occur along with IBM. Section 3 briefly mentions diagnosis and treatment, linking to videos from Johns Hopkins that give excellent descriptions. Section 4 includes an overview of the theories proposed to explain why IBM occurs—no cause or treatment has yet been discovered. Section 4 also includes a fairly scientific overview of the latest research on IBM that is intended more for doctors than patients. Section 5 looks at the physical accommodations and adaptations often required as IBM progresses. Section 6 (still under development) looks at the psychological aspects of dealing with a chronic, progressive, and debilitating illness like IBM. Finally, section 7 presents links that will take you to further explanations, discussions, and resources. There is a tremendous amount of information on this webpage and my suggestion is that you need to slowly work your way through it.

  This page is a good starting point for a person interested in IBM and contains information suitable to take to a family physician.

  The site provides two levels of information:

□ Basic introductions aimed at the IBM patient, his or her family, and caregivers;

□ Selected research on IBM intended for physicians.

  This webpage mentions several things several times, this reflects the fact that these things are important.

⧈ 1.1.3 About me.

⚀ I was a psychologist working for the government when, at age 40, I began to trip and fall. Then I noticed weakness in my hands and knees. After a three-year process of diagnosis, it was determined that I had IBM, and I retired on disability—that was in 2002. I had done a lot of research as part of my job, and when I got my diagnosis, I reviewed everything I could on IBM and created the webpage you are now reading. I try to help other patients with IBM to keep a realistic and positive outlook. This is always difficult when dealing with a chronic and debilitating disease without treatment.

▣ 1.2 Key information for new patients. If you have been diagnosed with inclusion body myositis here is what you need to know to begin with.

⧈ 1.2.1 General.

 This is an extremely rare, serious, and challenging disease.

 The disease strikes people later in life, usually developing after age 40. Most people develop IBM between the ages of roughly 50 and 70.

 Of every hundred patients, roughly 67 will be men, and 33 will be females.

 A survey done on IBM by the Yale School of Public Health found that over 91% of respondents indicated that they lived in their own house or apartment, versus 2.4% reporting that they lived in a relative's residence, 2.8% reporting that they lived in an assisted living facility and 3.3% reporting that they live somewhere different.

 Although people may feel the disease goes up and down, research has shown that it does not and slowly marches on.

⧈ 1.2.2 Impact on muscles.

 IBM is a disease that strikes and weakens the muscles. Not all muscles are impacted; for example, the heart is not affected. It does not affect the nerves.

 Over time, the disease will progress and get worse and worse. As more and more muscle cells are affected, the muscle becomes weaker and weaker, and more and more function is lost.

 As patients get older, they may need more and more help to accomplish the day-to-day functions of life like getting up in the morning, showering, going to the bathroom, eating, etc.

 The disease affects different people in different ways, and at different rates, so you cannot compare yourself with others.

□ Different muscle groups are affected at different rates.

□ The rate at which the disease progresses varies widely in patients.

□ The disease starts in different people at different ages.

□  It is clear that severity varies widely—there are very mild cases and, as well, there are very severe cases.

□ For some reason, the impact of IBM seems to be different in males versus females and as well, differs based on the age when you developed symptoms.

 In most cases, the muscles of the arms and legs are affected first, and weakness in the hands and tripping are common first symptoms.

 The disease usually leads to severe disability and often necessitates using a wheelchair.

 A common serious complication is weakness in swallowing (dysphagia) that can cause choking or aspiration (taking food into the lungs), causing pneumonia (sometimes a cause of death). Swallowing involvement is a critical factor that should be investigated after an IBM diagnosis.

 Another serious complication is respiratory impairment caused by weakness of the diaphragm. Respiratory involvement is a critical factor that should be investigated after an IBM diagnosis. Respiratory dysfunction can be identified, treated, and monitored.

 Depending on how you are affected, you will face various challenges:

□ If the disease affects your arms, you will have problems picking up objects and using your fingers.

□ If the disease affects your legs, you will have trouble falling, climbing stairs, etc.

□ If the disease affects your throat, you may have trouble swallowing.

□ If the disease affects the breathing muscles, you may have problems getting enough air, especially at night (which may cause chronically high carbon dioxide levels in the blood).

 An illustration, shown below, is helpful (after Greenberg, 2019).


⧈ 1.2.3 Cause of IBM.

 Doctors have not discovered what causes IBM.

 Over the past 50+ years, doctors have struggled to describe the disease accurately.

 Doctors don't understand what type of disease it is; many agree that it is an autoimmune disease. However, other doctors disagree.

 Two theories: IBM is either an autoimmune or degenerative disorder of the muscle.

 Recent research on the immune system's involvement strongly suggests that IBM is an autoimmune disorder. However, for some reason, drugs used to treat other autoimmune disorders are ineffective against IBM.

 Examination of muscle tissues under the microscope reveals that the muscle cells have been invaded by T cells, a type of white blood cell involved in the immune response against viruses and other pathogens.

 IBM does not appear to be directly genetic (it is not passed on to children); however, it seems genetics creates a predisposition to developing the disease.

⧈ 1.2.4 Diagnosis.

 Because the condition comes on very slowly, it may take years to notice that you are ill and seek help. You and those around you may attribute the symptoms to simply getting old.

 The diagnosis of this disease is challenging, and many patients describe going to many doctors. On average, it takes five years to arrive at a diagnosis.

 Doctors often mistake inclusion body myositis for a different disease called polymyositis, or, often, Amyotrophic lateral sclerosis (ALS).

⧈ 1.2.5 Treatment.

 Doctors have not developed any treatments that have been proven to slow down or stop the disease.

 The most effective thing you can do is watch for, and manage, complications and prevent injuries due to falls.

 Exercise programs specifically developed for each patient are now being recommended.

 Many companies sell stem cells, different diets, or supplements, but no research shows these are helpful.

⧈ 1.2.6 Impact on lifespan.

 If you have IBM, it tends to shorten your life by an average of three years compared to the population. Statistically, the median age of death is 84 compared to 87.5 in the population (Naddaf et al., 2021; Shelley et al., 2021).

 Shelley et al. (2021) found that when death could be attributed to IBM, it was predicted by three factors; the presence of dysphagia, being female and having a diagnosis after age 67.

 The most common causes of death in IBM patients are complications due to respiratory failure and aspiration pneumonia.

 Ongoing monitoring and awareness of dysphagia and respiratory involvement are highly recommended to the patient and their physicians.

⧈ 1.2.7 Classification of IBM.

⧈ 1.2.8  Blood tests in IBM.

⧈ 1.2.9 Possible confusion over:

⚀ Heart attacks:

□ One of the effects of the breakdown of muscle caused by IBM is that chemicals are released in the blood. These chemicals include Cardiac Troponin T (cTnT) and creatine kinase (CK). The problem arises when a patient with IBM is given a blood test and these chemicals appear raised, this has traditionally indicated a heart attack. If the doctor does not know that IBM leads to raising these levels, it can cause confusion that the patient has had, or is having, a heart attack.

⚀ Liver tests:

□ IBM may cause elevated levels of the liver enzymes, for example, aldolase, alanine transaminase (ALT) and aspartate transaminase (AST). These enzymes are released into the blood by damaged liver cells, so high levels of ALT and AST may be a sign of liver disease. Again, if the doctor does not know that IBM leads to raising these levels, it can cause confusion that the patient has liver issues.

⚀ Statin-induced muscle disease:

□ A rare side effect of the use of statin medications is a muscle disease called Statin-induced immune-mediated necrotizing myopathy (IMNM), also known as reductase (anti-HMGCR) myopathy. This is an inflammatory myopathy that is not the same as IBM. See: Statins and IBM. Also see: 2021 open access article.

⚀ Inclusion body myositis versus Hereditary inclusion body myopathy: see

⧈ 1.2.10 Brief History of IBM: A few highlights.

⧈ 1.2.11 How common is IBM?/IBM and aging.

⧈ 1.2.12 Genetics of IBM.

⚀ Genetic predisposition.

⚀ Familial IBM (fIBM)

□ Familial IBM refers to rare cases where (typical) IBM is seen in two or more patients within a single generation in a family.

□ The symptoms and features of fIBM are very similar to those seen in IBM. The familial occurrence of such a rare disorder likely highlights the importance of genetic predisposition in the causation of IBM.

⚀ Hereditary inclusion body myopathy (hIBM).

▣ 1.3 Recent reviews.

⧈ 1.3.1 A comprehensive review article – September 2022 (open).

⧈ 1.3.2 A 2022 review article from MDA.

⚀ As a pdf download.

⧈ 1.3.3 A 2021 review article (open).

▣ 1.4 Common questions.

▣ 1.5 Several introductory videos from the Johns Hopkins Myositis Center.

⧈ 1.5.1 Disease Overview.

⧈ 1.5.2 Signs & Symptoms.

⧈ 1.5.3 Lifestyle Options.

▣ 1.6 Bill's Information pages.

⧈ 1.6.1 An information page for patients, family and caregivers. (PDF).

⧈ 1.6.2 An information page to take to your family doctor. (PDF).

⧈ 1.6.3 Questions to ask your doctor. (PDF).


■ 2. Complications / Comorbidties.  


■ 3. Diagnosis and Treatment:

▣ 3.1 Diagnosis.

⧈ 3.1.1 Overview. Diagnosis. It is well known that diagnosing muscle conditions is challenging and especially IBM, because it is quite rare, and because the symptoms it presents are often quite varied.

⚀ This webpage will not focus on diagnosis. Diagnosis of IBM is a long, complicated process usually involving seeing several doctors and having numerous tests done. It is counterproductive to try to diagnose yourself using web pages or information from the Internet. Diagnosis is a job for medical specialists.

⚀ After going through the process myself and talking to other patients, the best advice I can give is that you must be patient and keep advocating for yourself. Diagnosis is not "black-and-white," and it is important not to give up as you move through the process. The average case takes five years to diagnose, and initially, incorrect diagnoses are often made. Be clear in your descriptions of your symptoms, keep good records and remember that a correct diagnosis is essential as it maps out what to expect in the future.

⚀ More information on the diagnosis of IBM can be found here: Johns Hopkins Medicine

⧈ 3.1.2 Diagnosis video from the Johns Hopkins Myositis Center.

▣ 3.2 Treatment.

⧈ 3.2.1 Overview. Based upon research, no treatment is recognized as effective for IBM (as of 2022). Based upon their experience and opinions, doctors may try medications with IBM patients however, this is a clinical judgment where any possible benefits must be weighed against potential side effects.

⧈ 3.2.2 Treatment video from the Johns Hopkins Myositis Center.

⧈ 3.2.3 A recent (2021) review article on treatment.

⚀ Summary: Thus far, no treatment for IBM has demonstrated a definite therapeutic effect, and effective treatment options in clinical practice are lacking. Trial design and ineffective therapies are likely to have contributed to these failures. Future studies should use a stratified approach and sensitive and relevant outcome measures to identify potential therapeutic targets.

⚀ Reference: Snedden, A. M., Lilleker, J. B., & Chinoy, H. (2021). In pursuit of an effective treatment: The past, present and future of clinical trials in inclusion body myositis. Current Treatment Options in Rheumatology. https://doi.org/10.1007/s40674-020-00169-4 (if you click on this link it will show you the article that you can then download)

⧈ 3.2.4 The best approach is to manage the complications that may arise from the disease. Evaluation of swallowing and respiration are critical, ongoing issues. Prevention of falls is an important consideration.

⧈ 3.2.5 "Standard of care for most patients with IBM involves strictly nonpharmacological management, including emotional support, physical therapy, education on fall precautions and exercise." From: Greenberg, 2019.

⧈ 3.2.6 "Currently, no evidence is available to support any specific treatment in clinical practice. To date, there are no effective or approved treatment options for inclusion body myositis" From: Hanna et al., 2019.

⧈ 3.2.7 Also see: Needham, M., & Mastaglia, F. L. (2016). Sporadic inclusion body myositis: A review of recent clinical advances and current approaches to diagnosis and treatment. Clinical Neurophysiology, 127(3), 1764-1773. https://doi.org/10.1016/j.clinph.2015.12.011

⧈ 3.2.8 Exercise in inclusion body myositis.

⚀  Also see: Exercise in Place—Myositis Support and Understanding (MSU)

⧈ 3.2.9 A cautionary note. There is a strong tendency for both doctors and patients to "want to do something"—anything—to try to slow down or reverse the symptoms of a major debilitating and chronic illness like IBM. For patients, it can be very frightening and frustrating to simply "do nothing." Caution must be used when no significant benefits of treatment can be demonstrated and when treatments all have significant potential side effects.


■ 4. Causes and Research.

▣ 4.1 Causes.

⧈ 4.1.1 After nearly 50 years of research, the basic causes of IBM remain unknown. There is no general consensus within the research community concerning the basic causes of inclusion body myositis. It appears that multiple factors work together to cause IBM (it is "a multifactorial disorder"). It is also very complicated to determine if an effect causes the disease or, if the effect is caused by the disease.

⧈ 4.1.2 Basic summary: A report prepared by Steven Greenberg for the National Organization for Rare Disorders gives a succinct overview of the causes of IBM.

      The cause of sIBM is unknown and complex. Researchers believe multiple immunological, genetic and environmental factors and factors related to aging all play a role in the development of the disorder. Researchers have identified two distinct processes – one autoimmune and one degenerative – that occur in individuals with sIBM. It appears likely that autoimmunity drives the disease and accounts for the minor “degenerative” pathological changes seen in sIBM skeletal muscle.
Numerous factors support that sIBM is an autoimmune disorder, especially the presence of certain inflammatory white blood cells in the muscle tissue of affected individuals. Autoimmune disorders occur when the body’s immune system mistakenly attacks healthy tissue. The inflammatory findings associated with sIBM led to it to be classified as an autoimmune inflammatory muscle disease along with other prominent inflammatory muscle diseases such as dermatomyositis and polymyositis. The identification of an autoantigen (NT5C1A) has confirmed IBM’s status as an autoimmune disease. However, sIBM, like a number of other autorimmune diseases, has not responded to some of the conventional therapies normally used to treat autoimmune disorders suggesting that distinct factors account for its refractory nature. In particular, cytotoxic T cells in sIBM muscle are highly differentiated and their phenotype overlaps with those of T cells in T-cell large granular lymphocytic leukemia, a similarly refractory disease.
In addition to the inflammatory process, researchers have emphasized that some muscle tissue of individuals with sIBM shows degenerative changes. Specifically, the muscle tissue of affected individuals sometimes contains sub-cellular compartments called vacuoles. These compartments have been reported to contain abnormal clumps of many different proteins. These clumps, often called “inclusion bodies”, give the disorder its name. This significant degenerative component has led some researchers to argue that sIBM is primarily a degenerative muscle disorder and not an inflammatory one. However, these changes are seen in other refractory autoimmune diseases (e.g., Sjogren syndrome and primary biliary cholangigits) and appear to be reflective of chronic exposure of tissues to highly T cell rich inflammatory environments. It is unknown what triggers or underlies the inflammatory or degenerative changes that characterize sIBM, a feature shared by all other autoimmune diseases.
Some individuals with sIBM may have a genetic predisposition that makes them more susceptible to developing sIBM. A genetic predisposition means that a person may carry a gene for a disease but it may not be expressed unless something in the environment triggers the disease. [Greenberg from the NORD Webpage] LINK

⧈ 4.1.3 Basic theories. Over the years, three major theories have been proposed to explain IBM. (presented in the order of likelihood based on contemporary research)

⚀ IBM appears to be an autoimmune disease: this disease damages the muscle cells and also causes protein abnormalities.

□ In autoimmune diseases, in response to some unknown cause, the immune system begins to produce antibodies that attack the body's tissues. Normally, the immune system is triggered by some foreign invader (like a virus), which causes the production of antibodies designed to attack and kill the invader. In autoimmune diseases, immune defenses attack normal body tissues. Common examples are rheumatoid arthritis, lupus, Type 1 diabetes, and Sjögren's syndrome. Treatment for autoimmune diseases generally focuses on reducing immune system activity.

□ For some reason, the medications that normally reduce the activity of the immune system have not improved the symptoms of IBM.

□ IBM is often also associated with other autoimmune disorders; commonly Sjögren's syndrome and rheumatoid arthritis.

□ The families of patients with IBM also often have various other autoimmune disorders (for example, Crohn's disease, rheumatoid arthritis, autoimmune hepatitis, lupus, etc.).

□ See: IBM as an autoimmune disease.

⚀ That something causes degeneration in the cells of the muscle. There are often holes seen in the muscle (vacuoles) and inclusion bodies of abnormal proteins (predominantly containing amyloid and TDP-43) although, it has not been shown that these bodies are responsible for the degeneration.

⚀ An older theory was that a virus is the cause, however, no virus has yet been clearly linked to causing IBM.

⧈ 4.1.4 More ideas on causes.

⚀ Over the years, abnormalities associated with part of the cell called the mitochondrion have been implicated and recent research has emphasized this aspect (see De Paepe, 2019).

⚀ It is possible that a yet undiscovered factor is the cause or trigger.

⚀ Until the basic causes are discovered, a specific treatment will remain elusive.

▣ 4.2 Research.

⧈ 4.2.1  Summary: Naturally, there is an overlap between causes and research. At this stage, research is primarily focused on finding the cause. Research also looks at trying to apply existing medications in clinical trials to see if they will help patients with IBM. I believe that this quotation from 2017 remains a good summary of the situation: "For the past two decades, the field of IBM research has been split with some researchers suggesting that IBM pathogenesis begins with inflammation leading to myodegeneration and others favouring a primary degenerative myopathy stimulating autoimmunity. Now with emerging therapies aimed at targeting muscle degeneration and other therapies focused on immune modulation, it is essential to understand the connection between these two pathologies. A siloed approach that ignores one or the other will not advance future therapeutics. Instead, additive therapies or dual acting therapies that focus on both aspects of disease pathogenesis will likely need to be employed."
From: http://doi.org/10.1111/nan.12384

⧈ 4.2.2 Trends: Many researchers seem to favour the idea that IBM is an autoimmune disorder. "Evidence that IBM is an autoimmune disease includes the presence of predisposing immunogenetic risk factors, a large number of antibody-secreting plasma cells within IBM muscle tissue, and the frequent occurrence of autoantibodies recognizing the NT5C1A protein in the blood of patients with IBM. Furthermore, the observation that cytotoxic CD8 + T cells surround and invade muscle fibres in IBM muscle specimens provided early evidence that muscle damage could be mediated by T cells. Indeed, subsequent studies revealed that CD8 + T cells are clonally expanded in muscle tissue and that the same clones are found in both blood and multiple muscles from the same patient, where they persist. Although the T cell targets remain unknown, these findings suggest that T cell stimulation by the relevant auto-antigen persists for years in these patients. Interestingly, some of the T cell clone identities are shared between different patients with IBM, suggesting a common as yet undefined target auto-antigen among those with IBM. Importantly, studies showed that both CD4+ and CD8 + T cells in patients with IBM have unusual properties, including aberrant loss of CD28 or CD5 expression with the gain of CD16, CD94 and CD57 expression that is associated with terminally differentiated T cells. Phenotypically similar to the abnormal lymphocytes seen in patients with T cell large granulocytic leukaemia, the infiltrating T cells in IBM would also be expected to have increased cytotoxic potential and resistance to apoptosis. These features may help explain why IBM is refractory to glucocorticoids and other immunomodulatory therapies but this population of T cells could also be a promising target for therapeutic intervention."
"In addition to the invasion of myofibres by CD8+ CD57+ T cells, IBM muscle specimens are notable for rimmed vacuoles and protein inclusions within muscle fibres. For example, in one study, aggregates of p62 and TDP43 proteins were found in 12 percent of IBM myofibres but only rarely in those of other IIM subtypes. Although other reports suggest that p62 accumulation may be a non-specific feature of IIM, TDP43 positivity is recognized as highly specific for IBM. Hence, IBM might have a considerable degenerative component, but it has not been shown whether the accumulation of these proteins would lead to muscle cell degeneration. Furthermore, it remains unclear whether these changes occur in response to intensive immune-mediated damage or reflect some other underlying non-immune pathological process." (Lundberg et al., 2021).

⧈ 4.2.3 General Muscle Research.

⚀ Muscles are very complex systems and research into their basic structures and functions continues.

⚀ The causes of some muscle diseases (like IBM) are unknown and in turn, few specific treatments are available. Until more specific treatments are developed, researchers are looking into trying to develop general approaches to enhance muscle function.

⚀ If researchers could boost muscle function it might be possible to offset the effects of the different muscle diseases. Even a small increase in function could be significant to the patient having one of these illnesses.

⚀ In normal muscle, there is a mechanism to stop muscle growth. Without this inhibitory system, muscle growth could go unchecked. Researchers are trying to take advantage of this inhibitory system. If this system could be short-circuited, then more muscle growth would occur. The basic goal is to have the body produce more muscle than normal. The underlying muscle disease will not be treated, but with more muscle being produced, the overall impact of the disease may be reduced. Even small gains might be significant for the affected patient.

⚀ An example of a general approach to increase muscle growth is a drug called Bimagrumab. This drug has been used to try to produce more muscle in various conditions. A report says it's safe to use but did not appear to work in IBM: See: (Hanna et al., 2019).

⧈ 4.2.4 IBM Research.

⚀ Research specifically focused on IBM attempts to understand what causes the disease and how it unfolds.

⚀ Most research on the treatment of IBM has looked at using existing medications and examining their impact on IBM. Generally speaking, no medication has shown significant improvements in IBM patients (see above).

⚀ Summary: IBM is a very complex and challenging disease to research. Much has been learned about the disease, but frustratingly, more remains unknown. The understanding of IBM and its causes is a very slowly evolving phenomenon.

⧈ 4.2.5 Current IBM Research.

⧈ 4.2.6 Past research.

⧈ 4.2.7 Functional assessment of IBM.


■ 5. Physical adaptation.


■ 6. Psychological aspects.    


■ 7. Further resources.

▣ 7.1 A key resource: Myositis Support and Understanding (MSU)

▣ 7.2 A key resource: The Myositis Association.

▣ 7.3 A brochure from the Myositis Association of America. (PDF).

▣ 7.4 Selections from Outlook (TMA).

▣ 7.5 IBM in Images.

▣ 7.6 Other Relevant Webpages:

⧈ 7.6.1 Web sites for IBM Information:

 Muscular Dystrophy Association (USA). LINK.

 Cure IBM is dedicated to inclusion body myositis awareness, education, and research. LINK.

 National Organization for Rare Disorders (NORD) LINK.

 Peter Frampton. LINK.

 IBM overview: LINK.

 Muscular Dystrophy UK IBM overview:
IBM Alert Card: LINK.

 National Institute of Neurological Disorders and Stroke (NINDS) site on IBM:. LINK.

 Washington University School of Medicine in St. Louis, MO, IBM Specialty Clinic devoted to inclusion body myositis. LINK.

 Wikipedia entry: LINK.

 IBM Facebook pages:

    □ IBM Facebook Page #1 (open):

    □ IBM Facebook Page #2 (membership):

 Clinical Trials for IBM:

    □ You can find information on the latest clinical trials on IBM by going to this website and entering inclusion body myositis on the search line: NIH Clinical Trials: http://clinicaltrials.gov/

 Yale IBM Registry: Yale IBM Registry.

 Webpage credibility.

  Jerry King's youtube IBM channel. (This is not my website).

  Seven warning signs of bogus science. (This is not my website).


▣ Website Miscellaneous:

⧈ How to Use PDF files:

 Note: some of the PDF files on this site are large and take considerable time to open. PDF files are like a photocopy of an article. You need to install a PDF reader (many computers already have one installed). If you click on a PDF file and have a reader, it will open automatically. If you need to install a reader, it is easy. You can get a free reader download at: http://get.adobe.com/reader/

⧈ Mission Statement:

 There are many excellent web sites that present information on various neuromuscular disorders. When I looked at the web, I was struck by how scattered the information was and how much of the information was very technical. Therefore, the primary intention of this site is to help integrate different sources and provide background to help the reader cope with complex medical jargon and methods. I am not trying to be comprehensive, and I do not want to be redundant and present information already covered elsewhere.

⧈ Disclaimer:

 I am not a medical doctor and this information is not intended to be read as medical advice nor is it a substitute for medical advice. Please consult your physician if you have medical concerns. I have done my best to offer a layman's interpretation of this material. Any opinions offered are personal and do not reflect those of my employer. Thanks.

⧈ Contact: For comments or improvements, please contact Bill at bill.tillier@gmail.com

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⧈ Page Created: April 06, 2001.