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Disease/ Disorder


A variety of muscle diseases affect the adult and elder population.

These conditions are:

  • Sarcopenia
  • Myosteatosis, which is the accumulation of fat within skeletal muscle including intermuscular adipose tissue, intramuscular tissue, and intramyocellular lipids.1
  • Idiopathic inflammatory myopathies, or myositis, which include dermatomyositis, polymyositis, necrotizing myopathy, and inclusion body myositis (IBM).
  • Polymyalgia rheumatica, which is not in itself an inflammatory muscle disease, but may mimic myositis.
  • Adult onset congenital myopathies and dystrophies including facioscapulohumeral (FSH) dystrophy, mitochondrial myopathy, McArdle disease and familial myopathies
  • Toxic and endocrine myopathies, including statin-induced and hypothyroidism myopathies.


  • Causes of adult and geriatric muscle diseases include immunological, paraneoplastic, genetic, and toxic-metabolic.
  • Sarcopenia is associated with inactivity, chronic illnesses, malnutrition, and metabolic effects of aging.
  • Myosteatosis occurs as a consequence of the metabolic effects of aging, sedentarism, and malnutrition.

 Epidemiology including risk factors and primary prevention

  • Incidence of sarcopenia is estimated between 10-29% in aging individuals, but this information is unreliable since universal definitions for sarcopenia continue to develop in response to ongoing research. Efforts have been made to clarify and reach a consensus. The most recent discussions highlight muscle strength as main the predictor of adverse outcomes, as defined by grip strength and low gait speed.2 As the global population continues to grow, the elderly demographic group is overtaking other age groups. It is expected that prevalence of sarcopenia will increase with current risk estimates in geriatric population at 45%. In addition to advancing age, female sex has been identified as a leading risk factor with modifiable factors such as physical activity, BMI, nutrition and several biomarkers such as decreased albumin, decreased testosterone, decreased IGF-1 and increased pro-inflammatory cytokines playing a key role. Prevention strategies center around macro and micronutrient optimization with creatine supplementation and resistive exercises as adjuvants.3
  • There is an increase in the amount of myosteatosis (fat accumulation within skeletal muscle) associated with aging. This has been further associated to increased mortality,1 chronic liver disease, hepatocellular carcinoma,4 insulin resistance, and chronic plaque psoriasis.5 Other associations are a current subject of research.
  • Inflammatory myopathies have an estimated yearly incidence of 7.8 per million/year, with the adult peak between ages 45 and 55. Females are more likely to be affected.
  • IBM has a yearly incidence of 2 to 5 cases per million adults with a peak at ages 50 to 70, with male predominance. IBM is considered the most prevalent idiopathic inflammatory myopathy in the geriatric population, although cancer related dermatomyositis is more common.
  • Statin-induced myopathy affects fewer than 5% and rhabdomyolysis occurs in less than 0.1% of patients, but risk increases with concomitant fibrate use.
  • Polymyalgia rheumatica has a yearly incidence of 20 cases per 100,000 people, most common in those with Northern European ancestry. Mean age of diagnosis is 70 years old and 75% of patients are female.


  • Sarcopenia is likely caused by multiple mechanisms, including environmental factors, inflammation, mitochondrial pathology, alterations in the neuromuscular junction, reduced satellite cell numbers, and hormonal changes.
  • Myosteatosis appears to develop independently of sarcopenia but may act synergistically. Myosteatosis may be caused by increased uptake, storage and transport of fatty acids, reduced fatty acid oxidation, and defective leptin signaling.6,7 Macrophage infiltration into skeletal muscle tissue may also lead to adipocyte hypertrophy, due to inhibition of adipocyte differentiation. Impaired mitochondrial function associated with aging may also result in a higher rate of storage of fatty acids. Another possible cause of myosteatosis is activation of quiescent muscle satellite cells into adipocytes. Neuromuscular changes may also lead to impaired muscle regeneration capacity.8
  • Idiopathic inflammatory myopathies most likely occur due to a combination of genetic and environmental factors. Environmental factors include infections (hepatitis B in polymyositis), malignancy (Dermatomyositis), and certain chemicals (D-penicillamine in polymyositis).
  • In polymyalgia rheumatica, the cause is unknown but genetic and environmental factors play a role in disease severity and susceptibility to treatment. Exposure to sunlight and viral infections are some of the potential environmental risk factors for polymyalgia rheumatica. Caucasians of Northern European descent are at higher risk for the disease. In Caucasians with polymyalgia rheumatica, it is linked to the HLA-DR4 allele.
  • Statins, except pravastatin, are metabolized via the cytochrome P-450 system, making this a potential cause of drug interactions. The lipophilic cerivastatin, lovastatin and simvastatin are more myotoxic. The mechanism of the myopathy is not clear but may be related to reduction in CoQ10 synthesis, which impairs muscle energy production.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

New onset/acute

Inflammatory myopathies present with worsening proximal muscle weakness and pain over several weeks to months. Steroid-induced myopathy exhibits proximal muscle weakness and may develop as early as the first week of patients receiving high dose corticosteroids.


  • Myosteatosis may occur within days of immobilization. It is reported that muscle fatty infiltration may increase up to 20% within 30 days of immobilization in young and healthy individuals
  • Polymyalgia rheumatica may present with new onset shoulder pain, morning stiffness for more than 45 minutes, with symptoms lasting at least several days to weeks. The disease is usually self-limiting, but untreated patients may develop impairments due to myalgias and muscle stiffness. Up to 21% of patients with polymyalgia rheumatica may suffer from giant cell arteritis.


  • Sarcopenia develops over the decades and presents clinically as a loss of muscle bulk and power. After 50 years of age there is a gradual decline in muscle mass. With age, thresholds for low physical performance and disability gradually become lower, but this may be ameliorated by lifestyle and nutritional modifications. Given that muscle is a metabolically active tissue, the loss of muscle mass may negatively affect muscle tissue’s metabolic functions.9  .
  • Increase in myosteatosis is related to decreased performance on functional measures, increased gait variability, progression of kyphosis, decreased balance, and risk of falls.  Myosteatosis may also negatively affect muscle tissue’s metabolic functions such as autocrine, paracrine, and endocrine signaling, glucose homeostasis, amino acid storage, and thermoregulation.1
  • Patients with polymyalgia rheumatica or other rheumatologic diseases who require chronic corticosteroid therapy should be monitored for medication side effects.
  • Muscular dystrophies and congenital myopathies are characterized by slowly progressive weakness and function loss.
  • Inclusion body myositis develops over the years in an insidious manner, with weakness and atrophy of the proximal lower extremity muscles and distal arms. Dysphagia may occur as disease progresses.



Specific secondary or associated conditions and complications

Malnutrition in advanced age is highly associated with sarcopenia with complications relating to the loss of the protective metabolic, immunomodulatory and mechanical roles of muscle. Specifically, sarcopenia is closely related to osteoporosis and either condition should trigger screening for the other.3

Myosteatosis is associated with an increased risk of developing insulin resistance and type-2 diabetes mellitus, arterial hypertension, and hyperlipidemia.

Development of dermatomyositis is usually associated with malignancy, with a cancer rate of 9-32% found among patients with dermatomyositis. Malignancies most commonly implicated in the development of dermatomyositis are ovarian, breast, stomach, colon, lung, melanoma, and non-Hodgkin lymphoma. Patients should undergo cancer screening after the diagnosis of dermatomyositis.

Essentials of Assessment


History is varied in these disorders and can help to narrow the differential diagnosis.

  • Sarcopenia and myosteatosis are associated to chronic diseases in the aging population such as rheumatic diseases, lung disease, chronic kidney and liver disease, congestive heart failure and malnutrition.
  • A history of cancer may be present in patients with dermatomyositis.
  • Family history may portend risk of a congenital disorder.
  • Medication use may be associated to toxic myopathies.
  • Rapid onset of shoulder pain and stiffness is a hallmark of polymyalgia rheumatica, although neck and pelvic muscle pain is common. Although not included in the new diagnostic criteria, constitutional signs such as low-grade fever, anorexia, fatigue, and weight loss can be seen are fairly common.

Physical examination

Physical examination may reveal muscle atrophy, swelling, weakness, and tenderness.

  • Patients with sarcopenia have decreased muscle bulk and strength and may specifically show slowed usual gait speed and decreased grip strength.2
  • Inclusion body myositis involves most commonly the long finger flexors, ankle dorsiflexors and quadriceps. In facioscapulohumeral muscular dystrophy, muscles involved are located in the facial, scapular, and proximal upper extremity muscles.
  • Focal muscle tenderness is characteristically seen with myositis.
  • Joint pathology as well as skin involvement is associated with rheumatological disorders.
  • Skin involvement such as scaly erythematous lesions in the finger joints (Gottron’s papules), and upper eyelid violaceus eruptions (heliotrope rash) are characteristic of dermatomyositis.

Functional assessment

  • In the case of sarcopenia, decreased muscle endurance and strength translates into a higher risk for falls, fractures, hospitalizations, disability, and decreased quality of life.
  • In myosteatosis, the presence of intermuscular fat impairs muscle function, with fat deposits compressing the motor unit, and subsequent loss of muscle strength.
  • Mobility limitations will vary according to the muscles involved.  Impaired loading response is observed in patients with knee extensor weakness such as those with inclusion body myositis. Muscular dystrophies, toxic, metabolic and autoimmune myopathies mostly express proximal weakness for which sit-to-stand assessment and stair climbing will be impaired.
  • Self-care limitations caused by proximal upper extremity weakness in FSH dystrophies and proximal myopathies include difficulty with grooming (due to inability to do activities above the shoulder level) or upper extremity dressing (due to impaired shoulder reach). Fine motor dexterity loss can be seen in inclusion body myositis due to distal muscle involvement.
  • Cognitive and behavior dysfunction is rare although assessment of affect is important considering the impact of pain and loss of function.

Laboratory studies

  • Evaluation of sarcopenia should include thyroid functions, albumin level, vitamin D level, growth hormone and, in men, serum testosterone.3
  • The ratio of creatinine to cystatin C is positively associated to muscle-rich fibers, and inversely associated with fat-rich muscle. Low creatinine-to-cystatin C ratio is associated with single-leg standing time.10
  • Serum creatinine phosphokinase (CPK) may be elevated in several myopathies and values are not specific for any muscle disease.
  • Rheumatological screen should include rheumatoid factor, anti-nuclear antibody, C-reactive protein, and erythrocyte sedimentation rate.
  • Genetic testing is indicated in the presence of family history or high clinical suspicion.
  • Erythrocyte sedimentation rate may be elevated in inflammatory myopathies.


The use of ultrasound is being investigated for muscle disease. Although accessible, ultrasound is unable to distinguish between intramyocellular and extramyocellular fat in patients with muscle fatty infiltration. Despite its limitations, ultrasound enables assessment of muscle cross sectional area, muscle thickness, pennation angle, muscle length, and echogenicity.

Studies elaborating on the use of quantitative ultrasound of finger flexors and quadriceps have yielded favorable results in its discrimination of patients with Inclusion body myositis vs Dermatomyositis, Polymyositis and clinically similar neuromuscular disorders. It has shown best results for discrimination with the Flexor Digitorum Profundus, with limitations in study design limiting diagnostic utility.11

Magnetic resonance imaging has the benefit of distinguishing several muscle groups, but is unable to accurately quantify muscle fat content. Magnetic resonance spectroscopy is a useful tool to measure intramyocellular lipids. Both imaging modalities are costly and not easily accessible in many centers.

Computed tomography allows the quantification of myosteatosis by way of the mean attenuation values of skeletal muscle. The midthigh is regularly used as an indicator of myosteatosis.12

Supplemental assessment tools

  • For sarcopenia the Strength, Assistance with walking, Rise from a chair, climb stairs and Falls (SARC-F) should be conducted annually beginning at age 65. It has been demonstrated to have high specificity for predicting functional deterioration and positive screening can trigger further assessment with grip strength and gait speed evaluation as per the Sarcopenia Definition and Outcomes Consortium (SDOC)3
  • EMG is helpful in identifying myopathy because it can both evaluate motor units and identify muscle necrosis and inflammation during spontaneous activity evaluation.
    • Abnormal spontaneous activity is greatest in proximal muscles in polymyositis/dermatomyositis, with the thoracic paraspinal muscles targeted because of the unlikelihood of degenerative spine disease.
    • Nerve conduction studies will most likely reveal no nerve dysfunction in pure muscle disease.
    • EMG is typically normal in polymyalgia rheumatica and sarcopenia.
  • Muscle biopsy is useful in distinguishing inflammatory muscle disease, dystrophies, vasculitis, and mitochondrial disorders. Statin-induced myopathies show nonspecific changes consistent with mitochondrial respiratory chain dysfunction (ragged red fibers, increased lipid, cytochrome-oxidase negative fibers).
  • Temporal artery biopsy should be done in a patient with polymyalgia rheumatic and headache, vision loss, and tenderness along the temporal artery.

Rehabilitation Management and Treatments

At different disease stages

New onset/acute

  • No effective medication treatment strategy has been discovered for IBM.
  • Polymyositis and dermatomyositis treatment is based on the presence of extradermal symptoms, with prednisone as the first line treatment; initial doses are continued for 2-4 weeks.  Steroid-sparing strategies for refractory myositis include methotrexate, azathioprine, mycophenolate mofetil, and IVIG. If steroid-sparing agents are used concomitantly. Prednisone at a dose of 0.5mg/kg may aid in induction of remission. If no extradermal symptoms are present, light protection and topical treatments may be used. However, Hydroxychloroquine has been used for the skin manifestations of dermatomyositis. 13
  • Minimizing statin dosage lowers the risk of myopathy. Risk factors for myopathies that are influenced by dosing include liver and renal disease, other medications, hypothyroidism, heavy alcohol use, and regular heavy exercise.
  • In the case of inflammatory myopathies, exercise such as aerobics, isometrics, range of motion, and functional exercise have shown efficacy in improving strength, aerobic capacity, endurance and function while decreasing fatigue during the acute and subacute phases of these diseases.
  • For polymyalgia rheumatica, prednisone at 10-20 mg daily will provide dramatic relief, typically in the first week of therapy. Lack of response should trigger further evaluation. The primary steroid sparing medication is methotrexate. Nonsteroidal anti-inflammatory medications may help sustain remission.


  • In a recent meta-analysis of patients with solid tumors, the prevalence of sarcopenia was found to be 35.3%. overall. The prevalence was higher than 50% in esophageal, urothelial, prostate, and thyroid cancers, cholangiocarcinoma, and sarcomas.14
  • Resistance training 3 times weekly in sarcopenia is effective in improving strength, muscle mass, and associated mobility deficits. In patients with sarcopenia secondary to androgen deprived prostate cancer patients, a 12-week resistance training intervention effectively improved sarcopenia, body fat percentage, strength and quality of life.
  • Creatine phosphate supplementation provides further benefit for sarcopenia. Experts recommend a higher daily protein intake of 1.1g/kg (body weight) per day if there is no renal insufficiency or other contraindications are present. Although still controversial, data shows enhancements in both skeletal muscle mass and function with leucine supplementation. As part of a multi- modal intervention, increasing dietary protein intake may support not only muscle mass maintenance but also bone health when calcium and vitamin D intakes are adequate.
  • Testosterone replacement in men with sarcopenia shows a definite improvement in muscle mass and strength. The reported side effect regarding an elevated risk for prostate cancer in combination with other potential side effects such as allergic reactions, fluid retention, gynecomastia, polycythemia, sleep apnea, loss of appetite, nausea, depression, or mood changes limits its usefulness in the treatment of sarcopenia and authors saw also no clear indication for androgen therapy use in the older persons to counter sarcopenia
  • In sarcopenia, growth hormone replacement therapy results in increases muscle mass but not in strength. Nonetheless, possible side effects of growth hormone replacement include fluid retention, joint swelling, joint pain, gynecomastia, orthostatic hypotension, increased risk of diabetes, and carpal tunnel syndrome. This puts into question its relative benefit vs. risk ratio.
  • Resistive training and aerobic exercise have good efficacy in improving strength and function in patients with chronic inflammatory myopathies.

Pre-terminal or end of life care

Studies have shown an association between sarcopenia, quality of life and depression in patients with newly diagnosed incurable cancer. Future efforts addressing sarcopenia at the time of diagnosis may improve outcome and quality of life.

Cutting Edge/ Emerging and Unique Concepts and Practice

Small trials with Ultrasound-Enhanced Electrical Impedance Tomography (US-EIT) have yielded promising results for its use as a new non-invasive method to assess diseased muscle.15

In the case of myosteatosis, a study in mice found that administration of anti-myostatin antibody resulted in increase in muscle mass and strength, and improved insulin sensitivity in old mice.16 Electrical impedance myography may be useful in measuring myosteatosis.17

Idiopathic Inflammatory Myopathy Classification Criteria:
The EULAR/ACR criteria have been developed and validated with a robust methodology, an improvement over previous criteria sets. The new IIM classification criteria are a valuable for the myositis disease activity core measures endorsed by the International Myositis Assessment and Clinical Studies Group (IMACS), and the recently published ACR/EULAR adult PM/DM and juvenile DM response criteria.

Gaps in the Evidence-Based Knowledge

  • There is a lack of studies on multidisciplinary rehabilitation and its impact on function in geriatric muscle disease. This deficiency is especially important in disorders without specific treatment, such as dystrophies, mitochondrial myopathies, congenital myopathies, and inclusion body myositis.
  • The extent to which life-long activity patterns and training could prevent age-related declines in strength capacities has not been prospectively examined in sarcopenia.
  • Diagnostic criteria for sarcopenia includes cut-offs that are yet to be validated. Future research may elaborate on standardization of the different diagnostic criteria.
  • It is unclear whether myosteatosis is reversible, and if so, to what extent. There is still no consensus on a standard measurement protocol to quantify and characterize myosteatosis.1
  • There is a lack of studies on severe disability in inflammatory myopathies, risks for severe disability, and the role of multidisciplinary treatment in its care.
  • Future research should focus on determining the optimal timing and intensity of efforts to assess and treat sarcopenia while working to improve the QOL and mood outcomes of patients with advanced cancer.
  • The threshold values for sarcopenia may need to be adjusted by extrinsic factors such as gender, stature or region to improve prediction.


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Original Version of the Topic

Anthony Chiodo, MD. Adult and Geriatric Muscle Disease. 12/27/2012.

Previous Revision(s) of the Topic

Edwardo Ramos, MD, Javier Gonzalez-Buonomo, MD,  Ana Ortiz-Santiago, MD. Adult and Geriatric Muscle Disease. 6/28/2018.

Author Disclosure

Edwardo Ramos, MD
Nothing to Disclose

Felix Perez Morciglio, MD
Nothing to Disclose

Ivan J. Perez Vicente, MD
Nothing to Disclose