15/03/24, 18.

59 Myopathy - StatPearls - NCBI Bookshelf

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

Myopathy
Authors

Hassan Nagy1; Karthika Durga Veerapaneni2.

Affiliations
1 Ain Shams University Hospitals
2 University of Arkansas Medical Sciences

Last Update: August 14, 2023.

Continuing Education Activity

Myopathies are a heterogeneous group of disorders primarily affecting the skeletal muscle structure, metabolism or channel function. They usually present
with muscle weakness interfering in daily life activities. Muscle pain is also a common finding and some myopathies are associated with rhabdomyolysis.
This activity reviews the classification, presentation patterns and highlights the role of interprofessional team in diagnosis and management of a suspected
muscle disorder.

Objectives:

Identify the presentation patterns of common myopathies.

Describe the diagnostic approach of a suspected myopathy.

Outline the management of a suspected myopathy.

Access free multiple choice questions on this topic.

Introduction
Myopathy is derived from the Greek words “myo” for muscle, and “pathy” for suffering which means muscle disease. The most common signs and
symptoms of myopathies include weakness, stiffness, cramps, and spasms. Myopathies are a heterogeneous group of disorders primarily affecting the
skeletal muscle structure, metabolism, or channel function. They usually present with muscle weakness interfering in daily life activities. Muscle pain is also
a common finding and some myopathies are associated with rhabdomyolysis.
https://www.ncbi.nlm.nih.gov/books/NBK562290/?report=printable 1/15
15/03/24, 18.59 Myopathy - StatPearls - NCBI Bookshelf

Etiology
The etiology of the myopathies is usually caused by a disruption in the muscle tissue integrity, and the metabolic stability which may be triggered by
inherited genetic diseases, or metabolic errors, certain drugs and toxins, bacterial or viral infections, inflammation, besides minerals, electrolytes, and
hormonal irregularities:

Inherited Myopathies

Mitochondrial Myopathies[1]

Mitochondrial encephalopathy, lactic acidosis, and strokelike syndrome (MELAS)

Kearns-Sayre syndrome

Others (Leber hereditary optic neuropathy; Myoclonic epilepsy with ragged red fibers; Leigh syndrome and neuropathy, ataxia, and retinitis
pigmentosa; mtDNA deletion and depletion syndromes; Chronic progressive external ophthalmoplegia; etc.)[1]

Congenital Myopathies

Nemaline myopathies[2]

Core myopathies

Centronuclear myopathies

Others[3]

Metabolic Myopathies[4]

Lipid myopathies (most common are carnitine palmitoyltransferase II deficiency, very-long-chain-acyl-CoA dehydrogenase deficiency,
trifunctional protein deficiency)

Glycogen storage disease myopathy (Acid maltase deficiency - Pompe disease, Debrancher deficiency - Cori disease - and muscle
phosphorylase deficiency - McArdle disease - are the most frequently encountered)

Channelopathies

Periodic paralysis (Hypokalemic, hyperkalemic, Andersen-Tawil syndrome)

Nondystrophic myotonias (p.e. paramyotonia congenita, Thomsen disease)

https://www.ncbi.nlm.nih.gov/books/NBK562290/?report=printable 2/15
15/03/24, 18.59 Myopathy - StatPearls - NCBI Bookshelf

Muscular Dystrophies[5]

Dystrophinopathies (Duchenne muscular dystrophy, Becker muscular dystrophy, Intermediate phenotype)

Myotonic muscular dystrophies (type 1 and type 2)

Facioscapulohumeral muscular dystrophies (type 1 and type 2)

Emery-Dreifuss muscular dystrophy

Limb-girdle muscular dystrophies

Oculopharyngeal muscular dystrophy

Congenital muscular dystrophy (most common being LAMA2-related, collagen VI-related and alfa-dystroglycan-related)

Distal myopathies

Acquired Myopathies

Toxic Myopathies

Necrotizing myopathies (statins, fibrates, immune checkpoint inhibitors, labetalol, propofol, alcohol, cyclosporine)[6][7]

Mitochondrial myopathies (some antiretrovirals)

Amphiphilic myopathies (chloroquine, hydroxychloroquine, amiodarone)

Antimicrotubular myopathies (vincristine)

Hypokalemic myopathies (diuretics, steroids, laxatives, alcohol, etc.)

Critical care-associated myopathies (corticosteroids, neuromuscular blockers)

Inflammatory myopathy (tumor necrosis alfa inhibitors, immune checkpoint inhibitors, statins, IFN-alfa, D-penicillamine, L-tryptophan,
hydroxyurea, imatinib lamotrigine, phenytoin)

Unknown mechanism (finasteride, omeprazole, isotretinoin)[7]

Immune-mediated or Idiopathic Inflammatory Myopathies

https://www.ncbi.nlm.nih.gov/books/NBK562290/?report=printable 3/15
15/03/24, 18.59 Myopathy - StatPearls - NCBI Bookshelf

Dermatomyositis

Antisynthetase syndrome

Immune-mediated necrotizing myopathy

Inclusion body myopathy

Overlap myositis (association with other connective tissue diseases as systemic lupus erythematosus, Sjogren syndrome, systemic sclerosis, and
rheumatoid arthritis)

Polymyositis[8]

Infectious Myopathies

Bacterial infections (Lyme disease, pyomyositis - Staphylococcus aureus)

Viral infections (Human immunodeficiency virus (HIV), Coxsackie A and B viruses, Influenza)

Parasitic infections (trichinosis, toxoplasmosis, cysticercosis)[9][10][11]

Fungal infection (Candida, Coccidiomycosis)[8]

Endocrine Myopathies [12]

Thyroid and parathyroid dysfunction (hyperthyroidism, hypothyroidism, hyperparathyroidism)

Adrenal dysfunction (Addison's disease, Cushing syndrome)

Diabetic muscle infarction

Electrolyte-mediated Mopathies (hypo- and hyperkalemia, hypercalcemia, hypermagnesemia, hypophosphatemia)

Myopathies associated with systemic disease (amyloidosis, sarcoidosis, vitamin D deficiency, critical care myopathy, idiopathic eosinophilic
myopathy, paraneoplastic)

NOTE: Rhabdomyolysis is a syndrome defined by skeletal muscle damage with CK elevation. It can occur with or without underlying muscle disease and
should not be considered as a primary myopathy.[8]

Epidemiology
https://www.ncbi.nlm.nih.gov/books/NBK562290/?report=printable 4/15
15/03/24, 18.59 Myopathy - StatPearls - NCBI Bookshelf

Inflammatory and endocrine myopathies are a more common type of myopathy in general which usually in middle-aged women> men. It was found that the
incidence rate of inflammatory myopathies varied between 1.16 to 19/million/year while the prevalence varied between 2.4 to 33.8 per 100,000 population.
[13]

The most common inherited myopathies are the dystrophinopathies, which are more common in male patients and affect every race and ethnicity equally.
Amongst them, Duchenne's and Becker's muscular dystrophy are the most prevalent which varied between 19.8 and 25.1 per 100,000 person-years.[14]
Mitochondrial myopathies affect 1 in 4300 people. Other forms of inherited myopathies are rare.[14]

History and Physical

Myopathies are typically involving motor impairment without no sensory symptoms. It presents as proximal muscle weakness, mainly in the pelvic girdle or
the shoulder girdle muscle groups. However, pelvic muscle group is more common and more severe. Comprehensive history alongside physical examination
is mandatory to identify and diagnose myopathies. Patients may complain of difficulty raising up from sitting position, climbing stairs or difficulty brushing
their hair, or practicing any above head activities. Some other myopathies will present in different muscle groups like thighs, back muscles, or fingers, and
could be possibly associated with other symptoms like myalgia, rashes, fatigue, or cramps. Muscle disease could also present with dark urine as a sign of
renal damage in the case of rhabdomyolysis, particularly after vigorous exercises like running marathons.

Polymyositis and dermatomyositis: Both of them affect women more than men, present with proximal weakness affects pelvic girdle more than shoulder
girdle. Polymyositis is associated with arthralgia while dermatomyositis is associated with other symptoms mainly skin manifestations including a purple
rash on the eyelids called heliotrope rash, an erythematous scaly rash appears on the dorsum of the fingers called Gottron's papules, a reddish rash appears
on the shoulder and the back known as Shawl sign, besides interstitial lung disease, Gastrointestinal vasculitis, and paraneoplastic syndrome underlying
malignancy.[15]

Hypothyroid and hyperthyroid myopathies: Both of them are associated with the thyroid disease whether it is hypo- or hyperthyroid disease, and both
present with proximal muscle weakness and peripheral neuropathy. Hypothyroid myopathy is associated with pseudohypertrophy, myoedema, and delayed
deep tendon reflexes. Hyperthyroid myopathy is associated with Grave's ophthalmopathy, goiter, and extraocular muscle weakness as well.[12][16][12]

Other types of acquired myopathies will represent within a group of symptoms associated with that particular disease like for example sarcoidosis
myopathy, amyloid myopathy, and critical illness myopathy. Duchenne muscular dystrophy, myotonic dystrophy 1,2, mitochondrial myopathies, Glycogen
storage diseases like (McArdle, Pompe's disease, etc) are inherited myopathies affect children and it is rare, and accompanied with severe systemic
complications. These patients' life expectancy is relatively limited depending on the severity of the disease and the complications.[17]

Evaluation
The complementary evaluation should be guided by clinical suspicion. Useful tests include:

https://www.ncbi.nlm.nih.gov/books/NBK562290/?report=printable 5/15
15/03/24, 18.59 Myopathy - StatPearls - NCBI Bookshelf

1) Laboratory studies

Complete blood count

Blood urea nitrogen and serum creatinine

Electrolytes (sodium, magnesium, potassium, calcium, phosphorus)

Aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), y-glutamyltransferase (GGT)

Creatine kinase (CK), myoglobin, and aldolase: CK the most useful blood test but levels may not correlate with the degree of muscle weakness.
Myopathies with enhanced regeneration or spared myofibers, such as in antisynthetase syndrome, dermatomyositis, and critical care myopathy, may
present with normal CK and selectively elevated aldolase.

C-reactive protein and erythrocyte sedimentation rate

Thyroid function tests

Anti-nuclear antigen (ANA) and myositis associated antibody panel (importantly -Jo1, -PL7, -PL12, -OJ for antisynthetase syndrome; TIF1-gamma, -
NXP2, -Mi2, -SAE, - MDA5 for dermatomyositis, - HMG-CoA, -SRP for immune-mediated necrotizing myopathy)

Urinalysis: positive hemoglobin dipstick without erythrocytes on microscopic evaluation is a sign of myoglobinuria

2) Electromyography (EMG) and nerve conduction study (NCS):[8]

In this context electrodiagnostic testing has many objectives:

1. it is useful to exclude alternative diagnoses such as neuromuscular junction or motor neuron disorders.

2. it can confirm the myopathic nature of the process if there is an identifiable pattern.

3. it helps characterized and stratify the severity of the disease

4. it can help to choose the best location to perform a muscle biopsy.

Motor NCS are usually normal unless there is a concomitant neuropathy. Exceptions to this include distal myopathies and critical care myopathy where low
compound muscle action potentials (CMAPs) with normal latencies and conduction velocities are seen. Sensory NCS are within normal range...Inclusion
body myositis is the exception since it can cause sensory abnormalities.

https://www.ncbi.nlm.nih.gov/books/NBK562290/?report=printable 6/15
15/03/24, 18.59 Myopathy - StatPearls - NCBI Bookshelf

Needle EMG is the most sensitive examination for myopathy. The presence of myotonic discharges and muscle membrane irritability (increased insertional
activity, fibrillation potentials, and positive sharp waves) helps to narrow the differential diagnosis as it is generally present in necrotizing myopathies
(inflammatory or toxic), myotonic dystrophies and a few metabolic and congenital myopathies. Repetitive stimulation and correlation with exercise may be
needed in the special case of channelopathies.

Complex repetitive discharges and decreased insertional activity are signs of a chronic process.

In some metabolic, congenital, endocrine myopathies, electrodiagnostic tests may be normal.

Of note, electrodiagnostic testing is not always needed if there is a strong suspicion of a myopathic disorder (p.e. suggestive clinical features with elevated
CK or positive family history), especially in the pediatric population. [18]

3) Electrocardiography (ECG): Findings suggestive of hypokalemia include the following:

Diffuse nonspecific ST-T wave changes

Increased PR interval

U waves

Wide QRS

4) Muscle biopsy: Muscle biopsies are categorized by three major components:[8]

Histological/histochemical

Myopathic vs. neuropathic patterns of disease

Presence of unique features that are clues to underlying pathophysiology and diagnosis

Myopathic pattern

Rounding and variation of myofiber size

Internal nuclei, fiber atrophy, degeneration and regenerating myofibers

Fatty replacement

Neuropathic pattern

https://www.ncbi.nlm.nih.gov/books/NBK562290/?report=printable 7/15
15/03/24, 18.59 Myopathy - StatPearls - NCBI Bookshelf

Evidence of denervation and re-innervation

Small, atrophic, angular fibers and target fibers

Re-innovation results in fiber type grouping

5) Muscle MRI: Magnetic resonance imaging of the muscles:[8]

Increased signal intensity within muscle tissue

May see muscle necrosis, degeneration, and/or inflammation

May see fatty replacement, an indicator of chronic muscle damage

Findings may help guide site selection for muscle biopsy

MRI offers a less invasive assessment tool in pediatric populations

Treatment / Management
Treatment for myopathy is generally supportive due to the nature of the etiology of the muscle disease including exercises, physical and occupational
therapies, nutrition, and dietetics, and may be genetic analysis and counseling.[19][20]

Inherited muscular dystrophies: Prednisone 0.75 mg/kg/day has presented improvement in muscle strength, increased muscle bulking, and slowed the
disease progression. It is also important to anticipate complications and treat them accordingly. In mitochondrial myopathies creatine monohydrate 5-10
g/day may benefit improving the symptoms, Coenzyme Q10 replacement still needs more consistent research results to prove significance.[21][18][21]

Acquired myopathies, in general, improve by treating the main causing disease whether it is a systemic disease like thyroid disease, sarcoidosis. Some
acquired myopathies will be caused by infection ( Bacterial, Viral, Fungal, Parasitic, or spirochetes) the myopathy symptoms improve by treating the
infection. Toxin or drug-related myopathy is also managed by the removal of the causative agent and avoiding it in the future. HIV-related myopathy is also
responding well to antiretroviral therapy HAART, and maybe steroids as well.[22][18]

Inflammatory myopathy and autoimmune related myopathies are treated mainly by immunomodulatory, immunosuppressants, and steroid drugs. It is proved
that steroids are better in comparison to immunomodulatory drugs due to side effects. Medications used are methotrexate, azathioprine, cyclosporin, and
cyclophosphamide besides oral dexamethasone and daily oral prednisolone. Unfortunately, some cases including IBMs are refractory to
immunosuppressants medication and steroids, and they continue to progress to more generalized weakness. High quality Randomised clinical trials are
needed to determine the effectiveness and toxicity of the immuno-mediated drugs in the treatment of these inflammatory myopathies.[23]

https://www.ncbi.nlm.nih.gov/books/NBK562290/?report=printable 8/15
15/03/24, 18.59 Myopathy - StatPearls - NCBI Bookshelf

Rhabdomyolysis: The ultimate goal for treatment in rhabdomyolysis is preventing the acute kidney injury by the myoglobin resulting from the muscle
damage. Aggressive hydration by IV fluids, and closely monitoring the kidney functions, and the electrolyte balance.[18]

Differential Diagnosis
Differential diagnosis of myopathy is extensive, as it varies depends on the associated symptoms:

Guillain-Barre syndrome: The typical patient with GBS, which in most cases will manifest as acute inflammatory demyelinating polyradiculoneuropathy
(AIDP), presents 2-4 weeks following a relatively benign respiratory or gastrointestinal illness with complaints of finger dysesthesias and proximal muscle
weakness of the lower extremities. The weakness may progress over hours to days to involve the arms, truncal muscles, cranial nerves, and muscles of
respiration.

Tick-borne diseases: The reference standard for the diagnosis of tickborne rickettsial diseases is the indirect immunofluorescence antibody (IFA) assay
using paired serum samples obtained soon after illness onset and 2-4 weeks later.

Lambert-Eaton myasthenic syndrome (LEMS): proximal muscle weakness, depressed tendon reflexes, post-tetanic potentiation, and autonomic changes
due to impairment in acetylcholine release.

Myasthenia gravis: an autoimmune disorder of peripheral nerves in which antibodies form against acetylcholine (ACh) nicotinic postsynaptic receptors at
the myoneural junction. A reduction in the number of ACh receptors results in a characteristic pattern of progressively reduced muscle strength with
repeated use of the muscle and recovery of muscle strength following a period of rest. The bulbar muscles are affected most commonly and most severely,
but most patients also develop some degree of fluctuating generalized weakness.

Other differentials include the following:

Malignant hyperthermia

Myotonia

Myositis ossificans

Myositis associated with the vasculitides

Paraneoplastic syndromes (eg. carcinomatous neuropathy, cachexia, myonecrosis)

Direct muscle damage (trauma, excessive exercise)

Nutritional deficiencies (vitamin E deficiency, malabsorption syndromes)

https://www.ncbi.nlm.nih.gov/books/NBK562290/?report=printable 9/15
15/03/24, 18.59 Myopathy - StatPearls - NCBI Bookshelf

Prognosis
The treatment goals for most myopathies are to slow or stop the progression of the disease concerning congenital, metabolic, and inflammatory myopathies.
Some of the inherited myopathies' complications could be fatal. The health-related quality of life within this category of myopathies such as inflammatory
and congenital myopathies is impaired. However. the prognosis of acquired myopathies is dependant on the etiology whether it is the severity of the
systemic disease or the nature of the infection, and the damage occurred due to a drug or a toxin. The acquired myopathies are well controlled by treating the
main disease.[24]

Complications
The complications of the various types of myopathies are largely attributed to the progression of the disease. Congenital, metabolic and hereditary
myopathies could have fatal complications like cardiomyopathies, recurrent infections, and sepsis, neuropathies, respiratory failure, or renal failures. On the
other hand, the complications of acquired myopathies are relatively limited to the etiology. For example, if it is infectious related then it is dependant on the
type of the infection or if it is related to drug or toxin, then it is dependant on the dose and the period, and so on. Here is a list of possible complications:

Death

Rhabdomyolysis

Heart arrhythmias

Paraneoplastic syndromes

Heart failure

Hypertension

Renal failure

Neuropathies: Seizures and cerebral dysplasias

Impaired movement

Bedsores

Infections and sepsis

Irreversible muscle wasting

Recurrent dysphagia
https://www.ncbi.nlm.nih.gov/books/NBK562290/?report=printable 10/15
15/03/24, 18.59 Myopathy - StatPearls - NCBI Bookshelf

Acute gastric dilation

Respiratory system failure

Endocrinopathies

Cataracts

Sensorineural hearing loss[25][26][27]

Deterrence and Patient Education

Some of the myopathic diseases are chronic and require lifestyle modification. It is highly encouraged to maintain a balanced diet that contacts a variety of
fruits and vegetables. In addition to a balanced diet, it is essential to stay active. Physical therapy and moderate exercise plans are recommended.
Particularly in patients with metabolic myopathies like lysosomal storage disease and glycogen storage disease, etc.. are encouraged to follow moderate
exercise plans besides diet plans that focus on decreasing the causative diet components.

Inflammatory muscle diseases are chronic diseases. Patients tend to benefit from regular exercise plans alongside medical therapy. Patients are advised to
continue to monitor the progression of the disease and the severity of the symptoms and maintain continuous medical care. Inherited myopathies are usually
associated with other complications. Anticipating complications is vital in the survival rate, and seeking immediate medical care in cases of emergencies like
cardiomyopathies, sepsis. etc.

Enhancing Healthcare Team Outcomes

Myopathies management is highly dependant on an interprofessional team of primary care physicians, family physicians, pediatricians, neurologists,
rheumatologists, nephrologists, cardiologists, and even orthopedics. There are also other health care providers that have a great share for the care of this
cohort of myopathic patients include dietitians, nutritionists, genetic counselors, mental health counselors, physical therapists, occupational therapists, and
speech therapists. It is pivotal to maintain interprofessional communication between all treatment team to slow the progression of different myopathies.

While the primary care physician or the family physician might be the first person who encounters the patient diagnosis with one of the chronic myopathies,
it takes all other specialists to participate in the treatment plans alongside with other medical providers mentioned above. The ultimate outcome to slow the
progression of the disease and help patients with inherited myopathies to cope with the disease and to delay the onset of the complications. The multi-
professional treatment team together improves the health-related quality of life for myopathic patients.

Review Questions

Access free multiple choice questions on this topic.

https://www.ncbi.nlm.nih.gov/books/NBK562290/?report=printable 11/15
15/03/24, 18.59 Myopathy - StatPearls - NCBI Bookshelf

Comment on this article.

References
1. DiMauro S. Mitochondrial myopathies. Curr Opin Rheumatol. 2006 Nov;18(6):636-41. [PubMed: 17053512]
2. de Winter JM, Ottenheijm CAC. Sarcomere Dysfunction in Nemaline Myopathy. J Neuromuscul Dis. 2017;4(2):99-113. [PMC free article:
PMC5467716] [PubMed: 28436394]
3. Nance JR, Dowling JJ, Gibbs EM, Bönnemann CG. Congenital myopathies: an update. Curr Neurol Neurosci Rep. 2012 Apr;12(2):165-74. [PMC free
article: PMC4491488] [PubMed: 22392505]
4. Smith EC, El-Gharbawy A, Koeberl DD. Metabolic myopathies: clinical features and diagnostic approach. Rheum Dis Clin North Am. 2011
May;37(2):201-17, vi. [PubMed: 21444020]
5. Wicklund MP. The muscular dystrophies. Continuum (Minneap Minn). 2013 Dec;19(6 Muscle Disease):1535-70. [PMC free article: PMC10564029]
[PubMed: 24305447]
6. Tomaszewski M, Stępień KM, Tomaszewska J, Czuczwar SJ. Statin-induced myopathies. Pharmacol Rep. 2011;63(4):859-66. [PubMed: 22001973]
7. Le Quintrec JS, Le Quintrec JL. Drug-induced myopathies. Baillieres Clin Rheumatol. 1991 Apr;5(1):21-38. [PubMed: 2070426]
8. Castro C, Gourley M. Diagnosis and treatment of inflammatory myopathy: issues and management. Ther Adv Musculoskelet Dis. 2012 Apr;4(2):111-20.
[PMC free article: PMC3383519] [PubMed: 22870499]
9. Crum-Cianflone NF. Bacterial, fungal, parasitic, and viral myositis. Clin Microbiol Rev. 2008 Jul;21(3):473-94. [PMC free article: PMC2493084]
[PubMed: 18625683]
10. Crum-Cianflone NF. Infection and musculoskeletal conditions: Infectious myositis. Best Pract Res Clin Rheumatol. 2006 Dec;20(6):1083-97.
[PubMed: 17127198]
11. El-Beshbishi SN, Ahmed NN, Mostafa SH, El-Ganainy GA. Parasitic infections and myositis. Parasitol Res. 2012 Jan;110(1):1-18. [PubMed:
21881948]
12. Szczęsny P, Świerkocka K, Olesińska M. Differential diagnosis of idiopathic inflammatory myopathies in adults - the first step when approaching a
patient with muscle weakness. Reumatologia. 2018;56(5):307-315. [PMC free article: PMC6263305] [PubMed: 30505013]
13. Meyer A, Meyer N, Schaeffer M, Gottenberg JE, Geny B, Sibilia J. Incidence and prevalence of inflammatory myopathies: a systematic review.
Rheumatology (Oxford). 2015 Jan;54(1):50-63. [PubMed: 25065005]
14. Mathis S, Tazir M, Magy L, Duval F, Le Masson G, Duchesne M, Couratier P, Ghorab K, Solé G, Lacoste I, Goizet C, Vallat JM. History and current
difficulties in classifying inherited myopathies and muscular dystrophies. J Neurol Sci. 2018 Jan 15;384:50-54. [PubMed: 29249377]
15. Ofori E, Ramai D, Ona M, Reddy M. Paraneoplastic Dermatomyositis Syndrome Presenting as Dysphagia. Gastroenterology Res. 2017
Aug;10(4):251-254. [PMC free article: PMC5593446] [PubMed: 28912913]
16. Vignesh G, Balachandran K, Kamalanathan S, Hamide A. Myoedema: A clinical pointer to hypothyroid myopathy. Indian J Endocrinol Metab. 2013
Mar;17(2):352. [PMC free article: PMC3683223] [PubMed: 23776921]
https://www.ncbi.nlm.nih.gov/books/NBK562290/?report=printable 12/15
15/03/24, 18.59 Myopathy - StatPearls - NCBI Bookshelf

17. Cardamone M, Darras BT, Ryan MM. Inherited myopathies and muscular dystrophies. Semin Neurol. 2008 Apr;28(2):250-9. [PubMed: 18351526]
18. Malik A, Hayat G, Kalia JS, Guzman MA. Idiopathic Inflammatory Myopathies: Clinical Approach and Management. Front Neurol. 2016;7:64. [PMC
free article: PMC4873503] [PubMed: 27242652]
19. Chiodo A. Acquired myopathy/dystrophies. PM R. 2013 May;5(5 Suppl):S74-80. [PubMed: 23584160]
20. Voet NB, van der Kooi EL, Riphagen II, Lindeman E, van Engelen BG, Geurts ACh. Strength training and aerobic exercise training for muscle disease.
Cochrane Database Syst Rev. 2010 Jan 20;(1):CD003907. [PubMed: 20091552]
21. Kley RA, Tarnopolsky MA, Vorgerd M. Creatine for treating muscle disorders. Cochrane Database Syst Rev. 2013 Jun 05;2013(6):CD004760. [PMC
free article: PMC6492334] [PubMed: 23740606]
22. Katzberg HD, Kassardjian CD. Toxic and Endocrine Myopathies. Continuum (Minneap Minn). 2016 Dec;22(6, Muscle and Neuromuscular Junction
Disorders):1815-1828. [PubMed: 27922495]
23. Choy EH, Hoogendijk JE, Lecky B, Winer JB. Immunosuppressant and immunomodulatory treatment for dermatomyositis and polymyositis. Cochrane
Database Syst Rev. 2005 Jul 20;(3):CD003643. [PubMed: 16034905]
24. Leclair V, Regardt M, Wojcik S, Hudson M., Canadian Inflammatory Myopathy Study (CIMS). Health-Related Quality of Life (HRQoL) in Idiopathic
Inflammatory Myopathy: A Systematic Review. PLoS One. 2016;11(8):e0160753. [PMC free article: PMC4978480] [PubMed: 27504827]
25. Friedrich O, Reid MB, Van den Berghe G, Vanhorebeek I, Hermans G, Rich MM, Larsson L. The Sick and the Weak: Neuropathies/Myopathies in the
Critically Ill. Physiol Rev. 2015 Jul;95(3):1025-109. [PMC free article: PMC4491544] [PubMed: 26133937]
26. Suresh E, Wimalaratna S. Proximal myopathy: diagnostic approach and initial management. Postgrad Med J. 2013 Aug;89(1054):470-7. [PubMed:
23596213]
27. Osias J, Manno E. Neuromuscular complications of critical illness. Crit Care Clin. 2014 Oct;30(4):785-94. [PubMed: 25257741]
Disclosure: Hassan Nagy declares no relevant financial relationships with ineligible companies.

Disclosure: Karthika Durga Veerapaneni declares no relevant financial relationships with ineligible companies.

https://www.ncbi.nlm.nih.gov/books/NBK562290/?report=printable 13/15
15/03/24, 18.59 Myopathy - StatPearls - NCBI Bookshelf

Figures

Figure 1 Small foci of coagulative necrosis can be recognised on haematoxylin and eosin (H&E) stained sections: ischaemic myocytes typically show
the hypereosinophilia that characterises early phases of coagulative necrosis. (A) The ischaemic myocytes are located in the left side of the panel; (B)
the ischemic myocytes are positioned bottom left; (C) low magnification view showing a small area of acute myocardial infarction in which granulocyte
infiltration is clearly visible among the myocytes showing coagulative necrosis (squared area and (D), inset at higher magnification). The front of the
myocardial ischemia is in the top half of the figure. Contributed by PubMed

Copyright © 2024, StatPearls Publishing LLC.

https://www.ncbi.nlm.nih.gov/books/NBK562290/?report=printable 14/15
15/03/24, 18.59 Myopathy - StatPearls - NCBI Bookshelf
This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ),
which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the
author and journal.

Bookshelf ID: NBK562290 PMID: 32965961

https://www.ncbi.nlm.nih.gov/books/NBK562290/?report=printable 15/15