It is not uncommon for drugs to damage muscle fibers. Particular families of drugs are known to induce myopathies on the molecular level, thus altering organelle function such as the mitochondria. Use of multiple drugs from these families in conjunction with one another can increase the risk of developing a myopathy. Many of the drugs associated with inducing myopathies in patients are found in rheumatology practice.

Many dietary factors and aberrations can induce ANIM. Chemical imbalances brought on by abnormal diets may either affect the muscle directly or induce abnormal functionality in upstream pathways.

- Excess Iodine consumption, especially in the form of kelp, can induce Hyperthyroidism. Hyperthyroidism is one of the most common ways to acquire ANIM. A hyperactive thyroid gland produces excessive amounts of hormones T3 and T4 leading to increased metabolism and increased sympathetic nervous system effects. The muscles exhibit a pathology similar to an overdose of epinephrine (commonly known as adrenaline). Patients with hyperthyroidism show weakness of shoulder girdle muscles in particular with this condition often being asymptomatic. More serious weakness of core and limb muscles may present.

- A dietary deficiency of vitamin D is most commonly associated with osteoporosis, but can cause ANIM as well. Vitamin D induced ANIM is most commonly associated with sleep deprivation as it induces tonsillar and adenotonsillar hypertrophy, as well as weakens the airway muscles. These changes induce sleep apnea and sleep disruption. Vitamin D induced ANM can also be associated with daytime impairment through this pathway.

Trauma to any muscle is also a common cause for acute ANIM. This is due to muscular contusions and partial or complete loss of function for affected muscle groups.

The pathogenesis of this disease is unclear. Arteriosclerosis obliterans has been postulated as the cause, along with errors of the clotting and fibrinolytic pathways such as antiphospholipid syndrome.

A large number of conditions may cause symptoms and signs similar to diabetic myonecrosis and include: deep vein thrombosis, thrombophlebitis, cellulitis, fasciitis, abscess, haematoma, myositis, pseudothrombophlebitis (ruptured synovial cyst), pyomyositis, parasitic myositis, osteomyelitis, calcific myonecrosis, myositis ossificans, diabetic myotrophy, muscle strain or rupture, bursitis, vasculitis, arterial occlusion, haemangioma, lymphoedema, sarcoidosis, tuberculosis, cat-scratch disease, amyloidosis, as well as tumours of lipoma, chondroma, fibroma, leiomyoma and sarcoma.

In post-menopausal women, the walls of the vagina become thinner (atrophic vaginitis). The mechanism for the age-related condition is not yet clear, though there are theories that the effect is caused by decreases in estrogen levels. This atrophy, and that of the breasts concurrently, is consistent with the homeostatic (normal development) role of atrophy in general, as after menopause the body has no further functional biological need to maintain the reproductive system which it has permanently shut down.

Masticatory muscle myositis (MMM) is an inflammatory disease in dogs affecting the muscles of mastication (chewing). It is also known as atrophic myositis or eosinophilic myositis. MMM is the most common inflammatory myopathy in dogs. The disease mainly affects large breed dogs. German Shepherd Dogs and Cavalier King Charles Spaniels may be predisposed. There is a similar disease of the eye muscles found in Golden Retrievers. Symptoms of acute MMM include swelling of the jaw muscles, drooling, and pain on opening the mouth. Ophthalmic signs may include third eyelid protrusion, red eyes, and exophthalmos (protruding eyeballs). In chronic MMM there is atrophy of the jaw muscles, and scarring of the masticatory muscles due to fibrosis may result in inability to open the mouth (trismus). The affected muscles include the temporalis, masseter, and pterygoid muscles. The disease is usually bilateral.

MMM is caused by the presence of 2M fibers in the muscles of the jaw. 2M fibers are not found elsewhere in the body. The immune system recognizes these proteins as foreign to the body and attacks them, resulting in inflammation. Diagnosis of MMM is through either biopsy of the temporalis or masseter muscles or the 2M antibody assay, in which blood serum of the possible MMM-dog is reacted with temporalis tissue of a normal dog, or both. False negatives by the 2M antibody assay may be obtained if MMM is end-stage with destruction of type 2M fibers and marked fibrosis. Treatment is usually with corticosteroids such as prednisone, often with decreasing doses for up to 4–6 months, and in the case of trismus, manual opening of the mouth under anesthesia. Feeding very soft or liquid food during this time is usually necessary. The ultimate degree of recovery of jaw function and muscle mass will depend upon the extent of damage to the muscle tissue. Recurrence of MMM may occur. Misdiagnosis of MMM as a retroorbital abscess based on physical examination and finding of trismus leads to inappropriate treatment with antibiotics, which will not impede the progress of MMM.

Macrophagic Myofasciitis, or MMF, is a rare muscle disease identified in 1993. The disease is characterized by microscopic lesions found in muscle biopsies that show infiltration of muscle tissue by PAS-positive macrophages.

Specific causes of MMF are unknown. Intramuscular injections of aluminium-containing vaccines have been implicated. Many of those affected with the disease had previously been treated for malaria with chloroquine or hydroxychloroquine.

Clinical symptoms include muscle pain, joint pain, muscle weakness, fatigue, fever, and muscle tenderness. A diagnosis can only be identified with an open muscle biopsy of the vaccinated muscle.

Studies at the University of Paris have shown that MMF lesions result when the aluminum hydroxide adjuvant from a vaccine remains embedded in the tissue and causes a steady immune reaction.

As of 2009 and with few exceptions, MMF had only been observed in France.

One drug in test seemed to prevent the type of muscle loss that occurs in immobile, bedridden patients.

Testing on mice showed that it blocked the activity of a protein present in the muscle that is involved in muscle atrophy. However, the drug's long-term effect on the heart precludes its routine use in humans, and other drugs are being sought.

Neuromuscular disease is a very broad term that encompasses many diseases and ailments that impair the functioning of the muscles, either directly, being pathologies of the voluntary muscle, or indirectly, being pathologies of nerves or neuromuscular junctions.

Neuromuscular diseases are those that affect the muscles and/or their direct nervous system control, problems with central nervous control can cause either spasticity or some degree of paralysis (from both lower and upper motor neuron disorders), depending on the location and the nature of the problem. Some examples of central disorders include cerebrovascular accident, Parkinson's disease, multiple sclerosis, Huntington's disease and Creutzfeldt–Jakob disease. Spinal muscular atrophies are disorders of lower motor neuron while amyotrophic lateral sclerosis is a mixed upper and lower motor neuron condition.

Muscular atrophy decreases qualities of life as the sufferer becomes unable to perform certain tasks or worsen the risks of accidents while performing those (like walking). Muscular atrophy increases the risks of falling in conditions such as inclusion body myositis (IBM) . Muscular atrophy affects a high number of the elderly.

There are many diseases and conditions which cause a decrease in muscle mass, known as atrophy, including activity, as seen when a cast is put on a limb, or upon extended bedrest (which can occur during a prolonged illness); cachexia - which is a syndrome that is a co-morbidity of cancer and congestive heart failure; chronic obstructive pulmonary disease; burns, liver failure, etc., and the wasting Dejerine-Sottas syndrome (HMSN Type III). Glucocorticoids, a class of medications used to treat allergic and other inflammatory conditions can induce muscle atrophy by increasing break-down of muscle proteins. Other syndromes or conditions which can induce skeletal muscle atrophy are liver disease, and starvation.

Neuromuscular disease can be caused by autoimmune disorders, genetic/hereditary disorders and some forms of the collagen disorder Ehlers–Danlos Syndrome, exposure to environmental chemicals and poisoning which includes heavy metal poisoning. The failure of the electrical insulation surrounding nerves, the myelin, is seen in certain deficiency diseases, such as the failure of the body's system for absorbing vitamin B-12

Diseases of the motor end plate include myasthenia gravis, a form of muscle weakness due to antibodies against acetylcholine receptor, and its related condition Lambert-Eaton myasthenic syndrome (LEMS). Tetanus and botulism are bacterial infections in which bacterial toxins cause increased or decreased muscle tone, respectively.Muscular dystrophies, including Duchenne's and Becker's, are a large group of diseases, many of them hereditary or resulting from genetic mutations, where the muscle integrity is disrupted, they lead to progressive loss of strength and decreased life span.

Further causes of neuromuscular diseases are :

Inflammatory muscle disorders

- Polymyalgia rheumatica (or "muscle rheumatism") is an inflammatory condition that mainly occurs in the elderly; it is associated with giant-cell arteritis(It often responds to prednisolone).

- Polymyositis is an autoimmune condition in which the muscle is affected.

- Rhabdomyolysis is the breakdown of muscular tissue due to any cause.

Tumors

- Smooth muscle: leiomyoma (benign)

- Striated muscle: rhabdomyoma (benign)

The most common causes of myalgia by injury are: sprains and strains.

The severity of symptoms vary widely even for the same type of CMT. There have been cases of monozygotic twins with varying levels of disease severity, showing that identical genotypes are associated with different levels of severity (see penetrance). Some patients are able to live a normal life and are almost or entirely asymptomatic. A 2007 review stated that "Life expectancy is not known to be altered in the majority of cases".

IOI or orbital pseudotumor is the second most common cause of exophthalmos following Grave’s orbitopathy and the third most common orbital disorder following thyroid orbitopathy and lymphoproliferative disease accounting for 5–17.6% of orbital disorders, There is no age, sex, or race predilection, but it is most frequently seen in middle-aged individuals. Pediatric cases account for about 17% of all cases of IOI.

Central core disease is inherited in an autosomal dominant fashion. Most cases have demonstrable mutations in the ryanodine receptor type 1 ("RYR1") gene, which are often "de novo" (newly developed). People with CCD are at risk for malignant hyperthermia (MH) when receiving general anesthesia.

Dejerine–Sottas neuropathy is caused by a genetic defect either in the proteins found in axons or the proteins found in myelin. Specifically, it has been associated with mutations in "MPZ", "PMP22", "PRX", and "EGR2" genes. The disorder is inherited in an autosomal dominant or autosomal recessive manner.

Multiple sclerosis (neurologic pain interpreted as muscular), Myalgic Encephalomyelitis (chronic fatigue syndrome), Myositis, Mixed connective tissue disease, Lupus erythematosus, Fibromyalgia syndrome, Familial Mediterranean fever, Polyarteritis nodosa, Devic's disease, Morphea, Sarcoidosis

There is no specific treatment but triggering anesthetics are avoided and relatives are screened for "RYR1" mutations as these may make them susceptible to MH.

The exact cause of IOI is unknown, but infectious and immune-mediated mechanisms have been proposed. Several studies have described cases where onset of orbital pseudotumor was seen simultaneously or several weeks after upper respiratory infections. Another study by Wirostko et al. proposes that organisms resembling Mollicutes cause orbital inflammation by destroying the cytoplasmic organelles of parasitized cells.

Orbital pseudotumor has also been observed in association with Crohn’s disease, systemic lupus erythematosus, rheumatoid arthritis, diabetes mellitus, myasthenia gravis, and ankylosing spondylitis all of which strengthen the basis of IOI being an immune-mediated disease. Response to corticosteroid treatment and immunosuppressive agents also support this idea.

Trauma has also been seen to precede some cases of orbital pseudotumor. However, one study by Mottow-Lippe, Jakobiec, and Smith suggests that the release of circulating antigens caused by local vascular permeability triggers an inflammatory cascade in the affected tissues.

Although these mechanisms have been postulated as possible causes of IOI, their exact nature and relationships to the condition still remain unclear.

The onset of TM requires toxic levels of the thyroxine hormone due to overproduction by the thyroid gland. Documented cases have only been diagnosed in conjunction with patients with hyperthyroidism. While hyperthyroidism is more common in women, the development of TM was more common among men with hyperthyroidism. Case studies of patients with diagnosed hyperthyroidism showed that only about half of them complained of symptoms characteristic of TM. Further examination as described above indicated that about 75% of the studied patients showed signs of muscle fiber degeneration. This indicates that either at the time of study some patients were in early stages of TM or the symptoms were insignificant patients.

Dejerine–Sottas disease, also known as Dejerine–Sottas syndrome, Dejerine–Sottas neuropathy, progressive hypertrophic interstitial polyneuropathy of childhood and onion bulb neuropathy (and, "hereditary motor and sensory polyneuropathy type III" and "Charcot–Marie–Tooth disease type 3"), is a hereditary neurological disorder characterised by damage to the peripheral nerves and resulting progressive muscle wasting. The condition is caused by mutations in a various genes and currently has no known cure.

The disorder is named for Joseph Jules Dejerine and Jules Sottas, French neurologists who first described it.

CMT is a result of genetic mutations in a number of genes. Based on the affected gene, CMT can be categorized into types and subtypes.

Hereditary motor and sensory neuropathies are relatively common and are often inherited with other neuromuscular conditions, and these co morbidities cause an accelerated progression of the disease.

Most forms HMSN affects males earlier and more severely than females, but others show no predilection to either sex. HMSN affects all ethnic groups. With the most common forms having no racial prediliections, but other recessively inherited forms tend to impact specific ethnic groups. Onset of HMSN in most common in early childhood, with clinical effects occurring before the age of 10, but some symptoms are lifelong and progress slowly. Therefore, these symptoms do not appear until later in life.

TM is directly related to thyroxine toxicity. It is believed this disorder is a direct result of hyperthyroidism, specifically hyperthyroidism caused by Graves' disease or a multinodular goiter. Both cause the thyroid gland to overproduce thyroxine. A multinodular goiter is a condition where the thyroid develops nodules. Overproduction of thyroxine is due to the enlargement of the thyroid gland. Graves' disease is an autoimmune condition where the immune system attacks the thyroid and induces overproduction of the thyroxine hormone.