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.

While the exact incidence is unknown, estimates range from 33 - 57 percent of patients staying in the ICU for longer than 7 days. More exact data is difficult to obtain, since variation exists in defining the condition.

The three main risk factors for CIP and CIM are sepsis and systemic inflammatory response syndrome (SIRS), and multi-organ failure. Reported rates of CIP/CIM in people with sepsis and SIRS range from 68 to 100 percent. Additional risk factors for developing CIP/CIM include: female gender, high blood sugar (hyperglycemia), low serum albumin, and immobility. A greater severity of illness increases the risk of CIP/CIM. Such risk factors include: multi-organ dysfunction, renal failure, renal replacement therapy, duration of organ dysfunction, duration of ICU stay, low albumin, and central neurologic failure.

Certain medications are associated with CIP/CIM, such as corticosteroids, neuromuscular blocking agents, vasopressors, catecholamines, and intravenous nutrition (parenteral nutrition). Research has produced inconsistent results for the impact of hypoxia, hypotension, hyperpyrexia, and increased age on the risk of CIP/CIM. The use of aminoglycosides is "not" an independent risk for the development of CIP/CIM.

Myasthenia gravis is the most common neuromuscular disease affecting function of the end plate in patients. It is present in 100 people out of 1,000,000 in the population, and its onset is usually in either younger or older individuals.(reference 14)

Acquired myasthenia gravis is the most common neuromuscular junction disease.(reference 7) Important observations were made by Patrick and Lindstrom in 1973 when they found that antibodies attacking the acetylcholine receptors were present in around 85% of cases of myasthenia gravis.(reference renamed form 13)(reference 36) The remaining diseases were also a result of antibody attacks on vital proteins, but instead of the acetylcholine receptor, the culprits were MuSK, a muscle-specific serum kinase, and lipoprotein receptor-related protein.(reference 36) So these mechanisms describe myasthenia gravis that is acquired, and not congenital, affecting these vital proteins by an immunological response against self-antigens. The cases not caused by antibodies against the acetylcholine receptors became by convention called seronegative myasthenia gravis.(reference 37) The term seronegative came about because scientists would be testing for acetylcholine receptor antibodies in patients that had myasthenia gravis resulting in negative tests in the serum. This does not imply that there are no antibodies present, but this terminology only became present because scientists were testing for the wrong antigen.(reference 36)(reference 38)

Neonatal myasthenia gravis is a very rare condition in which a mother with myasthenia gravis passes down her antibodies to her infant through the placenta, causing the it to be born with antibodies that will attach self-antigens.(reference 12)

Drug-induced myasthenia gravis is also a very rare condition in which pharmacological drugs cause a blockade or disruption of the NMJ machinery.(reference 12) Robert W. Barrons summarizes the possible causes of drug-induced myasthenia gravis: "Prednisone was most commonly implicated as aggravating myasthenia gravis, and D-penicillamine was most commonly associated with myasthenic syndrome. The greatest frequency of drug-induced neuromuscular blockade was seen with aminoglycoside-induced postoperative respiratory depression. However, drugs most likely to impact myasthenic patients negatively are those used in the treatment of the disease. These include overuse of anticholinesterase drugs, high-dose prednisone, and anesthesia and neuromuscular blockers for thymectomy."(reference 39)

Congenital syndromes affecting the neuromuscular junction are considered a very rare form of disease, occurring in 1 out of 200,000 in the United Kingdom.(reference 29) These are genetically inherited disorders. Symptoms are seen early since the affected individuals carry the mutation from birth. Congenital syndromes are usually classified by the location of the affected gene products. Congenital syndromes can have multiple targets affecting either the presynaptic, synaptic or postsynaptic parts of the neuromuscular junction.(reference 30) For example, if the malfunctioning or inactive protein is acetylcholinesterase, this would be classified as a synapse congenital syndrome.(reference 29)

Inclusion body myositis (IBM) is an inflammatory muscle disease characterized by slowly progressive weakness and wasting of both distal and proximal muscles, most apparent in the muscles of the arms and legs. There are two types: sporadic inclusion body myositis (sIBM), which is more common, and hereditary inclusion body myopathy (hIBM).

In sporadic inclusion body myositis [MY-oh-sigh-tis], two processes, one autoimmune and the other degenerative, appear to occur in the muscle cells in parallel. The inflammation aspect is characterized by the cloning of T cells that appear to be driven by specific antigens to invade muscle fibers. The degeneration aspect is characterized by the appearance of holes in the muscle cell vacuoles, deposits of abnormal proteins within the cells and in filamentous inclusions (hence the name inclusion body myositis).

Weakness comes on slowly (over months or years) and progresses steadily and usually leads to severe weakness and wasting of arm and leg muscles. It is more common in men than women. Patients may become unable to perform activities of daily living and most require assistive devices within 5 to 10 years of symptom onset. sIBM is not considered a disorder, but the risk of serious injury due to falls is increased. One common and potentially fatal complication is dysphagia. There is no effective treatment for the disease.

sIBM is a rare yet increasingly prevalent disease and is the most common cause of inflammatory myopathy in people over age 50. Recent research from Australia indicates that the incidence of IBM varies in different populations and ethnic groups. The authors found that the current prevalence was 14.9 per million in the overall population, with a prevalence of 51.3 per million population in people over 50 years of age. As seen in these numbers, sIBM is an age-related disease – its incidence increases with age and symptoms usually begin after 50 years of age. It is the most common acquired muscle disorder seen in people over 50, although about 20% of cases display symptoms before the age of 50.

sIBM is not inherited and is not passed on to the children of IBM patients. There are genetic features that do not directly cause IBM but that appear to predispose a person to getting IBM — having this particular combination of genes increases one's susceptibility to getting IBM. Some 67% of IBM patients have a particular combination of human leukocyte antigen genes in a section of the 8.1 ancestral haplotype in the center of the MHC class II region. sIBM is not passed on from generation to generation, although the susceptibility region of genes may be.

There are also several rare forms of hereditary inclusion body myopathy that are linked to specific genetic defects and that are passed on from generation to generation. Since these forms do not show features of muscle inflammation, they are classified as myopathies rather than forms of myositis. Because they do not display inflammation as a primary symptom, they may in fact be similar, but different diseases to sporadic inclusion body myositis. There are several different types, each inherited in different ways. See hereditary inclusion body myopathy.

A 2007 review concluded there is no indication that the genes responsible for the familial or hereditary conditions are involved in sIBM.

The long-term prognosis is uncertain, and has mostly to do with the underlying cause; i.e. autoimmune, paraneoplastic, etc. However, in recent years increased understanding of the basic mechanisms of NMT and autoimmunity has led to the development of novel treatment strategies. NMT disorders are now amenable to treatment and their prognoses are good. Many patients respond well to treatment, which usually provide significant relief of symptoms. Some cases of spontaneous remission have been noted, including Isaac's original two patients when followed up 14 years later.

While NMT symptoms may fluctuate, they generally don't deteriorate into anything more serious, and with the correct treatment the symptoms are manageable.

A very small proportion of cases with NMT may develop central nervous system findings in their clinical course, causing a disorder called Morvan's syndrome, and they may also have antibodies against potassium channels in their serum samples. Sleep disorder is only one of a variety of clinical conditions observed in Morvan's syndrome cases ranging from confusion and memory loss to hallucinations and delusions. However, this is a separate disorder.

Some studies have linked NMT with certain types of cancers, mostly lung and thymus, suggesting that NMT may be paraneoplastic in some cases. In these cases, the underlying cancer will determine prognosis. However, most examples of NMT are autoimmune and not associated with cancer.

Frequent contributing factors include: too much caffeine, high levels of anxiety, fatigue, dehydration, stress, overwork, and a lack of sleep. Use of certain drugs or alcohol may also be factors.

Magnesium deficiency.

Estimating the mortality rate based on the available literature is difficult. Several case reports have revealed an association between acquired partial lipodystrophy and other diseases.

Nephropathy, in the form of membranoproliferative glomerulonephritis, occurs in about 20% of patients. Usually, patients do not have clinically evident renal disease or abnormalities in renal function until they have had the disease for 8 or more years. Membranoproliferative glomerulonephritis usually presents with asymptomatic proteinuria or hematuria.

The disease may gradually progress. About 40-50% of patients develop end-stage renal disease over the course of 10 years. This condition is responsible for most recurrent hospital admissions in patients with acquired partial lipodystrophy. Rapid progression of renal disease in a pregnant patient was reported. Recurrent disease in transplanted kidneys is common, although there have been reports of successful transplantations.

Associated autoimmune diseases (e.g., systemic lupus erythematosus, thyroiditis) contribute significantly to increased morbidity in these patients compared with the general population. Although uncommon, insulin resistance increases cardiovascular risk. Susceptibility to bacterial infections probably results from a C3 deficiency (due to complement activation and consumption of C3). Low C3 levels may impair complement-mediated phagocytosis and bacterial killing.

The three causes of NMT are:

1. Acquired

2. Paraneoplastic

3. Hereditary

The acquired form is the most common, accounting for up to 80 percent of all cases and is suspected to be autoimmune-mediated, which is usually caused by antibodies against the neuromuscular junction.

The exact cause is unknown. However, autoreactive antibodies can be detected in a variety of peripheral (e.g. myasthenia gravis, Lambert-Eaton myasthenic syndrome) and central nervous system (e.g. paraneoplastic cerebellar degeneration, paraneoplastic limbic encephalitis) disorders. Their causative role has been established in some of these diseases but not all. Neuromyotonia is considered to be one of these with accumulating evidence for autoimmune origin over the last few years. Autoimmune neuromyotonia is typically caused by antibodies that bind to potassium channels on the motor nerve resulting in continuous/hyper-excitability. Onset is typically seen between the ages of 15–60, with most experiencing symptoms before the age of 40. Some neuromyotonia cases do not only improve after plasma exchange but they may also have antibodies in their serum samples against voltage-gated potassium channels. Moreover, these antibodies have been demonstrated to reduce potassium channel function in neuronal cell lines.

Around 250 cases have been reported since the recognition of this syndrome. It is a rare syndrome with no known prevalence, although it is more common than the generalized form of acquired lipodystrophy (Lawrence syndrome).

- Race: No clear relationship exists between incidence and race in this syndrome; however, most reported patients have been of European descent.

- Age: The median age of onset of lipodystrophy has been reported to be around seven years; however, onset occurring as late as the fourth or fifth decade of life also has been reported. The median age at presentation has been about 25 years, and women have been found to present later than men (age 28 for women, age 18 for men).

- Sex: Analysis of the pooled data revealed female patients were affected about four times more often than males.

CIP/CIM can lead to difficulty weaning a person from a mechanical ventilator, and is associated with increased length of stay in the ICU and increased mortality (death). It can lead to impaired rehabilitation. Since CIP/CIM can lead to decreased mobility (movement), it increases the risk of pneumonia, deep vein thrombosis, and pulmonary embolism.

Critically ill people that are in a coma can become completely paralyzed from CIP/CIM. Improvement usually occurs in weeks to months, as the innervation to the muscles are restored. About half of patients recover fully.

Many doctors commonly recommend a combined treatment of: a warm compress applied to the eyes (to relieve muscle tension, relax the muscles, and reduce swelling); a small dosage of antihistamine (to reduce any swelling that may be caused by an allergic reaction); increase bed rest (to allow muscles to rest); decrease exposure to computer screens, televisions, or harsh lighting (to allow muscles to rest); and monitor caffeine intake (too much caffeine can cause an adverse reaction such as eye twitching, but a controlled dose can serve as an effective treatment by increasing blood flow).

Parry–Romberg syndrome appears to occur randomly and for unknown reasons. Prevalence is higher in females than males, with a ratio of roughly 3:2. The condition is observed on the left side of the face about as often as on the right side.

The fact that some people affected with this disease have circulating antinuclear antibodies in their serum supports the theory that Parry–Romberg syndrome may be an autoimmune disease, specifically a variant of localized scleroderma. Several instances have been reported where more than one member of a family has been affected, prompting speculation of an autosomal dominant inheritance pattern. However, there has also been at least one report of monozygotic twins in which only one of the twins was affected, casting doubt on this theory. Various other theories about the cause and pathogenesis have been suggested, including alterations in the peripheral sympathetic nervous system (perhaps as a result of trauma or infection involving the cervical plexus or the sympathetic trunk), as the literature reported it following sympathectomy, disorders in migration of cranial neural crest cells, or chronic cell-mediated inflammatory process of the blood vessels. It is likely that the disease results from different mechanisms in different people, with all of these factors potentially being involved.

Antibodies against voltage-gated potassium channels (VGKC), which are detectable in about 40% of patients with acquired neuromytonia, have been implicated in Morvan’s pathophysiology. Raised serum levels of antibodies to VGKCs have been reported in three patients with Morvan’s Syndrome. Binding of serum from a patient with Morvan’s Syndrome to the hippocampus in a similar pattern of antibodies to known VGKC suggest that these antibodies can also cause CNS dysfunction. Additional antibodies against neuromuscular junction channels and receptors have also been described. Experimental evidence exists that these anti-VGKC antibodies cause nerve hyperexcitability by suppression of voltage gated K+ outward currents, whereas other, yet undefined humoral factors have been implicated in anti-VGKC antibody negative neuromyotonia. It is believed that antibodies to the Shaker-type K+ channels (the Kv1 family) are the type of potassium channel most strongly associated with acquired neuromyotonia and Morvan’s Syndrome.

Whether VGKC antibodies play a pathogenic role in the encephalopathy as they do in the peripheral nervous system is as yet unclear. It has been suggested that the VGKC antibodies may cross the blood–brain barrier and act centrally, binding predominantly to thalamic and striatal neurons causing encephalopathic and autonomic features.

In one case, a patient was diagnosed with both Morvan's syndrome and pulmonary hyalinizing granulomas (PHG). PHG are rare fibrosing lesions of the lung, which have central whorled deposits of lamellar collagen. How these two diseases relate to one another is still unclear.

Thymoma, prostate adenoma, and in situ carcinoma of the sigmoid colon have also been found in patients with Morvan’s Syndrome.

AGL with autoimmune origin is responsible for about 25% of all AGL reports. Those with autoimmune origin stems from other autoimmune diseases, most commonly with juvenile dermatomyositis and autoimmune hepatitis, but also occurs with rheumatoid arthritis, systemic lupus erythematous, and Sjogren syndrome.

This disease is endemic in Portuguese locations Póvoa de Varzim and Vila do Conde (Caxinas), with more than 1000 affected people, coming from about 500 families, where 70% of the people develop the illness. ll the analysed Portuguese families presented the same haplotype (haplotype I) associated with the Met 30 mutation. In northern Sweden, more specifically Piteå, Skellefteå and Umeå, 1.5% of the population has the mutated gene. There are many other populations in the world who exhibit the illness after having developed it independently.

About 25% of previously reported AGL is associated with panniculitis. Panniculitis is an inflammatory nodules of the subcutaneous fat, and in this type of AGL, adipose destruction originates locally at the infection or inflammation site and develops into generalized lipodystrophy.

A multitude of conditions may lead to the development of torticollis including: muscular fibrosis, congenital spine abnormalities, or toxic or traumatic brain injury.

A rough categorization discerns between congenital torticollis and acquired torticollis.

Other categories include:

- Osseous

- Traumatic

- CNS/PNS

- Ocular

- Non-muscular soft tissue

- Spasmodic

- Drug induced

The prognosis for Tropical spastic paraparesis indicates some improvement in a percentage of cases due to immunosuppressive treatment. A higher percentage will eventually lose the ability to walk within a ten-year interval.

The most common causes in young children are birth trauma and a type of cancer called neuroblastoma. The cause of about a third of cases in children is unknown.

For several decades, the term "tropical spastic paraparesis" was used to describe a chronic and progressive clinical syndrome that affected adults living in equatorial areas of the world. This condition was initially thought to be associated with infectious agents (such as Treponema pertenue and Treponema pallidum, which cause inflammation of the central nervous system) and with chronic nutritional deficiencies (such as avitaminosis) or exposure to potentially toxic foods (such as bitter cassava).

Tropical myeloneuropathies are classified as two separate syndromes: tropical ataxic neuropathy (TAN) and tropical spastic paraparesis (TSP). They are placed together because they are found in tropical countries, although tropical spastic paraparesis

has occurred in temperate countries (e.g., Japan).