The direct cause and pathophysiological basis of RMD is still unknown and can occur in children and adults of perfect or non-perfect health. Rare cases of adult RMD have developed due to head trauma, stress, and herpes encephalitis. Familial cases have been reported suggesting there may be some genetic aspect to the disorder; however, to date, this explanation has not been directly tested. As familial incidence rate is still relatively low, it is believed that behavioral aspects may play a larger role in RMD than family history and genetics. Many sufferers report no family history of the disorder. Another theory suggests that RMD is a learned, self-stimulating behavior to alleviate tension and induce relaxation, similar to tic movements.

An alternative theory suggests that the rhythmic movements help develop the vestibular system in young children, which can partially explain the high prevalence of RMD in infants. It has been seen that children who have underdeveloped vestibular systems benefit from performing RMD-like movements which stimulate the vestibular system

Sleep-related movements are commonly seen in children, especially infants. However, the majority of these movements stop as the child ages. Some 66% of infants of 9-months show RMD-like symptoms compared to only 8% of 4 year olds. The disorder is closely associated to mental retardation or other psychiatric disorders like Autism. More recent studies have shown there is a strong link between prolonged RMD and ADHD

PLMD is estimated to occur in approximately 4% of adults (aged 15–100), but is more common in the elderly, especially females, with up to 11% experiencing symptoms. PLMD appears to be related to restless legs syndrome (RLS) - a study of 133 people found that 80% of those with RLS also had PLMD. However the opposite is not true: many people who have PLMD do "not" also have restless legs syndrome.

It is mostly unknown what causes PLMD, but in many cases the patient also suffers from other medical problems such as Parkinson's disease or narcolepsy. Factors that increase the likelihood of PLMD in the absence of restless leg syndrome include being a shift worker, snoring, coffee drinking, stress, and use of hypnotics, particularly in the case of benzodiazepine withdrawal. For women, the presence of musculoskeletal disease, heart disease, obstructive sleep apnea, cataplexy, doing physical activities close to bedtime and the presence of a mental disorder were significantly associated with having a higher risk of both PLMD and restless legs syndrome.

The most comprehensive assessment so far has estimated RBD prevalence to be about 0.5% in individuals aged 15 to 100. It is far more common in males: most studies report that only about a tenth of sufferers are female. This may partially be due to a referral bias, as violent activity carried out by men is more likely to result in harm and injury and is more likely to be reported than injury to male bed partners by women, or it may reflect a true difference in prevalence as a result of genetic or androgenic factors. The mean age of onset is estimated to be about 60 years.

Various conditions are very similar to RBD in that sufferers exhibit excessive sleep movement and potentially violent behavior. Such disorders include sleepwalking and sleep terrors, which are associated with other stages of sleep, nocturnal seizures and obstructive sleep apnea which can induce arousals from REM sleep associated with complex behaviors. Because of the similarities between the conditions, polysomnography plays an important role in confirming RBD diagnosis.

It is now apparent that RBD appears in association with a variety of different conditions. Narcolepsy has been reported as a related disorder. Both RBD and narcolepsy involve dissociation of sleep states probably arising from a disruption of sleep control mechanisms. RBD has also been reported following cerebrovascular accident and neurinoma (tumor), indicating that damage to the brain stem area may precipitate RBD. RBD is usually chronic. However, it may be acute and sudden in onset if associated with drug treatment or withdrawal (particularly with alcohol withdrawal). 60% of RBD is idiopathic. This includes RBD that is found in association with conditions such as Parkinson's disease and dementia with Lewy bodies, where it is often seen to precede the onset of neurodegenerative disease. Monoamine oxidase inhibitors, tricyclic antidepressants, Selective serotonin reuptake inhibitors, and noradrenergic antagonists can induce or aggravate RBD symptoms and should be avoided in patients with RBD.

Surgery, such as the denervation of selected muscles, may also provide some relief; however, the destruction of nerves in the limbs or brain is not reversible and should be considered only in the most extreme cases. Recently, the procedure of deep brain stimulation (DBS) has proven successful in a number of cases of severe generalised dystonia. DBS as treatment for medication-refractory dystonia, on the other hand, may increase the risk of suicide in patients. However, reference data of patients without DBS therapy are lacking.

Symptomatic RBD is the more characteristically seen disorder. This category of RBD is strongly associated with neurodegenerative diseases. About 15% of Parkinson's patients also have RBD, 70% of multiple system atrophy patients also have RBD, and about 85% of Lewy body dementia patients also have RBD. Other reported neurological associations include Shy–Drager syndrome, olivopontocerebellar atrophy, multiple sclerosis, vascular encephalopathies, Tourette's syndrome, and Guillain–Barré syndrome. It is uncertain whether RBD precedes these neurodegenerative disorders, whether they coincide, or whether it follows these disorders. However, Mayo Clinic researchers have characterized RBD as the strongest predictor of whether a male patient is developing Lewy body dementia.

REM sleep behavior disorder or RBD is the most common REM sleep parasomnia in which muscle atonia is absent. This allows the individual to act out their dreams and may result in repeated injury—bruises, lacerations, and fractures—to themselves or others. Patients may take self-protection measures by tethering themselves to bed, using pillow barricades, or sleeping in an empty room on a mattress.

Demographically, 90% of RBD patients are males, and most are older than 50 years of age.

Typical clinical features of REM sleep behavior disorder are:

- Male gender predilection

- Mean age of onset 50–65 years (range 20–80 years)

- Vocalisation, screaming, swearing that may be associated with dreams

- Motor activity, simple or complex, that may result in injury to patient or bed-partner

- Occurrence usually in latter half of sleep period (REM sleep)

- May be associated with neurodegenerative disease

Acute RBD, occurs mostly as a result of a side-effect in prescribed medication—usually antidepressants. But if not then 55% of the time the cause is unknown the other 45% the cause is associated with alcohol.

Chronic RBD is idiopathic, meaning of unknown origin, or associated with neurological disorders. There is a growing association of chronic RBD with neurodegenerative disorders—Parkinson's disease, multiple system atrophy (MSA), or dementia—as an early indicator of these conditions by as much as 10 years.

Patients with narcolepsy also are more likely to develop RBD.

Functional neurological symptom disorder can mimic many other conditions. Some alternative diagnoses for FND include:

- Hemiplegic migraine

- Multiple sclerosis

- Motor neurone disease

- Parkinson's

- Autoimmune disorders

- Ehlers–Danlos syndrome

- Stroke

- Vitamin B12 deficiency or pernicious anaemia

- Myasthenia gravis

Parasomnias are a category of sleep disorders that involve abnormal movements, behaviors, emotions, perceptions, and dreams that occur while falling asleep, sleeping, between sleep stages, or during arousal from sleep. Most parasomnias are dissociated sleep states which are partial arousals during the transitions between wakefulness and NREM sleep, or wakefulness and REM sleep.

Mobility issues associated with falls and freezing of gait have a devastating impact in the lives of PD patients. Fear of falling in itself can have an incapacitating effect in PD patients and can result in social seclusion leaving patients largely isolated leading to depression. Immobility can also lead to osteoporosis which in-turn facilitates future fracture development. This then becomes a vicious circle with falls leading to immobility and immobility facilitating future falls. Hip fractures from falls are the most common form of fracture among PD patients. Fractures increase treatment costs associated with health care expenditures in PD. Also, when gait is affected it often heralds the onset of Lewy body dementia.

Spasmodic torticollis is one of the most common forms of dystonia seen in neurology clinics, occurring in approximately 0.390% of the United States population in 2007 (390 per 100,000). Worldwide, it has been reported that the incidence rate of spasmodic torticollis is at least 1.2 per 100,000 person years, and a prevalence rate of 57 per 1 million.

The exact prevalence of the disorder is not known; several family and population studies show that as many as 25% of cervical dystonia patients have relatives that are undiagnosed. Studies have shown that spasmodic torticollis is not diagnosed immediately; many patients are diagnosed well after a year of seeking medical attention. A survey of 59 patients diagnosed with spasmodic torticollis show that 43% of the patients visited at least four physicians before the diagnosis was made.

There is a higher prevalence of spasmodic torticollis in females; females are 1.5 times more likely to develop spasmodic torticollis than males. The prevalence rate of spasmodic torticollis also increases with age, most patients show symptoms from ages 50–69. The average onset age of spasmodic torticollis is 41.

Although not necessary for the diagnosis, individuals with intellectual disability are at higher risk for SMD. It is more common in boys, and can occur at any age.

Although essential tremor is often mild, people with severe tremor have difficulty performing many of their routine activities of daily living. ET is generally progressive in most cases (sometimes rapidly, sometimes very slowly), and can be disabling in severe cases.

In the past, the prognosis for patients with this disease had been very poor; with many patients suffering from severe disability or death. Now, patients are responding remarkably well to current treatments and the majority of patients go into spontaneous remission. For those that do not go into remission, the symptoms of hemiballismus can generally be very well controlled with medication.

Due to the rarity of this disorder, scientists know very little about the details of hemiballismus. There are still many unanswered questions such as:

•There appears to be a discrepancy between this disorder in humans and animals that has yet to be explained.

•Hemiballismus can also be induced by damage to other areas of the basal ganglia besides the subthalamic nucleus. Why is this? Research is being done in these areas in order to give scientists and clinicians a better model for this disease that will ultimately lead to better diagnosis and treatment of this disorder.

•Research is also being done on why certain treatments seem to help hemiballistic patients when they should seemingly do more harm. An example of this is why lesioning the globus pallidus seems to reduce hemiballistic movements.

•Why does blocking dopamine help reduce patients’ symptoms?

Geniospasm is movement disorder of the mentalis muscle.

It is a benign genetic disorder linked to chromosome 9q13-q21 where there are episodic involuntary up and down movements of the chin and lower lip. The movements consist of rapid fluttering or trembling at about 8 Hz superimposed onto a once per three seconds movement of higher amplitude and occur symmetrically in the V shaped muscle. The tongue and buccal floor muscles may also be affected but to a much lesser degree.

The movements are always present but extreme episodes may be precipitated by stress, concentration or emotion and commence in early childhood.

The condition is extremely rare and in a study in 1999 only 23 families in the world were known to be affected, although it may be under-reported. Inheritance is aggressively autosomal dominant. In at least two studies the condition appeared spontaneously in the families.

The condition responds very well to regular botulinus toxin injections into the mentalis muscle which paralyse the muscle but cause no impairment of facial expression or speech.

When other conditions lead to spasmodic torticollis, it is said that the spasmodic torticollis is secondary. A variety of conditions can cause brain injury, from external factors to diseases. These conditions are listed below:

- Perinatal (during birth) cerebral injury

- Kernicterus

- Cerebrovascular diseases

- Drug induced

- Central nervous system tumor

- Peripheral or central trauma

- Infectious or post infectious encephalopathies

- Toxins

- Metabolic

- Paraneoplastic syndromes

- Central pontine myelinolysis

Secondary spasmodic torticollis is diagnosed when any of the following are present: history of exogenous insult or exposure, neurological abnormalities other than dystonia, abnormalities on brain imaging, particularly in the basal ganglia.

Some research suggests that there may be a degree of inherited susceptibility to develop sleep bruxism. 21–50% of people with sleep bruxism have a direct family member who had sleep bruxism during childhood, suggesting that there are genetic factors involved, although no genetic markers have yet been identified. Offspring of people who have sleep bruxism are more likely to also have sleep bruxism than children of people who do not have bruxism, or people with awake bruxism rather than sleep bruxism.

There is a group called myoclonic dystonia where some cases are hereditary and have been associated with a missense mutation in the dopamine-D2 receptor. Some of these cases have responded well to alcohol.

Other genes that have been associated with dystonia include CIZ1, GNAL, ATP1A3, and PRRT2. Another report has linked THAP1 and SLC20A2 to dystonia.

Hyperkinesia, also known as hyperkinesis, refers to an increase in muscular activity that can result in excessive abnormal movements, excessive normal movements, or a combination of both. The word hyperkinesis comes from the Greek "hyper", meaning "increased," and "kinein", meaning "to move." Hyperkinesia is a state of excessive restlessness which is featured in a large variety of disorders that affect the ability to control motor movement, such as Huntington's disease. It is the opposite of hypokinesia, which refers to decreased bodily movement, as commonly manifested in Parkinson's disease. Many hyperkinetic movements are the result of improper regulation of the basal ganglia-thalamocortical circuitry. Overactivity of a direct pathway combined with decreased activity of an indirect pathway results in activation of thalamic neurons and excitation of cortical neurons, resulting in increased motor output. Often, hyperkinesia is paired with hypotonia, a decrease in muscle tone. Many hyperkinetic disorders are psychological in nature and are typically prominent in childhood. Depending on the specific type of hyperkinetic movement, there are different treatment options available to minimize the symptoms, including different medical and surgical therapies.

Many studies have reported significant psychosocial risk factors for bruxism, particularly a stressful lifestyle, and this evidence is growing, but still not conclusive. Some consider emotional stress to be the main triggering factor. It has been reported that persons with bruxism respond differently to depression, hostility and stress compared to people without bruxism. Stress has a stronger relationship to awake bruxism, but the role of stress in sleep bruxism is less clear, with some stating that there is no evidence for a relationship with sleep bruxism. However, children with sleep bruxism have been shown to have greater levels of anxiety than other children. People aged 50 with bruxism are more likely to be single and have a high level of education. Work-related stress and irregular work shifts may also be involved. Personality traits are also commonly discussed in publications concerning the causes of bruxism, e.g. aggressive, competitive or hyperactive personality types. Some suggest that suppressed anger or frustration can contribute to bruxism. Stressful periods such as examinations, family bereavement, marriage, divorce, or relocation have been suggested to intensify bruxism. Awake bruxism often occurs during periods of concentration such as while working at a computer, driving or reading. Animal studies have also suggested a link between bruxism and psychosocial factors. Rosales et al. electrically shocked lab rats, and then observed high levels of bruxism-like muscular activity in rats that were allowed to watch this treatment compared to rats that did not see it. They proposed that the rats who witnessed the electrical shocking of other rats were under emotional stress which may have caused the bruxism-like behavior.

Myoclonic dystonia or Myoclonus dystonia syndrome is a rare movement disorder that induces spontaneous muscle contraction causing abnormal posture. The prevalence of myoclonus dystonia has not been reported, however, this disorder falls under the umbrella of movement disorders which affect thousands worldwide. Myoclonus dystonia results from mutations in the SGCE gene coding for an integral membrane protein found in both neurons and muscle fibers. Those suffering from this disease exhibit symptoms of rapid, jerky movements of the upper limbs (myoclonus), as well as distortion of the body's orientation due to simultaneous activation of agonist and antagonist muscles (dystonia).

Myoclonus dystonia is caused by loss-of-function-mutations in the epsilon sarcoglycan gene (SGCE). The disease is dominantly inherited, however SGCE is an imprinted gene, so only the paternal allele is expressed. Therefore, children suffering from this disease inherit the mutation from the father. If the mutated allele is inherited from the mother, the child is not likely to exhibit symptoms.

While no cure has been found for myoclonus dystonia, treatment options are available to those suffering from the disease. Ethanol often ameliorates the symptoms well, and so the syndrome is also called "Alcohol-responsive dystonia". Alcohol may be substituted by benzodiazepines, such as clonazepam, which work through the same mechanism. Deep brain stimulation (DBS) is another viable option that can alleviate symptoms without the unwanted side effects of medications, and has been successful in treating other movement disorders.

Risk factors for Holmes tremor include excess exposure to heavy metals, such as mercury and lead, as well as an increased intake of various drugs and toxins. Researchers found that raising the dose of antidepressants or neuroleptics elevate the risk for developing Holmes tremor. Increasing intake of coffee, tea, or other stimulants can also cause for greater risk of development. Tremors depend on dosage and amount of exposure to these factors and will typically decrease dramatically if the intake is reduced. Hyperthyroidism and hyperglycemia also increase the likelihood of developing Holmes tremor.

In examining the causes of hemiballismus, it is important to remember that this disorder is extremely rare. While hemiballismus can result from the following list, just because a patient suffers from one of these disorders does not mean they will also suffer from hemiballismus.

Stroke

Hemisballismus as a result of stroke occurs in only about 0.45 cases per hundred thousand stroke victims. Even at such a small rate, stroke is by far the most common cause of hemiballismus. A stroke causes tissue to die due to a lack of oxygen resulting from an impaired blood supply. In the basal ganglia, this can result in the death of tissue that helps to control movement. As a result, the brain is left with damaged tissue that sends damaged signals to the skeletal muscles in the body. The result is occasionally a patient with hemiballismus.

Traumatic Brain Injury

Hemiballismus can also occur as a result of a traumatic brain injury. There are cases in which victims of assault or other forms of violence have developed hemiballismus. Through these acts of violence, the victim’s brain has been damaged and the hemiballistic movements have developed.

Amyotrophic Lateral Sclerosis

This disease causes neuronal loss and gliosis, which can include the subthalamic nucleus and other areas of the brain. Essentially any disorder that causes some form of neuronal loss or gliosis in the basal ganglia has the potential to cause hemiballismus.

Nonketotic Hyperglycemia

Patients with nonketotic hyperglycemia can develop hemiballismus as a complication to the disease through the development of a subthalamic nucleus lesion. This is the second most common reported cause of hemiballismus. It can be found primarily in the elderly and many of the reported cases have come from East Asian origin, which suggests that there may be some genetic disposition to development of hemiballismus as a result of hyperglycemia. Hemiballistic movements appear when blood glucose levels get too high and then subside once glucose levels return to normal. This time scale for this is usually several hours. In patients with this type of hemiballismus, imaging reveals abnormalities in the putamen contralateral to the movements as well as the globus pallidus and caudate nucleus. While the hyperglycemia itself is not the cause of the hemiballistic movements, it has been suggested that petechial hemorrhage or a decreased production of GABA and acetylcholine could result secondary to the hyperglycemia. One of these issues could be responsible for the hemiballistic movements.

Neoplasms

A neoplasm is an abnormal growth of cells. Cases have shown that if this occurs somewhere in the basal ganglia, hemiballismus can result.

Vascular malformations

Vascular malformations can cause abnormal blood flow to areas of the brain. If too little blood is delivered to the basal ganglia, a stroke can occur.

Tuberculomas

This is another form of tumor that can result in the brain as a result of a tuberculous meningitis infection. This type of tumor can also damage parts of the basal ganglia, sometimes resulting in hemiballismus.

Demyelinating plaques

Demyelinating plaques attack the myelin sheaths on neurons. This decreases the conduction velocity of the neurons, making the signals received by the basal ganglia garbled and incomplete. This disorganized signal can also cause the chaotic movements characterized by hemiballismus.

Complications from HIV infection

Patients with HIV often have complications that arise along with AIDS. Hypoglycemia due to pentamidine use in patients with AIDS has been known to cause hemiballismus. In some patients, hemiballismus has been the only visible symptom to alert the physician that the patients may have AIDS. It is typically a result of a secondary infection that occurs due to the compromised immune system and the most common infection causing hemiballismus is cerebral toxoplasmosis. Most of the lesions that result from this infection are found in the basal ganglia. As long as the diagnosis is not missed, this type of hemiballismus can be treated just as well as in patients without HIV.

Functional neurological disorder is a common problem, with estimates suggesting that up to a third of neurology outpatients having functional symptoms. In Scotland, around 5000 new cases of FND are diagnosed annually. Furthermore, non-epileptic seizures account for 1 in 7 referrals to neurologists after an initial seizure, and functional weakness has a similar prevalence to multiple sclerosis.