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.

A 1969 study of torsion dystonia patients found an average IQ 10 points higher than controls matched for age, sex and ethnic background.

The disease is more commonly found amongst Ashkenazi Jews. The occurrence of torsion dystonia in the Ashkenazi Jewish population as stated by the Department of Epidemiology and Public Health of Yale University School of Medicine in New Haven, CT; "Reports dating to the beginning of this century describe Ashkenazi Jewish (AJ) families with multiple cases of ITD either in siblings (Schwalbe 1908; Bernstein 1912; Abrahamson 1920) or in parents and offspring (Wechsler and Brock 1922; Mankowsky and Czerny 1929; Regensberg 1930). The first comprehensive evaluation of the mode of inheritance of ITD in Jewish and non-Jewish families was described by Zeman and Dyken (1967), who concluded that the disorder was inherited as an autosomal dominant with incomplete penetrance in both populations. Although they concluded that the gene frequency was higher in the AJ population than in non-Jews, no difference in mode of inheritance or disease mechanism was construed."

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.

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.

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.

This condition is very rare, only affecting one in two million people. It is more common in females than in males. There are several hundred cases in the United States, 25 known cases in the United Kingdom, and less than that in Australia and New Zealand.

In some cases Meige's syndrome can be reversed when it is caused by medication. It has been theorized that it is related to cranio-mandibular orthopedic misalignment, a condition that has been shown to cause a number of other movement disorders (Parkinon's, tourettes, and torticollis). This theory is supported by the fact that the trigeminal nerve is sensory for blink reflex, and becomes hypertonic with craniomandibular dysfunction. Palliative treatments are available, such as botulinum toxin injections.

Two other types, primary ciliary dyskinesia and biliary dyskinesia, are caused by specific kinds of ineffective movement of the body, and are not movement disorders.

Spastic thrusting of hip area can occur in Sodemytopic Parkinson's.

The main symptoms involve involuntary blinking and chin thrusting. Some patients may experience excessive tongue protrusion, squinting, light sensitivity, muddled speech, or uncontrollable contraction of the platysma muscle. Some Meige's patients also have "laryngeal dystonia" (spasms of the larynx). Blepharospasm may lead to embarrassment in social situations, and oromandibular dystonia can affect speech, making it difficult to carry on the simplest conversations. This can cause difficulty in both personal and professional contexts, and in some cases may cause patients to withdraw from social situations.

The condition tends to affect women more frequently than men.

"Primary dystonia" is suspected when the dystonia is the only sign and there is no identifiable cause or structural abnormality in the central nervous system. It is suspected to be caused by a pathology of the central nervous system, likely originating in those parts of the brain concerned with motor function, such as the basal ganglia, and the GABA (gamma-aminobutyric acid) producing Purkinje neurons. The precise cause of primary dystonia is unknown. In many cases it may involve some genetic predisposition towards the disorder combined with environmental conditions.

"Secondary dystonia" refers to dystonia brought on by some identified cause, such as head injury, drug side effect (e.g. tardive dystonia), or neurological disease (e.g. Wilson's disease).

Meningitis and encephalitis caused by viral, bacterial, and fungal infections of the brain have been associated with dystonia. The main mechanism is inflammation of the blood vessels, causing restriction of blood flow to the basal ganglia. Other mechanisms include direct nerve injury by the organism or a toxin, or autoimmune mechanisms.

Environmental and task-related factors are suspected to trigger the development of focal dystonias because they appear disproportionately in individuals who perform high precision hand movements such as musicians, engineers, architects, and artists. Chlorpromazine can also cause dystonia, which can be often misjudged as a seizure.

Neuroleptic drugs often cause dystonia, including oculogyric crisis.

Misfunction of the sodium-potassium pump may be a factor in some dystonias. The - pump has been shown to control and set the intrinsic activity mode of cerebellar Purkinje neurons. This suggests that the pump might not simply be a homeostatic, "housekeeping" molecule for ionic gradients; but could be a computational element in the cerebellum and the brain. Indeed, an ouabain block of - pumps in the cerebellum of a live mouse results in it displaying ataxia and dystonia. Ataxia is observed for lower ouabain concentrations, dystonia is observed at higher ouabain concentrations. A mutation in the - pump (ATP1A3 gene) can cause rapid onset dystonia parkinsonism. The parkinsonism aspect of this disease is thought to be attributable to malfunctioning - pumps in the basal ganglia; the dystonia aspect is thought to be attributable to malfunctioning - pumps in the cerebellum (that act to corrupt its input to the basal ganglia) possibly in Purkinje neurons.

Cerebellum issues causing dystonia is described by Filip et al. 2013: "Although dystonia has traditionally been regarded as a basal ganglia dysfunction, recent provocative evidence has emerged of cerebellar involvement in the pathophysiology of this enigmatic disease. It has been suggested that the cerebellum plays an important role in dystonia etiology, from neuroanatomical research of complex networks showing that the cerebellum is connected to a wide range of other central nervous system structures involved in movement control to animal models indicating that signs of dystonia are due to cerebellum dysfunction and completely disappear after cerebellectomy, and finally to clinical observations in secondary dystonia patients with various types of cerebellar lesions. It is proposed that dystonia is a large-scale dysfunction, involving not only cortico-basal ganglia-thalamo-cortical pathways, but the cortico-ponto-cerebello-thalamo-cortical loop as well. Even in the absence of traditional "cerebellar signs" in most dystonia patients, there are more subtle indications of cerebellar dysfunction. It is clear that as long as the cerebellum's role in dystonia genesis remains unexamined, it will be difficult to significantly improve the current standards of dystonia treatment or to provide curative treatment."

ET is one of the most common neurological diseases, with a prevalence of approximately 4% in persons age 40 and older and considerably higher among persons in their 60s, 70s, 80s, with an estimated 20% of individuals in their 90s and over. Aside from enhanced physiological tremor, it is the most common type of tremor and one of the most commonly observed movement disorders.

There are very few reported cases of PED, there are approximately 20 reported sporadic cases of PED and 9 PED families but there is some dispute on the exact number of cases. In addition it appears that PED becomes less severe with aging. Prior to onset of a PED episode some patients reported onset of symptoms including sweating, pallor, and hyperventilation. In brain scans it was observed that patients suffering form frequent PEDs there was increased metabolism in the putamen of the brain and decreased metabolism in the frontal lobe. Another study using subtraction single photon emission computed tomographic (SPECT) imaging technique which was coregistered with an MRI on a patient presented with PED symptoms showed increased cerebral perfusion in the primary somatosensory cortex area, and a mild increase in the region of the primary motor cortex and cerebellum. While all these correlations are not fully understand as to what exactly is happening in the brain it provides areas of interest to study further to hopefully understand PED more fully.

All PD associated subtypes have genetic contributions and are likely to run in a families genetic history due to dominant allele mutations. Mutations of identified genes have been leading areas of research in the study and treatment of paroxysmal dyskinesia. PKD, PNKD, and PED are classified as separate subtypes because they all have different presentations of symptoms, but also, because they are believed to have different pathologies.

Interestingly, studies on diseases that are similar in nature to PD have revealed insights into the causes of movement disorders. Hypnogenic paroxysmal dyskinesia is a form of epilepsy affecting the frontal lobe. Single genes have been identified on chromosomes 15, 20, and 21, which contribute to the pathology of these epilepsy disorders. Utilizing new knowledge about pathologies of related and similar disease can shed insight on the causal relationships in paroxysmal dyskinesia.

In most cases, PED is familial, but can also be sporadic. In familial cases, pedigrees examined have shown PED to be an autosomal-dominant inheritance trait. PED also has been associated with Parkinson's disease, epilepsy and migraines, although the exact relationship between these is unknown.

A suspected contributor to familial PED is a mutation in the GLUT1 gene, SLC2A1, which codes for the transporter GLUT1, a protein responsible for glucose entry across the blood–brain barrier. It is not thought that the mutation causes a complete loss of function of the protein but rather only slightly reduces the transporter's activity. In a study of PED patients, a median CSF/blood glucose ratio of .52 compared to a normal .60 was found. In addition, reduced glucose uptake by mutated transporters compared with wild-type in Xenopus oocytes confirmed a pathogenic role of these mutations.

Another recent study was performed to continue to look at the possible connection between PED and mutations on the SLC2A1 gene which codes for the GLUT1 transporter. While PED can occur in isolation it was also noted that it occurs in association with epilepsy as well. In this study the genetics of a five-generation family with history of PED and epilepsy were evaluated. From the results it was noted that most of the mutations were due to frameshift and missense mutations. When looking at homologous GLUT1 transporters in other species it was noted that serine (position 95), valine (position 140), and asparagine (position 317) were highly conserved and therefore mutations in these residues would most likely be pathogenic. Therefore, these are areas of interest when looking at what could lead to PED.All mutations that were observed appeared to only affect the ability of GLUT1 to transport glucose and not the ability for it to be inserted in the membrane. The observed maximum transport velocity of glucose was reduced anywhere from 3 to 10 fold.

A study was performed to determine if the mutation known for the PNKD locus on chromosome 2q33-35 was the cause of PED. In addition, other loci were observed such as the familial hemiplegic migraine (FHM) locus on chromosome 19p, or the familial infantile convulsions and paroxysmal choreoathetosis (ICCA). All three of these suspected regions were found to not contain any mutations, and were therefore ruled out as possible candidates for a cause of PED.

Paroxysmal Dyskinesia is not a fatal disease. Life can be extremely difficult with this disease depending on the severity. The prognosis of PD is extremely difficult to determine because the disease varies from person to person. The attacks for PKD can be reduced and managed with proper anticonvulsants, but there is no particular end in sight for any of the PD diseases. PKD has been described to cease for some patients after the age of 20, and two patients have reported to have a family history of the disease where PKD went into complete remission after the age of 23. With PNKD and PED, at this time, there is no proper way to determine an accurate prognosis.

X-linked dystonia parkinsonism is thought to result from a mutation of the TAF1 (TATA-binding protein-associated factor 1) gene at Xq13.1. It has an X-linked, recessive pattern of inheritance. Genetic analysis suggests that the responsible mutation was introduced into the Ilongo ethnic group of the Panay Island over 2000 years ago.

Current medical science does not precisely describe the causes of dystonia. Misfiring of neurons in the sensorimotor cortex, a thin layer of neural tissue that covers the brain, is thought to cause contractions. This misfiring may result from impaired inhibitory mechanisms during muscle contraction. When the brain tells a given muscle to contract, it simultaneously silences muscles that would oppose the intended movement. It appears that dystonia interferes with the brain's ability to inhibit those surrounding muscles, leading to loss of selectivity.

The sensorimotor cortex is organized as discrete "maps" of the human body. Under normal conditions, each body part (such as individual fingers) occupies a distinct area on these cortical maps. In dystonia, these maps lose their distinct borders and overlap occurs. Exploration of this initially involved over-training particular finger movements in non-human primates, which resulted in the development of focal hand dystonia. Examination of the primary somatosensory cortex in the trained animals showed grossly distorted representations of the maps pertaining to the fingers when compared to the untrained animals. Additionally, these maps in the dystonic animals had lost the distinct borders that were noted in the untrained animals.

Imaging studies in humans with focal dystonia have confirmed this finding. Also, synchronous afferent stimulation of peripheral muscles induces organizational changes in motor representations, characterized both by an increase in map size of stimulated muscles and a reduction in map separation, as assessed using transcranial magnetic stimulation.

The cross-connectivity between areas that are normally segregated in the sensory cortex may prevent normal sensorimotor feedback and so contribute to the observed co-contraction of antagonist muscle groups, and inappropriately timed and sequenced movements that underlie the symptoms of focal dystonia. It is hypothesized that a deficit in inhibition caused by a genetically mediated loss of inhibitory interneurons may be the underlying cause of the deficits observed in dystonia.

While usually painless, in some instances the sustained contraction and abnormal posturing in dystonia cause pain. Focal dystonia most typically affects people who rely on fine motor skills—musicians, writers, surgeons, etc. It is thought that the excessive motor training those skills require may contribute to the development of dystonia as their cortical maps become enlarged and begin to overlap. Focal dystonia is generally "task-specific," meaning that it is only problematic during certain activities.

Response to treatment is variable and the long-term and functional outcome is unknown. To provide a basis for improving the understanding of the epidemiology, genotype/phenotype correlation and outcome of these diseases their impact on the quality of life of patients, and for evaluating diagnostic and therapeutic strategies a patient registry was established by the noncommercial International Working Group on Neurotransmitter Related Disorders (iNTD).

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.

Focal dystonia is a neurological condition, a type of "dystonia", that affects a muscle or group of muscles in a specific part of the body, causing involuntary muscular contractions and abnormal postures. For example, in focal hand dystonia, the fingers either curl into the palm or extend outward without control. In musicians, the condition is called "musician's focal dystonia", or simply, "musician's dystonia". In sports, it is commonly referred to as the "yips".

Although all early reported cases occurred in the Philippines, X-linked dystonia parkinsonism has been diagnosed in the US, Canada, and Germany in people of Filipino descent. The prevalence in the Philippines has been estimated at 1/322,000 and as high as 1/4,000 in the province of Capiz's male population. As x-linked recessive disease, the majority of those affected are males with females generally asymptomatic carriers. In the largest described series, the mean age of onset was 39.7 years, the mean duration of illness was 16 years, and the mean age of death was 55.6 years.

To date, there is no single, universal treatment that has been found to cure myoclonus dystonia. However, there are several treatment methods that have been found to be effective for helping to reduce the symptoms associated with the syndrome.

Late-onset dyskinesia, also known as tardive dyskinesia, occurs after long-term treatment with an antipsychotic drug such as haloperidol (Haldol) or amoxapine (Asendin). The symptoms include tremors and writhing movements of the body and limbs, and abnormal movements in the face, mouth, and tongue including involuntary lip smacking, repetitive pouting of the lips, and tongue protrusions.

Rabbit syndrome is another type of chronic dyskinesia, while orofacial dyskinesia may be related to persistent replication of Herpes simplex virus type 1.

Dystonia is a neurological motor disorder that affects muscles and causes involuntary muscle spasms, and it occurs when the part of the brain called the basal ganglia malfunctions. The basal ganglia is located in the cerebrum and is responsible for controlling the coordination, speed, and fluidity of movement as well as suppressing involuntary or unwanted movements. Dystonias can be classified by the affected part(s) of the body.

1. General Dystonia - affects most or all of the body.

2. Focal Dystonia - localized to a specific part of the body.

3. Multifocal Dystonia - localized to two or more unrelated parts of the body.

4. Segmental Dystonia - localized to two or more adjacent parts of the body.

5. Hemidystonia - Involves the arm and leg on the same side of the body.

Body parts usually affected by focal dystonias include the neck, lower face, eyelids, or hands.

Typical treatments for dystonia include medication, surgery, and botox injections. Botox can reduce involuntary movements by blocking signals between muscles and nerves. When all other treatments are unsuccessful, surgery is usually used as a last resort (“Movement Disorders”).