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.

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.

An increased risk of tardive dyskinesia has been associated with smoking in some studies, although a negative study does exist. There seems to be a cigarette smoke-exposure-dependent risk for TD in antipsychotic-treated patients. Elderly patients are also at a heightened risk for developing TD, as are females and those with organic brain injuries or diabetes mellitus and those with the negative symptoms of schizophrenia. TD is also more common in those that experience acute neurological side effects from antipsychotic drug treatment. Racial discrepancies in TD rate also exist, with Africans and African Americans having higher rates of TD after exposure to antipsychotics. Certain genetic risk factors for TD have been identified including polymorphisms in the genes encoding the D, 5-HT and 5-HT receptors.

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.

"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.

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.

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

Primary spasmodic torticollis is defined as having no other abnormality other than dystonic movement and occasional tremor in the neck. This type of spasmodic torticollis is usually inherited. Studies have shown that the DYT7 locus on chromosome 18p in a German family and the DYT13 locus on chromosome 1p36 in an Italian family is associated with spasmodic torticollis. The inheritance for both loci is autosomal dominant. These loci are all autosomal dominantly inherited with reduced penetrance. Although these loci have been found, it is still not clear the extent of influence the loci have on spasmodic torticollis.

Tardive dyskinesia most commonly occurs in patients with psychiatric conditions who are treated with antipsychotic medications for many years. The average prevalence rate has been estimated to be around 30% for individuals taking antipsychotic medication, such as that used to treat schizophrenia. A study being conducted at the Yale University School of Medicine has estimated that "32% of patients develop persistent tics after 5 years on major tranquilizers, 57% by 15 years, and 68% by 25 years." More drastic data was found during a longitudinal study conducted on individuals 45 years of age and older who were taking antipsychotic drugs. According to this research study, 26% of patients developed tardive dyskinesia after just one year on the medication. Another 60% of this at-risk group developed the disorder after 3 years, and 23% developed "severe" cases of tardive dyskinesia within 3 years. According to these estimates, the majority of patients will eventually develop the disorder if they remain on the drugs long enough.

Elderly patients are more prone to develop tardive dyskinesia, and elderly women are more at-risk than elderly men. The risk is much lower for younger men and women, and also more equal across the sexes. Patients who have undergone electro-convulsive therapy or have a history of diabetes or alcohol abuse also have a higher risk of developing tardive dyskinesia.

Several studies have recently been conducted comparing the prevalence rate of tardive dyskinesia with second generation, or more modern, antipsychotic drugs to that of first generation drugs. The newer antipsychotics appear to have a substantially reduced potential for causing tardive dyskinesia. However, some studies express concern that the prevalence rate has decreased far less than expected, cautioning against the overestimation of the safety of modern antipsychotics.

A physician can evaluate and diagnose a patient with tardive dyskinesia by conducting a systematic examination. The physician should ask the patient to relax, and look for symptoms like facial grimacing, eye or lip movements, tics, respiratory irregularities, and tongue movements. In some cases, patients experience nutritional problems, so a physician can also look for a gain or loss in weight.

Apart from the underlying psychiatric disorder, tardive dyskinesia may cause afflicted people to become socially isolated. It also increases the risk of dysmorphophobia and can even lead to suicide. Emotional or physical stress can increase the severity of dyskinetic movements, whereas relaxation and sedation have the opposite effect.

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.

Acute dystonia is a sustained muscle contraction that sometimes appears soon after administration of antipsychotic medications. Any muscle in the body may be affected, including the jaw, tongue, throat, arms, or legs. When the throat muscles are involved, this type of dystonia is called an acute laryngospasm and is a medical emergency because it can impair breathing. Older antipsychotics such as Haloperidol or Fluphenazine are more likely to cause acute dystonia than newer agents. Giving high doses of antipsychotics by injection also increases the risk of developing acute dystonia.

Methamphetamine, other amphetamines and dopaminergic stimulants including cocaine and pemoline can produce choreoathetoid dyskinesias; the prevalence, time-frame and prognosis are not well established. Amphetamines also cause a dramatic increase in choreoathetoid symptoms in patients with underlying chorea such as Sydenham’s, Huntington’s, and Lupus. Long-term use of amphetamines may increase the risk of Parkinson's disease (PD): in one retrospective study with over 40,000 participants it was concluded that amphetamine abusers generally had a 200% higher chance of developing PD versus those with no history of abuse; the risk was much higher in women, almost 400%. There remains some controversy as of 2017.

Levodopa-induced dyskinesia (LID) is evident in patients with Parkinson's disease who have been on levodopa () for prolonged periods of time. LID commonly first appears in the foot, on the most affected side of the body. There are three main types that can be classified on the basis of their course and clinical presentation following an oral dose of :

- Off-period dystonia – correlated to the akinesia that occurs before the full effect of sets in, when the plasma levels of are low. In general, it occurs as painful spasms in the foot. Patients respond to therapy.

- Diphasic dyskinesia – occurs when plasma L-DOPA levels are rising or falling. This form occurs primarily in the lower limbs (though they can happen elsewhere) and is usually dystonic (characterized by apparent rigidity within muscles or groups thereof) or (characterized by involuntary movement of muscles) and will not respond to dosage reductions.

- Peak-dose dyskinesia – the most common form of levodopa-induced dyskinesia; it correlates with the plateau plasma level. This type usually involves the upper limbs more (but could also affect the head, trunk and respiratory muscles), is choreic (of chorea), and less disabling. Patients will respond to reduction but may be accompanied by deterioration of parkinsonism. Peak-dose L-DOPA-induced dyskinesia has been suggested to be associated with cortical dysregulation of dopamine signaling.

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.

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."

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.

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.

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".

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.

The medical treatment of essential tremor at the Movement Disorders Clinic at Baylor College of Medicine begins with minimizing stress and tremorgenic drugs along with recommending a restricted intake of beverages containing caffeine as a precaution, although caffeine has not been shown to significantly intensify the presentation of essential tremor. Alcohol amounting to a blood concentration of only 0.3% has been shown to reduce the amplitude of essential tremor in two-thirds of patients; for this reason it may be used as a prophylactic treatment before events during which one would be embarrassed by the tremor presenting itself. Using alcohol regularly and/or in excess to treat tremors is highly unadvisable, as there is a purported correlation between tremor and alcoholism. Alcohol is thought to stabilize neuronal membranes via potentiation of GABA receptor-mediated chloride influx. It has been demonstrated in essential tremor animal models that the food additive 1-octanol suppresses tremors induced by harmaline, and decreases the amplitude of essential tremor for about 90 minutes.

Two of the most valuable drug treatments for essential tremor are propranolol, a beta blocker, and primidone, an anticonvulsant. Propranolol is much more effective for hand tremor than head and voice tremor. Some beta-adrenergic blockers (beta blockers) are not lipid-soluble and therefore cannot cross the blood–brain barrier (propranolol being an exception), but can still act against tremors; this indicates that this drug’s mechanism of therapy may be influenced by peripheral beta-adrenergic receptors. Primidone’s mechanism of tremor prevention has been shown significantly in controlled clinical studies. The benzodiazepine drugs such as diazepam and barbiturates have been shown to reduce presentation of several types of tremor, including the essential variety. Controlled clinical trials of gabapentin yielded mixed results in efficacy against essential tremor while topiramate was shown to be effective in a larger double-blind controlled study, resulting in both lower Fahn-Tolosa-Marin tremor scale ratings and better function and disability as compared to placebo.

It has been shown in two double-blind controlled studies that injection of botulinum toxin into muscles used to produce oscillatory movements of essential tremors, such as forearm, wrist and finger flexors, may decrease the amplitude of hand tremor for approximately three months and that injections of the toxin may reduce essential tremor presenting in the head and voice. The toxin also may help tremor causing difficulty in writing, although properly adapted writing devices may be more efficient. Due to high incidence of side effects, use of botulinum toxin has only received a C level of support from the scientific community.

Deep brain stimulation toward the ventral intermediate nucleus of the thalamus and potentially the subthalamic nucleus and caudal zona incerta nucleus have been shown to reduce tremor in numerous studies. That toward the ventral intermediate nucleus of the thalamus has been shown to reduce contralateral and some ipsilateral tremor along with tremors of the cerebellar outflow, head, resting state and those related to hand tasks; however, the treatment has been shown to induce difficulty articulating thoughts (dysarthria), and loss of coordination and balance in long-term studies. Motor cortex stimulation is another option shown to be viable in numerous clinical trials.

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.

Treatment of tics present in conditions such as Tourette’s syndrome begins with patient, relative, teacher and peer education about the presentation of the tics. Sometimes, pharmacological treatment is unnecessary and tics can be reduced by behavioral therapy such as habit-reversal therapy and/or counseling. Often this route of treatment is difficult because it depends most heavily on patient compliance. Once pharmacological treatment is deemed most appropriate, lowest effective doses should be given first with gradual increases. The most effective drugs belong to the neuroleptic variety such as monoamine-depleting drugs and dopamine receptor-blocking drugs. Of the monoamine-depleting drugs, tetrabenazine is most powerful against tics and results in fewest side effects. A non-neuroleptic drug found to be safe and effective in treating tics is topiramate. Botulinum toxin injection in affected muscles can successfully treat tics; involuntary movements and vocalizations can be reduced, as well as life-threatening tics that have the potential of causing compressive myelopathy or radiculopathy. Surgical treatment for disabling Tourette’s syndrome has been proven effective in cases presenting with self-injury. Deep Brain Stimulation surgery targeting the globus pallidus, thalamus and other areas of the brain may be effective in treating involuntary and possibly life-threatening tics.

Pisa syndrome is predominantly caused by a prolonged administration or an overly dosed administration of antipsychotic drugs. Although antipsychotic drugs are known to be the main drugs that are concerned with this syndrome, several other drugs are reported to have caused the syndrome as well. Certain antidepressants, psychoactive drugs, and antiemetics have also been found to cause Pisa syndrome in patients.

Drugs found to have caused Pisa Syndrome:

- Atypical antipsychotic drugs- ex. clozapine, aripiprazole

- Tricyclic antidepressants- ex. clomipramine

- Psychoactive drugs

- Antiemetic drugs

- Cholinesterase inhibitors

- Galantamine

Based on the drugs that caused Pisa syndrome, it has been implicated that the syndrome may be due to a dopaminergic-cholinergic imbalance or a serotonergic or noradrenergic dysfunction. For the development of Pisa syndrome that cannot be alleviated by anticholinergic drugs, it has been considered that asymmetric brain functions or neural transmission may be the underlying mechanism. How these drugs interact with the biochemistry of the brain to cause the syndrome is unknown and a topic of current research.

Anticholinergic drugs have been reported to be extremely effective in 40% of the patients with the Pisa syndrome. Patients with Pisa syndrome that is resistant to anticholinergic drugs is mostly resolved by the reduction of the administration of the antipsychotic drugs as previously mentioned. While the specific pathology underlying idiopathic Pisa syndrome is unknown, the administration of anticholinergic drugs has provided resolution in known cases.

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 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.