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.

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.

It has been mapped to chromosome 2q31-36.

It has been associated with PNKD.

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 kinesigenic dyskinesia has been shown to be inherited in an autosomal dominant fashion. In 2011, the PRRT2 gene on chromosome 16 was identified as the cause of the disease. The researchers looked at the genetics of eight families with strong histories of PKD. They employed whole genome sequencing, along with Sanger sequencing to identify the gene that was mutated in these families. The mutations in this gene included a nonsense mutation identified in the genome of one family and an insertion mutation identified in the genome of another family. The researchers then confirmed this gene as the cause of PKD when it was not mutated in the genome of 1000 control patients. Researchers found PRRT2 mutations in 10 of 29 sporadic cases affected with PKD, thus suggests PRRT2 is the gene mutated in a subset of PKD and PKD is genetically heterogeneous. The mechanism of how PRRT2 causes PKD still requires further investigation. However, researchers suggest it may have to do with PRRT2's expression in the basal ganglia, and the expression of an associated protein, SNAP25, in the basal ganglia as well.

While not the same in all people, there are several common triggers that can precipitate an attack:

- Moderate to high consumption of stimulants, such as alcohol, caffeine, or nicotine.

- Low amounts of energy due to hunger, lack of sleep, illness, or physical fatigue.

- Moderate to high presence of stress.

- Menstruation and ovulation.

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.

Paroxysmal kinesigenic choreathetosis (PKC) also called paroxysmal kinesigenic dyskinesia (PKD) is a hyperkinetic movement disorder characterized by attacks of involuntary movements, which are triggered by sudden voluntary movements. The number of attacks can increase during puberty and decrease in a person's 20s to 30s. Involuntary movements can take many forms such as ballism, chorea or dystonia and usually only affect one side of the body or one limb in particular. This rare disorder only affects about 1 in 150,000 people with PKD accounting for 86.8% of all the types of paroxysmal dyskinesias and occurs more often in males than females. There are two types of PKD, primary and secondary. Primary PKD can be further broken down into familial and sporadic. Familial PKD, which means the individual has a family history of the disorder, is more common, but sporadic cases are also seen. Secondary PKD can be caused by many other medical conditions such as multiple sclerosis (MS), stroke, pseudohypoparathyroidism, hypocalcemia, hypoglycemia, hyperglycemia, central nervous system trauma, or peripheral nervous system trauma. PKD has also been linked with infantile convulsions and choreoathetosis (ICCA) syndrome, in which patients have afebrile seizures during infancy (benign familial infantile epilepsy) and then develop paroxysmal choreoathetosis later in life. This phenomenon is actually quite common, with about 42% of individuals with PKD reporting a history of afebrile seizures as a child.

The cause of AHC is unknown. It was initially thought to be a form of complicated migraine because of strong family histories of migraine reported in AHC cases. AHC has also been considered to be a movement disorder or a form of epilepsy. Suggested causes have included channelopathy, mitochondrial dysfunction, and cerebrovascular dysfunction. The disorder most closely related to AHC is familial hemiplegic migraine, and this was recently discovered to be caused by a mutation in a gene for calcium channel receptors. It is suspected that AHC may be caused by a similar channelopathy, and this is a current area of investigation into the cause of AHC. An association with "ATP1A2" mutation has been found in some patients, but other studies have found no mutations and thus a lack of evidence that mutations which cause AHC are in the same genes as mutations which cause familial hemiplegic migraine.

Because alternating hemiplegia of childhood is so rare, there is no increased risk of AHC for the children of siblings of someone with AHC, but it is believed to be autosomal dominant, by which a person with AHC has a 50% change of passing the disorder on to their children. AHC is questionably a progressive disease, because cognitive abilities do appear to decline over time. This cannot be completely determined however, because the mechanism of AHC's progression is unknown. It is likely that it is caused by a generalized cellular dysfunction caused by a mitochondrial disorder. However, studies involving mechanisms of AHC have been inconclusive. Experts currently researching this disorder believe that the cause of AHC is a mutated ion channel. This would make the cause difficult to find because one disrupted channel may be represented differently in different tissues. This mutation is suspected because the most closely related disease, FHM, is also caused by a mutated ion channel. A small number of genes which were suspected to carry a mutation for AHC have been screened for sodium channel protein mutations, ATP pump mutations, and excitatory amino acid transmitter mutations. None of these have yet been successful in determining the underlying cause of AHC.

One large study has identified the gene ATP1A3 as the likely genetic cause of this disorder. This gene is located on the long arm of chromosome 19 (19q13.31).

Published epidemiological data for akathisia are mostly limited to treatment periods preceding the arrival of second-generation antipsychotics. Sachdev (1995) reported an incidence rate of acute akathisia of 31% for 100 patients treated for 2 weeks with antipsychotic medications. Sachdev (1995) reported a prevalence range from 0.1% to 41%. In all likelihood, rates of prevalence are lower for current treatment as second-generation antipsychotics carry a lower risk of akathisia.

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.

Hemiplegic attacks can be brought on by particular triggers, and management of AHC often centers around avoiding common or known triggers. While triggers vary greatly from person to person, there are also some common ones which are prevalent in many patients. Common triggers include temperature changes, water exposure, bright lights, certain foods, emotional stress, and physical activity. While avoiding triggers may help, it cannot prevent all hemiplegic episodes because many occur without being triggered. Because attacks and other associated symptoms end with sleep, various sedatives can be used to help patients sleep.

Patients who develop PSH after traumatic injury have longer hospitalization and longer durations in intensive care in cases where ICU treatment is necessary. Patients often are more vulnerable to infections and spend longer times on ventilators, which can lead to an increased risk of various lung diseases. PSH does not affect mortality rate, but it increases the amount of time it takes a patient to recover from injury, compared to patients with similar injuries who do not develop PSH episodes. It often takes patients who develop PSH longer to reach similar levels of the brain activity seen in patients who do not develop PSH, although PSH patients do eventually reach these same levels.

The cause of benign paroxysmal torticollis in infants is thought to be migrainous. More than 50% of infants have a family history of migraine in first degree relatives. The cause is likely to be genetic.

The number of events that can lead to the development of PSH symptoms is many. The exact pathways or causes for the development of the syndrome are not known. Traumatic brain injury, hypoxia, stroke, anti-NMDA receptor encephalitis (although further associations are being explored), injury of the spinal cord, and many other forms of brain injury can cause onset of PSH. Even more obscure diseases such as intracranial tuberculoma have been seen to cause onset of paroxysmal sympathetic hyperactivity. It is observed that these injuries lead to the development of PSH or are seen in conjunction with PSH, but the pathophysiology behind these diseases and the syndrome is not well understood.

The mechanism of action of benign paroxysmal torticollis is not yet understood. It has been suggested that unilateral vestibular dysfunction or vascular disturbance in the brain stem may be responsible for the condition.

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.

Drugs that can trigger an oculogyric crisis include neuroleptics (such as haloperidol, chlorpromazine, fluphenazine, olanzapine), carbamazepine, chloroquine, cisplatin, diazoxide, levodopa, lithium, metoclopramide, lurasidone, domperidone, nifedipine, pemoline, phencyclidine ("PCP"), reserpine, and cetirizine, an antihistamine. High-potency neuroleptics are probably the most common cause in the clinical setting.

Other causes can include postencephalitic Parkinson's, Tourette's syndrome, multiple sclerosis, neurosyphilis, head trauma, bilateral thalamic infarction, lesions of the fourth ventricle, cystic glioma of the third ventricle, herpes encephalitis, kernicterus and juvenile Parkinson's.

Episodic ataxia (EA) is an autosomal dominant disorder characterized by sporadic bouts of ataxia (severe discoordination) with or without myokymia (continuous muscle movement). There are seven types recognised but the majority are due to two recognized entities. Ataxia can be provoked by stress, startle, or heavy exertion such as exercise. Symptoms can first appear in infancy. There are at least 6 loci for EA, of which 4 are known genes. Some patients with EA also have migraine or progressive cerebellar degenerative disorders, symptomatic of either familial hemiplegic migraine or spinocerebellar ataxia. Some patients respond to acetazolamide though others do not.

The various symptoms of EA are caused by dysfunction of differing areas. Ataxia, the most common symptom, is due to misfiring of Purkinje cells in the cerebellum. This is either due to direct malfunction of these cells, such as in EA2, or improper regulation of these cells, such as in EA1. Seizures are likely due to altered firing of hippocampal neurons (KCNA1 null mice have seizures for this reason).

In affected individuals presenting with the ICCA syndrome, the human genome was screened with microsatellite markers regularly spaced, and strong evidence of linkage with the disease was obtained in the pericentromeric region of chromosome 16, with a maximum lod score, for D16S3133 of 6.76 at a recombination fraction of 0. The disease gene has been mapped at chromosome 16p12-q12.This linkage has been confirmed by different authors. The chromosome 16 ICCA locus shows complicated genomic architecture and the ICCA gene remains unknown.

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.

Many other neurological conditions are associated with acanthocytosis but are not considered 'core' acanthocytosis syndromes. The commonest are:

- Pantothenate kinase-associated neurodegeneration, an autosomal recessive condition caused by mutations in "PANK2".

- Huntington's disease-like syndrome type 2, an autosomal dominant condition caused by mutations in "JPH3" that closely resembles Huntington's disease.

- Bassen-Kornzweig disease, or Bassen-Kornzweig Syndrome (see also History).

- Levine-Critchley syndrome (see History).

- Paroxysmal movement disorders associated with GLUT1 mutations.

- Familial acanthocytosis with paroxysmal exertion-induced dyskinesias and epilepsy (FAPED).

- Some cases of mitochondrial disease.

Choreoathetosis is the occurrence of involuntary movements in a combination of chorea (irregular migrating contractions) and athetosis (twisting and writhing).

It is caused by many different diseases and agents. It is a symptom of several diseases, including Lesch-Nyhan Syndrome, phenylketonuria, and Huntington disease.

Choreoathetosis is also a common presentation of dyskinesia as a side effect of levodopa-carbidopa in the treatment of Parkinson disease.

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.