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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

Akathisia is frequently associated with the use of dopamine receptor antagonist antipsychotic drugs. Understanding is still limited on the pathophysiology of akathisia, but it is seen to be associated with medications which block dopaminergic transmission in the brain. Additionally, drugs with successful therapeutic effects in the treatment of medication-induced akathisia have provided additional insight into the involvement of other transmitter systems. These include benzodiazepines, β-adrenergic blockers, and serotonin antagonists. Another major cause of the syndrome is the withdrawal observed in drug dependent individuals. Since dopamine deficiency (or disruptions in dopamine signalling) appears to play an important role in the development of RLS, a form of akathisia focused in the legs, the sudden withdrawal or rapidly decreased dosage of drugs which increase dopamine signalling may create similar deficits of the chemical which mimic dopamine antagonism and thus can precipitate RLS. This is why sudden cessation of opioids, cocaine, serotonergics, and other euphoria-inducing substances commonly produce RLS as a side-effect.

It has been correlated with Parkinson's disease and related syndromes. It is unclear, however, whether this is due more to Parkinson's or the drugs used to treat it, such as carbidopa/levodopa (levocarb).

Antidepressants can also induce the appearance of akathisia, due to increased serotonin signalling within the central nervous system. This also explains why serotonin antagonists are often a very effective treatment.

The 2006 UK study by Healy et al. observed that akathisia is often miscoded in antidepressant clinical trials as "agitation, emotional lability, and hyperkinesis (overactivity)". The study further points out that misdiagnosis of akathisia as simple motor restlessness occurs, but that this is more properly classed as dyskinesia.

It was discovered that akathisia involves increased levels of the neurotransmitter norepinephrine, which is associated with mechanisms that regulate aggression, alertness, and arousal.

The table below summarizes factors that can induce akathisia, grouped by type, with examples or brief explanations for each:

Movement disorders are clinical syndromes with either an excess of movement or a paucity of voluntary and involuntary movements, unrelated to weakness or spasticity. Movement disorders are synonymous with basal ganglia or extrapyramidal diseases. Movement disorders are conventionally divided into two major categories- "hyperkinetic" and "hypokinetic".

Hyperkinetic movement disorders refer to dyskinesia, or excessive, often repetitive, involuntary movements that intrude upon the normal flow of motor activity.

Hypokinetic movement disorders refer to akinesia (lack of movement), hypokinesia (reduced amplitude of movements), bradykinesia (slow movement) and rigidity. In primary movement disorders, the abnormal movement is the primary manifestation of the disorder. In secondary movement disorders, the abnormal movement is a manifestation of another systemic or neurological disorder.

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.

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).

Current research at the University of Utah is investigating whether sodium oxybate, also known as Gamma-Hydroxybutyric acid is an effective treatment for AHC. Thus far, only a small number of patients have been sampled, and no conclusive results are yet available. While some success has been had thus far with the drug, AHC patients have been known to respond well initially to other drugs, but then the effectiveness will decline over time. Currently, sodium oxybate is used as a narcolepsy-cataplexy treatment, though in the past it has been used controversially in nutritional supplements. This drug was chosen to test because of a possible link between the causes of narcolepsy-cataplexy and AHC.

Adiadochokinesia is a dyskinesia consisting of inability to perform the rapid alternating movements of diadochokinesia. Called also "adiadochocinesia", "adiadochokinesis", and "adiadokokinesia".

Compare with dysdiadochokinesia, which is an impairment of the ability to perform rapidly alternating movements.

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.

It has been mapped to chromosome 2q31-36.

It has been associated with PNKD.

Treatment depends upon the underlying disorder. Movement disorders have been known to be associated with a variety of autoimmune diseases.

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.

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.

Type 1 episodic ataxia (EA1) is characterized by attacks of generalized ataxia induced by emotion or stress, with myokymia both during and between attacks. This disorder is also known as episodic ataxia with myokymia (EAM), hereditary paroxysmal ataxia with neuromyotonia and Isaacs-Mertens syndrome. Onset of EA1 occurs during early childhood to adolescence and persists throughout the patient's life. Attacks last from seconds to minutes. Mutations of the gene KCNA1, which encodes the voltage-gated potassium channel K1.1, are responsible for this subtype of episodic ataxia. K1.1 is expressed heavily in basket cells and interneurons that form GABAergic synapses on Purkinje cells. The channels aid in the repolarization phase of action potentials, thus affecting inhibitory input into Purkinje cells and, thereby, all motor output from the cerebellum. EA1 is an example of a synaptopathy. There are currently 17 K1.1 mutations associated with EA1, Table 1 and Figure 1. 15 of these mutations have been at least partly characterized in cell culture based electrophysiological assays wherein 14 of these 15 mutations have demonstrated drastic alterations in channel function. As described in Table 1, most of the known EA1 associated mutations result in a drastic decrease in the amount of current through K1.1 channels. Furthermore, these channels tend to activate at more positive potentials and slower rates, demonstrated by positive shifts in their V½ values and slower τ activation time constants, respectively. Some of these mutations, moreover, produce channels that deactivate at faster rates (deactivation τ), which would also result in decreased current through these channels. While these biophysical changes in channel properties likely underlie some of the decrease in current observed in experiments, many mutations also seem to result in misfolded or otherwise mistrafficked channels, which is likely to be the major cause of dysfunction and disease pathogenesis. It is assumed, though not yet proven, that decrease in K1.1 mediated current leads to prolonged action potentials in interneurons and basket cells. As these cells are important in the regulation of Purkinje cell activity, it is likely that this results increased and aberrant inhibitory input into Purkinje cells and, thus, disrupted Purkinje cell firing and cerebellum output.

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).

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.