Tardive dyskinesia is characterized by repetitive, involuntary movements. Some examples of these types of involuntary movements include:

- Grimacing

- Tongue movements

- Lip smacking

- Lip puckering

- Pursing of the lips

- Excessive eye blinking

Rapid, involuntary movements of the limbs, torso, and fingers may also occur. In some cases, an individual's legs can be so affected that walking becomes difficult or impossible. These symptoms are the opposite of patients who are diagnosed with Parkinson's disease. Parkinson's patients have difficulty moving, whereas tardive dyskinesia patients have difficulty not moving.

Respiratory irregularity, such as grunting and difficulty breathing, is another symptom associated with tardive dyskinesia, although studies have shown that the prevalence rate is relatively low.

Tardive dyskinesia is often misdiagnosed as a mental illness rather than a neurological disorder, and as a result patients are prescribed neuroleptic drugs, which increase the probability that the patient will develop a severe and disabling case, and shortening the typical survival period.

Other closely related neurological disorders have been recognized as variants of tardive dyskinesia. Tardive dystonia is similar to standard dystonia but permanent. Tardive akathisia involves painful feelings of inner tension and anxiety and a compulsive drive to move the body. In some extreme cases, afflicted individuals experience so much internal torture that they lose their ability to sit still. Tardive tourettism is a tic disorder featuring the same symptoms as Tourette syndrome. The two disorders are extremely close in nature and often can only be differentiated by the details of their respective onsets. Tardive myoclonus, a rare disorder, presents as brief jerks of muscles in the face, neck, trunk, and extremities.

"AIMS Examination": This test is used when psychotropic medications have been prescribed because patients sometimes develop tardive dyskinesia due to prolonged use of antipsychotic medications. The Abnormal Involuntary Movement Scale (AIMS) examination is a test used to identify the symptoms of tardive dyskinesia (TD). The test is not meant to tell whether there is an absence or presence of tardive dyskinesia. It just scales to level of symptoms indicated by the actions observed. The levels range from none to severe. The AIMS examination was constructed in the 1970s to measure involuntary facial, trunk, and limb movements. It is best to do this test before and after the administration of the psychotropic drugs. Taking the AIMS consistently can help to track severity of TD over time.

Tardive dyskinesia (TD) is a disorder that results in involuntary, repetitive body movements. This may include grimacing, sticking out the tongue or smacking of the lips. Additionally there may be rapid jerking movements or slow writhing movements. In about 20% of people, decreased functioning results.

Tardive dyskinesia occurs in some people as a result of long-term use of neuroleptic medications (antipsychotics, metoclopramide). These medications are usually used for mental illness, but may also be given for gastrointestinal or neurological problems. The condition typically only develops after months to years of use. The diagnosis is based on the symptoms after ruling out other potential causes.

Efforts to prevent the condition include not using or using the lowest possible dose of neuroleptics. Treatment include stopping the neuroleptic medication if possible or switching to clozapine. Other medications such as valbenazine, tetrabenazine, or botulinum toxin may be used to lessen the symptoms. With treatment some see a resolution of symptoms while others do not.

Rates in those on atypical antipsychotics are about 20% while those on typical antipsychotics have rates of about 30%. Risk is greater in older people. The term "tardive dyskinesia" first came into use in 1964.

Extrapyramidal symptoms (EPS), also known as extrapyramidal side effects (EPSE), are drug-induced movement disorders that include acute and tardive symptoms. These symptoms include dystonia (continuous spasms and muscle contractions), akathisia (motor restlessness), parkinsonism (characteristic symptoms such as rigidity), bradykinesia (slowness of movement), tremor, and tardive dyskinesia (irregular, jerky movements). Antipsychotics are often discontinued due to inefficacy and intolerable side effects such as extrapyramidal symptoms.

Since it is difficult to measure extrapyramidal symptoms, rating scales are commonly used to assess the severity of movement disorders. The Simpson-Angus Scale (SAS), Barnes Akathisia Rating Scale (BARS), Abnormal Involuntary Movement Scale (AIMS), and Extrapyramidal Symptom Rating Scale (ESRS) are rating scales frequently used for such assessment and are not weighted for diagnostic purposes; these scales can help physicians weigh the benefit/expected benefit of a medication against the degree of distress which the side effects are causing the patient, aiding in the decision to maintain, reduce, or discontinue the causative medication/s.

Akathisia may range in intensity from a sense of disquiet or anxiety, to excruciating discomfort, particularly in the knees. Patients typically pace for hours because the pressure on the knees reduces the discomfort somewhat; once their knees and legs become fatigued and they are unable to continue pacing, they sit or lie down, although this does not relieve the akathisia. When misdiagnosis occurs in antipsychotic neuroleptic-induced akathisia, more antipsychotic may be prescribed, potentially worsening the symptoms. Neuro-psychologist Dennis Staker had drug-induced akathisia for two days. His description of his experience was this: "It was the worst feeling I have ever had in my entire life. I wouldn't wish it on my worst enemy." Many patients describe symptoms of neuropathic pain akin to fibromyalgia and restless legs syndrome. In Han et al. (2013), the authors describe restless legs syndrome's relation to akathisia, "Some researchers regard RLS as a 'focal akathisia' [in the legs]." Although these side effects disappear quickly and remarkably when the medication is stopped, tardive, or late-persisting akathisia may go on long after the offending drug is discontinued, sometimes for a period of years.

Healy, et al. (2006), described the following regarding akathisia: tension, insomnia, a sense of discomfort, motor restlessness, and marked anxiety and panic. Increased labile affect can result, such as weepiness.

Jack Henry Abbott (1981) describes the sensation:

In addition, not all observable restless motion is akathisia. For example, mania, agitated depression, and Attention Deficit Hyperactivity Disorder may look like akathisia, but the movements feel voluntary and not due to restlessness.

The extrapyramidal system regulates posture and skeletal muscle tone. Extrapyramidal symptoms (also called extrapyramidal side effects) get their name because they are symptoms of disorders in this system.

This is characterized by attacks of involuntary movements (dystonia, chorea, or ballism), which are typically triggered by sudden voluntary movements, but can also be triggered by involuntary movements as well (for example, hyperventilating). These voluntary movements usually involve whole body activity such as standing, walking, and running. The age of onset is typically in childhood or early adolescence with most cases reporting improvement or complete remission with aging. Attacks last from seconds to minutes and are known to be at higher risk of occurring during stress, fear, cold, heat, or menstruation.

The paroxysmal dyskinesias are mainly classified by their triggers and on the basis of the duration and frequency of the attacks. The three main types are paroxysmal kinesigenic dyskinesia (PKD), paroxysmal non-kinesigenic dyskinesia (PNKD) and paroxysmal exercise-induced (exertion-induced) dyskinesia (PED).

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.

Acute dystonia nearly always develops a few weeks after a dopamine blocking agent/medication has begun or a substantial increase in antipsychotic dosage. An acute dystonic reaction consists of sustained, painful muscular spasms, producing twisting of the trunk/body and abnormal posture. The most frequent occurrences of these spasms have been reported in the neck, tongue, and jaw. Oculogyric crisis and opisthotonus are also very common. Acute effects of dopamine antagonists also include Parkinsons-like symptoms, manifested by bradykinesia, pin rolling tremor, and rigidity of the body. These movements may fluctuate over hours and temporarily dissipate in response to reassurance, and the individual episodes may last minutes to hours. Acute reactions are more common in older patients and females. The pathophysiology underlying these reactions is unknown, but the movements usually occur during the period when blood medication level is dropping. The acute syndromes which occur due to prolonged exposure to a dopamine antagonist are collectively termed extrapyramidal symptoms, EPS.

Akathisia is a movement disorder characterized by a feeling of inner restlessness and inability to stay still. Usually the legs are most prominently affected. People may fidget, rock back and forth, or pace. Other may just feel uneasy. Complications include suicide.

Antipsychotics, particularly the first generation antipsychotics, are a leading cause. Other causes may include selective serotonin reuptake inhibitors, metoclopramide, reserpine, Parkinson’s disease, and untreated schizophrenia. It may also occur upon stopping antipsychotics. The underlying mechanism is believed to involve dopamine. Diagnosis is based on symptoms. It differs from restless leg syndrome in that akathisia is not associated with sleeping.

Treatment may include switching to an antipsychotic with a lower risk of the condition. Medications with tentative evidence of benefit include diphenhydramine, trazodone, benztropine, mirtazapine, and beta blockers. Vitamin B6 or correcting iron deficiency may also be useful. Around half of people on antipsychotics develop the condition. The term was first used by Ladislav Haškovec, who described the phenomenon in 1901. It is from Greek "a-" meaning "not" and "kathízein" meaning "to sit" or in other words an "inability to sit".

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.

The predominant symptom of Pisa syndrome is dystonia. Dystonia is a neurological movement disorder characterized by sustained muscle contraction leading to abnormal posture, twisting, and repetitive movement. In Pisa Syndrome specifically there is commonly a tonic flexion of the trunk of the body to one side, leading to a slight lean (reminiscent of the Leaning Tower of Pisa, hence the name "Pisa syndrome"). This is usually associated with a backward axial rotation of the spine and indifferent to markedly abnormal posture. Patients diagnosed with Pisa Syndrome usually experience either acute dystonia or tardive dystonia, also known as tardive dyskinesia. Differential diagnosis between the two may be hard to accomplish without a complete patient history, since both types of dystonia may occur simultaneously in a patient. These symptoms generally disappear after discontinuation of the antipsychotic drug. The time of onset of symptoms may vary depending on drug being administered and the neurological characteristics of the patient in question.

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.

Tardive dysphrenia, was proposed by the American neurologist Stanley Fahn, the head of the Division of Movements Disorders of the Neurological Institute of New York, in collaboration with the psychiatrist David V Forrest in the 1970s.

It originally was linked to a unique, rare, behavioral/mental neuroleptic drug-induced tardive syndrome observed in psychiatric patients (schizophrenia in particular) treated with the typical antipsychotic drugs or neuroleptics. Tardive dysphrenia is one of many neuroleptic-induced tardive syndromes, including tardive dyskinesia and the other already-recognized tardive dystonia, and tardive akathisia.

More recently, the Brazilian psychiatrist Leopoldo Hugo Frota, Adjunct Professor of Psychiatry at Federal University of Rio de Janeiro, extended the original Fahn's construct to enclose the — independently described but etiologically related concepts of — rebound psychosis, supersensitivity psychosis (Guy Chouinard) and schizophrenia pseudo-refractoriness (Heinz Lehmann & Thomas Ban) or secondary acquired refractoriness.

There is some disagreement in the psychiatric community regarding the diagnosis of tardive dysphrenia. Therefore, the following description should be considered general and tentative.

Paroxysmal kinesigenic dyskinesia is diagnosed using a strict set of guidelines. These criteria were studied and confirmed by Bruno et al. in a study of 121 individuals with PKD. The age at onset is between 1 and 20 years old. The attacks of involuntary movements last less than one minute and have a known trigger, usually a sudden voluntary movement. For example, if a PKD patient stands up or begins walking after being sedentary for a period of time, or a person goes from a walk to a run, it can trigger an attack. Persons with PKD do not lose consciousness during attacks and have a full memory of the entire attack. Lastly, people with the disorder have a good response to medication and are usually prescribed anticonvulsants. The study also found that patients with familial PKD exhibit symptoms that follow the diagnostic criteria closely, while sporadic PKD individuals may deviate slightly. Prior to criteria for diagnosis being set out, many patients with PKD were often diagnosed with some form of epilepsy. Many patients also experience an aura, similar to those experienced with epilepsy, preceding their attacks. Some patients describe it as a tingling sensation in the affected limb or “butterflies in their stomach.” Some individuals also have precipitants, such as stress and anxiety, that make it more likely for attacks to occur.

The above diagnostic criteria also set PKD apart from the other paroxysmal dyskinesias, which include paroxysmal nonkinesigenic dyskinesia (PNKD) and paroxysmal exercise-induced dyskinesia (PED). While PKD attacks last less than one minute, PNKD attacks last a few minutes to a few hours, and as the name suggests, the attacks do not occur because of a sudden voluntary movement like PKD. Additionally, PKD can almost always be managed with drug therapy, while PNKD is not as responsive to anticonvulsants. PED, on the other hand, separates itself from PKD in that it is caused by prolonged exercise. Attacks from PED will cease soon after exercise is stopped.

Tardive dysphrenia is characterized by a worsening of psychiatric symptoms that can be directly traced to the administration of antipsychotic medication.

Six symptoms are considered when diagnosing tardive dysphrenia:

A) The patient shows:

B) The symptoms are present for a full four weeks (full two weeks if successfully treated by immediate reinstitution or augmentation with a more potent drug and/or the rising of the previous drug) and contain any of these patterns:

C) Criteria A & B signs and symptoms emerge progressively with the administration of an oral antipsychotic drug or during the four-weeks period that follows its withdrawal (8 weeks for dépôt formulations).

D) There has been any exposure to a typical and/or atypical antipsychotic drug for at least three full months (full 12 weeks), or 1 full month (full 4 weeks) if the patient is sixty years old or older.

E) The clinical signs and symptoms cannot be attributed to another psychiatric condition, neurological condition, somatic illness, or severe stress. Also, exposure to other psychosis-inducing medicines must be excluded.

F) The signs and symptoms could not be better explained by an eventual previous psychiatric/neurological condition unfavorable natural evolution (i.e., Primary Refractory or poor prognosis Schizophrenia; severe Acute Mania; Dementia with Psychotic Symptoms) or by Neuroleptic Dysphoria.

Initial symptoms include restlessness, agitation, malaise, or a fixed stare. Then comes the more characteristically described extreme and sustained upward deviation of the eyes. In addition, the eyes may converge, deviate upward and laterally, or deviate downward. The most frequently reported associated findings are backwards and lateral flexion of the neck, widely opened mouth, tongue protrusion, and ocular pain. However it may also be associated with intensely painful jaw spasm which may result in the breaking of a tooth. A wave of exhaustion may follow an episode. The abrupt termination of the psychiatric symptoms at the conclusion of the crisis is most striking.

Other features that are noted during attacks include mutism, palilalia, eye blinking, lacrimation, pupil dilation, drooling, respiratory dyskinesia, increased blood pressure and heart rate, facial flushing, headache, vertigo, anxiety, agitation, compulsive thinking, paranoia, depression, recurrent fixed ideas, depersonalization, violence, and obscene language.

It is often not realized that in addition to the acute presentation, oculogyric crisis can develop as a recurrent syndrome, triggered by stress, and exposure to the above drugs.

Differentiating some kinds of atypical Parkinson: Northwest Parkinson Foundation

Before Parkinson's disease is diagnosed, the differential diagnoses include:

- AIDS can sometimes lead to the symptoms of secondary parkinsonism, due to commonly causing dopaminergic dysfunction. Indeed, parkinsonism can be a presenting feature of HIV infection.

- Corticobasal degeneration

- Creutzfeldt–Jakob disease

- Dementia pugilistica or "boxer's dementia" is a condition that occurs in athletes due to chronic brain trauma.

- Diffuse Lewy body disease

- Drug-induced parkinsonism ("pseudoparkinsonism") due to drugs such as antipsychotics, metoclopramide, sertraline, fluoxetine or the toxin MPTP

- Encephalitis lethargica

- Essential tremor, an illness which has some diagnostic overlap with Parkinson's disease

- Orthostatic tremor

- MDMA addiction and frequent use has been linked to Parkonsonism. Several cases have been reported where individuals are diagnosed with the syndrome after taking MDMA.

- Multiple system atrophy

- Pantothenate kinase-associated neurodegeneration, also known as neurodegeneration with brain iron accumulation or Hallervorden-Spatz syndrome

- Parkinson plus syndrome

- Progressive supranuclear palsy

- Toxicity due to substances such as carbon monoxide, carbon disulfide, manganese, paraquat, mercury, hexane, rotenone, Annonaceae, and toluene (inhalant abuse: "huffing")

- Vascular parkinsonism, associated with underlying cerebrovascular disease

- Wilson's disease is a genetic disorder in which an abnormal accumulation of copper occurs. The excess copper can lead to the formation of a copper-dopamine complex, which leads to the oxidation of dopamine to aminochrome. The most common manifestations include bradykinesia, cogwheel rigidity and a lack of balance.

- Paraneoplastic syndrome: neurological symptoms caused by antibodies associated with cancers

- Genetic

- Rapid onset dystonia parkinsonism

- Parkin mutation

- X-linked dystonia parkinsonism

- Autosomal recessive juvenile parkinsonism

Parkinsonism is a clinical syndrome characterized by tremor, bradykinesia, rigidity, and postural instability. Parkinsonism is found in Parkinson's disease (after which it is named), however a wide range of other causes may lead to this set of symptoms, including some toxins, a few metabolic diseases, and a handful of neurological conditions other than Parkinson's disease.

About 7% of people with parkinsonism have developed their symptoms following treatment with particular medications. Side effect of medications, mainly neuroleptic antipsychotics especially the phenothiazines (such as perphenazine and chlorpromazine), thioxanthenes (such as flupenthixol and zuclopenthixol) and butyrophenones (such as haloperidol), piperazines (such as ziprasidone), and rarely, antidepressants. The incidence of drug-induced parkinsonism increases with age. Drug-induced parkinsonism tends to remain at its presenting level, not progress like Parkinson's 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.

Episodes are relatively short-lived, lasting anywhere from 5–30 minutes, and in most cases disappear completely after cessation of the physical exercise. Most patients will experience 1 to 5 episodes per month, but some can have attacks daily. The muscles most often affected are usually in the legs and feet (75% of reported cases), but the upper body muscles such as the arms, face, neck, and trunk have also been observed to be affected during the episodes of dystonia. Age of onset is usually sometime in childhood, but can range from 1–30 years old. In one study it was found that the mean age of onset was around 8 years. Similarly in the study, the legs were the most common affected part of the body and the attacks were reported as stiffening and cramps by those affected.During an episode of PED patients find walking nearly impossible.Cerebral spinal fluid (CSF) analysis showed a two-fold increase of homovanillic acid and 5-hydroxyindoleacetic acid immediately following exercise compared to normal levels. This indicated that increased dopaminergic transmission could contribute to PED and other paroxysmal dyskinesias. Neurological examinations, EEG, and brain imaging are all normal in PED patients.

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.

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.

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.

The condition manifests itself as attacks lasting from a few minutes to several hours. Episodes only happen when the individual is awake, and they remain conscious throughout the attack. Symptoms are most severe in youth and lessen with age. Sufferers can have multiple attacks on a daily basis or may have periods of weeks or months between attacks. Symptoms experienced during attacks can vary and include dystonia, chorea, athetosis, ballismus, or a combination.