eMedicine Specialties > Neurology > Movement and Neurodegenerative Diseases

Tardive Dyskinesia

Author: James Robert Brasic, MD, MPH, Research Associate, Division of Nuclear Medicine, Russell H Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine
Coauthor(s): Brian Bronson, MD, Staff Physician, Department of Psychiatry, New York University Medical Center; Tristen T Chun, Division of Nuclear Medicine, Russell H Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine
Contributor Information and Disclosures

Updated: Oct 2, 2008

Introduction

Background

Tardive dyskinesias (TDs) are involuntary movements of the tongue, lips, face, trunk, and extremities that occur in patients treated with long-term dopaminergic antagonist medications. Although they are associated with the use of neuroleptics, TDs apparently existed before the development of neuroleptics. People with schizophrenia appear especially vulnerable to developing TDs after exposure to conventional neuroleptics, anticholinergics, toxins, substances of abuse, and other agents. TDs are most common in patients with schizophrenia, schizoaffective disorder, or bipolar disorder who have been treated with antipsychotic medication for long periods, but TDs occasionally occur in other patients as well. For example, people with fetal alcohol syndrome, other developmental disabilities, and other brain disorders are vulnerable to the development of tardive dyskinesias, even after receiving a single dose of the causative agent.

TDs may be differentiated from acute movement disorders that commonly occur in the same patient groups. The acute movement disorders that occur as manifestations of effects of neuroleptics and other dopamine antagonists include akathisia, acute dystonia, and other hyperkinetic dyskinesias. Acute effects of dopamine antagonists also include Parkinsonian syndromes manifested by bradykinesia, rigidity, and pill rolling tremor. The acute movement disorders resulting from exposure to dopamine antagonists are commonly termed extrapyramidal syndromes (EPS).

The occurrence of acute movement disorders upon exposure to dopamine antagonists is increased in female patients and older patients. Use of potent dopamine antagonists, prolonged exposure to dopamine antagonists, and prior occurrence of acute movement disorders on exposure to dopamine antagonists are also associated with an increased risk for the occurrence of acute movement adverse effects. Withdrawal dyskinesias may also occur as treatment with dopamine antagonists is decreased or withdrawn. They are often refractory to all therapeutic modalities. In addition to the prototypic orofacial dyskinesia, tardive syndromes also include a spectrum of hyperkinesias occurring during or after prolonged treatment with dopamine antagonists.

Bishnoi and colleagues provided evidence of the involvement of the adenosinergic receptor system in the development of TD in rodents. Haloperidol induced vacuous chewing movements, orofacial movements, and facial stereotypies in rate. These changes were reversed after treatment with adenosine or caffeine. These findings provide evidence that adenosine, a major inhibitory neurotransmitter in the central nervous system, plays a role in TD. Additionally, these results suggest potential therapeutic agents for clinical trials.1

Abnormalities of the dopamine receptor D2 (DRD2), the dopamine receptor D3 (DRD3), the dopamine transporter (DAT), and the manganese superoxide dismutase (MnSOD) genes have been hypothesized to play a role in TD.

Bishnoi and colleagues have demonstrated a beneficial effect of progesterone on an animal model of tardive dyskinesia. They hypothesize that the favorable effect of progesterone is modulated by means of the GABergic and neuroprotective actions of alloprogesterone, a metabolite of progesterone.2

The polymorphisms of the DRD2 gene, TaqI A and TaqI B, and associated haplotypes, were found to be associated with TD by Liou and colleagues.3 Bakker and colleagues report a possible association with a polymorphism of the DRD3 gene and TD.4

Dysfunction of the dopamine transporter has been hypothesized to play a role in the development of TD. However, Lafuente and colleagues did not find evidence of involvement of a polymorphism with a variable number of tandem repeats (VNTD) in the DAT gene (SLC6A3) in dyskinesias induced by antipsychotics.5 Thus, further research is needed to investigate the role of the dopamine transporter in the development and maintenance of TD.

Galecki and colleagues have reported the association of a polymorphism of the manganese superoxide dismutase (MnSOD) gene and TD.6

Pathophysiology

For most of the past century, movement disorders (ie, abnormal adventitious movements) have been categorized as extrapyramidal syndromes (EPSs) due to lesions of the extrapyramidal system of the central nervous system. The pyramidal system, controlling voluntary movements, includes precise anatomic pathways from the cortex to muscle. Voluntary movements through the pyramidal systems are visible. By contrast, extrapyramidal motor activities result in automatic movement and static, postural movement activities that are not noticeable. The extrapyramidal system includes theorized connections within the basal ganglia, the striatopallidonigral system, and other structures of the central nervous system that contribute to the regulation of movement, including related brainstem nuclei and the cerebellum.

An example of a classic disorder of the pyramidal system is a stroke, resulting in paralysis of an extremity. Corticospinal lesions above the pyramidal decussation typically result in paralysis of volitional movements of the contralateral half of the body and a fixed posture with flexion of the upper extremity and extension of the lower extremity. Bilateral corticospinal lesions of the upper pons and midbrain typically cause extension of all 4 extremities and decerebrate rigidity with dorsiflexion of the cervical and thoracolumbar spine. Unilateral lesions of the upper pons and midbrain often result in extension of the ipsilateral arm and leg.

Extrapyramidal dysfunction

Classic disorders of the extrapyramidal system include a variety of involuntary movement disorders. Some of these movement disorders include dyskinesias such as akathisia, chorea, dystonia, myoclonus, stereotypy, tic, and tremor.

[#Table1]Table 1. Classic Characterization of the Pyramidal and Extrapyramidal Systems
 

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Table
CharacteristicPyramidalExtrapyramidal
AnatomyPrecisely demarcated pathways from cortex to muscleHypothesized pathways among basal ganglia and other structures of the central nervous system
Physiologic movementsVoluntaryInvoluntary
Pathologic movementsParalysis, paresis, hyperreflexia, and spasticityAkathisia, athetosis, ballism, chorea, dystonia, myoclonus, stereotypy, tic, and tremor
CharacteristicPyramidalExtrapyramidal
AnatomyPrecisely demarcated pathways from cortex to muscleHypothesized pathways among basal ganglia and other structures of the central nervous system
Physiologic movementsVoluntaryInvoluntary
Pathologic movementsParalysis, paresis, hyperreflexia, and spasticityAkathisia, athetosis, ballism, chorea, dystonia, myoclonus, stereotypy, tic, and tremor

The pathophysiology of extrapyramidal disorders has been disputed because some extrapyramidal disorders may not involve lesions of the basal ganglia and, in addition, may not be involuntary. Because of the problems inherent in the concept of the extrapyramidal system, caution must be exercised in the classification of movement disorders as EPSs, and new approaches to the classification of movement disorders may be helpful.

Dyskinesia is a type of movement disorder that is subdivided into bradykinesias and hyperkinesias. Bradykinesias are characterized by abnormal slowness (eg, rigidity), difficulty initiating and terminating actions, and the masked facial expression of patients with Parkinson disease. Hyperkinesias are purposeless movements, including akathisia, chorea, dystonia, myoclonus, stereotypy, tic, and tremor.

The classification of movement disorders as bradykinesias and hyperkinesias is based on the observed phenomenology, etiology, and topography. Practitioners and researchers may be confounded by these classifications of movement disorders and may prefer instead to use clinical impressions. Methods of data analysis, including linear and logistic regression, linear discriminant function analysis, factor analysis, inverted factor analysis, tree approaches, dynamic clusters analysis, and principal component analysis, may facilitate the classification of these diseases.

Dopamine system

The pathophysiology of TD is not well understood. Central dopamine blockade is hypothesized to play a role in the pathogenesis of TD. Acute movement disorders are also hypothesized to result, in part, from the blockade of dopamine receptors by dopamine antagonists.

Several hypotheses have been proposed for the development of TD.

  • Striatal dopamine receptor supersensitivity may be responsible.
  • Chronic dopamine blockade may result in up-regulation of dopamine receptor responsiveness.
  • TD is hypothesized to result from compensatory supersensitivity of dopamine receptors following chronic blockade. Long-term blockade of dopamine D2 receptors in the basal ganglia by dopamine D2 antagonists (eg, neuroleptics) may produce TD.
  • When dopamine D2 -receptor blockade is reduced (even slightly), an exaggerated response of the postsynaptic dopamine D2 -receptor (even to low concentrations of dopamine) may result.
  • Striatal disinhibition of the thalamocortical pathway from imbalance of D1 and D2 receptors may be involved.
  • Neurodegeneration secondary to lipid peroxidation or excitotoxic mechanisms may be responsible.

Although the dopamine D2 receptor has traditionally been implicated in the pathogenesis of TD, mounting evidence indicates that, in some individuals, the dopamine D3, D4, and D5 receptors are involved.

Most likely, genetic traits produce a vulnerability to develop TD when a susceptible individual is exposed to particular agents. For example, the MscI polymorphism of the dopamine D3 receptor gene has been associated with the development of TD. Support for the hypothesis that TD may result from blockade of postsynaptic dopamine receptors in the basal ganglia and other parts of the brain exists in the form of the beneficial effects of increasing doses of neuroleptics for some patients with TD. Thus, dopamine antagonists may mask TD.

Nicotine may play a role in the pathophysiology of TS. Cigarette smokers appear to have increased metabolism of dopamine D2 antagonists. Nicotinic agonists appear to relieve dyskinesias in some people with Tourette syndrome (see Tourette Syndrome), a condition characterized by the presence of motor and phonic tics (see Tourette Syndrome and Other Tic Disorders). The relationship between TD and the use of cigarettes and other nicotinic agonists remains to be clarified.

In 2005, Tan and colleagues reported an inverse correlation of plasma levels of brain-derived neurotrophic factor and dyskinetic movements in people with schizophrenia with TD.7 Thus, brain-derived neurotrophic factor appears to have a protective effect in the nervous system against TD with people with schizophrenia.

Modestin and colleagues have observed that a fluctuating course of the illness characterizes people with tardive dyskinesia. They also report that length of illness is highly correlated with tardive dyskinesia.8

Bishoi and colleagues have noted that Curcumin, an antioxidant, may prevent the development of dyskinesias induced in animals by dopamine receptor blocking drugs.9

Clinical presentation

Patients often have movement disorders that may actually represent a mixture or overlap of several dyskinesia disorders (see Media file 2). Individuals treated with neuroleptics may demonstrate both acute and chronic effects, manifested by acute dyskinesias and TD. Individuals may simultaneously manifest akathisia and tics after long-term treatment with neuroleptics.

The diagnosis of acute and chronic dyskinesias may be difficult without a past history when seeing a patient for the first time. Precise documentation of a patient's complete movement history and medication history may facilitate accurate delineation of movement disorders. Therefore, a full neurologic and pharmacologic history may provide the basis to distinguish idiopathic Tourette disorder from acute medication-induced tardive tics.

Patients and families often cannot provide accurate histories; thus, firm diagnoses may be impossible. Because acute and tardive medication effects can be observed simultaneously, the distinction may be challenging in a clinical setting. Observing patients carefully on a regular basis with precise documentation at each visit, through structured rating instruments, of the phenomenology and topography of movements and the pharmacologic treatments helps to provide a basis for accurate future diagnosis of acute and TDs.

Genetic influences

A genetic basis for TD has not been identified. In particular, a functional polymorphism of the gene coding for human glutathione S-transferase P1 (GSTP1) does not appear to be associated with TD.10 Additionally, CYP3A4 and CYP2D6 gene polymorphisms are apparently unassociated with TD.11

General diagnosis

TD is common in individuals with psychotic disorders (eg, schizophrenias, schizoaffective disorders, bipolar disorders) who are treated with antipsychotic medications, especially dopamine antagonists, for many years.

Generally, TD is diagnosed if one of the following circumstances is present (see Media file 1):

  • A person who has taken neuroleptics for at least 3 months (1 mo if older than 60 y) develops at least 2 movements of at least mild intensity while taking a neuroleptic.
  • A person who has taken neuroleptics for at least 3 months (1 mo if older than 60 y) develops at least 1 movement of at least moderate intensity while taking a neuroleptic.
  • A person who has taken neuroleptics for at least 3 months (1 mo if older than 60 y) develops at least 2 movements of at least mild intensity within 4 weeks of the discontinuation of the neuroleptic.
  • A person who has taken neuroleptics for at least 3 months (1 mo if older than 60 y) develops at least 1 movement of at least moderate intensity within 4 weeks of the discontinuation of the neuroleptic.
  • A person who has taken neuroleptics for at least 3 months (1 mo if older than 60 y) develops at least 2 movements of at least mild intensity within 8 weeks of the discontinuation of a depot neuroleptic.
  • A person who has taken neuroleptics for at least 3 months (1 mo if older than 60 y) develops at least 1 movement of at least moderate intensity within 8 weeks of the discontinuation of a depot neuroleptic.

Frequency

United States

In 1997, Goetz estimated that TD occurs in approximately 15-30% of persons who receive long-term treatment with neuroleptics.12 TD is more likely to occur in individuals who have manifested acute adverse effects of exposure to dopamine antagonists. Frequency of the various subtypes varies markedly. For example, orofacial, buccolingual, and masticatory dyskinesias are common, but only 1-2% of people treated with dopamine antagonists develop tardive dystonia.

Orofacial TDs differ from peripheral TDs in the occurrence of comorbid acute movement disorders. Acute tremor, acute akathisia, and acute Parkinsonism are more common in people with peripheral TD. Distinguishing acute and TDs in an individual patient can represent a serious diagnostic challenge.

The prevalence of TD is higher in cigarette smokers.13

International

The international frequency is apparently similar to that of the United States.

Race

TD occurs in persons of every race.

  • Studies in different populations have identified overall prevalences of 1-65%.
  • Africans and African-Americans appear to be especially vulnerable to TD after exposure to low doses of neuroleptics for short durations.
  • However, drawing any conclusions on the basis of these results is difficult because different investigators conducted the studies in different settings. A number of other variables, such as therapeutic approaches, methodologic inconsistencies, diet, weather, and varied assessments, may also contribute to the differences in various racial groups.

Sex

Elderly female patients appear to be particularly susceptible. Young men are prone to develop tardive blepharospasm and tardive dystonia.

Age

TD occurs in all ages.

  • In 2001, Connor et al found that 5.9% of 95 young people aged 7-21 years receiving dopamine antagonist treatment for 3 months had TD.14
  • Advanced age is a major risk factor for TD. The prevalence of TD is 29% in elderly patients receiving dopamine antagonist treatment for 3 months and 26-67% in patients treated long term.

Clinical

History

Although TD has been observed after exposure to various substances (eg, L-dopa, amphetamine, metoclopramide), the prototype TD is the orofacial (ie, buccolingual, masticatory), hyperkinesias induced by neuroleptics (antipsychotic dopamine D2 -receptor blockers). People with other movement disorders and those with diabetes mellitus are at increased risk of TD.

Neuroleptic-induced TD is characterized by choreiform, athetoid, and rhythmic movements of the tongue, jaw, trunk, and extremities for at least 4 weeks that begin during treatment with neuroleptics or within 4 weeks of discontinuing neuroleptics. Diagnosis of neuroleptic-induced TD generally requires exposure to neuroleptics for at least 3 months. At least 1 month of exposure is typically required if the patient is aged 60 years or older. Oral and genital pain can be prominent manifestations of TD.

  • Neuroleptic-induced TD is excluded if symptoms and signs result from another neurologic or medical disorder, ill-fitted dentures, or other medications. For example, hyperthyroidism may manifest with choreiform movements of the limbs. Furthermore, it cannot be diagnosed if symptoms and signs result from an acute neuroleptic-induced movement disorder.
  • Antiparkinsonism agents usually do not improve neuroleptic-induced dyskinesias. Decreasing the dose of the neuroleptic may increase the movements temporarily. Increasing the dose of the neuroleptic diminishes movements in some patients thus masking the TD.
  • Although the neuroleptic dose may temporarily diminish the disorder, regular increments are needed to achieve apparent beneficial effects. Over a long-term period, maintaining and increasing doses of neuroleptics to mask TD may be ineffective. However, situations may exist in which masking of TD by continuing and escalating neuroleptic doses may be justified. Benefits and risks must be weighed. Neuroleptic-induced TDs are absent during sleep.

On initial examination, obtain a history of neurologic disorders that may involve the basal ganglia (eg, cerebrovascular disease, encephalitis, head trauma, neoplasms). Obtain a family history for hereditary dyskinesias associated with Huntington disease, Wilson disease, and torsion dystonia.

Inquire about medications, including amphetamines, L-dopa, and substances that may result in dyskinesias (see Table 2). Specifically note if antiemetic medications, especially metoclopramide (Reglan), prochlorperazine (Compazine), and related compounds are administered. Table 2 lists the medications reported to cause TD. Table 3 lists compounds associated with dyskinesias that usually resolve with dose reduction or discontinuation.

Medications causing tardive dyskinesia are as follows:

  • Antipsychotic agents (ie, neuroleptics)
    • Butyrophenones
      • Droperidol (Inapsine)
      • Haloperidol (Haldol)
      • Dibenzodiazepines
      • Loxapine (Daxolin, Loxitane)
    • Diphenylbutylpiperidines
      • Pimozide (Orap)
    • Indolones
      • Molindone (Moban)
    • Phenothiazines
      • Chlorpromazine (Thorazine)
      • Fluphenazine (Permitil, Prolixin)
      • Mesoridazine (Serentil)
      • Perphenazine (Trilafon)
      • Thioridazine (Mellaril)
      • Trifluoperazine (Stelazine)
    • Thioxanthenes
      • Thiothixene (Navane)
  • Newer atypical antipsychotic agents (sporadically linked to TDs)
    • Olanzapine (Zyprexa)
    • Quetiapine (Seroquel)
    • Risperidone (Risperdal)
    • Amisulpride (Solian)

[#Table3]Nonneuroleptic medications linked to dyskinesias are as follows:

  • Anticholinergics
    • Benzhexol
    • Biperiden (Akineton)
    • Ethopropazine
    • Orphenadrine (Norflex, Norgesic, Orphengesic)
    • Procyclidine
  • Antidepressants
    • Monoamine oxidase inhibitors (MAOIs)
      • Phenelzine (Nardil)
    • Selective serotonin reuptake inhibitors (SSRIs)
      • Fluoxetine (Prozac)
      • Sertraline (Zoloft)
    • Trazodone (Desyrel)
    • Tricyclic antidepressants
      • Amitriptyline (Elavil, Vanatrip)
      • Amitriptyline and perphenazine (Triavil)
      • Amoxapine (Asendin)
      • Doxepin (Sinequan)
      • Imipramine (Tofranil)
  • Antiemetics
    • Metoclopramide (Maxolon, Reglan)
    • Prochlorperazine (Compazine)
  • Antiepileptic drugs
    • Carbamazepine (Atretol, Epitol, Tegretol)
    • Ethosuximide (Zarontin)
    • Phenobarbital (Barbita, Luminal sodium, Solfoton)
    • Phenytoin (Dilantin)
  • Antihistamines
  • Antihistaminic decongestants
    • Combinations of antihistamines and sympathomimetics
  • Antimalarials
    • Chloroquine (Aralen)
  • Antiparkinson agents
    • Bromocriptine (Parlodel)
    • Levodopa (Dopar, L-Dopa, Larodopa)
    • Levodopa-carbidopa (Atamet, Sinemet)
  • Anxiolytics
    • Alprazolam (Xanax)
  • Biogenic amines
    • Dopamine (Intropin)
  • Mood stabilizers
    • Lithium (Cibalith-S, Eskalith, Lithane, Lithobid, Lithotabs, Lithonate)
  • Oral contraceptives
    • Estrogens
  • Stimulants
    • Amphetamine (Adderall)
    • Methylphenidate (Ritalin, Ritalin SR)
    • Caffeine

Unlike TD, Sydenham chorea is a disorder associated with a history of group A streptococcal infection and rheumatic fever in children.

Sydenham chorea typically affects children and adolescents 6 months or more after an infection with group A streptococci. Prompt administration of antibiotic therapy for infections with group A streptococci dramatically reduces the incidence of Sydenham chorea. The female-to-male ratio of Sydenham chorea is approximately 2:1.

This disease is characterized by the rapid onset of chorea, muscular weakness, hypotonia, dysarthria, obsessions, compulsions, and other behavioral and emotional disturbances. After an abrupt or insidious onset, Sydenham chorea worsens over 2-4 weeks and then resolves over 3-6 months. Chorea may persist after the episode has ended. One fifth of patients with Sydenham chorea experience a recurrence, typically within 2 years of the initial episode.

Hallervorden-Spatz disease occurs in patients aged 10-15 years, a different age group than that of persons with TD. Hallervorden-Spatz disease is an extremely rare, progressive neurogenetic disorder with autosomal recessive inheritance associated with dementia and death (approximately 20 y after onset). It is characterized by rigidity, dystonia, choreoathetosis, spasticity, foot deformity, and intellectual deterioration. It is associated with excessive iron deposition in the basal ganglia that can be observed on MRI.

Differentiate neuroleptic-induced TD from spontaneous dyskinesias and mannerisms of psychosis and other mental disorders. Several rating scales have been developed to identify the presence and severity of TD.

The most widely used instrument is the Abnormal Involuntary Movement Scale (AIMS) developed by the Psychopharmacology Research Branch of the National Institute of Mental Health. Because the AIMS can be readily administered in a few minutes, its use is recommended in patients who receive treatment with substances that may cause TD. Administer the AIMS at baseline before the institution of pharmacotherapy to document any movements present. Then administer the AIMS at least every 3 months during the course of treatment. Please refer to Media file 3 for the instructions and recording sheet for the AIMS.

Part of the AIMS assessment includes observation of the patient when he or she is distracted by other activities. Patients may suppress movements while concentrating intensely. Therefore, the administration of the AIMS can be supplemented by the requests to perform additional tasks during the AIMS. Movements may then be demonstrated when the patient is concentrating on the additional tasks.

  • For example, during the administration of item 5 of the AIMS assessment, have the patient sit in a chair with hands on knees, legs slightly apart, and feet flat on floor. Look at the entire body for movements while in this position (see Media file 3). Then ask the patient to count backwards from 30.
  • In addition, during the administration of item 5 of the AIMS assessment, ask the patient to sit with hands hanging unsupported; if the patient is male, with the hands between the legs, and if female and wearing a dress, with the hands hanging over the knees. Observe the hands and other body areas (see Media file 3). Then ask the patient to describe in detail the path traveled today. During this process ask the patient where the trip started, what streets were traveled, where turns were made, where the trip terminated, what floor and room were entered. These procedures stimulate the patient and may provoke the appearance of movement disorders.

To assess the appropriateness of treatment with antipsychotic medication, the Psychoactive Medication Quality Assurance Rating Survey (PQRS) can be used at initial assessment and then repeated annually (see Media file 4) and the PQRS Screening Criteria can be repeated monthly (see Media file 5).

Specific TDs (eg, orofacial dyskinesia, tardive akathisia, tardive blepharospasm, tardive dystonia, tardive myoclonus, tardive tics) resulting from long-term use of dopamine antagonists may occur concurrently.

Tardive akathisia manifests by repetitive tapping, squirming, and marching movements. It occurs as the dose of the dopamine antagonist is decreased after long-term treatment. People with akathisia complain of inner restlessness and the inability to remain still. Unlike other movement disorders, akathisia can be diagnosed solely on the subjective symptoms of the patient in the absence of any objective signs.

To elicit evidence of akathisia, ask the patient, "Do you have a sense of restlessness inside? Do you have an urge to move? Are you able to keep your feet still?" If the patient responds that those experiences are present, ask the patient to quantify the feelings as mild, moderate, or severe. Also ask the patient if the feelings are bothersome. If the patient finds the experiences to be distressing, again ask the patient to quantify the distress as mild, moderate, or severe. Tardive akathisia has been successfully treated with propranolol and other beta-blockers, biperiden, diazepam, clonidine, propoxyphene, codeine, and anticholinergics.

Blepharospasm (repetitive, forceful, sustained contraction of orbicularis oculi) may occur as an isolated finding. Meige syndrome refers to the occurrence of blepharospasm and dystonia of the lower face, jaw, and neck. Although blepharospasm has been reported with dopaminergic and sympathomimetic agents and antihistamines, it has also been associated with long-term treatment with dopamine antagonists. Tardive blepharospasm is the presence of repetitive sustained contractions of the orbicularis oculi for at least 1 month, developing during or within 3 months of discontinuation of treatment with dopamine antagonists (in the absence of other disease or familial causes). Symptoms of tardive blepharospasm fluctuate. Fatigue, anxiety, work, and light exacerbate tardive blepharospasm, while rest and sleep relieve it.

Tardive dystonia occurs in 1-2% of individuals during long-term treatment with dopamine antagonists. Differentiate tardive dystonia from acute dystonia, which occurs in the first days of neuroleptic treatment or after increasing the dose. Tardive dystonia presents as fixed posturing of the face and neck (eg, anterocollis, retrocollis, torticollis), extremities, and trunk. It may be localized, involving one or more body parts, or generalized. Unlike TD, tardive dystonia may improve with anticholinergic medication. Unlike TD, torsion dystonia is an inherited disorder with childhood onset typically occurring in people of Ashkenazi Jewish descent.

Tardive myoclonus, a rare disorder, presents as brief jerks of muscles in the face, neck, trunk, and extremities.

Tardive tourettism resembles Tourette syndrome and presents during or after treatment with dopamine antagonists. Typically, tardive tourettism begins in individuals older than 21 years, while Tourette syndrome commonly presents by age 7 years. This condition is characterized by frequent, multiple motor and vocal tics, echolalia, echopraxia, coprolalia, and copropraxia. Tics may be suppressed temporarily while inner tension builds; this inner tension is relieved by an explosion of tics. Tardive tourettism may occur with other TDs.

Tardive tremor is a hyperkinetic movement disorder associated with long-term treatment with dopamine antagonists. Kuo and Jankovic have reported the occurrence of tardive gait as a tardive dyskinesia.15

Physical

  • The neuroleptic-induced orofacial form constitutes the prototype of TD. This type is characterized by irregular movements of variable amplitude and low frequency.
  • Orofacial dyskinesias appear as involuntary, repetitive, and stereotyped facial grimacing and twisting and/or protrusion of the tongue.
  • The individual may initially be unaware of the movements. Family and friends may draw attention to the movements. Puckering, smacking, opening, and closing of the lips may occur constantly. The person may appear to be chewing or sucking on items. The movements resemble those of people with ill-fitting dentures.
  • Inquire about the use of dentures. Inquire if the person is aware of movements in the mouth, face, hands, and feet. Ask if dentures or teeth bother the patient. The tongue may protrude briefly out of the lips. If asked to maintain a protruded tongue, the person may be unable to keep the tongue out more than a second. Although the individual may attempt to disguise the movements by placing the hand to the mouth, in time, the movements become constant during waking hours and cannot be suppressed by the patient.
  • It is commonly associated with involuntary athetoid (slow, snakelike writhing) movements of the extremities, including wiggling, twisting, and tapping the fingers and toes. To perform a full assessment, ask the individual to remove shoes and socks so that the movements of the toes and feet can be observed fully. Movements typically become constant during waking hours. Often the individual cannot suppress the movements for more than a second.
  • TD is expressed in the tongue, cheeks, mandible, perioral area, and other regions of the face, fingers, and toes. Various facial movements (eg, lip smacking, chewing, sucking, puckering, tongue writhing, tongue protrusion, jaw opening, jaw closing, grimacing) are observed. TD may be observed in the upper face with excessive blinking and brow wrinkling.
  • Guitar and piano playing movements and other flexion and extension movements of the fingers and/or wrists can be observed. Flexion and extension movements of the ankles and toes are characteristic. Dyskinetic movements of the neck, trunk, and pelvis occasionally can occur. Jerking movements of the abdomen and diaphragm resulting in respiratory irregularity may occur.
  • Neuroleptic-induced TD is present at rest and diminishes or subsides when the affected body part is activated. For example, squeezing the hand of another person often eliminates finger dyskinesias, tongue protrusion commonly reduces tongue dyskinesias, and mouth opening diminishes orofacial dyskinesias. By pointing out the movements and asking the patient to stop, movements can be decreased. For example, by placing the patient's fingers on his or her lips, orofacial movements may be stopped.
  • Neuroleptic-induced TD is increased when the patient's attention is distracted away from the movements. This may occur when the examiner asks the patient to move a different body part. For example, finger dyskinesias are typically increased when the patient is asked to walk with arms resting comfortably at the sides of the body. Asking the patient to repeatedly touch the thumb to each finger sequentially in both hands may amplify TD in the tongue and the face. Provocative distracting movements may be necessary to induce movement in mild TD. Distraction of the patient is a component of the administration of the AIMS (see Media file 3).
  • Tardive akathisia includes the presence of subjective symptoms of restlessness and the urge to move. It refers to the inability to sit down or remain still. People with tardive akathisia exhibit constant pacing and moving of the hands and feet. They typically shift weight from one foot to the other when standing and swing legs when sitting.
    • Akathisia can be objectively and readily assessed in clinical settings by using the Hillside Akathisia Scale (see Media file 6). For this evaluation, examine the patient with bare feet and exposed hands so that movements of the extremities can be observed. Ask the patient to sit, stand, and lie still for 2 minutes in each position. While the patient is in each position, inquire about the presence of a sensation of inner restlessness and an urge to move. This can be accomplished by asking the patient after maintaining the designated position for a full minute, "Do you feel restless inside? Do you have the urge to move? Are you able to keep your feet still?" If the patient responds that these sensations are present, ask the patient to quantify the magnitude of the urge to move as mild, moderate, or severe.
    • Also, ask the patient if the urge to move is distressing. If the patient experiences distress, ask the patient to quantify the magnitude of the distress as mild, moderate, or severe. For clinical assessments, the individual may be assessed in the sitting and standing positions only. The evaluation in the lying position may be omitted. Score the evaluation at the conclusion of the assessment session.
    • Perform this assessment at the initial evaluation and then regularly throughout the course of treatment to determine beneficial and adverse effects.
  • Tardive blepharospasm manifests with findings similar to other forms of blepharospasm. Repetitive, forceful, and sustained contractions of the orbicularis oculi are observed. Dyskinetic blinking may occur.
  • Unlike tardive dystonia, torsion dystonia is characterized by twisting and sustained contractions of muscles resulting in rapid, repetitive, distressing movements. Torsion dystonia usually begins with inversions of the foot and spasm of the proximal limb muscles resulting in gait abnormalities. Scoliosis, torticollis, and tortipelvis may occur in torsion dystonia. Patients may experience considerable impairment in performing activities of daily living. Spasmodic torticollis presents in adults and is characterized by torticollis, anterocollis, or retrocollis.
  • Tardive tics may be observed in affected patients. Because the patient may suppress the tics temporarily, they may not be observed during the initial encounter.
  • Tardive tremor manifests as involuntary rhythmic sinusoidal movements of limbs, head, neck, or voice. Tardive tremors are persistent. Unlike cerebellar tremors, which are present on voluntary motion and not at rest, and psychogenic tremors, which diminish during the course of long examinations, tardive tremors are usually present at rest and with voluntary movement.
  • The presence of dementia in a patient in whom TD is suspected merits consideration of Huntington disease, Wilson disease, or a CNS neoplasm. The presence of hemiparesis, asymmetric reflexes, and other focal deficits indicates the need for further assessment to exclude structural brain lesions.
  • The presence of jaundice, hepatomegaly, abdominal pain, or Kayser-Fleischer rings in the cornea requires further assessment to exclude Wilson disease. Kayser-Fleischer rings may be observed best with a slit lamp examination. Ophthalmologic consultation is mandatory for patients in whom Wilson disease is suspected. It is characterized by the presence of choreiform movements, tremors, diminished dexterity, marked rigidity, dystonia, dysarthria, and neuropsychiatric manifestations. The presenting manifestation may be psychosis. Check serum ceruloplasmin and the copper transporter gene in every patient in whom Wilson disease is suspected.
  • Tachycardia, sweating, and a goiter suggest hyperthyroidism. TD may coexist with other neuroleptic-induced movement disorders, including parkinsonism (manifested by tremor, rigidity, and bradykinesia). Distinguish TD from acute dystonic reactions induced by medications and from neuroleptic withdrawal dyskinesias. Unlike TDs, withdrawal dyskinesias remit within a month of discontinuing neuroleptics.
  • Postural instability is common in Huntington disease but uncommon in neuroleptic-induced TD. Unlike TD, Huntington disease appears with chorea in the face and the proximal extremities. The term chorea implies a dancelike distinctive gait.
  • Characterization and classification of TDs and other movement disorders are facilitated by the administration of the Movement Disorders Checklist by trained raters to score the presence or absence of traits of movements (see Media file 7).
    • The Movement Disorders Checklist can be used readily by practitioners in clinical settings. Each different movement is rated separately on a distinct page with the Movement Disorders Checklist (see Media file 7).
    • With dichotomous random variables (ie, indicator functions, see Media file 8), algorithms in the form of linear regression equations express the relationships among dyskinesias and other movement disorders (see Media file 9). The formulation can be expressed as a Venn diagram (see Media file 2).
    • Therefore, every case of akathisia is also a case of stereotypy. Therefore, the presence of akathisia implies the presence of stereotypy.
    • Some cases of chorea can be classified as akathisia and stereotypy, while other cases of chorea can be classified as myoclonus. In addition, some cases of tics can also be classified as myoclonus. Some cases of dystonia can be classified as akathisia.
    • Media file 2 also indicates that tic is entirely separate and distinct from akathisia, chorea, dystonia, stereotypy, and tremor. Furthermore, Media file 2 demonstrates that tremor is distinct from the other movement disorders.
  • The presence of stereotypies can be assessed readily using the Timed Stereotypies Rating Scale (see Media file 10).
    • For this assessment, observe the patient with bare feet and exposed hands. Ask him or her to sit still in a chair for 10 minutes. Place a check mark on the score sheet (see Media file 10) the first time that each movement occurs during each 30-second interval of the 10-minute observation period. This can be accomplished by playing an audiotape dictating 30-second intervals of a 10-minute duration. (Download audio segment.) The tape may be played live in the presence of the patient. To avoid distracting the patient, the examiner may listen to the audiotape through headphones.
    • Another option is to videotape the patient for at least 10 minutes and then to rate the videotape with the audiotaped dictation of 30-second segments of a 10-minute duration later. Optimally, the patient is rated both live and on videotape. The videotape is rated by examiners blind to the status of the patient. Test-retest reliability can thus be determined by assessing the ratings of the live and videotape sessions.
    • Videotapes often miss crucial events, such as a tear or a jerk. In the blank spaces for other head/neck stereotypies in items 21 and 22 and for other stereotypies in items 49-60 at the end of the form, add additional movements of the patient (eg, extending arms at elbow and extending legs at knee). Also, in the blank spaces for other stereotypies in items 49-60 at the end of the form, add additional utterances of the patient (eg, grunts, snorts, throat clearing, vowels, syllables, words, sentences). The sessions may be videotaped. By using a toggle switch on a videocassette recorder, the videotapes may be played back frame-by-frame to facilitate the observation of each occurrence of every stereotypy.
    • Because some terms of the Timed Stereotypies Rating Scale may not be well known, we shall provide some further definitions. Item 9, the bonbon sign, is present when the patient presses the tip of the tongue against the cheek as if tasting a piece of candy in the mouth. Item 48, the Bronx cheer, is a colloquial euphemism for a sound occurring when air is forcefully expressed through tightly closed lips resembling the noise of a flatulent retort.

Causes

  • Long-term treatment with dopamine antagonists can cause TD. It can also be caused by both high-potency and low-potency traditional neuroleptics, including long-acting depot formulations (eg, decanoate and enanthate). Newer atypical antipsychotic agents, including olanzapine and risperidone, appear to carry less risk of TD.
  • The antiemetic metoclopramide, a potent D2 dopamine receptor antagonist, may cause TD, particularly in elderly patients.
  • TDs have also been reported with the use of antihistamines, fluoxetine, amoxapine (a tricyclic antidepressant), and other agents (see Table 2).
  • Psychogenic movement disorders are often florid and bizarre (see slides 35 and 38 of Media file 1 of Catatonia).
    • The motions of psychogenic movement disorders typically defy the boundaries that distinguish neurologic disorders. They usually do not resemble classic TD. Psychogenic movement disorders typically represent conversion disorders, neurologic symptoms expressed by a patient who believes that the symptoms are present (see slides 36 and 38 of Media file 1 of Catatonia). The patient is apparently physically healthy. Conversion disorders are not well understood (see slides 35 and 38 of Media file 1 of Catatonia).
    • Often a stress, positive or negative, has occurred in the life of the individual. People with psychogenic movement disorders often have experienced a major life event (eg, failure to attain an expected promotion, death of a loved one).
    • Malingering disorders may occur when an individual seeks disability and other compensation. Specifically, malingering occurs when the patient seeks a tangible reward for being sick. A person who malingers may seek to be excused from work or school because of the feigned illness. A person who malingers may seek compensation in the form of disability payments for the alleged illness (see slides 40 and 42-44 of Media file 1 of Catatonia).
    • Factitious disorder occurs when an individual feigns illness in order to assume the sick role. People with factitious disorders appear to seek the attention accorded to a patient. Factitious disorders are not well understood (see slides 40 and 42-44 of Media file 1 of Catatonia).
      • An extremely severe form of factious disorder is manifested as Munchausen syndrome. Munchausen syndrome is characterized by the apparently deliberate feigning of symptoms and signs. People with Munchausen syndrome may fabricate elaborate and bizarre stories. They may agree to multiple operations in an attempt to diagnose and treat the fabricated illnesses (see slides 40 and 42 of Media file 1 of Catatonia).
      • Munchausen syndrome by proxy occurs when a parent seeks treatment for a child, typically an infant who cannot speak. The parent fabricates a history of false symptoms for the healthy child leading to unnecessary diagnostic and therapeutic interventions (see slides 40 and 42 of Media file 1 of Catatonia). Munchausen syndrome by proxy is a form of child abuse. Suspected cases of Munchausen syndrome by proxy merit report to child protective services.
  • Although people with psychogenic movement disorders may seek and demand medication and surgery, they are likely to experience severe adverse effects. Therefore, avoid pharmacologic and surgical interventions in patients with psychogenic movement disorders.
  • Psychiatric consultation is indicated.

More on Tardive Dyskinesia

Overview: Tardive Dyskinesia
Differential Diagnoses & Workup: Tardive Dyskinesia
Treatment & Medication: Tardive Dyskinesia
Follow-up: Tardive Dyskinesia
Multimedia: Tardive Dyskinesia
References
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Further Reading

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Keywords

TD, buccolingual dyskinesia, orofacial dyskinesia, masticatory dyskinesia, extrapyramidal syndromes, EPS, antipsychotic medication, acute movement disorder, exposure to dopamine antagonists, long-term dopaminergic antagonist therapy, involuntary movement of the tongue, involuntary movement of the lips, involuntary movement of the face, involuntary movement of the trunk, involuntary movement of the extremities, schizophrenia, schizoaffective disorder, bipolar disorder, long-term treatment with neuroleptics, acute tremor, acute akathisia

acute Parkinsonism, tardive blepharospasm, tardive dystonia, neuroleptic-induced TD, choreiform movements, athetoid movements, rhythmic movements of tongue, rhythmic movements of jaw, rhythmic movements of trunk, rhythmic movements of extremities, cerebrovascular disease, encephalitis, head trauma, hereditary dyskinesias, Huntington disease, Wilson disease, torsion dystonia, orofacial dyskinesia, tardive akathisia, tardive myoclonus, tardive tics, Meige syndrome, anterocollis, retrocollis, torticollis, tardive tourettism 

echolalia, echopraxia, coprolalia, copropraxia, multiple motor and vocal tics, tardive tremor, facial grimacing, protrusion of tongue, involuntary athetoid movements of extremities, snakelike writhing of extremities, lip smacking, chewing, sucking, puckering, tongue writhing, jaw opening, jaw closing, grimacing, excessive blinking and brow wrinkling, brow wrinkling, guitar playing movements, piano playing movements, Hillside Akathisia Scale, dyskinetic blinking, scoliosis, tortipelvis, spasmodic torticollis, involuntary rhythmic sinusoidal movements of limbs, involuntary rhythmic sinusoidal movements of head, involuntary rhythmic sinusoidal movements of neck, Movement Disorders Checklist, stereotypy, Timed Stereotypies Rating Scale, Munchausen syndrome, bradykinesias, hyperkinesias, chorea

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Contributor Information and Disclosures

Author

James Robert Brasic, MD, MPH, Research Associate, Division of Nuclear Medicine, Russell H Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine
James Robert Brasic, MD, MPH is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Academy of Neurology, and Movement Disorders Society
Disclosure: Taylor and Francis Royalty Independent contractor; Wolters Kluver/Lippincott Williams & Wilkins Royalty Independent contractor

Coauthor(s)

Brian Bronson, MD, Staff Physician, Department of Psychiatry, New York University Medical Center
Disclosure: Nothing to disclose.

Tristen T Chun, Division of Nuclear Medicine, Russell H Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine
Disclosure: Nothing to disclose.

Medical Editor

Daniel H Jacobs, MD, Associate Professor of Neurology, University of Central Florida College of Medicine
Daniel H Jacobs, MD is a member of the following medical societies: American Academy of Neurology, American Society of Neurorehabilitation, and Society for Neuroscience
Disclosure: Teva Pharmaceutical Grant/research funds Consulting; Biogen Idex Grant/research funds Independent contractor; Serono EMD Royalty Speaking and teaching; Pfizer Royalty Speaking and teaching; Berlex Royalty Speaking and teaching

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Nestor Galvez-Jimenez, MD, MSc, MHA, Chairman, Department of Neurology, Program Director, Movement Disorders, Department of Neurology, Division of Medicine, Cleveland Clinic Florida
Nestor Galvez-Jimenez, MD, MSc, MHA is a member of the following medical societies: American Academy of Neurology, American College of Physicians, and Movement Disorders Society
Disclosure: Nothing to disclose.

Chief Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

 
 
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