AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

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.

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 Withdrawal dyskinesias may also occur as treatment with dopamine antagonists is decreased or withdrawn.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 (2006) 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.

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.

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 (2006). Bakker and colleagues (2006) report a possible association with a polymorphism of the DRD3 gene and TD.

Dysfunction of the dopamine transporter has been hypothesized to play a role in the development of TD. However, Lafuente and colleagues (2006) 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. Thus, further research is needed to investigate the role of the dopamine transporter in the development and maintenance of TD.

Galecki and colleagues (2006) have reported the association of a polymorphism of the manganese superoxide dismutase (MnSOD) gene and TD.

Pathophysiology

For most of the past century, movement disorders (ie, abnormal adventitious movements) have been categorized as 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.

Table 1. Classic Characterization of the Pyramidal and Extrapyramidal Systems

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. Thus, brain-derived neurotrophic factor appears to have a protective effect in the nervous system against TD with people with schizophrenia.

Clinical presentation

Patients often have movement disorders that may actually represent a mixture or overlap of several dyskinesia disorders. 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 (Shinkai, 2005). Additionally, CYP3A4 and CYP2D6 gene polymorphisms are apparently unassociated with TD (Tiwari, 2005)

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 Image 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. 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 (Yassa, 1987).

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.
• 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

Section 3 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

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 Figure 1). Specifically note if antiemetic medications, especially metoclopramide (Reglan), prochlorperazine (Compazine), and related compounds are administered. Figure 1 lists the medications reported to cause TD. Figure 2 lists compounds associated with dyskinesias that usually resolve with dose reduction or discontinuation.
• 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 Figure 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 Figure 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 Figure 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 Figure 4) and the PQRS Screening Criteria can be repeated monthly (see Figure 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.

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 Figure 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 Figure 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 Figure 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 Figure 7).
  • With dichotomous random variables (ie, indicator functions, see Figure 8), algorithms in the form of linear regression equations express the relationships among dyskinesias and other movement disorders (see Figure 9). The formulation can be expressed as a Venn diagram (see Image 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.
  • Image 2 also indicates that tic is entirely separate and distinct from akathisia, chorea, dystonia, stereotypy, and tremor. Furthermore, Image 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 Figure 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 Figure 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 Figure 2).
• Psychogenic movement disorders are often florid and bizarre (see slides 35 and 38 of Image 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 Image 1 of Catatonia). The patient is apparently physically healthy. Conversion disorders are not well understood (see slides 35 and 38 of Image 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 Image 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 Image 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 Image 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 Image 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.

DIFFERENTIALS

Section 4 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Other Problems to be Considered

Toxicity, Hallucinogen
Conversion disorder
Compulsions
Dyskinesias secondary to caffeine
Dyskinesias secondary to chloroquine
Dyskinesias secondary to estrogen
Dyskinesias secondary to lithium
Dyskinesias secondary to phenytoin
Dyskinesias secondary to schizophrenia
Factitious disorder
Fahr syndrome
Hyperthyroidism
Hypoparathyroidism
Malingering
Meige syndrome
Munchausen syndrome
Munchausen syndrome by proxy
Polycythemia rubra vera
Poorly fitting dentures
Somatization disorder
Spontaneous dyskinesias
Sydenham chorea
Syphilis
Systemic lupus erythematosus
Wilson disease
Dementia in Parkinson disease
Dementia in progressive supranuclear palsy
Pediatric epilepsy
Pediatric Gilles de la Tourette syndrome

WORKUP

Section 5 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Lab Studies

• Deficiency of serum ceruloplasmin due to an abnormal copper transporter gene characterizes Wilson disease. Urine copper collection may be abnormal. In addition, liver function tests and liver transaminases may be abnormal. Also, check the copper transporter gene in patients in whom Wilson disease is suspected.
• Thyroid function tests are indicated to exclude thyroid dysfunction.
• Evaluate tardive blepharospasm with serum biochemistry, serum copper, serum ceruloplasmin, thyroid function tests, and syphilis serology.
• Connective tissue disease screening tests are useful to exclude systemic lupus erythematosus and other vasculitides.
• Obtain red blood cell counts to exclude polycythemia rubra vera.
• Obtain serum calcium level.

Imaging Studies

• In TD, findings from brain CT and MRI are typically normal. However, these imaging studies may assist in the differential diagnosis.
• • In Huntington disease, atrophy of the caudate nucleus is commonly seen on CT and MRI of the brain. In Fahr syndrome, calcification is often seen in the brain, particularly in the basal ganglia.
  • Imaging results can also exclude neoplasm and cerebral infarction.
• Physiologic imaging studies (eg, positron emission tomography [PET]) of patients with TD may demonstrate increased glucose metabolism in the globus pallidus and precentral gyrus.
• Proton magnetic resonance spectroscopy has demonstrated neural damages in the left lenticular nucleus in a group of patients with TD.

Other Tests

• Evaluate tardive blepharospasm with electroencephalography, slit lamp examination, and a complete ophthalmologic evaluation.

Procedures

• Psychogenic movement disorders occasionally may be alleviated by the administration of a small intravenous injection of lorazepam or sodium amobarbital.
• • This procedure is not pathognomonic of psychogenic movement disorders. However, it may be helpful to confirm a diagnosis of a movement disorder due to hysteria, somatization disorder, somatoform disorder, or conversion disorders.
  • Typically, people who manifest psychogenic movement disorders have recent life experiences that are stressful. The life stresses can be both positive, such as a promotion, and negative, such as the death of a loved one.
  • Psychotherapy may then provide a more effective means of expressing the psychological distress often associated with psychogenic movement disorders.
  • People with psychogenic movement disorders may request and demand surgery and other treatments associated with morbidity and mortality. A prudent clinician withholds inappropriate treatments from people with psychogenic movement disorders.
• If infection is considered, lumbar puncture is indicated to obtain samples of cerebrospinal fluid for laboratory analysis.

TREATMENT

Section 6 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Medical Care

• Primary prevention of TD by using the lowest effective dose of neuroleptic for the shortest period of time is recommended. When TD is diagnosed, reduce or discontinue the causative agent if possible. The risk of a permanent movement disorder must be weighed against the risks of exacerbating psychosis. In addition, TD may initially worsen after discontinuing neuroleptics.
• Atypical neuroleptics may control psychosis while reducing the risk of TD. While traditional neuroleptics primarily block D₂ receptors, atypical neuroleptics bind variably to dopaminergic, serotonergic, alpha-adrenergic, histaminic, and muscarinic receptors.
  • In particular, clozapine has been recommended as treatment for patients with TD who require antipsychotics. Clozapine is one of the most effective atypical neuroleptics for treatment-refractory schizophrenia. Although clozapine has been associated with TD (Ertugrul and Demir, 2005), the incidence of TD with this and other atypical agents appears markedly less than that of traditional neuroleptics. The benefits of clozapine may result from its affinity for the D₄ receptor. However, risperidone and clozapine may be ineffective in treating negative and positive symptoms in some patients. Treatment with clozapine requires regular hematologic evaluation to avoid fatal agranulocytosis.
  • Administration of branched-chain amino acids has been reported to markedly reduce the movements of TD in a group of adult men with TD. This intervention in contraindicated in pregnant women. This promising treatment requires investigation in other locations to confirm its safety and efficacy.
• Other anecdotal treatments include vitamin E, levodopa, benzodiazepines, botulinum toxin, reserpine, tetrabenazine, and dopamine-depleting agents. Ondansetron, a selective 5-hydroxytryptamine-3 antagonist, has helped some individuals with TD. Discontinuation of treatment with anticholinergics may relieve TD. A controversial strategy to treat TD is continuing and/or increasing the dose of the dopamine antagonist.
• Tardive blepharospasm can respond favorably to reduction or cessation of dopamine antagonists. Individuals who must be treated with neuroleptics often respond favorably to atypical neuroleptics. Additional treatments to consider include anticholinergics, dopamine-depleting agents, benzodiazepines, clozapine, and botulinum toxin.
• For tardive tics, remove the causative neuroleptic if possible. If the patient cannot tolerate absence of the neuroleptic, substitute an atypical neuroleptic. Pimozide, clonidine, and haloperidol can be helpful in some patients with tardive tics.
• Clozapine has treated tardive tremor successfully. Propanolol is useful for tardive akathisia. In 2005, Ertugrul and Demir reported the occurrence of TD in a man treated with clozapine for a year; the man had previously received other dopamine antagonists. Previous exposure to dopamine antagonists may have contributed to the development of TD in the man.
• Clonazepam has been reported to successfully alleviate the symptoms of TD and spontaneous oral dyskinesia.

Consultations

• Consultation with an ophthalmologist is indicated to evaluate tardive blepharospasm and/or to exclude Wilson disease with slit lamp examination.
• For information about a neurologist in your area, please contact the American Academy of Neurology as follows:

  American Academy of Neurology
  1080 Montreal Avenue
  St Paul, MN 55116
  Telephone (800) 879-1960 or (651) 695-2717
  Fax (651) 695-2791

• Consultation with a movement-disorders specialist may help to clarify the diagnosis and treatment. For information about movement disorder experts in your area, please contact the Movement Disorder Society as follows:

  The Movement Disorder Society
  611 East Wells Street
  Milwaukee, WI 53202
  Telephone (414) 276-2145
  Fax (414) 276-3349

• Psychiatric consultation is indicated for people with possible psychogenic movement disorders (see slides 35 and 38 of Image 1 of Catatonia).
• Psychogenic movement disorders are some of the most bizarre and florid movement disorders. Typically, psychogenic movement disorders do not demonstrate the usual phenomenology and topology of TD (see slides 35 and 38 of Image 1 of Catatonia).
• Patients may have both psychogenic movement disorders and TD. The primary clinician tactfully and diplomatically must suggest to the patient that consultation to investigate psychological aspects may be helpful.
• • The patient should agree to psychiatric consultation before the specialist is asked to visit. If uncertain about the possible existence of a psychological component to a movement disorder, a prudent clinician requests psychiatric consultation.
  • A course of psychotherapy may have less morbidity than pharmacologic interventions.

MEDICATION

Section 7 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Reduction and cessation of the causative agents may relieve tardive symptoms. Anecdotal reports have suggested that various agents have helped individuals. No established medications exist to treat TD.

FOLLOW-UP

Section 8 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Patient Education

• For excellent patient education resources, visit eMedicine's Sleep Disorders Center. Also, see eMedicine's patient education article Restless Legs Syndrome.

MISCELLANEOUS

Section 9 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Medical/Legal Pitfalls

• Before administering any treatment that may block dopamine receptors, obtain informed written consent. In addition, all patients currently treated with dopamine antagonists, even those with schizophrenia treated with traditional neuroleptics for many years, merit re-evaluation for possible change of medication. Atypical antipsychotics, such as risperidone and clozapine, appear to have a lower risk of TD. Obtain written informed consent to acknowledge the risk of possible TD from patients treated with dopamine antagonists for any diagnosis including migraine, hiccups, and gastroesophageal reflux. Throughout the course of therapy, reevaluate the need for continuation of neuroleptics (see Table 1).
• Patients with TD who require continued treatment with a neuroleptic may benefit from atypical neuroleptics.
• Abrupt cessation of dopamine antagonists may lead to an acute exacerbation of symptoms (which presumably were controlled by medication).
• • Exercise caution in reducing and discontinuing treatment. Life-threatening conditions, such as malignant neuroleptic syndrome, are exceptions in which immediate discontinuation may be justified.
  • Abrupt cessation of treatment with dopamine antagonists may precipitate a florid psychosis with delusions, hallucinations, and suicidal and/or homicidal behavior. It is better to slowly taper the dose (by 10% increments of the original dose) while closely observing the patient for exacerbation of psychotic symptoms.
  • Total discontinuation is often difficult or impossible for people who have been pharmacologically treated. Some patients need a small dose of dopamine antagonists on a long-term basis. They may require hospitalization if the dopamine antagonist is discontinued completely.
  • Because Wilson disease is a treatable, preventable psychosis, evaluate patients with abdominal pain and mental dysfunction for Wilson disease. Obtain ophthalmologic consultation for patients in whom Wilson disease is suspected. Check serum ceruloplasmin and the copper transporter gene in patients who may have Wilson disease.
• Diagnosis and treatment of conditions that resemble TD (eg, seizure disorders, syphilis, thyroid disease, Wilson disease) constitute optimal medical practice.
• Although patients with psychogenic movement disorders, somatoform disorder, somatization disorder, hypochondriasis, hysteria, conversion disorder, malingering, Munchausen syndrome, and factitious disorders usually have manifestations that rule out TD, (see slides 35-36, 38, 40, and 42-44 of Image 1 of Catatonia) clinicians may be tempted to consider treatment for possible TD in people who have psychiatric and psychological problems. The desire of the clinician to offer a therapeutic intervention to an affected patient may be intensified by the requests and demands of patients for surgery and other help.
• Prudent clinicians must exercise extreme caution to avoid pharmacologic and surgical treatments for people with psychogenic movement disorders. Patients with psychogenic movement disorders are likely to experience extreme adverse effects and no beneficial effects from surgical and pharmacologic treatments. Tactful suggestion that stress may be contributing to the symptoms is appropriate. People with psychogenic movement disorders merit referral to mental health professionals for psychiatric and psychological interventions. In particular, surgery, including psychosurgery, is contraindicated for psychogenic movement disorders. Have the patient sit in a chair with hands on knees, legs slightly apart and feet flat on floor.
• Fully inform the patient (or the legal surrogate if the patient is incompetent) of the possible courses of action. Discuss with the patient the advantages and disadvantages of dopamine antagonist treatment. A written treatment plan that documents agreement with the treatment course between the clinician and patient is helpful. Regularly review and revise the treatment plan as needed.

Special Concerns

• Administration of any medication to pregnant women, including dopamine antagonists, may be dangerous to the fetus.
• • Before and during treatment, assess the need for treatment with psychoactive medication (see Figure 4).
• Obtain written informed consent from patients.

FIGURES

Figure 1. Medications Causing Tardive Dyskinesia

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) (Fountoulakis, 2006; Lin, 2006; Masdrakis, 2006; Peritogiannis, 2006)

Figure 2. Nonneuroleptic Medications Linked to Dyskinesias

• 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

Figure 3. Abnormal Involuntary Movement Scale (AIMS)
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(A) Examination procedure: Either before or after completing the examination procedure, observe the patient unobtrusively, at rest (eg, in waiting room). The chair to be used in this examination should be a hard, firm one without arms.

1. Ask the patient to remove shoes and socks.

2. Ask the patient if there is anything in his or her mouth (eg, gum, candy); if there is, to remove it.

3. Ask the patient about the current condition of his or her teeth. Ask the patient if he or she wears dentures. Do teeth or dentures bother the patient now?

4. Ask the patient whether he or she notices any movements in mouth, face, hands, or feet. If yes, ask to describe and to what extent they currently bother patient or interfere with his or her activities.

5. Have the patient sit in a chair with hands on knees, legs slightly apart and feet flat on floor. (Look at entire body for movements while in this position.)

6. Ask the patient to sit with hands hanging unsupported. If male, between legs, if female and wearing a dress, hanging over knees. (Observe hands and other body areas.)

7. Ask the patient to open mouth. (Observe tongue at rest in mouth.) Do this twice.

8. Ask the patient to protrude tongue. (Observe abnormalities of tongue movement.) Do this twice.

9. Ask the patient to tap thumb, with each finger, as rapidly as possible for 10 to 15 seconds; separately with right hand, then with left hand. (Observe facial and leg movements.)

10. Flex and extend patient's left and right arms (one at a time). (Note any rigidity.)

11. Ask the patient to stand up. (Observe in profile. Observe all body areas again, hips included.)

12. Ask the patient to extend both arms outstretched in front with palms down. (Observe trunk, legs, and mouth.)

13. Have the patient walk a few paces, turn and walk back to chair. (Observe hands and gait.) Do this twice.

(B) Rating sheet

Reproduced with permission from NIMH.

Figure 4. Psychoactive Medication Quality Assurance Rating Survey (PQRS)

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INSTRUCTIONS TO RATER:

• These guidelines apply to all items unless indicated otherwise.
• After reviewing the person's chart for the twelve (12) months before the rating date, circle Y if the stated item is true. For example, if the response to the item is NO, NOT APPLICABLE, NONE, DON'T KNOW, OTHER, or any response other than YES for an item, leave it blank.
• You may write any additional information on the backs of the pages.
• Key: *This criterion is required prior to treatment with psychoactive medications. †This criterion indicates that further investigation is required prior to treatment with psychoactive medication.