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Tardive Dyskinesia

Synonyms, Key Words, and Related Terms: buccolingual, orofacial dyskinesia, masticatory dyskinesia

James Robert Brasic, MD, Brian Bronson, MD, Daniel H Jacobs, MD, Francisco
Talavera, PharmD, PhD, Nestor Galvez-Jimenez, MD, Selim R Benbadis, MD,
Nicholas Lorenzo, MD

eMedicine Journal, February 5 2002, Volume 3, Number 2

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 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 neuroleptics, toxins, and other
agents. TDs are seen most commonly in patients with schizophrenia, schizoaffective
disorder, or bipolar disorder who are treated with antipsychotic medication, but they
occasionally are seen in other patients as well.

TDs may be differentiated from acute movement disorders that occur commonly 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 commonly
are 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 also are associated with an increased risk
for the occurrence of acute movement adverse effects. Withdrawal dyskinesias also may
occur as treatment with dopamine antagonists is decreased or withdrawn. They often are
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.

Pathophysiology: For most of this century, movement disorders (ie, abnormal

adventitious movements) have been categorized as extrapyramidal syndromes 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 decebrate 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

Characteristic Pyramidal Extrapyramidal

Precisely demarcated Hypothesized pathways among basal
Anatomy pathways from cortex to ganglia and other structures of the central
muscle nervous system
Voluntary Involuntary
Paralysis, paresis, Akathisia, athetosis, ballism, chorea,
hyperreflexia, and dystonia, myoclonus, stereotypy, tic, and
spasticity tremor

The pathophysiology of extrapyramidal disorders has been disputed, since 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 extrapyramidal syndromes, 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, are being
applied to 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 also are
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
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 receptor blockade is reduced (even slightly), an exaggerated
response of the postsynaptic dopamine 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.

While the dopamine D2 receptor traditionally has been implicated in the pathogenesis of
TD, mounting evidence exists that for 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.

Clinical presentation

Patients often exhibit movement disorders that actually may 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 simultaneously may manifest akathisia and tics after long-term treatment with

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. Thus, a full neurologic and pharmacologic history may provide the
basis to distinguish idiopathic Tourette disorder from acute medication-induced tardive

Often patients and families cannot provide accurate histories, thus firm diagnoses may be
impossible. Since 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 tardive


In the US: 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.

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 tardive
dyskinesias in an individual patient can represent a serious diagnostic challenge.

Internationally: International frequency is similar to that of the US.

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

Age: Advanced age is a major risk factor for TD. Prevalence in elderly patients treated
with dopamine antagonists is reportedly 29% after 3-12 months of treatment and 41%
after 10 years of treatment.


While TD has been observed following exposure to various substances (eg, L-

dopa, amphetamine, metoclopramide), the prototype TD is the orofacial (ie,
buccolingual, masticatory), hyperkinesias induced by neuroleptics (antipsychotic
dopamine receptor blockers).

Neuroleptic-induced TD is characterized by the presence of choreiform, athetoid,

and rhythmic movements of the tongue, jaw, trunk, and extremities for at least 4
weeks, beginning 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 typically is required if the patient is aged 60 years or older. Oral and
genital pain can be prominent manifestations of tardive dyskinesia.

o 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 present with choreiform
movements of the limbs. Furthermore, it cannot be diagnosed if symptoms
and signs result from an acute neuroleptic-induced movement disorder.

o 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.

o While this may diminish the disorder temporarily, regular increments in

neuroleptic dose may be 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.

Upon 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 identifies 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.

o 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.

o 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 presents in patients aged 10-15 years, and therefore

occurs in a different age group than 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.

o 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. Since the AIMS can be
administered readily 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.
o 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).
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.

o 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. Tardive akathisia has been
treated successfully with propranolol and other beta-blockers, biperiden,
diazepam, clonidine, propoxyphene, codeine, and anticholinergics.

o 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. While blepharospasm has been reported with dopaminergic and
sympathomimetic agents and antihistamines, it also has 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.

o 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.

o Tardive myoclonus, a rare disorder, presents as brief jerks of muscles in

the face, neck, trunk, and extremities.

o 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.
o Tardive tremor is a hyperkinetic movement disorder associated with long-
term treatment with dopamine antagonists.


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 initially may 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.
While 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 commonly is 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 typically are
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

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.
o Akathisia can be assessed objectively and readily in clinical settings using
the Hillside Akathisia Scale (see Figure 5). For this evaluation, examine
the subject with bare feet and exposed hands so that movements of the
extremities can be observed. Ask the subject to sit, stand, and lie still for 2
minutes in each position. While the subject is in each position, inquire
about the presence of a sensation of inner restlessness and an urge to
move. Score the evaluation at the conclusion of the assessment session.
o Perform this assessment at the initial evaluation and then regularly
throughout the course of treatment to determine beneficial and adverse

Tardive blepharospasm presents 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

Tardive tics may be observed in affected patients. Since 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 usually
are 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 or 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 presents with chorea in
the face and the proximal extremities. The term chorea implies a dance-like
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 6).
o 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 6).
o With dichotomous random variables (ie, indicator functions, see Figure 7),
algorithms in the form of linear regression equations express the
relationships among dyskinesias and other movement disorders (see
Figure 8). The formulation can be expressed as a Venn diagram (see
Picture 1).
o Thus, every case of akathisia is also a case of stereotypy. Therefore, the
presence of akathisia implies the presence of stereotypy.
o Some cases of chorea can be classified as akathisia and stereotypy, while
other cases of chorea can be classified as myoclonus. Additionally, some
cases of tics also can be classified as myoclonus. Some cases of dystonia
can be classified as akathisia and stereotypy.
o Picture 1 also indicates that tic is entirely separate and distinct from
akathisia, chorea, dystonia, stereotypy, and tremor. Furthermore, Picture 1
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 9).
o For this assessment, observe the subject with bare feet and exposed hands.
Ask the subject to sit still in a chair for 10 minutes. Place a check mark on
the score sheet (see Figure 9) 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 subject. To avoid distracting the subject,
the examiner may listen to the audiotape through headphones.
o Another option is to videotape the subject 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 subject is rated both live and
on videotape. The videotape is rated by examiners blind to the status of the
subject. Test-retest reliability thus can be determined by assessing the
ratings of the live and videotape sessions.
o Often videotapes miss crucial events, such as a tear or a jerk. In the blank
spaces in items 23-50 at the end of the form, add additional movements of
the subject (eg, toe wiggling, rubbing feet on floor, extending arms at
elbow, extending legs at knee, patting feet on floor). Also, on the blank
space at the end of the form add additional utterances of the subject (eg,
grunts, snorts, throat clearing, vowels, syllables, words, sentences). The
sessions may be videotaped. 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.


Long-term treatment with dopamine antagonists can cause TD. It also can be
caused by both high-potency and low-potency traditional neuroleptics, including
long-acting depot formulations (eg, decanoate). Newer atypical antipsychotic
agents, including clozapine 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 also have been reported with the use of antihistamines, fluoxetine,
amoxapine (a tricyclic antidepressant), and other agents (see Figure 2).
Psychogenic movement disorders often are florid and bizarre.

o The motions of psychogenic movement disorders typically defy the

boundaries that distinguish neurologic disorders. They usually do not
resemble classic TD.

o 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).

o Malingering and factitious disorders may occur when an individual seeks

disability and other compensation. Munchausen syndrome is characterized
by the apparently deliberate feigning of symptoms and signs.

o Although people with psychogenic movement disorders may seek

medication and surgery, they are likely to experience severe adverse
effects. Therefore, avoid pharmacologic and surgical interventions in
patients with psychogenic movement disorders.

o Psychiatric consultation is indicated.


Benign Childhood Epilepsy

Childhood Migraine Variants
Chorea Gravidarum
Chorea in Adults
Complex Partial Seizures
Cortical Basal Ganglionic Degeneration
Epilepsia Partialis Continua
Epilepsy in Adults with Mental Retardation
Epilepsy in Children with Mental Retardation
Epilepsy, Juvenile Myoclonic
Epileptiform Discharges
Essential Tremor
Frontal Lobe Epilepsy
HIV-1 Associated CNS Complications (Overview)
HIV-1 Associated Cerebrovascular Complications
Tourette Syndrome and Other Tic Disorders

Other Problems to be Considered:

Toxicity, Hallucinogen
Conversion disorder
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
Meige syndrome
Munchausen syndrome
Munchausen syndrome by proxy
Polycythemia rubra vera
Poorly fitting dentures
Somatization disorder
Spontaneous dyskinesias
Sydenham chorea
Systemic lupus erythematosus
Wilson disease
Dementia in Parkinson disease
Dementia in progressive supranuclear palsy
Pediatric epilepsy
Pediatric Gilles de la Tourette syndrome


Lab Studies:

Deficiency of serum ceruloplasmin due to an abnormal copper transporter gene

characterizes Wilson disease. Urine copper collection may be abnormal.
Additionally, liver function tests and liver transaminases may be abnormal. Also
check the copper transporter gene in patients in whom Wilson disease is

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:

Computed tomography (CT) scan and MRI of the brain typically are normal in
TD. However, these imaging studies may assist in differential diagnosis.

o In Huntington disease, atrophy of the caudate nucleus commonly is seen

on CT scan and MRI of the brain. Alternatively, in Fahr syndrome,
calcification often is seen in the brain, particularly in the basal ganglia.

o Imaging also can exclude neoplasm and cerebral infarction.

Physiologic imaging studies (eg, positron emission tomography) of patients with

TD 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 subjects with TD.

Other Tests:

Evaluate tardive blepharospasm with electroencephalography, slit lamp

examination, and a complete ophthalmologic evaluation.


Psychogenic movement disorders occasionally may be alleviated by the

administration of a small intravenous injection of lorazepam or sodium

o 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

o 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
o Psychotherapy then may provide a more effective means of expressing the
psychological distress often associated with psychogenic movement

o 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.


Medical Care:

Primary prevention of TD by using the lowest effective dose of neuroleptic for the
shortest period of time is recommended. Upon diagnosing TD, 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 initially may worsen after discontinuing neuroleptics.

Atypical neuroleptics may control psychosis while reducing the risk of TD. While
traditional neuroleptics primarily block D2 dopamine 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 in treatment-
refractory schizophrenia. While clozapine has been associated with TD, the
incidence of TD with this and other atypical agents appears markedly less than
with traditional neuroleptics. The beneficial effects of clozapine probably result
from its affinity for the dopamine D4 receptor. However, risperidone and
clozapine may be ineffective in treating negative and positive symptoms in some
patients. Also, treatment with clozapine requires regular hematologic evaluation
to avoid fatal agranulocytosis.

Other anecdotal treatments include vitamin E, levodopa, benzodiazepines,

botulinum toxin, reserpine, tetrabenazine, and dopamine-depleting agents.
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. Clonazepam has been reported to successfully alleviate the symptoms
of tardive dyskinesia as well as spontaneous oral dyskinesia.


Ophthalmologic consultation is indicated for tardive blepharospasm and/or to

exclude Wilson disease with slit lamp examination.

Psychiatric consultation is indicated for people with possible psychogenic

movement disorders.

o 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.

o 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.

o 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.

o A course of psychotherapy may have less morbidity than pharmacologic



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.


Medical/Legal Pitfalls:
Before administering any treatment that may block dopamine receptors, obtain
informed written consent. Additionally, 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).

o Exercise caution in reducing and discontinuing treatment. Life-threatening

conditions, such as malignant neuroleptic syndrome, are exceptions in
which immediate discontinuation may be justified.

o 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.

o Total discontinuation often is 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.

o Since 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, clinicians may be tempted to consider treatment
for possible TD for people who have psychiatric and psychological problems. The
desire of the clinician to offer a therapeutic intervention to a stricken 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.

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.

o Before and during treatment, assess the need for treatment with
psychoactive medication (see Figure 4).

o Obtain written informed consent from these patients.


Figure 1. Medications Causing Tardive Dyskinesia

Antipsychotic agents (ie, neuroleptics)

o Droperidol (Inapsine)
o Haloperidol (Haldol)
o Loxapine (Daxolin, Loxitane)
o Pimozide (Orap)
o Molindone (Moban)
o Chlorpromazine (Thorazine)
o Fluphenazine (Permitil, Prolixin)
o Mesoridazine (Serentil)
o Perphenazine (Trilofan)
o Thioridazine (Mellaril)
o Trifluoperazine (Stelazine)
o Thiothixene (Navane)

Newer atypical antipsychotic agents (sporadically linked to TDs)

Olanzapine (Zyprexa)
Quetiapine (Seroquel)
Risperidone (Risperdal)

Figure 2. Nonneuroleptic Medications Linked to Dyskinesias

o Benzhexol
o Biperiden (Akineton)
o Ethopropazine
o Orphenadrine (Norflex, Norgesic, Orphengesic)
o Procyclidine
o Monoamine oxidase inhibitors (MAOIs)
Phenelzine (Nardil)
o Selective serotonin reuptake inhibitors (SSRIs)
Fluoxetine (Prozac)
Sertraline (Zoloft)
o Trazodone (Desyrel)
o Tricyclic antidepressants
Amitriptyline (Elavil, Vanatrip)
Amitriptyline and perphenazine (Triavil)
Amoxapine (Ascendin)
Doxepin (Sinequan)
Imipramine (Tofranil)
o Metoclopramide (Maxolon, Reglan)
o Prochlorperazine (Compazine)
Antiepileptic drugs
o Carbamazepine (Atretol, Epitol, Tegretol)
o Ethosuximide (Zarontin)
o Phenobarbital (Barbita, Luminal sodium, Solfoton)
o Phenytoin (Dilantin)
Antihistaminic decongestants
o Combinations of antihistamines and sympathomimetics
o Chloroquine (Aralen)
Antiparkinson agents
o Bromocriptine (Parlodel)

o Levodopa (Dopar, L-Dopa, Larodopa)

o Levodopa-carbidopa (Atamet, Sinemet)
o Alprazolam (Xanax)
Biogenic amines
o Dopamine (Intropin)
Mood stabilizers
o Lithium (Cibalith-S, Eskalith, Lithane, Lithobid, Lithotabs, Lithonate)

Oral contraceptives
o Estrogens
o Amphetamine (Adderall)

o Methylphenidate (Ritalin, Ritalin SR)

o Caffeine

Figure 3. Abnormal Involuntary Movement Scale (AIMS)

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 patient to remove shoes and socks.

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

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

4. Ask patient whether he/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/her activities.

5. Have patient sit in 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 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

7. Ask patient to open mouth. (Observe tongue at rest in mouth.) Do this twice.
8. Ask patient to protrude tongue. (Observe abnormalities of tongue movement.)
Do this twice.

9. Ask 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

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

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

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

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

B) Rating Sheet

Patient Name Rater Name

Patient # Data Group: AIMS Evaluation Date
0: None
Complete the above examination procedure before
1: Minimal, may be extreme normal
making ratings.
2: Mild
For movement ratings, circle the highest severity
3: Moderate
4: Severe
1. Muscles of Facial Expression
e.g., movements of forehead, eyebrows, periorbital area,
Include frowning, blinking, smiling, and grimacing.
2. Lips and Perioral Area
Facial and e.g., puckering, pouting, smacking 01234
Movements 3. Jaw
e.g., biting, clenching, chewing, mouth opening, lateral 01234
4. Tongue
Rate only increase in movements both in and out of mouth, 01234
NOT the inability to sustain movement.
5. Upper (arms, wrists, hands, fingers)
Include choreic movements (i.e., rapid, objectively
purposeless, irregular, spontaneous), athetoid movements
(i.e., slow, irregular, complex, serpentine).
Extremity Do NOT include tremor (i.e., repetitive, regular,
Movements rhythmic).
6. Lower (legs, knees, ankles, toes)
e.g., lateral knee movement, foot tapping, heel dropping, 01234
foot squirming, inversion and eversion of the foot
Trunk 7. Neck, shoulders, hips
Movements e.g., rocking, twisting, squirming, pelvic gyrations

8. Severity of Abnormal Movements
9. Incapacitation Due to Abnormal Movements 01234
10. Patient's Awareness of Abnormal Movements
Rate only patient's report.

11. Current Problems with Teeth and/or Dentures

Dental 0: No 1: Yes
12. Does Patient Usually Wear Dentures?
0: No 1: Yes
Reproduced with permission from NIMH.

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

Person's Full Name

Person's Case Number


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
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.

*This criterion is required prior to treatment with psychoactive

+This criterion indicates that further investigation is required prior to
treatment with psychoactive medication.


1. Case number
2. Form number
3. Time number
4. Rater code number
5. Subject number
6. Rating date
7. Today's date
8. Person's sex is male. Y
9. Person's date of birth
10. Person's age in years
11. Person's street address
12. Person's apartment number
13. Person's city
14. Person's state, province, or region
15. Person's postal code
16. Person's telephone number
17. Person's racial/ethnic origin
1 = Asian
2 = African-American
3 = Hispanic
4 = Native American
5 = White
6 = Other
9 = Don't know
18. Person's living unit
19. Person's date of admission to this institution
20. Level of mental retardation
1 = Profound (IQ below 20 or 25)
2 = Severe (IQ 20-25 to 35-40)
3 = Moderate (IQ 35-40 to 50-55)
4 = Mild (IQ 50-55 to approximately 70)
5 = Borderline (IQ 71 to 84)
6 = Not retarded
9 = Don't know
21. Full scale IQ, as measured by standard individual
22. Person is deceased. Y

23. Primary clinician
24. Physician 1 managed medications for person
25. Physician 2 managed medications for person
26. Physician 3 managed medications for person


27. Record of previous diagnostic evaluation


28. Record of previous diagnostic evaluation Y



29. Comprehensive nonpsychiatric medical
evaluation is initiated.*
30. Comprehensive nonpsychiatric medical
evaluation is completed.*
31. Relevant nonpsychiatric medical assessment
components are completed.*


32. Comprehensive psychiatric evaluation is
33. Comprehensive psychiatric evaluation is
34. Relevant psychiatric assessment components are
35. Psychiatric diagnoses other than mental
retardation, if applicable, by Diagnostic and
Statistical Manual of Mental Disorders, Fourth
Edition, Text Revision (DSM-IV-TR) (American
Psychiatric Association, Washington, DC, 2000)
36. Psychiatric diagnoses other than mental
retardation, if applicable, by ICD-9-CM, International
Classification of Diseases, Ninth Revision, Clinical
Modification, Fourth Edition, 1994 (ICD-9-CM) Y
(Practice Management Information Corporation
(PMIC), Los Angeles, California, 1993)


37. Level of mental retardation is documented by IQ
derived from individual formal testing.*
38. Level of retardation is documented by adaptive


39. Focused behavioral evaluation is initiated.* Y
40. Focused behavioral evaluation is adequate for
initiating treatment.*
41. Behavioral symptoms related to any psychiatric
diagnoses are specified.*
42. Behavioral symptoms related to any medical
diagnoses are specified.*
43. Baseline behavioral symptoms similar to
treatment side effects are specified.*


44. Pulmonary disease is diagnosed. Y
45. Cardiovascular disease is diagnosed. Y
46. Cataracts are diagnosed. Y
47. The person is hepatitis A antigen positive. Y
48. The person is hepatitis B antigen positive. Y
49. Constipation is diagnosed. Y
50. Toe infection is diagnosed. Y
51. Ear/nose/throat disease is diagnosed. Y
52. Respiratory infection is diagnosed in the past year. Y
53. Central nervous system disease is diagnosed. Y
54. Seizures are diagnosed. Y
55. Endocrine disease is diagnosed. Y
56. Person ambulates with assistance. Y
57. Mental retardation due to disorders of metabolism
and nutrition is diagnosed.
58. Mental retardation due to infection (e.g., rubella)
or head trauma is diagnosed.
59. Cerebral malformations are diagnosed. Y
60. Down syndrome is diagnosed. Y
61. Fragile X syndrome is diagnosed. Y
62. Other chromosomal disorders are diagnosed. Y
63. One or more seizures are recorded during the past
twelve months.
64. Stereotypies are diagnosed. Y
65. Neuroleptic-related tardive or withdrawal
dyskinesias are diagnosed.
66. Additional medical diagnoses are given. Y
67. It is specified if medical diagnoses contribute to
target symptoms.
68. Another nonpsychiatric medical condition, other
than mental retardation, is diagnosed.
If yes, please list:

69. Other informal clinical symptom diagnoses, eg,

self-injurious behavior, are given.
70. Hierarchy of severity of medical diagnoses is


71. Autistic disorder is diagnosed. Y
72. Other pervasive developmental disorder is
73. Schizophrenia is diagnosed. Y
74. Depression is diagnosed. Y
75. Mania is diagnosed. Y
76. Self-injurious behavior has been recorded. Y
77. Aggression towards others has been recorded. Y
78. Suicide has been attempted in the past year. Y
79. Hyperactivity has been recorded in the past year. Y
80. Another nonmedical psychiatric diagnosis, other
than mental retardation is diagnosed.
If yes, please list:

81. Hierarchy of severity of psychiatric diagnoses is


82. Significant symptom observed by more than one
staff member.*
83. There is an obvious environmental cause for the
84. There is an obvious bias by the observer; others
do not agree.+
85. More than one significant symptom is observed. Y
86. A hierarchy of symptom priorities for treatment is
87. Target symptom(s) for treatment established.* Y
88. Baseline ratings of symptoms obtained by rating
89. Baseline ratings of symptoms obtained by
informal observation.*
90. Other target behavioral symptoms are identified.
If yes, please list:

91. Hierarchy of severity of target behavioral

symptoms is present.*

92. Only one available psychoactive treatment is
considered and reviewed.+
93. More than one available psychoactive treatment is
considered and reviewed.*
94. Beneficial and side effects of each psychoactive
treatment are reviewed.*
95. Sequence of psychoactive treatments is
96. Caution to do no harm to person in treatment
97. Informed consent is obtained prior to starting
psychoactive medication.*
98. Class of psychoactive medication selected in
relation to psychiatric diagnoses.*
99. Class of psychoactive medication selected in
relation to target behavioral symptom(s).*
100. Class of psychoactive medication selected in
relation to concurrent medical illnesses.*
101. Class of psychoactive medication selected in
relation to drug interactions.*
102. Psychoactive medication(s) excluded because
contraindicated or ineffective.
103. Psychoactive medication(s) retained as Y


104. Behavioral treatment plan is specified.* Y
105. Pharmacological treatment plan is specified.* Y
106. Duration of psychoactive treatments specified,
other than monthly renewals.*
107. Medication renewals are completed, based on
review of person's symptoms, at least monthly.*
108. Outcome criteria specified to determine
continuation of therapy.*
109. Time/method for determination of long-term side
effects specified.
110. Psychoactive medication review by preset
schedule, other than monthly medication renewals.
111. Psychoactive medication review by original
protocol schedule.
112. Psychoactive medication review by number of
113. Psychoactive medication review by long-term
side effects.*
114. Nonmedication influences reviewed: baseline
115. Nonmedication influences reviewed:
116. Nonmedication influences reviewed: concurrent


117. Psychoactive drug dosage in usual range
according to Physicians' Desk Reference (PDR)
(Forty-fourth Edition, Medical Economics Company,
Inc., Oradell, New Jersey, 1990).*
118. Psychoactive drug dosage in usual range
according to state manual.*
119. Psychoactive drug dosage in usual range Y
according to standard texts.*
120. Psychoactive drug dosage in usual range
according to scientific journals.*


121. Psychoactive drug dosage monitored by formal
protocol schedule.
122. Psychoactive drug dosage monitored by open
drug trial.
123. Psychoactive drug dosage monitored by plasma
drug levels.
124. Psychoactive drug dosage monitored by
consideration of other drugs currently taken.*
125. Appropriate beneficial behavioral effects are
126. Appropriate medication side effects are
127. Monitoring by staff observation, with chart
notes, at one site (day program or living unit).*
128. Monitoring by staff observation, with chart
notes, at two or more sites (including both day Y
program and living unit).
129. Monitoring by appropriate specific rating scales
filled out by assigned raters.
130. Monitoring by appropriate specific rating scales,
with raters by convenience.
131. Monitoring by open format. Y
132. Monitoring by single blind format. Y
133. Monitoring by double blind format. Y
134. Monitoring includes use of placebo. Y
135. Monitoring includes crossover of treatment

136. Drug holiday of at least four weeks each year Y
137. Drug holiday of at least four weeks this year
138. Drug holiday of at least four weeks this year
139. No drug holiday, with documentation supporting
this decision.
140. Attempt at drug holiday was discontinued, with

Reproduced with permission from Brasic, Young, Furman, et al.

Figure 5. Hillside Akathisia Scale [HAS Version 4]


TOTAL: _____





0 = Absent
1 = Questionable
2 = Present and easily controlled
3 = Present and barely controlled
4 = Present and not controllable

i L T
t y o
t i t
i n a
n g l
1. Patient has sensation of inner restlessness: ____ ____ ____ ____
2. Patient has the urge to move: ____ ____ ____ ____

3. Akathisia present in the head and trunk: ____ ____ ____ ____
4. Akathisia present in the hands and arms: ____ ____ ____ ____
5. Akathisia present in the feet and legs: ____ ____ ____ ____


0 = No akathisia
1 = Questionable
2 = Small amplitude movements, part of the time

3 = Small amplitude movements, all of the time OR large amplitude movements, part of
the time

4 = Large amplitude movements, all of the time


Severity of Akathisia:

Considering your total clinical experience with this particular population, how akathisic
is the patient at this time?

0 = Not assessed
1 = Normal, not akathisic

2 = Borderline akathisia
3 = Mildly akathisic

4 = Moderately akathisic
5 = Markedly akathisic

6 = Severely akathisic
7 = Among the most akathisic of patients
Global Improvement:
Rate total improvement whether or not, in your judgment, it is entirely due to drug

Compared to his/her condition at admission to the study, how much has he/she changed?

0 = Not assessed
1 = Very much improved
2 = Much improved
3 = Minimally improved

4 = No change
5 = Minimally worse

6 = Much worse
7 = Very much worse
Reproduced from Fleischhacker, Bergmann, Perovich, et al.

Figure 6. Movement Disorders Checklist

Instructions for Raters:

Fill out separate checklists for each different movement, posture, or utterance
observed. Do not rate two or more particular movements, postures, or utterances
on the same sheet. Please complete the following items based on all available
sources of information concerning each movement, posture, or utterance on the
rating date.




Item Characteristic No Yes Dont know

X1 Abnormal posture 0 1 9
X2 Abrupt 0 1 9
X3 Brief 0 1 9
X4 Can be suppressed 0 1 9
X5 Continuous 0 1 9
X6 Coordinated 0 1 9
X7 Feeling of restlessness 0 1 9
X8 Intermittent 0 1 9
X9 Movements flow randomly 0 1 9
X10 Oscillatory 0 1 9
X11 Patterned 0 1 9
X12 Present at rest 0 1 9
X13 Present when maintaining a posture 0 1 9
X14 Purposeless 0 1 9
X15 Regular 0 1 9
X16 Repetitive 0 1 9
X17 Ritualistic 0 1 9
X18 Shock-like 0 1 9
X19 Squeezing movements 0 1 9
X20 Sudden 0 1 9
X21 Sustained 0 1 9
X22 Twisting movements 0 1 9
X23 Urge to move 0 1 9

Figure 7. Definitions of Indicator Functions Utilizing the Items of the Movement

Disorders Checklist (See Figure 6)

Define the indicator functions, Yi and i, 1 < i < 23, to correspond to the items {Xi,
1 <= i <= 23} of the Movement Disorders Checklist (Figure
7) according to the following procedure:


1 if Xi = 1 on Figure 6 (1 <= i <= 23) (1)

Yi (Xi) =
{ 0 otherwise

Similarly, let

1 if Xi = 0 on Figure 6 (1 <= i <= 23) (2)

i (Xi) =
{ 0 otherwise

Then, define the additional indicator functions, Zj, 1 <= j <= 4, as follows:
1 if X14 = 1 or X17 = 1 (3)
Z1 (Xj) =
{ 0 otherwise

1 if X7 = 1 or X23 = 1 (4)
Z2 (Xj) =
{ 0 otherwise

1 if (X1 = 1) or (X16 = 1 and X19 = 1) or (X16 = 1 and X22 = 1) (5)

Z3 (Xj) =
{ 0 otherwise

1 if X12 = 1 or X13 = 1 (6)

Z4 (Xj) =
{ 0 otherwise

Figure 8. Algorithms to Classify Movement Disorders


Ai = a0 + a1Y1 + a2Y2 + . . . + a23Y23 + b11 + b22 + . . . + b2323 + c1Z1 + c2Z2 + . . . +


where a0 = 0, ai = 0 or 1, bi = 0 or 1, 1 <= i <= 23, and cj = 0 or 1, 1 <= j <= 4, are scalars,

and Yi, i, 1 <= i <= 23, and Zj, 1 <= j <= 4, are the indicator functions defined in
Equations (1) through (6) (See Figure 8).

Algorithm for stereotypy. Let

A1 = Y5 + Y6 + Y11 + Y16 + Z1 (8)

Then stereotypy is present ifY5 = Y6 + Y11 + Y16 + Z1 = 1 by Equation (3),

or, equivalently, if A1 = 5 by Equation (8).

Algorithm for akathisia. Let

A2 = Y5 + Y6 + Y11 + Y16 + Z1 + Z2 (9)

Note also that by Equation (8),

A 2 = A 1 + Z2 (10)

Then akathisia is present by Equation (9) if Y5 = Y6 = Y11 = Y16 = Z1 =Z2 =

1, or, equivalently, if both A1 = 5 and
Z2 = 1 by Equations (4), (8), and (9), or, equivalently, if A2 = 6 by
Equations (9) and (10).
Thus, all individuals with akathisia must also manifest stereotypy.

Algorithm for chorea. Let

A3 = Y2 + Y3 + Y5 + Y9 + 15 (11)
Then chorea is present if Y2 = Y3 = Y5 = Y9 = 15 = 1, or, equivalently, if A3
= 5 by Equation (11).

Algorithm for dystonia. Let

A4 = Y11 + Y21 + Z3 (12)

Then dystonia is present if Y11 = Y21 = Z3 = 1, or, equivalently, if A4 = 3 by

Equation (12).

Algorithm for myoclonus. Let

A5 = Y3 + Y18 + Y20 (13)

Then myoclonus is present if Y3 = Y18 = Y20 = 1, or, equivalently, if A5 = 3

by Equation (13).

Algorithm for tic. Let

A 6 = 5 + Y2 + Y3 + Y4 + Y8 (14)
Then tic is present if 5 = Y2 = Y3 = Y4 = Y8 = 1, or, equivalently, if A6 = 5
by Equation (14).

Algorithm for tremor. Let

A7 = Y10 + Z4 (15)

Then tremor is present if Y10 = Z4 = 1 by Equation (6), or, equivalently, if

A7 = 2 by Equation (15).
Figure 9. Timed Stereotypies Rating Scale

Although this rating scale can be used with a stopwatch, it is best used with a recording
of a 30-second interval timing (up to 10 min), which is available in MP3 format.
(Windows Media Player supports this format; MAC users can download an MP3 player
here.) Please download this MP3 audio file and dub it to a recording device (eg, tape
recorder) via the computer's audio output jack to create a copy to use when administering
the timed stereotypies rating scale.






0:00 0:30 1:00 1:30 2:00 2:30 3:00 3:30 4:00 4:30 5:00
2. Mouth
4. Forceful
5. Smelling,
6. Bronx
7. Biting
8. Chewing
9. Mouth
10. Teeth
11. Tongue
in & out
12. Tongue,
13. Hand
14. Finger
19. Tip-toe
20. Body
21. Head
22. Head
23. Other
24. Other
25. Other
26. Other
27. Other
28. Other
29. Other
30. Other
31. Other
32. Other
33. Other

34. Other



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Adams RD, Victor M: Principles of Neurology. 4th ed. NY: McGraw Hill;
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