Approach

TD is a clinical diagnosis based on a history of exposure to dopamine receptor-blocking agents, clinical observation of characteristic involuntary movements, and an absence of other conditions that might cause the signs and symptoms.

Be vigilant and judicious when prescribing drugs that could potentially block dopamine receptors.

For patients being treated with antipsychotics for conditions such as bipolar disorder or schizophrenia, at each visit assess for the symptoms of TD as part of the usual follow-up.[6][12][31][32] Use the Abnormal Involuntary Movement Scale for a structured assessment or use a semi-structured assessment, which should include the patient's (or carer's) account of abnormal movement and visual observation of psychomotor abnormalities.[4][12]

Consider other conditions that may mimic TD, such as tic disorder, levodopa-induced dyskinesia in patients with Parkinson's disease (drug-induced parkinsonism), facial chorea in patients with Huntington's disease, dystonia, stroke, severe hypoglycaemia, and other hyperkinetic movement disorders.[1][3][12]

History

Consider TD in a patient presenting with stereotypic involuntary oro-bucco-lingual movements that occur over a period of at least 4 weeks following use of a dopamine receptor-blocking agent for at least 3 months (or at least 1 month in people aged >60 years).[2] Although some drugs may cause TD after only a few days or weeks of exposure, there is usually a history of months of exposure (at least 3 months).

Signs and symptoms may develop during exposure to or following withdrawal of a causative drug (within 4 weeks of withdrawal from an oral drug, or within 8 weeks from a long-acting injectable drug).[2] Presentations can vary and there is a range in severity of symptoms.[4]

Take a comprehensive drug history, which may require a review of pharmacy or hospital records. This is one of the key aspects of diagnosing TD. Carefully document all drugs used in the past, even if the patient denies prior use of any dopamine receptor-blocking agents.

Antipsychotics (particularly typical antipsychotics) are the usual causative agents.[11][12] Several other drugs may also result in TD, for example:[5][13]

  • Chronic use of prokinetic agents (e.g., metoclopramide)

  • Selective serotonin-reuptake inhibitors (e.g., citalopram)

  • Serotonin-noradrenaline reuptake inhibitors (e.g., duloxetine)

  • Tricyclic antidepressants (e.g., amitriptyline)

  • Lithium

  • Cinnarizine (an antihistamine/calcium antagonist).

Consult your local drug formulary for a full list of drugs that may cause TD.

Consider the following weaker risk factors in your history taking, although these are not sufficient alone to make a diagnosis of TD:[3][4][5][6][11]

  • Age >50 years

  • Post-menopause

  • African-American ethnicity

  • Diabetes mellitus

  • Brain/central nervous system injury

  • Dementia

  • Smoking

  • Alcohol and substance misuse.

Rule out any history of trauma or surgery in the oro-bucco-lingual region. Although rare, patients may develop dyskinesia after peripheral injury to this area or after a dental procedure (edentulous dyskinesia).[33]

In a patient taking antipsychotics (or other potentially causative drugs), ask the patient or their family members or carers about the onset of the involuntary movements, any precipitants, and the impact on their overall health and quality of life.[6]

Physical examination

Visually assess the patient. Evaluate the patient for stereotypic involuntary movements involving the mouth and tongue (commonly referred to as oro-buccal-lingual dyskinesia). These may include:

  • A continuous chewing motion

  • Lip smacking

  • Lip puckering

  • Tongue writhing

  • Facial grimacing.

There are, however, many other types of involuntary movements, such as dystonia, tardive akathisia, tardive tremor, tardive tics (tourettism), tardive myoclonus, tardive chorea, and tardive parkinsonism that may be part of TD phenomenology. Some patients may have blepharospasm or transiently sustained jaw opening, deviation, or closure with jaw clenching and teeth grinding (bruxism) as part of cranial tardive dystonia.[3][5]

Patients may also develop tardive dystonia of the arms, legs, and trunk; the latter typically manifested by trunk arching (opisthotonus). Rarely, patients may develop choreic and athetoid movements of the trunk and limbs.[3][5] Some patients also develop chronic painful oral and genital sensations, which are termed tardive pain.[4]

Carefully document (preferably video) the involuntary movements. Rate the severity of the involuntary movements, for example, with the Abnormal Involuntary Movement Scale (AIMS) or Impact-TD.[34]

Consider referring the patient for a neurological consultation if unsure about the possible diagnosis of TD.[12] For example, due to an atypical presentation, a family history of other movement or neurodegenerative disorders (such as Huntington's disease), symptoms present of another neurological condition, or an unexpected response to treatment.[12]

Investigations

Do not routinely request investigations if a patient has the classic signs and symptoms of TD in the context of long-term use of causative drugs.

In patients with atypical features, consider appropriate investigations to rule out potential secondary causes. For example, in patients with:

  • Abrupt onset of symptoms or unilateral symptoms, request an urgent head computed tomography (CT) scan or magnetic resonance imaging (MRI) to rule out serious conditions such as stroke or severe hyperglycaemia (causing diabetic striatopathy).[35] The authors of this topic also recommend a comprehensive metabolic panel to rule out metabolic derangements.[36]

  • Cognitive impairment or eye movement abnormalities, request investigations for neurodegenerative conditions such as Huntington's disease (HD) and HD-like conditions. These include CAG repeat length, peripheral smear for acanthocytes, and MRI of the brain to look for caudate or striatal atrophy.

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