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Tardive dyskinesia
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Introduction
What does TD look like?
What are the risks of TD developing?
How common is TD?
Will TD disappear if medication is stopped?
What other options are there if TD appears?
Useful contacts
References
Introduction
Dyskinesia literally means ‘trouble moving’, and is used to describe involuntary jerky or slow writhing movements.
The term tardive dyskinesia (TD) is used to describe dyskinesia caused mainly by the use of antipsychotic drugs (also called neuroleptics or major tranquillisers), which are used to treat psychotic states such as occur in schizophrenia, and sometimes in bipolar disorder (manic depression) and severe depression. The term ‘tardive’ means delayed or late-appearing, reflecting the fact that symptoms start long after treatment has started.
Dyskinesia occasionally occurs in people who have never been treated with antipsychotic medication, [1] some of whom may have a first-degree relative (parent or sibling) with schizophrenia. [2] It may also be a side effect of drugs used to treat neurological or gastrointestinal disorders. [3]
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What does TD look like?
TD is characterised by repetitive involuntary purposeless muscle contractions that force parts of the body into abnormal, and sometimes painful, movements or postures. These movements and positions (called dystonias) can affect any part of the body, including the limbs, trunk, neck, eyelids, facial muscles and vocal cords. These movements are involuntary (they just happen) and are difficult or impossible to control.
The involuntary movements usually begin with the face, mouth, lips and tongue, and include grimacing, lip-smacking, tongue movements and rapid blinking. Involuntary movements may also involve the rest of the body and produce involuntary gestures, tics and writhing movements. Involuntary movements of the fingers may look as though the patient is playing an invisible guitar or piano.
TD is socially disabling and, at its worst, is severely physically disabling.
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What are the risks of TD developing?
TD is primarily associated with the older so-called ‘typical’ antipsychotic drugs such as chlorpromazine (Largactil) and haloperidol (Haldol, Dozic, Serenace), which also cause the so-called ‘extrapyramidal’ side effects (EPS) that mimic Parkinson’s disease. The risk of TD is lower with the newer ‘atypical’ antipsychotic drugs, such as olanzapine (Zyprexa) and risperidone (Risperdal).
The risk of TD is dose related, increasing with high doses of the older antipsychotic drugs. It mainly occurs in people who have been on moderate-to-high doses for periods of six months to two years or more. It rarely occurs with less than six months’ treatment at low doses, though there have been a few reports of TD occurring when low doses were prescribed for relatively short periods. The overall risk is five per cent of cases per year of treatment with ‘typical’ antipsychotic medications. [4]
Estimates for the risks of TD to long-term users of ‘typical’ antipsychotic drugs vary from 5 to 56 per cent; for people treated for four years or longer, a widely accepted estimate is 20 per cent. The risk is higher for people on depot preparations (slow-release formulations of drugs given as injections).
Psychiatric research shows that women, children, older people and people with mood disorders are at particular risk of TD. [5]
For people who show early signs of the neuromuscular adverse effects of antipsychotics, such as parkinsonism (e.g. shaking, stiffness, shuffling walk), there is a greater risk of developing TD. [6] People who develop Parkinson’s symptoms are likely to be given anti-Parkinson’s drugs, and use of these is therefore also associated with the development of TD. The World Health Organization has issued a statement saying that anti-Parkinson’s drugs should not be routinely given to people taking antipsychotics.
Stopping and starting antipsychotics may contribute to the risk of TD persisting once it has developed. [7]
Although it is currently not possible to predict who is at risk of getting TD with the use of antipsychotics, research is beginning to show that there may be genetic links, which may mean that people at risk can be identified in the future.[8]
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How common is TD?
The incidence (number of new cases per year) of TD is five per cent among people taking the older ‘typical’ antipsychotic drugs but less than one per cent per year in those taking the newer atypical antipsychotic drugs. The prevalence (number in any population) is 20 per cent of those taking the older anti-psychotic drugs. The risk is thought to be higher for women than men. [9]
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Will TD disappear if the medication is stopped?
TD may disappear if it is identified early and medication is stopped. Symptoms will improve spontaneously in about half of patients who discontinue antipsychotics at any time; although improvement is often delayed and may take up to five years. However, stopping medication is not possible for some people, and the risk of relapse or psychosis must be balanced against the risk of TD. If medication is to be stopped, it should be done by reducing the dose gradually, under medical supervision.
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What other options are there if TD appears?
A ‘typical’ antipsychotic might be substituted with one of the newer ‘atypical’ drugs, which have all been found to reduce symptoms of TD. If anti-Parkinson’s drugs are being prescribed for the adverse effects of the antipsychotics, then stopping these is advised. There is evidence that clonazepam (a benzodiazepine used in epilepsy) may be a useful treatment, and vitamin E appears to diminish TD in some cases.[10] A number of studies have suggested that vitamin B6 may also be helpful.[11]
TD is not necessarily progressive in all cases (i.e. it won’t necessarily get worse). Using the lowest possible dose of antipsychotic minimises the risk that TD will progress. Sometimes withdrawal dyskinesias occur when drugs are stopped. These are likely to diminish with time. TD may also be unmasked during drug withdrawal.
A consensus statement by The Royal College of Psychiatrists suggests use of a combination of moderate doses of a benzodiazepine and an antipsychotic in emergency situations where dangerous behaviour needs to be controlled rapidly, rather than high-dose antipsychotics.
For more information on antipsychotic drugs, see Mind’s booklet Making sense of antipsychotics.
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Useful contacts
ADDER (Action for Dystonia, Diagnosis, Epidemiology and Research)
Bath Cottage, Dinsdale Park, Middleton St George DL2 1DJ
tel: 01325 332 723, web: www.dystonia.co.uk
Choice and Medicine
web: www.choiceandmedication.org.uk
Website created by the UK Psychiatric Pharmacy Group and National Institute for Mental Health in England. Offers information about medications used in the mental health setting to help people make informed decisions about medication.
Dystonia Society
89 Albert Embankment, London SE1 7TP
helpline: 0845 458 6322 or 020 7793 3650 (Mon–Fri 10am–4pm)
tel: 0845 458 6211, web: www.dystonia.org.uk
Telephone service for people with dystonia (a condition dominated by involuntary sustained muscle spasms), their carers, the general public and health professionals. Provides information, advice, counselling, referrals and local contacts. Meetings, a membership scheme and a publications list are also available.
Rethink
89 Albert Embankment, London SE1 7TP
national advice service: 020 7840 3188 (Mon, Wed, Fri 10am–3pm, Tues, Thurs 10am–1pm)
tel: 0845 456 0455
email: advice@rethink.org web: www.rethink.org
A national mental health charity working with people affected by serious mental illness.
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References
[1] Gelder, M., Gath, D., Mayou, R. and Cowen, P., 1996, Oxford Textbook of Psychiatry, OUP.
[2] McCreadie, R. et al, 2003, ‘Spontaneous dyskinesia in first-degree relatives of chronically ill, never-treated people with schizophrenia’, British Journal of Psychiatry, vol 183, pp 45–9.
[3] National Institute of Neurological Disorders and Stroke: www.ninds.nih.gov/disorders/tardive/tardive.htm
[4] Chaplin, R., Potter, M., 1996, ‘Tardive dyskinesia: screening and risk disclosure’, Psychiatric Bulletin, vol 20, pp 714–16.
[5] Duncan, D., McConnell, H., Taylor, D., 1997, ‘Tardive dyskinesia – how is it prevented and treated?’, Psychiatric Bulletin, vol 21, pp 422–5.
[6] David Taylor, Chief Pharmacist, Maudsley Hospital, personal communication.
[7] Duncan, D., McConnell, H., Taylor, D., 1997, ‘Tardive dyskinesia – how is it prevented and treated?’, Psychiatric Bulletin, vol 21, pp 422–5.
[8] Bakker P. R., van Harten P. N., Van Os J., 2008, Antipsychotic-induced tardive dyskinesia and polymorphic variations in COMT, DRD2, CYP1A2 and MnSOD genes: a meta-analysis of pharmacogenetic interactions. Molecular Psychiatry vol 13, pp 544–56.
[9] Chaplin, R., Potter, M., 1996, ‘Tardive dyskinesia: screening and risk disclosure’, Psychiatric Bulletin, vol 20, pp 714–16.
[10] Duncan, D., McConnell, H., Taylor, D., 1997, ‘Tardive dyskinesia – how is it prevented and treated?’, Psychiatric Bulletin, vol 21, pp 422–5.
[11] Lerner V. et al, 2001, ‘Vitamin B6 helps quell neuroleptic-induced tardive dyskinesia’, Am J Psychiatry, vol 158, pp 1511–14.
This factsheet was written by Katherine Darton. Mind Information Unit, 2002. Updated November 2008.
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