| Tardive dyskinesia | |
|---|---|
| Other names | Linguofacial dyskinesia, tardive dystonia, tardive oral dyskinesia[1] |
 | |
| Tardive dyskinesia is believed to involve the neurotransmitter dopamine. | |
| Pronunciation | |
| Specialty | Neurology, psychiatry |
| Symptoms | Involuntary, repetitive body movements[1] |
| Causes | Neuroleptic medications (antipsychotics, metoclopramide)[1][2] |
| Diagnostic method | Based on symptoms after ruling out other potential causes[1] |
| Differential diagnosis | Huntington's disease, cerebral palsy, Tourette syndrome, dystonia[2] |
| Prevention | Using lowest possible dose of neuroleptic medication[3] |
| Treatment | Stopping neuroleptic medication if possible, switching to clozapine[1] |
| Medication | Valbenazine, tetrabenazine, botulinum toxin[1][4] |
| Prognosis | Variable[1] |
| Frequency | 20% (atypical antipsychotics) 30% (typical antipsychotics)[5] |
Tardive dyskinesia (TD) is a disorder that results in involuntary, repetitive body movements, which may include grimacing, sticking out the tongue, or smacking the lips.[1] Additionally, there may be rapid jerking movements or slow writhing movements.[1] In about 20% of people with TD, the disorder interferes with daily functioning.[3]
Tardive dyskinesia occurs in some people as a result of long-term use of dopamine-receptor-blocking medications such as antipsychotics and metoclopramide.[1][2] These medications are usually used for mental illness but may also be given for gastrointestinal or neurological problems.[1] The condition typically develops only after months to years of use.[1][3] The diagnosis is based on the symptoms after ruling out other potential causes.[1]
Efforts to prevent the condition include either using the lowest possible dose or discontinuing use of neuroleptics.[3] Treatment includes stopping the neuroleptic medication if possible or switching to clozapine.[1] Other medications such as valbenazine, tetrabenazine, or botulinum toxin may be used to lessen the symptoms.[1][4] With treatment, some see a resolution of symptoms, while others do not.[1]
Rates in those on atypical antipsychotics are about 20%, while those on typical antipsychotics have rates of about 30%.[5] The risk of acquiring the condition is greater in older people.[3] The term "tardive dyskinesia" first came into use in 1964.[3]
References edit
- ^ a b c d e f g h i j k l m n o p "Tardive dyskinesia". rarediseases.info.nih.gov. 1 June 2017. Archived from the original on 18 June 2017. Retrieved 10 June 2017.
- ^ a b c "Tardive Dyskinesia". NORD (National Organization for Rare Disorders). 2015. Archived from the original on 28 August 2017. Retrieved 11 June 2017.
- ^ a b c d e f Vijayakumar, D; Jankovic, J (May 2016). "Drug-Induced Dyskinesia, Part 2: Treatment of Tardive Dyskinesia". Drugs. 76 (7): 779–87. doi:10.1007/s40265-016-0568-1. PMID 27091214.
- ^ a b "Tardive Dyskinesia Information Page". National Institute of Neurological Disorders and Stroke. Archived from the original on 2017-07-04.
- ^ a b Carbon, M; Hsieh, CH; Kane, JM; Correll, CU (March 2017). "Tardive Dyskinesia Prevalence in the Period of Second-Generation Antipsychotic Use: A Meta-Analysis". The Journal of Clinical Psychiatry. 78 (3): e264–e278. doi:10.4088/jcp.16r10832. PMID 28146614.