Tardive dyskinesia associated with clozapine treatment

Bruscas, Maria Jesus; González, F García; Santos, José Luís; Sánchez, E. Pérez

doi:10.1016/j.pnpbp.2007.01.016

Cited by 9 publications

(2 citation statements)

References 11 publications

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“…In such cases switching to clozapine may reveal suppressed TD (Bruscas et al, 2007;Duggal and Mendhekar, 2007;Ertugrul and Demir, 2005;Li et al, 2009;Raguraman and Vijaysagar, 2007). In the few case reports suggesting that clozapine induces TD most of the patients had a history of long-term use of FGAs.…”

Section: B Switching To Clozapinementioning

confidence: 99%

Tardive Dyskinesia: Clinical Presentation and Treatment

Harten

Tenback

2011

International Review of Neurobiology

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Section: B Switching To Clozapinementioning

confidence: 99%

Tardive Dyskinesia: Clinical Presentation and Treatment

Harten

Tenback

2011

International Review of Neurobiology

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“…The exception is clozapine, the most atypical AAP (classified as an AAP even though it was already on the market in the 1960s); substantial evidence indicates it is almost free of extrapyramidal side effects, apart from akathisia. However, although the risk of TD is generally agreed to be lower with clozapine than with TAPs, evidence remains that even clozapine may cause new TD or intensify existing TD [18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37] (for review, see Hazari et al [38]). However, the decrease in TD prevalence rates with all other AAPs was much less than expected, and clinicians are cautioned not to overestimate the safety of AAPs [39].…”

Section: Introductionmentioning

confidence: 99%

Tardive Dyskinesia Associated with Atypical Antipsychotics: Prevalence, Mechanisms and Management Strategies

2018

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All antipsychotics, including the atypical antipsychotics (AAPs), may cause tardive dyskinesia (TD), a potentially irreversible movement disorder, the pathophysiology of which is currently unknown. The prevention and treatment of TD remain major challenges for clinicians. We conducted a PubMed search to review the prevalence and etiology of and management strategies for TD associated with AAPs. TD prevalence rates varied substantially between studies, with an estimated prevalence of around 20% in patients using AAPs. The risk of TD is lower with AAPs than with typical antipsychotics (TAPs) but remains a problem because AAPs are increasingly being prescribed. Important risk factors associated with TD include the duration of antipsychotic use, age, and ethnicity other than Caucasian. Theories about the etiology of TD include supersensitivity of the dopamine receptors and oxidative stress, but other neurotransmitters and factors are probably involved. Studies concerning the management of TD have considerable methodological limitations. Thus, recommendations for the management of TD are based on a few trials and clinical experience, and no general guidelines for the management of TD can be established. The best management strategy remains prevention. Caution is required when prescribing antipsychotics, and regular screening is needed for early detection of TD. Other strategies may include reducing the AAP dosage, switching to clozapine, or administering vesicular monoamine transporter (VMAT)-2 inhibitors. In severe cases, local injections of botulinum toxin or deep brain stimulation may be considered. More clinical trials in larger samples are needed to gather valid information on the effect of interventions targeting TD.

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