Evidence-based guideline: Treatment of tardive syndromes

Abstract

Objective: To make evidence-based recommendations regarding management of tardive syndromes (TDS), including tardive dyskinesias (TDD), by addressing 5 questions: 1) Is withdrawal of dopamine receptor blocking agents (DRBAs) an effective TDS treatment? 2) Does switching from typical to atypical DRBAs reduce TDS symptoms? 3) What is the efficacy of pharmacologic agents in treating TDS? 4) Do patients with TDS benefit from chemodenervation with botulinum toxin? 5) Do patients with TDS benefit from surgical therapy?Methods: PsycINFO, Ovid MEDLINE, EMBASE, Web of Science, and Cochrane were searched . Articles were classified according to a 4-tiered evidence-rating scheme; recommendations were tied to the evidence. Results and recommendations:Clonazepam probably improves TDD and ginkgo biloba probably improves TDS (both Level B); both should be considered as treatment. Risperidone may improve TDS but cannot be recommended as treatment because neuroleptics may cause TDS despite masking symptoms. Amantadine and tetrabenazine might be considered as TDS treatment (Level C). Diltiazem should not be considered as TDD treatment (Level B); galantamine and eicosapentaenoic acid may not be considered as treatment (Level C). Data are insufficient to support or refute use of acetazolamide, bromocriptine, thiamine, baclofen, vitamin E, vitamin B 6 , selegiline, clozapine, olanzapine, melatonin, nifedipine, fluperlapine, sulpiride, flupenthixol, thiopropazate, haloperidol, levetiracetam, quetiapine, ziprasidone, sertindole, aripiprazole, buspirone, yi-gan san, biperiden discontinuation, botulinum toxin type A, electroconvulsive therapy, a-methyldopa, reserpine, and pallidal deep brain stimulation as TDS treatments (Level U). Data are insufficient to support or refute TDS treatment by withdrawing causative agents or switching from typical to atypical DRBA (Level U). Tardive syndromes (TDS) are disorders that fulfill the following criteria: history of at least 3 months' total cumulative neuroleptic exposure during which the exposure can be continuous or discontinuous, presence of at least "moderate" abnormal involuntary movements in one or more body areas or at least "mild" movements in 2 or more body areas, and absence of other conditions that might produce abnormal involuntary movements.1 Various involuntary movements, including lingual-facial-buccal movements, are recognized as tardive dyskinesia (TDD) symptoms. TDS includes not only lingual-facial-buccal dyskinesia but also the variant forms, collectively termed tardive syndromes. [2][3][4][5][6][7][8] In this guideline, tardive dyskinesia encompasses all forms of persistent dyskinesia caused by dopamine receptor blocking agents (DRBAs).TDS prevalence is estimated to be 30% in outpatients with schizophrenia treated with neuroleptics.9-11 TDS †Deceased.

The Effects of Valbenazine in Participants with Tardive Dyskinesia

“…Often, however, this is not possible without exacerbation of the psychiatric disorder. 10 Medications such as clozapine, baclofen, tetrabenazine, and benzodiazepines have been anecdotally reported to improve TD, but evidence for their efficacy is limited. 10 Valbenazine, a novel and highly selective vesicular monoamine transporter 2 (VMAT2) inhibitor, is approved by the US Food and Drug Administration (FDA) for treatment of TD in adults.…”

“…10 Medications such as clozapine, baclofen, tetrabenazine, and benzodiazepines have been anecdotally reported to improve TD, but evidence for their efficacy is limited. 10 Valbenazine, a novel and highly selective vesicular monoamine transporter 2 (VMAT2) inhibitor, is approved by the US Food and Drug Administration (FDA) for treatment of TD in adults. On the basis of its pharmacologic profile, 11 it is hypothesized that the inhibitory effects of valbenazine may diminish monoamine neurotransmitter concentrations in the synaptic cleft, thereby reducing the availability of dopamine to hypersensitive postsynaptic receptors and reducing TD.…”

Antipsychotic-Induced Tardive Syndromes: Clinical Features and Treatment Approaches

“…Hipertiroidi, hiperparatiroidi ve hiperglisemi seyrek olarak atetoid hareketlere sebep olabilirler. 16,22,23 Mekanizması tam olarak bilinmemektedir. Nigrositriatal dopamin reseptör sisteminde aşırı duyarlılık, dopaminerjik ve kolinerjik sistemler arasındaki dengenin bozulması, sitriatonigral GABA'erjik nöronlarda işlev bozukluğu ve eksitotoksisite üzerinde durulmaktadır.…”

“…Yüksek dozlarda klonazepam, baklofen veya benzodiyazepin karışık sonuçlar vermiştir. 22,41 Distoni derin beyin stimülasyonuna da olumlu cevap verebilir. Bu, fokal distonisi olan hastalar için yararlı-dır.…”

Antipsychotikainduzierte tardive Syndrome

“…Die retrospektive Analyse der Daten von 108 nicht schizophrenen Patienten hat ergeben, dass nach Absetzen der TDauslösenden Medikation bei 13 % die TD nach 3 Jahren komplett verschwunden war [51]. Aufgrund dieser uneinheitlichen Datenlage kann ein Absetzen der antipsychotischen Therapie zur Behandlung der TD nicht eindeutig empfohlen werden [52]. Darüber hinaus kann das Absetzen eines Antipsychotikums die TD, zumindest initial für einige Wochen, verschlechtern [53,54].…”