Anticholinergic Challenge and Neuroleptic Withdrawal

Gárdos, George; Cole, Jonathan O.; Rapkin, Robert M.; LaBrie, Richard A.; Baquelod, Eleanor; Moore, Patricia; Sovner, Robert; Doyle, John B.

doi:10.1001/archpsyc.1983.01790220020003

Cited by 48 publications

(14 citation statements)

References 28 publications

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“…The neuroleptic withdrawal significantly increased dyskinesia and dysphoria, resulting in early therapy termination in 33% of patients and return to prior neuroleptics poststudy. 16 Another Class III study found no significant worsening of tardive dystonia (TD) or psychiatric relapse in patients with chronic schizophrenia randomized to placebo for 6 weeks or their regular injectable fluphenazine. 17 Short-term studies also suggest that TDS worsens during the first few weeks after neuroleptic withdrawal (Class III and IV studies).…”

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confidence: 99%

Evidence-based guideline: Treatment of tardive syndromes

et al. 2013

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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.

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confidence: 99%

Evidence-based guideline: Treatment of tardive syndromes

et al. 2013

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“…What is role of the type of TD (e.g., classical vs dystonia) on response? There is some suggestion that different types of TD will respond differently to agents, for example anticholinergics are helpful in dystonia [114], but can worsen classical oral-buccal-lingual dyskinesia [55]. Can the responsiveness to medications in TD be predicted by studies of genetic polymorphisms known to influence the risk and severity of TD [10]?…”

Section: Resultsmentioning

confidence: 99%

“…However, there is insufficient evidence that this leads to improvement [7]. In addition, such withdrawal of neuroleptics may worsen TD, at least initially [55][56][57][58] contributing to the belief (and, in turn, the practice) that neuroleptics can be used as symptomatic treatment for TD. The suppressive effects of first-generation neuroleptics on TD can be substantial (>60 % improvement), but several studies have suggested that this is only a temporary effect [25,59], triggering a spiraling of the dose upwards over time.…”

Section: Should Neuroleptics Be Used As a Therapeutic Agent For Td?mentioning

confidence: 99%

Tardive Dyskinesia: Therapeutic Options for an Increasingly Common Disorder

2014

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Tardive dyskinesia (TD) is a serious, often disabling, movement disorder that is caused by medications that block dopamine receptors (i.e., neuroleptics, anti-emetics). There is currently no standard treatment approach for physicians confronted with such patients. This may be the result of notions that TD is disappearing because of the switch to secondgeneration antipsychotic agents and that it is largely reversible.In this article we demonstrate that second-generation antipsychotics do, indeed, cause TD and, in fact, the frequency is likely higher than expected because of growing off-label uses and a tripling of prescriptions written in the last 10 years. In addition, studies demonstrate that TD actually remits in only a minority of patients when these drugs are withdrawn. Furthermore, neuroleptic agents are often utilized to treat TD, despite prolonged exposure being a risk factor for irreversibility. The outcome of these trends is a growing population afflicted with TD. We review non-neuroleptic agents that have shown positive results in small, early-phase, blinded trials, including tetrabenazine, amantadine, levetiracetam, piracetam, clonazepam, propranolol, vitamin B6, and Ginkgo biloba. Other options, such as botulinum toxin and deep brain stimulation, will also be discussed, and a suggested treatment algorithm is provided. While these agents are reasonable treatment options at this time there is a need, with a concerted effort between neurology and psychiatry, for full-scale drug development, including multicenter, randomized, blinded trials to confirm the effectiveness of the agents that were positive in phase 2 trials and the development of newer ones.

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“…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]. So es die Grunderkrankung zulässt, kann ein Versuch, die Dosis der antipsychotischen Medikation zu reduzieren, erfolgen.…”

Section: Behandlung Der Tardiven Dyskinesieunclassified