Neuroleptic‐Induced Tardive Dyskinesia Variants

Skidmore, Frank; Weiner, William J.; Burke, Robert E.

doi:10.1002/9780470753217.ch10

Cited by 10 publications

(12 citation statements)

References 88 publications

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“…TD movements can also result in limb chorea, trunk movements as rhythmic rocking or thrusting motions (referred to as pelvic dyskinesia when pelvic muscles are involved), and respiratory dyskinesia with altered rhythmical patterns leading to hyper-and hypoventilation that can be life threatening [11]. Other subtypes, occurring alone or combined, include tardive dystonia, akathisia, tics, tremor, and myoclonus [6,12]. The pathophysiology of TD remains elusive, though multiple hypotheses have been proposed (summarized in Table 1).…”

Section: Introductionmentioning

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 In addition, studies demonstrate that TD actually remits in only a minority of patients when these drugs are withdrawn.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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Section: Introductionmentioning

confidence: 99%

Tardive Dyskinesia: Therapeutic Options for an Increasingly Common Disorder

2014

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“…Second, there are many case reports of tardive syndromes in non-schizophrenic patients who have used antipsychotics for other indications, such as anxiety, personality disorders, hypochondriasis, or behavioral problems (Skidmore et al, 2005). Third, dopamine blocking agents are used in general practice and can induce movement disorders.…”

Section: Introductionmentioning

confidence: 99%

Tardive Dyskinesia: Clinical Presentation and Treatment

Harten

Tenback

2011

International Review of Neurobiology

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“…Our findings support suggestions that younger age and changes in antipsychotic treatment are risk factors but do not support treatment duration, total cumulative dose, or male sex as predictive of tardive onset dystonias. 1,32,33 There are several limitations to this report. Only 2 patients were observed to be experiencing an OGC episode by clinic staff; most were documented on the basis of patient and family member reports.…”

Section: Discussionmentioning

confidence: 91%

Incidence of Oculogyric Crisis and Long-Term Outcomes With Second-Generation Antipsychotics in a First-Episode Psychosis Program

Gardner

Abidi

Ursuliak³

et al. 2015

Journal of Clinical Psychopharmacology

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Oculogyric crisis (OGC) is an often recurrent dystonic adverse effect of antipsychotic treatment characterized by a sustained fixed upward gaze lasting minutes to hours. The risk of OGC has not been established. We prospectively estimated the incidence rate of OGC in an early intervention service for psychosis and provided details regarding the antipsychotics implicated, clinical presentation, and long-term outcomes of OGC. The Nova Scotia Early Psychosis Program provides comprehensive, team-based care to youth and young adults with schizophrenia spectrum disorder. For 6 years (April 2008 to March 2014), 452 new patients were admitted to the program and participated in an individualized program of care. Eight patients (4 females; mean age, 19.8 years) developed recurrent episodes of OGC after 3 months to 2 years of treatment with 1 or more second-generation antipsychotics, yielding an incidence rate of 1.8% (95% confidence interval, 0.9%-3.4%). Risperidone or olanzapine (alone or in combination with a second antipsychotic) seemed causative in each case. Also implicated in the onset or recurrence of oculogyric episodes were ziprasidone, quetiapine, clozapine, aripiprazole, and the first-generation antipsychotic loxapine. Follow-up ranged between 2 and 7 years. Episodes stopped after switching antipsychotic treatment in 4 cases and after stopping antipsychotic treatment in 2 cases. In the other 2 cases, recurrences were ongoing at last follow-up 2 and 6 years after onset with antipsychotic treatment continuing. We observed a high rate of tardive-onset, recurrent, and potentially chronic ocular dystonias in patients with first-episode psychosis caused by the use of second-generation antipsychotics.

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Neuroleptic‐Induced Tardive Dyskinesia Variants

Cited by 10 publications

References 88 publications

Tardive Dyskinesia: Therapeutic Options for an Increasingly Common Disorder

Tardive Dyskinesia: Therapeutic Options for an Increasingly Common Disorder

Tardive Dyskinesia: Clinical Presentation and Treatment

Incidence of Oculogyric Crisis and Long-Term Outcomes With Second-Generation Antipsychotics in a First-Episode Psychosis Program

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