Incidence of Tardive Dyskinesia With Atypical Versus Conventional Antipsychotic Medications: A Prospective Cohort Study

Department of Psychiatry, Yale University School of Medicine, 34 Park Street, New Haven, CT 06519, USA.
The Journal of Clinical Psychiatry (Impact Factor: 5.5). 02/2010; 71(4):463-74. DOI: 10.4088/JCP.07m03890yel
Source: PubMed


Most previous studies of the incidence of tardive dyskinesia with atypical antipsychotics compared with conventional antipsychotics have not had tardive dyskinesia as their primary focus. The current study aimed to compare the incidence of tardive dyskinesia with atypical vs conventional antipsychotics using methods similar to those from a previous prospective cohort study at our site in the 1980s.
Three hundred fifty-two initially tardive dyskinesia-free psychiatric outpatients (diagnosed at baseline using the Structured Clinical Interview for DSM-IV) were examined for a new diagnosis of tardive dyskinesia (using the Abnormal Involuntary Movement Scale and Glazer-Morgenstern criteria) every 6 months for up to 4 years at a community mental health center. At baseline, subjects were receiving conventional antipsychotics only (23%), atypicals only (64%), or both (14%). Only 26 subjects had never received conventional antipsychotics. Baseline evaluations were conducted from November 2000 through May 2003. Follow-ups were conducted through February 2005.
Compared with subjects treated with conventional antipsychotics alone since the previous visit, the adjusted tardive dyskinesia incidence rate-ratio for subjects treated with atypical antipsychotics alone was 0.68 (95% CI, 0.29-1.64). The incidence and prevalence of tardive dyskinesia was similar to previous findings at this site in the 1980s.
The incidence of tardive dyskinesia with recent exposure to atypical antipsychotics alone was more similar to that for conventional antipsychotics than in most previous studies. Despite high penetration of atypical antipsychotics into clinical practice, the incidence and prevalence of tardive dyskinesia appeared relatively unchanged since the 1980s. Clinicians should continue to monitor for tardive dyskinesia, and researchers should continue to pursue efforts to treat or prevent it.

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    • "SGAs is one-quarter that of FGAs, the results of this study suggest that the risk with SGAs is more than half that of FGAs (excluding clozapine patients) or more than two-thirds of the risk (including clozapine patients) [44]. The finding of surprisingly high rate of TD among clozapine patients in this study was attributed to certain confounding factors, such as confounding by indication (prescribing of clozapine to patients with TD or at-risk for TD), and should be interpreted with caution. "
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    ABSTRACT: Antipsychotic-induced extrapyramidal adverse effects are well recognized in the context of first-generation antipsychotic drugs. However, the introduction of second-generation antipsychotics, with atypical mechanism of action, especially lower dopamine receptors affinity, was met with great expectations among clinicians regarding their potentially lower propensity to cause extrapyramidal syndrome. This review gives a brief summary of the recent literature relevant to second-generation antipsychotics and extrapyramidal syndrome. Numerous studies have examined the incidence and severity of extrapyramidal syndrome with first- and second-generation antipsychotics. The majority of these studies clearly indicate that extrapyramidal syndrome does occur with second-generation agents, though in lower rates in comparison with first generation. Risk factors are the choice of a particular second-generation agent (with clozapine carrying the lowest risk and risperidone the highest), high doses, history of previous extrapyramidal symptoms, and comorbidity. Also, in comparative studies, the choice of a first-generation comparator significantly influences the results. Extrapyramidal syndrome remains clinically important even in the era of second-generation antipsychotics. The incidence and severity of extrapyramidal syndrome differ amongst these antipsychotics, but the fact is that these drugs have not lived up to the expectation regarding their tolerability.
    BioMed Research International 06/2014; 2014. DOI:10.1155/2014/656370 · 3.17 Impact Factor
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    • "Multiple risk factors of TD have been identified, including increased age, psychiatric diagnosis, female sex, a history of diabetes, organic brain damage, development of neurologic side effects, and the presence of negative symptoms related to SCZ.6 TD’s prevalence in patients has been differentiated between the use of first-generation/typical antipsychotics (FGAs/TAs) and second-generation/ atypical antipsychotics (SGAs/ATAs), with rates of 32.4% and 13.1%, respectively, based on short-term studies and haloperidol as prime comparator.6 In a recent, prospective, 4-year study, ATA use reduced the cumulative risk for TD by one-third relative to TAs.7 Nonetheless, the complication remains prevalent and a proportion of one-third of patients chronically exposed to antipsychotic drugs still display TD, despite ATA prescription alone or in combination.7 The annual risk remains greater in older adults, particularly in those living with a dementing illness.8 "
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    ABSTRACT: The aim of this review is to assess new, emerging, and experimental treatment options for tardive dyskinesia (TD). The methods to obtain relevant studies for review included a MEDLINE search and a review of studies in English, along with checking reference lists of articles. The leading explanatory models of TD development include dopamine receptor supersensitivity, GABA depletion, cholinergic deficiency, neurotoxicity, oxidative stress, changes in synaptic plasticity, and defective neuroadaptive signaling. As such, a wide range of treatment options are available. To provide a complete summary of choices we review atypical antipsychotics along with resveratrol, botulinum toxin, Ginkgo biloba, tetrabenazine, clonazepam, melatonin, essential fatty acids, zonisamide, levetiracetam, branched-chain amino acids, drug combinations, and invasive surgical treatments. There is currently no US Food and Drug Administration-approved treatment for TD; however, prudent use of atypical antipsychotics with routine monitoring remain the cornerstone of therapy, with experimental treatment options available for further management.
    Drug Design, Development and Therapy 11/2013; 7:1329-1340. DOI:10.2147/DDDT.S32328 · 3.03 Impact Factor
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    • "Atypical neuroleptics were initially thought to be at lower risk of inducing TDK; however, three prospective studies do not support this notion.47–49 Based on the dopamine hypersensitivity hypothesis (ie, prolonged dopamine antagonist therapy leads to dopamine hypersensitivity), both typical and atypical neuroleptic agents should suppress TDK, but the benefit is usually only in the short term and is greater with more potent agents.50 "
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    ABSTRACT: Tardive dyskinesia (TDK) includes orobuccolingual movements and "piano-playing" movements of the limbs. It is a movement disorder of delayed onset that can occur in the setting of neuroleptic treatment as well as in other diseases and following treatment with other drugs. The specific pathophysiology resulting in TDK is still not completely understood but possible mechanisms include postsynaptic dopamine receptor hypersensitivity, abnormalities of striatal gamma-aminobutyric acid (GABA) neurons, and degeneration of striatal cholinergic interneurons. More recently, the theory of synaptic plasticity has been proposed. Considering these proposed mechanisms of disease, therapeutic interventions have attempted to manipulate dopamine, GABA, acetylcholine, norepinephrine and serotonin pathways and receptors. The data for the effectiveness of each class of drugs and the side effects were considered in turn.
    Neuropsychiatric Disease and Treatment 09/2013; 9:1371-1380. DOI:10.2147/NDT.S30767 · 1.74 Impact Factor
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