Clinical Phenotype of Tardive Dyskinesia in Bipolar Disorder

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dc.coverageDOI: 10.1097/JCP.0000000000001532
dc.creatorGardea-Resendez, Manuel
dc.creatorTaylor-Desir, Monica J.
dc.creatorRomo-Nava, Francisco
dc.creatorBond, David
dc.creatorVallender, Eric J.
dc.creatorCuellar-Barboza, Alfredo B.
dc.creatorPrieto, Miguel L.
dc.creatorNunez, Nicolas
dc.creatorVeldic, Marin
dc.creatorOzerdem, Aysegul
dc.creatorSingh, Balwinder
dc.creatorMarkota, Matej
dc.creatorColby, Colin L.
dc.creatorCoombes, Brandon J.
dc.creatorBiernacka, Joanna M.
dc.creatorMcElroy, Susan L.
dc.creatorFrye, Mark A.
dc.date2022
dc.date.accessioned2025-11-18T19:41:50Z
dc.date.available2025-11-18T19:41:50Z
dc.description<p>Purpose Recognizing the negative impact that antipsychotic-induced movement disorders have on the quality of life and treatment outcomes in bipolar disorder (BD), this study aimed to assess clinical correlates and antipsychotic use patterns of tardive dyskinesia (TD+) in BD. Materials and Methods Participants with and without TD were included. Clinical variables were compared using t-test and χ2 test. Antipsychotic use patterns in TD+, including number of trials, mean doses, and estimated cumulative exposure, were assessed in a case-only analysis. Results The prevalence rate of TD was 5.1%. In comparison to the TD- group (n = 1074), TD+ participants (n = 58) were older, more likely to be female and have type I bipolar illness. There were 60.3% of the TD+ group that continued using antipsychotics at study entry and had a mean cumulative exposure to antipsychotics of 18.2 ± 15.6 years. Average dose, in haloperidol equivalents, was 5.9 ± 3.5 mg and 77.7% of the trials were second-generation antipsychotics. Conclusions This study confirms previously identified TD risk factors, such as age, sex, and bipolar subtype in a large BD cohort. Limitations included a cross-sectional design and the lack of tardive illness severity assessment. As atypical antipsychotics continue to be primary mood stabilization treatment, attempting to harmonize large data sets to identify additional biomarkers of tardive risk will optimize individualized care for patients with BD.</p>eng
dc.identifierhttps://investigadores.uandes.cl/en/publications/2c7a4a0e-045a-4fc3-b629-f27634503c6a
dc.identifier.urihttps://repositorio.uandes.cl/handle/uandes/52023
dc.languageeng
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.sourcevol.42 (2022) nr.2 p.159-162
dc.subjectantipsychotics
dc.subjectbipolar disorder
dc.subjecttardive dyskinesia
dc.subjectPhenotype
dc.subjectCross-Sectional Studies
dc.subjectTardive Dyskinesia/chemically induced
dc.subjectHumans
dc.subjectBipolar Disorder/chemically induced
dc.subjectQuality of Life
dc.subjectFemale
dc.subjectMale
dc.subjectAntipsychotic Agents/adverse effects
dc.subjectSDG 3 - Good Health and Well-being
dc.titleClinical Phenotype of Tardive Dyskinesia in Bipolar Disordereng
dc.typeArticleeng
dc.typeArtículospa
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