Pathophysiological mechanisms underlying antipsychotic-induced tardive dyskinesia

Purpose. To analyze the results of classical and modern studies reflecting the pathophysiological mechanisms of antipsychotic-induced tardive dyskinesia.Materials and methods. We searched for full-text publications in Russian and English in the databases of E-Library, PubMed, Web of Science and Spri...

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Main Authors: E. E. Vayman, N. A. Shnayder, N. G. Neznanov, R. F. Nasyrova
Format: Article
Language:English
Published: Siberian State Medical University (Tomsk) 2020-01-01
Series:Бюллетень сибирской медицины
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Online Access:https://bulletin.ssmu.ru/jour/article/view/2570
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author E. E. Vayman
N. A. Shnayder
N. G. Neznanov
R. F. Nasyrova
author_facet E. E. Vayman
N. A. Shnayder
N. G. Neznanov
R. F. Nasyrova
author_sort E. E. Vayman
collection DOAJ
description Purpose. To analyze the results of classical and modern studies reflecting the pathophysiological mechanisms of antipsychotic-induced tardive dyskinesia.Materials and methods. We searched for full-text publications in Russian and English in the databases of E-Library, PubMed, Web of Science and Springer published over the past decade, using keywords (tardive dyskinesia (TD), drug-induced tardive dyskinesia, antipsychotics (AP), neuroleptics, typical antipsychotics, atypical antipsychotics, pathophysiology, etiology and combinations of these words). In addition, the review included earlier publications of historical interest.Results. The lecture proposed theories of development of AP-induced TD, examining its effect on dopaminergic receptors, dopaminergic neurons, neurons of the basal ganglia, and other theories: activation of estrogen receptors, disorders of melatonin metabolism, disorders of the endogenous opioid system, oxidative stress with predominant oxidation processes, blockade of 5-HT2-receptors, a decrease in the pyridoxine level, genetic predisposition, interaction of AP with the brain trace element – iron, carbonyl stress and immune inflammation and the role of the neurotrophic factor.Conclusion. The disclosure of the mechanisms of AP-induced TD will allow the development of a strategy for personalized prevention and therapy of the considered neurological complication of the AP-therapy for schizophrenia in real clinical practice.
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spelling doaj-art-0b4fe7f7d22741a9823c11c37c9d76112025-08-04T16:45:42ZengSiberian State Medical University (Tomsk)Бюллетень сибирской медицины1682-03631819-36842020-01-0118416918410.20538/1682-0363-2019-4-169-1841578Pathophysiological mechanisms underlying antipsychotic-induced tardive dyskinesiaE. E. Vayman0N. A. Shnayder1N. G. Neznanov2R. F. Nasyrova3Bekhterev National Medical Research Center (NMRC) of Psychiatry and NeurologyBekhterev National Medical Research Center (NMRC) of Psychiatry and NeurologyBekhterev National Medical Research Center (NMRC) of Psychiatry and NeurologyBekhterev National Medical Research Center (NMRC) of Psychiatry and NeurologyPurpose. To analyze the results of classical and modern studies reflecting the pathophysiological mechanisms of antipsychotic-induced tardive dyskinesia.Materials and methods. We searched for full-text publications in Russian and English in the databases of E-Library, PubMed, Web of Science and Springer published over the past decade, using keywords (tardive dyskinesia (TD), drug-induced tardive dyskinesia, antipsychotics (AP), neuroleptics, typical antipsychotics, atypical antipsychotics, pathophysiology, etiology and combinations of these words). In addition, the review included earlier publications of historical interest.Results. The lecture proposed theories of development of AP-induced TD, examining its effect on dopaminergic receptors, dopaminergic neurons, neurons of the basal ganglia, and other theories: activation of estrogen receptors, disorders of melatonin metabolism, disorders of the endogenous opioid system, oxidative stress with predominant oxidation processes, blockade of 5-HT2-receptors, a decrease in the pyridoxine level, genetic predisposition, interaction of AP with the brain trace element – iron, carbonyl stress and immune inflammation and the role of the neurotrophic factor.Conclusion. The disclosure of the mechanisms of AP-induced TD will allow the development of a strategy for personalized prevention and therapy of the considered neurological complication of the AP-therapy for schizophrenia in real clinical practice.https://bulletin.ssmu.ru/jour/article/view/2570tardive dyskinesiadrug-induced tardive dyskinesiatheoriesantipsychoticspathophysiologypathogenesis
spellingShingle E. E. Vayman
N. A. Shnayder
N. G. Neznanov
R. F. Nasyrova
Pathophysiological mechanisms underlying antipsychotic-induced tardive dyskinesia
Бюллетень сибирской медицины
tardive dyskinesia
drug-induced tardive dyskinesia
theories
antipsychotics
pathophysiology
pathogenesis
title Pathophysiological mechanisms underlying antipsychotic-induced tardive dyskinesia
title_full Pathophysiological mechanisms underlying antipsychotic-induced tardive dyskinesia
title_fullStr Pathophysiological mechanisms underlying antipsychotic-induced tardive dyskinesia
title_full_unstemmed Pathophysiological mechanisms underlying antipsychotic-induced tardive dyskinesia
title_short Pathophysiological mechanisms underlying antipsychotic-induced tardive dyskinesia
title_sort pathophysiological mechanisms underlying antipsychotic induced tardive dyskinesia
topic tardive dyskinesia
drug-induced tardive dyskinesia
theories
antipsychotics
pathophysiology
pathogenesis
url https://bulletin.ssmu.ru/jour/article/view/2570
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AT nashnayder pathophysiologicalmechanismsunderlyingantipsychoticinducedtardivedyskinesia
AT ngneznanov pathophysiologicalmechanismsunderlyingantipsychoticinducedtardivedyskinesia
AT rfnasyrova pathophysiologicalmechanismsunderlyingantipsychoticinducedtardivedyskinesia