Open AccessPathophysiological mechanisms underlying antipsychotic-induced tardive dyskinesia
Author(s) -
Е. Э. Вайман,
Н. А. Шнайдер,
N. Neznanov,
Р. Ф. Насырова
Publication year - 2020
Publication title -
bûlletenʹ sibirskoj mediciny
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.135
H-Index - 3
eISSN - 1819-3684
pISSN - 1682-0363
DOI - 10.20538/1682-0363-2019-4-169-184
Subject(s) - tardive dyskinesia , antipsychotic , dyskinesia , medicine , neuroscience , dopaminergic , schizophrenia (object oriented programming) , psychology , neurochemical , bioinformatics , dopamine , psychiatry , parkinson's disease , disease , biology
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.