Role of ethnicity in the development of tardive dyskinesia

1996 ◽  
pp. 298-310
Author(s):  
Jonathan P. Lacro ◽  
Dilip V. Jeste
Keyword(s):  
Tardive Dyskinesia

scholarly journals Role of the basal ganglia and cerebral cortex in tardive dyskinesia: evidence from cerebrovascular accident.

1987 ◽  
Vol 50 (3) ◽  
pp. 367-368 ◽  
Author(s):  
A S Walters ◽  
M Katchen ◽  
J Fleishman ◽  
S Chokroverty ◽  
R Duvoisin
Keyword(s):  
Cerebral Cortex ◽  
Basal Ganglia ◽  
Tardive Dyskinesia ◽  
Cerebrovascular Accident

scholarly journals Putative role of pharmacogenetics to elucidate the mechanism of tardive dyskinesia in schizophrenia

2019 ◽  
Vol 20 (17) ◽  
pp. 1199-1223 ◽  
Author(s):  
Anton JM Loonen ◽  
Bob Wilffert ◽  
Svetlana A Ivanova
Keyword(s):  
Oxidative Stress ◽  
Tardive Dyskinesia ◽  
Genetic Variants ◽  
Long Term Potentiation ◽  
Specific Gene ◽  
Medium Spiny Neurons ◽  
Spiny Neurons ◽  
Long Term Treatment

Identifying biomarkers which can be used as a diagnostic tool is a major objective of pharmacogenetic studies. Most mental and many neurological disorders have a compiled multifaceted nature, which may be the reason why this endeavor has hitherto not been very successful. This is also true for tardive dyskinesia (TD), an involuntary movement complication of long-term treatment with antipsychotic drugs. The observed associations of specific gene variants with the prevalence and severity of a disorder can also be applied to try to elucidate the pathogenesis of the condition. In this paper, this strategy is used by combining pharmacogenetic knowledge with theories on the possible role of a dysfunction of specific cellular elements of neostriatal parts of the (dorsal) extrapyramidal circuits: various glutamatergic terminals, medium spiny neurons, striatal interneurons and ascending monoaminergic fibers. A peculiar finding is that genetic variants which would be expected to increase the neostriatal dopamine concentration are not associated with the prevalence and severity of TD. Moreover, modifying the sensitivity to glutamatergic long-term potentiation (and excitotoxicity) shows a relationship with levodopa-induced dyskinesia, but not with TD. Contrasting this, TD is associated with genetic variants that modify vulnerability to oxidative stress. Reducing the oxidative stress burden of medium spiny neurons may also be the mechanism behind the protective influence of 5-HT2 receptor antagonists. It is probably worthwhile to discriminate between neostriatal matrix and striosomal compartments when studying the mechanism of TD and between orofacial and limb-truncal components in epidemiological studies.

Late Onset Involuntary Movements in Chronic Schizophrenia: Relationship of ‘Tardive’ Dyskinesia to Intellectual Impairment and Negative Symptoms

1986 ◽  
Vol 149 (5) ◽  
pp. 616-620 ◽  
Author(s):  
J. L. Waddington ◽  
H. A. Youssef
Keyword(s):  
Tardive Dyskinesia ◽  
Negative Symptoms ◽  
Late Onset ◽  
Chronic Schizophrenia ◽  
Intellectual Impairment ◽  
Medication History ◽  
Involuntary Movements ◽  
Schizophrenic Patients ◽  
Relationship Of

Intellectual impairment, negative symptoms, and medication history were assessed in chronic schizophrenic patients with and without abnormal involuntary movements (tardive dyskinesia). Patients with involuntary movements had received neither longer nor more intensive treatment with neuroleptics or anticholinergics. However, the presence or absence of involuntary movements was prominently associated with the presence or absence of intellectual impairment/negative symptoms; these features are characteristic of the defect state/type II syndrome of schizophrenia, in which structural abnormalities of the brain may be over-represented. The role of subtle organic changes in conferring vulnerability to the emergence of such involuntary movements should be re-evaluated.

scholarly journals Pathophysiological mechanisms underlying antipsychotic-induced tardive dyskinesia

2020 ◽  
Vol 18 (4) ◽  
pp. 169-184
Author(s):  
E. E. Vayman ◽  
N. A. Shnayder ◽  
N. G. Neznanov ◽  
R. F. Nasyrova
Keyword(s):  
Tardive Dyskinesia ◽  
Dopaminergic Neurons ◽  
Neurological Complication ◽  
Carbonyl Stress ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Drug Induced ◽  
Pathophysiological Mechanisms ◽  
The Brain

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. 

scholarly journals 195 Current Use and Trends in the Management of Tardive Dyskinesia: Role of VMAT2 Inhibitors

CNS Spectrums ◽  
2018 ◽  
Vol 23 (1) ◽  
pp. 111-111
Author(s):  
Venkatesh Sreeram ◽  
Shanila Shagufta ◽  
Faisal Kagadkar ◽  
Mustafa Qureshi
Keyword(s):  
Tardive Dyskinesia ◽  
Atypical Antipsychotics ◽  
Intervention Studies ◽  
Treatment Modalities ◽  
Safety And Reliability ◽  
Probable Role ◽  
Botulinum Toxin Injections ◽  
Early Detection And Prevention ◽  
Funding Acknowledgements

AbstractObjectivesTardive Dyskinesia (TD) is a debilitating condition that requires prompt care and intervention. Studies demonstrated the probable role of Vesicular Monoamine Transport 2 (VMAT2) in the pathogenesis of TD and use of VMAT2inhibitors in managing TD. Our aim is to provide available data on the management of TD and to determine the efficacy ofvarious VMAT2 inhibitors for independent use. Also, to identify their use in combination and assess if there, any change inoutcome with early intervention.MethodsWe did a pivotal search of the scientific literature by querying PubMed and Google Scholar for studies on treatment modalities of TD including atypical antipsychotics and VMAT2 inhibitors. Also, references from publications were accessed for review.ResultsEarly detection and prevention are of paramount importance in managing TD. Cessate the antipsychotic been using andother dopamine blocking agents that probably implicated in causing the symptoms. Certain studies showed the use of new atypical antipsychotics like Paliperidone, Quetiapine in small titrated dose resolving the symptoms. According to the available data, using benzodiazepines, botulinum toxin injections and VMAT2 inhibitors like Valbenazine, Tetrabenazine, andDeutetrabenazine also managed TD with efficacy. Valbenazine has breakthrough global approval in resolving the symptoms. Although other VMAT2 inhibitors were used for TD earlier and showed to be effective in managing TD, larger trials are required showing their safety and reliability in efficacy.ConclusionsVMAT2 inhibitors were tested as efficacious in managing TD. Valbenazine and recently deutetrabenazine has been approved by US Food and Drug Administration (FDA) to treat TD. However, Tetrabenazine is yet to be approved by FDA. More clinical trials are required exploring their efficacy by comparing them or using them in combination. Our review also suggests timely detection and earlier intervening, especially if witnessed in children and adolescents would differ the outcome of TD.Funding AcknowledgementsNo funding.

Role of androgens in tardive dyskinesia

1991 ◽  
Vol 56 (1-4) ◽  
pp. 215-218
Author(s):  
Reuven Sandyk ◽  
Stanley R. Kay
Keyword(s):  
Tardive Dyskinesia
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