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Treatment of neurolept-induced tardive dyskinesia

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 pathophysiolog...

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Autor principal: Jankelowitz, Stacey K
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3783506/
https://www.ncbi.nlm.nih.gov/pubmed/24072972
http://dx.doi.org/10.2147/NDT.S30767
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author Jankelowitz, Stacey K
author_facet Jankelowitz, Stacey K
author_sort Jankelowitz, Stacey K
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description 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.
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spelling pubmed-37835062013-09-26 Treatment of neurolept-induced tardive dyskinesia Jankelowitz, Stacey K Neuropsychiatr Dis Treat Review 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. Dove Medical Press 2013 2013-09-16 /pmc/articles/PMC3783506/ /pubmed/24072972 http://dx.doi.org/10.2147/NDT.S30767 Text en © 2013 Jankelowitz. This work is published by Dove Medical Press Ltd, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Ltd, provided the work is properly attributed.
spellingShingle Review
Jankelowitz, Stacey K
Treatment of neurolept-induced tardive dyskinesia
title Treatment of neurolept-induced tardive dyskinesia
title_full Treatment of neurolept-induced tardive dyskinesia
title_fullStr Treatment of neurolept-induced tardive dyskinesia
title_full_unstemmed Treatment of neurolept-induced tardive dyskinesia
title_short Treatment of neurolept-induced tardive dyskinesia
title_sort treatment of neurolept-induced tardive dyskinesia
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3783506/
https://www.ncbi.nlm.nih.gov/pubmed/24072972
http://dx.doi.org/10.2147/NDT.S30767
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