Cargando…
An Oppositional Tolerance Account for Potential Cognitive Deficits Caused by the Discontinuation of Antidepressant Drugs
Depression is the leading cause of disability worldwide, making antidepressant drugs the most used psychiatric drugs in the USA. Withdrawal effects and rebound symptoms frequently occur after the reduction and/or discontinuation of these drugs. Although these phenomena have been investigated with re...
Autores principales: | , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Georg Thieme Verlag KG
2021
|
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8575552/ https://www.ncbi.nlm.nih.gov/pubmed/34293810 http://dx.doi.org/10.1055/a-1520-4784 |
_version_ | 1784595696620404736 |
---|---|
author | Colzato, Lorenza Zhang, Wenxin Walter, Henrik Beste, Christian Stock, Ann-Kathrin |
author_facet | Colzato, Lorenza Zhang, Wenxin Walter, Henrik Beste, Christian Stock, Ann-Kathrin |
author_sort | Colzato, Lorenza |
collection | PubMed |
description | Depression is the leading cause of disability worldwide, making antidepressant drugs the most used psychiatric drugs in the USA. Withdrawal effects and rebound symptoms frequently occur after the reduction and/or discontinuation of these drugs. Although these phenomena have been investigated with respect to the clinical symptomatology, no studies have systematically investigated the effects of withdrawal/rebound on general cognition. We present a novel framework based on the idea of allostatic adaptation, which allows to predict how different antidepressants likely impair different cognitive processes as a result of withdrawal and rebound effects. This framework relies on the assumptions that the type of cognitive impairments evoked by an antidepressant is determined by the targeted neurotransmitter systems, while the severity of deficits depends on its half-life. Our model predicts that the severity of detrimental cognitive withdrawal and rebound effects increases with a shorter half-life of the discontinued antidepressant drug. It further proposes drug-specific effects: antidepressants mainly targeting serotonin should primarily impair aversive and emotional processing, those targeting norepinephrine should impair the processing of alerting signals, those targeting dopamine should impair motivational processes and reward processing, and those targeting acetylcholine should impair spatial learning and memory. We hope that this framework will motivate further research to better understand and explain cognitive changes as a consequence of antidepressant discontinuation. |
format | Online Article Text |
id | pubmed-8575552 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Georg Thieme Verlag KG |
record_format | MEDLINE/PubMed |
spelling | pubmed-85755522021-11-10 An Oppositional Tolerance Account for Potential Cognitive Deficits Caused by the Discontinuation of Antidepressant Drugs Colzato, Lorenza Zhang, Wenxin Walter, Henrik Beste, Christian Stock, Ann-Kathrin Pharmacopsychiatry Depression is the leading cause of disability worldwide, making antidepressant drugs the most used psychiatric drugs in the USA. Withdrawal effects and rebound symptoms frequently occur after the reduction and/or discontinuation of these drugs. Although these phenomena have been investigated with respect to the clinical symptomatology, no studies have systematically investigated the effects of withdrawal/rebound on general cognition. We present a novel framework based on the idea of allostatic adaptation, which allows to predict how different antidepressants likely impair different cognitive processes as a result of withdrawal and rebound effects. This framework relies on the assumptions that the type of cognitive impairments evoked by an antidepressant is determined by the targeted neurotransmitter systems, while the severity of deficits depends on its half-life. Our model predicts that the severity of detrimental cognitive withdrawal and rebound effects increases with a shorter half-life of the discontinued antidepressant drug. It further proposes drug-specific effects: antidepressants mainly targeting serotonin should primarily impair aversive and emotional processing, those targeting norepinephrine should impair the processing of alerting signals, those targeting dopamine should impair motivational processes and reward processing, and those targeting acetylcholine should impair spatial learning and memory. We hope that this framework will motivate further research to better understand and explain cognitive changes as a consequence of antidepressant discontinuation. Georg Thieme Verlag KG 2021-07-22 /pmc/articles/PMC8575552/ /pubmed/34293810 http://dx.doi.org/10.1055/a-1520-4784 Text en The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial-License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/). https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License, which permits unrestricted reproduction and distribution, for non-commercial purposes only; and use and reproduction, but not distribution, of adapted material for non-commercial purposes only, provided the original work is properly cited. |
spellingShingle | Colzato, Lorenza Zhang, Wenxin Walter, Henrik Beste, Christian Stock, Ann-Kathrin An Oppositional Tolerance Account for Potential Cognitive Deficits Caused by the Discontinuation of Antidepressant Drugs |
title | An Oppositional Tolerance Account for Potential Cognitive Deficits Caused by the Discontinuation of Antidepressant Drugs |
title_full | An Oppositional Tolerance Account for Potential Cognitive Deficits Caused by the Discontinuation of Antidepressant Drugs |
title_fullStr | An Oppositional Tolerance Account for Potential Cognitive Deficits Caused by the Discontinuation of Antidepressant Drugs |
title_full_unstemmed | An Oppositional Tolerance Account for Potential Cognitive Deficits Caused by the Discontinuation of Antidepressant Drugs |
title_short | An Oppositional Tolerance Account for Potential Cognitive Deficits Caused by the Discontinuation of Antidepressant Drugs |
title_sort | oppositional tolerance account for potential cognitive deficits caused by the discontinuation of antidepressant drugs |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8575552/ https://www.ncbi.nlm.nih.gov/pubmed/34293810 http://dx.doi.org/10.1055/a-1520-4784 |
work_keys_str_mv | AT colzatolorenza anoppositionaltoleranceaccountforpotentialcognitivedeficitscausedbythediscontinuationofantidepressantdrugs AT zhangwenxin anoppositionaltoleranceaccountforpotentialcognitivedeficitscausedbythediscontinuationofantidepressantdrugs AT walterhenrik anoppositionaltoleranceaccountforpotentialcognitivedeficitscausedbythediscontinuationofantidepressantdrugs AT bestechristian anoppositionaltoleranceaccountforpotentialcognitivedeficitscausedbythediscontinuationofantidepressantdrugs AT stockannkathrin anoppositionaltoleranceaccountforpotentialcognitivedeficitscausedbythediscontinuationofantidepressantdrugs AT colzatolorenza oppositionaltoleranceaccountforpotentialcognitivedeficitscausedbythediscontinuationofantidepressantdrugs AT zhangwenxin oppositionaltoleranceaccountforpotentialcognitivedeficitscausedbythediscontinuationofantidepressantdrugs AT walterhenrik oppositionaltoleranceaccountforpotentialcognitivedeficitscausedbythediscontinuationofantidepressantdrugs AT bestechristian oppositionaltoleranceaccountforpotentialcognitivedeficitscausedbythediscontinuationofantidepressantdrugs AT stockannkathrin oppositionaltoleranceaccountforpotentialcognitivedeficitscausedbythediscontinuationofantidepressantdrugs |