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Treatment-resistant schizophrenia characterised by dopamine supersensitivity psychosis and efficacy of asenapine
Dopamine supersensitivity psychosis (DSP) frequently arises with long-term antipsychotic treatment and accounts for a significant proportion of treatment-resistant schizophrenia. The mechanism underlying DSP is thought to be a compensatory increase in dopamine receptor density in the striatum caused...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BMJ Publishing Group
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8051386/ https://www.ncbi.nlm.nih.gov/pubmed/33849886 http://dx.doi.org/10.1136/bcr-2021-242495 |
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author | Takao, Nagara Murai, Toshiya Fujiwara, Hironobu |
author_facet | Takao, Nagara Murai, Toshiya Fujiwara, Hironobu |
author_sort | Takao, Nagara |
collection | PubMed |
description | Dopamine supersensitivity psychosis (DSP) frequently arises with long-term antipsychotic treatment and accounts for a significant proportion of treatment-resistant schizophrenia. The mechanism underlying DSP is thought to be a compensatory increase in dopamine receptor density in the striatum caused by long-term antipsychotic treatment. Previous animal studies have reported that antipsychotics increase serotonin 5-HT2A receptor density in the striatum and that 5-HT2A receptor blockers suppress dopamine-sensitive psychomotor activity, which may be linked to the pathophysiology of DSP. In this paper, we describe a patient who was hospitalised with treatment-resistant schizophrenia. Following treatment with high-dose antipsychotic polypharmacy for 10 weeks, the patient experienced worsening of psychotic and extrapyramidal symptoms. The patient was then started on second-generation antipsychotic asenapine while other antipsychotics were tapered off, resulting in improvement of these symptoms. Retrospectively, we presumed that the high-dose antipsychotic polypharmacy caused DSP, which was effectively treated by the potent 5-HT2A receptor antagonism of asenapine. |
format | Online Article Text |
id | pubmed-8051386 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | BMJ Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-80513862021-04-26 Treatment-resistant schizophrenia characterised by dopamine supersensitivity psychosis and efficacy of asenapine Takao, Nagara Murai, Toshiya Fujiwara, Hironobu BMJ Case Rep Case Report Dopamine supersensitivity psychosis (DSP) frequently arises with long-term antipsychotic treatment and accounts for a significant proportion of treatment-resistant schizophrenia. The mechanism underlying DSP is thought to be a compensatory increase in dopamine receptor density in the striatum caused by long-term antipsychotic treatment. Previous animal studies have reported that antipsychotics increase serotonin 5-HT2A receptor density in the striatum and that 5-HT2A receptor blockers suppress dopamine-sensitive psychomotor activity, which may be linked to the pathophysiology of DSP. In this paper, we describe a patient who was hospitalised with treatment-resistant schizophrenia. Following treatment with high-dose antipsychotic polypharmacy for 10 weeks, the patient experienced worsening of psychotic and extrapyramidal symptoms. The patient was then started on second-generation antipsychotic asenapine while other antipsychotics were tapered off, resulting in improvement of these symptoms. Retrospectively, we presumed that the high-dose antipsychotic polypharmacy caused DSP, which was effectively treated by the potent 5-HT2A receptor antagonism of asenapine. BMJ Publishing Group 2021-04-13 /pmc/articles/PMC8051386/ /pubmed/33849886 http://dx.doi.org/10.1136/bcr-2021-242495 Text en © BMJ Publishing Group Limited 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. https://creativecommons.org/licenses/by-nc/4.0/This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) . |
spellingShingle | Case Report Takao, Nagara Murai, Toshiya Fujiwara, Hironobu Treatment-resistant schizophrenia characterised by dopamine supersensitivity psychosis and efficacy of asenapine |
title | Treatment-resistant schizophrenia characterised by dopamine supersensitivity psychosis and efficacy of asenapine |
title_full | Treatment-resistant schizophrenia characterised by dopamine supersensitivity psychosis and efficacy of asenapine |
title_fullStr | Treatment-resistant schizophrenia characterised by dopamine supersensitivity psychosis and efficacy of asenapine |
title_full_unstemmed | Treatment-resistant schizophrenia characterised by dopamine supersensitivity psychosis and efficacy of asenapine |
title_short | Treatment-resistant schizophrenia characterised by dopamine supersensitivity psychosis and efficacy of asenapine |
title_sort | treatment-resistant schizophrenia characterised by dopamine supersensitivity psychosis and efficacy of asenapine |
topic | Case Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8051386/ https://www.ncbi.nlm.nih.gov/pubmed/33849886 http://dx.doi.org/10.1136/bcr-2021-242495 |
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