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Motor learning deficits in cervical dystonia point to defective basal ganglia circuitry
Dystonia is conceptualized as a network disorder involving basal ganglia, thalamus, sensorimotor cortex and the cerebellum. The cerebellum has been implicated in dystonia pathophysiology, but studies testing cerebellar function in dystonia patients have provided equivocal results. This study aimed t...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8016965/ https://www.ncbi.nlm.nih.gov/pubmed/33795752 http://dx.doi.org/10.1038/s41598-021-86513-7 |
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author | Loens, Sebastian Verrel, Julius Herrmann, Vera-Maria Kienzle, Amrei Tzvi, Elinor Weissbach, Anne Junker, Johanna Münchau, Alexander Bäumer, Tobias |
author_facet | Loens, Sebastian Verrel, Julius Herrmann, Vera-Maria Kienzle, Amrei Tzvi, Elinor Weissbach, Anne Junker, Johanna Münchau, Alexander Bäumer, Tobias |
author_sort | Loens, Sebastian |
collection | PubMed |
description | Dystonia is conceptualized as a network disorder involving basal ganglia, thalamus, sensorimotor cortex and the cerebellum. The cerebellum has been implicated in dystonia pathophysiology, but studies testing cerebellar function in dystonia patients have provided equivocal results. This study aimed to further elucidate motor network deficits in cervical dystonia with special interest in the role of the cerebellum. To this end we investigated motor learning tasks, that differ in their dependence on cerebellar and basal ganglia functioning. In 18 cervical dystonia patients and 18 age matched healthy controls we measured implicit motor sequence learning using a 12-item serial reaction time task mostly targeting basal ganglia circuitry and motor adaptation and eyeblink conditioning as markers of cerebellar functioning. ANOVA showed that motor sequence learning was overall impaired in cervical dystonia (p = 0.01). Moreover, unlike healthy controls, patients did not show a learning effect in the first part of the experiment. Visuomotor adaptation and eyeblink conditioning were normal. In conclusion, these data lend support to the notion that motor learning deficits in cervical dystonia relate to basal ganglia-thalamo-cortical loops rather than being a result of defective cerebellar circuitry. |
format | Online Article Text |
id | pubmed-8016965 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-80169652021-04-07 Motor learning deficits in cervical dystonia point to defective basal ganglia circuitry Loens, Sebastian Verrel, Julius Herrmann, Vera-Maria Kienzle, Amrei Tzvi, Elinor Weissbach, Anne Junker, Johanna Münchau, Alexander Bäumer, Tobias Sci Rep Article Dystonia is conceptualized as a network disorder involving basal ganglia, thalamus, sensorimotor cortex and the cerebellum. The cerebellum has been implicated in dystonia pathophysiology, but studies testing cerebellar function in dystonia patients have provided equivocal results. This study aimed to further elucidate motor network deficits in cervical dystonia with special interest in the role of the cerebellum. To this end we investigated motor learning tasks, that differ in their dependence on cerebellar and basal ganglia functioning. In 18 cervical dystonia patients and 18 age matched healthy controls we measured implicit motor sequence learning using a 12-item serial reaction time task mostly targeting basal ganglia circuitry and motor adaptation and eyeblink conditioning as markers of cerebellar functioning. ANOVA showed that motor sequence learning was overall impaired in cervical dystonia (p = 0.01). Moreover, unlike healthy controls, patients did not show a learning effect in the first part of the experiment. Visuomotor adaptation and eyeblink conditioning were normal. In conclusion, these data lend support to the notion that motor learning deficits in cervical dystonia relate to basal ganglia-thalamo-cortical loops rather than being a result of defective cerebellar circuitry. Nature Publishing Group UK 2021-04-01 /pmc/articles/PMC8016965/ /pubmed/33795752 http://dx.doi.org/10.1038/s41598-021-86513-7 Text en © The Author(s) 2021 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Loens, Sebastian Verrel, Julius Herrmann, Vera-Maria Kienzle, Amrei Tzvi, Elinor Weissbach, Anne Junker, Johanna Münchau, Alexander Bäumer, Tobias Motor learning deficits in cervical dystonia point to defective basal ganglia circuitry |
title | Motor learning deficits in cervical dystonia point to defective basal ganglia circuitry |
title_full | Motor learning deficits in cervical dystonia point to defective basal ganglia circuitry |
title_fullStr | Motor learning deficits in cervical dystonia point to defective basal ganglia circuitry |
title_full_unstemmed | Motor learning deficits in cervical dystonia point to defective basal ganglia circuitry |
title_short | Motor learning deficits in cervical dystonia point to defective basal ganglia circuitry |
title_sort | motor learning deficits in cervical dystonia point to defective basal ganglia circuitry |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8016965/ https://www.ncbi.nlm.nih.gov/pubmed/33795752 http://dx.doi.org/10.1038/s41598-021-86513-7 |
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