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Right inferior frontal gyrus damage is associated with impaired initiation of inhibitory control, but not its implementation
Inhibitory control is one of the most important control functions in the human brain. Much of our understanding of its neural basis comes from seminal work showing that lesions to the right inferior frontal gyrus (rIFG) increase stop-signal reaction time (SSRT), a latent variable that expresses the...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
eLife Sciences Publications, Ltd
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9803357/ https://www.ncbi.nlm.nih.gov/pubmed/36583378 http://dx.doi.org/10.7554/eLife.79667 |
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author | Choo, Yoojeong Matzke, Dora Bowren, Mark D Tranel, Daniel Wessel, Jan R |
author_facet | Choo, Yoojeong Matzke, Dora Bowren, Mark D Tranel, Daniel Wessel, Jan R |
author_sort | Choo, Yoojeong |
collection | PubMed |
description | Inhibitory control is one of the most important control functions in the human brain. Much of our understanding of its neural basis comes from seminal work showing that lesions to the right inferior frontal gyrus (rIFG) increase stop-signal reaction time (SSRT), a latent variable that expresses the speed of inhibitory control. However, recent work has identified substantial limitations of the SSRT method. Notably, SSRT is confounded by trigger failures: stop-signal trials in which inhibitory control was never initiated. Such trials inflate SSRT, but are typically indicative of attentional, rather than inhibitory deficits. Here, we used hierarchical Bayesian modeling to identify stop-signal trigger failures in human rIFG lesion patients, non-rIFG lesion patients, and healthy comparisons. Furthermore, we measured scalp-EEG to detect β-bursts, a neurophysiological index of inhibitory control. rIFG lesion patients showed a more than fivefold increase in trigger failure trials and did not exhibit the typical increase of stop-related frontal β-bursts. However, on trials in which such β-bursts did occur, rIFG patients showed the typical subsequent upregulation of β over sensorimotor areas, indicating that their ability to implement inhibitory control, once triggered, remains intact. These findings suggest that the role of rIFG in inhibitory control has to be fundamentally reinterpreted. |
format | Online Article Text |
id | pubmed-9803357 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | eLife Sciences Publications, Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-98033572022-12-31 Right inferior frontal gyrus damage is associated with impaired initiation of inhibitory control, but not its implementation Choo, Yoojeong Matzke, Dora Bowren, Mark D Tranel, Daniel Wessel, Jan R eLife Neuroscience Inhibitory control is one of the most important control functions in the human brain. Much of our understanding of its neural basis comes from seminal work showing that lesions to the right inferior frontal gyrus (rIFG) increase stop-signal reaction time (SSRT), a latent variable that expresses the speed of inhibitory control. However, recent work has identified substantial limitations of the SSRT method. Notably, SSRT is confounded by trigger failures: stop-signal trials in which inhibitory control was never initiated. Such trials inflate SSRT, but are typically indicative of attentional, rather than inhibitory deficits. Here, we used hierarchical Bayesian modeling to identify stop-signal trigger failures in human rIFG lesion patients, non-rIFG lesion patients, and healthy comparisons. Furthermore, we measured scalp-EEG to detect β-bursts, a neurophysiological index of inhibitory control. rIFG lesion patients showed a more than fivefold increase in trigger failure trials and did not exhibit the typical increase of stop-related frontal β-bursts. However, on trials in which such β-bursts did occur, rIFG patients showed the typical subsequent upregulation of β over sensorimotor areas, indicating that their ability to implement inhibitory control, once triggered, remains intact. These findings suggest that the role of rIFG in inhibitory control has to be fundamentally reinterpreted. eLife Sciences Publications, Ltd 2022-12-30 /pmc/articles/PMC9803357/ /pubmed/36583378 http://dx.doi.org/10.7554/eLife.79667 Text en © 2022, Choo et al https://creativecommons.org/licenses/by/4.0/This article is distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use and redistribution provided that the original author and source are credited. |
spellingShingle | Neuroscience Choo, Yoojeong Matzke, Dora Bowren, Mark D Tranel, Daniel Wessel, Jan R Right inferior frontal gyrus damage is associated with impaired initiation of inhibitory control, but not its implementation |
title | Right inferior frontal gyrus damage is associated with impaired initiation of inhibitory control, but not its implementation |
title_full | Right inferior frontal gyrus damage is associated with impaired initiation of inhibitory control, but not its implementation |
title_fullStr | Right inferior frontal gyrus damage is associated with impaired initiation of inhibitory control, but not its implementation |
title_full_unstemmed | Right inferior frontal gyrus damage is associated with impaired initiation of inhibitory control, but not its implementation |
title_short | Right inferior frontal gyrus damage is associated with impaired initiation of inhibitory control, but not its implementation |
title_sort | right inferior frontal gyrus damage is associated with impaired initiation of inhibitory control, but not its implementation |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9803357/ https://www.ncbi.nlm.nih.gov/pubmed/36583378 http://dx.doi.org/10.7554/eLife.79667 |
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