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Neural correlates of impaired vocal feedback control in post-stroke aphasia

We used left-hemisphere stroke as a model to examine how damage to sensorimotor brain networks impairs vocal auditory feedback processing and control. Individuals with post-stroke aphasia and matched neurotypical control subjects vocalized speech vowel sounds and listened to the playback of their se...

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Autores principales: Behroozmand, Roozbeh, Bonilha, Leonardo, Rorden, Chris, Hickok, Gregory, Fridriksson, Julius
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8920755/
https://www.ncbi.nlm.nih.gov/pubmed/35092839
http://dx.doi.org/10.1016/j.neuroimage.2022.118938
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author Behroozmand, Roozbeh
Bonilha, Leonardo
Rorden, Chris
Hickok, Gregory
Fridriksson, Julius
author_facet Behroozmand, Roozbeh
Bonilha, Leonardo
Rorden, Chris
Hickok, Gregory
Fridriksson, Julius
author_sort Behroozmand, Roozbeh
collection PubMed
description We used left-hemisphere stroke as a model to examine how damage to sensorimotor brain networks impairs vocal auditory feedback processing and control. Individuals with post-stroke aphasia and matched neurotypical control subjects vocalized speech vowel sounds and listened to the playback of their self-produced vocalizations under normal (NAF) and pitch-shifted altered auditory feedback (AAF) while their brain activity was recorded using electroencephalography (EEG) signals. Event-related potentials (ERPs) were utilized as a neural index to probe the effect of vocal production on auditory feedback processing with high temporal resolution, while lesion data in the stroke group was used to determine how brain abnormality accounted for the impairment of such mechanisms. Results revealed that ERP activity was aberrantly modulated during vocalization vs. listening in aphasia, and this effect was accompanied by the reduced magnitude of compensatory vocal responses to pitch-shift alterations in the auditory feedback compared with control subjects. Lesion-mapping revealed that the aberrant pattern of ERP modulation in response to NAF was accounted for by damage to sensorimotor networks within the left-hemisphere inferior frontal, precentral, inferior parietal, and superior temporal cortices. For responses to AAF, neural deficits were predicted by damage to a distinguishable network within the inferior frontal and parietal cortices. These findings define the left-hemisphere sensorimotor networks implicated in auditory feedback processing, error detection, and vocal motor control. Our results provide translational synergy to inform the theoretical models of sensorimotor integration while having clinical applications for diagnosis and treatment of communication disabilities in individuals with stroke and other neurological conditions.
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spelling pubmed-89207552022-04-15 Neural correlates of impaired vocal feedback control in post-stroke aphasia Behroozmand, Roozbeh Bonilha, Leonardo Rorden, Chris Hickok, Gregory Fridriksson, Julius Neuroimage Article We used left-hemisphere stroke as a model to examine how damage to sensorimotor brain networks impairs vocal auditory feedback processing and control. Individuals with post-stroke aphasia and matched neurotypical control subjects vocalized speech vowel sounds and listened to the playback of their self-produced vocalizations under normal (NAF) and pitch-shifted altered auditory feedback (AAF) while their brain activity was recorded using electroencephalography (EEG) signals. Event-related potentials (ERPs) were utilized as a neural index to probe the effect of vocal production on auditory feedback processing with high temporal resolution, while lesion data in the stroke group was used to determine how brain abnormality accounted for the impairment of such mechanisms. Results revealed that ERP activity was aberrantly modulated during vocalization vs. listening in aphasia, and this effect was accompanied by the reduced magnitude of compensatory vocal responses to pitch-shift alterations in the auditory feedback compared with control subjects. Lesion-mapping revealed that the aberrant pattern of ERP modulation in response to NAF was accounted for by damage to sensorimotor networks within the left-hemisphere inferior frontal, precentral, inferior parietal, and superior temporal cortices. For responses to AAF, neural deficits were predicted by damage to a distinguishable network within the inferior frontal and parietal cortices. These findings define the left-hemisphere sensorimotor networks implicated in auditory feedback processing, error detection, and vocal motor control. Our results provide translational synergy to inform the theoretical models of sensorimotor integration while having clinical applications for diagnosis and treatment of communication disabilities in individuals with stroke and other neurological conditions. 2022-04-15 2022-01-29 /pmc/articles/PMC8920755/ /pubmed/35092839 http://dx.doi.org/10.1016/j.neuroimage.2022.118938 Text en https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) )
spellingShingle Article
Behroozmand, Roozbeh
Bonilha, Leonardo
Rorden, Chris
Hickok, Gregory
Fridriksson, Julius
Neural correlates of impaired vocal feedback control in post-stroke aphasia
title Neural correlates of impaired vocal feedback control in post-stroke aphasia
title_full Neural correlates of impaired vocal feedback control in post-stroke aphasia
title_fullStr Neural correlates of impaired vocal feedback control in post-stroke aphasia
title_full_unstemmed Neural correlates of impaired vocal feedback control in post-stroke aphasia
title_short Neural correlates of impaired vocal feedback control in post-stroke aphasia
title_sort neural correlates of impaired vocal feedback control in post-stroke aphasia
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8920755/
https://www.ncbi.nlm.nih.gov/pubmed/35092839
http://dx.doi.org/10.1016/j.neuroimage.2022.118938
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