Bilateral vestibulopathy causes selective deficits in recombining novel routes in real space

Abstract The differential impact of complete and incomplete bilateral vestibulopathy (BVP) on spatial orientation, visual exploration, and navigation-induced brain network activations is still under debate. In this study, 14 BVP patients (6 complete, 8 incomplete) and 14 age-matched healthy controls...

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Autores principales: Florian Schöberl, Cauchy Pradhan, Maximilian Grosch, Matthias Brendel, Florian Jostes, Katrin Obermaier, Chantal Sowa, Klaus Jahn, Peter Bartenstein, Thomas Brandt, Marianne Dieterich, Andreas Zwergal
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Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/034260c7c82a45ff88090b0eb36c22fb
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spelling oai:doaj.org-article:034260c7c82a45ff88090b0eb36c22fb2021-12-02T13:57:26ZBilateral vestibulopathy causes selective deficits in recombining novel routes in real space10.1038/s41598-021-82427-62045-2322https://doaj.org/article/034260c7c82a45ff88090b0eb36c22fb2021-01-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-82427-6https://doaj.org/toc/2045-2322Abstract The differential impact of complete and incomplete bilateral vestibulopathy (BVP) on spatial orientation, visual exploration, and navigation-induced brain network activations is still under debate. In this study, 14 BVP patients (6 complete, 8 incomplete) and 14 age-matched healthy controls performed a navigation task requiring them to retrace familiar routes and recombine novel routes to find five items in real space. [18F]-fluorodeoxyglucose-PET was used to determine navigation-induced brain activations. Participants wore a gaze-controlled, head-fixed camera that recorded their visual exploration behaviour. Patients performed worse, when recombining novel routes (p < 0.001), whereas retracing of familiar routes was normal (p = 0.82). These deficits correlated with the severity of BVP. Patients exhibited higher gait fluctuations, spent less time at crossroads, and used a possible shortcut less often (p < 0.05). The right hippocampus and entorhinal cortex were less active and the bilateral parahippocampal place area more active during navigation in patients. Complete BVP showed reduced activations in the pontine brainstem, anterior thalamus, posterior insular, and retrosplenial cortex compared to incomplete BVP. The navigation-induced brain activation pattern in BVP is compatible with deficits in creating a mental representation of a novel environment. Residual vestibular function allows recruitment of brain areas involved in head direction signalling to support navigation.Florian SchöberlCauchy PradhanMaximilian GroschMatthias BrendelFlorian JostesKatrin ObermaierChantal SowaKlaus JahnPeter BartensteinThomas BrandtMarianne DieterichAndreas ZwergalNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-16 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Florian Schöberl
Cauchy Pradhan
Maximilian Grosch
Matthias Brendel
Florian Jostes
Katrin Obermaier
Chantal Sowa
Klaus Jahn
Peter Bartenstein
Thomas Brandt
Marianne Dieterich
Andreas Zwergal
Bilateral vestibulopathy causes selective deficits in recombining novel routes in real space
description Abstract The differential impact of complete and incomplete bilateral vestibulopathy (BVP) on spatial orientation, visual exploration, and navigation-induced brain network activations is still under debate. In this study, 14 BVP patients (6 complete, 8 incomplete) and 14 age-matched healthy controls performed a navigation task requiring them to retrace familiar routes and recombine novel routes to find five items in real space. [18F]-fluorodeoxyglucose-PET was used to determine navigation-induced brain activations. Participants wore a gaze-controlled, head-fixed camera that recorded their visual exploration behaviour. Patients performed worse, when recombining novel routes (p < 0.001), whereas retracing of familiar routes was normal (p = 0.82). These deficits correlated with the severity of BVP. Patients exhibited higher gait fluctuations, spent less time at crossroads, and used a possible shortcut less often (p < 0.05). The right hippocampus and entorhinal cortex were less active and the bilateral parahippocampal place area more active during navigation in patients. Complete BVP showed reduced activations in the pontine brainstem, anterior thalamus, posterior insular, and retrosplenial cortex compared to incomplete BVP. The navigation-induced brain activation pattern in BVP is compatible with deficits in creating a mental representation of a novel environment. Residual vestibular function allows recruitment of brain areas involved in head direction signalling to support navigation.
format article
author Florian Schöberl
Cauchy Pradhan
Maximilian Grosch
Matthias Brendel
Florian Jostes
Katrin Obermaier
Chantal Sowa
Klaus Jahn
Peter Bartenstein
Thomas Brandt
Marianne Dieterich
Andreas Zwergal
author_facet Florian Schöberl
Cauchy Pradhan
Maximilian Grosch
Matthias Brendel
Florian Jostes
Katrin Obermaier
Chantal Sowa
Klaus Jahn
Peter Bartenstein
Thomas Brandt
Marianne Dieterich
Andreas Zwergal
author_sort Florian Schöberl
title Bilateral vestibulopathy causes selective deficits in recombining novel routes in real space
title_short Bilateral vestibulopathy causes selective deficits in recombining novel routes in real space
title_full Bilateral vestibulopathy causes selective deficits in recombining novel routes in real space
title_fullStr Bilateral vestibulopathy causes selective deficits in recombining novel routes in real space
title_full_unstemmed Bilateral vestibulopathy causes selective deficits in recombining novel routes in real space
title_sort bilateral vestibulopathy causes selective deficits in recombining novel routes in real space
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/034260c7c82a45ff88090b0eb36c22fb
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