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Functional Plasticity after Unilateral Vestibular Midbrain Infarction in Human Positron Emission Tomography

The aim of the study was to uncover mechanisms of central compensation of vestibular function at brainstem, cerebellar, and cortical levels in patients with acute unilateral midbrain infarctions presenting with an acute vestibular tone imbalance. Eight out of 17 patients with unilateral midbrain inf...

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Autores principales: Becker-Bense, Sandra, Buchholz, Hans-Georg, Baier, Bernhard, Schreckenberger, Mathias, Bartenstein, Peter, Zwergal, Andreas, Brandt, Thomas, Dieterich, Marianne
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5100888/
https://www.ncbi.nlm.nih.gov/pubmed/27824897
http://dx.doi.org/10.1371/journal.pone.0165935
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author Becker-Bense, Sandra
Buchholz, Hans-Georg
Baier, Bernhard
Schreckenberger, Mathias
Bartenstein, Peter
Zwergal, Andreas
Brandt, Thomas
Dieterich, Marianne
author_facet Becker-Bense, Sandra
Buchholz, Hans-Georg
Baier, Bernhard
Schreckenberger, Mathias
Bartenstein, Peter
Zwergal, Andreas
Brandt, Thomas
Dieterich, Marianne
author_sort Becker-Bense, Sandra
collection PubMed
description The aim of the study was to uncover mechanisms of central compensation of vestibular function at brainstem, cerebellar, and cortical levels in patients with acute unilateral midbrain infarctions presenting with an acute vestibular tone imbalance. Eight out of 17 patients with unilateral midbrain infarctions were selected on the basis of signs of a vestibular tone imbalance, e.g., graviceptive (tilts of perceived verticality) and oculomotor dysfunction (skew deviation, ocular torsion) in F18-fluordeoxyglucose (FDG)-PET at two time points: A) in the acute stage, and B) after recovery 6 months later. Lesion-behavior mapping analyses with MRI verified the exact structural lesion sites. Group subtraction analyses and comparisons with healthy controls were performed with Statistic Parametric Mapping for the PET data. A comparison of PET A of acute-stage patients with that of healthy controls showed increases in glucose metabolism in the cerebellum, motion-sensitive visual cortex areas, and inferior temporal lobe, but none in vestibular cortex areas. At the supratentorial level bilateral signal decreases dominated in the thalamus, frontal eye fields, and anterior cingulum. These decreases persisted after clinical recovery in contrast to the increases. The transient activations can be attributed to ocular motor and postural recovery (cerebellum) and sensory substitution of vestibular function for motion perception (visual cortex). The persisting deactivation in the thalamic nuclei and frontal eye fields allows alternative functional interpretations of the thalamic nuclei: either a disconnection of ascending sensory input occurs or there is a functional mismatch between expected and actual vestibular activity. Our data support the view that both thalami operate separately for each hemisphere but receive vestibular input from ipsilateral and contralateral midbrain integration centers. Normally they have gatekeeper functions for multisensory input to the cortex and automatic motor output to subserve balance and locomotion, as well as sensorimotor integration.
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spelling pubmed-51008882016-11-18 Functional Plasticity after Unilateral Vestibular Midbrain Infarction in Human Positron Emission Tomography Becker-Bense, Sandra Buchholz, Hans-Georg Baier, Bernhard Schreckenberger, Mathias Bartenstein, Peter Zwergal, Andreas Brandt, Thomas Dieterich, Marianne PLoS One Research Article The aim of the study was to uncover mechanisms of central compensation of vestibular function at brainstem, cerebellar, and cortical levels in patients with acute unilateral midbrain infarctions presenting with an acute vestibular tone imbalance. Eight out of 17 patients with unilateral midbrain infarctions were selected on the basis of signs of a vestibular tone imbalance, e.g., graviceptive (tilts of perceived verticality) and oculomotor dysfunction (skew deviation, ocular torsion) in F18-fluordeoxyglucose (FDG)-PET at two time points: A) in the acute stage, and B) after recovery 6 months later. Lesion-behavior mapping analyses with MRI verified the exact structural lesion sites. Group subtraction analyses and comparisons with healthy controls were performed with Statistic Parametric Mapping for the PET data. A comparison of PET A of acute-stage patients with that of healthy controls showed increases in glucose metabolism in the cerebellum, motion-sensitive visual cortex areas, and inferior temporal lobe, but none in vestibular cortex areas. At the supratentorial level bilateral signal decreases dominated in the thalamus, frontal eye fields, and anterior cingulum. These decreases persisted after clinical recovery in contrast to the increases. The transient activations can be attributed to ocular motor and postural recovery (cerebellum) and sensory substitution of vestibular function for motion perception (visual cortex). The persisting deactivation in the thalamic nuclei and frontal eye fields allows alternative functional interpretations of the thalamic nuclei: either a disconnection of ascending sensory input occurs or there is a functional mismatch between expected and actual vestibular activity. Our data support the view that both thalami operate separately for each hemisphere but receive vestibular input from ipsilateral and contralateral midbrain integration centers. Normally they have gatekeeper functions for multisensory input to the cortex and automatic motor output to subserve balance and locomotion, as well as sensorimotor integration. Public Library of Science 2016-11-08 /pmc/articles/PMC5100888/ /pubmed/27824897 http://dx.doi.org/10.1371/journal.pone.0165935 Text en © 2016 Becker-Bense et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Becker-Bense, Sandra
Buchholz, Hans-Georg
Baier, Bernhard
Schreckenberger, Mathias
Bartenstein, Peter
Zwergal, Andreas
Brandt, Thomas
Dieterich, Marianne
Functional Plasticity after Unilateral Vestibular Midbrain Infarction in Human Positron Emission Tomography
title Functional Plasticity after Unilateral Vestibular Midbrain Infarction in Human Positron Emission Tomography
title_full Functional Plasticity after Unilateral Vestibular Midbrain Infarction in Human Positron Emission Tomography
title_fullStr Functional Plasticity after Unilateral Vestibular Midbrain Infarction in Human Positron Emission Tomography
title_full_unstemmed Functional Plasticity after Unilateral Vestibular Midbrain Infarction in Human Positron Emission Tomography
title_short Functional Plasticity after Unilateral Vestibular Midbrain Infarction in Human Positron Emission Tomography
title_sort functional plasticity after unilateral vestibular midbrain infarction in human positron emission tomography
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5100888/
https://www.ncbi.nlm.nih.gov/pubmed/27824897
http://dx.doi.org/10.1371/journal.pone.0165935
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