The effects of deefferentation without deafferentation on functional connectivity in patients with facial palsy
Identifieur interne : 000D59 ( Main/Merge ); précédent : 000D58; suivant : 000D60The effects of deefferentation without deafferentation on functional connectivity in patients with facial palsy
Auteurs : Carsten M. Klingner [Allemagne] ; Gerd F. Volk [Allemagne] ; Stefan Brodoehl [Allemagne] ; Otto W. Witte [Allemagne] ; Orlando Guntinas-Lichius [Allemagne]Source :
- NeuroImage : Clinical [ 2213-1582 ] ; 2014.
Abstract
Cerebral plasticity includes the adaptation of anatomical and functional connections between parts of the involved brain network. However, little is known about the network dynamics of these connectivity changes. This study investigates the impact of a pure deefferentation, without deafferentation or brain damage, on the functional connectivity of the brain. To investigate this issue, functional MRI was performed on 31 patients in the acute state of Bell's palsy (idiopathic peripheral facial nerve palsy). All of the patients performed a motor paradigm to identify seed regions involved in motor control. The functional connectivity of the resting state within this network of brain regions was compared to a healthy control group. We found decreased connectivity in patients, mainly in areas responsible for sensorimotor integration and supervision (SII, insula, thalamus and cerebellum). However, we did not find decreased connectivity in areas of the primary or secondary motor cortex. The decreased connectivity for the SII and the insula significantly correlated to the severity of the facial palsy. Our results indicate that a pure deefferentation leads the brain to adapt to the current compromised state during rest. The motor system did not make a major attempt to solve the sensorimotor discrepancy by modulating the motor program.
Url:
DOI: 10.1016/j.nicl.2014.08.011
PubMed: 25379413
PubMed Central: 4215462
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Klingner</name><affiliation wicri:level="1"><nlm:aff id="aff1">Hans Berger Clinic of Neurology, Jena University Hospital, Germany</nlm:aff><country xml:lang="fr">Allemagne</country><wicri:regionArea>Hans Berger Clinic of Neurology, Jena University Hospital</wicri:regionArea><wicri:noRegion>Jena University Hospital</wicri:noRegion><wicri:noRegion>Jena University Hospital</wicri:noRegion><wicri:noRegion>Jena University Hospital</wicri:noRegion></affiliation></author><author><name sortKey="Volk, Gerd F" sort="Volk, Gerd F" uniqKey="Volk G" first="Gerd F." last="Volk">Gerd F. Volk</name><affiliation wicri:level="1"><nlm:aff id="aff2">Department of Otorhinolaryngology, Jena University Hospital, Germany</nlm:aff><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Otorhinolaryngology, Jena University Hospital</wicri:regionArea><wicri:noRegion>Jena University Hospital</wicri:noRegion><wicri:noRegion>Jena University Hospital</wicri:noRegion><wicri:noRegion>Jena University Hospital</wicri:noRegion></affiliation></author><author><name sortKey="Brodoehl, Stefan" sort="Brodoehl, Stefan" uniqKey="Brodoehl S" first="Stefan" last="Brodoehl">Stefan Brodoehl</name><affiliation wicri:level="1"><nlm:aff id="aff1">Hans Berger Clinic of Neurology, Jena University Hospital, Germany</nlm:aff><country xml:lang="fr">Allemagne</country><wicri:regionArea>Hans Berger Clinic of Neurology, Jena University Hospital</wicri:regionArea><wicri:noRegion>Jena University Hospital</wicri:noRegion><wicri:noRegion>Jena University Hospital</wicri:noRegion><wicri:noRegion>Jena University Hospital</wicri:noRegion></affiliation></author><author><name sortKey="Witte, Otto W" sort="Witte, Otto W" uniqKey="Witte O" first="Otto W." last="Witte">Otto W. Witte</name><affiliation wicri:level="1"><nlm:aff id="aff1">Hans Berger Clinic of Neurology, Jena University Hospital, Germany</nlm:aff><country xml:lang="fr">Allemagne</country><wicri:regionArea>Hans Berger Clinic of Neurology, Jena University Hospital</wicri:regionArea><wicri:noRegion>Jena University Hospital</wicri:noRegion><wicri:noRegion>Jena University Hospital</wicri:noRegion><wicri:noRegion>Jena University Hospital</wicri:noRegion></affiliation></author><author><name sortKey="Guntinas Lichius, Orlando" sort="Guntinas Lichius, Orlando" uniqKey="Guntinas Lichius O" first="Orlando" last="Guntinas-Lichius">Orlando Guntinas-Lichius</name><affiliation wicri:level="1"><nlm:aff id="aff2">Department of Otorhinolaryngology, Jena University Hospital, Germany</nlm:aff><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Otorhinolaryngology, Jena University Hospital</wicri:regionArea><wicri:noRegion>Jena University Hospital</wicri:noRegion><wicri:noRegion>Jena University Hospital</wicri:noRegion><wicri:noRegion>Jena University Hospital</wicri:noRegion></affiliation></author></analytic><series><title level="j">NeuroImage : Clinical</title><idno type="eISSN">2213-1582</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Cerebral plasticity includes the adaptation of anatomical and functional connections between parts of the involved brain network. However, little is known about the network dynamics of these connectivity changes. This study investigates the impact of a pure deefferentation, without deafferentation or brain damage, on the functional connectivity of the brain. To investigate this issue, functional MRI was performed on 31 patients in the acute state of Bell's palsy (idiopathic peripheral facial nerve palsy). All of the patients performed a motor paradigm to identify seed regions involved in motor control. The functional connectivity of the resting state within this network of brain regions was compared to a healthy control group. We found decreased connectivity in patients, mainly in areas responsible for sensorimotor integration and supervision (SII, insula, thalamus and cerebellum). However, we did not find decreased connectivity in areas of the primary or secondary motor cortex. The decreased connectivity for the SII and the insula significantly correlated to the severity of the facial palsy. Our results indicate that a pure deefferentation leads the brain to adapt to the current compromised state during rest. The motor system did not make a major attempt to solve the sensorimotor discrepancy by modulating the motor program.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Albert, N B" uniqKey="Albert N">N.B. Albert</name></author><author><name sortKey="Robertson, E M" uniqKey="Robertson E">E.M. Robertson</name></author><author><name sortKey="Miall, R C" uniqKey="Miall R">R.C. Miall</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Biswal, B" uniqKey="Biswal B">B. Biswal</name></author><author><name sortKey="Yetkin, F Z" uniqKey="Yetkin F">F.Z. Yetkin</name></author><author><name sortKey="Haughton, V M" uniqKey="Haughton V">V.M. Haughton</name></author><author><name sortKey="Hyde, J S" uniqKey="Hyde J">J.S. 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