Disrupted functional connectivity of the default mode network due to acute vestibular deficit
Identifieur interne : 002127 ( Pmc/Corpus ); précédent : 002126; suivant : 002128Disrupted functional connectivity of the default mode network due to acute vestibular deficit
Auteurs : Carsten M. Klingner ; Gerd F. Volk ; Stefan Brodoehl ; Otto W. Witte ; Orlando Guntinas-LichiusSource :
- NeuroImage : Clinical [ 2213-1582 ] ; 2014.
Abstract
Vestibular neuritis is defined as a sudden unilateral partial failure of the vestibular nerve that impairs the forwarding of vestibular information from the labyrinth. The patient suffers from vertigo, horizontal nystagmus and postural instability with a tendency toward ipsilesional falls. Although vestibular neuritis is a common disease, the central mechanisms to compensate for the loss of precise vestibular information remain poorly understood. It was hypothesized that symptoms following acute vestibular neuritis originate from difficulties in the processing of diverging sensory information between the responsible brain networks. Accordingly an altered resting activity was shown in multiple brain areas of the task-positive network. Because of the known balance between the task-positive and task-negative networks (default mode network; DMN) we hypothesize that also the DMN is involved.
Here, we employ functional magnetic resonance imaging (fMRI) in the resting state to investigate changes in the functional connectivity between the DMN and task-positive networks, in a longitudinal design combined with measurements of caloric function. We demonstrate an initially disturbed connectedness of the DMN after vestibular neuritis. We hypothesize that the disturbed connectivity between the default mode network and particular parts of the task-positive network might be related to a sustained utilization of processing capacity by diverging sensory information. The current results provide some insights into mechanisms of central compensation following an acute vestibular deficit and the importance of the DMN in this disease.
Url:
DOI: 10.1016/j.nicl.2014.08.022
PubMed: 25379422
PubMed Central: 4215422
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