Global multisensory reorganization after vestibular brain stem stroke.

Julian Conrad,Valerie Kirsch,Thomas Stephan,Rainer Boegle,Marianne Dieterich,Ozan Eren,Iskra Stefanova‐Brostek,Peter Zu Eulenburg,Maximilian Habs,Marco Duering,Frank Wollenweber,Matthias Ertl,Sandra Becker‐Bense

doi:10.1002/acn3.51161

Abstract

ObjectivePatients with acute central vestibular syndrome suffer from vertigo, spontaneous nystagmus, postural instability with lateral falls, and tilts of visual vertical. Usually, these symptoms compensate within months. The mechanisms of compensation in vestibular infarcts are yet unclear. This study focused on structural changes in gray and white matter volume that accompany clinical compensation.MethodsWe studied patients with acute unilateral brain stem infarcts prospectively over 6 months. Structural changes were compared between the acute phase and follow‐up with a group of healthy controls using voxel‐based morphometry.ResultsRestitution of vestibular function following brain stem infarcts was accompanied by downstream structural changes in multisensory cortical areas. The changes depended on the location of the infarct along the vestibular pathways in patients with pathological tilts of the SVV and on the quality of the vestibular percept (rotatory vs graviceptive) in patients with pontomedullary infarcts. Patients with pontomedullary infarcts with vertigo or spontaneous nystagmus showed volumetric increases in vestibular parietal opercular multisensory and (retro‐) insular areas with right‐sided preference. Compensation of graviceptive deficits was accompanied by adaptive changes in multiple multisensory vestibular areas in both hemispheres in lower brain stem infarcts and by additional changes in the motor system in upper brain stem infarcts.InterpretationThis study demonstrates multisensory neuroplasticity in both hemispheres along with the clinical compensation of vestibular deficits following unilateral brain stem infarcts. The data further solidify the concept of a right‐hemispheric specialization for core vestibular processing. The identification of cortical structures involved in central compensation could serve as a platform to launch novel rehabilitative treatments such as transcranial stimulations.

Highlights

Acute central vestibular syndrome manifests with rotational vertigo, spontaneous nystagmus (SPN), tilts of the subjective visual vertical (SVV), and postural instability with lateral falls
Patients with acute central vestibular syndrome suffer from vertigo, spontaneous nystagmus, postural instability with lateral falls, and tilts of visual vertical
This study focused on structural changes in gray and white matter volume that accompany clinical compensation

Summary

Introduction

Acute central vestibular syndrome manifests with rotational vertigo, spontaneous nystagmus (SPN), tilts of the subjective visual vertical (SVV), and postural instability with lateral falls. The sensory signals are conveyed from the vestibular end organs to the vestibular nuclei in the pontomedullary brain stem and via several bilateral pathways with multiple crossings to the thalamus. They reach the multisensory integration centers of the temporoparietal cortex.[11,12,13,14,15] The posterior insula with the parietal opercular cortex (OP2), the posterior insular and retroinsular cortex were reliably identified as the core regions of the multisensory vestibular network in humans.[14,16,17,18,19] These regions show a right-hemispheric preponderance for vestibular signal processing in right-handed humans.[18]

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