Structural Changes in the Human Brain following Vestibular Neuritis Indicate Central Vestibular Compensation

Abstract

Vestibular neuritis (VN) is a sudden unilateral vestibular failure (UVF) with a variable course. Caloric hyporesponsiveness often persists, and it is largely unknown why patients with the same degree of hyporesponsiveness show different functional recovery. As the peripheral vestibular deficit alone does not seem to determine functional recovery, it was the aim of this study to elucidate whether structural (morphological) brain changes (1) contribute to central vestibular compensation, and (2) account for the variability of clinical recovery in VN. Structural global gray-matter volume (GMV) changes in 15 VN patients were compared with age-matched controls. Morphometric changes in multisensory vestibular cortices, which may be related to functional disability scores, were hypothesized. Patients were examined with neuro-otological tests and clinical scores to assess vestibular disability. Using voxel-based morphometry (VBM, SPM2), categorical comparison revealed GMV increase in patients' multisensory vestibular cortices [insula, inferior parietal lobe (IPL), superior temporal gyrus (STG)], cerebellum, and motion-sensitive areas in the middle temporal area (MT). GMV decrease was found in the midline pontomedullary junction. Simple regression analysis revealed (1) GMV increase in insula and retroinsular vestibular cortex and STG with improving clinically assessed vestibular deficits, and (2) GMV increase in insula vestibular cortex and STG with improving self-assessed vestibular impairment. For the first time, these data suggest structural cortical plasticity in multisensory vestibular-cortex areas in VN that are related to clinical vestibular function and vertigo. As increase of GMV was related to an improvement of vestibular function, structural alterations may be related to central vestibular compensation.

Predictors of development of chronic vestibular insufficiency after vestibular neuritis

“…As well, previous study on this subject has shown that maintenance of symmetric head rotation with EMG monitoring produce reliably reproducible results, the VEMP amplitude being the best criteria [20]. On the other hand, significant structural cortical alterations related to central vestibular compensation are observed in patients following acute vestibular lesions [21]. Conventional vestibular testing, however, focuses on reflex responses and therefore provides little insight into the functioning of the substantial vestibulo-cortical projection-responsible for sensations of rotation and vertigo [22].…”

Structural brain changes following peripheral vestibulo-cochlear lesion may indicate multisensory compensation

“…Neuro-otological sig3ns of vestibular imbalance were assessed in a standardised fashion using a clinical vestibular score (CVS) 10. This score is based on clinical examination covering (1) spontaneous nystagmus, (2) head-shaking nystagmus, (3) gaze-evoked nystagmus, (4) positional nystagmus, (5) head impulse test,22 (6) ataxia of stance, (7) lateropulsion, (8) lateropulsion during gait without horizontal head movements, (9) ataxia of gait with horizontal head movements, (10) tandem gait ataxia, (11) ataxia on body rotation (180°) and (12) the Fukuda stepping test.…”

“…All high-resolution anatomical 3D images were acquired, preprocessed and analysed, as described elsewhere 10. T1-weighted three-dimensional gradient echos acquired with a fast low-angle shot sequence (FLASH) (TR=15 ms, TE=5 ms, flip angle 30°, acquisition matrix 256×256, isotropic voxel=1 mm 3 ) were acquired on a 1.5 T scanner (Siemens Symphony, Erlangen, Germany) with a standard head coil to reduce possible inhomogeneities and geometric variations due to magnetic field and gradient differences.…”

Neurobiological Mechanisms of Acute Vertigo

“…Three months after acute vestibular neuritis, voxel-based morphometry of MR-images demonstrated gray-matter volume increases within the multisensory vestibular cortical areas (insula, inferior parietal lobe, superior temporal gyrus), the cerebellum and motion-sensitive areas such as the middle temporal area MT /V5 [67]. At the same time, gray-matter volume decreases were found in the midline pontomedullary junction (i.e.…”

“…the inhibitory brainstem commissural pathways interconnecting the MVN), which may either be a consequence of peripheral vestibular denervation or resulting from VC in order to rebalance the commissural inhibitory system. Taking into account that in this study a link between the amount of graymatter volume increase in the vestibular cortical areas and the decrease in vestibular complaints / deficits could be established, it suggests that the structural (volumetric) alterations found indeed reflect VC [67]. Except for gray-matter volume increases in the medial temporal gyrus bilaterally, gray-matter volume changes were not related to the degree of the peripheral vestibular deficit.…”