Abstract
Why vestibular compensation (VC) after an acute unilateral vestibular loss is the neuro-otologist’s best friend is the question at the heart of this paper. The different plasticity mechanisms underlying VC are first reviewed, and the authors present thereafter the dual concept of vestibulo-centric versus distributed learning processes to explain the compensation of deficits resulting from the static versus dynamic vestibular imbalance. The main challenges for the plastic events occurring in the vestibular nuclei (VN) during a post-lesion critical period are neural protection, structural reorganization and rebalance of VN activity on both sides. Data from animal models show that modulation of the ipsilesional VN activity by the contralateral drive substitutes for the normal push–pull mechanism. On the other hand, sensory and behavioural substitutions are the main mechanisms implicated in the recovery of the dynamic functions. These newly elaborated sensorimotor reorganizations are vicarious idiosyncratic strategies implicating the VN and multisensory brain regions. Imaging studies in unilateral vestibular loss patients show the implication of a large neuronal network (VN, commissural pathways, vestibulo-cerebellum, thalamus, temporoparietal cortex, hippocampus, somatosensory and visual cortical areas). Changes in gray matter volume in these multisensory brain regions are structural changes supporting the sensory substitution mechanisms of VC. Finally, the authors summarize the two ways to improve VC in humans (neuropharmacology and vestibular rehabilitation therapy), and they conclude that VC would follow a “top-down” strategy in patients with acute vestibular lesions. Future challenges to understand VC are proposed.
Highlights
Why vestibular compensation (VC) after an acute unilateral vestibular loss is the neuro-otologist’s best friend is the question at the heart of this paper
The main challenges for the plastic events occurring in the vestibular nuclei (VN) during a post-lesion critical period are neural protection, structural reorganization and rebalance of VN activity on both sides
Data from animal models show that modulation of the ipsilesional VN activity by the contralateral drive substitutes for the normal push–pull mechanism
Summary
The vestibular syndrome after a unilateral vestibular loss is made of both static symptoms, observed in a stationary subject, and dynamic symptoms seen only when the patient moves his/her head or his/her whole body in space [12] (Fig. 1a) The static deficits constitute the ocular-tilt reaction, that is, a combination of ocular motor signs (spontaneous vestibular nystagmus, skew deviation, eye cyclotorsion), postural signs (head and body tilt to the lesion side), and perceptive signs (vertigo, tilt of the subjective visual vertical). The static syndrome results from the combination of the effects of the horizontal canal and utricular lesions, and is more accentuated in the frontal than in the sagittal plane [19] This static syndrome is fully compensated in unilateral vestibular loss patients with a longer time constant (3 months for the postural and ocular motor deficits, up to 1 year for the perception of verticality) [11, 12, 20], compared to animal models (1 week in the rat, mice and guinea pig, 6 weeks in the cat). The dual concept of brain orchestration of ‘‘neurobiological signatures, or melodies’’ and ‘‘behavioural signatures, or melodies’’ has been proposed to explain the recovery of the static and dynamic functions, respectively [21] It will be shown in the following that the former depends on the vestibular aetiology, while the latter depends on the patients themselves
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