Recovery after Vestibular Lesions: From Animal Models to Patients

Abstract

Gaze and postural stabilization is the result of a complex multisensory integration, which can be defined as the process of matching multiple internal representations of an external event (head and/or trunk rotation), obtained from different sensory modalities, into a unique intrinsic frame of reference in which appropriate motor commands can be coded. Despite the importance of the labyrinths, their lesions are not rare. They result in static and dynamic deficits. What is remarkable is that some of these deficits recover in mammalian species, including humans: the vestibular compensation process refers to the complete or partial normalization of the static and dynamic postural and ocular motor deficits. In the following, only two aspects of vestibular compensation will be discussed: (1) the relationship between the recovery of the vestibulo-ocular reflexes and the postlesional plasticity of the intrinsic membrane properties of the medial vestibular nucleus, and (2) the relationship between the postural recovery and the vestibular control of the skeletal geometry at large. Subsequently, the results of investigations in animal models will be related to some clinical findings. While such an exercise is highly speculative, it points to new directions for clinical research and vestibular rehabilitation.

The intrinsic plasticity of medial vestibular nucleus neurons during vestibular compensation—a systematic review and meta-analysis

“…This process may be acute (less than 2 weeks) or chronic (greater than 2 weeks). The animal model widely used to study vestibular compensation is experimentally induced UVD [2,23].…”

Vestibular Lesion-Induced Developmental Plasticity in Spinal Locomotor Networks during Xenopus laevis Metamorphosis

“…For example, an acute ablation of vestibular endorgans or vestibular nerve transection on one side (unilateral labyrinthectomy, UL) causes deficits in both postural and oculomotor reflexes (for a review, see [6]) that recover after several weeks. Vestibular compensation, which has been proposed to account for such functional restorations in terrestrial species (see [7]), consists of a gradual re-equilibration of activity in the brainstem vestibular nuclei of the two sides and implicates the use of body proprioceptive information ascending from the spinal cord (see [8]). However, although such compensatory plasticity has been extensively studied in brainstem nuclei, surprisingly very little is known about the long-term effects of a vestibular lesion on downstream locomotor networks in the spinal cord.…”