Abstract
This article is a Vietnamese translation/adaptation of a review by Lacour, Helmchen, and Vidal (2016, Journal of Neurology) on vestibular compensation following acute unilateral vestibular loss. Vestibular compensation is described as a remarkable self-recovery mechanism involving neuroprotection, structural reorganization, and rebalancing of neural activity in both vestibular nuclei. The process unfolds in three stages: Recovery (restoration of pre-lesion functional connections, mainly through VOR recovery via peripheral receptor regeneration and synaptic strengthening), Adaptation (reduction of asymmetry through repeated activation signals at peripheral and central levels), and Substitution (the most powerful mechanism, encompassing sensory substitution and behavioral changes). The article distinguishes between static deficits (nystagmus, postural tilt, positional vertigo), which typically recover quickly and completely within weeks to months, and dynamic deficits (gaze instability during movement, ataxia), which recover more slowly and incompletely, requiring central nervous system reorganization. Neurotransmitters including GABA, glycine, and glutamate play key roles in restoring symmetry between the two vestibular nuclei; pharmacological agents (e.g., Tanganil/Acetyl-DL-Leucine) can accelerate this rebalancing. Stress hormones (cortisol, ACTH) also influence compensation, with excessive stress or comorbid anxiety/depression impairing recovery. Early, individualized vestibular rehabilitation is recommended during the window of neural plasticity to optimize outcomes.
