Abstract
Vestibular compensation (VC) refers to the functional responses and recovery processes essential for controlling posture and eye movements following damage to the vestibular system. Since damaged peripheral vestibular receptors and nerves cannot regenerate, VC relies primarily on synaptic and neuronal plasticity within the brainstem vestibular nuclei, cerebellum, and related brain regions. The article describes two categories of deficits following unilateral peripheral vestibular lesions: "static" signs, which resolve rapidly, and "dynamic" signs, which compensate more slowly and often incompletely. At the cellular level, unilateral deafferentation causes an immediate loss of resting discharge in ipsilateral medial vestibular nucleus (MVN) neurons, followed by gradual recovery through four proposed mechanisms: (1) altered responsiveness to GABAergic inhibitory signals; (2) increased intrinsic excitability of MVN neurons; (3) synaptic reorganization of excitatory pathways; and (4) cerebellar modulation, particularly via the nodulus. Stress and hypothalamic-pituitary-adrenal axis activity also influence VC through glucocorticoids and neurosteroids, though findings on dexamethasone's efficacy remain inconsistent. Regarding treatment, few pharmacological agents have demonstrated a clear promoting effect on VC. Antihistamines and calcium channel blockers (flunarizine, cinnarizine) primarily act as vestibular suppressants rather than compensation enhancers. Acetyl-DL-leucine (marketed as Tanganil), a glutamate precursor, has shown efficacy in promoting VC and is widely used in Vietnamese clinical practice. Vestibular rehabilitation exercises also play a key role by compensating for afferent deficits and enhancing neural plasticity through appropriate stress responses.
