Mechanisms of neuroimmune crosstalk in vestibular disorders: Linking inflammation with neural circuit dysfunction (Review)

Vestibular disorders such as vestibular migraine (VM) and Menière's disease (MD) involve complex interactions between inflammation and neural circuit dysfunction. Emerging evidence highlights neuroimmune crosstalk as a unifying pathophysiological framework. The present review synthesized current knowledge on inflammatory cytokine networks; neuropeptide signaling including calcitonin gene‑related peptide and histamine; glial responses; and systemic immune influences including the gut‑vestibular axis. Emerging evidence suggests potentially distinct immunological profiles may differentiate VM from MD. Illustrative examples include elevated IL‑1β and macrophage‑derived C‑X‑C motif chemokine ligand (CXCL)8 in MD, whereas CXCL10 acting through the PI3K/AKT signaling pathway has been implicated in VM pathogenesis. However, direct comparative studies remain limited and findings across cytokine studies show some heterogeneity. These observations support the concept of mechanism‑based subtyping as a promising framework requiring further validation. Neuroinflammation has dual effects on vestibular compensation, with appropriately calibrated responses promoting recovery and excessive or suppressed inflammation impairing plasticity. The present review integrates molecular, cellular and systemic neuroimmune mechanisms to provide a cohesive framework linking inflammation with vestibular neural circuit dysfunction. The purpose of the present study was to inform future biomarker development and precision therapeutic strategies for vestibular disorders.