Otoconial repositioning alters brain connectivity in benign paroxysmal positional vertigo patients.

ObjectiveTo explore the changes in brain network functional connectivity (FC) in patients with benign paroxysmal positional vertigo (BPPV) before and after otoconial repositioning treatment, and to analyze the correlation between FC and the Dizziness Handicap Inventory (DHI) score, thereby elucidating the neural basis of BPPV from a central mechanism perspective.MethodsA prospective cohort design was adopted, including 29 BPPV patients (BPPV group) and 29 healthy controls (control group). Resting-state brain network data were collected using 44-channel functional near-infrared spectroscopy (fNIRS), and the FC intensity of the whole brain and regions of interest (ROIs) was calculated. FC detection and DHI scoring were performed in the BPPV group before and 7 days after repositioning. Group comparisons were conducted using t-tests or Mann-Whitney U tests, and correlations were analyzed using Pearson analysis.ResultsThe whole-brain FC in the BPPV group before repositioning (0.52 ± 0.20) was significantly lower than that in the control group (0.64 ± 0.18) (t = −4.32, P < 0.01). Seven days after repositioning, the FC of the visual cortex V1, V2 + V3, and somatosensory cortex increased compared with that before treatment (P < 0.05), but did not return to normal levels (P < 0.05). The DHI score was negatively correlated with whole-brain FC (r = −0.62, P < 0.01).ConclusionfNIRS revealed characteristic FC alterations in BPPV: acute-phase decreases, partial sensory cortex recovery post-repositioning, and delayed prefrontal recovery. FC correlated negatively with symptom severity, suggesting its potential as an objective biomarker. These findings provide insights into central mechanisms and support neuroregulation-assisted therapy development.