Background: Chronic subjective tinnitus affects 15-20% of adults globally, with 3-5% experiencing severe quality-of-life impairment. Sound therapy (ST) is a core intervention, but its neuromodulatory mechanisms remain incompletely characterized due to the lack of objective biomarkers.
Methods: Following PRISMA guidelines, we systematically searched PubMed, Web of Science, Embase, and other databases (1977-2025) for randomized controlled trials (RCTs) investigating ST effects on EEG spectral power in tinnitus patients. Inclusion criteria required pre/post-ST EEG data in delta (0.5-4 Hz) and alpha (8-14 Hz) bands. Two independent reviewers extracted data and assessed bias using Cochrane tools. Standardized mean differences (SMDs) with 95% confidence intervals (CIs) were pooled via fixed/random-effects models.
Results: Two RCTs (n=71 patients) met inclusion criteria. Post-ST, the intervention group showed non-significant trends toward increased delta (SMD=0.11, 95% CI: [-0.40, 0.62], P=0.67) and alpha (SMD=0.09, 95% CI: [-0.41, 0.60], P=0.72) power. Between-group analyses revealed greater alpha enhancement in customized ST versus controls (SMD=0.40, 95% CI: [-0.12, 0.91], P=0.13; I2=39%). Alpha changes demonstrated moderate consistency across studies (I2=39%, P=0.19).
Conclusion: ST induces measurable delta/alpha power modulation, suggesting enhanced inhibitory neurotransmission and attentional regulation. While statistical significance was limited by sample size, these trends support EEG as a tool for objective treatment monitoring. We propose a "dual-band synergistic neuromodulation" framework: ST concurrently suppresses pathological hyperexcitability and potentiates slow-wave inhibition. Standardized EEG protocols and longitudinal validation are critical for advancing precision tinnitus therapeutics.
Keywords: biomarkers; electroencephalography; meta-analysis; neuromodulation; sound therapy; tinnitus.
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