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.

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.

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).

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.