Abstract

Noise-induced cochlear synaptopathy (CS) is defined as a permanent loss of synapses in the auditory nerve pathway following noise exposure. Several studies using auditory brainstem response (ABR) have indicated the presence of CS and increased central gain in tinnitus patients with normal hearing thresholds (TNHT), but the results were inconsistent. This meta-analysis aimed to review the evidence of CS and its pathological changes in the central auditory system in TNHT. Published studies using ABR to study TNHT were reviewed. PubMed, EMBASE, and Scopus databases were selected to search for relevant literature. Studies (489) were retrieved, and 11 were included for meta-analysis. The results supported significantly reduced wave I amplitude in TNHT, whereas the alternations in wave V amplitude were inconsistent among the studies. Consistently increased V/I ratio indicated noise-induced central gain enhancement. The results indicated the evidence of noise-induced cochlear synaptopathy in tinnitus patients with normal hearing. However, inconsistent changes in wave V amplitude may be explained by that the failure of central gain that triggers the pathological neural changes in the central auditory system and/or that increased central gain may be necessary to generate tinnitus but not to maintain tinnitus.

Highlights

  • Tinnitus is defined as a phantom sound without any corresponding external acoustic stimulus (Langguth et al, 2013)

  • The results showed no significant difference in wave V amplitude between tinnitus participants and controls (SMD = 0.09, 95% confidence interval (CI): −0.30, 0.48, p = 0.65) and large heterogeneity (Chi2 = 106.33, p < 0.001, I2 = 85%)

  • This review investigated whether the auditory brainstem response (ABR) changes in tinnitus patients with normal hearing are consistent across studies

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Summary

Introduction

Tinnitus is defined as a phantom sound without any corresponding external acoustic stimulus (Langguth et al, 2013). Tinnitus is often reported by patients with elevated hearing thresholds and, hyperactivity along the peripheral, and central auditory pathways after cochlear damage has been proposed as the primary cause (Jastreboff, 1990; Rauschecker et al, 2010; Roberts et al, 2010). It seems contradictory, that some 8– 27.5% of tinnitus patients show a relatively normal performance in pure-tone audiometry (Sanchez et al, 2005; Zhao et al, 2010; Sheldrake et al, 2015). This suggests that normal hearing audiometry does not necessarily indicate normal cochlear function.

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