European Journal of Cardiovascular Medicine

Noise-induced hearing loss (NIHL) is a growing public health concern, particularly among adolescents and young adults due to increased exposure to recreational noise through personal listening devices, concerts, and occupational hazards (1). Traditionally, NIHL has been diagnosed through pure tone audiometry, which identifies threshold elevations at specific frequencies. However, emerging evidence suggests that significant neural damage can occur in the cochlea even when audiometric thresholds remain within the normal range—a condition now referred to as cochlear synaptopathy or “hidden hearing loss” (2,3).

Cochlear synaptopathy is characterized by the degeneration of ribbon synapses between inner hair cells and type I afferent auditory nerve fibers without apparent damage to outer hair cells (4). This synaptic loss primarily affects low spontaneous rate fibers that are crucial for encoding sound in noisy environments, which explains why individuals with this condition often report difficulty understanding speech in background noise despite normal hearing thresholds (5). As a result, standard audiometric testing may fail to detect these subtle neural deficits.

To identify cochlear synaptopathy in humans, researchers have turned to objective and behavioral measures. Electrocochleography (ECochG), a technique that records electrical potentials from the cochlea and auditory nerve, has been employed to assess synaptic integrity. Specifically, the summating potential (SP) to action potential (AP) ratio has emerged as a sensitive indicator of synaptic loss (6). Additionally, speech-in-noise (SIN) tests offer a functional assessment of a person's ability to comprehend speech in adverse listening environments and may reveal deficits that are not evident in quiet conditions (7).

This study aims to assess cochlear synaptopathy in young adults with chronic noise exposure by evaluating the SP/AP ratio through ECochG and analyzing their performance in SIN tests. These measures could enhance the early detection of noise-induced neural damage, thereby facilitating timely preventive strategies.

A total of 60 participants, aged 18 to 25 years, were recruited and divided into two groups. Group A (n=30) comprised individuals with a history of chronic noise exposure (e.g., use of personal listening devices exceeding 4 hours per day for more than 2 years, regular attendance at loud events). Group B (n=30) included age- and gender-matched individuals with minimal recreational or occupational noise exposure. All participants had clinically normal hearing thresholds (≤25 dB HL) across standard audiometric frequencies (250–8000 Hz).

Audiological Evaluation
Basic audiological assessments were carried out in a sound-treated room. Pure tone audiometry was performed using a calibrated diagnostic audiometer to confirm normal hearing thresholds. Tympanometry was conducted to ensure normal middle ear status, and participants with abnormal tympanograms or a history of otological disorders were excluded.

Electrocochleography (ECochG)
ECochG recordings were obtained using a commercially available auditory evoked potential system. The extratympanic approach was used with tiptrodes placed in the ear canal. A click stimulus of 100 μs duration was delivered at 90 dB nHL through insert earphones at a rate of 11.1 clicks per second. Responses were averaged over 1500 sweeps. The summating potential (SP) and action potential (AP) were measured, and the SP/AP ratio was calculated for each subject. Increased SP/AP ratios were considered suggestive of cochlear synaptopathy.

Speech-in-Noise (SIN) Testing
Speech-in-noise ability was assessed using the Quick Speech-in-Noise (QuickSIN) test. Participants were asked to repeat key words from a series of sentences presented in multi-talker babble noise at decreasing signal-to-noise ratios (SNRs), beginning from +25 dB SNR to 0 dB SNR. The SNR loss was calculated based on the number of correctly repeated words and was used as an indicator of difficulty in understanding speech in noisy environments.

Statistical Analysis
Data were analyzed using SPSS version 25.0. Descriptive statistics were computed for demographic and test variables. Independent t-tests were used to compare SP/AP ratios and QuickSIN scores between the two groups. Pearson’s correlation was used to assess the relationship between SP/AP ratio and SNR loss. A p-value of <0.05 was considered statistically significant.

The study included 60 participants divided equally into two groups. Group A consisted of 30 individuals with a history of chronic noise exposure, and Group B included 30 age-matched controls with minimal exposure. Both groups had normal hearing thresholds on pure tone audiometry.

Electrocochleography Findings

The SP/AP ratio was significantly higher in Group A compared to Group B. The mean SP/AP ratio in Group A was 0.54 ± 0.08, while it was 0.34 ± 0.06 in Group B, indicating a possible neural deficit in noise-exposed individuals (p < 0.001). This suggests that participants in Group A may be exhibiting early signs of cochlear synaptopathy despite normal audiograms.

Table 1. Comparison of SP/AP Ratios Between Groups

(Table 1: Comparison of SP/AP ratios between noise-exposed individuals and controls.)

Speech-in-Noise (SIN) Performance

Participants in Group A showed significantly poorer performance on the QuickSIN test. The mean SNR loss was 9.3 ± 1.4 dB in Group A, compared to 3.7 ± 1.2 dB in Group B (p < 0.001), indicating a notable decline in speech perception in noisy environments among those with noise exposure.

Table 2. QuickSIN SNR Loss in Both Groups

(Table 2: Speech-in-noise scores showing SNR loss in dB among the two groups.)

Correlation Between SP/AP Ratio and SNR Loss

A significant positive correlation was found between SP/AP ratio and SNR loss across all participants (Pearson’s r = 0.72, p < 0.001), suggesting that greater synaptic dysfunction is associated with increased difficulty in understanding speech in noise.

Table 3. Correlation Between SP/AP Ratio and SNR Loss

(Table 3: Pearson correlation indicating a strong association between electrophysiological and behavioral indicators of cochlear synaptopathy.)

These findings support the hypothesis that noise exposure in young adults leads to subclinical auditory nerve damage, which can be detected using ECochG and SIN testing even when standard audiograms appear normal.

The present study aimed to evaluate cochlear synaptopathy in young adults with chronic noise exposure using electrocochleography (ECochG) and speech-in-noise (SIN) testing. Despite having normal hearing thresholds on pure tone audiometry, participants with a history of high noise exposure demonstrated elevated SP/AP ratios and poorer SIN performance, indicating the presence of subclinical auditory neural deficits consistent with “hidden hearing loss.”

Our findings align with the growing body of literature suggesting that noise exposure can lead to synaptic degeneration in the cochlea without overt threshold shifts (1,2). Kujawa and Liberman (2009) first demonstrated in animal models that even temporary threshold shifts from noise exposure can result in irreversible synaptic damage and auditory nerve fiber loss, a condition later referred to as cochlear synaptopathy (3). Subsequent histological studies in humans have confirmed similar synaptic loss in aging and noise-exposed individuals (4,5).

In the current study, participants in Group A exhibited significantly higher SP/AP ratios compared to controls, consistent with previous research indicating that increased SP/AP ratios may reflect synaptic loss or auditory nerve dysfunction (6,7). ECochG has emerged as a valuable tool for assessing neural integrity, with SP/AP ratio being particularly sensitive to early neural changes not detected by routine audiometry (8). Our findings support its utility in identifying cochlear synaptopathy in young, noise-exposed populations.

Speech-in-noise (SIN) testing, which assesses real-world communication ability, further reinforced the presence of hidden hearing loss in the noise-exposed group. Group A participants had significantly greater SNR loss on the QuickSIN test compared to controls. This aligns with previous studies reporting that individuals with cochlear synaptopathy often struggle to understand speech in noisy environments, despite normal audiograms (9,10). These difficulties are thought to arise from the loss of low-spontaneous-rate auditory nerve fibers, which are crucial for encoding speech in noise (11,12).

The strong positive correlation observed between SP/AP ratios and SNR loss (r = 0.72) suggests a direct relationship between neural damage and functional listening difficulties. Similar correlations have been reported in earlier studies using auditory brainstem responses (ABRs) and SIN performance as surrogate measures of neural integrity (13,14). Our data strengthen the evidence for combining electrophysiological and behavioral assessments for early detection of synaptopathy.

The demographic targeted in this study—young adults—represents a critical group, as early neural damage from chronic exposure to recreational noise may predispose them to accelerated hearing deterioration with age (15). This underscores the importance of implementing preventive strategies such as public education on safe listening practices, regulation of personal audio device output, and regular auditory screenings using sensitive tools like ECochG and SIN tests.

However, this study has certain limitations. The sample size was relatively small, and the cross-sectional design precludes causal inferences. Additionally, while ECochG provides valuable information about cochlear and neural function, it cannot directly quantify synaptic counts, and inter-subject variability in anatomy and electrode placement may affect amplitude measurements. Future studies incorporating longitudinal follow-up, larger cohorts, and complementary techniques such as auditory brainstem response (ABR) testing and otoacoustic emissions (OAEs) are warranted.

In conclusion, our findings support the hypothesis that cochlear synaptopathy exists in young adults exposed to prolonged noise and can be effectively identified using ECochG and SIN assessments. These tools may be integrated into early diagnostic protocols for individuals at risk of developing noise-induced auditory dysfunction, even when conventional hearing tests show no abnormalities.

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