(PP507) Neural Adaptive Properties Among Individuals at Risk for Hidden Hearing Loss

Loud sound exposure is shown to cause cochlear synaptopathy (hidden hearing loss). To develop sensitive clinical electrophysiologic measures, we evaluated the neural adaptive properties using the click train paradigm among normal-hearing college-age students who participated in marching band for at least five years (high-risk group) and non-marching band group with the group low noise-exposure history (low-risk group). The results indicate no difference in click-train-induced neural adaptation functions between groups despite reduced wave I amplitude for the high-risk group. These results suggest that structural and functional modifications consequent to cochlear synaptopathy do not alter the mechanisms mediating neural adaptation.


Summary: 

Rationale/

Purpose:

Recent studies in animals suggest that even moderate levels of noise exposure can damage synaptic ribbons between the inner hair cells and auditory nerve fibers without affecting audiometric thresholds, giving rise to the use of the term “hidden hearing loss” (HHL). Given the pervasive exposure to occupational and recreational noise in the general population, it is likely that individuals afflicted with HHL will go unidentified unless sensitive clinical measures are developed to diagnose this condition. The objective of the project is to search for sensitive clinical electrophysiologic measures for early detection of HHL by measuring neural adaptive properties using the click train paradigm among normal-hearing college-age students who participated in marching band for at least five years (high-risk group) and non-marching band group with the group low noise-exposure history (low-risk group).

Hypothesis:

Reduced neuronal population consequent to cochlear synaptopathy may render the population response more susceptible to adaptation. We hypothesize that inefficiencies in synaptic processing associated with recreational overexposure among high-risk groups may alter the characteristics of neural adaptation as reflected in the changes in ABR latency and amplitude and the time course and response recovery from adaptation. The absence of the expected changes would suggest that structural and functional changes consequent to synaptopathy do not alter the mechanisms mediating neural adaptation.

Methods:

ABRs were obtained using click trains consisting of five identical clicks with an inter-click interval (ICI) of 12 msec and three inter-train intervals (ITI) of 25, 50, and 100 msec. Participants were young normal-hearing individuals who participated in the marching band for at least five years (high-risk group) and non-marching band group with low noise-exposure history (low-risk group).

Results:

The results of this experiment demonstrated that (i) a different pattern of latency and amplitude change for wave I and wave V for both fixed and variable ITI conditions; (ii) although the wave I amplitude for individual click in the train is smaller for high-risk group, the normalized amplitude change within the train (across individual click number) and ITI is comparable between groups suggesting that the nature of the transition from un-adapted to adapted response properties is very similar between groups.  

Conclusion:

No differences in adaptive properties between groups suggest that the extent to which adaptation reflects activity from hair cell nerve junction, the processes at the synaptic level relevant to adaptation, are not different for the two groups. To conclude, the reduction in synapses and the number of fibers (consistent with synaptopathy) may only decrease the auditory nerve output but does not appear to alter synaptic processes relevant to click-train-induced neural adaptation.