an investigation of hidden hearing loss due to noise ... ›...
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An Investigation of Hidden Hearing Loss due to Noise Exposure in Young Adults with Normal Hearing
G. Prendergast, H. Guest, D. Hall, K. Kluk-de Kort, A. Léger, A. Hickox, M. Heinz, K. Munro & C. Plack**Manchester Centre for Audiology and Deafness (ManCAD)
School of Psychological Sciences, University of Manchester, UK
What is hidden hearing loss (HHL)?
References
Moser T. Predoehl F. & Starr A. (2013). Review of hair cell synapse defects in sensorineural hearing impairment. Otol. Neurotol. 34:995-1004.
Kujawa S.G. & Liberman M.C. (2009). Adding insult to injury: cochlear nerve degeneration after "temporary" noise-induced hearing loss. J Neurosci. 29:14077-85.
Schaette R. & McAlpine D. (2011). Tinnitus with a normal audiogram: physiological evidence for hidden hearing loss and computational model.J Neurosci. 31:13452-7.
Lutman M.E. Davis A.C. Ferguson M.A. (2008). Epidemiological evidence for the effectiveness of the noise at work regulations. Health and Safety Executive. RR669
What is the evidence for HHL?“Hidden Hearing Loss” describes a change in the auditory system as a result of cochlear synaptopathy.
Cochlear synaptopathy is the loss of synapses (connections) between inner hair cells in the ear and auditory nerve fibres that carry sound information to the brain. This loss of synapses occurs as part of the natural ageing process and also due to noise exposure.
Pure-tone audiometry is the standard diagnostic test of hearing and this measures the sensitivity of the inner and outer hair cells. Cochlear synaptopathy is not detectable via pure-tone audiometry. Hence, many people may have noise damage to their hearing that is not being detected.
Figure 1: Schematic showing the site of cochlear synaptopathy in the inner ear (taken from Moser et al., 2013).
Taken from Kujawa and Liberman (2009).Figure 2 (above): Wave I of the ABR was measured at a series of sound levels.Figure 3 (left): synaptic ribbon counts in an exposed and non-exposed animal
The measurements at 1 day post-exposure (shown in red) demonstrate a temporary threshold shift.
3-days and 8-weeks post exposure the ABR response at low sound levels returns to normal. At high sound levels there remains a reduction in the response (blue and black).
Further investigation confirmed that after 64 weeks, 50% nerve fibre loss had occurred.
Is HHL related to tinnitus?
Primary evidence comes from experiments on rodents. Kujawa & Liberman (2009) exposed mice to 100 dB SPL noise (8-16 kHz) for 2 hours. Wave I of the electrophysiological auditory brainstem response (ABR) was used as a measure of auditory nerve function.
Schaette & McAlpine (2011) measured ABR responses in a group of audiometrically matched tinnitus and non-tinnitus listeners. Figures 4 and 5 are taken from this study.
Figure 4 (right): Shows average ABR waveforms for non-tinnitus and tinnitus participants (upper and lower waveforms respectively).
The bar plots show that the growth in wave I magnitude as level increases is not as large in the tinnitus group as for the normal-hearing controls.
Figure 5 (left): Schematic of what Schaette & McAlpine believe may be occurring. In the tinnitus group, the reduction in wave I is caused by a loss of auditory nerve fibres and an increase in “central gain” results in a normal wave V, but is also the cause of the tinnitus.
It is unclear as to whether noise induced hidden hearing loss occurs in listeners with clinically normal hearing.
If hidden hearing loss does occur in humans it is unclear the extent to which this is a problem across the population. It is also unclear what perceptual problems may result from a loss of auditory nerve function.
We are currently conducting a large scale project at the University of Manchester to address some of these issues and better understand if hidden hearing loss can be reliably measured in humans and what the consequences may be.
Current ManCAD study
129 audiometrically normal listeners (mean across ears < 20 dB HL 0.25-8 kHz) have participated in our study.
Noise exposure is assessed using a noise exposure questionnaire (Lutman et al 2008).
A number of electrophysiological and behavioural measures are collected.
Figure 6: Shows the participants' noise exposure scores as a function of age.
Currently there is no evidence from this young cohort with good audiological thresholds that noise exposure is related to a change in ABR, although we have found much poorer sensitivity to quiet sounds at very high frequencies in the noise exposed group (beyond the normal clinical frequency range).
It remains unclear the extent to which synaptopathy exists in humans and how it might be best detected.
Figure 7: Grand average ABRs are shown for the 28 individuals with the highest (red) and lowest (blue) noise exposure scores.
Wave I