Evidence of “hidden hearing loss” following noise exposures that produce robust TTS and ABR wave-I amplitude reductions

Abstract

In animals, noise exposures that produce robust temporary threshold shifts (TTS) can produce immediate damage to afferent synapses and long-term degeneration of low spontaneous rate auditory nerve fibers. This synaptopathic damage has been shown to correlate with reduced auditory brainstem response (ABR) wave-I amplitudes at suprathreshold levels. The perceptual consequences of this "synaptopathy" remain unknown but have been suggested to include compromised hearing performance in competing background noise. Here, we used a modified startle inhibition paradigm to evaluate whether noise exposures that produce robust TTS and ABR wave-I reduction but not permanent threshold shift (PTS) reduced hearing-in-noise performance. Animals exposed to 109 dB SPL octave band noise showed TTS >30 dB 24-h post noise and modest but persistent ABR wave-I reduction 2 weeks post noise despite full recovery of ABR thresholds. Hearing-in-noise performance was negatively affected by the noise exposure. However, the effect was observed only at the poorest signal to noise ratio and was frequency specific. Although TTS >30 dB 24-h post noise was a predictor of functional deficits, there was no relationship between the degree of ABR wave-I reduction and degree of functional impairment.

Effects of noise exposure on auditory brainstem response and speech-in-noise tasks: a review of the literature

“…These exposures typically employ a short-term noise exposure, with rodent subjects typically exposed to octave band noise for two-hours. Across rodents, the two-hour duration sound exposure level needed to induce cochlear synaptopathy has varied, with higher sound levels needed in the guinea pig (106 dB SPL, see Lin et al 2011) and rat (109 dB SPL, see Lobarinas, Spankovich, and Le Prell 2017) than in the mouse (100 dB SPL, see Kujawa and Liberman, 2009;Fernandez et al 2015). In the absence of noise exposure, age-related cochlear synaptopathy is also reliably observed.…”

Effects of Recreational Noise on Threshold and Suprathreshold Measures of Auditory Function

“…[7][8][9] Data from rodents and data that are emerging from primate models suggest it is unlikely that there would be a significant risk of synaptic damage in humans from concerts or other equivalent recreational exposures that result in small TTSs. 12,21,22,51 However, any inference related to the potential hazard associated with a single loud recreational event must be made with caution. Unlike animals tested in laboratory models that include a single acute exposure, humans experience noise exposure on a repeat basis, and they may experience noise exposure in combination with other hazards (such as during chemical exposure in the workplace).…”

Dynamic gain adjustments in descending corticofugal outputs from auditory cortex compensate for cochlear nerve synaptic damage

“…Enhanced central gain and functional recovery following selective cochlear afferent lesions is more rapid and robust at higher stages of central processing. At the level of the auditory nerve compound action potential, sound-evoked response amplitudes directly report the extent of cochlear afferent loss with no observable regulation of gain 15,42,46,55,56 . Similarly, measurements of brainstem far-field evoked potentials and brainstem acoustic reflexes show minimal gain enhancement at the earliest stations of central auditory processing following selective cochlear afferent lesions 42,57,58 , though some studies have reported enhanced acoustic startle and medial olivocochlear reflexes after a moderate presumed loss of cochlear afferent synapses 59,60 .…”