Otoacoustic emissions and medial olivocochlear suppression during auditory recovery from acoustic trauma in humans.

It is well known that the large inter-individual susceptibility to noise exposure makes it impossible to predict the degree of hearing loss which will develop after any given intense noise exposure. The acoustic trauma which sometimes occurs affects cochlear mechanisms, the damage being most probably due to deactivation of the active processes of the outer hair cells (OHCs), which receive direct efferent innervation. The present report is of a follow-up study involving young military personnel recovering auditively from impulse noise exposure, and seeks to assess changes in cochlear status by means of otoacoustic emissions (OAEs) and their modulation by the medial olivocochlear (MOC) system. The study investigated the relationship between recovery of cochlear function and variables that could serve as predictors of vulnerability to noise-induced hearing loss (NIHL). Thirty-six subjects with unilateral NHIL above 4 kHz were included. Normal and affected ears were compared with respect to click-evoked and spontaneous OAEs (CEOAEs and SOAEs, respectively) and for contralateral CEOAE suppression. Measurements were obtained: (i) just after the traumatic exposure (D0); (ii) 3 days after this first measurement (D3); and (iii) 30 days after (D30). Significant improvement in the 4, 6 and 8 kHz thresholds was observed for the affected ear, with large inter-subject variability. No significant change was observed in CEOAE amplitude or MOC suppression, whereas incidence of SOAE was found to increase in the affected ear, leading to higher SOAE prevalence on this side I month after the intense noise exposure. There was no significant correlation between NIHL at 4, 6 and 8 kHz and MOC functioning on D0, but significant correlations were obtained between audiometric threshold improvement by D3 and contralateral CEOAE suppression, with better recovery in subjects with greater MOC suppressive action. The MOC system could be an underlying mechanism in post-traumatic auditory threshold recovery.