LAUSR

BACKGROUND New research in animal models indicates that even at lower intensities, noise exposure can induce defects in the synapses of the auditory pathway. However, only very high levels of noise exposure lead to mechanical hair cell damage with lesions of the inner ear and measurable hearing loss (audiogram; distortion product otoacoustic emissions, DPOAE). This paper revises the literature, starting with a case study. CASE HISTORY A 41-year-old patient suffered from hearing loss and tinnitus in the right ear following a car accident with airbag deployment. Hearing loss recovered partially, tinnitus and difficulties in speech discrimination persisted. Audiometry showed typical high-frequency hearing loss (40 dB) and tonal tinnitus (8 kHz). Although DPOAE and ABR potentials (auditory brainstem response, wave III and V) were completely normal 6 months after the accident, there was no detectable cochlear action potential (CAP) in electrocochleography (ECochG). DISCUSSION These findings indicate recovery of initial hair cell damage, whereas synaptic transformation remains reduced and slight hearing loss and poor speech perception in complex listening situations persist. This phenomenon has been described as "hidden hearing loss" in newer literature. Although similar retrocochlear lesions in the auditory pathway could be detected in animal models, valid data in humans are currently lacking because no adequate diagnostic methods are available. CONCLUSION Noise trauma initially results in hair cell damage. After recovery, hearing loss may persist, which can be due to synaptic lesions in the first neuron. An adequate testbattery has to be developped.