Professional musicians (PMs) are at high risk of developing hearing loss (HL) and other audiological symptoms such as tinnitus, hyperacusis, and diplacusis. The aim of this systematic review is to (A) assess the risk of developing HL and audiological symptoms in PMs and (B) evaluate if different music genres (Pop/Rock Music—PR; Classical Music—CL) expose PMs to different levels of risk of developing such conditions. Forty-one articles including 4618 PMs were included in the study. HL was found in 38.6% PMs; prevalence was significantly higher among PR (63.5%) than CL (32.8%) PMs; HL mainly affected the high frequencies in the 3000-6000 Hz range and was symmetric in 68% PR PMs and in 44.5% CL PMs. Tinnitus was the most common audiological symptom, followed by hyperacusis and diplacusis. Tinnitus was almost equally distributed between PR and CL PMs; diplacusis was more common in CL than in PR PMs, while prevalence of hyperacusis was higher among PR PMs. Our review showed that PR musicians have a higher risk of developing HL compared to CL PMs; exposure to sounds of high frequency and intensity and absence of ear protection may justify these results. Difference in HL symmetry could be explained by the type of instruments used and consequent single-sided exposure.

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We observed a MELAS patient who came to our Clinical Center for moderate SNHL. The ABR from this patient displayed waves (Figure 1) with amplitude and latency too reduced to be considered within the normal range, but not completely absent as it would be expected considering his auditory threshold in pure tone audiometry (PTA).In an attempt to explain this observation, we reviewed the literature on the temporal bone aspect of MELAS patients. Loss of Spiral Ganglions (SGs) and atrophy of Stria Vascularis (SV) are typical findings in temporal bone of patients with MELAS even when the Organ of Corti is entirely preserved.In SGs and SV mitochondria are abundant [7], as they are necessary to support the high metabolic functions of these structures. In MELAS, mitochondria that have been damaged (by deletion/mutation in their DNA) increase the Redox Oxidative Species (ROS) concentration [8] and cell apoptosis [9] which reduce the number of inner ear cells (SG, VS and Hair cells) and, cause a malfunction of the remaining cells.ABR reflects the way the auditory signal travels from the retrocochlear portion (synapse, SGs, cochlear nerve and cochlear nuclei) (Waves I, III) to the cortex (wave V); if all the structures in the retro-cochlear hearing pathways function correctly, the ABR displays normal amplitude and latency; but damage in even one of the structures causes abnormal ABR latency and/or amplitude, which in turn alter the overall signal shape.We think that the abnormal ABR of our patient can be explained by the altered functions of residual SGs, which cannot sufficiently amplify the signal to generate an actual ABR wave. The numerous mitochondrial mutations observed in the temporal bone of patients with MELAS [10][11] support the idea that the residual SGs do not function well enough to allow a correct transmission of the impulse, which in turn leads to an abnormal ABR. Arguably, the high ABR variability in MELAS patients reported in the literature [2,3,4,6] is due to the stochastic segregation of mitochondria during embryogenesis; the concentration of damaged mitochondria could differ among patients just due to