Recent neuroscience research suggests that tinnitus may reflect synaptic loss in the cochlea that does not express in the audiogram but leads to neural changes in auditory pathways that reduce sound level tolerance (SLT). Adolescents (N = 170) completed a questionnaire addressing their prior experience with tinnitus, potentially risky listening habits, and sensitivity to ordinary sounds, followed by psychoacoustic measurements in a sound booth. Among all adolescents 54.7% reported by questionnaire that they had previously experienced tinnitus, while 28.8% heard tinnitus in the booth. Psychoacoustic properties of tinnitus measured in the sound booth corresponded with those of chronic adult tinnitus sufferers. Neither hearing thresholds (≤15 dB HL to 16 kHz) nor otoacoustic emissions discriminated between adolescents reporting or not reporting tinnitus in the sound booth, but loudness discomfort levels (a psychoacoustic measure of SLT) did so, averaging 11.3 dB lower in adolescents experiencing tinnitus in the acoustic chamber. Although risky listening habits were near universal, the teenagers experiencing tinnitus and reduced SLT tended to be more protective of their hearing. Tinnitus and reduced SLT could be early indications of a vulnerability to hidden synaptic injury that is prevalent among adolescents and expressed following exposure to high level environmental sounds.Tinnitus (chronic ringing of the ears) reduces quality of life for millions worldwide. Although the majority of cases are diagnosed after the age of 50 years, persistent tinnitus can occur at any age including in childhood and adolescence 1 . Neuroscience research suggests that most cases of tinnitus are caused, not by pathological increased auditory nerve activity in the cochlea related to otological disease, but by neuroplastic changes that occur in central auditory pathways following deafferentation of those pathways by damage to the cochlear transduction mechanism (inner and outer hair cells and their stereocilia) or to auditory nerve fibers (ANFs) that convey sound information from ribbon synapses on inner hair cells to the brain [2][3][4][5] . Damage to these cochlear structures (sensorineural hearing loss) can increase thresholds for sound detection measured by the clinical audiogram, and accordingly, audiometric hearing loss putatively caused by noise exposure or the aging process is present in most tinnitus sufferers 6 . However, not all tinnitus patients have abnormal audiograms. Cochlear pathology in these cases may involve, not low-threshold ANFs that are tapped by the audiogram, but high-threshold ANFs that depolarize (fire) only to suprathreshold sounds. Studies in a mouse model of hearing loss found that ~45% of ribbon synapses on high-threshold ANFs were permanently lost following exposure to a level of sound similar to that of some discotheques, with no loss of ribbon synapses on low threshold ANFs or persisting structural damage to cochlear hair cells or their stereocilia [7][8][9][10] . Consequently, wave I of the auditory br...

There was no evidence of minimal hearing damage in the audiometry and OAE. Nonetheless, the decreased LDL in adolescents with constant tinnitus suggests that their auditory system is more sensitive. Therefore, this may be the first sign of vulnerability to sounds. Future medium- to long-term monitoring of these students may show whether they will begin a process of functional impairment, altering hearing thresholds, and OAE.

Purpose To analyze the performance of normal-hearing adults with communication complaints in the Dichotic Sentences Test. Methods We selected from the database 15 normal-hearing participants with normal results in the Digits Dichotic Test, aged between 19 and 44 years, right-handed, who reported communicative complaints. The Dichotic Sentences Test was applied using two protocols consisting of four different combinations of lists called sequences 1 and 2, in the following order: training, divided attention step, right and left directed attention steps. Results In the first application sequence, the average performance in the divided attention step was 84.7% for the right ear and 60.67% for the left, with statistical difference between ears. The asymmetry between ears varied from -50% to 60%. In the directed attention step, the average performance was 99.33% for the right ear and 98% for the left, with no statistical difference. In the second application sequence, there was a tendency for better results, more pronounced for the left ear, with no statistical significance, with the performance variation and asymmetry between ears remaining high. In the comparison between the sequences, in the divided attention step, it was found that, for the right ear, 40% of the individuals did not vary, 33% performed worse, and 26.7% performed better; for the left ear, 6.6% did not vary, 20% performed worse, and 73.33% performed better. There was result stability in the directed attention step. Conclusion The normal-hearing adults with communication complaints presented a heterogeneous profile, especially in the divided attention step, with a marked difference between ears and response variability.