In rodents, exposure to high-level noise can destroy synapses between inner hair cells and auditory nerve fibers, without causing hair cell loss or permanent threshold elevation. Such “cochlear synaptopathy” is associated with amplitude reductions in wave I of the auditory brainstem response (ABR) at moderate-to-high sound levels. Similar ABR results have been reported in humans with tinnitus and normal audiometric thresholds, leading to the suggestion that tinnitus in these cases might be a consequence of synaptopathy. However, the ABR is an indirect measure of synaptopathy and it is unclear whether the results in humans reflect the same mechanisms demonstrated in rodents. Measures of noise exposure were not obtained in the human studies, and high frequency audiometric loss may have impacted ABR amplitudes. To clarify the role of cochlear synaptopathy in tinnitus with a normal audiogram, we recorded ABRs, envelope following responses (EFRs), and noise exposure histories in young adults with tinnitus and matched controls. Tinnitus was associated with significantly greater lifetime noise exposure, despite close matching for age, sex, and audiometric thresholds up to 14 kHz. However, tinnitus was not associated with reduced ABR wave I amplitude, nor with significant effects on EFR measures of synaptopathy. These electrophysiological measures were also uncorrelated with lifetime noise exposure, providing no evidence of noise-induced synaptopathy in this cohort, despite a wide range of exposures. In young adults with normal audiograms, tinnitus may be related not to cochlear synaptopathy but to other effects of noise exposure.
Objective: This study sought to investigate whether the size of the target used in the horizontal vHIT has an effect on the saccade profile of healthy subjects, and to expand upon previous work linking age to the existence of small vHIT saccades. Methods: Forty eight participants were recruited between 18 and 77 years of age, with no history of vestibular, oculomotor or neurological conditions and a visual acuity of at least 0.3 LogMAR. Participants underwent four consecutive horizontal vHIT trials using the standard target size and three smaller targets. VOR gain and metrics for saccadic incidence, peak eye velocity and latency were then extracted from results. Results: Target size was a statistically significant influence on saccade metrics. As target size increased, saccadic incidence decreased while peak eye velocity and latency increased. However, a potential order effect was also discovered, and once this was corrected for the remaining effect of target size was small and is likely clinically insignificant. The effect of age was much stronger than target size; increasing age was strongly positively correlated with saccadic incidence and showed a medium size correlation with peak velocity, though not with saccadic latency. Conclusion: While this study suggests that target size may have a statistically significant impact on the vHIT saccade profile of normal subjects, age has a greater influence on the incidence and size of small vHIT saccades.
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