Dataset Information

Severe Temporal Hyper-Activated States Caused by Noise in Tinnitus and Hyperacusis with Normal Hearing.

ABSTRACT: Lots of neuroimaging and animal studies have revealed that tinnitus and hyperacusis share the same patterns in the bottom up central auditory process. The aim was to identify the abnormal central patterns commonly observed in both tinnitus and hyperacusis in humans. We investigated two cases of normal hearing: a tinnitus patient and a hyperacusis patient. We compared the differences between the severe temporal hyper-activated state (STHS), with spikes, fast beta and gamma frequencies after noise exposure, and the mild temporal hyper-activated state (MTHS), in no sound exposed condition. The power of the gamma band in the two cases was increased in both auditory cortices compared to the other brain regions. Our results of human with normal hearing were the first to identify how tinnitus and hyperacusis caused by sound are abnormally active and how they maintain constant pathological states.

SUBMITTER: Bae EB

PROVIDER: S-EPMC6646893 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature

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Severe Temporal Hyper-Activated States Caused by Noise in Tinnitus and Hyperacusis with Normal Hearing.

Bae Eun Bit EB Lee Jun Ho JH

Journal of audiology & otology 20190625 3

Lots of neuroimaging and animal studies have revealed that tinnitus and hyperacusis share the same patterns in the bottom up central auditory process. The aim was to identify the abnormal central patterns commonly observed in both tinnitus and hyperacusis in humans. We investigated two cases of normal hearing: a tinnitus patient and a hyperacusis patient. We compared the differences between the severe temporal hyper-activated state (STHS), with spikes, fast beta and gamma frequencies after noise ...[more]

PMID: 31234248

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Project description:PurposeMany workers in developing countries are exposed to unsafe occupational noise due to inadequate health and safety practices. We tested the hypotheses that occupational noise exposure and aging affect speech-perception-in-noise (SPiN) thresholds, self-reported hearing ability, tinnitus presence, and hyperacusis severity among Palestinian workers.MethodPalestinian workers (N = 251, aged 18-70 years) without diagnosed hearing or memory impairments completed online instruments including a noise exposure questionnaire; forward and backward digit span tests; hyperacusis questionnaire; the short-form Speech, Spatial and Qualities of Hearing Scale (SSQ12); the Tinnitus Handicap Inventory; and a digits-in-noise (DIN) test. Hypotheses were tested via multiple linear and logistic regression models, including age and occupational noise exposure as predictors, and with sex, recreational noise exposure, cognitive ability, and academic attainment as covariates. Familywise error rate was controlled across all 16 comparisons using the Bonferroni-Holm method. Exploratory analyses evaluated effects on tinnitus handicap. A comprehensive study protocol was preregistered.ResultsNonsignificant trends of poorer SPiN performance, poorer self-reported hearing ability, greater prevalence of tinnitus, greater tinnitus handicap, and greater severity of hyperacusis as a function of higher occupational noise exposure were observed. Greater hyperacusis severity was significantly predicted by higher occupational noise exposure. Aging was significantly associated with higher DIN thresholds and lower SSQ12 scores, but not with tinnitus presence, tinnitus handicap, or hyperacusis severity.ConclusionsWorkers in Palestine may suffer from auditory effects of occupational noise and aging despite no formal diagnosis. These findings highlight the importance of occupational noise monitoring and hearing-related health and safety practices in developing countries.Supplemental materialhttps://doi.org/10.23641/asha.22056701.

Project description:ObjectivesTo determine whether suprathreshold measures of auditory function, such as distortion-product otoacoustic emissions (DPOAEs) and auditory brainstem responses (ABRs), are correlated with noise exposure history in normal-hearing human ears. Recent data from animal studies have revealed significant deafferentation of auditory nerve fibers after full recovery from temporary noise-induced hearing loss. Furthermore, these data report smaller ABR wave I amplitudes in noise-exposed animal ears when compared with non-noise-exposed control animals or prenoise exposure amplitudes in the same animal. It is unknown whether a similar phenomenon exists in the normal-hearing, noise-exposed human ear.DesignThirty normal-hearing human subjects with a range of noise exposure backgrounds (NEBs) participated in this study. NEB was quantified by the use of a noise exposure questionnaire that extensively queried loud sound exposure during the previous 12 months. DPOAEs were collected at three f2s (1, 2, and 4 kHz) over a range of L2s. DPOAE stimulus level began at 80 dB forward-pressure level and decreased in 10 dB steps. Two-channel ABRs were collected in response to click stimuli and 4 kHz tone bursts; one channel used an ipsilateral mastoid electrode and the other an ipsilateral tympanic membrane electrode. ABR stimulus level began at 90 dB nHL and was decreased in 10 dB steps. Amplitudes of waves I and V of the ABR were analyzed.ResultsA statistically significant relationship between ABR wave I amplitude and NEB was found for clicked-evoked ABRs recorded at a stimulus level of 90 dB nHL using a mastoid recording electrode. For this condition, ABR wave I amplitudes decreased as a function of NEB. Similar systematic trends were present for ABRs collected in response to clicks and 4 kHz tone bursts at additional suprathreshold stimulation levels (≥70 dB nHL). The relationship weakened and disappeared with decreases in stimulation level (≤60 dB nHL). Similar patterns were present for ABRs collected using a tympanic membrane electrode. However, these relationships were not statistically significant and were weaker and more variable than those collected using a mastoid electrode. In contrast to the findings for ABR wave I, wave V amplitude was not significantly related to NEB. Furthermore, there was no evidence of a systematic relationship between suprathreshold DPOAEs and NEB.ConclusionsA systematic trend of smaller ABR wave I amplitudes was found in normal-hearing human ears with greater amounts of voluntary NEB in response to suprathreshold clicks and 4 kHz tone bursts. These findings are consistent with the data from previous work completed in animals, where the reduction in suprathreshold responses was a result of deafferentation of high-threshold/low-spontaneous rate auditory nerve fibers. These data suggest that a similar mechanism might be operating in human ears after exposure to high sound levels. However, evidence of this damage is only apparent when examining suprathreshold wave I amplitude of the ABR. In contrast, suprathreshold DPOAE level was not significantly related to NEB. This was expected, given noise-induced auditory damage findings in animal ears did not extend to the outer hair cells, the generator for the DPOAE response.

Dataset Information

Severe Temporal Hyper-Activated States Caused by Noise in Tinnitus and Hyperacusis with Normal Hearing.

Publications

Severe Temporal Hyper-Activated States Caused by Noise in Tinnitus and Hyperacusis with Normal Hearing.

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