High-Frequency Cochlear Amplifier Dysfunction: A Dominating Contribution to the Cognitive-Ear Link

Objective: The objective of this study was to investigate the role of the high-frequency cochlear dysfunction in the cognitive-ear link.Methods: Seventy-four presbycusis patients (PC group) and seventy-one age-, sex-, and education-level matched normal hearing controls (NH group) were recruited in this study. Participants underwent a battery of cognitive tests estimated by Montreal Cognitive Assessment (MoCA), Stroop Color-Word Interference Test (Stroop), Symbol Digit Modalities Test (SDMT), Auditory Verbal Learning Test (AVLT), and Trail-Making Test (TMT-A and B), as well as auditory tests including distortion product otoacoustic emission (DPOAE), pure tone (PT) thresholds, and speech reception thresholds (SRT). Data were analyzed using the factor analysis, partial correlation analysis, multiple linear regression models, and mediation models.Results: Distortion product otoacoustic emission detection amplitudes and PT thresholds performed worse gradually from low to high frequencies in both the NH and PC groups. High-frequency DPOAE (H-DPOAE) was significantly correlated with cognitive domains in the PC group (AVLT: r = 0.30, p = 0.04; SDMT: r = 0.36, p = 0.01; Stroop: r = –0.32, p = 0.03; TMT-A: r = –0.40, p = 0.005; TMT-B: r = –0.34, p = 0.02). Multiple linear regression models showed that H-DPOAE predicted cognitive impairment effectively for aspects of memory (R2 = 0.27, 95% CI, 0.03 to 1.55), attention (R2 = 0.32, 95% CI, –6.18 to –0.40), processing speed (R2 = 0.37, 95% CI, 0.20 to 1.64), and executive function (TMT-A: R2 = 0.34, 95% CI, –5.52 to 1.03; TMT-B: R2 = 0.29, 95% CI, –11.30 to –1.12). H-DPOAE directly affected cognition and fully mediated the relationship between pure tone average (PTA)/SRT and cognitive test scores, excluding MoCA.Conclusion: This study has demonstrated that the high-frequency cochlear amplifier dysfunction has a direct predictive effect on the cognitive decline and makes a large contribution to the cognitive-ear link.

The Effects of Clinical Factors and Neonatal Morbidities on Hearing Screening Among Neonatal Admissions

Background: Hearing loss is an important disorder affecting newborns admitted to NICU. A national hearing screening program using otoacoustic emission testing is an essential tool to identify hearing loss early in neonates enabling early intervention to avoid further challenges of pediatric deafness. On the other hand, a delay of the auditory pathway maturation in preterm babies compared to term newborns has already been suggested in the literature. Taking this information into account, in this paper, we aim to identify the best time to perform NICU infant hearing screening tests. Objectives: We aim to study the clinical factors and neonatal morbidities that may affect neonatal hearing screening results using otoacoustic emission test, in order to decrease the false positive test results that increase parental anxiety and increase the need for subsequent investigations. Methods: This is a prospective cross-sectional study that included 204 infants who were admitted to a tertiary referral hospital NICU unit between September 2017 and May 2018. Both transient evoked otoacoustic emissions (TEOAE) and distortion product otoacoustic emission (DPOAE) screening tests were performed in order to screen hearing loss. Results: Our study included 204 infants, 52.9% of which were males and 47.1% females. There were correlations between both hyperbilirubinemia and ventilation ≥5 days and the failure rate of the first OAE test results among NICU infants where the P-values were (p=0.0133) and (p=0.0456) respectively. Moreover, 165 babies (80.9%) passed the first OAE with a mean birth weight of 2759 gram and mean maternal age of 30.6 years, while 39 babies (19.1%) failed the test with a mean birth weight of 2436 gram and mean maternal age of 32 years. There was no statistically significant relation between both maternal age and birth weight with failure of the first screening test. Conclusion: Our study suggests a higher failure rate of the first OAE in NICU infants who had hyperbilirubinemia or ventilation ≥5 days. Therefore, our recommendation is to postpone the first phase of hearing screening for those infants until the first scheduled vaccine appointment to achieve high compliance to attendance and decrease distress to the family that can be associated with false-negative results of the test.

Deletion of Oncomodulin Gives Rise to Early Progressive Cochlear Dysfunction in C57 and CBA Mice

Ca2+ signaling is a major contributor to sensory hair cell function in the cochlea. Oncomodulin (OCM) is a Ca2+ binding protein (CaBP) preferentially expressed in outer hair cells (OHCs) of the cochlea and few other specialized cell types. Here, we expand on our previous reports and show that OCM delays hearing loss in mice of two different genetic backgrounds: CBA/CaJ and C57Bl/6J. In both backgrounds, genetic disruption of Ocm leads to early progressive hearing loss as measured by auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE). In both strains, loss of Ocm reduced hearing across lifetime (hearing span) by more than 50% relative to wild type (WT). Even though the two WT strains have very different hearing spans, OCM plays a considerable and similar role within their genetic environment to regulate hearing function. The accelerated age-related hearing loss (ARHL) of the Ocm KO illustrates the importance of Ca2+ signaling in maintaining hearing health. Manipulation of OCM and Ca2+ signaling may reveal important clues to the systems of function/dysfunction that lead to ARHL.

Effects of Calcitonin-Gene-Related-Peptide on Auditory Nerve Activity

Calcitonin-gene-related peptide (CGRP) is a lateral olivocochlear (LOC) efferent neurotransmitter. Depression of sound-driven auditory brainstem response amplitude in CGRP-null mice suggests the potential for endogenous CGRP release to upregulate spontaneous and/or sound-driven auditory nerve (AN) activity. We chronically infused CGRP into the guinea pig cochlea and evaluated changes in AN activity as well as outer hair cell (OHC) function. The amplitude of both round window noise (a measure of ensemble spontaneous activity) and the synchronous whole-nerve response to sound (compound action potential, CAP) were enhanced. Lack of change in both onset adaptation and steady state amplitude of sound-evoked distortion product otoacoustic emission (DPOAE) responses indicated CGRP had no effect on OHCs, suggesting the origin of the observed changes was neural. Combined with results from the CGRP-null mice, these results appear to confirm that endogenous CGRP enhances auditory nerve activity when released by the LOC neurons. However, infusion of the CGRP receptor antagonist CGRP (8–37) did not reliably influence spontaneous or sound-driven AN activity, or OHC function, results that contrast with the decreased ABR amplitude measured in CGRP-null mice.

Effect of Radiofrequency Waves of Mobile Phones on Distortion Product Otoacoustic Emissions

Objective The prolonged exposure to electromagnetic fields of mobile phones can damage the cochlear hair cells, which can be detected by otoacoustic emission (OAE). To know the effect of mobile phones on hearing, the young volunteers were subjected to prolonged mobile phone usage and changes in OAE were recorded. Materials and Methods Twenty-eight volunteers with normal hearing were made to talk one full hour continuously on the mobile phone. Distortion product otoacoustic emission (DPOAE) was measured prior to the usage of mobile phones and immediately after the use (post-exposure 1) and 24 hours after the use (post-exposure 2). The values were compared. Results Out of the 28 volunteers, 20 were females and 8 were males. Twenty-one volunteers preferred the right ear while using mobile phones, 7 preferred the left ear. There was no statistically significant difference between the baseline DPOAE values and values of post-exposure 1 and 2 when only the preferred ear was taken into consideration. When the preferred ear was compared with nonpreferred ear, a statistically significant difference was found only in the low frequencies between the pre-exposure and post-exposure 1 values. Conclusion This study shows there was no significant correlation between OAE and prolonged mobile phone exposure when the preferred ear was not considered.

Inner hair cell dysfunction in Klhl18 mutant mice leads to low frequency progressive hearing loss

Age-related hearing loss in humans (presbycusis) typically involves impairment of high frequency sensitivity before becoming progressively more severe at lower frequencies. Pathologies initially affecting lower frequency regions of hearing are less common. Here we describe a progressive, predominantly low-frequency recessive hearing impairment in two mutant mouse lines carrying different mutant alleles of the Klhl18 gene: a spontaneous missense mutation (Klhl18lowf) and a targeted mutation (Klhl18tm1a(KOMP)Wtsi). Both males and females were studied, and the two mutant lines showed similar phenotypes. Threshold for auditory brainstem responses (ABR; a measure of auditory nerve and brainstem neural activity) were normal at 3 weeks old but showed progressive increases from 4 weeks onwards. In contrast, distortion product otoacoustic emission (DPOAE) sensitivity and amplitudes (a reflection of cochlear outer hair cell function) remained normal in mutants. Electrophysiological recordings from the round window of Klhl18lowf mutants at 6 weeks old revealed 1) raised compound action potential thresholds that were similar to ABR thresholds, 2) cochlear microphonic potentials that were normal compared with wildtype and heterozygous control mice and 3) summating potentials that were reduced in amplitude compared to control mice. Scanning electron microscopy showed that Klhl18lowf mutant mice had abnormally tapering of the tips of inner hair cell stereocilia in the apical half of the cochlea while their synapses appeared normal. These results suggest that Klhl18 is necessary to maintain inner hair cell stereocilia and normal inner hair cell function at low frequencies.

Does Oral Monosodium Glutamate Have a Cochleotoxic Effect? An Experimental Study

<b><i>Introduction:</i></b> The effect of orally consumed monosodium glutamate (MSG), which is a common additive in the food industry, on the cochlea has not been investigated. The present study aimed to investigate the possible cochleotoxic effects of oral MSG in guinea pigs using electrophysiological, biochemical, and histopathological methods. <b><i>Methods:</i></b> Thirty guinea pigs were equally divided into control and intervention groups (MSG 100 mg/kg/day; MSG 300 mg/kg/day). At 1 month, 5 guinea pigs from each group were sacrificed; the rest were observed for another month. Electrophysiological measurements (distortion product otoacoustic emission [DPOAE] and auditory brainstem response [ABR]), glutamate levels in the perilymph and blood samples, and histopathological examinations were evaluated at 1 and 2 months. <b><i>Results:</i></b> Change in signal-to-noise ratio at 2 months was significantly different in the MSG 300 group at 0.75 kHz and 2 kHz (<i>p</i> = 0.013 and <i>p</i> = 0.044, respectively). There was no statistically significant difference in ABR wave latencies of the guinea pigs given MSG compared to the control group after 1 and 2 months; an increase was noted in ABR thresholds, although the difference was not statistically significant. In the MSG groups, moderate-to-severe degeneration and cell loss in outer hair cells, support cells, and spiral ganglia, lateral surface junction irregularities, adhesions in stereocilia, and partial loss of outer hair cell stereocilia were noted. <b><i>Conclusion:</i></b> MSG, administered in guinea pigs at a commonly utilized quantity and route of administration in humans, may be cochleotoxic.

Effect of Caffeine on Otoacoustic Emissions

Introduction Caffeine is consumed everyday in a variety of ways by a large population around the world, including coffee, tea, and soft drinks. Therefore, there is a significant need to explore the effects of caffeine on human auditory system. The present study aimed to investigate the effect of caffeine on cochlea using distortion product otoacoustic emission (DPOAE). Materials and Methods Thirty-three young adults were recruited for the study. The effect of caffeine on cochlea was assessed using DPOAE at frequencies between 1 to 10 kHz before and after caffeine consumption. Results The signal to noise ratio of DPOAE was compared before and after coffee intake, which revealed no significant differences. Conclusion The current study results suggest that caffeine has no effect on cochlear functioning.

Measuring Distortion-Product Otoacoustic Emission With a Single Loudspeaker in the Ear: Stimulus Design and Signal Processing Techniques

The distortion-product otoacoustic emission (DPOAE) is a backward propagating wave generated inside the cochlea during the wave amplification process. The DPOAE signal can be detected rapidly under relatively noisy conditions. In recent years, the earphone industry demonstrated interest in adopting DPOAE as an add-on feature to make their product “intelligent” of inner-ear status. However, a technical challenge remains to be tackled—the loudspeaker in an earphone generates its own cubic distortion at the same frequency as DPOAE. Unfortunately, the intensity of loudspeaker distortion is typically comparable to that of the DPOAE, if not higher. In this research, we propose two strategies, namely compensation and cancellation, to enable DPOAE measurement with a single loudspeaker. The compensation strategy exploits the part of the growth function of the loudspeaker distortion which is almost linear, and thus suppresses the distortion it generates while retaining a larger portion of DPOAE in the residual signal. The cancellation strategy utilizes a one-dimensional Volterra filter to remove the cubic distortion from the loudspeaker. Testing on normal-hearing ears shows that the compensation strategy improved the DPOAE-to-interference ratio by approximately 7 dB, resulting in a cross-correlation of 0.62 between the residual DPOAE level and the true DPOAE level. Meanwhile, the cancellation strategy directly recovered both the magnitude and the phase of DPOAE, reducing the magnitude estimation error from 15.5 dB to 3.9 dB in the mean-square sense. These pilot results suggest that the cancellation strategy may be suitable for further testing with more subjects.