Neural correlates of auditory processing following exposure to an augmented acoustic environment

Thesis (Ph. D.)--University of Rochester. Dept. of Biomedical Engineering, 2010.Each year as many as 3/1000 children are diagnosed with congenital sensorineural hearing loss. Common in these children are delays in grammar comprehension, vocabulary retention and speech development, related to temporal processing abilities. Studies in a mouse model of congenital sensorineural hearing loss suggest that early exposure to an augmented acoustic environment (AAE) limits outer hair cell death and maintains peripheral auditory thresholds. However, there have been no studies on the effects of AAE on neural encoding in the central auditory system. The goal of these experiments is to investigate midbrain auditory processing in a mouse model (the DBA strain) of sensorineural hearing loss, and determine the effects of AAE exposure. It is clear that sound exposure during the early developmental period has profound effects on neural processing in the central auditory system of normal-hearing subjects. Questions remain on the effects of such sound exposure on a model of hearing impairment. In Aim I of this study we presented a novel temporal AAE containing silent gaps embedded in noise bursts to DBA mice and examined the frequency representation, intensity encoding and temporal processing in the auditory midbrain. Mice were exposed to a traditional AAE stimulus, a novel temporal AAE stimulus, or no stimulus from birth to P30. Auditory brainstem responses (ABRs) and distortion product otoacoustic emissions (DPOAEs) were recorded to assess peripheral auditory function. To assess the effects on central auditory processing we recorded neural activity from a 16-channel electrode in the inferior colliculus (IC). We confirmed peripheral preservation with AAE exposure, and expanded these results to demonstrate outer hair cell functional preservation. In the midbrain we demonstrated that IC neurons showed decreased thresholds, that high best-frequency units were maintained, tuning sharpness was improved, excitatory drive was increased and most importantly, units displayed shorter neural gap thresholds. Additionally, only mice exposed to our novel temporal AAE demonstrated significantly shortened mean gap threshold at low carrier levels, and in the presence of continuous background noise. To be useful as a therapeutic intervention the effect of onset time on central auditory function must be examined. Additionally, it is not known if the improvements provided by AAE exposure will remain after exposure cessation. In Aim II of this study we asked whether delaying the exposure onset or altering its duration influence the improvements in neural processing noted above. Again DBA mice were exposed to a traditional AAE stimulus or no stimulus from birth to P60. Two additional groups were included, one exposed for 30 days followed by 30 days of no exposure (On/Off), the other not exposed until P30 followed by 30 days of exposure (Off/On). All animals were tested at P60. Again ABRs and DPOAEs were recorded to assess peripheral auditory function, and central auditory processing was measured using a 16-channel electrode in the IC. We determined that the onset time of exposure is of little importance in demonstrating improvements in both peripheral and central auditory system. However, continued exposure is essential to maintain the beneficial effects and limit functional loss. Our results demonstrate that AAE preserves peripheral structure and function and improves central auditory processing, that a targeted temporal AAE can improve neural correlates of temporal processing, and that the timing of AAE is essential in delaying the progression of sensorineural hearing loss. These experiments pave the way for possible therapeutic intervention in children suffering congenital sensorineural hearing loss

Pediatric trainees systematically under-report duty hour violations compared to electronic health record defined shifts.

Duty hour monitoring is required in accredited training programs, however trainee self-reporting is onerous and vulnerable to bias. The objectives of this study were to use an automated, validated algorithm to measure duty hour violations of pediatric trainees over a full academic year and compare to self-reported violations. Duty hour violations calculated from electronic health record (EHR) logs varied significantly by trainee role and rotation. Block-by-block differences show 36.8% (222/603) of resident-blocks with more EHR-defined violations (EDV) compared to self-reported violations (SRV), demonstrating systematic under-reporting of duty hour violations. Automated duty hour tracking could provide real-time, objective assessment of the trainee work environment, allowing program directors and accrediting organizations to design and test interventions focused on improving educational quality

Loss of the Cochlear Amplifier Prestin Reduces Temporal Processing Efficacy in the Central Auditory System

Active mechanical amplification of sound occurs in cochlear outer hair cells (OHCs) that change their length with oscillations of their membrane potential. Such length changes are the proposed cellular source of the cochlear amplifier, and prestin is the motor protein responsible for OHC electromotility. Previous findings have shown that mice lacking prestin displayed a loss of OHC electromotility, subsequent loss of distortion-product otoacoustic emissions, and a 40–60 dB increase in hearing thresholds. In this study we were interested in studying the functional consequences of the complete loss of cochlear amplification on neural coding of frequency selectivity, tuning, and temporal processing in the auditory midbrain. We recorded near-field auditory evoked potentials and multi-unit activity from the inferior colliculus (IC) of prestin (−/−) null and prestin (+/+) wild-type control mice and determined frequency response areas (FRAs), tuning sharpness, and gap detection to tone bursts and silent gaps embedded in broadband noise. We were interested in determining if the moderate to severe sensorineural hearing loss associated with the loss of motor protein prestin would also impair auditory midbrain temporal-processing measures, or if compensatory mechanisms within the brainstem could compensate for the loss of prestin. In prestin knockout mice we observed that there are severe impairments in midbrain tuning, thresholds, excitatory drive, and gap detection suggesting that brainstem and midbrain processing could not overcome the auditory processing deficits afforded by the loss of OHC electromotility mediated by the prestin protein