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Hearing Disorders: HELP
Articles by Gary W. Harding
Based on 3 articles published since 2009
(Why 3 articles?)

Between 2009 and 2019, G. W. Harding wrote the following 3 articles about Hearing Disorders.
+ Citations + Abstracts
1 Article Time course of organ of Corti degeneration after noise exposure. 2017

Bohne, Barbara A / Kimlinger, Melissa / Harding, Gary W. ·Washington University in St. Louis, Department of Otolaryngology, Box 8115, 660 South Euclid Avenue, St. Louis, MO 63110, USA. Electronic address: bohneb@ent.wustl.edu. · St. Louis University, One North Grand Blvd., St. Louis, MO 63103, USA. · Washington University in St. Louis, Department of Otolaryngology, Box 8115, 660 South Euclid Avenue, St. Louis, MO 63110, USA. ·Hear Res · Pubmed #27890677.

ABSTRACT: From our permanent collection of plastic-embedded flat preparations of chinchilla cochleae, 22 controls and 199 ears from noise-exposed animals were used to determine when, postexposure, hair cell (HC) and supporting cell (SC) degeneration were completed. The exposed ears were divided into four groups based on exposure parameters: 0.5- or 4-kHz octave band of noise at moderate (M) or high (H) intensities. Postexposure survival ranged from <1 h to 2.5 y. Ears fixed ≤ 0-12 h postexposure were called 'acute'. For 'chronic' ears, postexposure survival was ≥7 d for groups 0.5M and 4M, ≥ 1 mo for the 4H group and ≥7 mo for the 0.5H group. The time course of inner-ear degeneration after noise exposure was determined from data in the 0.5H and 4H groups because these groups contained ears with intermediate survival times. Outer hair cells (OHCs) began dying during the exposure. OHC loss slowed down beyond 1 mo but was still present. Conversely, much inner hair cell loss was delayed until 1-3 wk postexposure. Outer pillar and inner pillar losses were present at a low level in acute ears but increased exponentially thereafter. These results are the first to demonstrate quantitatively that hair cells (HCs) and supporting cells (SCs) may continue to degenerate for months postexposure. With short postexposure survivals, the remaining SCs often had pathological changes, including: buckled pillar bodies, shifted Deiters' cell (DC) nuclei, detachment of DCs from the basilar membrane and/or splitting of the reticular lamina. These pathological changes appeared to allow endolymph and perilymph to intermix in the fluid spaces of the organ of Corti, damaging additional HCs, SCs and nerve fibers. This mechanism may account for some postexposure degeneration. In ears exposed to moderate noise, some of these SC changes appeared to be reversible. In ears exposed to high-level noise, these changes appeared to indicate impending degeneration.

2 Article Calibrated finger rub auditory screening test (CALFRAST). 2009

Torres-Russotto, D / Landau, W M / Harding, G W / Bohne, B A / Sun, K / Sinatra, P M. ·Department of Neurology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA. drtorres@unmc.edu ·Neurology · Pubmed #19414727.

ABSTRACT: BACKGROUND: Determination of auditory function is a fundamental part of a complete neurologic examination. Disability from permanent hearing loss is common in the general population. Current bedside auditory tests are unreliable and cumbersome. We evaluated the calibrated finger rub auditory screening test (CALFRAST) as a routine diagnostic tool. METHODS: The sound spectrum and mean peak intensities of standard finger rub were measured, as well as background noise. CALFRAST overlapped the frequency spectrum of normal speech. Patients and companions were recruited from a neurology clinic. With arms extended, two stimulus intensities were presented: strong finger rub (CALFRAST-Strong 70) and the faintest rub that the examiner could hear (CALFRAST-Faint 70). With subjects' eyes closed, each ear's CALFRAST threshold was ascertained and then compared with its audiometric measure. The normal threshold was considered to be 25 dB. Validity, reliability, and discrimination abilities were obtained using standard methods. RESULTS: Two hundred twenty-one subjects (442 ears; 58% women) were examined. Ages ranged from 18 to 88 years, with a mean of 46 years. Eighty-five subjects (39%) had some degree of hearing loss. Both specificity and positive predictive value of CALFRAST-Strong 70 were 100%. Both sensitivity and negative predictive value of CALFRAST-Faint 70 were 99%, with a negative likelihood ratio <0.1. Area under the receiver operating characteristic curve was 0.94, consistent with excellent discrimination ability. Both intrarater and interrater reliability were excellent, both kappa >0.8. Subjects' self-assessment of hearing was unreliable. CONCLUSION: The calibrated finger rub auditory screening test (CALFRAST) is simple, accurate, inexpensive, and reliable. As a routine screening tool, CALFRAST may contribute to more efficient identification of auditory impairment.

3 Article Relation of focal hair-cell lesions to noise-exposure parameters from a 4- or a 0.5-kHz octave band of noise. 2009

Harding, Gary W / Bohne, Barbara A. ·Department of Otolaryngology, Box 8115, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA. hardingg@ent.wustl.edu ·Hear Res · Pubmed #19393307.

ABSTRACT: In a previous study, we examined the relation between total energy in a noise exposure and the percentage losses of outer (OHC) and inner (IHC) hair cells in the basal and apical halves of 607 chinchilla cochleae [Harding, G.W., Bohne, B.A., 2004a. Noise-induced hair-cell loss and total exposure energy: analysis of a large data set. J. Acoust. Soc. Am. 115, 2207-2220]. The animals had been exposed continuously to either a 4-kHz octave band of noise (OBN) at 47-108 dB SPL for 0.5h-36 d, or a 0.5-kHz OBN at 65-128 dB SPL for 3.5h-433 d. Interrupted exposures were also employed with both OBNs. Post-exposure recovery times ranged from 0 to 913 days. Cluster analysis was used to separate the data into three magnitudes of damage. The data were also separated into recovery times of 0 days (acute) and >0 days (chronic) and the apical and basal halves of the organ of Corti (OC). A substantial part of these hair-cell losses occurred in focal lesions (i.e., >or=50% loss of IHCs, OHCs or both over a distance of >or=0.03 mm). This aspect of the damage from noise was not included in the previous analysis. The present analysis describes, within the same three clusters, the apex-to-base distribution of 1820 focal lesions found in 468 of 660 (71%) noise-exposed cochleae. In these cochleae, OC length in mm was converted to percent distance from the apex. The lesion data were analyzed for location in percent distance from the apex and size (mm) of the lesions. In 55 of 140 (39%) non-noise-exposed, control OCs, there were 186 focal hair-cell lesions, the characteristics of which were also determined. Focal lesions with hair-cell loss >or=50% involved predominantly OHCs, IHCs only, or both OHCs and IHCs (i.e., combined OHC-IHC lesions). The predominantly OHC and combined lesions were pooled together for the analysis. The distributions of lesion location (in percent distance from the apex), weighted by lesion size (in percent of OC length) were tallied in 2%-distance bins. In controls, focal lesions were uniformly distributed from apex to base and 70% of them were pure IHC lesions. In cochleae exposed to the 4-kHz OBN, lesions were distributed throughout the basal half of the OC. In cochleae exposed to the 0.5-kHz OBN, lesions occurred in both halves of the OC. With continuous exposures, 74% of the lesions were predominantly OHC or combined lesions. With interrupted exposures, 52% of the lesions were OHC or combined lesions. Lesion size was generally larger in the chronic compared to acute cochleae with similar exposures. There was a minimum total energy at which focal lesions began to appear and slightly higher energies resulted in nearly all exposed cochleae having focal lesions.