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Product Otoacoustic Emissions (product + otoacoustic_emission)
Kinds of Product Otoacoustic Emissions Selected AbstractsAuditory function and hearing loss in children and adults with Williams syndrome: Cochlear impairment in individuals with otherwise normal hearing,AMERICAN JOURNAL OF MEDICAL GENETICS, Issue 2 2010Jeffrey A. Marler Abstract Hearing loss is common in school-age individuals with Williams syndrome (WS) and extensive in adults. Prior studies with relatively small sample sizes suggest that hearing loss in WS has an early onset and may be progressive, yet the auditory phenotype and the scope of the hearing loss have not been adequately characterized. We used standard audiometric tools: Otoscopy, tympanometry, air-conduction (bone conduction when available) behavioral testing, and distortion product otoacoustic emissions (DPOAEs) to measure hearing sensitivity and outer hair cell function. We tested 81 individuals with WS aged 5.33,59.50 years. Sixty-three percent of the school-age and 92% of the adult participants had mild to moderately-severe hearing loss. The hearing loss in at least 50% was sensorineural. DPOAE testing corroborated behavioral results. Strikingly, 12 of 14 participants with hearing within normal limits bilaterally had 4,000-Hz DPOAE input/output (DPOAE IO) functions indicative of outer hair cell damage and impaired cochlear compression. Our results indicate that hearing loss is very common in WS. Furthermore, individuals with WS who have "normal" hearing as defined by behavioral thresholds may actually have sub-clinical impairments or undetected cochlear pathology. Our findings suggest outer hair cell dysfunction in otherwise normal hearing individuals. The DPOAE IO in this same group revealed growth functions typically seen in groups with noise-induced damage. Given this pattern of findings, individuals with WS may be at increased risk of noise-induced hearing loss. Recommendations regarding audiological testing for individuals with WS and accommodations for these individuals in both academic and nonacademic settings are provided. © 2010 Wiley-Liss, Inc. [source] Systemic steroid reduces long-term hearing loss in experimental pneumococcal meningitis,THE LARYNGOSCOPE, Issue 9 2010Lise Worsøe MD Abstract Objectives/Hypothesis: Sensorineural hearing loss is a common complication of pneumococcal meningitis. Treatment with corticosteroids reduces inflammatory response and may thereby reduce hearing loss. However, both experimental studies and clinical trials investigating the effect of corticosteroids on hearing loss have generated conflicting results. The objective of the present study was to determine whether systemic steroid treatment had an effect on hearing loss and cochlear damage in a rat model of pneumococcal meningitis. Study Design: Controlled animal study of acute bacterial meningitis. Methods: Adult rats were randomly assigned to two experimental treatment groups: a group treated with systemic steroid (n = 13) and a control group treated with saline (n = 13). Treatment was initiated 21 hours after infection and repeated once a day for three days. Hearing loss and cochlear damage were assessed by distortion product otoacoustic emissions (DPOAE), auditory brainstem response (ABR) at 16 kHz, and spiral ganglion neuron density. Results: Fifty-six days after infection, steroid treatment significantly reduced hearing loss assessed by DPOAE (P < .05; Mann-Whitney) and showed a trend toward reducing loss of viable neurons in the spiral ganglion (P = .0513; Mann-Whitney). After pooling data from day 22 with data from day 56, we found that systemic steroid treatment significantly reduced loss of spiral ganglion neurons (P = .0098; Mann-Whitney test). Conclusions: Systemic steroid treatment reduces long-term hearing loss and loss of spiral ganglion neurons in experimental pneumococcal meningitis in adult rats. The findings support a beneficial role of anti-inflammatory agents in reducing hearing loss and cochlear damage in meningitis. Laryngoscope, 2010 [source] Cochlear delays measured with distortion product otoacoustic emissionsCLINICAL OTOLARYNGOLOGY, Issue 4 2000S. Schneider Objective. To investigate the generation place and mechanism of distortion product otoacoustic emissions (DPOAEs) by measuring their delays. Materials and methods. Two tones with the frequencies f1 and f2 (f1 < f2) were presented to the ear canal of a guinea-pig by two telephones. The frequency of one of the tones was varied while the other was kept constant. The amplitude and phase of four DPOAEs (2f1,f2, 3f1,2f2, 4f1,3f2 and 2f2,f1) were measured as a function of frequency. From the phase vs. frequency relation of the DPOAE the cochlear delay is calculated, which is related to the place where the emission is generated. Results. Delays that were determined by varying the f1 frequency appear to be equal for all four distortion products. When the f2 frequency is varied, the delays of the DPOAEs with frequencies 2f1,f2, 3f1,2f2, 4f1,3f2 and 2f2,f1 are significantly larger than the delays of the DPOAE with frequency 2f2,f1. Conclusion. The DPOAEs 2f1,f2, 3f1,2f2 and 4f1,3f2 are generated at the same cochlear place, close to the characteristic place of the f2 frequency. The DPOAE with frequency 2f2,f1 comes from a more basal location in the cochlea. [source] |