86 research outputs found
Fitting model of ABR age dependency in a clinical population of normal hearing children
The purpose of this study was to present a simple and powerful fitting model that describes age-dependent changes of auditory brainstem responses (ABR) in a clinical population of normal hearing children. A total of 175 children (younger than 200Â weeks postconceptional age) were referred for audiologic assessment with normal ABR results. ABR parameters of normal hearing children between 2003 and 2008 were included. The results of the right ears recorded at 90Â dB nHL were analyzed. A simple and accurate fitting model was formulated based on these data. A very similar age-dependent effect was found for peaks III and V, and IâIII and IâV intervals; latencies decrease as postconceptional age increases. It shows that the total age-dependent effect will be completed after 1.5â2Â years. The age-dependent effect can be modeled by a relatively simple and accurate exponential function. This fitting model can be easily implemented to analyze ABR results of infants in daily clinical practice. We speculate about the underlying physiological processes
Incidence and clinical value of prolonged IâV interval in NICU infants after failing neonatal hearing screening
Infants admitted to neonatal intensive care units (NICUs) have a higher incidence of perinatal complications and delayed maturational processes. Parameters of the auditory brainstem response (ABR) were analyzed to study the prevalence of delayed auditory maturation or neural pathology. The prevalence of prolonged IâV interval as a measure of delayed maturation and the correlation with ABR thresholds were investigated. All infants admitted to the NICU Sophia Childrenâs Hospital between 2004 and 2009 who had been referred for ABR measurement after failing neonatal hearing screening with automated auditory brainstem response (AABR) were included. The ABR parameters were retrospectively analyzed. Between 2004 and 2009, 103 infants were included: 46 girls and 57 boys. In 58.3% (60 infants) of our population, the IâV interval was recordable in at least one ear at first diagnostic ABR measurement. In 4.9%, the IâV interval was severely prolonged. The median ABR threshold of infants with a normal or mildly prolonged IâV interval was 50Â dB. The median ABR threshold of infants with a severely prolonged IâV interval was 30Â dB. In conclusion, in case both peak I and V were measurable, we found only a limited (4.9%) incidence of severely prolonged IâV interval (â„0.8Â ms) in this high-risk NICU population. A mild delay in maturation is a more probable explanation than major audiologic or neural pathology, as ABR thresholds were near normal in these infants
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Auditory neuropathy in childhood.
ObjectivesAuditory neuropathy is a recently described disorder in which patients demonstrate hearing loss for pure tones, impaired word discrimination out of proportion to pure tone loss, absent or abnormal auditory brainstem responses, and normal outer hair cell function as measured by otoacoustic emissions and cochlear microphonics. We have identified eight pediatric patients having hearing deficits that are most likely due to a neuropathy of the eighth nerve. In this study, the results of audiologic testing performed with these eight children are described.Study designRetrospective review of audiologic findings in eight children with auditory neuropathy.MethodsEach subject was tested with pure tone and speech audiologic testing, auditory brainstem response, and click-evoked otoacoustic emissions. Results of these tests were tabulated and summarized.ResultsPure tone audiologic testing revealed five children with upsloping sensorineural hearing loss, two with high frequency loss, and one with a mild, flat configuration. Six children demonstrated poor word discrimination scores, and the other two had fair to good word discrimination. All eight subjects had normal distortion product and transient otoacoustic emissions. All eight children demonstrated absent or marked abnormalities of brainstem auditory evoked potentials. These findings suggest that while cochlear outer hair cell function is normal, the lesion is located at the eighth nerve.ConclusionsRecent advances in otoacoustic emissions testing permit differentiation of neural deafness from sensory deafness. This paper describes the clinical presentation and audiologic findings in pediatric auditory neuropathy, as well as the recommended management of these patients. Otolaryngologists should be aware of this disorder and implications for its management, which differs from treatment of sensorineural hearing loss
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Temporal and speech processing deficits in auditory neuropathy.
Auditory neuropathy affects the normal synchronous activity in the auditory nerve, without affecting the amplification function in the inner ear. Patients with auditory neuropathy often complain that they can hear sounds, but cannot understand speech. Here we report psychophysical tests indicating that these patients' poor speech recognition is due to a severe impairment in their temporal processing abilities. We also simulate this temporal processing impairment in normally hearing listeners and produce similar speech recognition deficits. This study demonstrates the importance of neural synchrony for auditory perceptions including speech recognition in humans. The results should contribute to better diagnosis and treatment of auditory neuropathy
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Auditory neuropathy.
Ten patients presented as children or young adults with hearing impairments that, by behavioural and physiological testing, were compatible with a disorder of the auditory portion of the VIII cranial nerve. Evidence of normal cochlear outer hair cell function was provided by preservation of otoacoustic emissions and cochlear microphonics in all of the patients. Auditory brainstem potentials showed evidence of abnormal auditory pathway function beginning with the VIII nerve: the potentials were absent in nine patients and severely distorted in one patient. Auditory brainstem reflexes (middle ear muscles; crossed suppression of otoacoustic emissions) were absent in all of the tested patients. Behavioural audiometric testing showed a mild to moderate elevation of pure tone threshold in nine patients. The extent of the hearing loss, if due to cochlear receptor damage, should not have resulted in the loss of auditory brainstem potentials. The shape of the pure tone loss varied, being predominantly low frequency in five patients, flat across all frequencies in three patients and predominantly high frequency in two patients. Speech intelligibility was tested in eight patients, and in six was affected out of proportion to what would have been expected if the pure tone loss were of cochlear origin. The patients were otherwise neurologically normal when the hearing impairment was first manifest. Subsequently, eight of these patients developed evidence for a peripheral neuropathy. The neuropathy was hereditary in three and sporadic in five. We suggest that this type of hearing impairment is due to a disorder of auditory nerve function and may have, as one of its causes, a neuropathy of the auditory nerve, occurring either in isolation or as part of a generalized neuropathic process
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