Behavioral auditory sensitivity11/5/2023 They attributed the speech perception scores that are disproportionate to pure tone hearing loss to these suprathreshold temporal processing deficits.Īnother factor that is reported to be related to speech perception abilities in these individuals is cortical evoked event related potentials. These temporal processing abnormalities had significant correlation with speech perception abilities. Rance et al also reported poor performance on the task involving timing cues (TMTF, temporal aspects of frequency discrimination) in a group of 14 children with AN. They also found a correlation between temporal modulation transfer function (TMTF) and speech perception abilities in their patients. Zeng et al reported the abnormal results on two measures of temporal perception in their group of children with AN: (i) gap detection threshold (identification of silence embedded in within the bursts of noise) and (ii) temporal modulation transfer function (measure of sensitivity to slow and fast amplitude fluctuation). Speech perception abilities in these patients appear to depend on the extent of suprathreshold temporal distortions of cues rather than access to speech spectrum, unlike the patients with sensory hearing loss. Some patients perform at the levels expected for patients with comparable degrees of sensory hearing loss and others show speech understanding which is disproportionate to their degree of hearing loss. Speech perception ability in these patients also varies considerably. Therefore, AN consists of many varieties depending on the sites of lesion. Some possible sites of lesion that could produce the audiometric and electrophysiological profile of AN include: inner hair cells, synaptic junction between inner hair cell and type I afferent nerve fibers, spiral ganglion cells, specific damage or demyelinization of type I auditory nerve fibers. Though the audiometric and electrophysiological findings are consistent with the 'retro outer hair cell dysfunction' exact site(s) of the pathology is yet to be determined. Presence of outer hair cell integrity in evoked otoacoustic emission or cochlear microphonics.Ībsence of synchronized neural activity at the level of 8 th nerve and brainstem. The clinical findings that define auditory neuropathy are The presence of MMN may not be directly linked to presence of behavioral discrimination and to speech perception capabilities at least in adults with auditory neuropathy.Īuditory neuropathy (AN) is recently described hearing disorder characterized by abnormal auditory nerve functioning in presence of normal cochlear receptor hair cell activity. Individuals with auditory neuropathy have severely affected temporal processing.Ģ. Many of the subjects with auditory neuropathy showed normal MMN even though they could not discriminate the stimulus contrast behaviorally. None of the measured evoked potential parameters correlated with the speech perception scores. In majority of individuals with auditory neuropathy P 1/N 1, P 2/N 2 complex and mismatch negativity could be elicited with normal amplitude and latency. Results revealed a significant correlation between temporal processing deficits and speech perception abilities. Auditory evoked potentials measures were, recording of P 1/N 1, P 2/N 2 complex and mismatch negativity (MMN). Psychophysical tests included measurement of open set speech identification scores, just noticeable difference for transition duration of syllable /da/ and temporal modulation transfer function. We studied the auditory evoked potentials and psychophysical abilities in 14 adults with auditory neuropathy to characterize their perceptual capabilities. The disproportionate loss of auditory percept in presence of normal cochlear function is suggestive of impairment of auditory neural synchrony. Speech perception abilities in these individuals are disproportionate to their hearing sensitivity and reported to be dependent on cortical evoked potentials and temporal processing abilities. Auditory neuropathy is a disorder characterized by no or severely impaired auditory brainstem responses in presence of normal otoacoustic emissions and/or cochlear microphonics.
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