Abstract
Auditory temporal processes in quiet are impaired in auditory neuropathy (AN) similar to normal hearing subjects tested in noise. N100 latencies were measured from AN subjects at several tone intensities in quiet and noise for comparison with a group of normal hearing individuals. Subjects were tested with brief 100 ms tones (1.0 kHz, 100-40 dB SPL) in quiet and in continuous noise (90 dB SPL). N100 latency and amplitude were analyzed as a function of signal intensity and audibility. N100 latency in AN in quiet was delayed and amplitude was reduced compared to the normal group; the extent of latency delay was related to psychoacoustic measures of gap detection threshold and speech recognition scores, but not to audibility. Noise in normal hearing subjects was accompanied by N100 latency delays and amplitude reductions paralleling those found in AN tested in quiet. Additional N100 latency delays and amplitude reductions occurred in AN with noise. N100 latency to tones and performance on auditory temporal tasks were related in AN subjects. Noise masking in normal hearing subjects affected N100 latency to resemble AN in quiet. N100 latency to tones may serve as an objective measure of the efficiency of auditory temporal processes.
Highlights
Auditory neuropathy (AN) describes patients with dysfunction of the auditory nerve in the presence of preserved cochlear outer hair-cell receptor functions (Starr et al, 1996)
In the presence of noise, N100 potentials to tones were progressively delayed and amplitudes reduced compared to tones in quiet starting at 90 dB SPL (SNR= 0)
The results of the present study demonstrate that auditory cortical N100 potentials to 1.0 kHz tones are prolonged in latency and reduced in amplitude in Auditory Neuropathy (AN) compared to normal hearing subjects
Summary
Auditory neuropathy (AN) describes patients with dysfunction of the auditory nerve in the presence of preserved cochlear outer hair-cell receptor functions (Starr et al, 1996). The diagnosis of AN is based primarily on physiological measures of function of auditory nerve and brainstem pathways, cochlear outer hair cells, and auditory middle-ear muscles. The criteria include: (1) absence or marked abnormalities of auditory brainstem responses (ABRs) beyond that expected for the degree of hearing loss; (2) preserved outer hair-cell activity including otoacoustic emissions (OAEs) and/or cochlear microphonics (CMs); and (3) absence of acoustic and preserved, non-acoustic middle-ear muscle reflexes (Berlin et al, 2003; Starr et al, 1996; 2001). Speech perception in other etiologies of AN are necessary to define if these defects are present
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