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.

Distortion product otoacoustic emission suppression tuning curves in human adults and neonates.

Distortion product otoacoustic emission (DPOAE) iso-suppression tuning curves (STC) were generated in 15 normal-hearing adults and 16 healthy term-born neonates for three f2 frequencies. The 2f1-f2 DPOAE was elicited using f2/f1 = 1.2, LI = 1.2, LI = 65 and L2 = 50 dB SPL. A suppressor tone was presented at frequencies ranging from 1 octave below to 1/4 octave above f2 and varied in level until DPOAE amplitude was reduced by 6 dB. The suppressor level required for 6 dB suppression was plotted as function of suppressor frequency to generate a DPOAE STC. Forward-masked psychoacoustic tuning curves (PTC) were obtained for three of the adult subjects. Results indicate that DPOAE STCs are stable and show minimal inter- and intra-subject variability. The tip of the STC is consistently centered around the f2 region and STCs are similar in shape, width (Q10) and slope to VIIIth-nerve TCs. PTCs and STCs measured in the same subject showed similar trends, although PTCs had narrower width and steeper slope. Neonatal STCs were recorded at 3000 and 6000 Hz only and were comparable in shape, width and slope to adult STCs. Results suggest: (1) suppression of the 2f1-f2 DPOAE may provide an indirect measure of cochlear frequency resolution in humans and (2) cochlear tuning, and associated active processes in the cochlea, are mature by term birth for at least mid- and high-frequencies. These results provide significant impetus for continued study of DPOAE suppression as a means of evaluating cochlear frequency resolution in humans.

Possible origins of the non-monotonic intensity discrimination function in forward masking.

A non-monotonic intensity discrimination function in forward masking has been recently reported [Zeng et al. (1991) Hear. Res. 55, 223-230; Zeng and Turner (1992) J. Acoust Soc. Am. 92, 782-787] in which just-noticeable-differences (jnds) in intensity are largest for midlevel tones and smaller for soft and loud tones following an intense narrow-band noise. One hypothesis was that this midlevel hump reflects the contribution of low-spontaneous rate (SR) neurons to intensity coding, based on the differential recovery from forward masking of low-SR and high-SR neurons [Relkin and Doucet (1991) Hear. Res. 55, 215-222]. The present study conducted three experiments stimulating different stages of the auditory system in an attempt to determine the peripheral and central origins of the midlevel hump. First, in two cochlear implant (CI) listeners, the forward masker produced a midlevel hump on the intensity discrimination function, suggesting that the synapses between the hair cell and the eighth nerve are probably not responsible for the hump, as they are bypassed and the eighth nerve is stimulated directly. Second, in auditory brainstem implant (ABI) listeners, the forward masker produced no midlevel hump, but the masked jnds were larger than those without a masker. The absence of the midlevel hump in the ABI listeners suggests that the occurrence of the hump requires physiological mechanisms in the auditory nerve transmission, or the intrinsic processing circuits of the cochlear nuclei, or both. Third, in normal-hearing listeners, an ipsilateral, 90 dB SPL, pure-tone forward masker produced a midlevel hump, which is similar to that using a narrow-band noise masker; whereas a contralateral forward masker produced essentially no midlevel hump, suggesting that binaural interactions at superior olivary complex and more central sites are probably not responsible.

Recovery from prior stimulation. II: Effects upon intensity discrimination.

We obtained just-noticeable differences (jnds) for the intensity of pure tones following a forward masker. The masker was a 100-ms burst of narrow-band noise centered at 1000 Hz presented at 90 dB SPL; the pure-tone signal was at 1000 Hz and was 25 ms in duration. The masker-signal delay was 100 ms. Under these conditions, there is no threshold shift for the detection of the pure-tone signal following the forward masker. In contrast with the absence of a forward-masker effect upon detection thresholds, unusually large midlevel (40-60 dB SPL) jnds were observed. These large midlevel jnds were measured as a function of signal delay, revealing that they are not completely recovered to the normal (unmasked) values by 400 ms. We interpret these data as a consequence of the slower recovery of low-spontaneous rate, high-threshold neurons following prior stimulation (Relkin and Doucet, 1990). These experiments may therefore provide psychophysical evidence that the low-spontaneous rate, high-threshold neurons are a necessary physiological component in the coding of the large dynamic range for intensity. In addition, the present data provide evidence that the assumption that the effect of forward masking is limited to 100-200 ms is inappropriate, as this recovery time does not necessarily apply to suprathreshold tasks.