Cortical evoked response to gaps in noise: within-channel and across-channel conditions.

OBJECTIVES: The objective of this study was to describe the cortical evoked response to silent gaps in a group of young adults with normal hearing using stimulus conditions identical to those used in psychophysical studies of gap detection. Specifically, we sought to examine the P1-N1-P2 auditory evoked response to the onsets of stimuli (markers) defining a silent gap for within-channel (spectrally identical markers) and across-channel (spectrally different markers) conditions using four perceptually-equated gap durations. It was hypothesized that (1) P1, N1, and P2 would be present and consistent for 1st marker (before the gap) onsets; (2) for within-channel markers, P1, N1, and P2 would be present for 2nd marker (after the gap) onsets only when the gap was of a duration equal to or larger than the behaviorally measured gap detection threshold; and (3) for the across-channel conditions, P1, N1, and P2 would be present for 2nd marker onsets regardless of gap duration. This is expected due to the additional cue of frequency change following the gap.

DESIGN: Twelve young adults (mean age 26 years) with normal hearing participated. Within-channel and across-channel gap detection thresholds were determined using an adaptive psychophysical procedure. Next, cortical auditory evoked potentials (P1-N1-P2) were recorded with a 32-channel Neuroscan electroencephalogram system using within-channel and across-channel markers identical to those used for the psychophysical task and four perceptually weighted gap durations: (1) individual listener's gap detection threshold; (2) above gap detection threshold; (3) below gap detection threshold; and (4) a 1-ms gap identical to the gap in the standard interval of the psychophysical task. P1-N1-P2 peak latencies and amplitudes were analyzed using repeated-measures analyses of variance. A temporal-spatial principal component analysis was also conducted.

RESULTS: The latency of P2 and the amplitude of P1, N1, and P2 were significantly affected by the acoustic characteristics of the 2nd marker as well as the duration of the gap. Larger amplitudes and shorter latencies were generally found for the conditions in which the acoustic cues were most salient (e.g., across-channel markers, 1st markers, large gap durations). Interestingly, the temporal-spatial principal component analysis revealed activity elicited by gap durations equal to gap detection threshold in the latency regions of 167 and 183 ms for temporal-parietal and right-frontal spatial locations.

CONCLUSIONS: The cortical response to a silent gap is unique to specific marker characteristics and gap durations among young adults with normal hearing. Specifically, when the onset of the 2nd marker is perceptually salient, the amplitude of the P1-N1-P2 response is relatively larger and the P2 latency is relatively shorter than for nonsalient 2nd marker onsets, providing noninvasive, nonbehavioral indicators of the neural coding of this important temporal cue in the thalamic-cortical region of the central auditory system. Gap duration appears to be most clearly indicated by P1 and T-complex amplitude.