An investigation of sensory deficits underlying the aphasia-like behavior of macaques with auditory cortex lesions.

Bilateral auditory cortex lesions in Japanese macaques result in an aphasia-like deficit in which the animals are unable to discriminate two forms of their coo vocalizations. To determine whether this deficit is sensory in nature, two monkeys with bilateral lesions were tested for their ability to discriminate frequency and frequency change. The results indicated that although the animals were able to discriminate between sounds of different frequencies, they were unable to determine whether a sound was changing in frequency. Because the animals' coo vocalizations differ primarily in the predominant direction of their frequency change and not in their absolute frequency content, the aphasia-like deficit of animals with bilateral auditory cortex lesions appears to be a sensory disorder.

"Central" auditory gap detection: a spatial case.

Normal listeners were tested for their temporal auditory gap detection thresholds using free-field presentation of white-noise stimuli delivered from the left (L) and right (R) poles of the interaural axis. The noise bursts serving as the leading and trailing markers for the silent period were presented in either the same (LL,RR) or different (LR,RL) auditory locations. The duration of the leading marker was a second independent variable. Gap thresholds for stimuli in which the markers had the same location were low, and usually were independent of the duration of the leading marker. Gap thresholds for the LR and RL conditions were longer. These gap thresholds were sensitive to the duration of the leading marker, and increased as the leading marker duration decreased. This finding is consistent with the hypothesis that a relative timing operation mediates gap detection when the markers activate different perceptual channels. The present data suggest that this timing process can operate on perceptual channels emerging from central nervous system processing.