This paper reviews the literature on the Nl wave of the human auditory evoked potential. It concludes that at least six different cerebral processes can contribute to (he negative wave recorded from the scalp with a peak latency between 50 and 150 ms: a component generated in the auditory‐cortex on the supratemporal plane, a component generated in the association cortex on the lateral aspect of the temporal and parietal cortex, a component generated in the motor and premotor cortices, the mismatch negativity, a temporal component of the processing negativity, and a frontal component of the processing negativity, The first three, which can be considered ‘true’ N1 components, are controlled by the physical and temporal aspects of the stimulus and by the general state of the subject. The other three components are not necessarily elicited by a stimulus but depend on the conditions in which the stimulus occurs. They often last much longer than the true N1 components that they overlap.
Auditory evoked potentials were recorded from the vertex of subjects who listened selectively to a series of tone pips in one ear and ignored concurrent tone pips in the other ear. The negative component of the evoked potential peaking at 80 to 110 milliseconds was substantially larger for the attended tones. This negative component indexed a stimulus set mode of selective attention toward the tone pips in one ear. A late positive component peaking at 250 to 400 milliseconds reflected the response set established to recognize infrequent, higher pitched tone pips in the attended series.
Ten patients presented as children or young adults with hearing impairments that, by behavioural and physiological testing, were compatible with a disorder of the auditory portion of the VIII cranial nerve. Evidence of normal cochlear outer hair cell function was provided by preservation of otoacoustic emissions and cochlear microphonics in all of the patients. Auditory brainstem potentials showed evidence of abnormal auditory pathway function beginning with the VIII nerve: the potentials were absent in nine patients and severely distorted in one patient. Auditory brainstem reflexes (middle ear muscles; crossed suppression of otoacoustic emissions) were absent in all of the tested patients. Behavioural audiometric testing showed a mild to moderate elevation of pure tone threshold in nine patients. The extent of the hearing loss, if due to cochlear receptor damage, should not have resulted in the loss of auditory brainstem potentials. The shape of the pure tone loss varied, being predominantly low frequency in five patients, flat across all frequencies in three patients and predominantly high frequency in two patients. Speech intelligibility was tested in eight patients, and in six was affected out of proportion to what would have been expected if the pure tone loss were of cochlear origin. The patients were otherwise neurologically normal when the hearing impairment was first manifest. Subsequently, eight of these patients developed evidence for a peripheral neuropathy. The neuropathy was hereditary in three and sporadic in five. We suggest that this type of hearing impairment is due to a disorder of auditory nerve function and may have, as one of its causes, a neuropathy of the auditory nerve, occurring either in isolation or as part of a generalized neuropathic process.
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