Helen J. Neville

Bitemporal lesions dissociate auditory evoked potentials and perception.

Authors:

  • David L. Woods

  • Robert T. Knight

  • Helen J. Neville

Date: 1984

PubMed: 6199182

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Abstract:

We studied auditory evoked potentials (AEPs) in an 82-year-old female patient who became suddenly deaf following the second of two strokes. The patient showed markedly elevated pure tone thresholds, was unable to discriminate sounds and could not understand speech. Brain-stem auditory evoked potentials (BAEPs) were normal. CT scans revealed bilateral lesions of the superior temporal plane which included auditory cortex. Two experiments were performed. In the first, tones, complex sounds and speech stimuli were presented at intensities above and below the patient's perceptual threshold. P1, N1 and P2 components were elicited by each of the stimuli--whether or not they were perceived. In particular, stimuli presented below threshold evoked large amplitude, short latency responses comparable to those produced in a control subject. In a second experiment, the refractory properties of the N1-P2 were examined using trains of tones. They were also found to be similar to those of normal subjects. Shifts in the pitch of the tones near the end of the train (when refractory effects were maximal) evoked N1-P2s with enhanced amplitudes, although the change in pitch was not perceived by the patient. In both experiments AEP scalp topographies were normal. The results suggest that bitemporal lesions of auditory cortex can dissociate auditory perception and long-latency auditory evoked potentials. A review of evoked potential studies of cortical deafness suggests that the neural circuits responsible for N1-P2 generation lie in close proximity to those necessary for auditory perception.


The effects of frontal cortex lesions on event-related potentials during auditory selective attention.

Authors:

  • Robert T. Knight

  • Steven A Hillyard

  • David L. Woods

  • Helen J. Neville

Date: 1981

PubMed: 6172256

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Abstract:

We compared electrophysiological indices of auditory selective attention in control subjects and in patients with unilateral lesions of the dorsolateral frontal lobes. In control subjects, ERPs following attended tones showed an enhanced negativity from 80 to 500 msec post-stimulus which had a different topographic distribution than the N120. Lesions of the frontal lobes reduced the attention-related negativity and impaired behavioral performance. The ERP reductions were equivalent in recordings obtained from electrodes placed over the damaged and intact cortex. A difference was noted between left and right frontal groups as a function of ear of delivery of the stimuli. Patients with left frontal lesions showed reduced attention effects following tones presented to either ear. Patients with right frontal lesions showed intact attention effects to right ear tones, but no attention-related negativity to left ear tones. When the left and right frontal groups were considered together, tones in ignored channels produced larger responses when presented to the ear contralateral to damaged cortex. These results underline the important role of the frontal lobes in processes of selective attention. Although the endogenous negativity produced in selective attention tasks does not appear to originate in dorsolateral frontal cortex, the frontal lobes exhibit a modulating influence upon it. In addition, the endogenous attention related negativity and exogenous N120 components apparently arise from different neural generators.


The effects of frontal and temporal-parietal lesions on the auditory evoked potential in man.

Authors:

  • Robert T. Knight

  • Steven A Hillyard

  • David L. Woods

  • Helen J. Neville

Date: 1980

PubMed: 6159179

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Abstract:

We compared the properties of long-latency auditory evoked potentials (AEPs) in patients with unilateral lesions of the dorsolateral frontal cortex (N = 10) or temporal-parietal cortex (N = 10) to those of a group of age-matched normal subjects. Extensive lesions of the frontal cortex had no effect on AEP amplitudes, scalp distributions or refractory properties. However, following frontal lesions AEPs were larger to tones presented in the ear contralateral to the lesion than they were for tones presented ipsilaterally. Following unilateral temporal-parietal lesions, the N1 component (98 msec latency) was markedly reduced in amplitude at all scalp sites, and no increase in N1 amplitude occurred with lengthening ISIs. The P2 component (200 msec), however, showed the same amplitude and refractory properties as in the normal subjects. The results underline the critical role played by the cortex of the posterior-superior temporal plane and the adjacent cortex of the parietal lobe in the production of the N1 component.