Source locations of pattern-specific components of human visual evoked potentials. I. Component of striate cortical origin
Source locations of pattern-specific components of human visual evoked potentials. I. Component of striate cortical origin
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DOI:
10.1007/bf00233371
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发表时间:
2004
影响因子:
2
通讯作者:
D. Jeffreys;J. Axford
中科院分区:
文献类型:
--
作者:
D. Jeffreys;J. Axford
A study was made of the transverse distributions of human scalprecorded potentials evoked by the brief presentation of a pattern into different regions of a continuously illuminated diffuse field. The first two components of these visual evoked potentials (VEPs), designated C.I. (latency 65–80 msec) and C. II (latency 90–110 msec), were both greatly influenced by the retinal location of the stimulus pattern. In an initial study of the VEP waveforms with 12 subjects, followed by a more detailed investigation of the distribution of the individual components in 4 subjects, the following results were found.1.Corresponding peaks (C. I and C. II) of the VEPs to stimulation of the upper and lower half-fields were inverted in polarity.2.For the left and right half-field VEPs, the transverse distribution of C. I, but not of C. II, showed a polarity reversal across the midline.3.Consistent differences were observed between the distributions of C. I for adjacent upper and lower quadrants, as well as between those for adjacent horizontal and vertical octants of the upper field.4.Subjects differed in the degree of left-right asymmetry shown. There was also a much greater degree of interindividual consistency of quadrant and upper and lower half-field VEPs than for full-field or left and right half-field responses.5.For C. I, an additive relationship was demonstrated between the half-field and the constituent quadrant VEP distributions.These results indicate that C. I and C. II have spatially separate sources. Assuming a simple dipolar model based on the known retinotopic organization of the striate cortex, it is shown that the measured distributions are compatible with the hypothesis that component C. I, but not C. II, originates in striate cortex, from surface negative cortical activity.