What is the physiologic basis of visual evoked potential (VEP)?

Updated: Oct 25, 2019
  • Author: Andrew B Evans, MD; Chief Editor: Selim R Benbadis, MD  more...
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Answer

Answer

The generator site for VEPs is believed to be the peristriate and striate occipital cortex. Prolongation of P100 latency is the most common abnormality and usually represents an optic nerve dysfunction. VEP is clearly more sensitive than physical examination in detecting optic neuritis.

Ikeda et al investigated current source generators (dipoles) of human VEP to pattern-onset stimuli. [1] A visual stimulus (a checkerboard pattern) was presented for 250 msec in each of the 8 quadrants. Central and peripheral parts of each of the 4 quadrant fields were evaluated. The VEPs, consisting of initial positive-late negative waves, were recorded mainly on the occipital region contralateral to stimulated visual fields. The initial positive waves of VEP were divided into the following 2 components:

  • Early component with an approximate peak latency of 70-90 msec

  • Late component with an approximate peak latency of 100-120 msec

The results from these analyses of VEP indicated topographic localization of the dipoles around the calcarine fissure. [1] This was comparable to the retinotopy of the human occipital lobe based on clinicopathologic studies.

In a multicenter study, Brigell et al described the pattern VEP using standardized techniques, concluding that the peak latency of pattern-reversal VEP is a sensitive measure of conduction delay in the optic nerve caused by demyelination. [2] To establish whether pattern-reversal VEP could be standardized for use as a measure in multicenter therapeutic trials for optic neuropathy or multiple sclerosis (MS), the investigators evaluated stimulus and recording variables at 4 centers.

Overall, pattern-reversal VEPs were recorded from 64 healthy subjects and 15 patients with resolved optic neuritis; the results showed equivalent latency and amplitude data from all centers, indicating that the VEP test can be standardized satisfactorily for multicenter clinical trials. [2] Furthermore, the authors concluded that the N70 and P100 peak latencies and N70-P100 interocular amplitude difference were sensitive measures of resolved optic neuritis.

Abboud et al, in a study that used flash VEP to assess left-right asymmetry in the potential amplitude on the scalp in brain-damaged patients who had sustained a stroke, determined that the VEP amplitude was smaller over the ischemic hemisphere than over the intact hemisphere. [3] This finding indicates that the left-right asymmetry in scalp VEPs of patients after brain damage may be a result of changes in the conductivity of the volume conductor, attributable to the ischemic region between the source and the electrodes.

Ipata et al, in a study designed to assess interhemispheric visual transfer of information in humans, obtained estimates of interhemispheric transfer time that ranged from 5.77 to 12.54 msec, depending on the type of component and the location of the electrode sites. [4] More anterior locations yielded shorter values, and overall transfer time tended to be 7 msec shorter for the N70 component than for the P100 component.


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