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Editors Selection IGR 8-4

Electrophysiology: mfVEP

Comment by Vittorio Porciatti on:

15100 Comparison between multifocal and conventional VEP latency changes secondary to glaucomatous damage, Grippo TM; Hood DC; Kanadani FN et al., Investigative Ophthalmology and Visual Science, 2006; 47: 5331-5336

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The electrical activity of RGCs under distress may be reduced and delayed. Since Visually Evoked Potentials (VEPs) are known to be delayed in glaucoma, VEP latency might represent a vehicle for detecting abnormal RGC function and monitoring neuroprotection. Two recent VEP studies in glaucoma patients appear to conflict with each other on this point. Rodarte et al. (2006)¹ reported that VEP latency measured by multifocal VEPs (mfVEPs) shows average delays of few milliseconds and extensive overlap between control and patients. By contrast, Parisi et al.² reported that the mean latency of conventional VEPs (cVEP) was 28 ms longer in glaucoma patients than in normal controls, and that the distribution of latencies in patients did not overlap with that of the control group. To better understand the nature for these discrepancies, Grippo et al. (1103) compared latencies of cVEPs and mfVEPs in the same eyes of 47  glaucoma patients and 22 control subjects. They found only modest increase of both cVEP and mfVEP latencies (about 6 ms) and that only 12-17% of the readings exceeding the range of controls. The authors conclude that a delayed VEP is not a good indicator of damaged, as opposed to dead, RGCs or there are relatively few patients who exhibit evidence of damaged RGCs.

As to VEP delay as indicator of RGC damage, one should take into account that VEP abnormalities in glaucoma may result from neuronal damage occurring at retinal as well as postretinal level. VEP latency delays in glaucoma appear to have a substantial postretinal component, since delays in the Pattern Electroretinogram (PERG) account for only a portion of the delay measured at cortical (VEP) level.^3,4 Furthermore, neuronal damage may differentially affect magnocellular, parvocellular, and koniocellular pathways.⁵ Indeed, VEPs in response to pattern stimuli that emphasize the activity of different visual channels such as blue-yellow or red-green chromatic patterns may result remarkably delayed (20-50 ms) and more sensitive (50-75%) to glaucoma damage than do responses to achromatic pattern reversal stimuli.^3,6,7 So it may not be too surprising that the cVEP delay reported by Parisi et al. is longer than that mfVEP delay reported by Rodarte et al. and Grippo et al., given that the experimental conditions were different. What is more surprising is the lack of overlap in VEP latency between glaucoma patients and controls reported by Parisi et al. Possibly, this may be due to the particular selection of patients and controls, as the authors themselves acknowledge.

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