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Delays in signal conduction are not great enough to be useful clinically
In this issue of the BJO (p 1132) the paper by Rodarte et al reports on the effect of glaucoma on the multifocal multichannel visual evoked potential (mfVEP), specifically its effect on signal latency.1 Many previous publications have established that there is a loss of mfVEP amplitude in glaucoma.2–5 This paper confirms that there are also some measurable effects on latency, but the delays in signal conduction are not great enough to be useful clinically with only 40% showing significant change. As a relative negative finding this is important if the mfVEP is to be used in the diagnostic setting.
It is consistent with our understanding of the mechanisms of cell death in glaucoma, where demyelination is not a feature, in contrast to optic neuritis where marked latency delays are the hallmark. In fact in our recent study,6 large mfVEP latency delays in the recovery phase of a first episode of optic neuritis may even be predictive of the later onset of multiple sclerosis. A recent paper by Danesh-Meyer et al has also reported mfVEP amplitude reductions in compressive optic neuropathy,7 with some latency delays but not as marked as in optic neuritis (personal communication). The relative losses of amplitude versus delay may help separate not only disease types, but possibly prognosis in these conditions. It had been hoped that latency delays in glaucoma may be useful as an early marker in glaucoma, since there are many previous studies on the conventional VEP (cVEP) where some delays were identified. Also, latency has greater reproducibility and less inter-subject variability so would therefore be a useful parameter to measure. Unfortunately, this study confirms that the delays are not substantial enough to use in diagnosis. We …
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