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Editors Selection IGR 8-4
Electrophysiology: PERG in OHT
Comment by Vittorio Porciatti on:
25145 Electrophysiological evidence of early functional damage in glaucoma and ocular hypertension, North RV; Jones AL; Drasdo N et al., Investigative Ophthalmology and Visual Science, 2010; 51: 1216-1222
Over the past thirty years, a large body of evidence concurred in showing that the Pattern Electroretinogram (PERG) is altered in OHT and in the early stages of human and experimental glaucoma. North (177) et al. further confirmed this notion in 23 patients with OHT and 30 patients with early OAG. They also confirmed that the PERG is not unique among electrophysiological measures to show alterations in these groups of patients. The photopic negative response (PhNR) ‐ elicited by either a red light on a blue background or by a blue light alternating with a green background ‐ was also altered to some extent. North et al. also used OCT to measure the full retinal thickness and the RNFL thickness, and found significant, but modest correlations between the imaging and electrophysiological measures.
While technically sound, this study adds little weight to the stateof- the-art in this area of research. As a confirmatory contribution, it does not discuss a number of relevant reports on PERG applications in clinical and experimental glaucoma, including structure-function relationships and the effect of IOP-lowering treatment. As an original contribution, it does not fulfil its intended purpose 'to quantify early retinal ganglion cell (RGC) damage in early glaucoma.' In addition, experimental data do not support the conclusion that 'electrophysiology can be used to quantify RGC dysfunction that occurs before cell death.' Quantification was addressed by comparing within-function relative losses (PERG vs PhNRs); however, this comparison has limitations because of lack of spatial congruency between measures (PERG is local, PhNRs are full field). A modest correlation between the imaging and electrophysiological measures per se cannot provide any indication about relative loss of RGC function vs RGC death or support statements such as 'structural changes to the optic nerve head and the attenuation of ERG parameters occur at different points in the pathologic process.' It is unfortunate that the authors did not take advantage of PERG and RNFL data to match congruent retinal locations and calculate relative PERG and RNFL losses from normal, as it has been done in other studies (IOVS 47: 3904; Doc Ophthalmol 120: 187).
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