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Editors Selection IGR 8-2
Electrophysiology: Effect diabetes on PERG
Comment by Stuart Graham on:
26083 The PERG in diabetic glaucoma suspects with no evidence of retinopathy, Ventura LM; Golubev I; Feuer WJ et al., Journal of Glaucoma, 2010; 19: 243-247
Ventura et al. (693) examined the compounding effect of diabetic status on the interpretation of pattern electroretinogram (PERG) recordings in a group of glaucoma suspects who were being followed using the PERGLA paradigm. The PERG reflects ganglion cell function and it is known that both glaucoma and diabetes can reduce PERG signals, the latter indirectly presumably via inner retinal vascular changes. The purpose of this study was to determine if the effects are additive. The PERGLA conterphase stimulus creates a steady state PERG, and phase shift is determined from Fourier transform as a measure of latency. The authors include control data from a previously collected set of 48 age matched normals with no diabetes (Ophth 2005, no systemic disease). There were 174 glaucoma suspects, who represent an undefined mixture of OHT and suspect discs. Eighteen of these had an existing diagnosis of diabetes and did not have any visible retinopathy and these were compared with the remainder of the cohort.
The mean PERG amplitude of both glaucoma suspects and the diabetic group was significantly (P < 0.01) smaller than that of controls. Further the mean PERG amplitude of diabetic patients was significantly (P < 0.05) smaller again than that of the glaucoma suspects alone. The figure showing the raw amplitudes shows a wide scatter of data points in the diabetic glaucoma group (21 subjects rather than the 18 in the Methods). Therefore attributing an additional degree of diabetes specific signal reduction for any individual would not be possible. However, the authors conclude that the interpretation of PERG results must consider any underlying diagnosis of diabetes, even in the absence of retinopathy. PERGLA phase shift did not show any significant changes (although this cannot be appreciated as Figure 1F appears to show exactly the same data points as the normals in Figure 1D).
Whether or not diabetes increases susceptibility to glaucomatous damage cannot be determined from this study. There are other reports suggesting that hyperglycaemia might even be protective (see Quigley, Arch Ophth 2009; 127: 227-228 for a review). There does appear to be a further reduction in PERG amplitude attributable to the diabetes, but this may be a local effect and not necessarily translate into increased RGC cell death.
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