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. Author manuscript; available in PMC: 2009 Sep 29.
Published in final edited form as: Invest Ophthalmol Vis Sci. 2008 Mar 7;49(7):2985–2992. doi: 10.1167/iovs.07-1651

FIGURE 3.

FIGURE 3

Clinical electrophysiology of control (blue lines) and 7-second pNAION-induced (red lines) eyes. Top: VEP in both eyes at baseline (before induction) and at 1, 2, and 9 weeks after induction. At baseline, the VEPs were equal in the two eyes; however, at 1 week, there was a reduction in the VEP amplitude from the pNAION eye, whereas the VEP amplitude in the control eye remained normal. The reduction in VEP amplitude in the pNAION eye persisted at 2 and 9 weeks, whereas the VEP amplitude in the control eye remained normal. Note that the latency of the P100 peak remained normal in both eyes throughout the period of observation. Bottom: PERG of control and 7-second pNAION eyes during the same period as the VEP. At baseline, the PERG was normal in both eyes and remained normal in both eyes 1 week after induction; however, by 2 weeks after induction, there was a large reduction in the N95 PERG amplitude in the pNAION eye compared with the control eye, suggesting that intraocular RGC function declined after the ON infarct. This reduction was still present at 9 weeks. The delay in PERG reduction suggests that, at least in this animal, RGC damage did not occur immediately.