Impaired visual function in glaucoma

Objective: This work aims to evaluate whether glaucomatous visual field defects could be related to an impaired retinal function, to a delayed neural conduction in postretinal visual pathways, or both. Methods: Visual field by Humphrey perimeter (central 24-2 threshold test) and simultaneous recordings of visual evoked potential (VEP) and pattern electroretinogram (PERG) were assessed in 21 subjects with open angle glaucoma (POAG) and in 15 age-matched controls (C). Results: VEP: in POAG eyes we found P100 latency significantly (P<0.01) delayed when compared with controls and correlated with mean deviation (index of global visual field damage, MD) of 24-2 Humphrey perimetry (P<0.001); the P100 amplitudes were significantly (P<0.01) lower in POAG eyes than in control eyes and correlated with MD (P<0.001). PERG: POAG eyes showed P50 latency significantly (P<0.01) delayed when compared with controls and correlated with MD (P=0.002); the P50 and N95 amplitudes were significantly (P<0.01) lower in POAG than in control eyes and correlated with MD (P50: P=0.006; N95: P=0.002). Retinocortical time (RCT: difference between VEP P100 and PERG P50 latencies) and latency window (LW: difference between VEP N75 and PERG P50 latencies) were significantly (P<0.01) longer in POAG eyes than in control eyes and correlated with MD (RCT: P<0.001; LW: P<0.001). No significant correlations (P>0.05) were found between electrophysiological parameters and the corrected pattern standard deviation (index of localized visual field damage) of 24-2 Humphrey perimetry Conclusion: In patients with open angle glaucoma the reduction of the index of global visual field damage (MD) could be ascribed to two sources of functional impairment: one retinal (impaired PERG) and one postretinal (delayed RCT and LW). In the postretinal impairment, a postsynaptic degeneration at the level of the lateral geniculate nucleus could be suggested.