Both II and IO analyses revealed a lack of structure-function relationship in OHT, suggesting that, at this disease stage, PERG losses appear to affect primarily retinal/optic nerve head function. In EG they reflect both dysfunction and RNFL loss.

Luminance flicker-evoked RF(onh) is abnormally reduced in patients with OHT or EOAG, indicating an impairment of neurally mediated vasoactivity. The data suggest that PERG-derived neural activity and flicker-evoked RF(onh) can be independently altered early in the disease process.

Although this study cannot provide evidence for long-term benefit of EGCG supplementation in OAG, and the observed effect is small, the results suggest that EGCG might favourably influence inner retinal function in eyes with early to moderately advanced glaucomatous damage.

The results suggest a significant alteration of both ChBVel and ChBF in EMG, which does not appear to be associated with the severity of central retinal dysfunction. These findings may contribute to a better understanding of the pathophysiology of early glaucomatous damage in EMG and have implications for the treatment of this pathologic condition.

To investigate pattern electroretinogram changes in treated ocular hypertension, we evaluated pattern electroretinogram recordings of 48 hypertensive eyes following an 8-month timolol maleate therapy. During treatment, 27 of 48 eyes had normalized intraocular pressures (15–18 mm Hg), while 21 retained elevated values (21–25 mm Hg). Twenty-eight eyes with untreated hypertension (22–25 mm Hg) lasting at least 8 months, as well as 32 untreated, normotensive eyes served as controls. When compared to untreated normotensive controls, timolol-treated eyes with either elevated or normalized intraocular pressures showed reductions in the mean electroretinographic amplitudes. However, these amplitude reductions were substantially greater in treated eyes with elevated pressures as compared to those with normalized ones. Untreated hypertensive controls showed pattern electroretinogram reductions, with respect to normal values, that were comparable to those of treated hypertensive eyes, but larger than those of treated normotensive ones. These results indicate that, in treated ocular hypertension, pattern electroretinogram losses tend to be associated with moderately increased intraocular pressures in the range of 21–25 mm Hg. Electro retinographic abnormalities may be, at least in part, prevented only by lowering intraocular pressure into a normal range.