Structure-function relationship between handheld photopic negative response and macular GCIPL thickness in chronic optic neuropathy.

PURPOSE: To determine whether photopic negative response (PhNR) parameters obtained using a handheld electroretinography (ERG) device reflect quantitative indicators of residual retinal ganglion cell (RGC)-driven inner retinal function and how these functional measures relate to OCT-derived structural metrics in chronic unilateral non-glaucomatous optic neuropathy (ON).

METHODS

In this retrospective observational study, 27 patients (54 eyes) with unilateral chronic ON were examined using handheld full-field photopic ERG (RETeval™, LKC Technologies) without pupil dilation or corneal electrodes. Several ERG parameters, including the PhNR72 amplitude, PhNR minimum amplitude, P-ratio, and W-ratio, were analyzed. Optical coherence tomography (OCT)-derived ganglion cell-inner plexiform layer (GCIPL) and retinal nerve fiber layer (RNFL) thicknesses, and Humphrey field analyzer (HFA) indices were acquired on the same day. Linear mixed-effects models accounting for intereye correlation and false discovery rate (FDR) correction were used to assess structure-function relationships.

RESULTS

ON eyes showed significantly reduced PhNR72 and PhNR minimum amplitudes, and lower P-ratio (PhNR72/b-wave) and W-ratio (PhNR minimum/(b-wave minus a-wave) (all p < 0.01) compared with unaffected eyesof the patients. In multivariable models, the W-ratio was independently associated with GCIPL thickness in the inferotemporal sector (β = 0.45; 95% CI, 0.22-0.68; FDR-adjusted p < 0.05), whereas no significant associations were found with RNFL thickness or HFA indices.

CONCLUSIONS

Handheld photopic ERG-derived PhNR parameters, particularly the W-ratio, are selectively associated with GCIPL thickness, suggesting preferential coupling with RGC-driven inner retinal function rather than axonal or field-level measures. Thus, portable ERG provides a practical functional biomarker complementary to OCT for evaluating residual RGC-driven inner retinal function in chronic ON.