Assessment of contrast gain signature in inferred magnocellular and parvocellular pathways in patients with glaucoma

PurposeContrast gain signatures of inferred magnocellular and parvocellular postreceptoral pathways were assessed for patients with glaucoma using a contrast discrimination paradigm developed by Pokorny and Smith. The potential causes for changes in contrast gain signature were investigated using model simulations of ganglion cell contrast responses.MethodsFoveal contrast discrimination thresholds were measured with a pedestal-Δ-pedestal paradigm developed by Pokorny and Smith [Pokorny, J., & Smith, V. C. (1997). Psychophysical signatures associated with magnocellular and parvocellular pathway contrast gain. Journal of the Optical Society of America A, 14(9), 2477–2486]. Stimuli were 27 ms luminance increments superimposed on 227 ms pulsed Δ-pedestals. Contrast thresholds and contrast gain signatures mediated by the inferred magnocellular (MC) and parvocellular (PC) pathways were assessed using linear fits to contrast discrimination thresholds at either lower or higher Δ-pedestal contrasts, respectively. Twenty-seven patients with glaucoma were tested, as well as 16 age-similar control subjects free of eye disease.ResultsContrast sensitivity and contrast gain signature mediated by the inferred MC pathway were lower for the glaucoma group, and reduced contrast gain signature was correlated with reduced contrast sensitivity (r2 = 45%, p < .0005). These two parameters mediated by the inferred PC pathway were little affected for the glaucoma group. Model simulations suggest that the reduced contrast sensitivity and contrast gain signature were consistent with the hypothesis that reduced MC ganglion cell dendritic complexity can lead to reduced effective retinal illuminance, and hence increased semi-saturation contrast of the ganglion cell contrast response functions.ConclusionsThe contrast sensitivity and contrast gain signature of the inferred MC pathway were reduced in patients with glaucoma. The results were consistent with a model of ganglion cell dysfunction due to reduced synaptic density.