In our younger subjects, photopic CS showed significant correlation with the thickness measurements of peripheral macular IRL, GCC and cpRNFL (
Table 2). Inner retinal layer thickness (the same substructure mentioned for the older age group), was the only independent contributor to CS measured in the central 10° of the visual field (
Table 3;
Fig.) and was able to explain up to 28% of the variance in photopic CS but not in mesopic CS. It is difficult to find an explanation for this because the variability in CS was similar under mesopic and photopic conditions and a loss of GCs in young subjects is unlikely. Contrary to the positive association found for the older group, correlation between IRL thickness and CS was negative for this younger group, meaning that the thickening noted gave rise to worse CS function. Although correlation between mesopic CS and peripheral IRL thickness in the younger eyes was not significant, when the regression lines of the two age groups were compared the interaction term was significant (
P = 0.0001). Relationships between both photopic and mesopic CS and peripheral IRL were significantly different for each age group and the model was able to explain 37% and 36% of the variability in photopic and mesopic CS, respectively. The IRL thickening noted in some, supposedly healthy, young eyes could perhaps be attributed to increased glial tissue. Astroglial cells are strategically located to sense hypoxia in the inner layers of retina.
36 They defend the retina from damage through a process called reactive gliosis designed to maintain retinal homeostasis.
36 In mild to moderate forms of gliosis, cells may undergo hypertrophy (larger cell body size or thickening) and the enlargement of processes, yet if the trigger is removed, the cells could revert back to their former condition without altering the tissue.
37 The molecular changes that take place in the adult retina induced by damage occur rapidly, within minutes or hours.
36 In young healthy retinas, stress can be produced by external or internal factors such as smoking, dietary fat, or exposure to blue light
38 (e.g., emitted by electronic displays). Therefore, in some of our young subjects we propose that transient thickening of the macular IRL may have been responsible for the reduction observed in CS. In contrast, cpRNFL thickness could not be associated here with CS. This confirms the results of the single study conducted in healthy young subjects
39 and suggests that macular IRL thickness measures are better predictors of visual function than cpRNFL in healthy subjects. It should be noted that in our study, macular IRL and cpRNFL thicknesses were only moderately related (rho = 0.39,
P = 0.0166) in young subjects.