Research Information System
CURRENT EYE RESEARCH, vol.44, no.11, pp.1271-1277, 2019 (SCI-Expanded)
Purpose: To evaluate the effect of multiple sclerosis (MS) on the amplitude of accommodation (AA) and retinal nerve fiber layer (RNFL) thickness. Materials and Methods: A total of 25 MS patients with visual-evoked potential (VEP) abnormalities (MS/+VEP Group), 25 MS patients without VEP abnormalities (MS/-VEP Group), and 25 controls (Control Group) were enrolled. Only findings from the right eye of the participants were included in the analysis. Each participant underwent a pattern-reversal visual-evoked potential (PVEP) recording, an RNFL thickness analysis by optic coherence tomography (OCT) in all quadrants, and a measurement of amplitude of accommodation (AA) with minus lens technique. The AA and the RNFL thickness were compared between the groups. Results: The mean age and sex distributions did not differ significantly across the groups (p= .788, p= .906, respectively). The mean AA was 5.36 +/- 0.7 D in MS/+VEP group, 6.06 +/- 1.4 D in MS/-VEP group, and 6.4 +/- 0.9 D in control group (p= .002). The difference in the mean AA values between MS/+VEP and control groups were significant (p = .002). AA was significantly correlated with age, P100 latency and amplitude values in MS/+VEP group (r = -0.832, p < .001; r = -0.596, p = .002 and r = 0.498, p = .011, respectively). In a multivariable regression model, age and P100 latency were significant parameters for affecting AA in patients with MS (p < .001 and p = .001). In another multivariable regression model, age and average RNFL thickness were significant parameters for affecting AA in patients with MS (p < .001 and p = .010). Conclusions: We found that the AA was lower in MS patients with VEP abnormalities compared to age-matched healthy individuals. P100 latency was a significant parameter for predicting AA in MS/+VEP group. These results suggest that MS patients with VEP abnormalities might experience presbyopia earlier in life than people without MS, probably due to the chronic demyelination of neural pathways.