Neurodegeneration in PD is not restricted to the brain, but also occurs in the retina. Accordingly, patients with PD can gradually develop visual problems. The changes in the different retinal layers can be easily assessed using OCT . In the current study, SD-OCT was used as a quantitative measure to evaluate retinal structures and morphology in patients with PD.
The present study revealed reduced macular thickness and macular volume in patients with PD compared with healthy controls. This was in agreement with previous studies that reported thinning of macula [6, 10,11,12,13,14,15].
The current study also revealed reduced GCC thickness in patients with PD compared to healthy controls. This was in agreement with Moschos and Chatziralli (2017)  who reported a significant reduction in the average GCC thickness in patients with PD compared to controls. Other studies using segmentation analysis also observed significant thinning of the GCL in patients with PD [8, 16]. GCL atrophy is thought to be a component of RNFL loss, which is suggested to produce consecutive degeneration of the RGC layer and its axons as the disease progresses [17, 18].
The results of our study revealed reduction in the RNFL thickness in the temporal, superotemporal, inferotemporal and nasal quadrants in PD patients compared to healthy controls. However, our study could not find differences regarding the thicknesses of the superonasal and inferonasal quadrants between the two groups. This was supported by the first OCT study in PD by Inzelberg et al. (2004)  who reported thinned average RNFL, specifically in the inferior and temporal quadrants in a small group of 10 PD patients. Satue et al. (2013)  further revealed significant differences in the inferior, inferotemporal and superotemporal RNFL thicknesses in patients with PD compared to controls using SD-OCT. Moreover, Moschos and Chatziralli  observed a significant reduction in the average RNFL thickness as well as the superior and temporal quadrants, in PD patients compared to controls. The significant reduction in the temporal fibers may suggest a mitochondrial pattern of retinal axonal loss in PD. This may support the role of mitochondrial dysfunction in the pathogenesis of PD . Other studies showed significant RNFL thinning in PD patients in all quadrants [21,22,23,24].
The RNFL comprises mainly non-myelinated axons of RGCs, so RNFL thickness measurements provide a relatively direct assessment of the axons and axonal damage. PD causes axonal damage in the RNFL, along with retinal thinning that can be detected using SD-OCT .
Contrary to our study, some studies have failed to find changes in the inner macular thickness or macular volume [25,26,27]. Sen et al. (2014)  also reported no significant difference in the average GCC thickness among patients with PD and controls. Moreover, some studies did not find difference in the RNFL thickness between PD patients and healthy controls [25, 27, 29, 30]. This discrepancy may be explained by the different OCT equipment used by these studies, which can affect retinal measurements. Different sample sizes and retinal segmentation algorithms may account for these discrepant findings.
The results of our study revealed that long duration of the disease was associated with decreased macular volume, inferior and temporal parafoveal thicknesses and GCC thickness. This was in agreement with a study conducted by Garcia-Martin et al. (2014)  which revealed that the inner retinal layer thicknesses was significantly thinner in PD patients with disease duration longer than 10 years compared to those with shorter disease duration. This study reported that thickness inversely correlated with longer disease duration.
The results of our study also showed a significant negative correlation between the UPDRS scores and the macular volume, inferior and nasal parafoveal thicknesses, as well as the GCC measurements, and nasal and temporal RNFL thicknesses. Our results are supported by a study done by Altintaş et al. (2008)  who reported an inverse correlation between the foveal thickness measured by TD-OCT and the UPDRS total and motor scores. Another study conducted by Satue et al. (2014)  revealed an inverse correlation between the inner inferior macular thickness measured using the Cirrus OCT device and the UPDRS scores.
The results of our study also revealed a significant inverse correlation between all macular thickness measurements, GCC thickness and temporal RNFL thickness assessed by SD-OCT and the scores on the HY scale. In agreement with our study, Garcia-Martin et al. (2014)  reported that both the RNFL and macular thicknesses were negatively correlated with the HY scores. Pilat et al. (2016)  also reported a negative correlation between the RNFL and central retinal thicknesses and the HY scores. Moreover, Satue et al. (2014)  found that most macular thickness measurements assessed by Spectralis OCT are correlated with the HY scores.
Contrary to our study, some studies failed to detect correlations between structural parameters using OCT and disease duration or severity assessed by either HY scale or UPDRS [8, 20, 30,31,32].
These discrepant findings may be partly explained by the difference in terms of the stage and severity of the disease. In the study conducted by Aydin et al. (2017) , the median HY score of PD patients was 1 and the median UPDRS score was 24, while the median HY score was 3 and the median UPDRS score was 49.5 in our study. Also, La Morgia et al. (2013) and Roth et al. (2014) [20, 30] included patients with mild disease (mean UPDRS scores were 25.9 ± 12.4 and 19 ± 10, respectively). In our study, the mean UPDRS score was 48.59 ± 14.94. Moreover, Aydin et al. (2017)  included a relatively small number of patients (25 PD patients) and 29 healthy controls which may account for some of the discrepant results.
The results of our study revealed no significant difference in the OCT parameters between the treated and untreated patients with PD. Previous researchers did not find significant correlations between retinal thickness and levodopa dosages [26, 33]. Sen et al. (2014)  found no significant difference in the thickness of retina between the treated and untreated groups although the disease in patients with treated PD was more severe than in the untreated group. They suggested that levodopa may have a protective effect on retina in patients with PD.
In addition, by using the multivariate linear regression analysis, we found that the HY scale was a significant predictor for the reduction of the average GCC thickness and macular volume.
The main limitations of the study included that it would be of more interest if we could compare the RNFL thinning pattern in PD patients with that of secondary parkinsonism, a longitudinal study using repeated OCT on the same patients will offer better data on the course of the disease, and we did not have the opportunity to use electroretinogram (ERG) due to financial issues and hence could not evaluate the functional impairment in visual processing along with OCT changes.