## 5 Discussion  
A literature review over the last decade was conducted in order to elucidate the diagnostic value of OCT in a setting of clinically evident Parkinsonism. Original articles dealing with the potential utility of OCT implementation within a group of patients presenting with Parkinsonian features were identified and reviewed. Despite the fact that [PERSON] et al. first applied OCT within a group of patients with PD almost twenty years ago [25], ongoing research regarding the potential role of OCT in patients presenting with Parkinsonism is still characterized by inconsistency, and has yielded conflicting results. To date, no reliable OCT biomarkers able to distinguish between PD and atypical Parkinsonian syndromes in clinical practice have been developed. The assessment of RNFL and macular thickness, as well as the evaluation of single retinal layers, constitute OCT measures that are both readily accessible and reproducible, able to visualize subtle retinal changes as surrogate markers of brain abnormalities. There is growing evidence that different disease entities are coupled with distinct alterations of retinal morphology [26]. Being called a window to the brain [27; 28], the eyes, and more specifically, the retinal microstructure, may reflect the underlying pathology of each patient's disorder, thus providing unique insights into the neurodegenerative process [29; 30; 31]. Until now, specific diagnostic protocols utilizing OCT techniques have been developed in order to provide useful information regarding PD diagnosis [32]. Notably, various CNS disorders, multiple sclerosis and PD being among them, may have an impact on the optic nerve and the retina, which both embryologically originate from the diencephalon, with clinically evident visual disturbances [13; 33; 34; 35; 36]. Although reductions in RNFL thickness and the thickness of the macular layers have been linked to nigral dopaminergic depletion [37], indicating a similar pathophysiology mechanism to PD, retinal thinning was also demonstrated within the course of neurological diseases with a distinct etiological basis, including multiple sclerosis, neuromyleitis optica, and Alzheimer's disease [38; 39; 40; 41]. Thus, dopaminergic loss may not be solely responsible for RNFL and macular thickness reduction, as has been reported among patients presenting with neurological disorders without dopaminergic loss as well, making retinal thinning a rather non-specific degeneration marker [42; 43; 44]. There is growing evidence that OCT may serve as an early diagnostic tool among patients with PSP, independent of the disease's clinical phenotypes [45]. Indeed, pRNFL reflecting the degree of retinal axonal degeneration has been shown to be significantly thinner within a group of patients with PSP than healthy controls [45; 46; 47; 48]. Highlighting the positive correlation between retinal thinning and PSP severity and duration, non-motor symptoms, and cognitive performance, researchers have pointed out the potential role of OCT as a monitoring marker of disease progression [45; 46; 48], although contradictory results were yielded from another study [47]. Similarly, retinal microstructure alterations and, more specifically, a degree of retinal thinning, has been demonstrated within groups of patients with MSA when compared with healthy individuals [49; 50; 51; 52; 53]. Interestingly, retinal thickness reductions were found to be more marked among patients with the MSA-P subtype than those presenting with the MSA-C subtype, which is strongly linked to clinical severity of the disease [54]. According to a recent meta-analysis, a distinct pattern of retinal changes has been observed in patients with MSA when compared with patients with PD [55]. As far as retinal morphology in patients with PD is concerned, retinal thinning was demonstrated through OCT [56; 57], located periappillary [25], in the fovea [58], or in different retinal areas [59; 60; 61; 62; 63; 64; 65; 66; 67; 68].