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While the most prominent symptoms of Parkinson's disease stem from loss of neurons in the nigrostriatal pathway, there exist other dopaminergic cellular networks in the nervous system that may be affected by dopamine deficiency and in particular the amacrine retinal cells. Indeed, visual dysfunction is not uncommon in Parkinson's Disease (PD), and several publications have reported deficiencies in visual acuity, color discrimination, contrast sensitivity and motion perception. To shed some light in the retinal manifestations of the disease, the authors of this study investigated retinal structure and function in a cohort of PD patients, using tools and methods that are part of the routine assessment of glaucoma patients, including a full ocular examination, 24-2 SITA visual fields and OCT RNFL measurements. They identified 24 patients with reliable second visual fields and high-quality OCT scans and enrolled additionally 24 sex and agematched controls.
No anatomical differences and no structural defects were detected in the RNFLs of PD patients, but the perimetric findings were consistent and statistically significant: patients with Parkinson's disease had higher MDs and PSDs and lower Mean Sensitivities both in their superior and their inferior hemifields compared to controls. In addition their Mean Sensitivity was lower in the superior vs. the inferior hemifield. The Glaucoma Hemifield Test was outside normal limits in 73% of the cases, with frequent evidence of perimetric defects commonly seen in glaucoma, like arcuate defects, nasal steps or paracentral scotomata. Of note, no correlation was found between perimetric defects and the severity scores commonly used in PD, like the Mini Mental State Examination or the Hoehn and Yahn scale. In the discussion the authors consider the potential mechanisms underlying these findings and in particular the fact that dopaminergic deficiency may affect the retinal amacrine, horizontal and ganglion cell circuitry, thus modifying the receptive field output of the retina. They consider that this is a more likely explanation of the observed defects, at least in their patient sample, than motor dysfunction or impaired visual processing in the brain.
Frequent evidence was found in patients with Parkinson's disease or perimetric defects commonly seen in glaucoma
The implications of the study may be far reaching for the neuroscientist seeking to identify biomarkers for PD. From the glaucomatologist's perspective its main merit is to highlight that visual field findings in Parkinson's disease may mimic glaucomatous perimetric defects, representing a differential diagnosis challenge with true glaucomatous damage in these patients.