Asterios Chrysou1, Nomdo M Jansonius2, Teus van Laar3. 1. Department of Neurology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands. Electronic address: a.chrysou@rug.nl. 2. Department of Ophthalmology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands. Electronic address: n.m.jansonius@umcg.nl. 3. Department of Neurology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands. Electronic address: t.van.laar@umcg.nl.
Abstract
BACKGROUND: Patients with Parkinson's disease experience visual symptoms, partially originating from retinal changes. Since 2011, multiple case-control studies using spectral-domain OCT, which allows for studying individual retinal layers, have been published. The aim of this study was to substantiate the occurrence, extent, and location of retinal degeneration in Parkinson's by meta-analysis. METHODS: Spectral-domain OCT case-control data were collected by performing a search in PubMed and Embase with terms: "optical coherence tomography" and "parkinson", up to November 5th, 2018. Studies with fewer than 10 patients or controls were excluded. We performed a random effects meta-analysis. Heterogeneity was evaluated with I2 statistics; publication bias with Egger's and Begg's tests. RESULTS: Out of 77 identified studies, 36 were included, totaling 1916 patients and 2006 controls. A significant thinning of the peripapillary retinal nerve fiber layer (d = -0.42; 95% confidence interval -0.54 to -0.29) and the combined ganglion cell and inner plexiform layers (d = -0.40; -0.72, to -0.07) was found. The inner nuclear layer and outer plexiform layer did not show significant changes. Heterogeneity ranged from 3 to 92%; no publication bias was found. CONCLUSIONS: Parkinson's patients show significant thinning of the inner retinal layers, resembling changes found in glaucoma and other neurodegenerative diseases like Alzheimer's. Study of different cell layers in-vivo is possible by moving from time-to spectral domain OCT. Retinal degeneration may be affiliated with neurodegenerative pathology overall, and could serve as a biomarker in neurodegenerative disorders. Longitudinal research including clinical correlations is needed to determine usefulness in Parkinson's disease.
BACKGROUND:Patients with Parkinson's disease experience visual symptoms, partially originating from retinal changes. Since 2011, multiple case-control studies using spectral-domain OCT, which allows for studying individual retinal layers, have been published. The aim of this study was to substantiate the occurrence, extent, and location of retinal degeneration in Parkinson's by meta-analysis. METHODS: Spectral-domain OCT case-control data were collected by performing a search in PubMed and Embase with terms: "optical coherence tomography" and "parkinson", up to November 5th, 2018. Studies with fewer than 10 patients or controls were excluded. We performed a random effects meta-analysis. Heterogeneity was evaluated with I2 statistics; publication bias with Egger's and Begg's tests. RESULTS: Out of 77 identified studies, 36 were included, totaling 1916 patients and 2006 controls. A significant thinning of the peripapillary retinal nerve fiber layer (d = -0.42; 95% confidence interval -0.54 to -0.29) and the combined ganglion cell and inner plexiform layers (d = -0.40; -0.72, to -0.07) was found. The inner nuclear layer and outer plexiform layer did not show significant changes. Heterogeneity ranged from 3 to 92%; no publication bias was found. CONCLUSIONS:Parkinson'spatients show significant thinning of the inner retinal layers, resembling changes found in glaucoma and other neurodegenerative diseases like Alzheimer's. Study of different cell layers in-vivo is possible by moving from time-to spectral domain OCT. Retinal degeneration may be affiliated with neurodegenerative pathology overall, and could serve as a biomarker in neurodegenerative disorders. Longitudinal research including clinical correlations is needed to determine usefulness in Parkinson's disease.
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