Retinal imaging effectively measures risk for cognitive decline in Parkinson’s disease
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Patients with idiopathic Parkinson’s disease who had lower retinal thickness at baseline demonstrated an increased risk for cognitive decline after 3 years, suggesting layer thickness could have predictive value.
Researchers, who specifically looked at macular ganglion-inner plexiform layer complex (GCIPL) and peripapillary retinal nerve fiber layer (pRNFL) thickness, published the findings in Annals of Neurology.
“It’s been known for years that retinal alterations are present in Parkinson’s disease, and a thinning of inner retinal layers has been associated with disease severity in previous studies,” Ane Murueta-Goyena, PhD, of the neurodegenerative diseases group at BioCruces Bizkaia Health Research Institute in Spain, told Healio Neurology. “Considering that the retina can be imaged through noninvasive techniques, such as optical coherence tomography (OCT), during the past two decades a lot of efforts have been made to evaluate the usefulness of retinal measurements for the diagnosis and prognosis of Parkinson’s disease.”
However, there are no validated biomarkers currently for cognitive progression in Parkinson’s disease, she continued.
“It is known that early compromise of visuospatial abilities delineates the progression to Parkinson’s disease dementia, but the identification of reliable and minimally invasive biomarkers is urgent for the design and evaluation of preventive strategies and clinical trials targeting cognitive decline in this population,” Murueta-Goyena said.
Murueta-Goyena and colleagues used a prospective, longitudinal evaluation of Spectralis retinal OCT, Montreal Cognitive Assessment (MoCA) and Unified Parkinson’s Disease Rating Scale (UPDRS) score data to assess the change in retinal thickness over time and its value in predicting cognitive functioning.
“OCT is readily available in ophthalmology departments and is fast, non-invasive and comfortable for the patient,” Murueta-Goyena said.
The researchers enrolled participants with idiopathic Parkinson’s disease (n = 42), dementia with Lewy bodies (n = 4), E46K-SNCA mutation carriers (n = 4) and controls (n = 17). They included the cohorts of patients with dementia with Lewy bodies and E46K-SNCA mutation carriers as well as the control cohort “as a strategy to identify [Parkinson’s disease] patients with worse prognosis.”
Researchers also compared participant data with a dataset collected from 250 healthy volunteers to evaluate age-related changes in macular OCT measurements.
At baseline, researchers gathered data on disease duration, Hoehn & Yahr scale score, UPDRS part III score (UPDRS III), a motor examination, and Levodopa equivalent daily dose (LEDD) data. They used linear mixed models to estimate the reduction rates of macular ganglion-inner plexiform layer complex (GCIPL) and peripapillary retinal nerve fiber layer (pRNFL) thickness.
During the follow-up period, 17 patients (idiopathic Parkinson’s disease, n = 14; dementia with Lewy bodies, n =1; E46K-SNCA, n = 2) saw UPDRS III score changes of 5 or more points. Motor decline correlated only with baseline UPDRS III scores (OR = .897, P = .016). Mean MoCA scores decreased from baseline among patients with idiopathic Parkinson’s disease (24.8 vs. 23.3; multivariate linear mixed-effects regression models, P = .01), carriers of E46-SNCA (19 vs. 15.5) and dementia with Lewy bodies (24 vs. 16).
“Interestingly, cognitive worsening was not associated with initial MoCA score or any other demographic or disease-related clinical variable,” the researchers wrote.
The rate of low contrast visual acuity deterioration was most prominent in participants who were carriers of E46-SNCA (-37.4% change) and had dementia with Lewy bodies (-20.5% change) compared with patients with idiopathic Parkinson’s disease (20% change) and controls (29.4% change).
Among patients with idiopathic Parkinson’s disease, pRNFL and GCIPL thickness decreased. The average pRNFL thickness decrease was significant in patients with idiopathic Parkinson’s disease (-.55 µm/year; P < .001), but not in controls (-.15 µm/year, P = .192). GCIPL thickness in the parafoveal region (1- to 3-mm ring) presented the largest reduction rate. The annualized atrophy rate was 0.63 m in patients with idiopathic Parkinson’s disease and 0.23 m in controls (P < .0001).
Murueta-Goyena and colleagues found that retinal thickness was associated with cognitive decline. Patients with idiopathic Parkinson’s disease with lower parafoveal GCIPL and pRNFL thickness at baseline demonstrated a greater risk for cognitive decline at 3 years (RR = 3.49 [95% CI, 1.10-11.1] and RR = 3.28 [95% CI, 1.03 – 10.45], respectively). Classifying patients according to their visual outcomes at baseline demonstrated that the risk for worsening of general cognition was almost five times higher among patients with visual dysfunction (RR = 4.69; 95% CI, 1.34-16.5), even after adjusting for confounders (RR = 4.79; 95% CI, 0.91-21.18). They did not find significant associations between retinal thickness and motor deterioration.
“As far as we know, this is the first study demonstrating that a single timepoint measurement with a noninvasive technique can predict cognitive decline in Parkinson’s disease,” Murueta-Goyena said. “Our results provide a real breakthrough in the field of retinal imaging with OCT for monitoring neurodegeneration and predicting subsequent cognitive worsening in Parkinson’s disease. In the near future, OCT could be used in Parkinson’s disease to make clinical decisions.”