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. 2009 May;65(5):569-76.
doi: 10.1002/ana.21614.

Microvascular lesions in the brain and retina: The age, gene/environment susceptibility-Reykjavik study

Affiliations

Microvascular lesions in the brain and retina: The age, gene/environment susceptibility-Reykjavik study

Chengxuan Qiu et al. Ann Neurol. 2009 May.

Abstract

Objective: To investigate whether the severity and location of cerebral white matter hyperintensities (WMHs) and brain infarcts are correlated with the signs of retinal microvascular abnormalities in the elderly.

Methods: The study included 4,176 men and women (mean age, 76 years) who participated in the Age, Gene/Environment Susceptibility (AGES)-Reykjavik Study. Digital retinal images of both dilated eyes were taken and evaluated for the presence of retinal focal arteriolar signs (focal arteriolar narrowing and arteriovenous nicking) and retinopathy lesions (retinal blot hemorrhages and microaneurysms). Brain magnetic resonance imaging scans were acquired and evaluated for the presence and distribution of cerebral infarcts and WMHs. Logistic and multinomial logistic models were constructed to estimate the association of retinal microvascular signs to brain lesions.

Results: Controlling for demographic and major cardiovascular risk factors, we found that retinal focal arteriolar signs, but not retinopathy lesions, were significantly associated with an increasing load of subcortical and periventricular WMHs. The strongest association was found between retinal arteriolar signs and a heavier WMH load, specifically in the subcortical frontal lobe, and periventricular frontal and parietal caps. There was a tendency toward bilateral retinal focal arteriolar narrowing being more strongly associated with the heavier load of subcortical WMHs. Arteriovenous nicking was significantly associated with subcortical infarcts.

Interpretation: In older adults, retinal focal arteriolar signs, but not retinopathy lesions, are correlated with the load of diffuse WMHs, particularly those located in the subcortical frontal lobe, and the periventricular frontal and parietal caps of the brain.

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Conflict of interest statement

Conflict of interest: The authors have no conflict of interest in connection with this study.

Figures

Fig 1
Fig 1
Burden (one eye or both eyes affected vs. no lesion) of retinal focal arteriolar narrowing (A), AV nicking (B), and retinopathy lesions (C) in relation to the severity of cerebral white matter hyperintensities (WMHs) in subcortical (quartiles) and periventricular (tertiles) areas: odds ratios were derived from multi-adjusted multinomial logistic models, in which people with no retinal lesion held as reference for the modeling. # Reference group; * p<0.05; § p<0.01.
Fig 2
Fig 2
Retinal focal arteriolar changes (arteriolar narrowing or AV nicking) and retinopathy lesions (retinal hemorrhages or microaneurysms), each alone or in combination, in relation to the severity of cerebral white matter hyperintensities (WMHs) in subcortical (quartiles) and periventricular (tertiles) areas: odds ratios were derived from multi-adjusted multinomial logistic models, in which people with no retinal lesion held as reference for the modeling. # Reference group; § p<0.01.

References

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