PubMed ID: 19475677
Author(s): Qiu C, Cotch MF, Sigurdsson S, Klein R, Jonasson F, Klein BE, Garcia M, Jonsson PV, Harris TB, Eiriksdottir G, Kjartansson O, van Buchem MA, Gudnason V, Launer LJ. Microvascular lesions in the brain and retina: The age, gene/environment susceptibility-Reykjavik study. Ann Neurol. 2009 May;65(5):569-76. doi: 10.1002/ana.21614. PMID 19475677
Journal: Annals Of Neurology, Volume 65, Issue 5, May 2009
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.