BACKGROUND AND PURPOSE:The association of perivascular spaces in the centrum semiovale with amyloid accumulation among patients with Alzheimer disease-related cognitive impairment is unknown. We evaluated this association in patients with Alzheimer disease-related cognitive impairment and b -amyloid deposition, assessed with [ 18 F] florbetaben PET/CT. MATERIALS AND METHODS: MR imaging and [ 18 F] florbetaben PET/CT images of 144 patients with Alzheimer disease-related cognitive impairment were retrospectively evaluated. MR imaging-visible perivascular spaces were rated on a 4-point visual scale: a score of $3 or ,3 indicated a high or low degree of MR imaging-visible perivascular spaces, respectively. Amyloid deposition was evaluated using the brain b -amyloid plaque load scoring system. RESULTS: Compared with patients negative for b -amyloid, those positive for it were older and more likely to have lower cognitive function, a diagnosis of Alzheimer disease, white matter hyperintensity, the Apolipoprotein E « 4 allele, and a high degree of MR imaging-visible perivascular spaces in the centrum semiovale. Multivariable analysis, adjusted for age and Apolipoprotein E status, revealed that a high degree of MR imaging-visible perivascular spaces in the centrum semiovale was independently associated with b -amyloid positivity (odds ratio, 2.307; 95% CI, 1.036-5.136; P ¼ .041). CONCLUSIONS:A high degree of MR imaging-visible perivascular spaces in the centrum semiovale independently predicted b -amyloid positivity in patients with Alzheimer disease-related cognitive impairment. Thus, MR imaging-visible perivascular spaces in the centrum semiovale are associated with amyloid pathology of the brain and could be an indirect imaging marker of amyloid burden in patients with Alzheimer disease-related cognitive impairment.

PurposeTo investigate the incidence and preoperative clinical features of reactivated Graves' orbitopathy (GO) after orbital decompression.MethodsThis study included patients with GO who underwent orbital decompression for disfiguring proptosis and not compressive optic neuropathy and received postoperative follow-up care for more than 12 months. Patients who experienced active inflammatory signs within 6 months of decompression were excluded from analysis. The demographic characteristics, ophthalmic manifestations, and biochemical parameters of the patients were analyzed for association with reactivation of GO by logistic regression analysis.ResultsOut of the 92 patients included in this study, seven (7.6%) experienced reactivation of GO after orbital decompression. The mean time interval between surgery and reactivation of GO was 36.3±14.3 weeks. Univariate logistic regression analysis identified age, existing smoking habits, and modified NOSPECS and Gorman scores as significant factors for the reactivation of GO. The results of multivariate logistic regression analysis revealed that smoking and modified NOSPECS and Gorman scores were associated with the reactivation of GO.ConclusionsQuitting smoking is important for the prevention of reactivation of GO after orbital decompression. Patients with severe symptoms, especially those with restrictive myopathy, should be carefully monitored for reactivation of GO after orbital decompression.