Background and Purpose: The association of retinal microvascular abnormalities with the total cerebral small vessel disease (cSVD) burden found on brain MRI has not been determined. In the present study, we examined whether the retinopathy score could predict the total cSVD burden in ischemic stroke/transient ischemic attack (TIA) patients. A simple practical diagnostic tool may help identify candidates for MRI screening. Methods: We consecutively collected clinical data including retinal photography and cerebral MRI of ischemic stroke/TIA patients from August 2016 to August 2017 at our stroke center. The retinopathy score was assessed by the Keith-Wagener-Barker grading system for analyzing retinal microvascular abnormalities. To evaluate the total cSVD burden, the total cSVD score was assessed by awarding one point for the presence of each marker of cSVD on MRI. The clinical characteristics and retinopathy score were analyzed across patients for each total cSVD score. The association between the retinopathy score and the total cSVD score was analyzed. Results: Among the 263 enrolled patients, the frequency of hypertension in patients with a total cSVD score of 2, 3, or 4 was higher than that in patients with a score of 0 (69.5, 71.7, and 89.2% vs. 45.2% respectively, all P < 0.05). The retinopathy score was related to the total cSVD score (r = 0.687, P < 0.001). Adjusted multivariate ordinal regression showed that the retinopathy score was independently correlated with the total cSVD score (odds ratio [OR], 4.18; 95% confidence interval [CI], 3.07–5.70) after adjustment for age, history of hypertension, previous stroke/TIA and current smoking. The c statistics were 0.30 (95% CI, 0.24–0.37; P < 0.05), 0.46 (95% CI, 0.39–0.53; P = 0.303), 0.79 (95% CI, 0.72–0.86; P < 0.001), and 0.81 (95% CI, 0.74–0.88; P < 0.001) for predicting the total cSVD score of 1, 2, 3, and 4 respectively. Conclusions: These results suggest that retinal microvascular abnormalities have predictive value for severe total cSVD burden in ischemic stroke/TIA patients.

Many patients show poor outcomes following endovascular reperfusion therapy (ERT), and poor cortical venous outflow is a risk factor for these poor outcomes. We investigated the association between the outflow of the internal jugular vein (IJV) and baseline cortical venous outflow and the outcomes after ERT. We retrospectively enrolled 78 patients diagnosed with an acute anterior circulation stroke and successful ERT. Poor IJV outflow on the affected side was defined as stenosis ≥50% or occlusion of ipsilateral IJV, and poor outflow of bilateral IJVs was defined as stenosis ≥50% or occlusion of both IJVs. Poor cortical venous outflow was defined as a cortical vein opacification score (COVES) of 0 on admission. Multivariate analysis showed that poor outflow of IJV on the affected side was an independent predictor for hemorrhagic transformation. The poor outflow of bilateral IJVs was an independent risk factor for poor clinical outcomes. These patients also had numerical trends of a higher incidence of symptomatic intracranial hemorrhage, midline shift >10 mm, and in-hospital mortality; however, statistical significance was not observed. Additionally, poor IJV outflow was an independent determinant of poor cortical venous outflow. For acute large vessel occlusion patients, poor IJV outflow is associated with poor baseline cortical venous outflow and outcomes after successful ERT.

Objectives: Hypertension (HBP) is a risk factor for the development of motor and cognitive functions in Parkinson disease (PD) patients, but the specific mechanism is unclear. This study investigated white matter structural network abnormalities and their mediation effect of cognitive decline in patients with PD and HBP. Methods: PD patients with HBP and normal blood pressure (HBP and non-HBP) underwent conventional and multi-shell diffusion magnetic resonance imaging (MRI) at baseline. Cognitive function was evaluated using the Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) at baseline and 12-month follow-up. Enlarged perivascular spaces (EPVS) in the basal ganglia and midbrain were assessed at baseline. White matter structural network based on the diffusion MRI was constructed. The mediation effect and correlations of EPVS and the network metrics with cognitive function were analyzed. Results: At 12-month follow-up, the cognitive decline was found in the HBP group. Global connectivity was impaired in the HBP group. The number and maximum diameter of EPVS were higher in the HBP group. The nodal connectivity was impaired in the HBP group and associated with the cognitive function at baseline and follow-up. Both global and nodal network metrics, as well as the counts of EPVS mediated the effect of HBP on the cognitive decline. Conclusions: The PD patients with HBP had worse cognitive function. Hypertensive impairment of white matter connectivity may be the underlying mechanism of cognitive decline in PD patients.