Objective—: Carotid intraplaque hemorrhage (IPH) is associated with cardiovascular events. Calcification, which frequently accompanies IPH, may play a role in IPH occurrence. In this study, we aimed to investigate the associations between calcification characteristics and IPH in carotid plaques. Approach and results—: One hundred seventeen patients with cerebrovascular symptoms and carotid plaques detected by ultrasound were recruited and underwent multicontrast magnetic resonance imaging. Advanced carotid plaques with composition measured by magnetic resonance imaging were included in the analysis. Carotid calcifications were divided into the following categories: surface, mixed, and deep calcification. They were also classified into single and multiple calcifications according to quantity. Logistic regression models utilizing generalized estimating equations were performed to evaluate the relationship between calcification and IPH. Of 117 subjects, 85 with 142 plaques were included in the final analysis, whereas 32 were excluded because of lack of plaque compositions. Of the 142 plaques, 40 (28.2%) had IPH. Plaques with IPH showed greater prevalence of calcification than those without (87.5% versus 55.9%; P =0.005). After adjusting for age, low-density lipoprotein, maximum wall thickness, and maximum soft plaque thickness, multiple calcifications (odd ratio, 10.1; 95% confidence interval, 3.3–30.4), surface calcification (odd ratio, 29.4; 95% confidence interval, 4.1–210.8), and mixed calcifications (odd ratio, 27.9; 95% confidence interval, 7.3–107.1) were found to be strongly associated with the presence of IPH (all P <0.05). Conclusions—: Surface calcification and multiple calcifications in carotid atherosclerotic plaques are independently associated with the presence of IPH, suggesting that both quantity and location of calcification may play important roles in the occurrence of IPH. These findings may provide novel insights for understanding mechanisms of IPH.

BACKGROUND AND PURPOSE: An accurate evaluation of the World Health Organization grade and cellular proliferation is particularly important in meningiomas. Our aim was to prospectively evaluate and compare diffusional kurtosis imaging, DTI, and DWI metrics in determining the grade and cellular proliferation of meningiomas. MATERIALS AND METHODS: Ninety-six consecutive patients with histopathologically confirmed meningiomas were included in this study. Mean kurtosis, radial kurtosis, axial kurtosis, fractional anisotropy, mean diffusivity, and ADC were semiautomatically obtained in the solid components of tumors. Each normalized diffusion value was compared between high-grade meningiomas and low-grade meningiomas using the Mann-Whitney U test. Receiver operating characteristic, multiple logistic regression, and Pearson correlation analysis were used for statistical evaluations. RESULTS: Diffusional kurtosis imaging metrics (mean kurtosis, radial kurtosis, and axial kurtosis) were significantly higher in high-grade meningiomas than in low-grade meningiomas (P ≤ .001). Mean diffusivity and ADC were significantly lower in high-grade meningiomas than in low-grade meningiomas (P = .003 and .002). Mean kurtosis had significantly greater area the under curve values than mean diffusivity and fractional anisotropy in differentiating high-grade meningiomas from low-grade meningiomas (P = .038 and .002). Mean kurtosis was the only variable that could be used to independently differentiate high-grade meningiomas and low-grade meningiomas (P < .001). Significant correlations were found between the Ki-67 labeling index and kurtosis metrics (P < .001), as well as for mean diffusivity and ADC (P = .004, and .007). CONCLUSIONS: Compared with other diffusion metrics, mean kurtosis may serve as an optimal parameter for evaluating and predicting the meningioma grade. Moreover, diffusion metrics may potentially reflect cellular proliferation.

Objective: Differentiation of glioblastomas from solitary brain metastases using conventional MRI remains an important unsolved problem. In this study, we introduced the conception of the cerebral blood flow (CBF) gradient in peritumoral edema—the difference in CBF values from the proximity of the enhancing tumor to the normal-appearing white matter, and investigated the contribution of perfusion metrics on the discrimination of glioblastoma from a metastatic lesion.

Growing evidence highlights the roles of glymphatic system and peripheral inflammation in Parkinson’s disease (PD). We evaluated their interrelationship and potential mechanisms contributing to motor symptoms using DTI-ALPS and inflammatory markers (leukocyte, lymphocyte, neutrophil counts, neutrophil-to-lymphocyte ratio [NLR], and platelet-to-lymphocyte ratio [PLR]) in 134 PD patients (52 tremor-dominant [TD], 62 postural instability and gait difficulty [PIGD]) and 81 healthy controls (HC, 33 with inflammatory markers). PD exhibited lower DTI-ALPS than HC (1.43 ± 0.19 vs. 1.52 ± 0.21, p = 0.001). DTI-ALPS was negatively correlated with NLR, PLR, and neutrophils in PD (all p < 0.05) and with neutrophils in PIGD (β = –0.043, p = 0.048), and positively correlated with lymphocytes in TD (β = 0.105, p = 0.034). DTI-ALPS mediated the relationship between peripheral inflammation (NLR and neutrophils) and MDS-UPDRS III score in PD. Overall, glymphatic dysfunction correlates with peripheral inflammation and may mediate effects of inflammation on motor symptoms in PD, with distinct inflammation profiles between TD and PIGD.