Shanhua Han

Background/Objectives: Neural compensation, in which healthy brain regions take over functions lost due to lesions, is a potential biomarker for functional recovery after stroke. However, previous neuroimaging studies often speculated on neural compensation simply based on greater measures in patients (compared to healthy controls) without demonstrating a more direct link between these measures and the functional recovery. Because taking over the function of a lesion region means taking on a similar role as that lesion region in its functional network, the present study attempted to explore neural compensation based on the similarity of functional connectivity (FC) patterns between a healthy regions and lesion regions. Methods: Seventeen stroke patients (13M4F, 63.2 ± 9.1 y.o.) underwent three resting-state functional MRI (rs-fMRI) sessions during rehabilitation. FC patterns of their lesion regions were derived by lesion network analysis; and these patterns were correlated with healthy FC patterns derived from each brain voxel of 51 healthy subjects (32M19F, 61.0 ± 14.3 y.o.) for the assessment of pattern similarity. Results: We identified five healthy regions showing decreasing FC similarity (29–54%, all corrected p < 0.05, effect size η²: 0.10–0.20) to the lesion network over time. These decreasing similarities were associated with increasing behavioral scores on activities of daily living (ADL, p < 0.001, η² = 0.90), suggesting greater neural compensation at early-stage post-stroke and reduced compensation toward the end of effective rehabilitation. Conclusions: Besides direct FC measures, the present results propose an alternative biomarker of neural compensation in functional recovery from stroke. For sensorimotor recoveries like ADL, this biomarker could be more sensitive than direct measures of lesion connectivity in the motor network.

Objective: To compare the quantitative susceptibility mapping (QSM) susceptibility values and pathology composition with different types of thrombi in the middle cerebral artery (MCA), and assess the value of susceptibility weight imaging in thrombus component diagnosis in stroke. Materials and methods: This study included 15 patients (73.47 ± 10.7 years; 6 males and 9 females) who underwent magnetic resonance imaging before mechanical thrombectomy due to acute middle cerebral artery occlusion between January 2017 and December 2019. All patients had the susceptibility vessel sign (SVS) on SWI (susceptibility weighted imaging), and the thrombus susceptibility was measured by signal processing in nuclear magnetic resonance SPIN software. The retrieved thrombi underwent histopathologic analysis, and the correlation between thrombus susceptibility and the pathologic composition was analyzed by two independent Kolmogorov–Smirnov tests. The location and length of thrombi were evaluated on both SWI and DSA, and the correlation was explored using two independent samples Wilcoxon rank test. The correlations between susceptibility and the infarct core volumes (ADC < 620 mm²/s volume map), hypoperfusion volumes (Tmax > 6 s volume map), 90-day modified Rankin scale (mRS), and the National Institutes of Health Stroke Scale (NIHSS) at admission were analyzed by Spearman’s correlation analysis. Results: Among the 15 retrieved thrombi, the mean thrombus susceptibility of RBC-dominant and fibrin-dominant thrombi were 209.88 ± 11.32 and 155.70 ± 28.20 (ppb), respectively (p = 0.037). The average distance of the proximal end of the thrombi to the midline was 24.67 ± 8.43 mm and 24.62 ± 8.44 mm, as measured by SWI and DSA (digital subtraction angiography), respectively (p < 0.001). The correlation between thrombus susceptibility was weakly negatively correlated with ADC < 620 mm²/s volume map (r = 0.356, p = 0.193) and poorly correlated with Tmax > 6 s volume map (r = 0.252, p = 0.365), 90-day mRS (r = 0.182, p = 0.517), and NIHSS at admission (r = 0.262, p = 0.345). Conclusions: The measurements of the Quantitative susceptibility value of thrombi may help predict the composition of thrombi in patients with acute middle cerebral artery occlusion. QSM provides a more accurate method to evaluate the thrombi.

To automatically and quantitatively evaluate the venous oxygen saturation (SvO2) in cerebral ischemic tissues and explore its value in predicting prognosis. A retrospective study was conducted on 48 AIS patients hospitalized in our hospital from 2015–2018. Based on quantitative susceptibility mapping and perfusion-weighted imaging, this paper measured the cerebral SvO2 in hypoperfusion tissues and its change after intraarterial rt-PA treatment. The cerebral SvO2 in different hypoperfusion regions between the favorable and unfavorable clinical outcome groups was analyzed using an independent t-test. Relationships between cerebral SvO2 and clinical scores were determined using the Pearson correlation coefficient. The receiver operating characteristic process was conducted to evaluate the accuracy of cerebral SvO2 in predicting unfavorable clinical outcomes. Cerebral SvO2 in hypoperfusion (Tmax > 4 and 6 s) was significantly different between the two groups at follow-up (p < 0.05). Cerebral SvO2 and its changes before and after treatment were negatively correlated with clinical scores. The positive predictive value, negative predictive value, accuracy, and area under the curve of the cerebral SvO2 were higher than those predicted by the ischemic core. Therefore, the cerebral SvO2 of hypoperfusion regions was a stronger imaging predictor of unfavorable clinical outcomes after stroke.

This study investigated the quantitative distribution of cerebral venous oxygen saturation (SvO2) based on quantitative sensitivity mapping (QSM) and determined its prognostic value in patients with acute ischemic stroke (AIS). A retrospective study was conducted on 39 hospitalized patients. Reconstructed QSM was used to calculate the cerebral SvO2 of each region of interest (ROI) in the ischemic hemisphere. The intraclass correlation coefficient (ICC) and Bland–Altman analysis were conducted to define the best resolution of the distribution map. The correlation between the cerebral SvO2 in hypoxic regions (SvO2_ROI < 0.7) and clinical scores was obtained by Spearman and power analysis. The associations between cerebral SvO2 and unfavorable prognosis were analyzed using multivariate logistic regression. Excellent agreement was found between the cerebral SvO2 in hypoxic regions with a resolution of 7.18 × 7.18 × 1.6 mm³ and asymmetrically prominent cortical veins regions (ICC: 0.879 (admission), ICC: 0.906 (discharge)). The cerebral SvO2 was significantly negative with clinical scores (all |r| > 0.3). The cerebral SvO2 and its changes at discharge were significantly associated with an unfavorable prognosis (OR: 0.812 and 0.866). Therefore, the cerebral SvO2 in hypoxic regions measured by the quantitative distribution map can be used as an indicator for evaluating the early prognosis of AIS.

Mild cognitive impairment (MCI) occurs frequently in many end stage renal disease (ESRD) patients, may significantly worsen survival odds and prognosis. However, the exact neuropathological mechanisms of MCI combined with ESRD are not fully clear. This study examined functional connectivity (FC) alterations of the default-mode network (DMN) in individuals with ESRD and MCI. Twenty–four individuals with ESRD identified as MCI patients were included in this study; of these, 19 and 5 underwent hemodialysis (HD) and peritoneal dialysis (PD), respectively. Another group of 25 age-, sex- and education level-matched subjects were recruited as the control group. All participants underwent resting-state functional MRI and neuropsychological tests; the ESRD group underwent additional laboratory testing. Independent component analysis (ICA) was used for DMN characterization. With functional connectivity maps of the DMN derived individually, group comparison was performed with voxel-wise independent samples t-test, and connectivity changes were correlated with neuropsychological and clinical variables. Compared with the control group, significantly decreased functional connectivity of the DMN was observed in the posterior cingulate cortex (PCC) and precuneus (Pcu), as well as in the medial prefrontal cortex (MPFC) in the ESRD group. Functional connectivity reductions in the MPFC and PCC/Pcu were positively correlated with hemoglobin levels. In addition, functional connectivity reduction in the MPFC showed positive correlation with Montreal Cognitive Assessment (MoCA) score. Decreased functional connectivity in the DMN may be associated with neuropathological mechanisms involved in ESRD and MCI.