Background Accumulating evidence indicates regional structural changes in the white matter (WM) of brains in patients with blepharospasm (BSP); however, whether large‐scale WM structural networks undergo widespread reorganization in these patients remains unclear. Objective We investigated topology changes and global and local features of large‐scale WM structural networks in BSP patients compared with hemifacial spasm (HFS) patients or healthy controls (HCs). Methods This cross‐sectional study applied graph theoretical analysis to assess deterministic diffusion tensor tractography findings in 41 BSP patients, 41 HFS patients, and 41 HCs. WM structural connectivity in 246 cortical and subcortical regions was assessed, and topological parameters of the resulting graphs were calculated. Networks were compared among BSP, HFS, and HCs groups. Results Compared to HCs, both BSP and HFS patients showed alterations in network integration and segregation characterized by increased global efficiency and modularity and reduced shortest path length. Moreover, increased nodal efficiency in multiple cortical and subcortical regions was found in BSP and HFS patients compared with HCs. However, these differences were not found between BSP and HFS patients. Whereas all participants showed highly similar hub distribution patterns, BSP patients had additional hub regions not present in either HFS patients or HCs, which were located in the primary head and face motor cortex and basal ganglia. Conclusions Our findings suggest that the large‐scale WM structural network undergoes an extensive reorganization in BSP, probably due to both dystonia‐specific abnormalities and facial hyperkinetic movements. © 2021 International Parkinson and Movement Disorder Society

White matter abnormalities in blepharospasm (BSP) have been evaluated using conventional intra-voxel metrics, and changes in patterns of cortical thickness in BSP remain controversial. We aimed to determine whether local diffusion homogeneity, an inter-voxel diffusivity metric, could be valuable in detecting white matter abnormalities for BSP; whether these changes are related to disease features; and whether cortical thickness changes occur in BSP patients. Diffusion tensor and structural magnetic resonance imaging were collected for 29 patients with BSP and 30 healthy controls. Intergroup diffusion differences were compared using tract-based spatial statistics analysis and measures of cortical thickness were obtained. The relationship among cortical thickness, diffusion metric in significantly different regions, and behavioral measures were further assessed. There were no significant differences in cortical thickness and fractional anisotropy between the groups. Local diffusion homogeneity was higher in BSP patients than controls, primarily in the left superior longitudinal fasciculus, corpus callosum, left posterior corona radiata, and left posterior thalamic radiata (P < 0.05, family-wise error corrected). The local diffusion homogeneity values in these regions were positively correlated with the Jankovic rating scale (r s = 0.416, P = 0.031) and BSP disability index (r s = 0.453, P = 0.018) in BSP patients. These results suggest that intra-and inter-voxel diffusive parameters are differentially sensitive to detecting BSP-related white matter abnormalities and that local diffusion homogeneity might be useful in assessing disability in BSP patients.

Background High white blood cell (WBC) count and high blood glucose level are risk factors for mortality and pneumonia after acute ischemic stroke (AIS). We investigated the combined effect of high WBC count and high blood glucose level on hospital admission and in-hospital mortality and pneumonia in acute AIS patients. Methods A total of 3124 AIS patients enrolled from December 2013 to May 2014 across 22 hospitals in Suzhou city were included in the present study. We divided patients into four groups according to their level of WBC count and blood glucose: NWNG (normal WBC count and normal glucose), NWHG (normal WBC count and higher glucose), HWNG (higher WBC count and normal glucose), and HWHG (higher WBC count and higher glucose). Cox proportional hazard model and logistic regression model were used to estimate the combined effect of WBC count and blood glucose on all-cause in-hospital mortality and pneumonia in AIS patients. Results HWHG was associated with a 2.22-fold increase in the risk of in-hospital mortality in comparison to NWNG (adjusted hazard ratio [HR] 2.22; 95% confidence interval [CI], 1.21–4.07; P trend = 0.003). The risk of pneumonia was significantly higher in patients with HWHG compared to those with NWNG (adjusted odds ratio [OR] 2.61; 95% CI, 1.66–4.10; P trend < 0.001). The C-statistic for the combined WBC count and blood glucose was higher than WBC count or blood glucose alone for prediction of in-hospital mortality and pneumonia (all p < 0.01). Conclusions High WBC count combined with high blood glucose level at admission was independently associated with in-hospital mortality and pneumonia in AIS patients. Moreover, the combination of WBC count and blood glucose level appeared to be a better predictor than WBC count or blood glucose alone. Electronic supplementary material The online version of this article (10.1186/s12974-019-1422-7) contains supplementary material, which is available to authorized users.

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Objective:To assess the risk of glucose-6-phosphate dehydrogenase (G6PD) on stroke prognosis, we compared outcomes between stroke patients with and without G6PD deficiency.Methods:The study recruited 1251 patients with acute ischemic stroke. Patients were individually categorized into G6PD-deficiency and non-G6PD-deficiency groups according to G6PD activity upon admission. The primary endpoint was poor outcome at 3 months defined by a modified Rankin Scale (mRS) score ≥ 2 (including disability and death). Secondary outcomes included the overall mRS scores at 3 months, and in-hospital death and all death within 3 months. Logistic regression and Cox models, adjusted for potential confounders, were fitted to estimate the association of G6PD deficiency with the outcomes.Results:Among 1251 patients, 150 (12.0 %) were G6PD deficient. Patients with G6PD deficiency had higher proportions of large-artery atherosclerosis (odds ratio [OR] 1.53, 95% confidence interval [CI] 1.09-2.17) and stroke history (OR 1.93, 95% CI 1.26-2.90) compared to the non-G6PD-deficient group. The two groups differed significantly in the overall mRS-score distribution (adjusted common OR 1.57, 95% CI 1.14-2.17). Patients with G6PD deficiency had higher rates of poor outcome at 3 months (adjusted OR 1.73, 95% CI 1.08-2.76; adjusted absolute risk increase 13.0%, 95% CI 2.4%-23.6%). The hazard ratio of in-hospital death for patients with G6PD-deficiency was 1.46 (95% CI 1.37-1.84).Conclusions:G6PD deficiency is associated with the risk of poor outcome at 3 months after ischemic stroke and may increase the risk of in-hospital death. These findings suggest the rationality of G6PD screening in patients with stroke.

Pristella maxillaris is known as the X-ray fish based on its translucent body. However, the morphological characteristics and the molecular regulatory mechanisms of these translucent bodies are still unknown. In this study, the following three phenotypes, a black-and-gray body color or wild-type (WT), a silvery-white body color defined as mutant I (MU1), and a fully transparent body with a visible visceral mass named as mutant II (MU2), were investigated to analyze their chromatophores and molecular mechanisms. The variety and distribution of pigment cells in the three phenotypes of P. maxillaris significantly differed by histological assessment. Three types of chromatophores (melanophores, iridophores, and xanthophores) were observed in the WT, whereas MU1 fish were deficient in melanophores, and MU2 fish lacked melanophores and iridophores. Transcriptome sequencing of the skin and peritoneal tissues of P. maxillaris identified a total of 166,089 unigenes. After comparing intergroup gene expression levels, more than 3,000 unigenes with significantly differential expression levels were identified among three strains. Functional annotation and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses of the differentially expressed genes (DEGs) identified a number of candidates melanophores and iridophores genes that influence body color. Some DEGs that were identified using transcriptome analysis were confirmed by quantitative real-time PCR. This study serves as a global survey of the morphological characteristics and molecular mechanism of different body colors observed in P. maxillaris and thus provides a valuable theoretical foundation for the molecular regulation of the transparent phenotype.

BackgroundExecutive dysfunction has been observed in patients with left-sided anterior corona radiata infarction. However, whether left-sided posterior corona radiata infarction could cause executive dysfunction is unclear. Also, whether secondary damage in the left frontal white matter following ipsilateral posterior corona radiata infarct is causal or not and contributes to the occurrence and development of executive dysfunction, is still uncertain.MethodsTwelve patients with posterior corona radiata infarction underwent diffusion tensor imaging (DTI) and an executive functional assessment at week 1 (W1), week 4 (W4), and week 12 (W12) after onset. Color duplex sonography and Transcranial Duplex Scanning (TCD) were performed at W1 and W12. Twelve healthy volunteers of similar ages and educational histories were examined as controls and assessed once.ResultsIn the patients, we observed an increased mean diffusivity (MD) and a decreased fractional anisotropy (FA) in the left frontal white matter from W1 to W12. There were no significant changes in cerebral blood flow in patients between W1 and W12 according to the result of Color duplex sonography and TCD. Patients showed progressively impaired executive function during 12 weeks. Significant correlations were found between increased MD and decreased FA in the left frontal white matter with impaired degree of executive function.ConclusionsThis study demonstrates that DTI detected secondary damage in left-sided frontal white matter in patients with acute infarction at the ipsilateral posterior corona radiata. This change may be correlated with executive functional changes in these patients.

Background and purpose Aspirin is the first recommended antiplatelet agent to prevention secondary stroke, but its safety and efficacy in stroke patients with glucose-6-phosphate dehydrogenase deficiency remain unclear. We sought to evaluate its safety and efficacy in ischemic stroke patients with and without glucose-6-phosphate dehydrogenase deficiency. Methods Patients with ischemic stroke receiving aspirin (100 mg/day) for three months were recruited for a multicenter, prospective, cohort study. Blood glucose-6-phosphate dehydrogenase activity was examined after stroke. Safety outcomes including acute hemolysis, moderate-to-severe bleeding, and death (vascular, all-cause), and efficacy outcome indicated as stroke recurrence were evaluated at three months. Risk factors associated with moderate-to-severe bleeding and all-cause death were determined using multivariate or Cox regression analysis. Results Among the included 1121 patients, 81 of 130 glucose-6-phosphate dehydrogenase deficient and 576 of 991 glucose-6-phosphate dehydrogenase normal patients received aspirin for three months. Acute hemolysis was observed in one of the glucose-6-phosphate dehydrogenase deficient and in none of the glucose-6-phosphate dehydrogenase normal patients ( p = 0.876). The rates of moderate-to-severe bleeding were 2.5% and 0.3% ( p = 0.045), and the percentages of all-cause death were 6.2% and 1.4% ( p = 0.008) in the glucose-6-phosphate dehydrogenase deficient and glucose-6-phosphate dehydrogenase normal patients. Stroke recurrence rate was similar in the two groups (2.5% vs. 1.7%; p = 0.608). Glucose-6-phosphate dehydrogenase deficiency was significantly associated with increased risk of moderate-to-severe bleeding (adjust p = 0.048) and all-cause death during aspirin use (adjust p = 0.008). Conclusions Long-term low-dose aspirin therapy might relate to worse safety outcomes in patients with glucose-6-phosphate dehydrogenase deficiency and large clinical trials are needed to further confirm these findings.