Objective To investigate the regulatory mechanism of the central nervous system in patients with refractory overactive bladder (rOAB) using diffusion tensor imaging (DTI) and graph theory analysis. Methods A total of 43 rOAB patients (rOAB group) and 46 matched healthy controls (HC group) were recruited during May and Nov.2024. All participants were scanned with DTI, and surveyed with the overactive bladder symptom score (OABSS), and overactive bladder questionnaire (OAB-q). Their age, gender, height, weight, and educational years were collected.DTI plus graph theory analysis was employed to explore the alterations in global and local topological properties of the brain structural network in rOAB patients. Brain regions showing significant group differences in structural metrics [specifically, the right paracentral lobule (PCL.R) ]were further used as seed points for functional connectivity (FC) analysis. Correlations between the nodal clustering coefficient (NCp) of the identified region, FC strength, OABSS, and OAB-q score were investigated. Results The OABSS [8 (6,10) vs.0 (0,1) ]and OAB-q [71 (53,80) vs.20 (19,24) ]were higher in the rOAB group than the HC group (P<0.001). Graph theory analysis revealed no statistically significant differences in global network metrics between the two groups (P>0.05). However, the NCp was significantly higher in the PCL.R of rOAB group compared to HC group (P<0.05, FDR-corrected).FC analysis using the PCL.R as a seed region demonstrated significantly reduced FC value in the left cerebellar crus Ⅱ (Cerebelum_Crus2_L) of the rOAB group (P<0.05, FDR-corrected). Partial correlation analysis showed that the NCp of PCL.R was positively correlated with both OABSS (r=0.255, P=0.018) and OAB-q score (r=0.257, P=0.017). Conversely, the FC of Cerebelum_Crus2_L was significantly negatively correlated with OABSS (r=-0.545, P<0.001) and OAB-q score (r=-0.535, P<0.001). Conclusion Patients with rOAB exhibit distinct brain structural network alterations compared to healthy individuals, primarily manifestation in the NCp value of PCL.R increased, and the FC intensity of Cerebelum_Crus2_L is significantly weakened. These alterations in the topological properties of the structural network may be implicated in the pathogenesis of rOAB.

Objective To investigate the correlation between total burden of cerebral small vessel disease (CSVD) and cognitive impairment in patients with acute basal ganglia infarction. Methods Patients with acute basal ganglia infarction for the first time were enrolled, and the general data of the enrolled patients were collected. Patients were assessed by Montreal cognitive assessment (MoCA). Based on MoCA assessment, patients were then divided into cognitive impairment (CI) group and non-cognitive impairment (NCI) group. CSVD total load scores were conducted afterwards in order to analyze the correlation between the total load of different degrees of cerebral small vessel disease and cognitive impairment. Results A total of 178 patients were enrolled in this study: 135 in the CI group and 43 in the NCI group. There were significant differences in age (t=4.11, P=0.04) but not in high-density lipoprotein (t=2.92, P=0.09), and glycosylated hemoglobin C (t=3.02, P=0.08) between the two groups. The infarct volume was larger in the CI group (CI group: 424.72±36.55, NCI group: 227.02±34.62, t=4.022, P=0.046). There were significant differences in a sing1e lentiform nucleus (χ2=19.08, P<0.01), caudal Nucleus(χ2=9.97, P<0.01), infarction at the site of internal capsule(χ2=3.85, P=0.05), the infarct site involved lentiform nucleus, internal capsule and caudate nucleus at(χ2=4.30, P=0.04), and numbers of patients with moderate-to-severe internal carotid artery stenosis (χ2=4.14, P=0.04) as well as numbers of patients with moderate-to-severe intracranial artery stenosis (χ2=4.19, P=0.04). Similarly, there were significant differences in CSVD total burden (t=3.62, P<0.01), deep white matter hyperintensity (t=9.02, P<0.01), and cerebral microbleeds (t=5.54, P=0.02) between CI group and NCI group. The comparisons on MoCA score, visuospatial and execution, attention, language, generalization and abstraction, memory and orientation but not naming were statistically significant between the two groups. The logistic regression equation showed that CSVD total burden (OR=0.316, 95%Cl: 0.185~0.541, P<0.001), age (OR=0.924, 95%Cl: 0.884~0.967, P=0.001) and infarct volume (OR=0.924, 95%Cl: 0.884~0.967, P=0.001), (95%Cl: 1.000~1.003, P=0.047) was significantly associated with cognitive impairment in patients with acute basal ganglia infarction. Conclusion High CSVD total load score, older age and larger infarct volume may be risk factors for cognitive impairment in patients with acute basal ganglia infarction.

Nasopharyngeal carcinoma (NPC) is a common head and neck malignant tumor with high incidence in southern China. Local recurrence is one of the main failure modes of locally advanced NPC. The dose-escalation after radical radiotherapy for locally advanced NPC remains controversial. In the era of modern radiotherapy, the mainstream treatment mode of locally advanced NPC is neoadjuvant chemotherapy plus concurrent chemoradiotherapy. There is no consensus on whether to prescribe dose-escalation, how and when to conduct dose-escalation, how much dose to prescribe for patients with residual lesion proved by MRI or pathology. How to accurately determine the target volume and dose / fraction to maximize the local control of the tumor are the directions of clinical practice for locally advanced NPC, which remain to be further studied.