Hypothalamic lesions in neuromyelitis optica spectrum disorders: exploring a scoring system based on magnetic resonance imaging.

PURPOSE: We propose a scoring system for early diagnosis of sleep abnormalities in neuromyelitis optica spectrum disorders (NMOSD) with hypothalamic lesions based on magnetic resonance imaging (MRI). MATERIALS AND METHODS: We evaluated MRI features of 45 patients with hypothalamic lesions identified from two cohorts. Univariate logistic regression analysis identified factors associated with sleepiness, which were subsequently used to develop a scoring system. Interrater reliability was determined using intraclass correlation coefficient (ICC). Correlations between scores and clinical features were analyzed. RESULTS: In total, 48.9% of 45 patients with hypothalamic lesions exhibited sleepiness. The number of involved slices, maximum width/length of hypothalamic lesions, and boundaries extending beyond the hypothalamus were associated with sleepiness (all p < 0.05). The sensitivity and specificity of the scoring system were 68.2% and 87.0%, respectively. The ICC values for the maximum width and length measurement of hypothalamic lesions were 0.82 and 0.81, respectively. Daily sleep time and Epworth sleepiness scale scores were positively correlated with MRI-based scores (p < 0.05, 95% confidence interval (CI) 0.69-0.93 and p < 0.05, 95% CI 0.55-0.88, respectively). CONCLUSION: A scoring system based on MRI features was developed to provide diagnosis of sleepiness in NMOSD with hypothalamic lesions earlier than other measures.

Gut microbiota from patients with arteriosclerotic CSVD induces higher IL-17A production in neutrophils via activating RORγt.

The intestinal microbiota shape the host immune system and influence the outcomes of various neurological disorders. Arteriosclerotic cerebral small vessel disease (aCSVD) is highly prevalent among the elderly with its pathological mechanisms yet is incompletely understood. The current study investigated the ecology of gut microbiota in patients with aCSVD, particularly its impact on the host immune system. We reported that the altered composition of gut microbiota was associated with undesirable disease outcomes and exacerbated inflammaging status. When exposed to the fecal bacterial extracts from a patient with aCSVD, human and mouse neutrophils were activated, and capacity of interleukin-17A (IL-17A) production was increased. Mechanistically, RORγt signaling in neutrophils was activated by aCSVD-associated gut bacterial extracts to up-regulate IL-17A production. Our findings revealed a previously unrecognized implication of the gut-immune-brain axis in aCSVD pathophysiology, with therapeutic implications.