White matter hyperintensities had a correlation with the cerebral perfusion level, but no correlation with the severity of large vessel stenosis in the anterior circulation.

OBJECTIVE: The contribution of large vessel stenosis to the development of white matter hyperintensities (WMHs) has not been fully elucidated. This study aims to explore the correlation between ipsilateral white matter hyperintensities (WMHs) and the severity of large vessel stenosis in the anterior circulation and cerebral perfusion level, as well as analyze the factors influencing WMHs. METHODS: A cross-sectional study of 150 patients with unilateral anterior circulation large vessel stenosis of ≥50% was conducted. The severity of ipsilateral WMHs was assessed by Fazekas scale on T2-weighted image and/or fluid-attenuated inversion recovery MR imaging, vascular stenosis severity was evaluated on computed tomography angiography images, and the level of cerebral perfusion was rated according to a staging system for abnormal cerebral perfusion based on CTP results. The relationships between the stenosis severity, cerebral perfusion level and ipsilateral WMHs severity were analyzed. A multivariate logistic regression analysis was performed to determine the factors independently influencing WMHs. RESULTS: Among 150 patients (mean age, 63.12 ± 10.55 years), there was a statistically significant positive correlation between cerebral perfusion level and the severity of DWMHs and PWMHs (Gamma = 0.561, p < .001; Gamma = 0.600, p < .001), and a positive correlation between cerebral perfusion level and the severity of vascular stenosis (Gamma = 0.495, p < .001).While, there was no statistically significant correlation between the severity of vascular stenosis and the severity of DWMHs and PWMHs (Gamma = 0.188, p = .08; Gamma = 0.196, p = .06). The multivariate logistic regression analysis results demonstrated that age (OR = 1.047, 95% CI 1.003-1.093; p = .035), stroke/TIA history (OR = 2.880, 95% CI 1.154-7.190; p = .023) and stage II of cerebral perfusion (OR = 2.880, 95% CI 1.154-7.190; p = .023) were independent influencing factors on ipsilateral DWMHs. Age (OR = 1.051, 95% CI 1.009-1.094; p = .018), and stage II of cerebral perfusion (OR = 12.871, 95% CI 3.576-46.322; p < .001) were factors independently influencing ipsilateral PWMHs. CONCLUSION: White matter hyperintensities may be attributed to cerebral hypoperfusion secondary to vascular stenosis but not directly to the severity of stenosis in the large vessels of anterior circulation. Moreover, longitudinal studies with sequential imaging exams may further reveal the impact of cerebral perfusion secondary to vascular stenosis on the development and progression of WMHs.

Clinical epidemiological characteristics of nitrous oxide abusers: A single-center experience in a hospital in China.

PURPOSE: This study investigated the clinical epidemiological characteristics of nitrous oxide (N2 O) abusers in a hospital in China, which have not been systematically reported. METHODS: The characteristics of patients abusing N2 O who were examined and treated at the Affiliated Hospital of Xuzhou Medical University from January 2017 to December 2020 were analyzed. RESULTS: A total of 61 patients (average age: 21.7 ± 3.2 years; 42 male and 19 female) were enrolled; 60.7% of the patients had an education level of high school or lower, and most (59.0%) had no stable occupation. The mean exposure time was 8.5 ± 7.7 months (range: 1-36 months). Only 52.5% of the abusers reported the physician of the relevant exposure history at the first time of visiting the doctor. The main clinical type was mixed (49.2%). The most common clinical manifestation was distal limb numbness (80.3%). The most frequent outcome was peripheral neuropathy (59%) and subacute combined degeneration (36%). Serum homocysteine level was elevated in 67.5% (27/40) of the patients, while 44.4% (20/45) showed reduced vitamin B12. Note that 61% (22/36) showed abnormal signals in the posterior or lateral funiculus of the spinal cord, and 97% (31/32) of the patients showed peripheral nerve damage by electromyography. In all cases, symptoms were alleviated after halting N2 O intake and receiving nutritional neurotherapy. CONCLUSIONS: N2 O abuse can lead to nervous system damage, especially peripheral nerve and spinal cord damage. A full understanding of its clinical epidemiological characteristics is helpful for clinicians to make a timely and clear diagnosis.