ObjectiveTo investigate the relationship between the level of homocysteine (HCY) and the overall burden of cerebral small vessel disease (CSVD) in patients with ischemic stroke.MethodsA total of 322 patients with first-ever ischemic stroke admitted to the People’s Hospital of Deyang City between January 2016 and December 2017 were enrolled. The patients’ demographic information, clinical information, and serum HCY concentration were collected after admission. The presence or absence of a CSVD was assessed by MRI and the overall burden score for the CSVD was determined. Multivariate logistic regression analysis was used to assess whether serum HCY level was associated with the overall burden of CSVD.ResultsThe median level of HCY was 13.2 μmol/L (inter-quartile range: 4.3 to 22.6 μmol/L). Univariate analysis showed that the difference of HCY levels among patients with different total CSVD scores was statistically significant (F=6.874, P=0.001); Spearman correlation analyses showed that the HCY level grouped by quartiles was correlated to the number of lacunar infarctions (rs=0.267, P=0.001), Fazekas score of white matter lesions (rs=0.122, P=0.042), and enlarged perivascular space (EPV) score (rs=0.319, P=0.001), but was not correlated to cerebral microhemorrhage (rs=?0.010, P=0.869). After multivariate regression analysis to adjust the effects of other factors, compared with the patients with HCY levels in the lowest quartile group, the patients with HCY levels in the highest quartile group were more likely to develop lacunar infarction [odds ratio (OR)=1.892, 95% confidence interval (CI) (1.012, 2.987)], white matter lesions [OR=1.548, 95%CI (1.018, 1.654)], severe EPV [OR=6.347, 95%CI (3.592, 13.978)], and the increase in the CSVD score [OR=2.981, 95%CI (1.974, 5.398)].ConclusionIn patients with ischemic stroke, elevated HCY levels may be associated with the overall burden of the CSVD.
Cerebral small vessel disease (CSVD) encompasses a group of progressive disorders involving the small vessels of the brain with complex etiologies. Inflammation plays a pivotal role in both the onset and progression of CSVD. In age-related CSVD, chronic inflammation can exacerbate brain tissue damage by impairing endothelial function and disrupting the blood-brain barrier. In contrast, in inflammatory CSVD subtypes driven primarily by immune dysregulation, inflammation itself constitutes the core pathogenic mechanism. These subtypes present with diverse clinical manifestations, posing significant challenges for diagnosis and treatment. A deeper understanding of the inflammatory mechanisms involved in CSVD and the unresolved issues in this field may provide new avenues for personalized interventions and improved prognosis.
Cerebral small vessel disease refers to a series of clinical, imaging, and pathological syndromes caused by various factors affecting small blood vessels in the brain. Cognitive impairment is one of the most common complications of cerebral small vessel disease. Current researches have found that cognitive impairment is related to various factors such as hypoxia. Hyperbaric oxygen therapy can achieve certain therapeutic effects by improving hypoxia. This article reviews the pathogenesis of cerebral small vessel disease, biomarkers of cerebral small vessel disease, research progress on hyperbaric oxygen therapy for cognitive impairment, and focuses on the research progress of hyperbaric oxygen therapy for mild cognitive impairment and dementia, providing more references for clinical treatment.
ObjectiveTo explore the correlation between urinary disorders and imaging changes of cerebral small vessel diseases (CSVDs) in community-dwelling populations.MethodsA cross-sectional analysis was conducted on participants enrolled in the Shunyi study from June 2013 to April 2016. Eligible participants were community-dwelling populations aged ≥35 years with interpretable magnetic resonance imaging scans and no history of stroke or urinary system diseases. Data on demographic characteristics, vascular risk factors, cognitive functions, and urinary disorders (including any form of urinary disorders, incontinence, daytime urination frequency, and nocturnal urination frequency) were collected. Imaging changes including white matter hyperintensities (WMHs), lacunes, cerebral microbleeds (CMBs), perivascular spaces (PVSs), and brain volume were measured using 3 T magnetic resonance imaging. Logistic regression model analysis was performed to identify the potential correlations between urinary disorders and imaging markers of CSVD.ResultsA total of 916 participants (with a mean age of 57.4 years; 36.2% were males) were finally enrolled in this study based on the enrollment criteria. CSVD imaging changes of WMHs, lacunes, CMBs, PVSs or brain volume were not associated with any form of urinary disorders in multivariable models (P>0.05). CSVD imaging changes were not associated with presence of urinary incontinence (P>0.05). In terms of urinary frequency, the CSVD imaging changes were not related to nocturnal urinary frequency (P>0.05). However, lower brain volume was correlated with daytime urination frequency [3-5 vs. <3 times per day: odds ratio (OR)=2.520, 95% confidence interval (CI) (1.278, 4.972), P=0.008; >5 vs. <3 times per day: OR=3.115, 95%CI (1.317, 7.372), P=0.010].ConclusionBrain atrophy may affect daytime urination frequency in community-dwelling populations.
ObjectiveTo investigate the association between the imaging markers of ischemic cerebral small vessel disease and the occurrence of large hemispheric infarction (LHI).MethodsWe consecutively enrolled the patients with cerebral infarction in the middle cerebral artery blood supply area who admitted to the Department of Neurology, West China Hospital, Sichuan University between January 1st, 2015 and March 30th, 2016, and underwent head CT/MRI scans within one month of onset. LHI was defined as: the hypodensity was larger than 1/2 of the blood supply area of middle cerebral artery or more than 1/3 of the cerebral hemisphere within 6 hours on head CT at admission, or the infarction area was larger than 2/3 of the ipsilateral hemisphere on head MRI at admission. The basic clinical data and imaging data were collected, and the independent predictors of LHI and its independent correlation with ischemic cerebrovascular disease were explored by univariate and multivariate analyses.ResultsA total of 503 patients were included, 111 (22.1%) with LHI and 392 (77.9%) with non-LHI. Compared with the non-LHI patients, the LHI patients had a lower prevalence of white matter lesions, a lower Fazekas score, a lower prevalence of Fazekas score > 1, a lower prevalence of lacunae, a lower proportion of diabetes mellitus, a higher atrial fibrillation proportion of history, a shorter time from onset to treatment, a higher National Institute of Health Stroke Scale (NIHSS) score at admission, and a lower Glasgow Coma scale score; the distributions of TOAST types and locations of vascular stenosis were different (P<0.05). Multivariate analyses showed that white matter lesions [odds ratio (OR)=0.182, 95% confidence interval (CI) (0.050, 0.660), P=0.010], higher Fazekas score [OR=0.770, 95% CI (0.611, 0.970), P=0.027], and Fakazes score > 1 [OR=0.490, 95%CI (0.259, 0.928), P=0.029] were independent protective factors of LHI, while lacunae was not an independent factor of LHI [OR=0.583, 95% CI (0.265, 1.279), P=0.178]. Higher NIHSS score and history of atrial fibrillation were independent risk factors for LHI (P<0.001).ConclusionsThe occurrence and severity of white matter lesions (higher Fazekas score and Fazekas score > 1) are more in non-LHI group, and are independently related to the occurrence of LHI. The results suggest that ischemic preconditioning may have a protective effect on brain.
Objective To investigates the metabolic changes in serum between patients with normal cognition of cerebral small vessel disease (CSVD) and those with cognitive impairment of CSVD. It aims to identify distinct metabolic pathways of CSVD-related cognitive impairment, which can provide new research directions for the diagnosis and treatment of this disease. Methods Serum samples from CSVD patients diagnosed in the Department of Neurology, West China Hospital of Sichuan University between July 2021 and December 2023 were used in this study. According to the patients’ Montreal Cognitive Assessment scores, they were divided into cognitively unimpaired CSVD group and cognitively impaired CSVD group. Untargeted metabolomic detection was performed using ultra-high performance liquid chromatography-tandem mass spectrometry. Quality control of the metabolomic data was conducted through correlation analysis of quality control samples. This study constructed an orthogonal partial least squares-discriminant analysis model to examine the relationship between metabolites and sample groups. Different metabolites were selected based on the criteria of P<0.05 and variable importance in projection >1, which were then subjected to metabolic pathway enrichment analysis. Results A total of 157 CSVD patients were included, including 51 cognitively unimpaired CSVD patients and 106 cognitively impaired CSVD patients. Untargeted metabolomics analysis, conducted in both positive and negative ion modes, identified a total of 68 significantly different metabolites between the cognitively unimpaired and cognitively impaired CSVD groups. These metabolites primarily consisted of lipids and lipid-like molecules, amino acids and their metabolites, and steroid hormones. Among these, the serum levels of 21 metabolites were increased in patients with CSVD-related cognitive impairment, while the levels of 47 metabolites were decreased. Further enrichment analysis revealed that these differential metabolites were predominantly enriched in 11 metabolic pathways, which included signaling pathways such as sphingolipid metabolism, protein digestion and absorption, and amino acid biosynthesis. Conclusions Compared with cognitively unimpaired CSVD patients, those with cognitive impairment showed increased levels of endogenous sphingolipids, such as phytosphingosine, and decreased levels of essential amino acids, including valine and leucine, in their serum. This suggests that lipid metabolism reprogramming and energy metabolism disturbances may be the main metabolic features in CSVD-related cognitive impairment. These different metabolites not only serve as promising biomarker candidates for CSVD-related cognitive impairment, but also offer new directions for investigating its pathological mechanisms.