Brain Hemorrhages最新文献

Objective

Cerebral vasospasm remains a major determinant of delayed cerebral ischemia (DCI) and poor outcomes after aneurysmal subarachnoid hemorrhage (SAH). This study was aimed to investigate if a matricellular protein pigment epithelium-derived factor (PEDF) can be a biomarker of angiographic vasospasm (aVSP) after SAH.

Methods

In 197 consecutive patients with aneurysmal SAH, plasma PEDF concentrations were serially measured at days 1–12 post-SAH.

Results

Plasma PEDF concentrations in SAH patients were elevated compared with patients with unruptured cerebral aneurysms, and especially higher in patients with admission World Federation of Neurological Surgeons (WFNS) grades IV–V. However, higher plasma PEDF concentrations at days 1–3 and 10–12 were associated with no development of aVSP. In an analysis limited to 72 non-sedated patients with preoperative WFNS grades I–III, plasma PEDF concentrations were also significantly higher in patients with neither DCI nor aVSP. Multivariate analysis showed that increased plasma PEDF concentration at days 1–3 was an independent predictor of no development of aVSP.

Conclusion

This was the first study to measure plasma PEDF concentrations and to show the relationships with aVSP development in SAH patients. PEDF may act protectively against aVSP, and serve as a negative biomarker and a target for drug discovery for aVSP.

Objective

This study aims to analyze the profile of patients with chronic subdural hematoma (cSDH) and to verify the factors associated with hematoma size.

Methods

We conducted a single-center, retrospective and observational case series of consecutive patients who underwent surgical treatment for cSDH at the Hospital de Clínicas de Passo Fundo, between 2018 and 2022. Data were extracted from the patients’ history records and imaging exams available. Patients’ characteristics were grouped and described through their respective prevalence. The relationship between patients’ characteristics and outcome (discharge or death) was analyzed using Fisher's exact test. Hematoma size was described in millimeters using means, and the relationship between hematoma size, patient age and hematoma side was tested using Student's t test.

Results

A total of 95 individuals were included in the study. Of these, 66.3 % were male and 7.4 % died. The mean age was 72 years. The most common symptoms and history findings were history of trauma (69.9 %), motor deficit (68.4 %) and cognitive deficit (26.3 %). The average hematoma size was similar on both sides, and showed an increasing trend with aging. The size of cSDH was also greater in those who presented motor deficits.

Conclusion

Surgically treated patients with cSDH had high rates of cognitive deficit, motor deficit and history of trauma. In addition, mortality rate was considered low and the size of hematoma was associated with age and motor deficits.

Background

Hematoma growth rarely occurs after 24 h in patients with intracerebral hemorrhage (ICH). Here we report a case with delayed hematoma growth caused by thrombocytopenia.

Case presentation

A 68-year-old leukemia patient presented with sudden left-sided weakness. Initial computed tomography scans revealed a small basal ganglia hemorrhage without early expansion. However, three days later, there was a significant hematoma expansion coupled with thrombocytopenia. The patient's condition remained stable after treatment. Our case suggests that hematoma expansion may occur even 3 days after symptom onset in patients with ICH.

Conclusion

This underscores the significance of promptly recognizing and closely monitoring delayed hematoma growth in cases of ICH associated with leukemia to facilitate timely intervention.

Background

Anterior cranial fossa dural arteriovenous fistulas (ACF-dAVFs) usually drain into the superior sagittal sinus (SSS) via the cortical veins. More rarely, the ACF-dAVF drains posteriorly into the olfactory vein, which points deeply into the basal vein of Rosenthal.

Case presentation

Here, we report a previously unreported case of ACF-dAVF with basal ganglia hemorrhage as the clinical symptom, in which the fistula drained posteriorly into the straight sinus via the olfactory vein, the basal vein of Rosenthal and the Galen vein. Obstruction of the draining vein leads to the formation of a venous bulb in the mid-basal vein of Rosenthal, which eventually causes basal ganglia hemorrhage.

Conclusion

This case highlights the importance of careful consideration of ACF-dAVF draining posteriorly via the olfactory vein, which may lead to differential diagnosis of basal ganglia hemorrhage.

Objective

We aimed to evaluate the association between admission glucose-to-lymphocyte ratio (GLR) and 28-day all-cause mortality in critically ill patients with non-traumatic SAH.

Methods

Data were extracted from the Medical Information Mart for Intensive Care IV database. The primary outcome was 28-day all-cause mortality. Cox regression analysis, Kaplan-Meier curves, restricted cubic spline curves, subgroup analysis and sensitivity analysis were used to assess the relationship between GLR and patient outcome.

Results

A total of 530 patients were included in this study. The Kaplan-Meier curves demonstrated that SAH patients in the high-GLR group (GLR ≧7.4) had a lower 28-day survival rate. A linear relationship was found between GLR and 28-day mortality. Multivariable Cox regression revealed that admission GLR was independently associated with 28-day mortality in critically ill SAH patients (hazard ratio [HR] = 1.03, 95 % confidence interval [CI] = 1.01–1.06, P = 0.011). SAH patients in the high-GLR group had a higher risk of 28-day mortality, compared with those in the low-GLR group (HR = 1.62, 95 % CI = 1.10–2.37, P = 0.015). Subgroup and sensitivity analyses supported the robustness of our results.

Conclusion

High GLR levels at admission were associated with increased 28-day all-cause mortality in critically ill SAH patients.

The integration of bioinformatics analysis into intracerebral hemorrhage (ICH)research represents a paradigm shift in our approach to understanding, diagnosing, and treating this complex neurological disorder. By leveraging the power of bioinformatics, the scientific community is poised to make significant strides in combating this devastating condition, ultimately improving patient outcomes and quality of life. This study provides a comprehensive overview of the application of bioinformatics tools and techniques in elucidating the genetic, molecular, and environmental underpinnings of ICH. Through a detailed examination of genomic sequencing, transcriptomics, proteomics, and machine learning, we explore how these bioinformatics approaches have contributed to identifying genetic variants, understanding molecular pathways, and discovering biomarkers related to ICH. Challenges such as data complexity, integration of multi-omics data, and the translation of bioinformatics findings into clinical practice are discussed, alongside ethical considerations surrounding data privacy and patient consent. This study underscores the critical role of bioinformatics in advancing our understanding of ICH, offering insights into its pathophysiology, and paving the way for personalized medicine and targeted therapeutic interventions.

Astrocytes, the most prevalent cells in the central nervous system, significantly contribute to the normal physiological functions of the brain. Following cerebral infarction, these astrocytes undergo activation, transforming into reactive astrocytes, ultimately leading to the formation of glial scars. These scars play a crucial role in the intricate process of brain injury. Given their involvement in neuroprotection, regulation of scarring, facilitation of nerve regeneration, preservation of the blood–brain barrier, promotion of angiogenesis, and modulation of the immune response post-cerebral infarction, researchers have proposed an array of therapeutic strategies directed towards targeting astrocytes. This review delves into the beneficial functions of reactive astrocytes in the context of cerebral infarction, exploring corresponding treatment strategies that capitalize on these insights.

Objective

Intracerebral hemorrhage (ICH) is a severe stroke that can adversely affect patient outcomes due to the accompanying inflammatory response. As a result, there is a growing interest in studying inflammation in ICH. We systematically reviewed relevant articles using the Web of Science to understand the literature on this subject. This study aims to provide a comprehensive overview of the field through bibliometric analysis, highlight its current status, identify frontiers, and speculate on future directions.

Methods

We conducted a bibliometric analysis of the global English literature on inflammation related to ICH research based on the Web of Science from 1993 to the present to address publication trends and research hotspots.

Results

A total of 885 publications were included from 1993 to 2023. These articles were authored by 7375 researchers from 1639 organizations in 68 countries and published in 571 journals. Collectively, they cited 48,980 references from 5621 journals. The author who published the most articles was Dr. Zhang, John H. Interestingly, 6 of the top ten most published authors were from China. Regarding the countries that published the most articles, China was at the top of the list, followed by the United States. The most frequently used keywords were “Inflammation”, “Neuroinflammation”, and “Microglia”. Regarding journal publication and reference citations, Stroke was the most published and cited journal.

Conclusions

Over the past 30 years, there has been considerable progress in scientific research concerning inflammation in the context of ICH. The pivotal themes of these studies have been immune cells and inflammatory mediators. It is worth noting, however, that most of the published literature on inflammation in ICH pertains to preclinical studies, with comparatively fewer clinical investigations. Several challenges must be addressed to translate these promising research achievements into clinical practice.

Blood-brain barrier (BBB) damage is a major pathological change after intracerebral hemorrhage (ICH) and is both the cause and result of brain edema and the inflammatory response post-ICH. Cerebral immune cells (CICs), including microglia, pericytes, and astrocytes play a crucial role in the damage and protection of the BBB after ICH. Recent evidence suggests that peripheral immune cells (PICs) also play an important role in BBB damage and protection, brain edema, and neurological function impairment. Therefore, regulating interactions between glial cells and immune cells is expected to alleviate ICH-induced BBB damage. In this review, we first introduce the role of CICs, endothelial cells (ECs), oligodendrocytes (OLs), and PICs in BBB damage and protection after ICH, focusing on their polarization and inflammatory response. Next, we specifically discuss the crosstalk between CICs and PICs, such as the brain-spleen axis and brain-gut axis after ICH. Finally, we suggest that glial cells, PICs and, meningeal lymphatic system may be potential targets for alleviating BBB damage after ICH, and discuss some molecular targets and potential strategies for alleviating BBB damage after ICH by modulating CICs, ECs, and PICs.