Brain Hemorrhages最新文献

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.

Objective

Delayed cerebral ischemia (DCI) is one of the most feared complications in aneurysmal subarachnoid hemorrhage (SAH). Animal models are crucial to studying the disease mechanisms and potential treatments. DCI in rodents was thought to not exist; herein we examine literature and our experience with DCI in rodents.

Methods

Daily behavioral performance was assessed every day from day 1 to up to 7 days post-SAH on mice from 5 different studies that used the endovascular perforation model. Performance was graded using an 8-test sensorimotor neuroscore previously described. The daily neuroscore was then used to identify the incidence and timing of delayed neurological deficits (DND), a clinical surrogate for DCI. A total number of 298 mice (134 males, 164 females) were subjected to SAH. Fifty-one mice had histological staining done to identify infarct volume.

Results

The overall incidence of DND was 33.9%; 27.6% in males and 39.0% in females, but this difference was not statistically significant. The overall incidence of delayed death was 21.1%, and there was no significant difference for delayed mortality in females versus male mice. There is a non-statistically significant trend towards increased infarct volume in mice suffering DND.

Conclusions

Mice with endovascular puncture induced SAH develop DND at rates comparable to human patients. Future work needs to correlate the DND seen with decreased regional cerebral blood flow, another hallmark of DCI, but in spite of this need, researchers may use the murine models to test therapies for DCI after SAH.

Cerebral veins are responsible for the outflow drainage of brain interstitial fluid (ISF). The importance of cerebral venous drainage has been emphasized in various neurological diseases. Impaired venous outflow may lead to brain edema, blood–brain barrier (BBB) disruption, inflammatory responses and hemorrhagic complications. With the development of imaging technologies, several imaging-based signs for venous assessment are proposed. Therapies targeting cerebral venous drainage have shown beneficial outcomes in cerebral venous sinus thrombosis (CVST) in clinic, however more insight into the cellular and molecular level should be elucidated. Here we review the pathological changes following cerebral venous drainage impairment, summary the advances in image-based evaluation, address the potential molecular mechanisms, and discuss venous drainage-focused therapies. A better understanding of cerebral venous drainage and its underlying mechanism will promote the pharmacological development and clinical management of CVST.