Cytokines and subarachnoid hemorrhage
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PROVIDER: S-EPMC10657139 | biostudies-literature | 2023 Jan
REPOSITORIES: biostudies-literature
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Project description:ObjectiveTo perform two scoping systematic reviews of the literature on cytokine measurement in cerebral microdialysis (CMD) and cerebrospinal fluid (CSF) in aneurysmal subarachnoid hemorrhage (SAH) patients, aiming to summarize the evidence relating cytokine levels to pathophysiology, disease progression, and outcome.MethodsTwo separate systematic reviews were conducted: one for CMD cytokines and the second for CSF cytokines.Data sourcesArticles from MEDLINE, BIOSIS, EMBASE, Global Health, Scopus, Cochrane Library (inception to October 2016), reference lists of relevant articles, and gray literature were searched.Study selectionTwo reviewers independently identified all manuscripts utilizing predefined inclusion/exclusion criteria. A two-tier filter of references was conducted.Data extractionPatient demographic and study data were extracted to tables.ResultsThere were 9 studies identified describing the analysis of cytokines via CMD in 246 aneurysmal SAH patients. Similarly, 20 studies were identified describing the analysis of CSF cytokines in 630 patients. The two scoping systematic reviews demonstrated the following: (1) limited literature available on CMD cytokine measurement in aneurysmal SAH with some preliminary data supporting feasibility of measurement and potential association between interleukin (IL)-6 and patient outcome. (2) Various CSF measured cytokines may be associated with patient outcome at 3-6 months, including IL-1ra, IL-6, IL-8, and tumor necrosis factor-alpha. (3) There is a small literature body supporting an association between acute/subacute CSF transforming growth factor levels and the development of chronic hydrocephalus at 2-3 months.ConclusionThe evaluation of CMD and CSF cytokines is an emerging area of the literature in aneurysmal SAH. Further large prospective multicenter studies on cytokines in CMD and CSF need to be conducted.
| S-EPMC5550693 | biostudies-literature
Project description:Aneurysmal subarachnoid hemorrhage (SAH) is a worldwide health burden with high fatality and permanent disability rates. The overall prognosis depends on the volume of the initial bleed, rebleeding, and degree of delayed cerebral ischemia (DCI). Cardiac manifestations and neurogenic pulmonary edema indicate the severity of SAH. The International Subarachnoid Aneurysm Trial (ISAT) reported a favorable neurological outcome with the endovascular coiling procedure compared with surgical clipping at the end of 1 year. The ISAT trial recruits were primarily neurologically good grade patients with smaller anterior circulation aneurysms, and therefore the results cannot be reliably extrapolated to larger aneurysms, posterior circulation aneurysms, patients presenting with complex aneurysm morphology, and poor neurological grades. The role of hypothermia is not proven to be neuroprotective according to a large randomized controlled trial, Intraoperative Hypothermia for Aneurysms Surgery Trial (IHAST II), which recruited patients with good neurological grades. Patients in this trial were subjected to slow cooling and inadequate cooling time and were rewarmed rapidly. This methodology would have reduced the beneficial effects of hypothermia. Adenosine is found to be beneficial for transient induced hypotension in 2 retrospective analyses, without increasing the risk for cardiac and neurological morbidity. The neurological benefit of pharmacological neuroprotection and neuromonitoring is not proven in patients undergoing clipping of aneurysms. DCI is an important cause of morbidity and mortality following SAH, and the pathophysiology is likely multifactorial and not yet understood. At present, oral nimodipine has an established role in the management of DCI, along with maintenance of euvolemia and induced hypertension. Following SAH, hypernatremia, although less common than hyponatremia, is a predictor of poor neurological outcome.
| S-EPMC4463029 | biostudies-other
Project description:The diagnosis of cerebral vasospasm after Subarachnoid-Hemorrhage is currently very difficult, additional tools such as blood biomarkers are necessary. We tested the ability of gene expression profiles of blood cells to predict vasospasm. 32 patients suffering subarachnoid-hemorrhage were included in this prospective monocentre study. They were grouped according to have a complicated cerebral vasospasm (Vasospasm) or not (Control) and Paired according to age (+/- 10 years), sex, Fisher grade (+/- 1), location, smoking (at least 3 first parameters). Gene expression profiles of blood cells were determined using 25,000~gene microarray. Blood sample: 2.5 mL harvested in PAXgene® Blood RNA tubes (PreAnalytix) RNA extraction: PAXgene® Blood RNA kit (Qiagen). We used a Universel Reference RNA (Stratagene). RNA amplification and labelling: kit Amino Allyl MessageAmp II (Ambion). We hybridized 4 microarrays per patient using pangenomic microarrays from the "Réseau National des Génopôles" (Illkirch, France). 2 slides were hybridized with reference RNA labelled Cy3 and patient RNA labelled Cy5, and 2 slides were hybridized with reference RNA labelled Cy5 and patient RNA labelled Cy3. Hybridation : Agilent protocol with few modifications : 750 ng of each labelled RNA were hubriddized at 60°C during 17 hours in an Aglient hybridization oven. After washings, Slides were scanned with a GenePix 4000B scanner (Molecular Devices). Image intensity data were extracted with GenePix Pro 6.0 analysis software. Quantification of Cy3 and Cy5 and selection of good spots were performed using the MAIA software (Novikov E and Barillot E. Software package for automatic microarray image analysis (MAIA). The ACUITY software was then used to normalize log ratios Cy3/Cy5 with Lowess non linear normalization, to filter out genes not present in at least 3 slides out of 4, to evaluate the reproducibility of the 4 microarrays of each patient (hierarchical clustering, Self Organizing Maps). Statistical analyses to insure reproducibility was performed using Excel (correlation coefficients, ANOVA). Only slides that passed all reprocubility tests were validated.
2014-05-08 | E-GEOD-37924 | biostudies-arrayexpress
Project description:Aneurysmal subarachnoid hemorrhage is a neurologic emergency that requires immediate patient stabilization and prompt diagnosis and treatment. Early measures should focus on principles of advanced cardiovascular life support. The aneurysm should be evaluated and treated in a comprehensive stroke center by a multidisciplinary team capable of endovascular and, operative approaches. Once the aneurysm is secured, the patient is best managed by a dedicated neurocritical care service to prevent and manage complications, including a syndrome of delayed neurologic decline. The goal of such specialized care is to prevent secondary injury, reduce length of stay, and improve outcomes for survivors of the disease.
| S-EPMC8147706 | biostudies-literature
Project description:The diagnosis of cerebral vasospasm after Subarachnoid-Hemorrhage is currently very difficult, additional tools such as blood biomarkers are necessary. We tested the ability of gene expression profiles of blood cells to predict vasospasm.
2014-05-08 | GSE37924 | GEO
Project description:To investigate the difference proteins after subarachnoid hemorrhage in human CSF.
2022-01-13 | PXD030593 | Pride
Project description:Purpose: Subarachnoid hemorrhage (SAH) is fatal in approximately 40% of cases. However, among survivors up to 95% experience permanent disabilities: post-SAH syndrome, which include impaired memory, executive functions, emotional and cognitive disturbances. Up to 45% of SAH patients are unable to continue with their professional activities. The long-term cognitive deficits result from morphological brain damage, including atrophy of the temporomesial/hippocampal area, which correlates with decreased neurocognitive scores. The mechanisms of the remote brain damage following SAH remain unknown, which hinders the progress in identifying new therapeutic targets. To unveil the leading mechanisms of permanent cognitive abnormalities following SAH and origin of atrophy of the temporomesial/hippocampal area, we analyzed SAH-induced specific hippocampal genomic pathways, which may lead to long term morphological damage. methods: Hippocampal RNA of SAH and Control groups, obtained 4 days after SAH induced by perforation of the circle of Willis in mice, was processed and sequenced. Using the next-generation RNA sequencing we determined differentially expressed genes in the bilateral whole hippocampus remote from SAH and applied different functional analyses and clustering tools to determine the main molecular pathways. Results: Differential gene expression analysis detected 642 upregulated and 398 down-regulated genes (false discovery rate <0.10) in SAH compared to Control group. Functional analyses using IPA suite, Gene Ontology terms, REACTOME pathways, and MsigDB Hallmark gene set collections revealed suppression of oligodendrocytes/myelin related genes, and overexpression of genes related to complement system along with genes related to innate and adaptive immunity, and extracellular matrix reorganization. Interferon regulatory factors, TGF-β1 and BMP, were identified as major orchestrating elements in the hippocampal tissue response. The MEME-Suite identified binding motifs of Krüppel-like factors, zinc finger transcription factors, and interferon regulatory factors as overrepresented DNA promoter motifs. Conclusion: Our findings suggest that damage of the entorhinal cortex by the subarachnoid blood remotely triggers specific hippocampal response, which may include suppression of oligodendrocytes functioning due to anterograde degeneration of hippocampal afferents accompanied. Identification of the prominent molecular hippocampal pathways may lead to the development of new therapeutic approaches for the treatment of long-term SAH consequences.
2021-08-11 | GSE167110 | GEO
Project description:BackgroundSubarachnoid hemorrhage (SAH) survivors experience significant neurological disability, some of which is under-recognized by neurovascular clinical teams. We set out to objectively determine the occurrence of hearing impairment after SAH, characterize its peripheral and/or central origin, and investigate likely pathological correlates.MethodsIn a case-control study (n = 41), participants were asked about new onset hearing difficulty 3 months post-SAH, compared with pre-SAH. Formal audiological assessment included otoscopy, pure tone audiometry, a questionnaire identifying symptoms of peripheral hearing loss and/or auditory processing disorder, and a test of speech understanding in noise. A separate cohort (n = 21) underwent quantitative susceptibility mapping (QSM) of the auditory cortex 6 months after SAH, for correlation with hearing difficulty.ResultsTwenty three percent of SAH patients reported hearing difficulty that was new in onset post-SAH. SAH patients had poorer pure tone thresholds compared to controls. The proportion of patients with peripheral hearing loss as defined by the World Health Organization and British Audiological Society was however not increased, compared to controls. All SAH patients experienced symptoms of auditory processing disorder post-SAH, with speech-in-noise test scores significantly worse versus controls. Iron deposition in the auditory cortex was higher in patients reporting hearing difficulty versus those who did not.ConclusionThis study firmly establishes hearing impairment as a frequent clinical feature after SAH. It primarily consists of an auditory processing disorder, mechanistically linked to iron deposition in the auditory cortex. Neurovascular teams should inquire about hearing, and refer SAH patients for audiological assessment and management.
| S-EPMC6414479 | biostudies-literature
Project description:Cortical spreading depolarizations (SD) are strongly associated with worse tissue injury and clinical outcomes in the setting of aneurysmal subarachnoid hemorrhage (SAH). Animal studies have suggested a causal relationship, and new therapies to target SDs are starting to be tested in clinical studies. A recent set of single-center randomized trials assessed the effect of the phosphodiesterase inhibitor cilostazol in patients with SAH. Cilostazol led to improved functional outcomes and SD-related metrics in treated patients through a putative mechanism of improved cerebral blood flow. Another promising therapeutic approach includes attempts to block SDs with, for example, the NMDA receptor antagonist ketamine. SDs have emerged not only as a therapeutic target but also as a potentially useful biomarker for brain injury following SAH. Additional clinical and preclinical experimental work is greatly needed to assess the generalizability of existing therapeutic trials and to better delineate the relationship between SDs, SAH, and functional outcome.
| S-EPMC7283429 | biostudies-literature
Project description:Subarachnoid hemorrhage is a devastating sequela of aneurysm rupture. Because it disproportionately affects younger patients, the population impact of hemorrhagic stroke from subarachnoid hemorrhage is substantial. Secondary brain injury is a significant contributor to morbidity after subarachnoid hemorrhage. Initial hemorrhage causes intracranial pressure elevations, disrupted cerebral perfusion pressure, global ischemia, and systemic dysfunction. These initial events are followed by two characterized timespans of secondary brain injury: the early brain injury period and the delayed cerebral ischemia period. The identification of varying microglial phenotypes across phases of secondary brain injury paired with the functions of microglia during each phase provides a basis for microglia serving a critical role in both promoting and attenuating subarachnoid hemorrhage-induced morbidity. The duality of microglial effects on outcomes following SAH is highlighted by the pleiotropic features of these cells. Here, we provide an overview of the key role of microglia in subarachnoid hemorrhage-induced secondary brain injury as both cytotoxic and restorative effectors. We first describe the ontogeny of microglial populations that respond to subarachnoid hemorrhage. We then correlate the phenotypic development of secondary brain injury after subarachnoid hemorrhage to microglial functions, synthesizing experimental data in this area.
| S-EPMC11318405 | biostudies-literature