Inflammation and Anti-Inflammatory Targets after Aneurysmal Subarachnoid Hemorrhage

Muhammad, Sajjad; Hänggi, Daniel

doi:10.3390/ijms22147355

Cited by 25 publications

(25 citation statements)

References 40 publications

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“…Delayed cerebral ischemia (DCI) is a late complication occurring typically 4–14 days after the onset of an SAH induced by a combination of angiographic vasospasm, arterial constriction and thrombosis, as well as cortical spreading ischemia [ 8 ]. DCI is an important factor affecting about 30% of survivors and seems to be a major contributor to poor outcomes after an aSAH [ 9 ]. Gusdon et al [ 8 ].…”

Section: Discussionmentioning

confidence: 99%

Exploration of Risk Factors for Poor Prognosis of Non-Traumatic Non-Aneurysmal Subarachnoid Hemorrhage

et al. 2022

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Background: Subarachnoid hemorrhage (SAH) is a devastating neurological disease associated with high rates of mortality and disability. Aneurysms are the main cause of non-traumatic subarachnoid hemorrhages. However, non-traumatic non-aneurysmal subarachnoid hemorrhage (naSAH), another clinical type of SAH, has been poorly studied for its prognosis and risk factors. Method and result: We collected demographic and clinical variables for 126 naSAH and 89 aneurysmal subarachnoid hemorrhage (aSAH) patients, including age and gender; hospitalization days; hematological indicators; clinical score scales; past medical history; and personal history. We found that the monocytes in naSAH (0.50 ± 0.26) patients were lower than in aSAH patients (0.60 ± 0.27). The prevalence of diabetes in naSAH (30.2%) patients was higher than in aSAH (14.5%) patients. The naSAH patients were divided into good and poor outcome groups based on the modified Rankin Scale at the 90th day (90-day mRS) after discharge. A univariate analysis showed that there were significant differences in age, white blood cell count (WBC), monocyte count, D-dipolymer, neuron-specific enolase (NSE), random blood glucose (RBG), aspartate transaminase (AST), urea and free triiodothyronine (FT3) between the two groups. A logistic regression showed that aging and high level NSE were independent risk factors for a poor outcome. The predictive ability of age (area under curve (AUC) = 0.71) and NSE (AUC = 0.68) were analyzed by a receiver operating characteristic (ROC) curve. The results of the logistic regression suggested that age, D-dipolymer, NSE, RBG, urea and FT3 distinguished and predicted the prognosis of naSAH. The discriminant analysis of the above variables revealed that the discriminant accuracy was 80.20%. Conclusions: Compared with aSAHs, naSAHs are more likely to occur in patients with diabetes, and the level of monocytes is lower. Moreover, the prognosis of elderly patients with an naSAH is relatively poor, and the level of NSE in the course of the disease also reflects the prognosis. Multivariate comprehensive analysis is helpful to judge the prognosis of patients at a small cost.

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Section: Discussionmentioning

confidence: 99%

Exploration of Risk Factors for Poor Prognosis of Non-Traumatic Non-Aneurysmal Subarachnoid Hemorrhage

et al. 2022

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“…35,91 Damage-associated molecular pattern molecules, including hemoglobin, are released in SAH, and their role in initiating inflammatory cascades suggests they may be promising therapeutics targets to avoid associated post-SAH complications such as headache. 91 Cyclooxygenase-2 is a principal enzyme in the conversion of arachidonic acid to prostaglandins and is over-expressed in endothelial cells after SAH. 35 In animal models, COX-2 inhibitors are attributed to effective edema and inflammation prevention, which may be part of the multi-modal pathophysiology of post-SAH headache.…”

Section: Pre-clinical Studies and Emerging Treatmentsmentioning

confidence: 99%

Headache persisting after aneurysmal subarachnoid hemorrhage: A narrative review of pathophysiology and therapeutic strategies

et al. 2022

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Objective This narrative review of the literature concerns persistent headache attributed to past non‐traumatic subarachnoid hemorrhage (SAH), based off demographic and clinical features, what are pathophysiologic mechanisms by which these headaches occur, which medical and interventional treatments have the most evidence for pain alleviation, and what pre‐clinical evidence is there for emerging treatments for these patients. Background Following initial stabilization and treatment of spontaneous SAH, most commonly due to aneurysmal rupture, headache in the immediate inpatient setting and persisting after discharge are an important cause of morbidity. These headaches often receive heterogenous treatment of uncertain efficacy, and the risk factors and pathophysiology of their development has received little study. Methods A narrative review of current literature discussing post‐SAH headache was conducted using a literature search in PubMed with search term combinations including “post subarachnoid hemorrhage pain”, “subarachnoid hemorrhage headache”, and “post subarachnoid hemorrhage headache”. Clinical studies mentioning headache after SAH and/or treatment in the abstract/title were included through March, 2022. Results and Conclusion Post‐SAH headaches are shown to decrease quality of life, have a multi‐modal pathophysiology in their occurrence, and only a select few medications (reviewed herein) have been demonstrated to have efficacy in alleviation of these headaches, while also harboring possible risks including vasospasm and re‐bleeding. An effective treatment paradigm of these headaches will include trials of evidence‐based therapeutics, rapid reduction of opioid medications if not effective, and consideration of multi‐modal pain control strategies including nerve blocks.

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“…Subarachnoid hemorrhage (SAH) is a clinical condition caused by rupture of intracranial blood vessels and direct inflow of blood into the subarachnoid space; the mortality rate of this condition is estimated to be approximately 50% ( 1 ). The pathophysiologic mechanism of SAH is complex and multifactorial.…”

Section: Introductionmentioning

confidence: 99%

The role of the astrocyte in subarachnoid hemorrhage and its therapeutic implications

Zhao²,

Yao³

et al. 2022

Front. Immunol.

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Subarachnoid hemorrhage (SAH) is an important public health concern with high morbidity and mortality worldwide. SAH induces cell death, blood−brain barrier (BBB) damage, brain edema and oxidative stress. As the most abundant cell type in the central nervous system, astrocytes play an essential role in brain damage and recovery following SAH. This review describes astrocyte activation and polarization after SAH. Astrocytes mediate BBB disruption, glymphatic–lymphatic system dysfunction, oxidative stress, and cell death after SAH. Furthermore, astrocytes engage in abundant crosstalk with other brain cells, such as endothelial cells, neurons, pericytes, microglia and monocytes, after SAH. In addition, astrocytes also exert protective functions in SAH. Finally, we summarize evidence regarding therapeutic approaches aimed at modulating astrocyte function following SAH, which could provide some new leads for future translational therapy to alleviate damage after SAH.

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Inflammation and Anti-Inflammatory Targets after Aneurysmal Subarachnoid Hemorrhage

Abstract: Aneurysmal subarachnoid hemorrhage (aSAH), with a crude worldwide incidence of around 7 [...]

Cited by 25 publications

References 40 publications

Exploration of Risk Factors for Poor Prognosis of Non-Traumatic Non-Aneurysmal Subarachnoid Hemorrhage

Exploration of Risk Factors for Poor Prognosis of Non-Traumatic Non-Aneurysmal Subarachnoid Hemorrhage

Headache persisting after aneurysmal subarachnoid hemorrhage: A narrative review of pathophysiology and therapeutic strategies

The role of the astrocyte in subarachnoid hemorrhage and its therapeutic implications

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