White matter T2 hyperintensities and blood‐brain barrier disruption in the hyperacute stage of subarachnoid hemorrhage in male mice: The role of lipocalin‐2

Toyota, Yasunori; Wei, Jialiang; Xi, Guohua; Keep, Richard F.; Hua, Ya

doi:10.1111/cns.13221

Cited by 28 publications

(30 citation statements)

References 30 publications

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“…A stable internal environment is necessary for normal nerve function 1,2 . Damage to the blood‐brain barrier is a major part of the pathophysiological process of many nervous system diseases, such as multiple sclerosis, stroke, Alzheimer's disease, vascular dementia, cerebral small vessel disease, traumatic brain injury, and epilepsy 3‐12 …”

Section: Introductionmentioning

confidence: 99%

Endothelial glycocalyx as an important factor in composition of blood‐brain barrier

2020

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The blood‐brain barrier is a dynamic and complex neurovascular unit that protects neurons from somatic circulatory factors as well as regulates the internal environmental stability of the central nervous system. Endothelial glycocalyx is a critical component of an extended neurovascular unit that influences the structure of the blood‐brain barrier and plays various physiological functions, including an important role in maintaining normal neuronal homeostasis. Specifically, glycocalyx acts in physical and charge barriers, mechanical transduction, regulation of vascular permeability, modulation of inflammatory response, and anticoagulation. Since intact glycocalyx is necessary to maintain the stability and integrity of the internal environment of the blood‐brain barrier, damage to glycocalyx can lead to the dysfunction of the blood‐brain barrier. This review discusses the role of glycocalyx in the context of the substantial literature regarding the blood‐brain barrier research, in order to provide a theoretical basis for the diagnosis and treatment of neurological diseases as well as point to new breakthroughs and innovations in glycocalyx‐dependent blood‐brain barrier function.

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Section: Introductionmentioning

confidence: 99%

Endothelial glycocalyx as an important factor in composition of blood‐brain barrier

2020

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“…Several studies even applied micro‐CT, DSA to longitudinally monitor vasospasm and tried to reveal the progression after SAH 26 . Besides, early brain injury (EBI) encompasses the entire brain injury occurring within 72 h after SAH, which is related to oxidative stress, neuroinflammation, neuronal death, blood‐brain barrier (BBB) damage, autophagy–apoptosis, and ferroptosis 27–30 . Although timely and effective treatment is implemented, the SAH‐induced neurological impairments are permanent in individual.…”

Section: Discussionmentioning

confidence: 99%

Development of a nomogram for predicting clinical outcome in patients with angiogram‐negative subarachnoid hemorrhage

Zhang

et al. 2021

CNS Neurosci Ther

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To the best of our knowledge, this is the largest clinical retrospective study in AN‐SAH patients, and is the first time to establish accurate predictive models paired with bleeding pattern. Background Angiogram‐negative subarachnoid hemorrhage (AN‐SAH) has a definite incidence of delayed cerebral ischemia (DCI) and poor clinical outcomes. The purpose is to screen independent factors and establish a nomogram to guide the clinical therapy and assess post‐discharge prognosis. Methods We identified 273 consecutive patients referred to our institute from 2013 to 2018 for AN‐SAH. A nomogram to predict poor outcomes was formulated based on the multivariable models of independent risk factors. The accuracy and discrimination of nomograms were determined in training and internal validation cohorts. Results The overall poor outcome rates of AN‐SAH were 14.3% and 8.7% at 3 months and 12 months, respectively. In addition, perimesencephalic AN‐SAH (PAN‐SAH) presented with a more unfavorable prognosis compared with non‐perimesencephalic AN‐SAH (NPAN‐SAH). The clinical prognosis was associated with the World Federation of Neurosurgical Societies scale (WFNS) (odds ratio, 3.82 [95% CI, 1.15‐12.67] for 3‐month outcome; and odds ratio, 31.69 [95% CI, 3.65‐275.43] for 12‐month outcome), Subarachnoid hemorrhage Early Brain Edema Score (SEBES) (odds ratio, 10.39 [95% CI, 1.98‐54.64] for 3‐month outcome; odds ratio, 10.01 [95% CI, 1.87‐53.73] for 12‐month outcome), and symptomatic vasospasm (odds ratio, 3.16 [95% CI, 1.03‐9.70] for 3‐month outcome; odds ratio, 5.15 [95% CI, 1.34‐19.85] for 12‐month outcome). The nomogram was constructed based on the above features, which represented great predictive value in clinical outcomes. Conclusions Symptomatic vasospasm, high WFNS, cerebral edema, and NPAN‐SAH after hemorrhage were associated with poor outcome of AN‐SAH. The nomogram with WFNS (3‐5), SEBES (3‐4), vasospasm, and NPAN‐SAH represented a practical approach to provide individualized risk assessment for AN‐SAH patients.

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“…Since most blood spread into the subarachnoid space without direct nervous tract disruption, white matter injury after SAH is initially considered to be the consequence of blood-brain barrier disruption (27,28) and neurotoxicity of blood disintegration (29). Physical factors such as biological stress, mainly caused by elevated intracranial pressure, attack the whole brain in the acute phase, while biochemical factors including thrombin, excitatory amino acids, and inflammatory cytokines lead to subsequent white matter injury after SAH (Figure 1).…”

Section: Potential Pathophysiology Mediated Secondary White Matter Injury After Sahmentioning

confidence: 99%

Secondary White Matter Injury and Therapeutic Targets After Subarachnoid Hemorrhage

Gao

Zhou

et al. 2021

Front. Neurol.

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Aneurysmal subarachnoid hemorrhage (SAH) is one of the special stroke subtypes with high mortality and mobility. Although the mortality of SAH has decreased by 50% over the past two decades due to advances in neurosurgery and management of neurocritical care, more than 70% of survivors suffer from varying degrees of neurological deficits and cognitive impairments, leaving a heavy burden on individuals, families, and the society. Recent studies have shown that white matter is vulnerable to SAH, and white matter injuries may be one of the causes of long-term neurological deficits caused by SAH. Attention has recently focused on the pivotal role of white matter injury in the pathophysiological processes after SAH, mainly related to mechanical damage caused by increased intracerebral pressure and the metabolic damage induced by blood degradation and hypoxia. In the present review, we sought to summarize the pathophysiology processes and mechanisms of white matter injury after SAH, with a view to providing new strategies for the prevention and treatment of long-term cognitive dysfunction after SAH.

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White matter T2 hyperintensities and blood‐brain barrier disruption in the hyperacute stage of subarachnoid hemorrhage in male mice: The role of lipocalin‐2

Cited by 28 publications

References 30 publications

Endothelial glycocalyx as an important factor in composition of blood‐brain barrier

Endothelial glycocalyx as an important factor in composition of blood‐brain barrier

Development of a nomogram for predicting clinical outcome in patients with angiogram‐negative subarachnoid hemorrhage

Secondary White Matter Injury and Therapeutic Targets After Subarachnoid Hemorrhage

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