Ischemic Cerebral Edema and the Blood-Brain Barrier

1974 ◽  
Vol 30 (6) ◽  
pp. 461 ◽  
Author(s):  
Michael D. O'Brien
Keyword(s):  
Blood Brain Barrier ◽  
Cerebral Edema ◽  
Brain Barrier ◽  
Blood Brain

scholarly journals Cerebral Edema Formation After Stroke: Emphasis on Blood–Brain Barrier and the Lymphatic Drainage System of the Brain

2021 ◽  
Vol 15 ◽  
Author(s):  
Sichao Chen ◽  
Linqian Shao ◽  
Li Ma
Keyword(s):  
Blood Brain Barrier ◽  
Cerebral Edema ◽  
Lymphatic System ◽  
Vasogenic Edema ◽  
Lymphatic Vessels ◽  
Drainage System ◽  
Brain Barrier ◽  
Edema Formation ◽  
Blood Brain ◽  
The Brain

Brain edema is a severe stroke complication that is associated with prolonged hospitalization and poor outcomes. Swollen tissues in the brain compromise cerebral perfusion and may also result in transtentorial herniation. As a physical and biochemical barrier between the peripheral circulation and the central nervous system (CNS), the blood–brain barrier (BBB) plays a vital role in maintaining the stable microenvironment of the CNS. Under pathological conditions, such as ischemic stroke, the dysfunction of the BBB results in increased paracellular permeability, directly contributing to the extravasation of blood components into the brain and causing cerebral vasogenic edema. Recent studies have led to the discovery of the glymphatic system and meningeal lymphatic vessels, which provide a channel for cerebrospinal fluid (CSF) to enter the brain and drain to nearby lymph nodes and communicate with the peripheral immune system, modulating immune surveillance and brain responses. A deeper understanding of the function of the cerebral lymphatic system calls into question the known mechanisms of cerebral edema after stroke. In this review, we first discuss how BBB disruption after stroke can cause or contribute to cerebral edema from the perspective of molecular and cellular pathophysiology. Finally, we discuss how the cerebral lymphatic system participates in the formation of cerebral edema after stroke and summarize the pathophysiological process of cerebral edema formation after stroke from the two directions of the BBB and cerebral lymphatic system.

scholarly journals Application of Blood-Brain Barrier Permeability Imaging in Global Cerebral Edema

2016 ◽  
Vol 37 (9) ◽  
pp. 1599-1603 ◽  
Author(s):  
J. Ivanidze ◽  
O.N. Kallas ◽  
A. Gupta ◽  
E. Weidman ◽  
H. Baradaran ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Cerebral Edema ◽  
Brain Barrier ◽  
Barrier Permeability ◽  
Blood Brain Barrier Permeability ◽  
Blood Brain ◽  
Brain Barrier Permeability

Abstract P335: Post-Treatment Blood-Brain Barrier Disruption is Associated With Cerebral Edema and Extends Into Penumbral Tissue in Anterior Circulation Large Vessel Occlusion

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Felix Ng ◽  
Gagan Sharma ◽  
Leonid Churilov ◽  
Nawaf Yassi ◽  
Timothy Kleinig ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Blood Brain Barrier ◽  
Cerebral Edema ◽  
Post Treatment ◽  
Large Vessel ◽  
Brain Barrier ◽  
Large Vessel Occlusion ◽  
Anterior Circulation ◽  
Vessel Occlusion ◽  
Blood Brain

Background: Blood Brain Barrier (BBB) disruption is central to vasogenic edema development after ischemia in preclinical studies. We investigated the relationship between BBB disruption and cerebral edema in patients receiving reperfusion therapies for anterior circulation large vessel occlusion. Methods: In a post-hoc pooled analysis of the Tenecteplase versus Alteplase before Endovascular Therapy for Ischemic Stroke (EXTEND-IA TNK) part 1 and 2 multicenter RCTs, the DWI lesion on 24h post-treatment MRI and peri-infarct salvaged penumbra derived from pre-treatment CT-Perfusion (CTP) were segmented and registered to 24h MR Perfusion. A validated permeability measure (percentage of measured cerebral blood volume lost due to T1 effect from gadolinium leakage across the BBB) was calculated for each ROI. The association between post-treatment BBB disruption in the infarct and cerebral edema assessed on a trichotomized ordinal scale of negligible (<1mm midline shift), mild (≥1 to <5mm) or severe (≥5mm) was analyzed using ordinal logistic regression. Results: Of 220 patients analyzed, median (IQR) BBB disruption was 2.36(1.4-4.1)% in the infarct, 1.61(1.0-2.6)% in salvaged penumbra and 0.98(0.7-1.5)% in normal brain (p<0.001). There were 119 (54.1%) patients with negligible, 90 (40.8%) mild and 11 (5.0%) severe cerebral edema at 24h. In multivariable analysis, infarct BBB disruption was associated with increased cerebral edema (cOR=1.11 per%, 95%CI 1.02-1.21;p=0.012, adjusted for age, admission NIHSS and reperfusion (mTICI2b/3 or >50% reperfusion on early CTP 2h post-lysis). Infarct BBB disruption correlated with follow-up infarct volume (rho=0.37;p<0.001), and was associated with parenchymal hematoma (aOR=1.18, 95%CI 1.00-1.40;p=0.048) and worse outcome assessed on 90-day modified Rankin Scale (cOR=1.16 per%, 95%CI 1.08-1.26;p<0.001, adjusted for age, admission NIHSS and reperfusion). Conclusions: BBB disruption after reperfusion treatment extends beyond the infarct lesion, and is associated with cerebral edema development, hemorrhagic transformation and poor outcome. Further studies to evaluate BBB integrity as an imaging biomarker and potential therapeutic target in malignant cerebral edema after ischemic stroke are needed.

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