Mechanism and Therapy of Brain Edema after Intracerebral Hemorrhage

Zheng, Haiping; Chen, Chunli; Zhang, Jie; Hu, Zhiping

doi:10.1159/000445170

Cited by 201 publications

(185 citation statements)

References 112 publications

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“…12,30 Microglia have multiple capabilities that can critically impact hemorrhagic brain injury, including the production of proinflammatory cytokines. 6,31 Recent studies have demonstrated that activation of microglia contributes to brain injury after ICH 30,[32][33][34] and that removal of microglia attenuates hemorrhagic brain injury. 19 In line with these findings, ICH triggered a predominant expression of the transcriptor AP-1 in microglia in conjunction with upregulation of IL-6 and TNF-α, well-known proinflammatory cytokines that amplify local inflammation, further supporting a detrimental role of microglia in acute ICH injury.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of activator protein 1 attenuates neuroinflammation and brain injury after experimental intracerebral hemorrhage

Wei

Zhu

et al. 2019

CNS Neurosci Ther

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Aims Intracerebral hemorrhage (ICH) is a devastating type of stroke without specific treatment. Activator protein 1 (AP‐1), as a gene regulator, initiates cytokine expression in response to environmental stimuli. In this study, we investigated the relationship between AP‐1 and neuroinflammation‐associated brain injury triggered by ICH. Methods Intracerebral hemorrhage mice were developed by autologous blood or collagenase infusion. We measured the dynamics of AP‐1 in mouse brain tissues during neuroinflammation formation after ICH. The effects of the AP‐1 inhibitor SR11302 on brain injury and neuroinflammation as well as the underlying mechanisms were investigated in vivo and in vitro. Results AP‐1 was significantly upregulated in mouse brain tissue as early as 6 hours after ICH, accompanied by elevations in proinflammatory factors, including interleukin (IL)‐6, IL‐1β, and tumor necrosis factor (TNF)‐α. Inhibition of AP‐1 using SR11302 reduced neurodeficits and brain edema at day 3 after ICH. SR11302 ablated microglial IL‐6 and TNF‐α production and brain‐infiltrating leukocytes in ICH mice. In addition, SR11302 treatment diminished thrombin‐induced production of IL‐6 and TNF‐α in cultured microglia. Conclusions Inhibition of AP‐1 curbs neuroinflammation and reduces brain injury following ICH.

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Section: Discussionmentioning

confidence: 99%

Inhibition of activator protein 1 attenuates neuroinflammation and brain injury after experimental intracerebral hemorrhage

Wei

Zhu

et al. 2019

CNS Neurosci Ther

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“…The latter concept is explained as the cause of the most characteristic posterior reversible encephalopathy syndrome (PRES) lesion. In hypertensive encephalopathy, brain edema can cause stimulation of stretch receptors in the fourth ventricle, which can make the hypertension worse8). These theories suggest that hypertensive encephalopathy can have different characteristics depending on the underlying diseases, because each etiology has a different contributing factor for hypertension.…”

Section: Introductionmentioning

confidence: 99%

Clinical characteristics of hypertensive encephalopathy in pediatric patients

et al. 2017

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PurposeThe aim of this study was to assess the clinical characteristics of hypertensive encephalopathy according to the underlying etiologies in children.MethodsWe retrospectively evaluated 33 pediatric patients who were diagnosed as having hypertensive encephalopathy in Chonbuk National University Children's Hospital. Among the patients, 18 were excluded because of incomplete data or because brain magnetic resonance imaging (MRI) was not performed. Finally, 17 patients were enrolled and divided into a renal-origin hypertension group and a non-renal-origin hypertension group according to the underlying cause. We compared the clinical features and brain MRI findings between the 2 groups.ResultsThe renal group included renal artery stenosis (4), acute poststreptococcal glomerulonephritis (2), lupus nephritis (2), and acute renal failure (1); the nonrenal group included essential hypertension (4), pheochromocytoma (2), thyrotoxicosis (1), and acute promyelocytic leukemia (1). The mean systolic blood pressure of the renal group (172.5±36.9 mmHg) was higher than that of the nonrenal group (137.1±11.1 mmHg, P<0.05). Seizure was the most common neurologic symptom, especially in the renal group (P<0.05). Posterior reversible encephalopathy syndrome (PRES), which is the most typical finding of hypertensive encephalopathy, was found predominantly in the renal group as compared with the nonrenal group (66.6% vs. 12.5%, P<0.05).ConclusionWe conclude that the patients with renal-origin hypertension had a more severe clinical course than those with non-renal-origin hypertension. Furthermore, the renal-origin group was highly associated with PRES on brain MRI.

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“…Brain atrophy may also contribute to a larger hematoma volume on presentation because of a less effective tamponade effect [9,26] . Additional damage might derive from an excess of local neuroinflammatory response due to dysregulation of aging microglia [31] possibly through acceleration in the formation of brain edema [32] . We actually observed a wide range of values for admission hematoma volume in oldest-old subjects and data dispersion was already noticeable for the old-old.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Age on Characteristics and Mortality of Intracerebral Hemorrhage in the Oldest-Old

et al. 2016

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Background: Incidence of acute intracerebral hemorrhage (ICH) increases with age, but there is a lack of information about ICH characteristics in the oldest-old (age ≥85 years). In particular, there is a need for information about hematoma volume, which is included in most clinical scales for prediction of mortality in ICH patients. Many of these scales also assume that, independent of ICH characteristics, the oldest-old have a higher mortality than younger elderly patients (age 65-74 years). However, supporting evidence from cohort studies is limited. We investigated ICH characteristics of oldest-old subjects compared to young (<65 years), young-old (65-74 years) and old-old (75-84 years) subjects. We also investigated whether age is an independent mortality predictor in elderly (age ≥65 years) subjects with acute ICH. Methods: We retrospectively collected clinical and neuroimaging data of 383 subjects (age 34-104 years) with acute supratentorial primary ICH who were admitted to an Italian Stroke Unit (SU) between October 2007 and December 2014. Measured ICH characteristics included hematoma location, volume and intraventricular extension of hemorrhage on admission CT scan; admission Glasgow Coma Scale ≤8 and hematoma expansion (HE) measured on follow-up CT-scans obtained after 24 h. General linear models and logistic models were used to investigate the association of age with ICH characteristics. These models were adjusted for pre-admission characteristics, hematoma location and time from symptom onset to admission CT scan. Limited to elderly subjects, Cox models were used to investigate the association of age with in-SU and 1-year mortality: the model for in-SU mortality adjusted for pre-admission and ICH admission characteristics and the model for 1-year mortality additionally adjusted for functional status and disposition at SU discharge. Results: Independent of pre-admission characteristics, hematoma location and time from symptom onset to admission CT-scan, oldest-old subjects had the highest admission hematoma volume (p < 0.01). Age was unrelated to all other ICH characteristics including HE. In elderly patients, multivariable adjusted risk of in-SU and 1-year mortality did not vary across age categories. Conclusions: Oldest-old subjects with acute supratentorial ICH have higher admission hematoma volume than young and young-old subjects but do not differ for other ICH characteristics. When taking into account confounding from ICH characteristics, risk of in-SU and 1-year mortality in elderly subjects with acute supratentorial ICH does not differ across age categories. Our findings question use of age as an independent criterion for stratification of mortality risk in elderly subjects with acute ICH.

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Mechanism and Therapy of Brain Edema after Intracerebral Hemorrhage

Cited by 201 publications

References 112 publications

Inhibition of activator protein 1 attenuates neuroinflammation and brain injury after experimental intracerebral hemorrhage

Inhibition of activator protein 1 attenuates neuroinflammation and brain injury after experimental intracerebral hemorrhage

Clinical characteristics of hypertensive encephalopathy in pediatric patients

The Effect of Age on Characteristics and Mortality of Intracerebral Hemorrhage in the Oldest-Old

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