Brain Edema XIII

Hoff, Julian T.; Keep, Richard F.; Xi, Guohua; Hua, Ya

doi:10.1007/3-211-30714-1

Cited by 12 publications

(2 citation statements)

References 20 publications

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“…Matrix metalloproteinase‐9 mediates vascular leakage in the brain by rearranging tight junction (Bauer et al., 2010). Proinflammatory mediators, such as oxidative mediators, adhesion molecules, cytokines, and chemokines, act directly on brain endothelial cells causing the loosening of the junction complexes between endothelial cells (Stamatovic et al., 2006). …”

Section: Discussionmentioning

confidence: 99%

“…Systemic inflammation is also present in patients with COPD (Furutate et al., 2016). These factors can eventually conspire to increase blood–brain barrier (BBB) permeability (Bailey, Bärtsch, Knauth, & Baumgartner, 2009; Bauer, Burgers, Rabie, & Marti, 2010; Heo, Han, & Lee, 2005; Schoch, Fischer, & Marti, 2002; Stamatovic, Dimitrijevic, Keep, & Andjelkovic, 2006). Nicotine has also been implicated in BBB changes (Paulson et al., 2010).…”

Section: Introductionmentioning

confidence: 99%

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Vasogenic cerebral edema associated with the disability in activities of daily living in patients with chronic obstructive pulmonary disease

et al. 2018

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IntroductionThe aim of this study was to explore whether patients with chronic obstructive pulmonary disease (COPD) develop vasogenic cerebral edema, and whether this edema contributes to the COPD‐related disability.MethodsEighteen stable patients with COPD and 17 matched healthy volunteers were enrolled. Apparent diffusion coefficient (ADC) values were calculated by voxel‐based analysis using DTI‐Studio software based on diffusion tensor imaging. COPD‐related disability was calculated using activities of daily living (ADL) scale.ResultsIn patients with COPD, ADC increased in the white matter fiber tracts including the bilateral anterior cingulum and posterior corpus callosum and in the white matter fibers connecting the bilateral insular cortices, sub‐lobar cortices, and pars triangularis cortices and the left rectus and olfactory gyrus. However, after further controlling for cigarette smoking, the difference in ADC values in the posterior corpus callosum between groups disappeared. Patients with COPD had significantly higher scores in ADL than that in controls. Moreover, ADL scores were positively correlated with the increased regional ADC values.ConclusionVasogenic cerebral edema occurs in patients with COPD. Cigarette smoking may be a risk factor for COPD‐related vasogenic edema. Vasogenic cerebral edema may be related to the COPD‐related ADL impairment.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Vasogenic cerebral edema associated with the disability in activities of daily living in patients with chronic obstructive pulmonary disease

et al. 2018

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Cerebral Intraparenchymal Hemorrhage

Gross

Jankowitz

Friedlander

2019

JAMA

245

177

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pontaneous intraparenchymal hemorrhage (IPH) is relatively common and has devastating consequences. Recognition of risk factors (eg, hypertension), early distinction from an ischemic event, and identification of clinical features that can worsen IPH complications is important in optimizing outcomes from IPH. This review examines the pathophysiology of and management options for IPH, with the intent of helping clinicians better manage the condition. IPH accounts for 6.5% to 19.6% of cases of stroke 1,2 but is associated with the greatest rate of mortality; 1-year survival from IPH is approximately 40%, 3-5 and 10-year survival is 24%. 4 Across several studies, the rate of functional independence at follow-up varied from 12% to 39%. 5 A meta-analysis of 36 studies reported an incidence of IPH of 24.6 per 100 000 person-years (range, 1.8-129.6), and the rate was significantly higher in Asian and older populations. 5 MethodsThe PubMed database was searched on September 1, 2018, using the terms intracerebral hemorrhage and intraparenchymal hemorrhage, for English-language studies of the pathophysiology, epidemiology, and management of IPH published after January 1, 2015. Large population epidemiologic studies, randomized trials, and formal treatment guidelines were reviewed. Relevant references published before January 1, 2015, were extracted and also reviewed. Studies providing only aggregate data for all types of hemorrhagic stroke (including subarachnoid hemorrhage) were excluded. This review was based on 77 referenced articles, including 11 clinical trials, 10 meta-analyses, 41 observational studies, 2 guidelines, and 13 other reports.

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Pediatric Traumatic Brain Injury and Microvascular Blood-Brain Barrier Pathology

Fullerton,

Hay,

Bryant-Craig

et al. 2024

JAMA Netw Open

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ImportancePediatric traumatic brain injury (TBI) is a major cause of morbidity and mortality, with an increased risk of catastrophic outcome compared with adult TBI, including diffuse brain swelling and so-called second impact syndrome. Nevertheless, the biological substrates driving adverse outcomes in pediatric TBI remain poorly described.ObjectiveTo compare neuropathological evidence of brain swelling and blood-brain barrier (BBB) disruption after moderate or severe acute TBI in adult vs pediatric case material.Design, Setting, and ParticipantsIn this retrospective case series, cases of pediatric (aged 3-18 years) and adult (aged ≥19 years) TBI were accrued from January 1, 1979, to December 31, 2005, and underwent laboratory-based assessment of autopsy material from the Glasgow TBI Archive. Data analysis was performed from January 2019 to January 2024.ExposuresSingle moderate or severe TBI.Main Outcomes and MeasuresEvaluation of representative brain tissue sections stained for markers of endothelia (CD34) and BBB integrity (fibrinogen and immunoglobin G).ResultsEighty-one pediatric patients (mean [SD] age, 12.1 [4.6] years; 50 [62%] male) and 62 adult patients (mean [SD] age, 38.7 [12.9] years; 35 [56%] male) were studied. At autopsy, when present, brain swelling was more often diffuse and bilateral among pediatric patients (64 of 81 cases [83%]) when compared with adult patients (21 of 62 [34%]) (P &lt; .001). Histologic evidence of BBB disruption was common in material from both adult (57 of 62 [91%]) and pediatric (65 of 81 [80%]) (P = .06) patients. In pediatric patients, however, this was a predominantly microvascular, capillary-level pathology, which was a less common finding in adult case material (mean [SD], 84.7% [8.6%] vs 31.2% [7.7%]; P &lt; .001).Conclusions and RelevanceThis autopsy case series of patients dying in the acute phase after single moderate or severe TBI provides neuropathological evidence of age-dependent differences in vascular pathology. Specifically, although BBB disruption in pediatric material was typically confined to microvascular, capillary-level vessels, in adult case material, BBB disruption more typically involved larger-diameter vessels. This observation of distinct microvascular pathology in pediatric acute TBI requires further investigation. In the meantime, this study presents an intriguing potential candidate pathology contributing to diffuse brain swelling in this age group.

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Brain Edema XIII

Cited by 12 publications

References 20 publications

Vasogenic cerebral edema associated with the disability in activities of daily living in patients with chronic obstructive pulmonary disease

Vasogenic cerebral edema associated with the disability in activities of daily living in patients with chronic obstructive pulmonary disease

Cerebral Intraparenchymal Hemorrhage

Pediatric Traumatic Brain Injury and Microvascular Blood-Brain Barrier Pathology

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