Biphasic Pathophysiological Response of Vasogenic and Cellular Edema in Traumatic Brain Swelling

Barzó, Pál; Marmarou, Anthony; Fatouros, Panos P.; Hayasaki, K.; Corwin, Frank

doi:10.1007/978-3-7091-6837-0_37

Cited by 30 publications

(31 citation statements)

References 11 publications

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“…We demonstrated prominent brain edema in the adult and P21 brains at 24 h after TBI, a finding consistent with that reported by others at various ages (Adelson et al, 2001;Barzo et al, 1997;Kempski, 2001). Recent clinical studies suggest that young children are particularly susceptible to diffuse brain swelling after severe TBI (Bauer et al, 1999).…”

Section: Brain Edema In the Developing Brainsupporting

confidence: 87%

Age-Dependent Differences in Glutathione Peroxidase Activity after Traumatic Brain Injury

Fan

Yamauchi²,

Noble³

et al. 2003

Journal of Neurotrauma

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Children younger than 4 years old have worse outcome after traumatic brain injury (TBI) compared to older children and adults. This increased susceptibility may in part be due to differences in the response to oxidative stress. We hypothesized that the immature brain does not have an adequate compensatory response to injury from oxidative stress. To begin to address this hypothesis, we first compared the general dimensions and water content in postnatal day 21 (P21) and adult murine brain in the naive state as well as after injury (edema). We examined glutathione peroxidase (GPx ) activity in cortical and subcortical regions in P21 and adult murine brain following a controlled cortical impact. Brain dimensions including areas of the mantle and hemispheres were similar in each of these groups. The thickness of the cortical mantle was significantly greater in the immature brain as compared to the mature brain (p = 0.01, respectively). Brain edema was assessed through changes in water content, and the response to oxidative challenge was identified by changes in GPx activity. The P21 brain was similar in vulnerability to posttraumatic brain edema when compared to adult. GPx activity in the adult brain was increased within 24 h post-injury in the cortex, thalamus and hippocampus (ANOVA, p < 0.05), whereas there was no compensatory increase in GPx activity in P21 brain, although baseline levels had reached adult levels developmentally. These findings support our hypothesis and illuminate the important role of oxidative stress after TBI in the immature brain that warrants further study.

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Section: Brain Edema In the Developing Brainsupporting

confidence: 87%

Age-Dependent Differences in Glutathione Peroxidase Activity after Traumatic Brain Injury

Fan

Yamauchi²,

Noble³

et al. 2003

Journal of Neurotrauma

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“…This cellular edema results in a proportional decrease in the local apparent diffusion coefficient (ADC, see Glossary) that can be measured by brain magnetic resonance imaging (MRI, see Glossary). Thus, a reduction in ADC is a measure of local cytotoxic cerebral edema [146,147]. The intracellular space increase cannot occur without a reduction in the space occupied by the ECM, as gelatins are not compressible.…”

Section: Edema Mri Diffusion Changes Seizures and Anticonvulsant Rmentioning

confidence: 99%

Chloride Dysregulation, Seizures, and Cerebral Edema: A Relationship with Therapeutic Potential

Glykys

Dzhala

Egawa

et al. 2017

Trends in Neurosciences

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Pharmaco-resistant seizures and cytotoxic cerebral edema are serious complications of ischemic and traumatic brain injury. Intraneuronal Cl− concentration ([Cl−]i) regulation impacts both cell volume homeostasis and Cl− permeable GABAA receptor-dependent membrane excitability. Understanding the pleiotropic molecular determinants of neuronal [Cl−]i –cytoplasmic impermeant anions, polyanionic extracellular matrix (ECM) glycoproteins, and plasmalemmal Cl− transporters– could help identify novel anti-convulsive and neuroprotective targets. The cation-Cl− cotransporters and ECM metalloproteinases may be particularly druggable targets for intervention. Here, we establish a paradigm that accounts for recent data regarding the complex regulatory mechanisms of neuronal [Cl−]i and how these mechanisms impact neuronal volume and excitability. We propose approaches to modulate [Cl−]i that are relevant for two common clinical sequela of brain injury: edema and seizures.

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“…Both vasogenic and cytotoxic edema contribute to traumatic brain swelling (Barzo et al, 1997). Vasogenic edema forms immediately after injury and becomes widespread at later times; cellular edema begins to develop soon after injury and becomes dominant at 1-2 weeks postinjury (Barzo et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Quantitative Analysis of Microvascular Alterations in Traumatic Brain Injury by Endothelial Barrier Antigen Immunohistochemistry

Lin

Ginsberg

Zhao

et al. 2001

Journal of Neurotrauma

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Endothelial barrier antigen (EBA) is a protein triplet located in the plasma membrane of microvascular endothelium and selectively expressed in the normal nervous system. In this study, microvascular alterations following traumatic brain injury were studied using EBA immunohistochemistry. Anesthetized, physiologically regulated, normothermic Sprague-Dawley rats received moderate (1.5-2.0 atm) parieto-occipital parasagittal fluid-percussion traumatic brain injury (TBI). Control rats were subjected to similar anesthesia and physiological monitoring. Seven days after operative procedures, brains were perfusion-fixed, and coronal sections were reacted for EBA immunohistochemistry using a monoclonal antibody to rat EBA. Selected sections were reacted for isolectin B4 histochemistry. Computerized image analysis was used to compute numbers of EBA-immunopositive vascular profiles and mean vascular profile areas. In control brains, virtually all brain microvessels were clearly and positively immunostained, and antibody binding was specific for blood vessels. In rats with TBI, EBA immunoreactivity was greatly reduced in the zone of cortical contusion. Within the core contusion, fractional areas occupied by vascular profiles were markedly reduced (on average, by 57%), vascular profile counts were diminished, and lectin histochemistry revealed a robust inflammatory response with abundant macrophages. Taken together, these findings were thought to indicate frank microvascular destruction. At adjacent peri-contusional sites, the intensity of EBA immunostaining was also diminished; and vascular profile counts were reduced at adjacent cortical sites and homologous contralateral sites. The latter findings were interpreted as sublethal microvascular alterations possibly related to cerebral edema. The present results confirm that EBA is a specific immunohistochemical marker of normal central nervous system microvessels; that it is suitable for use in formaldehyde-fixed material; and that it is useful in quantitatively assessing microvascular alterations observed at contusional, peri-contusional and more remote sites following traumatic brain injury.

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Biphasic Pathophysiological Response of Vasogenic and Cellular Edema in Traumatic Brain Swelling

Cited by 30 publications

References 11 publications

Age-Dependent Differences in Glutathione Peroxidase Activity after Traumatic Brain Injury

Age-Dependent Differences in Glutathione Peroxidase Activity after Traumatic Brain Injury

Chloride Dysregulation, Seizures, and Cerebral Edema: A Relationship with Therapeutic Potential

Quantitative Analysis of Microvascular Alterations in Traumatic Brain Injury by Endothelial Barrier Antigen Immunohistochemistry

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