Mechanisms of cerebral edema in traumatic brain injury: therapeutic developments

Donkin, James; Vink, Robert

doi:10.1097/wco.0b013e328337f451

Cited by 322 publications

(260 citation statements)

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“…Edema‐induced deficits in spatiotemporal organization and muscle function may contribute to the impairment of ADL in patients with COPD. Our findings support the hypothesis that cerebral edema is involved in the morbidity and mortality associated with hypoxic disease (Donkin & Vink, 2010). ADC values may be a relevant prognostic biomarker for morbidity and mortality.…”

Section: Discussionsupporting

confidence: 91%

“…Vasogenic edema is the result of water movement from the vasculature to the brain parenchyma (Donkin & Vink, 2010). Vascular endothelial growth factor (Boeck et al., 2015), free radicals (Rossman et al., 2013), matrix metalloproteinase‐9 (Vlahos et al., 2012), and systemic inflammation (Furutate et al., 2016) have been found to play a role in the modulation of BBB permeability after hypoxic stress in COPD.…”

Section: Discussionmentioning

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: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

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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“…So far, 13 isoforms have been identified, many of which are present in the brain. In particular, Aqp-4 has demonstrated to be highly expressed in astrocytes compared to neurons (Nielsen et al, 1997 andRash et al, 1998), and has been proven to play a role in the pathogenesis of brain edema in several cerebral diseases: trauma (Donkin and Vink, 2010), brain tumors (Nico and Ribatti, 2011) and cerebrovascular disease (Badaut et al, 2011). Moreover, Aqp function is coupled with ion channels in order to maintain ionic homeostasis, especially K + (Nagelhus et al, 1999 andRao et al, 2011).…”

Section: Water Channelsmentioning

confidence: 99%

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Bosoi

Rose

2013

Neurochemistry International

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Hepatic encephalopathy (HE) is a complex neuropsychiatric syndrome that typically develops as a result of acute liver failure or chronic liver disease. Brain edema is a common feature associated with HE. In acute liver failure, brain edema contributes to an increase in intracranial pressure, which can fatally lead to brain stem herniation. In chronic liver disease, intracranial hypertension is rarely observed, even though brain edema may be present. This discrepancy in the development of intracranial hypertension in acute liver failure versus chronic liver disease suggests that brain edema plays a different role in relation to the onset of HE. Furthermore, the pathophysiological mechanisms involved in the development of brain edema in acute liver failure and chronic liver disease are dissimilar. This review explores the types of brain edema, the cells, and pathogenic factors involved in its development, while emphasizing the differences in acute liver failure versus chronic liver disease. The implications of brain edema developing as a neuropathological consequence of HE, or as a cause of HE, are also discussed. HighlightsBrain edema is a common feature in ALF and CLD. HE is inconsistently associated with the presence of brain edema. Fibrous and protoplasmic astrocytes are differentially implicated in the pathogenesis of HE. The pathogenesis of HE is multifactorial causing an array of neurological symptoms.

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“…Cerebral edema in the neurointensive care setting can occur with a heterogenous group of neurological diseases, which typically fall under the categories of metabolic [1, 2], infectious [3], neoplastic [4], cerebrovascular [5][6][7], and traumatic [8,9] brain injury. Irrespective of the inciting process, cerebral edema results in the pathological accumulation of fluid in the brain's intracellular and extracellular spaces.…”

Section: Overview Of Perturbations In Brain Fluid Homeostasismentioning

confidence: 99%

Novel Treatment Targets for Cerebral Edema

2012

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Cerebral edema is a common finding in a variety of neurological conditions, including ischemic stroke, traumatic brain injury, ruptured cerebral aneurysm, and neoplasia. With the possible exception of neoplasia, most pathological processes leading to edema seem to share similar molecular mechanisms of edema formation. Challenges to brain-cell volume homeostasis can have dramatic consequences, given the fixed volume of the rigid skull and the effect of swelling on secondary neuronal injury. With even small changes in cellular and extracellular volume, cerebral edema can compromise regional or global cerebral blood flow and metabolism or result in compression of vital brain structures. Osmotherapy has been the mainstay of pharmacologic therapy and is typically administered as part of an escalating medical treatment algorithm that can include corticosteroids, diuretics, and pharmacological cerebral metabolic suppression. Novel treatment targets for cerebral edema include the Na(+)-K(+)-2Cl(−) co-transporter (NKCC1) and the SUR1-regulated NC Ca-ATP (SUR1/TRPM4) channel. These two ion channels have been demonstrated to be critical mediators of edema formation in brain-injured states. Their specific inhibitors, bumetanide and glibenclamide, respectively, are well-characterized Food and Drug Administration-approved drugs with excellent safety profiles. Directed inhibition of these ion transporters has the potential to reduce the development of cerebral edema and is currently being investigated in human clinical trials. Another class of treatment agents for cerebral edema is vasopressin receptor antagonists. Euvolemic hyponatremia is present in a myriad of neurological conditions resulting in cerebral edema. A specific antagonist of the vasopressin V1A-and V2-receptor, conivaptan, promotes water excretion while sparing electrolytes through a process known as aquaresis.Keywords Cerebral edema . Hyponatraemia . Osmotherapy . NKCC1 . SUR1/TRPM4 . Vaptan . Glyburide Overview of Perturbations in Brain Fluid HomeostasisCerebral edema in the neurointensive care setting can occur with a heterogenous group of neurological diseases, which typically fall under the categories of metabolic [1, 2], infectious [3], neoplastic [4], cerebrovascular [5][6][7], and traumatic [8,9] brain injury. Irrespective of the inciting process, cerebral edema results in the pathological accumulation of fluid in the brain's intracellular and extracellular spaces. This occurs secondary to alterations in the complex interplay between 4 distinct fluid compartments within the cranium; fluid is present within: 1) the blood in the cerebral blood vessels, 2) the cerebrospinal fluid in the ventricular system and subarachnoid space, 3) the interstitial fluid of the brain parenchyma, and 4) the intracellular fluid of the neurons and glia. These fluid compartments are not isolated, and specific movements of solutes and water from one compartment to another occur under normal conditions. When dysregulation of this normally tightly controlled fluid balance...

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Mechanisms of cerebral edema in traumatic brain injury: therapeutic developments

Cited by 322 publications

References 65 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

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Novel Treatment Targets for Cerebral Edema

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