Systemic manifestations of traumatic brain injury

Gaddam, Samson Sujit Kumar; Buell, Thomas J.; Robertson, Claudia S.

doi:10.1016/b978-0-444-52892-6.00014-3

Cited by 48 publications

(42 citation statements)

References 130 publications

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“…As TBI patients exhbit and increased susceptibility to peripheral infection 60 , we investigated the response to Cr , a clinically relevant enteric infection, in the context of chronic brain injury. Moderate TBI did not alter the host immune reponse to Cr infection in the colon as rates of colonization, clearance, and upregulation of Th1/Th17 cytokines in response to Cr were similar in infected sham and TBI mice.…”

Section: Discussionmentioning

confidence: 99%

Bidirectional brain-gut interactions and chronic pathological changes after traumatic brain injury in mice

Elise

Smith

Desai

et al. 2017

Brain, Behavior, and Immunity

128

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Objectives Traumatic brain injury (TBI) has complex effects on the gastrointestinal tract that are associated with TBI-related morbidity and mortality. We examined changes in mucosal barrier properties and enteric glial cell response in the gut after experimental TBI in mice, as well as effects of the enteric pathogen Citrobacter rodentium (Cr) on both gut and brain after injury. Methods Moderate-level TBI was induced in C57BL/6 mice by controlled cortical impact (CCI). Mucosal barrier function was assessed by transepithelial resistance, fluorescent-labelled dextran flux, and quantification of tight junction proteins. Enteric glial cell number and activation were measured by Sox10 expression and GFAP reactivity, respectively. Separate groups of mice were challenged with Cr infection during the chronic phase of TBI, and host immune response, barrier integrity, enteric glial cell reactivity, and progression of brain injury and inflammation were assessed. Results Chronic CCI induced changes in colon morphology, including increased mucosal depth and smooth muscle thickening. At day 28 post-CCI, increased paracellular permeability and decreased claudin-1 mRNA and protein expression were observed in the absence of inflammation in the colon. Colonic glial cell GFAP and Sox10 expression were significantly increased 28 days after brain injury. Clearance of Cr and upregulation of Th1/Th17 cytokines in the colon were unaffected by CCI; however, colonic paracellular flux and enteric glial cell GFAP expression were significantly increased. Importantly, Cr infection in chronically-injured mice worsened the brain lesion injury and increased astrocyte- and microglial-mediated inflammation. Conclusion These experimental studies demonstrate chronic and bidirectional brain-gut interactions after TBI, which may negatively impact late outcomes after brain injury.

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Section: Discussionmentioning

confidence: 99%

Bidirectional brain-gut interactions and chronic pathological changes after traumatic brain injury in mice

Elise

Smith

Desai

et al. 2017

Brain, Behavior, and Immunity

128

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“…9 The impact of TBI on systemic blood vessel function, however, has not been studied directly, and there is a knowledge gap between clinical evidence of the effects of trauma on endothelial markers and laboratory measurement of endothelial function after trauma. To address this, we used a well-established TBI model to assess the functional consequences of trauma on endotheliumdependent vasodilation and pressure-induced constriction (myogenic tone) in mesenteric arteries.…”

Section: +mentioning

confidence: 99%

“…1 Survivors of TBI often experience profound catecholamine surges and additional systemic complications such as hypertension, pulmonary edema, and cardiomyopathy. [2][3][4][5][6][7][8][9] Notably, endothelial dysfunction secondary to systemic inflammation and shock is widely believed to contribute to systemic complications in severe trauma, 9,10 yet there have been no studies that directly measure endothelial function in systemic blood vessels after head trauma.…”

Section: Introductionmentioning

confidence: 99%

Traumatic Brain Injury Causes Endothelial Dysfunction in the Systemic Microcirculation through Arginase-1–Dependent Uncoupling of Endothelial Nitric Oxide Synthase

Villalba

Sackheim

Nuñez

et al. 2017

Journal of Neurotrauma

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Endothelial dysfunction is a hallmark of many chronic diseases, including diabetes and long-term hypertension. We show that acute traumatic brain injury (TBI) leads to endothelial dysfunction in rat mesenteric arteries. Endothelial-dependent dilation was greatly diminished 24 h after TBI because of impaired nitric oxide (NO) production. The activity of arginase, which competes with endothelial NO synthase (eNOS) for the common substrate l-arginine, were also significantly increased in arteries, suggesting that arginase-mediated depletion of l-arginine underlies diminished NO production. Consistent with this, substrate restoration by exogenous application of l-arginine or inhibition of arginase recovered endothelial function. Moreover, evidence for increased reactive oxygen species production, a consequence of l-arginine starvation-dependent eNOS uncoupling, was detected in endothelium and plasma. Collectively, our findings demonstrate endothelial dysfunction in a remote vascular bed after TBI, manifesting as impaired endothelial-dependent vasodilation, with increased arginase activity, decreased generation of NO, and increased O 2 -production. We conclude that blood vessels have a ''molecular memory'' of neurotrauma, 24 h after injury, because of functional changes in vascular endothelial cells; these effects are pertinent to understanding the systemic inflammatory response that occurs after TBI even in the absence of polytrauma.

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“…[1] It is often associated with aneurysmal subarachnoid hemorrhage, TBI, seizures, and stroke. [2345678] The entity often remains under diagnosed or undiagnosed in routine clinical practice. [2] Although the condition was described more than four decades ago, the exact incidence, pathophysiology, and the criteria for diagnosis remain unclear even today.…”

Section: Discussionmentioning

confidence: 99%

Neurogenic pulmonary edema in traumatic brain injury

Rajagopal¹,

Swaminathan²,

Vetrivel³

2017

Indian Journal of Critical Care Medicine

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A 29-year-old male admitted with severe traumatic brain injury following a road traffic accident was sedated and ventilated uneventfully for 72 h. On the fourth posttrauma day, after stopping sedation to assess readiness for extubation, he developed sudden onset desaturation; arterial blood gas showed severe diffusion defect with very low PaO2/FiO2 ratio following an episode of generalized tonic-clonic seizure. The differential diagnoses and further management are discussed.

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Systemic manifestations of traumatic brain injury

Cited by 48 publications

References 130 publications

Bidirectional brain-gut interactions and chronic pathological changes after traumatic brain injury in mice

Bidirectional brain-gut interactions and chronic pathological changes after traumatic brain injury in mice

Traumatic Brain Injury Causes Endothelial Dysfunction in the Systemic Microcirculation through Arginase-1–Dependent Uncoupling of Endothelial Nitric Oxide Synthase

Neurogenic pulmonary edema in traumatic brain injury

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