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Use of diffusion tensor imaging to assess the impact of normobaric hyperoxia within at-risk pericontusional tissue after traumatic brain injury.



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Veenith, Tonny V 
Carter, Eleanor L 
Grossac, Julia 
Newcombe, Virginia F 
Outtrim, Joanne G 


Ischemia and metabolic dysfunction remain important causes of neuronal loss after head injury, and we have shown that normobaric hyperoxia may rescue such metabolic compromise. This study examines the impact of hyperoxia within injured brain using diffusion tensor imaging (DTI). Fourteen patients underwent DTI at baseline and after 1 hour of 80% oxygen. Using the apparent diffusion coefficient (ADC) we assessed the impact of hyperoxia within contusions and a 1 cm border zone of normal appearing pericontusion, and within a rim of perilesional reduced ADC consistent with cytotoxic edema and metabolic compromise. Seven healthy volunteers underwent imaging at 21%, 60%, and 100% oxygen. In volunteers there was no ADC change with hyperoxia, and contusion and pericontusion ADC values were higher than volunteers (P<0.01). There was no ADC change after hyperoxia within contusion, but an increase within pericontusion (P<0.05). We identified a rim of perilesional cytotoxic edema in 13 patients, and hyperoxia resulted in an ADC increase towards normal (P=0.02). We demonstrate that hyperoxia may result in benefit within the perilesional rim of cytotoxic edema. Future studies should address whether a longer period of hyperoxia has a favorable impact on the evolution of tissue injury.


This is the final published version of the article. It was originally published by NPG in Journal of Cerebral Blood Flow & Metabolism here:


Adult, Aged, Brain, Brain Injuries, Diffusion Tensor Imaging, Female, Humans, Male, Middle Aged, Oxygen, Oxygen Inhalation Therapy, Young Adult

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J Cereb Blood Flow Metab

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SAGE Publications
Medical Research Council (G0701532)
Medical Research Council (G0600986)
Medical Research Council (G9439390)
Medical Research Council (G0001237)
Medical Research Council (G0600986/1)
Medical Research Council (G0701532/1)
Dr TV Veenith was supported by clinical research training fellowship from National institute of Academic Anaesthesia and Raymond Beverly Sackler studentship. VFJN is supported by an NIHR academic clinical fellowship. JPC was supported by Wellcome trust project grant. DKM is supported by an NIHR Senior Investigator Award. This work was supported by a Medical Research Council (UK) Program Grant (Acute brain injury: heterogeneity of mechanisms, therapeutic targets and outcome effects (G9439390 ID 65883)), the UK National Institute of Health Research Biomedical Research Centre at Cambridge, and the Technology Platform funding provided by the UK Department of Health.