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

Change log
Veenith, TV 
Carter, EL 
Grossac, J 

Ischaemia and metabolic dysfunction remain important causes of neuronal loss following 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 following one 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 oedema 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 following hyperoxia within contusion, but an increase within pericontusion (p < 0.05). We identified a rim of perilesional cytotoxic oedema 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 oedema. Future studies should address whether a longer period of hyperoxia has a favourable impact on the evolution of tissue injury.

Normobaric Hyperoxia, Diffusion tensor imaging, Contusion, Traumatic brain injury, Penumbra
Journal Title
International Journal of Diabetes and Metabolism
Conference Name
Journal ISSN
Volume Title
Publisher DOI
Publisher URL
MRC (G0701532)
MRC (G0600986)
MRC (G9439390)
MRC (G0001237)
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.