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dc.contributor.authorVeenith , Tonny V
dc.date.accessioned2020-01-15T10:27:54Z
dc.date.available2020-01-15T10:27:54Z
dc.date.issued2020-02-24
dc.date.submitted2019-06-01
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/300900
dc.description.abstractCerebral ischaemia is a frequent finding in post mortem studies following traumatic brain injury (TBI), but clinical studies using 15oxygen positron emission tomography (15O PET) suggest that classical ischaemia is uncommon beyond the first 24 hours after injury. Evidence of metabolic failure in the absence of classical ischaemia may represent ongoing neuronal dysfunction and progressive neuronal loss. Any therapeutic intervention that mitigates such metabolic derangements before they result in irreversible neuronal injury may improve tissue fate and improve the functional outcome for patients. Energy failure was spatially defined, characterised, and mapped using 15O and 18Fluoromisinidazole ([18F] FMISO) positron emission tomography. This enabled differentiation of classical ischaemia, diffusion hypoxia, and established infarction, and provided data on the dominant local mechanism at any given time after TBI. My thesis also aimed to examine the utility of diffusion tensor imaging and whole-brain proton MR spectroscopy (WB 1H MRS) as imaging biomarkers to investigate normobaric hyperoxia as a therapeutic option following traumatic brain injury (TBI). Using ([18F] FMISO PET evidence of tissue hypoxia consistent with microvascular ischaemia was found across the injured brain. The impact of normobaric hyperoxia (NBH) was examined in a clinical TBI cohort using diffusion tensor imaging and WB 1H MRS. Some evidence of benefit was found within the perilesional brain, but further studies should examine the value of a longer period of exposure to NBH and whether this has implications for functional outcome.
dc.description.sponsorshipAAGBI, MRC, Wellcome trust
dc.formatPDF
dc.language.isoen
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectTraumatic Brain Injury
dc.subjectNeurotrauma
dc.subjectProton Spectroscopy
dc.subjectDTI
dc.titleEnergy failure following traumatic brain injury: Potential mechanisms and impact of normobaric hyperoxia
dc.typeThesis
dc.type.qualificationlevelDoctoral
dc.type.qualificationnameDoctor of Philosophy (PhD)
dc.publisher.institutionUniversity of Cambridge
dc.publisher.departmentDepartment of Medicine
dc.date.updated2020-01-08T22:12:51Z
dc.identifier.doi10.17863/CAM.47974
dc.contributor.orcidVeenith , Tonny V [0000-0002-4125-8804]
dc.publisher.collegeWolfson College
dc.type.qualificationtitlePhD
cam.supervisorColes , Jonathan
cam.supervisorMenon , David
cam.thesis.fundingtrue


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Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)
Except where otherwise noted, this item's licence is described as Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)