| Summary: | Traumatic brain injury (TBI) causes significant morbidity and mortality. Modern neurocritical care management utilises several monitoring techniques to identify or predict secondary insults but many of these techniques have significant limitations. The ideal cerebral monitor would be a non-invasive system able to provide realtime quantitative haemodynamic and metabolic information at multiple sites with high temporal and spatial resolution. Near infrared spectroscopy (NIRS) fulfils many of these requirements and has great potential as a cerebral monitoring tool. In addition to measurements of oxy- and deoxy-haemoglobin concentration, NIRS can monitor changes in mitochondrial redox state by measuring changes in oxidised cytochrome c oxidase (oxCCO) concentration. This is an attractive monitoring target as it is intimately involved in adenosine triphosphate synthesis and cellular homeostasis, yet few studies exist which investigate oxCCO concentration changes in either the normal or injured adult human brain. This thesis explores the use of NIRS, and in particular measurement of oxCCO concentration changes, for monitoring patients with TBI. Cerebral metabolism in both health and TBI is described and current monitoring tools and treatment strategies used in TBI are discussed. Studies investigating NIRS measurements in the brains of healthy volunteers during changes in arterial oxygen and carbon dioxide tension are described in order to determine the ability of NIRS to detect these physiological perturbations and to characterise the resulting metabolic changes. Spectroscopic data are analysed to investigate the methodology used to calculate oxCCO concentration changes. NIRS is used to monitor patients with TBI during normobaric hyperoxygenation and non-invasively measured NIRS variables are compared with those acquired using invasive cerebral monitoring devices. Correlations are shown between non-invasive measures of mitochondrial redox state and invasive measures of cellular redox state. NIRS can monitor changes in cerebral physiology after TBI and has the potential to guide neuroprotective strategies on the neurocritical care unit.
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