Novel Non-invasive Optical Monitoring of Brain Haemodynamics and Metabolism Following Acute Brain Injury
Lead Research Organisation:
University College London
Department Name: Institute of Neurology
Abstract
Following severe head injury and brain haemorrhage, one of the key difficulties facing clinicians is knowing whether we are supplying the injured brain with adequate levels of blood and oxygen, and knowing whether that oxygen is being used effectively. Existing methods of monitoring are either invasive (involving insertion of probes in to the brain) and only monitor a small portion of injured tissue, or do not provide information in a timely fashion, and require the dangerous transfer of unwell patients to remote scanning units.
NIRS is a non-invasive method that involves shining light through tissue, and analysing the characteristics of that light to deduce changes in the concentration of important molecules within that tissue; two such molecules are haemoglobin - involved in the carriage of oxygen - and cytochrome oxidase - which is crucial to energy production within cells. I wish to use a novel combination of NIRS techniques in healthy volunteers and patients who have suffered severe head injuries and brain haemorrhages in order to look at changes in haemoglobin and cytochrome oxidase. This knowledge will be useful in characterising the nature of brain injury, and may lead to the development of new clinical monitors in order to guide clinical treatment.
NIRS is a non-invasive method that involves shining light through tissue, and analysing the characteristics of that light to deduce changes in the concentration of important molecules within that tissue; two such molecules are haemoglobin - involved in the carriage of oxygen - and cytochrome oxidase - which is crucial to energy production within cells. I wish to use a novel combination of NIRS techniques in healthy volunteers and patients who have suffered severe head injuries and brain haemorrhages in order to look at changes in haemoglobin and cytochrome oxidase. This knowledge will be useful in characterising the nature of brain injury, and may lead to the development of new clinical monitors in order to guide clinical treatment.
Technical Summary
Traumatic brain injury (TBI) and subarachnoid haemorrhage (SAH) are important neurosurgical diseases that carry significant mortality, morbidity and cost to society. Following TBI, primary brain injury was traditionally considered to be that irreversible damage immediately produced by initial insults, although a number of processes are responsible for its early evolution. Secondary injury is the cerebral damage caused by additional injury processes following primary injury, although the two may overlap in timescale.
Following SAH, a variety of pathophysiological processes conspire to cause cell death, including significant intracranial hypertension in the hyperacute phase, disordered cerebrovascular autoregulation, the development of hydrocephalus and delayed cerebral ischaemia due to arterial vasospasm.
Although distinct diseases with significant differences in the pathophysiological determinants of cell death, both TBI and SAH are linked by the fact that cellular hypoxia/ischaemia is a central process by which neuronal death results.
Modern neurointensive care attempts to minimise the development and impact of these injuries by implementing management strategies aimed at maximising cellular survival. These strategies are centred on the prevention, early detection and treatment of cerebral hypoxia and ischaemia, and when implemented within specialist units lead to improved patient outcomes following TBI. Following SAH, the need for specific monitoring and therapy is widely acknowledged, though there is controversy regarding the optimum regime to prevent and treat ischaemic complications.
Current approaches to the detection of cerebral hypoxia/ischaemia are problematic. Invasive methods are by nature focal, and potentially insensitive to insults remote to the invasive probes. Conversely, global measures of oxygenation detect global perturbations but are insensitive to regional ischaemia. Imaging techniques can provide useful information, but their utility is restricted in the management of critical care patients by virtue of their limited availability, remote nature - requiring the transfer of critically ill patients to radiology suites - and inadequate temporal resolution.
Can optical techniques for the non-invasive measurement of cerebral haemodynamics and metabolism be refined and employed in patients who have suffered subarachnoid haemorrhage (SAH)? What are the effects on arterial hyperoxia and carbon dioxide manipulation on cerebral haemodynamics and metabolism following severe TBI and SAH?
Using novel instrumentation designed in-house and undertaking studies on healthy volunteers, patients in the neurosurgical intensive care unit and in the laboratory, I will answer these questions. This will prove crucial in turning near infrared spectroscopy in to a viable clinical tool to individualise treatment and identify therapeutic windows in a wide range of brain disease.
Following SAH, a variety of pathophysiological processes conspire to cause cell death, including significant intracranial hypertension in the hyperacute phase, disordered cerebrovascular autoregulation, the development of hydrocephalus and delayed cerebral ischaemia due to arterial vasospasm.
Although distinct diseases with significant differences in the pathophysiological determinants of cell death, both TBI and SAH are linked by the fact that cellular hypoxia/ischaemia is a central process by which neuronal death results.
Modern neurointensive care attempts to minimise the development and impact of these injuries by implementing management strategies aimed at maximising cellular survival. These strategies are centred on the prevention, early detection and treatment of cerebral hypoxia and ischaemia, and when implemented within specialist units lead to improved patient outcomes following TBI. Following SAH, the need for specific monitoring and therapy is widely acknowledged, though there is controversy regarding the optimum regime to prevent and treat ischaemic complications.
Current approaches to the detection of cerebral hypoxia/ischaemia are problematic. Invasive methods are by nature focal, and potentially insensitive to insults remote to the invasive probes. Conversely, global measures of oxygenation detect global perturbations but are insensitive to regional ischaemia. Imaging techniques can provide useful information, but their utility is restricted in the management of critical care patients by virtue of their limited availability, remote nature - requiring the transfer of critically ill patients to radiology suites - and inadequate temporal resolution.
Can optical techniques for the non-invasive measurement of cerebral haemodynamics and metabolism be refined and employed in patients who have suffered subarachnoid haemorrhage (SAH)? What are the effects on arterial hyperoxia and carbon dioxide manipulation on cerebral haemodynamics and metabolism following severe TBI and SAH?
Using novel instrumentation designed in-house and undertaking studies on healthy volunteers, patients in the neurosurgical intensive care unit and in the laboratory, I will answer these questions. This will prove crucial in turning near infrared spectroscopy in to a viable clinical tool to individualise treatment and identify therapeutic windows in a wide range of brain disease.