Abstract
The aetiology and management of secondary deterioration in patients with acute traumatic or ischaemic brain injury remain serious challenges for clinicians and also for basic neuroscientists. The occurrence of spreading depolarization events and some of their features in the cerebral cortex in patients with traumatic brain injury and aneurysmal subarachnoid haemorrhage, as documented in recent papers, represent a novel pathophysiological mechanism in this setting. The history and definitions of two critically different patterns of depolarization are reviewed on the basis of their physiology and pathophysiology, particularly the responses of the cerebral microcirculation to depolarization as seen in the laboratory. It is now becoming possible to conduct similar assessments in the brain-injured patient. Currently the recorded incidence of depolarization events in patients undergoing craniotomy for traumatic contusions is in the region of 50-60%, rising to 72% following major subarachnoid haemorrhage. Realization of the therapeutic potential of the new findings will depend on clear knowledge of the impact of the different patterns of depolarization on outcome. Meantime, current results call for even stricter attention during clinical management of acute brain injury to secondary factors such as body temperature and plasma glucose.
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