Abstract
As a brain injury mechanism, direct modes of brain damage such as tissue laceration, ischemia, and hypoxia grouped as primary brain injuries, and secondary brain injuries such as brain edema [18], cerebral blood flow (CBF) disturbances [20,25], reduced cerebral perfusion pressure (CPP) [10], and elevation of intracranial pressure (ICP) [20] have been discussed. Formation of free radicals, blood-brain barrier (BBB) dysfunction [7,26], release of neurotoxic excitatory amino acids [1,3,11,19,22–24], and increased levels of intracellular Ca2+ [4] have been demonstrated as promoting factors of this brain injury mechanism.Therefore, these pathophysiological changes have been considered as initial targets of treatment in the intensive care unit (ICU). This management concept for treatment of severely brain-injured patients has long been supported by many animal studies. However, in recent clinical studies of severely brain-injured patients, a hypothalamus- pituitary-adrenal (HPA) axis neurohormonal brain injury mechanism was observed (Fig. 6) [5,6,8,13–15].
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Hayashi, N., Dietrich, D.W. (2004). Secondary Brain Injury Mechanism of Hypothalamus—Pituitary—Adrenal Axis Neurohormonal Activation in Severely Brain-Injured Patients. In: Brain Hypothermia Treatment. Springer, Tokyo. https://doi.org/10.1007/978-4-431-53953-7_24
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DOI: https://doi.org/10.1007/978-4-431-53953-7_24
Publisher Name: Springer, Tokyo
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