Cortical depolarization (CD) of the cerebral cortex could be developed under various pathophysiological conditions. In
animal models, CD was recorded under partial or complete ischemia as well as when cortical spreading depression (SD)
was induced externally or by internal stimulus. The development of CD in patients and the changes in various metabolic
parameters, during CD, was rarely reported.
Brain metabolic, hemodynamic, ionic and electrical responses to the CD event are dependent upon the O2 balance in the
tissue. When the O2 balance is negative (i.e. ischemia), the CD process will be developed due to mitochondrial
dysfunction, lack of energy and the inhibition of Na+-K+-ATPase. In contradiction, when oxygen is available (i.e.
normoxia) the development of CD after induction of SD will accelerate mitochondrial respiration for retaining ionic
homeostasis and normal brain functions.
We used the multiparametric monitoring approach that enable real time monitoring of mitochondrial NADH redox state,
microcirculatory blood flow and oxygenation, extracellular K+, Ca2+, H+ levels, DC steady potential and
electrocorticogram (ECoG). This monitoring approach, provide a unique tool that has a significant value in analyzing the
pathophysiology of the brain when SD developed under normoxia, ischemia, or hypoxia. We applied the same
monitoring approach to patients suffered from severe head injury or exposed to neurosurgical procedures.
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