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remaining members of the vasculature to adequately perfuse the brain. The second most useful application of EEG monitoring in skull base cases is to detect emboli which is representated by reduced activity and to define the degree of burst suppression if barbiturate brain protection is instituted. The functioning of the cerebral cortex is extremely sensitive to changes in arterial oxygenation and insufficient cerebral blood flow or an inadequate partial pressure of oxygen; this sensitivity is rapidly reflected in the EEG. Oxidative metabolism supplies the energy for maintainance of the membrane potential of nerve cells and the EEG is directly dependent on the transmembrane potentials of neurons; thus it reflects disturbances of cerebral metabolism such as hypoxia. Some factors that may contribute to ischemic events in cranial base tumor patients are decreased oxygen-carrying capacity due to hypovolemia or decreased cerebral perfusion pressure due to factors associated with decreased systemic arterial pressure, increased intracranial pressure, or mechanical obstruction of cerebral vessels. We routinely provide two channels of continuous EEG monitoring during cranial base cases. The electrode configuration is P3/F3 and P4/F4, which provides 2 parasagittal planes. The typical pattern seen in these measures during cerebral hypoperfusion is a reduction or loss in high frequency activity and the appearance of large amplitude slow waves in the delta (1-4Hz). Other concurrent factors that may alter the EEG are changes in depth of anesthesia, temperature changes, and changes in CO2 content. These factors may be recognized by their relatively slow onset, lasting for several minutes, in contrast to the ishemic changes which generally occur within seconds. One must keep in mind that there are situations where the EEG may be acutely depressed upon injection of an anesthetic that rapidly passes the blood-brain barrier. Such situations may be found in high-dose opioid anesthesia when fentanyl induces an immediate and marked reduction of fast frequency activity in the EEG with an increase in the low frequency, high amplitude activity in the delta range. Decreased frequency with increased amplitude implies an ischemic event to the cortex, widespread frequency slowing and decreased amplitude usually implies brain stem ischemia. Once this rather brief window of opportunity of approximately 5 min has passed, other more permanent and devastating changes occur. After isoelectricity occurs on the EEG, DC potential shifts can occur, and tissue surrounding the central, most ischemic area demonstrates transient or sustained depolarizations. These processes consume energy and spread through peri-ischemic regions, increasing the area of ischemic damage. Other changes during this time period include declining intracellular pH, release of excitatory neurotransmitters, activation of calcium channels, severe imbalance between metabolism/blood flow, and induction of genes expressing mediators of this process. Many changes occur in the EEG before isoelectricity occurs, and these changes seem related to the (Continued on page 109)
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