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systems being monitored.
Potential problems with anesthesia for intraoperative monitoring can usually be solved or avoided by the neurophysiologic monitoring team and the anesthesia team communicating their needs to one another both before and during the operation.
Another prerequisite for successful use of intraoperative neurophysiologic monitoring techniques is that the surgeon understand and be able to interpret the information presented by the neurophysiologic monitoring team, and that the surgeon be prepared to make the appropriate changes in the surgical procedure. It has, for various reasons, been difficult to quantify the benefits of intraoperative monitoring. However, it is generally agreed that proper use of neurophysiologic monitoring techniques can help reduce the incidence of permanent neurologic deficits. It is also widely recognized that this monitoring during neurosurgical procedures can help the surgeon (1) identify important neural structures when the anatomy has been distorted by disease processes or injury and (2) detect when specific neural pathways have been manipulated. Intraoperative neurophysiologic monitoring has contributed to improvements in surgical methods because monitoring allows, for the first time, direct identification of exactly which surgical manipulations cause injuries.
EEG correlates to the anesthetic depth produced by both inhaled and intravenous anesthetic agents. EEG, which is a measure of cerebral electrical activity, is exquisitely sensitive to decreases in cerebral blood flow, confirmed with the use of intra-arterially injected xenon-133. There were no EEG changes seen with blood flow above 30 mL/100 g brain per minute, minor changes with flow between 18 and 30 mL, an major changes with flow below 17 mL. The degree of EEG change reflected the severity of flow reduction and was reversible with prompt restoration of blood flow. The normal EEG in an awake patient demonstrates slightly asymmetric 8 to 13-Hz, 50 mV sinusoidal alpha waves in both the occipital and parietal regions. These waves wax and wane spontaneously and disappear rapidly when patients open their eyes and concentrate on a task or thought. Beta waves, which are faster than 13 Hz and are of lower amplitude occur in the frontal regions symmetrically. When the normal patient is asleep, the rhythm slows symmetrically, and vertex sharp wave and sleep spindles appear. If the sleep is induced by barbiturates, an increase in the fast frequencies occurs. General anesthetic agents including nitrous oxide, enflurane, and pentothal, cause similar changes in the EEG. At the initial stages of analgesia, the alpha rhythm abates and the voltage of bet activity increases. Beta activity then becomes generalized, of higher voltage, and intermixed with 3 to 7-Hz activity. As anesthesia deepens slow activity becomes predominant and progressively increases in amplitude and decreases in frequency. Anesthesia results in a burst-suppression pattern. At the deepest level of anesthesia, all EEG ac (Continued on page 106)
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