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abnormalities present in their preoperative tracing.  The EEG following induction of general anesthesia but prior to carotid cross clamping demonstrates normal fast activity and amplitude over both hemispheres. Two minutes following clamping of the right carotid artery; loss of fast activity and amplitude was seen over the right hemisphere (F4-O4, C4-P4, F8-T4, T4-T6). Similar, but less profound changes were also present over the left hemisphere (F7-T3, T3~T5, F3-C3, C3-P3).  A shunt was immediately placed that restored the EEG tracing to normal within 3 minutes.
The presence of an occluded carotid artery contralateral to the endarterectomy significantly increases the chances of mono- or even bihemispheric ischemia during carotid cross clamping. The angiographic determination of inadequate collateral circulation is also a predictor of intraoperative ischemia.  It has been found that even in patients with a completely occluded contralateral carotid artery, the majority can be operated on safely without the use of a shunt. There are also patients who would appear to have good collateral circulation by angiographic criteria who develop significant cerebral ischemia during carotid cross-clamping. Therefore, although the preoperative angiogram may be helpful in alerting the surgeon to a patient at increased risk of ischemia, it is inadequate alone to determine the need for a shunt. Brief periods of hypotension may cause significant hemispheric ischemia ipsilateral to a critically stenosed carotid artery. Changes in the EEG tracing indicative of cerebral ischemia most typically appear within 2 minutes of carotid cross-clamping and mandate placement of an intraluminal shunt. Once flow is restored via the shunt, the EEG should normalize within 3 to 5 minutes. In those patients in whom the baseline EEG tracing is abnormal, especially if a prior stroke has occurred, the EEG is a far less sensitive indicator of additional hemispheric ischemia. The EEG can help identify patients who are unlikely to tolerate direct carotid occlusion and may need an extracranial-to-intracranial bypass procedure prior to carotid sacrifice.   Meyer and Muzzi have described a method of cerebral protection in which EEG monitoring is used to titrate the inspired concentration of isoflurane to achieve EEG isoelectricity.  If an injury to a carotid artery occurs during
tumor resection and it is desired to place the patient under pentobarbital protection, the neurophysiologists must be prepared to provide a measure of burst suppression from both ongoing electroencephalographic activity and median nerve evoked potentials. Thus the need for EEGs must have been anticipated prior to the draping of the patient. The functioning of the cerebral cortex is extremely sensitive to changes in arterial oxygenation and insufficient CBF or inadequate partial pressure of oxygen; this sensitivity is rapidly reflected in the EEG.  The major use in monitoring EEG during skull base surgery is related to clamping and bypassing of the internal carotid artery in patients who failed a preoperative blood flow study.  Associated with this decreased availability of blood maybe hypoxia caused by an inability of the

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