Preoperative cerebrovascular symptoms and electroencephalographic abnormalities do not predict cerebral ischemia during carotid endarterectomy.

BACKGROUND AND PURPOSE: The purpose of this prospective study was to establish (1) whether patients with neurological symptoms scheduled for carotid endarterectomy had an increased incidence of electroencephalographic (EEG) abnormalities during awake baseline recordings, (2) whether these symptoms and EEG abnormalities predicted ischemic EEG pattern changes at carotid artery cross-clamp, and (3) whether there was an association between age, presence of EEG baseline abnormalities, and ischemic pattern changes at carotid artery cross-clamp. METHODS: We reviewed the medical record of each patient scheduled to undergo carotid endarterectomy and recorded the patient's age and history of previous neurological symptoms. We then continuously monitored and analyzed 16 channels of anteroposterior bipolar EEG and two of referential derivations from at least 5 minutes before induction of anesthesia and throughout the operation. RESULTS: We completed 394 consecutive studies. Preoperative neurological symptoms were related to EEG abnormalities in awake patients (P < .001) and to EEG asymmetries in anesthetized patients (P < .001). Abnormal awake EEG findings were associated with asymmetries after anesthesia (P < .0001). Twenty-eight percent of both symptomatic (70/249) and asymptomatic (41/145) patients had EEG ischemic pattern changes at carotid artery cross-clamp. Neither neurological symptoms nor EEG abnormalities were associated with age or the development of EEG ischemic pattern changes at carotid artery cross-clamp. CONCLUSIONS: Despite the strong association between a history of cerebral ischemic symptoms and preoperative EEG abnormalities in patients undergoing carotid endarterectomy, patients who have suffered strokes or transient ischemic events are at no greater risk of having EEG evidence of cerebral ischemia during carotid artery cross-clamp than patients without symptoms and with normal baseline EEGs. We conclude that preoperative EEG abnormalities in symptomatic patients are not due to age or to insufficiency of regional cerebral blood flow.

Epileptiform activity during opioid anesthesia.

The proconvulsant properties of exogenously administered opioids in man are not established. We prospectively evaluated relationships between epileptiform activity and opioid dose in 20 patients undergoing coronary artery revascularization. Baseline electroencephalograms were performed before surgery. Ten subjects were given fentanyl and 10 sufentanil, at 100 micrograms/kg and 10 micrograms/kg, respectively, in 4 divided doses, 3 min apart. Midazolam (4 mg) was given 3 min after the last dose of narcotic. Serum opioid concentrations were measured by radioimmunoassay. Within 3 min of the first opioid dose, 19 of 20 patients developed epileptiform activity, characterized by generalized single and multiphasic, low-to-moderate voltage spike discharges, similar in appearance to benign epileptiform transients of sleep (BETS). Despite continuously increasing serum concentrations of opioid, the number of spike discharges initially increased during the first and second dose intervals and then declined during the third and fourth dose intervals. This dissociation between epileptiform discharges and measured serum opioid concentration was unexpected and remained unexplained. Spike activity was consistently attenuated (P = 0.000003) within 20 sec of midazolam administration. Abrupt cessation of discharges after administration of the anticonvulsant, midazolam, suggests an epileptogenic mechanism for the opioid-induced activity.

Loss of somatosensory evoked potentials during intramedullary spinal cord surgery predicts postoperative neurologic deficits in motor function [corrected].

STUDY OBJECTIVES: To estimate the sensitivity and specificity of somatosensory evoked potentials (SSEPs) for predicting new postoperative motor neurologic deficits during intramedullary spinal cord surgery; to establish whether SSEPs more accurately predicted postoperative deficits in position and vibration sense than in strength. DESIGN: Prospective open and retrospective study. SETTING: University-affiliated hospital. PATIENTS: 20 patients with intramedullary spinal cord tumors scheduled for surgery with intraoperative SSEPs. INTERVENTIONS: Median, ulnar, and tibial nerve cortical and subcortical SSEPs were recorded continuously. MEASUREMENTS AND MAIN RESULTS: Conventional intraoperative SSEP criteria considered indicative of neurologic injury were modified and defined as either the complete and permanent loss of the SSEP or the simultaneous amplitude reduction of 50% or greater in the nearest recording electrode rostral to the surgical site and 0.5 millisecond increase in the central latency. Our definition required confirmation of both amplitude and latency changes on a repeated average. All patients had 1 or more SSEPs, which were reproducible and sufficiently stable for analysis throughout the operation. Six patients developed new postoperative neurologic deficits. One had new motor deficits in an extremity from which no baseline SSEPs could be elicited. In each of the other 5 patients, significant SSEP changes preceded the postoperative motor deficits in the extremity or extremities monitored. In no patient without a new postoperative motor deficit was there a significant change in the SSEP. In only 2 of these 5 patients was there a documented postoperative loss or diminution in vibration or position sense. CONCLUSIONS: Intraoperative SSEP changes during intramedullary spinal cord surgery are a sensitive predictor of new postoperative motor deficits, but such changes may not correlate reliably with postoperative deficits in position or vibration sense. In this setting SSEP monitoring serves primarily to reassure the operating team that, when the SSEPs remain constant, the surgery has not caused additional injury.

Computer-derived density spectral array in detection of mild analog electroencephalographic ischemic pattern changes during carotid endarterectomy.

The purpose of this prospective study was twofold: 1) to determine the sensitivity and specificity of computer-derived density spectral array in detecting analog electroencephalographic (EEG) ischemic pattern changes during carotid artery cross-clamping in patients undergoing carotid endarterectomy; and 2) to assess the ability of density spectral array to identify such changes in comparison with the degree and type of change seen in the analog EEG ischemic pattern. Sixteen channels of anteroposterior bipolar and two to four channels of referential electroencephalography with four channels of density spectral array were monitored simultaneously during carotid endarterectomy in 103 patients under general anesthesia. Two "observers" interpreted the density spectral array and the analog electroencephalograms, one during and immediately after the operations and the other 6 months after completion of all surgery. Analyses were conducted to establish both the number of patients with analog EEG ischemic changes and the number of ischemia events during carotid artery cross-clamping. Observer A indicated that the density spectral array identified analog EEG ischemic changes in 21 of 29 patients, for a sensitivity of 72% (specificity 99%), whereas Observer B's results showed that the density spectral array identified analog EEG ischemic changes in 16 of 27 patients, for a sensitivity of 59% (specificity 96%). Density spectral array detection of analog EEG ischemic changes based on severity classifications were 61% and 18% in the mild group, 70% and 71% in the moderate group, and 95% in the severe group, indicating a relationship between density spectral array sensitivity and severity of analog EEG ischemic change, with p = 0.02 and p = 0.004 for the two observers. The kappa statistics for observer reproducibility were highly significant, with k = 0.95 for analog EEG ischemic changes and 0.85 for density spectral array changes. It is concluded that density spectral array does not reliably detect mild analog EEG pattern changes of cerebral ischemia and is not a reliable substitute for 16-channel analog EEG monitoring of cerebral ischemia during carotid endarterectomy.

Somatosensory evoked potentials sensitivity relative to electroencephalography for cerebral ischemia during carotid endarterectomy.

BACKGROUND AND PURPOSE: The relation between electroencephalographic pattern changes and cerebral ischemia during carotid endarterectomy under general anesthesia is well established. Pattern changes seen on somatosensory evoked potentials under the same conditions are reported to be more sensitive indicators of cerebral ischemia. We estimated the sensitivity and specificity of somatosensory evoked potentials relative to electroencephalography for detecting cerebral ischemia during carotid endarterectomy under general anesthesia. METHODS: We simultaneously monitored electroencephalographs and somatosensory evoked potentials in 53 carotid endarterectomies performed on 51 patients under general anesthesia, and we determined the extent to which somatosensory evoked potentials detected cerebral ischemia defined by electroencephalographic pattern changes at the time of carotid cross-clamp. RESULTS: Twenty-three of the 53 cases studied had electroencephalographic evidence of ischemia following carotid cross-clamp. Ten of these 23 cases had an increased somatosensory evoked potential latency of 0.1 msec or greater (sensitivity 0.43). One of these 23 patients had a decrease in somatosensory evoked potential amplitude of 50% or greater (sensitivity 0.04). Of the 30 subjects who had no electroencephalographic evidence of ischemia, 13 had either no change or a decrease in somatosensory evoked potential latency (specificity 0.45). None of these 30 cases had a significant decrease in somatosensory evoked potential amplitude (specificity 1.0). If somatosensory evoked potential latencies were a sensitive method for detecting cerebral ischemia (true sensitivity of 0.95 or higher), the probability of only 10 subjects having somatosensory evoked potential latency increases would be less than 0.001. Therefore, our observed sensitivity cannot be attributed to chance. CONCLUSIONS: We conclude that measuring somatosensory evoked potentials is not a sensitive method for detecting cerebral ischemia during carotid endarterectomy.