(Stroke. 1995;26:1210-1214.)
© 1995 American Heart Association, Inc.
Articles |
Preoperative Cerebrovascular Symptoms and Electroencephalographic Abnormalities Do Not Predict Cerebral Ischemia During Carotid Endarterectomy
From the Departments of Anesthesia and Neurology (L.A.K., M.L.-B.) and Anesthesia (K.M.), Massachusetts General Hospital, Harvard Medical School, Boston, and the Department of Statistics (A.Z.), Harvard University, Cambridge, Mass.
Correspondence to Lee A. Kearse, Jr, PhD, MD, Department of Anesthesia, Massachusetts General Hospital, 32 Fruit St, Boston, MA 02114.
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Abstract |
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 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
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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.
Key Words: anesthesia • carotid endarterectomy • cerebral ischemia • electroencephalography
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The correlation between electroencephalographic (EEG) changes and cerebral ischemia during carotid endarterectomy under general anesthesia is well established.1 2 3 4 No study, however, has described the baseline EEG abnormalities of patients undergoing carotid endarterectomy in relation to the patients' neurological symptoms or history of strokes or established a clear relationship between those EEG abnormalities and the intraoperative presence of EEG patterns of cerebral ischemia. The purpose of this prospective study was threefold: (1) to characterize and compare the type, distribution, and incidence of EEG abnormalities in patients with and without neurological symptoms undergoing carotid endarterectomy; (2) to determine whether there was any correlation between the presence of preoperative neurological symptoms and the categories of baseline EEG abnormalities and EEG asymmetries after induction of anesthesia and whether these symptoms, EEG abnormalities, and asymmetries were related to the incidence of ischemic events at carotid artery cross-clamp; and (3) to evaluate the relationship between these EEG abnormalities and patients' age.
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Subjects and Methods |
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The study was approved by the Subcommittee on Human Studies. Written informed consent for the surgery with routine EEG monitoring was obtained from each patient who was scheduled for carotid endarterectomy. During a period of 2 years, 421 consecutive studies were completed. Twenty-five subjects with known seizure disorders or who were taking psychotropic medications were excluded from the study, leaving 396 patients whose EEGs were analyzed. Patients' ages ranged from 43 to 91 years, with a mean of 73 years.
Before each operation, the patient's medical record was reviewed and the admitting diagnosis and reason for surgery were recorded. Also recorded were the patient's handedness, medical history, medications, and physical examination. All data were first entered onto a patient profile form, then after surgery into a computer database for analysis.
Preoperative evaluation of each patient included a physical examination with a neurological assessment, an electrocardiogram, and an angiogram of the cervical carotid and vertebral arteries. Two hundred fifty-one patients were considered to be symptomatic, defined as having had a transient ischemic attack, a mild acute stroke, or worsening of an old stroke within 6 months before surgery. The remaining 145 patients all had severe internal carotid artery stenosis defined by radiographic criteria as greater than 80% narrowing of the intravascular lumen.
Twenty-three Grass E5GH gold cup electrodes were applied with collodion
on each patient's scalp according to the International 10-20 System
and were filled with a conduction gel. Electrode impedances were kept
at less than 2000 
. A Nihon Kohden model 4321 electroencephalograph
was used to record 16 bipolar channels of EEG in an anteroposterior
montage and two channels of EEG referenced either to the second
cervical vertebra or average reference. The remaining channels were
used for recording the electrocardiogram and the radial arterial blood
pressure. A high-frequency filter was set at 70 Hz with the time
constant at 0.3 seconds, and a 60-Hz notch filter was used when
necessary. At least 5 minutes of awake baseline EEG recordings were
made before induction of anesthesia but after preoperative medication.
These recordings were completed with the patient lying supine on the
operating room table with his or her eyes closed.
For each operation, the EEG was assessed and interpreted for awake baseline abnormalities, anesthetic-induced changes, and patterns of cerebral ischemia. The EEG was evaluated continuously from the baseline recording and throughout the induction of anesthesia and the operation, until the patient was again awake and appropriately responsive to simple commands. Although this on-line interpretation by either an electroencephalographer or EEG technologist provided information to the surgeons and anesthesiologists regarding patterns of cerebral ischemia during the surgery, a second reading of the EEG by one of the electroencephalographers was performed after surgery to identify in detail the EEG features analyzed in this study. This second interpretation was completed without the information from the patient profile and was used in the study.
The reactive alpha activity of the EEG was analyzed for each patient by determining the highest frequency range and mean frequency observed in EEG channels P3-O1, P4-O2, P7-O1, and P8-O2. Patients revealing a drowsy EEG pattern were aroused. Patients with low-voltage fast records were considered normal. Marked hemispheric asymmetries in alpha rhythm voltage and in beta activity were considered abnormal. Any organized theta or delta activity unassociated with drowsiness that was observed in the awake EEG tracings was also considered abnormal. The location of the abnormal slowing was categorized into focal (for example, anterior or posterior temporal), regional (for example, temporal, parietal, anterior, posterior), hemispheric, and generalized. Although distinctions were made in terms of the severity of the EEG abnormalities (for example, infrequent, intermittent, or persistent left temporal theta slowing), for the purposes of this study all patients with baseline EEG abnormalities, whether mild or severe, were scored as abnormal and the distribution of the abnormalities noted.
All data regarding the specific anesthetic, including the amount and timing of its administration, were recorded on a worksheet for future analysis. EEG asymmetries induced by those anesthetics were noted and the location of focal, regional, or hemispheric asymmetries in amplitude and frequencies were identified and recorded. These asymmetries were compared with the baseline normal and abnormal awake EEGs. EEG pattern changes of cerebral ischemia as defined by several authors1 2 3 4 5 that occurred at carotid artery cross-clamp were reported as present or absent. The criteria for EEG ischemic patterns at carotid artery cross-clamp included ipsilateral or generalized loss or diminution of the alpha and beta fast frequencies, with or without concomitant ipsilateral or generalized increases in theta and delta slowing.
Each patient was monitored intraoperatively with a radial artery catheter, an electrocardiograph, a pulse oximeter, an oral temperature probe, and a capnograph. Oral diazepam was given approximately 90 minutes before induction of anesthesia at a dose (0.05 mg/kg) unlikely to produce measurable drug-induced effects that would interfere with our method of scoring the awake baseline EEG tracings.6 Anesthesia consisted of thiopental (3 to 5 mg/kg) or propofol (2 to 3 mg/kg), followed by 60% to 70% nitrous oxide in oxygen, an opioid, isoflurane at low concentrations (0.2% to 0.5%), and a muscle relaxant. Systolic blood pressure was maintained within 20% of average preoperative values with infusions of phenylephrine and nitroglycerin, as necessary, and the end-tidal CO2 at low normal values (34 to 40 mm Hg). The delivered concentration of the inhalational agents or infusion of narcotics was held constant throughout the cross-clamp period. If there were EEG pattern changes consistent with cerebral ischemia at carotid artery cross-clamp, the surgeons placed an intraluminal bypass shunt proximal and distal to the cross-clamp. In some operations the systolic blood pressure was raised with phenylephrine in an effort to normalize the EEG before a shunt was placed. The surgery performed consisted of angioplasty of the carotid bifurcation and the initial segment of the internal carotid artery with or without a vein-patch graft.
To assess the relationships among patients' ages and symptoms with EEG
findings at awake baseline, after induction of anesthesia, and at
carotid artery cross-clamp, 
2, Fisher's exact,
and ANOVA tests were performed, with P<.05 considered
significant.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Complete data were available for 394 of the 396 patients. The data from two patients were eliminated because of inadequate baseline awake EEG recordings. A total of 203 right and 191 left carotid endarterectomies were performed. Sixty-three percent of all patients were considered to be symptomatic, with 208 having hemispheric transient ischemic attacks and 41 strokes.
There was a close correlation between patients' cerebrovascular symptoms and abnormal baseline EEGs (P<.001). These EEG abnormalities were related to the appropriate contralateral side of the symptoms (P<.0005), whether the symptoms were due to strokes (P<.0002) or to transient ischemic attacks (P<.0001). The association between EEG and patients' symptoms persisted after induction of anesthesia (P<.001), with EEG abnormalities specifically related to the contralateral side of symptoms in patients with transient ischemic attacks (P<.0001) and strokes (P<.0001). Abnormal awake EEG findings were associated with asymmetries after anesthesia (P<.0001). In addition, both the side of the baseline EEG abnormalities and EEG asymmetries after induction of anesthesia correlated with the ipsilateral side on which the surgery was performed (P<.0002 and P<.00001, respectively). Twenty-eight percent of both symptomatic (70/249) and asymptomatic (41/145) patients had EEG ischemic pattern changes at carotid artery cross-clamp. No association was found between neurological symptoms or preoperative EEG abnormalities and ischemic pattern changes at carotid artery cross-clamp. EEG pattern changes of cerebral ischemia after carotid artery cross-clamp were independent of the baseline EEG abnormality, EEG asymmetries after induction of anesthesia, and history of transient ischemic attacks and strokes.
Twenty-four percent of all patients had abnormal baseline awake
EEGs, and 69% had EEG asymmetries after induction of anesthesia. A
strong association between abnormal baseline EEGs and EEG asymmetries
after induction of anesthesia (P=.001) was demonstrated. An
example of a patient with an abnormal awake baseline EEG whose
asymmetry persisted after anesthesia and who developed ischemic
EEG changes at carotid cross-clamp is shown in the
Figure
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Table 1 shows the distribution of EEG abnormalities by
age group in the baseline awake EEGs of our patients. As seen in Table 2, the number of EEG asymmetries after induction of
anesthesia was approximately three times greater than the number of
preoperative EEG abnormalities. There was an increase with age in the
number of preoperative EEGs that were abnormal and in the number of EEG
asymmetries after induction of anesthesia, but these findings were not
statistically significant. There were also more abnormalities
present in the EEG derivations on the left, but these differences
did not achieve statistical significance. Although there was a slight
decrease in the mean and in the ranges of posterior alpha activity in
these patients by decade, this decrease did not reach statistical
significance. There was, therefore, no relationship between the
presence of EEG abnormalities or diminution of the posterior alpha
frequencies and age. There was also no association between the
patients' age and preoperative symptoms, and age was not associated
with EEG ischemic changes at carotid artery cross-clamp.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Our data revealed a significant association between patients' cerebrovascular symptoms and an increase in the incidence of awake baseline EEG abnormalities. In contrast, we found that the preoperative cerebrovascular symptoms and EEG abnormalities had no significant relation to the presence of EEG ischemic pattern changes at carotid artery cross-clamp. We had anticipated that, if reduced or ischemic cerebral blood flow were the cause of the abnormal baseline EEG slow-wave content, occlusion of the major arterial vessel ipsilateral to the positive EEG findings would exacerbate those findings and be associated with an increased incidence of EEG ischemic pattern changes at carotid artery occlusion. That these EEG abnormalities showed no statistically significant association with EEG changes of cerebral ischemia at carotid artery occlusion suggests that the principal cause of the preoperative EEG abnormalities was not reduced or ongoing ischemic regional cerebral blood flow but a fixed "injury," sufficiently stable to remain unchanged, even in the setting of an acute reduction in ipsilateral regional cerebral blood flow.
Although some investigators have reported an association between increased EEG slow-wave activity and decreased regional cerebral blood flow in patients with strokes or transient ischemic attacks,7 other investigators have found that this correlation, if present, depended on the location of the brain injury, the duration of symptoms, the timing of the EEG relative to the onset of symptoms, and the specific vascular territories examined.8 9 10 11 Moreover, the relationship between EEG slow-wave activity and regional cerebral blood flow after strokes may evolve over several years.12 Our results support the findings of Nagata and coinvestigators,8 who demonstrated a poor correlation between awake EEG abnormalities and regional cerebral blood flow in patients after transient ischemic attacks and who reported that cerebral circulation may return to normal or near normal after stroke or transient ischemic attacks, despite findings of residual EEG abnormalities or neurological deficits.
Because we found no statistically significant, age-related baseline EEG changes, whether measured by the ranges in or mean frequency of the posterior alpha activity or by the presence of regional slowing, our results contrast with reports attributing reductions in alpha frequency and increases in temporal slowing to normal aging.13 14 15 16 17 18 19 20 21 In addition, the absence of a significant association between age and propensity toward having EEG ischemic pattern changes at carotid artery cross-clamp among patients with and without preoperative EEG abnormalities argues against the concept of a closely "coupled" relationship between EEG slow-wave activity in awake elderly individuals and reduced or insufficient (ischemic) regional cerebral blood flow.22 23 We conclude that the preoperative EEG abnormalities, whether focal, regional, or hemispheric, and EEG asymmetries after induction of anesthesia are probably attributable to parenchymal injury and not to age or to chronic insufficiencies in cerebral blood flow.
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Acknowledgments |
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We thank Danielle Antin-Ozerkis and Jason Hartman for their assistance in collecting data and Mary Farr for her help in the preparation of the manuscript.
Received January 6, 1995; revision received March 22, 1995; accepted March 22, 1995.
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References |
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