Anesth Analg 2000;90:148
© 2000 International Anesthesia Research Society
REGIONAL ANESTHESIA AND PAIN MANAGEMENT
The Anticonvulsant Effects of Volatile Anesthetics on Lidocaine-Induced Seizures in Cats
Kohei Murao, MD,
Koh Shingu, MD,
Koichi Tsushima, MD,
Kazuyo Takahira, MD,
Sakahiro Ikeda, MD, and
Shin-ichi Nakao, MD
Department of Anesthesiology, Kansai Medical University Hospital, Moriguchi, Osaka, Japan
Address correspondence and reprint requests to Koh Shingu, MD, Department of Anesthesiology, Kansai Medical University Hospital, Fumizono-cho 10–15, Moriguchi, Osaka 570-8507, Japan. Address e-mail to shingu{at}takii.kmu.ac.jp
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Abstract
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Large concentrations of sevoflurane and isoflurane, but not halothane, induce spikes in the electroencephalogram. To elucidate whether these proconvulsant effects affect lidocaine-induced seizures, we compared the effects of sevoflurane, isoflurane, and halothane in cats. Fifty animals were allocated to 1 of 10 groups: 70% nitrous oxide (N2O), 0.6 minimum alveolar anesthetic concentration (MAC) + 70% N2O, 1.5 MAC + 70% N2O, and 1.5 MAC of each volatile agent in oxygen. Lidocaine 4 mg · kg-1 · min-1 was infused IV under mechanical ventilation with muscle relaxation. Electroencephalogram in the cortex, amygdala, and hippocampus and multiunit activities in the midbrain reticular formation (R-MUA) were recorded. Lidocaine induced spikes first from the amygdala or hippocampus in the 70% N2O and halothane groups and from the cortex in the sevoflurane and isoflurane groups. Lidocaine induced seizures in all cats in the 70% N2O and 0.6 MAC + N2O groups. Seizure occurrence was reduced in the 1.5 MAC + N2O group (P < 0.05 versus 70% N2O). The onset of seizure was delayed in the 0.6 MAC + N2O and 1.5 MAC groups for sevoflurane and isoflurane, but not for halothane, compared with the 70% N2O group (P < 0.05). Lidocaine increased R-MUA with seizure by 130% ± 56% in the 70% N2O group. The increase of R-MUA with seizure was more suppressed in the volatile anesthetic groups than in the 70% N2O group (P < 0.05). In the present study, sevoflurane and isoflurane attenuated seizure when the blood lidocaine concentration was accidentally increased.
Implications: Increasingly, epidural blockade is combined with general anesthesia to achieve stress-free anesthesia and continuous pain relief in the postoperative period. In the present study, sevoflurane and isoflurane attenuated seizure when the blood lidocaine concentration was accidentally increased.
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Introduction
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The use of regional anesthesia has become increasingly popular for reducing intraoperative general anesthetic requirements. The accidental intravascular injection of a local anesthetic may cause serious complications, including seizures. Volatile anesthetics enhance GABAA receptor activities (1) and have anticonvulsant actions (2,3). The anticonvulsant actions may be mediated by their depressive actions on the central nervous system (CNS), partly by enhancing GABAA receptor activities. A few reports compare the potency of the anticonvulsant actions of volatile anesthetics on local anesthetic-induced seizures (4,5). However, enflurane, isoflurane, and sevoflurane have proconvulsant actions, in that large concentrations induce spontaneous spikes on an electroencephalogram (EEG), and generalized seizure is evoked during deep enflurane and sevoflurane anesthesia in cats (6). It is not known whether these proconvulsant actions affect their anticonvulsant actions on local anesthetic-induced seizures. Oshima et al. (7) reported that enflurane had anticonvulsant actions in several epilepsy animal models, but they did not investigate a local anesthetic-induced seizure model.
We previously reported that background neuronal activity in the midbrain reticular formation, an index of general CNS activities, was suppressed by volatile anesthetics, and that suppression with sevoflurane and isoflurane was significantly greater than that with halothane (8,9). We hypothesized that the greater the depressive actions of volatile anesthetics on general CNS activities, the greater the anticonvulsant actions. In addition, the proconvulsant actions of sevoflurane and isoflurane may be counteracted by their greater depressive actions on general CNS activity. We studied this hypothesis by comparing the actions of sevoflurane, isoflurane, and halothane on lidocaine-induced seizure in cats.
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Methods
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Fifty cats weighing 2.6–3.2 kg were used in this study, which was approved by our institutional committee on animal research. Each animal was anesthetized by placing it in a 50-L box filled with 5% sevoflurane in oxygen; sevoflurane anesthesia was then maintained via a face mask. Catheters were inserted into bilateral cephalic veins and into a femoral artery. After 1 mg of vecuronium had been injected, the trachea was intubated. The lungs were ventilated mechanically using a nonrebreathing ventilator (Acoma, Tokyo, Japan) to maintain an end-tidal carbon dioxide (CO2) concentration of 30–35 mm Hg. Anesthesia was maintained with 3.5% sevoflurane in oxygen. Vecuronium was injected as required. The animal was then placed on a stereotaxic apparatus. Stainless steel screws, 2.0 mm in diameter, were inserted in the frontal bone of the skull (reference electrode) and over the temporal and occipital cortex to record the cortical electroencephalogram (EEG). Two parallel stainless steel wire electrodes, 0.2 mm in diameter, insulated with epoxylite resin except at the tips, with a vertical separation of 0.5–1.0 mm at the tips, were inserted into bilateral midbrain reticular formation [A2, L3, H-2, according to the atlas of Snider and Niemer (10)] to record the reticular multiunit activity (R-MUA). The same type of wire electrodes were also inserted into bilateral dorsal hippocampus (A2, L8, H9) and the medial amygdala (A12, L9, H-6). Each set of the electrodes was connected to a socket that was fixed to the skull with dental cement. After sevoflurane had been discontinued, a mixture of 70% nitrous oxide (N2O) in oxygen was administered for 30 min (control period), during which period no noxious stimuli was applied to cats.
Animals were then allocated to 1 of 10 groups (five cats in each group): 70% N2O, 0.6 minimum alveolar anesthetic concentration (MAC) of a volatile anesthetic + 70% N2O, 1.5 MAC of a volatile anesthetic + 70% N2O, and 1.5 MAC of a volatile anesthetic. The volatile anesthetics studied were sevoflurane, isoflurane, and halothane. The 1 MAC values in cats were 2.6% for sevoflurane (11), 1.6% for isoflurane, and 1.2% for halothane (12) .
The EEG was recorded on an eight-channel polygraph (Nihon-Koden, Tokyo, Japan), and the R-MUA and arterial blood pressure were recorded on an oscillograph (Nihon-Koden). The firing of reticular neurons was measured using a R-MUA technique as described previously (13). This technique registers neuronal discharges from a 1-mm radius around the tip of the electrode (14). The level of R-MUA was measured as the distance from the multiunit tracing to the input short. End-tidal concentrations of each volatile anesthetic and CO2 were measured by using an infrared anesthetic gas monitor (Capnomac Ultima, Datex, Helsinki, Finland), which was calibrated each day. Rectal temperature was maintained at 37–39°C by using a warm water mattress and heating lamp. Systolic arterial pressure was maintained >70 mm Hg by an IV infusion of noradrenaline 0.1 mg · kg-1 · h-1.
Lidocaine was infused at the rate of 4 mg · kg-1 · min-1 IV 30 min after an appropriate mixture of gas had been given (baseline period). The infusion of lidocaine induced sporadic spikes, then repetitive spikes, which were synchronized in all sites of recording and were interrupted by flat EEG. We judged that seizure was induced when repetitive spikes were observed. The time from the infusion of lidocaine to the occurrence of sporadic spikes and seizure was measured. The infusion of lidocaine was continued until seizures developed, at which time arterial blood was taken and its lidocaine concentration was measured. The blood sample was immediately centrifuged, and plasma (0.2 mL) was stored at -30°C until lidocaine concentration measurement by using a fluorescent immunoassay. If repetitive spikes did not develop within 1 h, the infusion of lidocaine was terminated.
The anticonvulsant actions of the gas mixture were evaluated with onset time of spikes and seizure, the number of cats with seizure activity on the EEG, arterial plasma concentration of lidocaine when seizure developed, and increase of R-MUA associated with the seizure. R-MUA was expressed as a percentage of that obtained during exposure to 70% N2O (control period) in each animal.
Data are presented as mean ± SD. The occurrence of seizure was analyzed by using the 
2 test. Other data were analyzed by using analysis of variance and the Newman-Keuls test for multiple comparisons. P < 0.05 was considered significant.
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Results
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In the control period, EEG patterns were not different among groups. Before the infusion of lidocaine (baseline period), EEG patterns were different among groups: the 0.6 MAC + N2O groups of sevoflurane and isoflurane showed slow waves on the EEG; the 1.5 MAC halothane groups with or without N2O showed high-voltage slow waves in cortical EEG and sporadic spikes or sharp waves in amygdaloid and hippocampal EEG; the 1.5 MAC and 1.5 MAC + N2O groups of sevoflurane and isoflurane showed sporadic spikes on the EEG, which were synchronized in all sites of recording, and the background EEGs were almost isoelectric. Rhythmic low-voltage oscillations were shown on the background EEGs in the 1.5 MAC and 1.5 MAC + N2O groups of the sevoflurane and isoflurane groups, which were dominant in amygdaloid and hippocampal EEG and remarkable in the 1.5 MAC + N2O group compared with the 1.5 MAC groups. Volatile anesthetics suppressed R-MUA in the baseline period. The suppression in R-MUA was dose-dependent for sevoflurane and isoflurane, and the suppression was significantly greater in the sevoflurane and isoflurane groups than in halothane groups (P < 0.05) (Table 1). Although baseline R-MUA was not different between the 1.5 MAC + N2O and 1.5 MAC groups for halothane and sevoflurane, the 1.5 MAC isoflurane group showed greater suppression of R-MUA (P < 0.05) (Table 1).
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Table 1. Effects of Anesthetics on the Tetraphasic Changes in Multiunit Activity in the Midbrain Reticular Formation (R-MUA)
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Lidocaine induced tetraphasic changes on the EEGs and R-MUA in the 70% N2O group (Figure 1). The initial stage was represented by diffuse high-voltage slow waves on the EEG and suppression of the R-MUA. The second stage was represented by low-voltage fast waves in cortical EEG, low-voltage fast waves or rhythmic waves in amygdaloid and hippocampal EEGs, and activation of the R-MUA. The third stage was represented by the reappearance of slow waves and the occurrence of sporadic spikes on the EEG and suppression of the R-MUA. The fourth stage was represented by an epileptiform EEG and synchronized increases of the R-MUA with repetitive spikes on the EEG. Seizure developed 528 ± 69 s after the initiation of the lidocaine infusion, and R-MUA increased by 130% ± 56% with seizure activity. The arterial blood lidocaine concentration at this point was 44 ± 10 µg/mL.
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Figure 1. Effects of lidocaine 4 mg · kg-1 · min-1 on the electroencephalogram (EEG) and midbrain reticular multiunit activity (R-MUA) in a cat in the 70% N2O group. A, Cortical (Cx) EEG and R-MUA. Changes in the level of neuronal unit firing were measured as the distance from the multiunit tracing to the input short line. The upward shift of the tracing indicates the increase in the firing rate of units, and the downward shift indicates the decrease. The R-MUA and Cx EEG, in which changes in the amplitudes are shown, show sequential changes in four stages. The initial stage consists of suppression of the R-MUA associated with high amplitudes in the Cx EEG. The second stage consists of activation of the R-MUA associated with low amplitudes in the Cx EEG. The third stage consists of suppression of the R-MUA associated with high amplitudes in the Cx EEG. The fourth stage consists of repeated activation of the R-MUA associated with high amplitudes in the Cx EEG. The start of the lidocaine infusion is indicated by an arrow. B, Changes on the EEG recorded from the Cx, amygdala (Amy), and dorsal hippocampus (DH) in each phase during the lidocaine infusion. Baseline = before the lidocaine infusion, Stage 1 = the stage of initial depression, Stage 2 = the stage of excitation, Stage 3 = the stage of late depression, Stage 4 = the stage of seizure.
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Seizure was induced in five cats in the 0.6 MAC + N2O groups and in four cats in the 1.5 MAC groups. In the 1.5 MAC + N2O groups, seizure was observed in only one cat for sevoflurane, none for isoflurane, and two for halothane (P < 0.05 versus the 70% N2O group) (Table 2). Although the onset time of spikes in the volatile anesthetic groups was not different from that in the 70% N2O group, it was delayed in all groups (P < 0.05), except the 0.6 MAC + N2O and 1.5 MAC halothane groups. The arterial lidocaine concentration in the volatile anesthetic groups was higher than that in the 70% N2O group (P < 0.05). The increase of R-MUA associated with seizure activity was more suppressed in the volatile anesthetics groups than in the 70% N2O group (P < 0.05) (Table 1), but there was no dose-dependency in the increase of R-MUA associated with seizure activity among volatile anesthetic groups.
Lidocaine induced tetraphasic changes in R-MUA in all study groups. In the volatile anesthetic groups, R-MUA was significantly more depressed than in the 70% N2O group at all stages (Table 1, Figure 2). However, the EEG did not show characteristic tetraphasic changes during the lidocaine infusion in the volatile anesthetic groups (Figure 2). Characteristic rhythmic waves in amygdaloid EEG, which indicate activation, were observed during the second stage in the 0.6 MAC + N2O groups, but not in the 1.5 MAC + N2O or 1.5 MAC groups. Lidocaine induced burst-suppression and isoelectric EEG during the third stage of R-MUA. In the 1.5 MAC + N2O and 1.5 MAC groups of sevoflurane and isoflurane, spikes were shown before the infusion of lidocaine; these spikes diminished transiently with the infusion of lidocaine (Figure 2). Sporadic spikes reappeared in the cortical EEG, then synchronized in all sites of recording (Figure 3). In the 70% N2O and halothane groups, lidocaine initially induced spikes in the amygdala and hippocampus (Figure 3).
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Figure 2. Effects of lidocaine infusion 4 mg · kg-1 · min-1 on the cortical electroencephalogram (EEG; upper trace) and midbrain reticular multiunit activity (R-MUA; lower trace) in each group. The tetraphasic changes in R-MUA are seen in all groups. Both sevoflurane and isoflurane 1.5 MAC and 1.5 MAC + N2O show high-amplitude traces in the cortical EEG before the lidocaine infusion, and they are abolished transiently during the lidocaine infusion. A horizontal line designated "control" and an underline in each trace show the levels of R-MUA during the control period (anesthesia with 70% N2O) and input short in each animal, respectively, and an arrow indicates when the lidocaine infusion was initiated.
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Figure 3. Electroencephalograms (EEGs) on the cortex (Cx), amygdala (Amy), and dorsal hippocampus (DH) during the initiation of spikes (a) and when the spikes were synchronized in all sites (b) during the lidocaine infusion in the 1.5 MAC groups. Spikes originate from the Cx in the sevoflurane and isoflurane groups and from the Amy and DH in the halothane group.
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Discussion
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Sevoflurane, isoflurane, and halothane significantly reduced the occurrence of lidocaine-induced seizure in the 1.5 MAC + N2O groups and suppressed the increase of R-MUA associated with seizures. These results indicate that all the volatile anesthetics studied have anticonvulsant actions on lidocaine-induced seizures. Furthermore, 1.5 MAC + N2O prevented the occurrence of seizure in more cats than 1.5 MAC, which suggests an anticonvulsant action of N2O when used in combination with volatile anesthetics.
Fukuda et al. (4) reported an equipotency between sevoflurane and isoflurane for attenuating bupivacaine-induced seizures in rats. Badgwell et al. (5) did not observe any difference in anticonvulsant actions between halothane and isoflurane in bupivacaine-induced seizure in pigs. They also reported a high incidence of ventricular dysrhythmias in halothane anesthesia. The increase of bupivacaine in the brain might have been delayed by cardiac dysrhythmia in that group and may have exaggerated halothane’s anticonvulsant action. We infused lidocaine and did not observe any ventricular dysrhythmia during the study. High concentrations of sevoflurane or isoflurane induce spontaneous spikes on the EEG (6,8), and generalized convulsion can be evoked by peripheral somatic stimulation during deep sevoflurane anesthesia in cats (6). In addition, epileptoid EEGs have been reported in patients anesthetized with sevoflurane (15,16). These proconvulsant actions of sevoflurane, and possibly isoflurane, could lead one to suspect that they enhance lidocaine-induced seizures. However, the present study showed that it is unlikely. Rather, isoflurane and sevoflurane showed similar or more potent anticonvulsant actions than halothane on lidocaine-induced seizures in cats, because the onset of seizure was significantly delayed by sevoflurane and isoflurane, but not by halothane, in the 0.6 MAC + N2O and 1.5 MAC groups. The CNS sites at which seizures originate are different among different seizure-inducing drugs. Although sevoflurane- and enflurane-induced seizures originate from the cerebral cortex (6,17), lidocaine-induced seizures involve limbic structures (17–20). Therefore, it is possible that the proconvulsant effects of sevoflurane, and perhaps isoflurane, did not enhance the lidocaine-induced seizure. The present results show that volatile anesthetics depressed R-MUA and that the suppression at 1.5 MAC in the baseline period was greater for sevoflurane and isoflurane than for halothane. This is consistent with previous studies (8,9). The potent depressive actions of sevoflurane and isoflurane on spontaneous CNS activities may have counteracted their proconvulsant actions in the present seizure model. However, the correlation between the effects on the R-MUA and anticonvulsant actions of anesthetics requires more investigation.
Seizures were was induced in significantly fewer cats in the 1.5 MAC + N2O groups than in the 0.6 MAC + N2O groups, which suggests a dose-dependency in the anticonvulsant actions of volatile anesthetics. However, no dose-dependency was observed in the onset of seizure and in the lidocaine concentration at the onset of seizure. This discrepancy in dose-dependencies indicates that there might be a range of appropriate lidocaine brain levels for inducing seizures and that, when the brain level of lidocaine increases over this range, neuronal excitability might be too suppressed to spread seizure activities throughout the brain. The onset of spikes induced by lidocaine was not affected by volatile anesthetics. This indicates that the lidocaine-induced generation of spikes is not suppressed by volatile anesthetics and N2O, and that the mechanisms for the generation of spikes and for the spread of epileptic activity throughout the brain are different. The resistance in the generation of lidocaine-induced spikes to volatile anesthetics could be due to the regional difference of depression in the CNS by volatile anesthetics. Isoflurane and sevoflurane depress activities in the cortex, rather than the limbic structures (6), where lidocaine-induced spikes originate.
Seizures were induced in fewer cats in the 1.5 MAC + N2O groups than in the 1.5 MAC groups. This indicates an anticonvulsant action of N2O. DeJong et al. (21) also reported that N2O increased the convulsive threshold of lidocaine in cats.
In addition, 1.5 MAC sevoflurane and isoflurane induced sporadic spikes on EEGs before the infusion of lidocaine, and these spikes disappeared during the infusion of lidocaine when the R-MUA increased (the second phase). These results suggest that lidocaine itself has an anticonvulsant action, as previously reported (22,23).
Lidocaine induced tetraphasic changes in R-MUA under general anesthesia that were similar those under the nonanesthetic conditions reported by Seo et al. (24) and Shibata et al. (25). They showed that behavior and variables of the cardiovascular systems correlated with the excitatory and depressive phases of the R-MUA. We could not observe these changes in the present study, in which animals received a muscle relaxant and the blood pressure was controlled by an infusion of noradrenaline. Therefore, we could not determine whether behavioral and circulatory changes could indicate acute toxicity of local anesthetics or whether they were masked during general anesthesia. Seo et al. (24) showed that the tetraphasic actions could be modified by the infusion rate of lidocaine and that the depressive phases of the tetraphasic changes were skipped by high rates of infusion of lidocaine at 8–16 mg · kg-1 · mg-1. Shibata et al. (25) also reported similar modifications by high infusion rates of other local anesthetics. In the present study, we revealed that lidocaine has excitatory and depressive actions on the R-MUA, even under general anesthesia with volatile anesthetics and N2O, and that these actions are resistant to general anesthetics.
In conclusion, halothane, isoflurane, sevoflurane, and N2O have anticonvulsant actions on lidocaine-induced seizures in cats. The tetraphasic action of lidocaine on the R-MUA is resistant to volatile anesthetics.
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Acknowledgments
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Supported in part by Grant-in-Aid for Scientific Research 08457415 from the Ministry of Education, Science and Culture, Japan.
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Accepted for publication August 30, 1999.
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Abstract
Introduction
