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Anesth Analg 2000;91:989-995
© 2000 International Anesthesia Research Society

GENERAL ARTICLES

The Epileptogenic Properties of the Volatile Anesthetics Sevoflurane and Isoflurane in Patients with Epilepsy

Takehiko Iijima, DDS, DMSc, PhD*, Zenkou Nakamura, DDS, DMSc{dagger}, Yasuhide Iwao, MD, DMSc*, and Hiroshi Sankawa, MD, DMSc*

*Department of Anesthesiology, Kyorin University School of Medicine; and {dagger}Section of Dentistry, Tokyo Metropolitan Higashiyamato Medical Center for the Severely Disabled, Tokyo, Japan

Address correspondence and reprint requests to Takehiko Iijima, DDS, DMSc, PhD, Department of Anesthesiology, Kyorin University of Medicine, 6-20-2 Sinkawa Mitaka, Tokyo 181-8611, Japan. Address e-mail to iijmt{at}kyorin-u.ac.jp


   Abstract
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 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
No study comparing epileptogenicity of sevoflurane to other volatile anesthetics has been performed. We compared the epileptogenic properties of sevoflurane to isoflurane in patients with epilepsy. In 24 mentally and/or physically disabled patients, 12 with epilepsy and 12 without epilepsy, electroencephalograms were recorded under anesthesia with 1.0 minimum alveolar anesthetic concentration (MAC), 1.5 MAC, and then 2.0 MAC sevoflurane or isoflurane under three ventilatory conditions: (A) 100% oxygen, and end-tidal CO2 partial pressure (ETCO2) = 40 mm Hg, (B) 50% oxygen, 50% nitrous oxide, ETCO2 = 40 mm Hg, and (C) 100% oxygen, ETCO2 = 20 mm Hg. Spike activity was evaluated as a spike-and-wave index (% durations of spike and wave). The spike-and-wave index increased (P < 0.05) from 1.99% ± 0.96% during 1.0 MAC sevoflurane to 6.14% ± 4.45% during 2.0 MAC sevoflurane in (A) in the epilepsy group, while no spike activity was observed in the nonepilepsy group. Only a few spikes were observed under isoflurane anesthesia, 0.04% ± 0.04% in (A), with no spikes in (B) and (C). Supplementation with 50% nitrous oxide or hyperventilation (P < 0.05) suppressed the occurrence of spikes. Sevoflurane has a stronger epileptogenic property than isoflurane, but nitrous oxide or hyperventilation counteracts this specific epileptogenic property.

Implications: The stronger epileptogenicity of sevoflurane than isoflurane was confirmed in a controlled study in patients with epilepsy. Hyperventilation and supplementation of nitrous oxide under sevoflurane anesthesia suppressed epileptogenicity. A combination of sevoflurane and nitrous oxide may be a safer method for seizure-prone patients than the use of sevoflurane alone.


   Introduction
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 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Inhibition of glutamate release from presynaptic nerve terminals or activation of inhibitory GABAergic pathways may explain the depressant effect of many volatile anesthetics (1–4). However, enflurane has an excitatory effect and occasionally evokes convulsions (5,6). Halogenated methyl ether anesthetics seem to exert a dual-phase effect in a dose-dependent manner involving partial excitation and depression (7).

Sevoflurane and isoflurane are widely used volatile anesthetics. Electroencephalographic (EEG) abnormalities as well as tremors, clonus, and seizure-like motor activity, have been reported with these anesthetics (8–10) and there are reports (11,12) about their epileptogenic properties in animal experiments. So far, however, there has been no comparative study of epileptogenic properties of these anesthetics in humans. Elucidation of such effects would be useful when choosing suitable anesthetics for surgical intervention in patients with epilepsy. We therefore examined the epileptogenic properties of sevoflurane and isoflurane in epileptic and nonepileptic patients and the effects of hyperventilation and supplementation with nitrous oxide.


   Methods
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 Methods
Results
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We studied 24 patients (13 men and 11 women, aged 16 to 41 yr, ASA physical status I or II) (Table 1), who were scheduled for dental treatment under general anesthesia. Our study was approved by the Institutional Human Studies Committee of Tokyo Metropolitan Higashiyamato Medical Center for the Severely Disabled. Informed consent for participation in the study was obtained from the parents of the patients. All of the patients were mentally handicapped. They were allocated to two groups. Group I consisted of 12 patients with a history of epilepsy (Table 1), all of whom were treated with anticonvulsant medication. Six patients in this group had focal seizures, and the other six patients had generalized seizures. Group II consisted of 12 patients without a history of epilepsy (Table 1). None of the patients had habitually used medication affecting the EEG, e.g., psychotropic drugs or tranquilizers.


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  		Table 1. Background of the Subjects
 
The epileptic patients did not take anticonvulsants on the morning before the examination, and no premedication was given. Anesthesia was induced by mask inhalation of oxygen 2 L/min, nitrous oxide 4 L/min, and incremental doses of 0.5% to 4.0% volatile anesthetic (sevoflurane or isoflurane). Tracheal intubation was performed after neuromuscular block with vecuronium bromide 0.1 mg/kg IV. No further administration of muscle relaxant was required during anesthesia.

Silver/silver chloride gel-filled electrodes were secured by using the international standard electrode placement (10–20) system to the left and right parietal (FP3 and FP4), left and right temporal (T3 and T4), left and right frontal (F7 and F8), left and right central (C3 and C4), left and right occipital (O1 and O2), and vertex (Fz and Pz) regions. A reference electrode was installed on the earlobe (A1, A2) on the same side.

The patients’ lungs were mechanically ventilated throughout the procedures. Ventilatory conditions were adjusted as follows. Ventilatory condition A: 100% oxygen with end-tidal carbon dioxide partial pressure (ETCO2) 40 mm Hg. Ventilatory condition B: 50% oxygen and 50% nitrous oxide with ETCO2 40 mm Hg. Ventilatory condition C: 100% oxygen with ETCO2 20 mm Hg. Under each of these conditions, the anesthetic dose was adjusted to 1.0, 1.5, or 2.0 minimum alveolar anesthetic concentration (MAC). To prevent motion artifacts, the dental procedure was stopped temporarily, and EEGs were recorded for more than 3 min after the end-tidal concentration of the inhaled anesthetic and ETCO2 had become stable for more than 5 min under each ventilatory condition. Approximately 3 mo later, EEGs were again recorded under anesthesia using isoflurane under the same conditions as those used for sevoflurane. These patients required multiple dental treatments to complete the prosthetic procedure.

EEGs were recorded with a Neurofax EEG-5514TM (Nihon Kohden Corp., Tokyo, Japan). Electrode impedance was maintained below 5 k{Omega}. EEG data were high-pass filtered to 120 Hz by using noise filter settings. EEG data were recorded on paper by a pen-recorder, and stored on digital audio tape (RD-200T PCM Data RecorderTM; TEAC Corp., Tokyo, Japan) for subsequent analysis.

The 1-min period of EEG data before incision was divided into 5-s epochs and subjected to fast Fourier transformation (FFT) analysis by using a DP1100 signal processorTM (NEC Medical Systems Ltd., Tokyo, Japan). The frequency band stages used were {delta} (0.2–3.8 Hz), {theta} (4.0–7.8 Hz), {alpha} (8.0–12.8 Hz), and ß (13.0–35.0 Hz). One epoch was analyzed for 1 min, and 12 epochs were added. The power value at each frequency band stage was calculated with FFT. For evaluation of the background EEG under each measurement condition, the power value of each site and {delta} ratio ({alpha} + ß)/{delta} were averaged.

The EEGs were analyzed visually by a pediatric neurologist (HH) who was blinded to the group assignment. The occurrence of both focal epileptiform discharges (number of sharp waves, spikes, polyspikes, spike-wave complexes) and generalized discharges (duration of paroxysms) was counted for each patient. According to the method of Guey et al. (13), the percent duration of paroxysms with each activity was established as follows: the individual spike-and-wave index = (sum of durations of paroxysms per activity/total duration of activity in question) x 100.

SAS version 6.11TM (SAS Institute, Cary, NC) was used for statistical evaluation. All values are expressed as the mean ± SEM. Differences in physiologic values between the two groups were assessed by paired Student’s t-tests. For the multiplex comparative assay, multivariate analysis of variance was used for comparisons among the three ventilatory conditions and three MACs, and Fisher’s protected least square difference was used as a post hoc test. Differences at P < 0.05 were considered statistically significant.


   Results
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 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
Delta ratios decreased (P < 0.05) during ventilatory condition A with both sevoflurane and isoflurane (Fig. 1). There was no significant difference in the {delta} ratio between the two anesthetics under each ventilatory condition, or between Groups I and II. Delta ratios in both groups under ventilatory conditions B and C were significantly lower than under ventilatory condition A (P < 0.05).



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  		Figure 1. Changes in {delta} ratio ([{alpha} + ß]/{delta}). Group I, patients with epilepsy, n = 12 and Group II, patients without epilepsy, n = 12. A power spectral analysis was performed with fast Fourier transformation, using a 5-s epoch; 12 epochs were averaged to produce a power spectrum. The relative power of {alpha}, ß, and {delta} frequency bands was used for calculation of the {delta} ratio. The {delta} ratio decreased significantly (*P < 0.05; post hoc test, Fisher’s protected least squares difference) from the control conditions under condition A. There were no significant differences between sevoflurane and isoflurane under conditions A, B, and C. Values are means ± SEM. MAC = minimum alveolar anesthetic concentration.

 
Seven patients (58%) given sevoflurane and 3 patients (25%) given isoflurane showed epileptiform patterns under ventilatory condition A in Group I. Six patients (50%) who received sevoflurane and one patient (8%) who received isoflurane showed epileptiform patterns under ventilatory condition B. Seven patients given sevoflurane (58%) and one patient given isoflurane (8%) showed an epileptiform pattern under ventilatory condition C. In Group II (n = 12), no epileptiform pattern was observed under any of the conditions, irrespective of whether sevoflurane or isoflurane was used (Table 2).


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  		Table 2. The Findings of the Electroencephalogram and Spike-and-Wave Index in Each Subject
 
The spike-and-wave index increased significantly from 1.99% ± 0.96% (1.0 MAC sevoflurane) to 6.14% ± 4.45% (2.0 MAC sevoflurane) (P < 0.01) under ventilatory condition A in Group I, whereas it decreased in a dose-dependent manner during isoflurane anesthesia (P > 0.05) (Fig. 2). Under ventilatory condition B, the spike-and-wave index increased slightly from 0.89% ± 0.56% (1.0 MAC sevoflurane) to 1.41% ± 0.59% (2.0 MAC sevoflurane) (P > 0.05), whereas it was 0.04% ± 0.04% during 1.0 MAC isoflurane. No spike activity was observed during 2.0 MAC isoflurane (Fig. 2). Under ventilatory condition C, the spike-and-wave index decreased slightly from 1.25% ± 0.57% (1.0 MAC sevoflurane) to 0.59% ± 0.31% (2.0 MAC sevoflurane) (P > 0.05), whereas it was 0.01% ± 0.01% during 1.0 MAC isoflurane. No spike activity was observed during 2.0 MAC isoflurane (Fig. 2). No spike activity was observed under all conditions in Group II.



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  		Figure 2. Changes in spike-and-wave index (%). A: at O2 = 100% and normocapnia, condition A; B: at O2 = 50%, N2O = 50% and normocapnia, condition B; C: at O2 = 100% and hypocapnia, condition C. Note that the amount of spike activity increased significantly (*P < 0.05) under 2.0 minimum alveolar anesthetic concentration (MAC) of sevoflurane, but did not increase under 2.0 MAC of isoflurane under condition A. No spike activity was observed with isoflurane under conditions A and B. The spike-and-wave index of sevoflurane was significantly higher than that of isoflurane under each condition (*P < 0.05; multivariate analysis of variance). Values are means ± SEM. The MACs correspond to the MAC of each volatile anesthetic alone.

 
There was no significant difference in the number of appearances of the epileptiform pattern between patients with partial seizures and those with generalized seizures. Four of the six patients with generalized seizures had an epileptiform pattern (Fig. 3). Two patients showed a generalized epileptiform pattern and two a focal pattern (Table 2). However, four of the six patients with partial seizures showed an epileptiform pattern, and all of these were focal. No specific epileptiform pattern was observed for any specific ventilatory condition or volatile anesthetic.



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  		Figure 3. Representative electroencephalograms (Fz) under sevoflurane and isoflurane anesthesia (Patient No. 5) when the ventilatory condition was (A)- end-tidal CO2 partial pressure = 40 mm Hg. Note that spike activity increased markedly under 2.0 minimum alveolar anesthetic concentration (MAC) of sevoflurane, whereas isoflurane did not induce spike activity.

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
Increasing doses of inhaled anesthetics shifts the EEG from a slowing pattern to a burst suppression, and finally enters a state of isoelectricity. Spike activity was often observed during sevoflurane anesthesia in the phase between the burst suppression pattern and isoelectricity. We rarely observed such spike activity during isoflurane anesthesia, even before isoelectricity occurred.

It is likely that the mechanism of depression of neuronal activity differs between sevoflurane and isoflurane. There may be a window during which spikes are likely to be evoked before total suppression of neuronal activity under sevoflurane anesthesia. Enflurane exerts its epileptogenicity through N-methyl-D-aspartate (NMDA) receptors, as suggested by a study in which spikes were abolished after NMDA receptor blockade in hippocampal slices (14). Sevoflurane has a similar molecular structure and contains seven fluoride atoms, which are related to its excitatory properties (7). Therefore, the epileptogenic property of sevoflurane may be exerted through the same mechanism. However, no data on the direct effect of sevoflurane on NMDA receptors are available.

The difference in NMDA receptor excitability between isoflurane and sevoflurane needs to be examined to clarify the underlying difference in their mechanisms of epileptogenicity. There appears to be different cell types that act in opposite ways on stimulation of the same receptor. In fact, two different cell types showing opposite responses to dopamine receptor stimulation are known to exist in the globus pallidus (15). Ethanol is also an NMDA receptor antagonist, and has been confirmed to exert a biphasic effect in a dose-dependent manner (16). Sevoflurane conceivably acts in the same manner.

The MAC concentration we used was 1.71% for sevoflurane (from the data obtained from Japanese patients (17) and 1.15% for isoflurane. The MAC for sevoflurane is reported to be 2.05% in the United States (18,19). These differences may be attributable to the age of the study subjects. The MAC for sevoflurane we used may be a smaller dose than that for isoflurane. We examined the {delta} ratio for quantitative analysis of the extent of neuronal suppression, but found no significant difference in the {delta} ratio between the two anesthetics (1.71% sevoflurane, 1.15% isoflurane). Thus, we assumed that there was no significant difference of depth of anesthesia between the two anesthetics (20).

The addition of nitrous oxide suppressed the incidence of spikes in our study. This result is consistent with previous reports in which nitrous oxide itself suppresses neuronal activity (21) and its combination with isoflurane completely suppressed spike activity (22,23). In contrast, the combination with nitrous oxide was reported to increase spike activity in cats during sevoflurane anesthesia (24). Others reported that seizure activity evoked by enflurane was suppressed by combination with nitrous oxide in the cat (25). We speculate that these differences are attributable to the depth of anesthesia.

Hyperventilation is generally used to evoke seizures. In contrast, we observed that the incidence of spikes was suppressed during hyperventilation. Respiratory alkalosis itself produces a slower EEG pattern, which we also observed as lowering of the {delta} ratio. Perhaps the combination of volatile anesthetics and hyperventilation exerts suppressive effects on neuronal activity. This suppression pattern seems to be similar to that of nitrous oxide.

The pattern of epileptogenicity evoked by sevoflurane was dependent on the individual pattern of epilepsy. We did not observe a focal pattern of epileptic spikes in patients who originally showed a global pattern of epilepsy, and vice versa. Sevoflurane itself seemed to sensitize an individual to their own pattern of epilepsy, and did not evoke a sevoflurane-specific epileptogenic pattern.

The epileptogenicity of inhaled anesthetics does not usually cause complications in paralyzed patients during anesthesia. Our findings in this study, however, may become important when spikes are intentionally evoked while searching for an ictal focus during epilepsy surgery or when selecting an anesthetic for treatment of refractory status epilepticus (26,27).

Our study was not randomized for the order of administration of volatile anesthetics. The interval between the two experimental events was three months. Therefore, the first anesthetic should not have influenced the second one. The baseline EEG was not significantly different between the two tests, which was confirmed quantitatively by FFT analysis. Anesthesia for dental treatment for the patients was repeated several times before this study because of multiple dental caries. Therefore, the study was done in the midst of repeated anesthesia.

In conclusion, we have observed a high susceptibility to spike activity during sevoflurane anesthesia in comparison with isoflurane. Such spike activity can be abolished by additional inhalation of nitrous oxide or hyperventilation.


   Acknowledgments
 
We thank Hiroshi Hamaguchi, MD, for assistance with evaluation of the EEGs, and Hiroko Ishii, PhD, for assistance with the EEG editing.


   References
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

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Accepted for publication June 5, 2000.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press