Effect of Dexmedetomidine on Electrocorticography During Epilepsy Surgery under Isoflurane or Propofol Anesthesia: A Prospective, Randomized Trial

Abstract

Objectives

Avoiding or minimizing the interference of anesthetic agents with electrocorticography (ECoG) signals during ECoG-guided epilepsy surgery is vital to the successful resection of the epileptogenic area. Most agents in routine use have widely variable effects like suppression, enhancement, or no impact on the ECoG signals. Dexmedetomidine is reported to have no influence, or minimal depressant effect, on the signals, but studies evaluating its effect on intraoperative ECoG are limited. This study evaluates the effect of dexmedetomidine on ECoG signals during ECoG-guided epilepsy surgeries conducted under either isoflurane-based or propofol-based anesthesia regimens. It also assesses the safety of dexmedetomidine use in these combination forms by determining its impact on hemodynamic parameters, recovery from anesthesia, and incidence of intraoperative awareness.

Materials and Methods

Thirty epilepsy patients, randomized into Group-I (dexmedetomidine-isoflurane, n = 15) and Group-P (dexmedetomidine-propofol, n = 15), underwent ECoG-guided epilepsy surgeries. After dural reflection, dexmedetomidine was administered as a bolus of 1 μg/kg, and ECoG signals were recorded before and after the bolus via brain surface grids. Dexmedetomidine infusion of 0.5 μg/kg/h was thereafter continued throughout surgery in both groups. The effect of dexmedetomidine on ECoG scores, hemodynamic parameters, anesthesia emergence times, and incidence of intraoperative awareness was evaluated in both groups and compared.

Results

Dexmedetomidine did not cause ECoG suppression when administered with either propofol or isoflurane anesthesia. However, it caused a significant increase in the ECoG score in Group-I (baseline: 1.8 ± 0.7; post-dexmedetomidine: 2.1 ± 0.9; p = 0.02), while there was no change in scores in Group-P (baseline: 2.0 ± 0.7; post-dexmedetomidine: 2.10 ± 0.7; p = 0.16). The anesthesia emergence time was within defined normal limits in both groups; however, in Group-I, it was significantly longer than that in Group-P (p = 0.03). The hemodynamic parameters were not affected by dexmedetomidine, and there was no incidence of awareness in both groups.

Conclusion

Dexmedetomidine, when used with propofol anesthesia, had no effect on the intraoperative ECoG signals, hemodynamic parameters, and anesthesia recovery time. Use of dexmedetomidine with isoflurane anesthesia also did not cause ECoG suppression, but significantly augmented the ECoG scores, while normal hemodynamic and recovery status were maintained. There was no incident of intraoperative awareness in either group. As per this study, the dexmedetomidine-propofol anesthetic regimen appears to be suitable for use in ECoG-guided epilepsy surgeries. However, the ECoG-enhancing effect observed with dexmedetomidine when used with isoflurane necessitates further research for validation and to understand its clinical implications.

Keywords

epilepsy surgery - electrocorticography - dexmedetomidine - isoflurane - propofol - anesthesia

Introduction

Intraoperative electrocorticography (ECoG) guidance during epilepsy surgery is used for precisely identifying the epileptogenic focus and ascertaining the adequacy of surgical resection.[1] Interference with the ECoG signals, mainly suppression, can lead to incorrect mapping and subsequent unsuccessful surgery. Commonly used anesthetic drugs are known to interfere with ECoG signals by causing excitation or inhibition of epileptiform discharges.[2] [3] [4] [5] [6] To minimize interference, the anesthetic drugs are temporarily discontinued, or their doses reduced, before obtaining ECoG recordings[3] [7] [8]; however, this action may lead to intraoperative awareness,[9] an unpleasant experience described as “postoperative recall of sensory perception during anesthesia.”[10] A suitable anesthetic drug for ECoG-guided epilepsy surgery would thus be one that has no influence, or minimal depressant effect, on intraoperative ECoG signals without requiring dose reduction.

Dexmedetomidine, an α-2 agonist drug with neuroprotective properties, is commonly used as a sedative or an anesthetic adjuvant in neurosurgical patients. It is currently generating interest as a potentially useful drug for epilepsy surgeries due to its reported absence of influence, or minimally depressant effect, on ECoG signals.[7] [8] [11] [12] [13] The effect of dexmedetomidine on intraoperative ECoG signals has also been studied.[7] [8] [11] [12] As dexmedetomidine is not used as a sole anesthetic agent, its effect on ECoG has been evaluated in combination with other anesthetic agents like sevoflurane[11] and propofol.[7] [8] Evaluation of more such combinations of dexmedetomidine with various commonly used anesthetic agents will enable identification of a suitable anesthetic regimen for epilepsy surgeries.

We undertook this prospective, randomized study with the primary objective of evaluating the effect of dexmedetomidine used in combination with either isoflurane- or propofol-based anesthetic regimen on intraoperative ECoG in patients undergoing ECoG-guided epilepsy surgeries. We hypothesized that dexmedetomidine used with either of these anesthetic regimens would have no influence on intraoperative ECoG signals. The secondary objective of this study was to determine the safety of using dexmedetomidine in these combination regimens by assessing its effects on hemodynamic parameters, anesthesia recovery time, and incidence of intraoperative awareness.

Materials and Methods

After obtaining approval from the Institutional Ethics Committee, consecutive patients in the age group of 12 to 60 years and requiring ECoG-guided epilepsy surgery for drug-resistant epilepsy were selected for the study. A single neurologist evaluated all eligible patients through clinical assessment, magnetic resonance imaging, video electroencephalography (EEG), or positron emission tomography. The decision to perform epilepsy surgery was taken collectively by the epilepsy team comprising the neurologist, neurosurgeon, neuro-radiologist, and neuro-anesthesiologist. Patients with bradyarrhythmias, hypotension, uncontrolled hypertension, pregnancy, hepatic and renal impairment, cardiac disease, morbid obesity, and known allergy to anesthetic drugs were excluded. This study was conceived as a pilot feasibility trial to evaluate the change in ECoG score with a dexmedetomidine bolus administered with propofol versus the isoflurane anesthetic agent. A sample size of 15 participants per group was chosen based on anticipated recruitment feasibility within the study period and to provide preliminary estimates of variability for future definitive sample size calculations.

Conduct of Study

Using a computer-generated randomization method and sealed opaque envelopes, the recruited patients were randomized into two groups: (1) Isoflurane group (Group-I), who received dexmedetomidine-isoflurane anesthesia, and (2) Propofol group (Group-P), who received dexmedetomidine-propofol anesthesia. All personnel present in the operating room (OR), except the neuro-anesthesia team, were unaware of the anesthetic regimen allotted to the study patients. Standard neurosurgical monitoring and additional bispectral index (BIS) to monitor the anesthetic depth were used for surgery. General anesthesia (GA) was induced in both groups with an intravenous (IV) bolus of fentanyl 2 µg/kg, thiopentone 3 to 5 mg/kg, and atracurium 0.5 mg/kg, and maintained with infusions of fentanyl (0.5 µg/kg/hour) and atracurium (5–7 µg/kg/hour), nitrous oxide (N₂O) and oxygen mixture (50:50), and BIS-guided doses of isoflurane and propofol targeting a BIS value of 40 to 60. Following craniotomy and dural reflection, the BIS was kept at 60 to 70 with an isoflurane end-tidal concentration of 0.3 to 0.5% in Group-I, and a propofol dose of 25 to 50 µg/kg/min in Group-P, and ECoG recording was started. Signals were obtained from brain surface strips or grid, and depth electrodes were placed at various locations depending on the surgical requirement. ECoG recording was done for 2 minutes on a 64-channel recording device (Nicolet Viasys, USA version 5.32), and analyzed in real time by the ECoG team, comprising a neurologist and an ECoG technician, present in the operating room; this team was also blinded to the anesthetic regimen used. Following the initial recording, dexmedetomidine (Neon, Neon Laboratories Ltd., Mumbai, India), in a bolus dose of 1 µg/kg, was infused over 5 minutes in both groups. A second ECoG recording was obtained at each of the prior locations, 5 minutes after dexmedetomidine administration, to align with its rapid distribution half-life (∼6 minutes) and onset of central effects. The data collected from both recordings were interpreted collectively by the ECoG team, and in case of disagreement or uncertainty, the neurologist's opinion prevailed. Dexmedetomidine was thereafter continued as an infusion of 0.5 µg/kg/h for the remaining surgery in both groups, along with BIS-titrated doses of isoflurane and propofol to maintain the BIS value at 40 to 60. Dexmedetomidine, fentanyl, and atracurium infusions were stopped at the end of dura closure, and N₂O, isoflurane, or propofol were stopped at the time of Mayfield head clamp removal. Neuromuscular blockade was reversed with neostigmine (50–70 µg/kg) and glycopyrrolate (8–10 µg/kg) when the patient started breathing, and tracheal extubation was done when the patient obeyed commands. IV paracetamol 15 mg/kg was used for postoperative analgesia. The Consort Diagram for methodology is depicted in [Fig. 1].

Fig. 1 CONSORT flow diagram.

Data Recorded in Both Groups

• ECoG signals: recorded just before administering dexmedetomidine bolus (baseline/ pre-dexmedetomidine) and 5 minutes after the end of the bolus dose (post-dexmedetomidine).

• Heart rate (HR), mean arterial pressure (MAP), and BIS value: recorded at (1) baseline, (2) every minute during bolus administration, (3) five minutes after the end of the bolus dose, and (d) every 15 minutes thereafter till the end of surgery.

• Time to anesthesia emergence: measured as the duration between the stoppage of N₂O till regaining consciousness[14]; this usually correlates with a BIS of 90 or higher.

• Incidence of intraoperative awareness: considered as per definition in the Modified Brice Questionnaire.[15]

• Intraoperative complications: seizures and inadvertent electrode migration or malposition during surgery.

Interpretation of Data Collected

• ECoG scores were graded based on the method described by Mathern et al.[16] ECoG score 0: presence of regular activity; ECoG score 1: presence of normal background of mixed γ, β, and α frequencies of moderate to low amplitude (usually < 20–30 mV), and a few observed low-amplitude spikes; ECoG score 2: presence of background of mixed α, β, and δ frequencies but of low to moderate amplitude with loss of fast (>20 Hz) background frequencies, and often observed repeated but non-continuous spikes, poly-spikes or paroxysmal fast activity of medium amplitude; ECoG score 3: presence of mostly 6 to 20 Hz background frequencies with some localized nearly continuous interictal epileptiform features of moderate amplitude, or persistent repetitive spiking, and very rarely, capture of electrographic seizures; ECoG score 4: presence of slow (<6 Hz) background frequencies with continuous synchronous features of moderate to high amplitude, and multiple independent epileptiform abnormalities like poly-spikes, paroxysmal fast activity, and electrographic seizures which could be recorded; ECoG score 5: detection of slow rhythmic, usually synchronous background (<4 Hz) and often of high amplitude, and continuous synchronized or independent high-amplitude epileptiform abnormalities observed in multiple cortical sites, and rarely recorded ictal discharges but observed in surrounding cortex. The mean ECoG scores were compared before and after dexmedetomidine administration in each group. Post-dexmedetomidine scores higher than pre-dexmedetomidine scores indicated ECoG augmentation, while lower scores indicated ECoG suppression.

• Hemodynamic parameters (HR and MAP) changes of ± 20% from baseline were considered abnormal.

• A BIS value of 40 to 60 suggested adequate anesthetic depth; values below or above this range were considered as indicating increased and decreased anesthetic depths, respectively.

• Intraoperative awareness was evaluated as per the criteria described in the Modified Brice Questionnaire.

• Delayed emergence was considered if the patient was not obeying simple verbal commands 20 to 30 minutes after cessation of anesthesia.[17]

Statistical Analysis

The collected data were transformed into variables, coded, and entered into Microsoft Excel. Statistical evaluation was performed using SPSS PC 25 version. Normality of data was tested by the Kolmogorov-Smirnov test. Quantitative data were expressed as the mean and standard deviation (SD), depending on the distribution's normality. The difference between two comparable groups was tested by Student's t-test (unpaired) or Mann-Whitney “U”-test. The Wilcoxon signed-rank test was used for comparison between pre-dexmedetomidine and post-dexmedetomidine data. The qualitative data were expressed in percentages, and statistical differences between the proportions were tested by the chi-squared test or Fisher's exact test. A p-value less than 0.05 was considered statistically significant.

Results

Preoperative Data

The preoperative demographic characteristics were comparable between Group-I (15 patients) and Group-P (15 patients), and no patient had any comorbid condition ([Table 1]). The distribution of epileptogenic lesions was also comparable between the groups ([Table 2]).

Table 1 Comparison of demographic characteristics between Group I and Group P

Demographic characteristics	Group-I (n = 15)	Group-P (n = 15)	p-Value
Male	8 (53.3%)	6 (40%)	0.46
Female	7 (46.67%)	9 (60%)
Mean age in years	26.47 ± 7.44	24.53 ± 8.28	0.69
Weight in kg	60.4 ± 15.53	57.07 ± 14.05	0.71

Table 2 Distribution of types of epileptogenic lesions in Group-I and Group-P

Diagnosis	Group-I (n = 15)	Group-P (n = 15)
Left MTS	4 (26.67%)	6 (40%)
Right MTS	7 (46.67%)	7 (46.67%)
Left FCD	2 (13.33%)	0
Left hippocampal gliosis	1 (6.67%)	0
Left parietooccipital sclerosis	1 (6.67%)	0
Left temporal DNET	0	1 (6.67%)
Right frontal FCD	0	1 (6.67%)

Abbreviations: DNET, dysembryoplastic neuroepithelial tumor; FCD, focal cortical dysplasia; MTS, mesial temporal sclerosis.

ECoG Data

The ECoG scores, expressed as mean, are depicted in [Fig. 2]. In Group-I, the pre-dexmedetomidine mean score was 1.8 ± 0.7, and the post-dexmedetomidine mean score was 2.1 ± 0.9; the increase in ECoG score following dexmedetomidine administration was statistically significant (p = 0.02). In Group-P, the pre-dexmedetomidine mean score was 2.0 ± 0.7, and the post-dexmedetomidine mean score was 2.10 ± 0.7 with no significant change observed in ECoG scores (p = 0.16). On intergroup comparison, the pre-dexmedetomidine ECoG scores and the post-dexmedetomidine scores were comparable between the groups (p = 0.99 and p = 0.36, respectively).

Fig. 2 Comparison of mean ECoG scores before and after dexmedetomidine in Group-I and Group-P.

Hemodynamic Parameters and BIS Values

In Group-I, the pre-dexmedetomidine HR was 68 ± 8.14, and the post-dexmedetomidine HR was 67 ± 11.1, with no significant change in HR (p = 0.26). The pre-dexmedetomidine MAP was 88.7 ± 9.52, and the post-dexmedetomidine MAP was 81.1 ± 8.95, showing no significant change in MAP (p = 0.82). Similarly, in Group-P, the pre-dexmedetomidine HR was 71.8 ± 9.81, and the post-dexmedetomidine HR was 64.9 ± 13.2, with no significant alteration in HR (p = 0.28). The pre-dexmedetomidine MAP was 86.7 ± 4.92, and the post-dexmedetomidine MAP was 81.7 ± 8.09, with no significant alteration in MAP (p = 0.25). The mean ± SD values of HR and MAP were comparable between the two groups and remained within normal limits throughout surgery ([Fig. 3]). BIS values were maintained at 60 to 70 just prior to administering dexmedetomidine and were comparable between the groups (Group-I, 65 ± 4; Group-P, 64.2 ± 2.48; p = 0.08). BIS measured at 1-minute intervals during dexmedetomidine bolus infusion declined similarly in both groups (mean decline in BIS was 10.3 in Group-I and 9.6 in Group-P). Following dexmedetomidine administration, the BIS values were in the range of 40 to 60 and were comparable between the two groups. (Group-I, 52.3 ± 6.28; Group-P, 51.9 ± 7.09; p = 0.0.65). BIS values remained in the range of 40 to 60 at the 15-minute reading, and during all subsequent readings throughout surgery.

Fig. 3 Comparison of hemodynamic parameters between Group-I and Group-P at different intervals: (A) heart rate (HR) comparison, (B) mean arterial pressure (MAP) comparison.

Recovery from Anesthesia

The time to emergence was within the normal range in both groups, but on inter-group comparison, time to emergence was significantly longer in Group-I compared with that in Group-P (Group-I, 14.4 ± 3.7 minutes; Group-P, 7.33 ± 2.05 minutes; p = 0.03).

• Intraoperative awareness was not observed in any patient.

• Intraoperative complications: seizures or inadvertent electrode migration/malposition were not observed in any patient.

Discussion

In this study, we observed that administration of dexmedetomidine did not suppress the epileptiform activity when used with either isoflurane- or propofol-based anesthetic regimens, but caused significant augmentation of activity when used in the isoflurane regimen. The hemodynamic parameters were not altered by the addition of dexmedetomidine to either of the anesthetic regimens. The time to emergence from anesthesia was within defined normal limits in both groups, but was significantly longer with isoflurane than with propofol. A decrease in the BIS value was observed with dexmedetomidine administration, which was comparable in both groups. There was no incident of intraoperative awareness in any patient.

No suppression of intraoperative ECoG signals by dexmedetomidine, observed in both anesthesia regimens, partially supports our hypothesis. This non-inhibitory effect of dexmedetomidine on interictal epileptiform activity is attributed to its lack of action on the gamma-aminobutyric acid (GABA) receptor-mediated pathway, which is linked to epileptiform discharges.[13] [18] Some earlier authors have also reported no suppression of intraoperative ECoG signals.[7] [8] [11] [12] Dexmedetomidine-propofol combination was used by Souter et al as sedation during awake craniotomy for seizure area resection in six patients,[7] and by Pacreu et al for GA in one patient undergoing right selective amygdalohippocampectomy[8]; both case reports revealed no ECoG suppression with the use of dexmedetomidine, thus enabling accurate mapping of epileptic foci. Chaitanya et al studied the effects of a single bolus of dexmedetomidine used alone during surgery for drug-resistant epilepsy and found no suppression of ECoG, but a significant increase in the mean spike rate of ECoG.[12] Oda et al used a single dose infusion of dexmedetomidine and sevoflurane combination in patients undergoing surgery for temporal lobe epilepsy and found that dexmedetomidine decreased the median frequency of ECoG without affecting spike activity.[11] We noticed that dexmedetomidine caused no inhibition of the intraoperative ECoG signals in its normally used dose, thereby suggesting a potential suitability of this drug in ECoG-guided epilepsy surgery.

Our second observation regarding significant augmentation of ECoG scores by dexmedetomidine in the isoflurane anesthetic regimen is a serious concern, even though no seizures were observed; our ECoG score increased up to 3, which is below a defined seizure threshold score of 4 and above.[16] Dexmedetomidine-induced increased epileptiform activity has been attributed to a reduction in noradrenaline secretion and modulation of inhibitory neurotransmitters that potentially lower the seizure threshold, and is the same as that seen with sleep deprivation.[19] [20] Some prior studies have also reported ECoG augmentation with dexmedetomidine showing as a significant increase in mean spike rate of ECoG without seizures,[12] increased spike frequency without seizures,[20] subclinical seizures and an increase in spike and wave activity,[7] and increased interictal epileptiform activity of 4 foci.[13] Prior evidence reveals that clonidine, another α-2 agonist drug, also increases the epileptic discharges in animals and humans,[21] and it has been implied that α-2 agonists may either have no effect or cause enhancement of epileptiform discharges in patients with medically intractable seizures.[13] Though dexmedetomidine has shown proconvulsant activities in animals,[22] [23] there is, so far, sparse evidence of such effects in humans.[24] However, an ECoG-enhancing effect of dexmedetomidine deserves more attention because it could be its potential adverse effect in terms of inducing epileptic seizures.[20] Whether dexmedetomidine causes selective ECoG augmentation when used with different anesthetic agents, as was observed in its combination with isoflurane but not with propofol or sevoflurane in an earlier study,[11] deserves further investigation. In our study, a possible contribution to ECoG enhancement by isoflurane, known to have neuro-excitatory effects,[25] also needs to be considered and explored further.

Combining dexmedetomidine with other anesthetic agents raises safety concerns regarding hemodynamic stability and timely recovery from anesthesia. Some studies have reported episodes of bradycardia and hypotension, though transient and self-corrected, due to the sympatholytic effects of dexmedetomidine.[11] [26] We did not observe any significant intraoperative hemodynamic alterations in either group. Emergence from anesthesia occurred within 20 minutes in all our patients, which is consistent with acceptable neurosurgical recovery timelines.[17] However, on comparison, a significantly longer emergence time was seen in the isoflurane group, which is more likely due to isoflurane's known delayed anesthesia washout[27] [28] [29] rather than any sedative prolongation from dexmedetomidine.

Development of intraoperative awareness is a possibility due to the commonly followed protocol of anesthetic dose reduction to minimize interference with ECoG signals. An 8% incidence of intraoperative awareness has been previously reported when BIS was maintained at 70 or higher before starting ECoG recording.[9] This side effect may have been obviated in our study by the additional sedation provided by dexmedetomidine, which decreased the BIS from a value of 60 to 70 to 40 to 60. Use of dexmedetomidine is known to reduce the requirements of the concurrent anesthetic agents, and we too observed that this lower BIS value could be maintained throughout the remaining surgery using minimal doses of propofol and isoflurane. However, analysis of BIS requires caution in the presence of dexmedetomidine, which can have a confounding effect on BIS interpretation due to its own sedative effect contributing to the lower BIS. No alternate anesthetic depth monitor was available to us, and we additionally used hemodynamic monitoring for assessment of anesthetic depth. With BIS and hemodynamic monitoring, we did not find any evidence suggestive of a lighter plane of anesthesia in our patients. Furthermore, postoperative assessment using the Modified Brice Questionnaire for the detection of any episodes of intraoperative awareness also did not reveal any such incident.

There were various limitations in our study. The sample size was small, based on convenience sampling, due to the lack of prior data for formal sample size calculation and the limited availability of eligible patients. The dexmedetomidine bolus was administered over 5 minutes instead of the standard 10 minutes due to logistical constraints. We used manual analysis of ECoG recordings, which can potentially introduce an interpretation bias. Formal inter-rater reliability metrics were not available to us, but a combined analysis and interpretation of the data by the neurologist and the EEG technician helped mitigate the interpretation bias. We only had BIS as the anesthetic depth monitor, which can show misleading values in the presence of dexmedetomidine. These limitations suggest that while our findings are promising, they should be interpreted with caution and corroborated with larger, well-powered studies.

Conclusion

This study further adds to the limited existing literature on the effects of dexmedetomidine on intraoperative ECoG signals and is among the few early studies evaluating dexmedetomidine as part of combined anesthetic regimens. The results endorse prior findings of a non-suppressant effect of dexmedetomidine on intraoperative ECoG signals. Due to its sedative effect, dexmedetomidine additionally helps in minimizing ECoG interference by enabling the use of concomitant anesthetic drugs in lower doses, while preventing any consequent intraoperative awareness. However, dexmedetomidine-induced ECoG augmentation, observed in this study and earlier, needs additional research for validation and to ascertain if dexmedetomidine has any proconvulsant propensity. Our observation of possible differential ECoG-enhancing effects of dexmedetomidine when combined with various anesthetic agents also warrants further evaluation to enable selection of the safest anesthetic combination regimen. Based on the present study, we feel that the dexmedetomidine-propofol combination appears to be a suitable anesthetic regimen for routine anesthesia practice in ECoG-guided epilepsy surgeries.

Conflict of Interest

None declared.

Acknowledgments

The authors thank Ms. Priti Dhingra and Mr. Anand Kumar, ECoG technicians, for assistance in ECoG recordings.

• References

• 1 Roessler K, Heynold E, Buchfelder M, Stefan H, Hamer HM. Current value of intraoperative electrocorticography (iopECoG). Epilepsy Behav 2019; 91: 20-24
• 2 Bindra A, Chouhan RS, Prabhakar H, Dash HH, Chandra PS, Tripathi M. Comparison of the effects of different anesthetic techniques on electrocorticography in patients undergoing epilepsy surgery - a bispectral index guided study. Seizure 2012; 21 (07) 501-507
• 3 Chui J, Manninen P, Valiante T, Venkatraghavan L. The anesthetic considerations of intraoperative electrocorticography during epilepsy surgery. Anesth Analg 2013; 117 (02) 479-486
• 4 Kacar Bayram A, Yan Q, Isitan C, Rao S, Spencer DD, Alkawadri R. Effect of anesthesia on electrocorticography for localization of epileptic focus: literature review and future directions. Epilepsy Behav 2021; 118: 107902
• 5 Hisada K, Morioka T, Fukui K. et al. Effects of sevoflurane and isoflurane on electrocorticographic activities in patients with temporal lobe epilepsy. J Neurosurg Anesthesiol 2001; 13 (04) 333-337
• 6 Schneider F, Herzer W, Schroeder HW. et al. Effects of propofol on electrocorticography in patients with intractable partial epilepsy. J Neurosurg Anesthesiol 2011; 23 (02) 150-155
• 7 Souter MJ, Rozet I, Ojemann JG. et al. Dexmedetomidine sedation during awake craniotomy for seizure resection: effects on electrocorticography. J Neurosurg Anesthesiol 2007; 19 (01) 38-44
• 8 Pacreu S, Vilà E, Moltó L, Bande D, Rueda M, Fernández Candil JL. Anaesthesia management in epilepsy surgery with intraoperative electrocorticography. Manejo anestésico en la cirugía de epilepsia con electrocorticografía intraoperatoria. Rev Esp Anestesiol Reanim (Engl Ed) 2018; 65 (02) 108-111
• 9 Mei HA, Ho DN. Intraoperative awareness in epileptic patients during cerebral cortex electroencephalography measurement under general anesthesia. J Dalian Med Univ 2013; 35 (01) 61-64
• 10 Sandhu K, Dash H. Awareness during anaesthesia. Indian J Anaesth 2009; 53 (02) 148-157
• 11 Oda Y, Toriyama S, Tanaka K. et al. The effect of dexmedetomidine on electrocorticography in patients with temporal lobe epilepsy under sevoflurane anesthesia. Anesth Analg 2007; 105 (05) 1272-1277
• 12 Chaitanya G, Arivazhagan A, Sinha S. et al. Dexmedetomidine anesthesia enhances spike generation during intra-operative electrocorticography: a promising adjunct for epilepsy surgery. Epilepsy Res 2015; 109: 65-71
• 13 Talke P, Stapelfeldt C, Garcia P. Dexmedetomidine does not reduce epileptiform discharges in adults with epilepsy. J Neurosurg Anesthesiol 2007; 19 (03) 195-199
• 14 Cascella M, Bimonte S, Di Napoli R. Delayed emergence from anesthesia: what we know and how we act. Local Reg Anesth 2020; 13: 195-206
• 15 Moonesinghe SR, Walker EM, Bell M. SNAP-1 Investigator Group. Design and methodology of SNAP-1: a Sprint National Anaesthesia Project to measure patient reported outcome after anaesthesia. Perioper Med (Lond) 2015; 4: 4
• 16 Mathern GW, Cepeda C, Hurst RS, Flores-Hernandez J, Mendoza D, Levine MS. Neurons recorded from pediatric epilepsy surgery patients with cortical dysplasia. Epilepsia 2000; 41 (Suppl. 06) S162-S167
• 17 Nicolas B, Patrick R. Supratentorial masses: anesthetic considerations. In: Cottrell JE, Young WJ. eds. Cottrell and Young's Neuroanesthesia. 5th ed.. Mosby; 2010: 184-202
• 18 Bortel A, Yao ZS, Shmuel A. A rat model of somatosensory-evoked reflex seizures induced by peripheral stimulation. Epilepsy Res 2019; 157: 106209
• 19 Yavuz M, İyiköşker P, Mutlu N. et al. Dexmedetomidine, an alpha 2A receptor agonist, triggers seizures unilaterally in GAERS during the pre-epileptic phase: Does the onset of spike-and-wave discharges occur in a focal manner?. Front Neurol 2023; 14: 1231736
• 20 Mason KP, O'Mahony E, Zurakowski D, Libenson MH. Effects of dexmedetomidine sedation on the EEG in children. Paediatr Anaesth 2009; 19 (12) 1175-1183
• 21 Kirchberger K, Schmitt H, Hummel C. et al. Clonidine and methohexital-induced epileptic magnetoencephalographic discharges in patients with focal epilepsies. Epilepsia 1998; 39 (08) 841-849
• 22 Miyazaki Y, Adachi T, Kurata J, Utsumi J, Shichino T, Segawa H. Dexmedetomidine reduces seizure threshold during enflurane anaesthesia in cats. Br J Anaesth 1999; 82 (06) 935-937
• 23 Mirski MA, Rossell LA, McPherson RW, Traystman RJ. Dexmedetomidine decreases seizure threshold in a rat model of experimental generalized epilepsy. Anesthesiology 1994; 81 (06) 1422-1428
• 24 Kubota T, Fukasawa T, Kitamura E. et al. Epileptic seizures induced by dexmedetomidine in a neonate. Brain Dev 2013; 35 (04) 360-362
• 25 Watts AD, Herrick IA, McLachlan RS, Craen RA, Gelb AW. The effect of sevoflurane and isoflurane anesthesia on interictal spike activity among patients with refractory epilepsy. Anesth Analg 1999; 89 (05) 1275-1281
• 26 Chaitanya G, Arivazhagan A, Sinha S. et al. Hemodynamic effects of dexmedetomidine during intra-operative electrocorticography for epilepsy surgery. J Neurosci Rural Pract 2014; 5 (Suppl. 01) S17-S21
• 27 Ittichaikulthol W, Pausawasdi S, Srichintai P, Sarnvivad P. Propofol vs isoflurane for neurosurgical anesthesia in Thai patients. J Med Assoc Thai 1997; 80 (07) 454-460
• 28 Prabhakar H, Singh GP, Mahajan C, Kapoor I, Kalaivani M, Anand V. Intravenous versus inhalational techniques for rapid emergence from anaesthesia in patients undergoing brain tumour surgery. Cochrane Database Syst Rev 2016; 9 (09) CD010467
• 29 Miura Y, Kamiya K, Kanazawa K. et al. Superior recovery profiles of propofol-based regimen as compared to isoflurane-based regimen in patients undergoing craniotomy for primary brain tumor excision: a retrospective study. J Anesth 2012; 26 (05) 721-727

Publication History

Article published online:
19 November 2025