Interictal magnetoencephalography and the irritative zone in the electrocorticogram.

Magnetoencephalography (MEG) is considered a useful tool for planning electrode placement for chronic intracranial subdural electrocorticography (ECoG) in candidates for epilepsy surgery or even as a substitute for ECoG. MEG recordings are usually interictal and therefore, at best, reflect the interictal ECoG. To estimate the clinical value of MEG, it is important to know how well interictal MEG reflects interictal activity in the ECoG. From 1998 to 2008, 38 candidates for ECoG underwent a 151-channel MEG recording and 3D magnetic resonance imaging as a part of their presurgical evaluation. Interictal MEG spikes were identified, clustered, averaged and modelled using the multiple signal classification algorithm and co-registered to magnetic resonance imaging. ECoG was continuously recorded with electrode grids and strips for approximately 1 week. In a representative sample of awake interictal ECoG, interictal spikes were identified and averaged. The different spikes were characterized and quantified using a combined amplitude and synchronous surface-area measure. The ECoG spikes were ranked according to this measure and plotted on the magnetic resonance imaging surface rendering. Interictal spikes in MEG and ECoG were allocated to a predefined anatomical brain region and an association analysis was performed. All interictal MEG spikes were associated with an interictal ECoG spike. Overall, 56% of all interictal ECoG spikes had an interictal MEG counterpart. The association between the two was >or=90% in the interhemispheric and frontal orbital region, approximately 75% in the superior frontal, central and lateral temporal regions, but only approximately 25% in the mesial temporal region. MEG is a reliable indicator of the presence of interictal ECoG spikes and can be used to plan intracranial electrode placements. However, a substantial number of interictal ECoG spikes are not detected by MEG, and therefore MEG cannot be considered a substitute for ECoG.

The intracarotid amobarbital or Wada test: unilateral or bilateral?

OBJECTIVE: In the Netherlands, presurgical screening for temporal lobe epilepsy (TLE) includes the intracarotid amobarbital procedure (IAP), consisting of two consecutive injections of amobarbital, ipsilateral and contralateral to the epileptic focus. We studied whether a bilateral IAP has added value to a unilateral, ipsilateral IAP. METHODS: This population-based study included 183 consecutive patients referred for screening for TLE surgery who underwent bilateral IAP. Using multivariable modeling, we assessed the added value of bilateral IAP on the decision for surgery, resection size, amygdalohippocampectomy, post-operative seizure freedom, memory performance, and IQ change. RESULTS: Given the results from the unilateral IAP, the bilateral IAP had added prognostic value for postoperative change in verbal memory (P < 0.01) and verbal IQ (P < 0.01), especially if patients had a left-sided focus. In contrast, information provided by the contralateral IAP was not associated with decision-making or surgical strategy. CONCLUSIONS: A bilateral IAP has added value in predicting post-operative verbal memory and IQ. A bilateral IAP is currently not used to guide surgical strategy, but may be used for this purpose when verbal capacity is of particular concern in patients with a left-sided focus. In other cases, IAP is best performed unilaterally.

Cognitive impairment in tuberous sclerosis complex is a multifactorial condition.

OBJECTIVE: In patients with tuberous sclerosis complex (TSC), associations between tuber number, infantile spasms, and cognitive impairment have been proposed. We hypothesized that the tuber/brain proportion (TBP), the proportion of the total brain volume occupied by tubers, would be a better determinant of seizures and cognitive function than the number of tubers. We investigated tuber load, seizures, and cognitive function and their relationships. METHODS: Tuber number and TBP were characterized on three-dimensional fluid-attenuated inversion recovery MRI with an automated tuber segmentation program. Seizure histories and EEG recordings were obtained. Intelligence equivalents were determined and an individual cognition index (a marker of cognition that incorporated multiple cognitive domains) was calculated. RESULTS: In our sample of 61 patients with TSC, TBP was inversely related to the age at seizure onset and to the intelligence equivalent and tended to be inversely related to the cognition index. Further, a younger age at seizure onset or a history of infantile spasms was related to lower intelligence and lower cognition index. In a multivariable analysis, only age at seizure onset and cognition index were related. CONCLUSIONS: Our systematic analysis confirms proposed relationships between tuber load, epilepsy and cognitive function in tuberous sclerosis complex (TSC), but also indicates that tuber/brain proportion is a better predictor of cognitive function than tuber number and that age at seizure onset is the only independent determinant of cognitive function. Seizure control should be the principal neurointervention in patients with TSC.

Overlapping neurologic and cognitive phenotypes in patients with TSC1 or TSC2 mutations.

OBJECTIVE: The purpose of this study was to systematically analyze the associations between different TSC1 and TSC2 mutations and the neurologic and cognitive phenotype in patients with tuberous sclerosis complex (TSC). METHODS: Mutation analysis was performed in 58 patients with TSC. Epilepsy variables, including EEG, were classified. A cognition index was determined based on a comprehensive neuropsychological assessment. On three-dimensional fluid-attenuated inversion recovery MR images, an automated tuber segmentation program detected and calculated the number of tubers and the proportion of total brain volume occupied by tubers (tuber/brain proportion [TBP]). RESULTS: As a group, patients with a TSC2 mutation had earlier age at seizure onset, lower cognition index, more tubers, and a greater TBP than those with a TSC1 mutation, but the ranges overlapped considerably. Familial cases were older at seizure onset and had a higher cognition index than nonfamilial cases. Patients with a mutation deleting or directly inactivating the tuberin GTPase activating protein (GAP) domain had more tubers and a greater TBP than those with an intact GAP domain. Patients with a truncating TSC1 or TSC2 mutation differed from those with nontruncating mutations in seizure types only. CONCLUSIONS: Although patients with a TSC1 mutation are more likely to have a less severe neurologic and cognitive phenotype than those with a TSC2 mutation, the considerable overlap between both aspects of the phenotype implies that prediction of the neurologic and cognitive phenotypes in individuals with tuberous sclerosis complex should not be based on their particular TSC1 or TSC2 mutation.

Epilepsy surgery in tuberous sclerosis: the Dutch experience.

INTRODUCTION: Epilepsy associated with tuberous sclerosis complex (TSC) is drug resistant in more than half of the patients. Epilepsy surgery may be an alternative treatment option, if the epileptogenic tuber can be identified reliably and if seizure reduction is not at the expense of cognitive or other functions. We report the pre-surgical identification of the epileptogenic tuber and post-surgical outcome of patients with TSC in The Netherlands. METHODS: Twenty-five patients underwent the pre-surgical evaluation of the Dutch Comprehensive Epilepsy Surgery Programme, including a detailed seizure history, interictal and ictal video EEG registrations, 3D FLAIR MRI scans and neuropsychological testing. Suitability of the candidates was decided in consensus. Seizure outcome, scored with the Engel classification, and cognition were reassessed at fixed post-surgery intervals. RESULTS: Epilepsy surgery was performed in six patients. At follow-up, four patients had Engel classification 1, two had classification 4. Improved development and behaviour was perceived by the parents of two patients. Epilepsy surgery was not performed in 19 patients because seizures were not captured, ictal onset zones could not be localised or were multiple, interictal EEG, video EEG and MEG results were not concordant, or seizure burden had diminished during decision making. A higher cognition index was found in the surgical patients compared to the non-surgical candidates. CONCLUSIONS: Epilepsy surgery can be performed safely and successfully in patients in whom semiology, interictal EEG, ictal EEG, MEG and the location of tubers are concordant. In other cases the risk of surgery should be weighed against the chance of seizure relief and in case of children subsequent impact on neurodevelopment.

[Intracranial EEG monitoring for epilepsy surgery using electrode grids--results in the first 22 Dutch patients]. / Intracranieel eeg-onderzoek met elektrodematjes ten behoeve van epilepsiechirurgie; resultaten bij de eerste 22 patiënten.

OBJECTIVE: Description of initial experiences with subdural electrode grids in patients with refractory focal epilepsy as additional diagnostic tool for epilepsy surgery. Using these electrodes, the attacks were recorded during a number of days and the cerebral cortex was electrically stimulated in order to map the functional areas. DESIGN: Retrospective. METHOD: Data were collected from patients in whom subdural electrode grids had been placed between 1 September 1999 and 31 August 2004. All patients underwent a neurological examination and a neuropsychological test before the implantation. At the follow-up examination, the results with regard to function and the frequency of attacks were noted, as well as the complications. RESULTS: Electrodes were placed in 22 patients: 9 women and 13 men with an average age of 27 years (range: 5-42). The implantation lasted for an average of 7 days (range: 3-10). In 4 patients, increased seizures during implantation required intravenous anticonvulsant treatment. Severe but transitory complications were seen in 4 patients (meningitis, subdural haematoma and ischaemia). 19 patients underwent a therapeutic resection. A postoperative decline in language skills was noted in 1 patient, while another 2 scored poorer in verbal tests. A permanent decline in sensorimotor function was seen in 1 patient, but this had been foreseen. Of the 16 operated patients with a duration of follow-up of at least 1 year, so were (practically) free of attacks, and another 3 patients had significantly fewer attacks. CONCLUSION: Registration with intracranial electrodes makes it possible to treat epileptic patients surgically by excision of brain tissue near critical areas. Such intensive monitoring is, however, not without risk and this must be weighed against the potential benefits.

Cerebrovascular reserve capacity is preserved in a population-based sample of patients with type 2 diabetes mellitus.

BACKGROUND AND PURPOSE: Type 2 diabetes mellitus (DM2) is associated with an increased risk of stroke. DM2 is also associated with cognitive impairments. Vascular dysfunction, such as impaired cerebrovascular reserve capacity (CVR), may be a determinant of these changes, but previous studies on CVR in DM2 have provided variable results in selected populations of patients. We aimed to examine CVR in a population-based sample of DM2 patients. METHODS: The CO(2) reactivity of the middle cerebral artery was examined using transcranial Doppler ultrasonography in 81 DM2 patients and 38 controls. In DM2 patients CVR was correlated with diabetic parameters, vascular risk factors and cognitive functioning. RESULTS: CVR was similar in patients and controls (51 vs. 49%). Within the DM2 group, there was no statistically significant relationship between CVR and DM duration, HbA(1c), albuminuria, blood pressure, intima-media thickness and cognition. CVR tended to be lower in diabetic patients with retinopathy [46 vs. 55%, mean difference: -7.9 (confidence interval -18.0, 2.2)]. CONCLUSION: We conclude that CVR is not impaired in unselected patients with DM2 and probably does not, therefore, play a major role in the aetiology of cognitive impairment.

Seizure detection in adult ICU patients based on changes in EEG synchronization likelihood.

INTRODUCTION: Seizures are common in Intensive Care Unit (ICU) patients, and may increase neuronal injury. PURPOSE: To explore the possible value of synchronization likelihood (SL) for the automatic detection of seizures in adult ICU patients. METHODS: We included EEGs from ICU patients with a variety of diagnoses. The gold standard for further analyses was the consensus judgment of three clinical neurophysiologists who classified 150 scalp EEG epochs as "definitely epileptiform," "definitely non epileptiform," or "uncertain." SL estimates the statistical interdependencies between two time series, such as two EEG channels. We computed the average synchronization by calculating the SL between one channel and every other channel, and taking the mean of these values. RESULTS: The mean SL in the 38 "definitely epileptiform" epochs ranged from 0.095 to 0.386 (mean 0.189; SD 0.066). In the 34 "definitely nonepileptiform" epochs the mean SL ranged from 0.087 to 0.158 (mean 0.115; SD 0.016; p < 0.0005). The area under the ROC curve was 0.812 (95% Confidence Interval 0.725 to 0.898). CONCLUSION: The mean SL may distinguish between seizure and nonseizure epochs, and may prove helpful to monitor epileptic activity in ICU patients.

Recovery of amplitude integrated electroencephalographic background patterns within 24 hours of perinatal asphyxia.

OBJECTIVE: To assess the time course of recovery of severely abnormal initial amplitude integrated electroencephalographic (aEEG) patterns (flat trace (FT), continuous low voltage (CLV), or burst suppression (BS)) in full term asphyxiated neonates, in relation to other neurophysiological and neuroimaging findings and neurodevelopmental outcome. METHODS: A total of 190 aEEGs of full term infants were reviewed. The neonates were admitted within 6 hours of birth to the neonatal intensive care unit because of perinatal asphyxia, and aEEG recording was started immediately. In all, 160 infants were included; 65 of these had an initial FT or CLV pattern and 25 an initial BS pattern. Neurodevelopmental outcome was assessed using a full neurological examination and the Griffiths' mental developmental scale. RESULTS: In the FT/CLV group, the background pattern recovered to continuous normal voltage within 24 hours in six of the 65 infants (9%). All six infants survived the neonatal period; one had a severe disability, and five were normal at follow up. In the BS group, the background pattern improved to normal voltage in 12 of the 25 infants (48%) within 24 hours. Of these infants, one died, five survived with moderate to severe disability, two with mild disability, and four were normal. The patients who did not recover within 24 hours either died in the neonatal period or survived with a severe disability. CONCLUSION: In this study there was a small group of infants who presented with a severely abnormal aEEG background pattern within six hours of birth, but who achieved recovery to a continuous normal background pattern within the first 24 hours. Sixty one percent of these infants survived without, or with a mild, disability.

Cortisol, depression and reduced cortico-cortical cross-talk in Cushing's syndrome.

In the present report assumed relationships between hypercortisolism, depression and cortico-cortical cross-talk in Cushing's syndrome were investigated. Electroencephalographic (EEG) recordings and depression ratings from three patients diagnosed with mild, moderate and severe hypercortisolism were obtained. Reductions in cortico-cortical cross-talk as quantified by EEG coherence together with increases in depression were observed in the moderate and severe as compared to the mild hypercorticolism state. These findings provide preliminary evidence for the hypothesis that loss of cortico-cortical cross-talk might be linked to hypercortisolism and the severity of depressive symptoms.

Synaptosomal glutamate and GABA transport in patients with temporal lobe epilepsy.

High-affinity glutamate and GABA transporters found in the plasma membrane of neurons and glial cells terminate neurotransmission by rapidly removing extracellular transmitter. Impairment of transporter function has been implicated in the pathophysiologic mechanisms underlying epileptogenesis. We characterized glutamate and gamma-aminobutyric acid (GABA) transport in synaptosomes, isolated from neocortical and hippocampal biopsies of patients with temporal lobe epilepsy (TLE). We analyzed K(+)-evoked release in the presence and absence of Ca(2+) to determine vesicular and transporter-mediated release, respectively. We also analyzed (3)H-glutamate and (3)H-GABA uptake, the effect of glutamate uptake inhibitors L-trans-pyrrolidine-2,4-dicarboxylic acid (tPDC) and DL-threo-beta-benzyloxyaspartate (TBOA), and GABA uptake inhibitor N-(4,4-diphenyl-3-butenyl)-3-piperidinecarboxylic acid (SK&F 89976-A). Neocortical synaptosomes from TLE patients did not show vesicular glutamate release, strongly reduced transporter-mediated release, and an increased basal release compared to that in rat synaptosomes. Furthermore, basal release was less sensitive to tPDC, and (3)H-glutamate uptake was reduced compared to that in rat synaptosomes. Vesicular GABA release from neocortical synaptosomes of TLE patients was reduced compared to that in rat synaptosomes, whereas transporter-mediated release was hardly affected. Furthermore, basal GABA release was more than doubled, but neither basal nor stimulated release were increased by SK&F 89976-A, which did significantly increase both types of GABA release in rat synaptosomes. Finally, (3)H-GABA uptake by synaptosomes from TLE patients was reduced significantly in hippocampus (0.19 +/- 0.04%), compared to that in neocortex (0.32 +/- 0.04%). Control experiments with human peritumoral cortical tissue suggest that impaired uptake of glutamate, but not of GABA, was caused in part by the hypoxic state of the biopsy. Our findings provide evidence for impaired function of glutamate and GABA transporters in human TLE.

Measurement of the conductivity of skull, temporarily removed during epilepsy surgery.

The conductivity of the human skull plays an important role in source localization of brain activity, because it is low as compared to other tissues in the head. The value usually taken for the conductivity of skull is questionable. In a carefully chosen procedure, in which sterility, a stable temperature, and relative humidity were guaranteed, we measured the (lumped, homogeneous) conductivity of the skull in five patients undergoing epilepsy surgery, using an extended four-point method. Twenty-eight current configurations were used, in each of which the potential due to an applied current was measured. A finite difference model, incorporating the geometry of the skull and the electrode locations, derived from CT data, was used to mimic the measurements. The conductivity values found were ranging from 32 mS/m to 80 mS/m, which is much higher than the values reported in other studies. Causes for these higher conductivity values are discussed.

Collateral flow and ischemic brain lesions in patients with unilateral carotid artery occlusion.

OBJECTIVE: To investigate the association between ischemic brain lesions and intracranial collateral blood flow in patients with unilateral occlusion of the internal carotid artery (ICA). METHODS: Sixty-eight consecutive patients were included. Ischemic lesions on MRI were identified on hard copies, and volume measurements of the lesions were performed on an MR workstation. Intracranial collateral pathways were studied with MR angiography, digital subtraction angiography, and transcranial Doppler sonography. RESULTS: The presence of collateral flow via the anterior communicating artery (ACoA) was associated with a reduction in prevalence (p = 0.01) and volume (p = 0.008) of internal border zone infarcts in the hemisphere ipsilateral to the occluded ICA. Absence of collateral blood flow via the circle of Willis was associated with an increase in prevalence (p = 0.007) and volume (p = 0.005) of internal border zone infarcts. No association between any collateral flow pattern in the circle of Willis and periventricular lesions or lacunar, territorial, or external border zone infarcts was found. No association between collateral flow via the ophthalmic artery or leptomeningeal vessels with any type of ischemic lesion was found. CONCLUSION: Collateral flow via the ACoA is associated with a reduction of the prevalence and volume of internal border zone lesions but not with any other type of ischemic lesion. The presence of a functional posterior communicating artery or secondary collateral pathways is not associated with the prevalence of any type of ischemic lesion.

Quantitative cerebral perfusion MRI and CO2 reactivity measurements in patients with symptomatic internal carotid artery occlusion.

Quantitative perfusion MRI is a promising new technique capable of offering information on cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time (MTT). However, it is still unclear how these perfusion parameters relate to the underlying physiological indicators and how they compare to conventional techniques. The purpose of this study was to investigate how quantitative perfusion MRI is related to the cerebrovascular reactivity as measured by transcranial Doppler ultrasonography (TCD) in combination with a CO2 stimulus in patients with a symptomatic occlusion of the internal carotid artery (ICA). Thirty-nine patients with transient or minor disabling retinal or hemispheric ischemic symptoms and an occlusion of the ICA underwent quantitative perfusion MRI and CO2 reactivity measurements by TCD. Perfusion parameters were correlated with cerebrovascular reactivity measurements and compared with measurements of control subjects. The results of this study show a negative correlation between the cerebrovascular reactivity and the time to bolus peak (TBP) both for gray (r = -0.26, P = 0.035) and white matter (r = -0.28, P = 0.026). No correlation between resting CBV, CBF, or MTT and cerebrovascular reactivity was found. Our results indicate that an increase in TBP reflects a poor development of collateral flow, which is supported by a relatively low CO2 reactivity in these patients.

Collateral circulation via the ophthalmic artery or leptomeningeal vessels is associated with impaired cerebral vasoreactivity in patients with symptomatic carotid artery occlusion.

BACKGROUND AND PURPOSE: In patients with carotid artery occlusion (CAO), collateral flow may reduce the risk of ischemic stroke. Collateral flow via the ophthalmic artery (OphthA) and flow via leptomeningeal vessels have been considered secondary collaterals, which are recruited only if the primary collateral circulation via the circle of Willis is insufficient. The aim of this study was to investigate whether patients with symptomatic CAO who have secondary in addition to primary collaterals have a worse flow state of the brain than those without secondary collaterals, as measured by vascular reactivity testing. METHODS: We studied 70 patients with symptomatic CAO who were independent for their daily activities. In all patients, collateral circulation through the circle of Willis was present. Vascular reactivity, measured by means of transcranial Doppler sonography with carbogen inhalation, was compared between patients with and without secondary collaterals. RESULTS: CO2 reactivity was lower in 64 patients with (mean +/- standard deviation 8 +/- 14%) than in 6 patients without secondary collaterals (33 +/- 18%) resulting in a mean difference of 24% (95% confidence interval 12-37%; p < 0.01). CONCLUSIONS: Patients with symptomatic CAO with collateral circulation through the OphthA or through leptomeningeal vessels in addition to collaterals via the circle of Willis have a worse hemodynamic status of the brain than those with Willisian collaterals only. Therefore the presence of these collaterals may indicate insufficiency of collateral blood flow via the circle of Willis.

Diazepam-enhanced beta activity in Sturge Weber syndrome: its diagnostic significance in comparison with MRI.

OBJECTIVES: This study was performed to assess the extent of functional involvement of the affected hemisphere in Sturge Weber syndrome in comparison with the uninvolved hemisphere. To this end beta activity in the electroencephalogram (EEG) was measured, both before and after administration of diazepam intravenously (i.v.). METHODS: In 9 patients asymmetry in beta band activity was studied before and after diazepam administration. Several beta bands and asymmetry parameters were calculated. beta band asymmetries were compared with structural abnormalities (magnetic resonance imaging, MRI). RESULTS: Total beta activity was reduced in the involved hemisphere in all patients after diazepam administration. In 3 patients functional abnormalities were found in brain regions that were structurally intact. CONCLUSIONS: Decreased diazepam-enhanced beta activity in the EEG is a sensitive criterion of functional abnormality. In patients with subtle structural abnormalities diazepam-enhanced EEG may have added value in diagnosing functional involvement and in monitoring disease progression in patients.

EEG evidence for shunt requirement during carotid endarterectomy: optimal EEG derivations with respect to frequency bands and anesthetic regimen.

Currently there is no consensus on the derivations that should be used for EEG monitoring during carotid endarterectomy (CEA). The aim of this study was to determine which derivations distinguish the best between patients requiring a shunt and patients who do not need a shunt. Four predefined frequency bands and two regimens for general anesthesia (isoflurane versus propofol) were used. EEG data (16 channels) were obtained from 152 EEGs recorded during carotid endarterectomy. Analog EEG signals of preclamp and clamp periods of 100 seconds were digitized to compute power spectra. Changes in power during clamping were calculated for all possible derivations in four predefined frequency bands and were expressed as Z-scores. For each derivation, the area under the receiver operating characteristics curve was calculated. Derivations with the greatest area under the receiver operating characteristics curve were considered to distinguish the best between the shunt and the nonshunt groups formed in retrospect on the basis of consensus between three independent and experienced board-certified electroencephalographers. The two different anesthetic regimens resulted in different patterns of EEG changes because of clamping. The optimal derivations to differentiate between the shunt and the nonshunt groups also differed for the two anesthetic regimens, although for both conditions, anterior head regions were especially preferred. The optimal derivations are given for each anesthetic regimen.

The existence of two sources in rolandic epilepsy: confirmation with high resolution EEG, MEG and fMRI.

In benign rolandic epilepsy seizure semiology suggests that the epileptic focus resides in the lower sensorimotor cortex. Previous studies involving dipole modeling based on 32 channel EEG have confirmed this localization. These studies have also suggested that two distinct dipole sources are required to adequately describe the typical interictal spikes. Since in benign epilepsy invasive validation is prohibited, this study tries to further establish these results using a multi-modal approach, involving 32 channel EEG, high resolution 84 channel EEG, 151 channel MEG and fMRI. From one patient interictal spikes were recorded and analyzed using the MUSIC algorithm in a realistic volume conductor model. In an fMRI experiment the same patient performed voluntary tongue movements, thus mimicking a typical seizure. Results show that EEC, MEG and fMRI localization converge on the same area in the lower part of the sensorimotor cortex, and that high resolution EEG clearly reveals two distinct sources, one in the post- and one in the pre-central cortex.

Activation of interictal spiking in mesiotemporal lobe epilepsy by propofol-induced sleep.

The objective of this study was to test whether low-dose propofol increases the number of interictal spikes in patients with mesiotemporal lobe epilepsy, and to determine whether this is the result of intrinsic properties and is restricted to the primary epileptogenic focus. Controlled infusion of propofol in step-up/-down target concentrations of 0, 0.3, 0.6, and 0.8 mg/L was administered to 10 patients during a 3.5-hour daytime EEG registration. The number of spikes were counted and related to propofol concentration and sleep level. Results were compared with a spontaneous, nocturnal first sleep cycle in 9 of 10 patients. All patients entered nonrapid eye movement 1 sleep during propofol administration, and 8 reached nonrapid eye movement 2 sleep. In 7 patients who showed spikes, spikes were related to sleep (P < 0.05) and not to increasing (P = 0.1) or decreasing (P = 0.5) propofol concentration. Six of nine patients showed more spikes during spontaneous (nocturnal) sleep than during propofol-induced sleep. Contralateral spiking was not suppressed selectively. Low-dose propofol is a safe means of increasing spiking in these patients because it induces sleep. There were no signs of an intrinsic epileptogenicity of propofol or a selective effect on ipsilateral spikes. Controlled sleep induction will increase the yield of interictal spikes during short interictal recordings such as in magnetoencephalography.