EEG Discharges Research Articles

Nitric oxide production is enhanced in rat brain before oxygen-induced convulsions

Central nervous system oxygen toxicity (CNS O 2 toxicity) is preceded by release of hyperoxic vasoconstriction, which increases regional cerebral blood flow (rCBF). These increases in rCBF precede the onset of O 2-induced convulsions. We have tested the hypothesis that hyperbaric oxygen (HBO 2) stimulates NO production in the brain that leads to hyperemia and anticipates electrical signs of neurotoxicity. We measured rCBF and EEG responses in rats exposed at 4 to 6 atmospheres (ATA) of HBO 2 and correlated them with brain interstitial NO metabolites (NO x ) as an index of NO production. During exposures to hyperbaric oxygen rCBF decreased at 4 ATA, decreased for the initial 30 min at 5 ATA then gradually increased, and increased within 30 min at 6 ATA. Changes in rCBF correlated positively with NO x production; increases in rCBF during HBO 2 exposure were associated with large increases in NO x at 5 and 6 ATA and always preceded EEG discharges as a sign of CNS O 2 toxicity. In rats pretreated with l-NAME, rCBF remained maximally decreased throughout 75 min of HBO 2 at 4, 5 and 6 ATA. These data provide the first direct evidence that increased NO production during prolonged HBO 2 exposure is responsible for escape from hyperoxic vasoconstriction. The finding suggests that NO overproduction initiates CNS O 2 toxicity by increasing rCBF, which allows excessive O 2 to be delivered to the brain.

Proof of principle trials: EEG surrogate endpoints

Pivotal studies in man require prolonged administration to demonstrate efficacy for most seizure types. Earlier evidence of human efficacy can be of value for decision making, and EEG surrogate endpoints can be of value in this respect. Studies of spontaneous EEG discharges under standard recording conditions can demonstrate meaningful acute EEG effects of antiepileptic drugs (AEDs). These require a rapidly effective formulation of the product, preferably intravenous. The EEG recording conditions are standardised and the subject is required to perform a task to maintain a constant level of vigilance. The outcome measure of efficacy is spike count per minute or, if the discharges are more protracted (as generalised no spike and wave), the percentage of recording time occupied by discharges. Sub-acute experiments are conducted under less rigorously standardised conditions, but over longer periods, using ambulatory monitoring or telemetry to record the EEG. The photoparoxysmal responses (PPRs) of photosensitive subjects, evoked using a standardised stimulation protocol, are subject to less variability than spontaneous epileptiform activity. The PPR is elicited over a range of flash rates that can be used as a measure of sensitivity, and an effective treatment will reduce the range or abolish the PPR. Reduction in photosensitivity is demonstrable after a single dose of various AEDs, at clinically relevant plasma concentrations, even using drugs that are not generally effective for long-term treatment of photosensitive epilepsy. Evoked potential and nerve conduction studies and electronystagmography can be used to assess possible neurotoxicity, and quantitative EEG analysis can be employed to assess sedative effects.

Sudden unexpected death in epilepsy

Sudden unexpected death in epilepsy

Subclinical rhythmic EEG discharge of adults: SREDA in two children

Subclinical rhythmic electroencephalogram (EEG) discharge is an uncommon rhythmic EEG pattern that has been reported to occur in adults. It is thought to be a nonspecific finding with little clinical significance. This article reports this EEG pattern in two children and suggests it be called subclinical rhythmic EEG discharge of adults and children.

Combined influence of cyclic arousability and EEG synchrony on generalized interictal discharges within the sleep cycle

Purpose: to analyze the activating role of cyclic alternating pattern (CAP) and EEG synchrony on generalized interictal paroxysms in the first part of the night, when all sleep patterns are represented. Methods: nocturnal polysomnographic investigation was accomplished on a randomized series of 18 subjects with an active form of primary generalized epilepsy (PGE), but only six patients showed a complete and regular profile of the first two sleep cycles (SCs). Completeness and regularity of the selected SCs consisted in the absence of intervening wakefulness, in the presence of all sleep stages, and in the identification of three main units, (a) a descending branch, dominated by the build-up of EEG synchrony in the transition from light to deep non-rapid eye movement (NREM) sleep; (b) a trough, where the magnitude of EEG synchrony is greatest and gives rise to stages 3 and 4; (c) an ascending branch characterized by a decrease of EEG synchrony preceding the onset of rapid eye movement (REM) sleep. Generalized paroxysms were evaluated in terms of discharge rates (number of interictal bursts per minute of sleep) and distribution within the investigated sleep parameters. Results: the discharge rates decreased from SC1 to SC2, with higher values quantified during NREM sleep (mean, 2.8) compared with REM sleep (mean, 0.8). Both SCs showed a progressive decrease of activation across the three units, from the highest discharge rates reached during the descending branches (mean, 3.6) to the more attenuated discharge rates during the troughs (mean, 2.4) down to the lowest rates during the ascending limbs (mean, 1.1). The magnitude of activation during the descending branches was closely related to the CAP condition (mean, 5.2) and to the powerful effect of phase A (mean, 13.9). The great majority (82%) of EEG discharges occurring in phase A were distributed within the A1 subtypes (identified by sequences of k-complexes or delta bursts). Conclusions: within the first two SCs, the features of NREM sleep endowed with the major activating power on generalized bursts are represented by the rise of EEG synchrony (descending branch) and by the A phases of CAP involved in the regulation of its build-up.

Idiopathic generalized epilepsy with generalized and other seizures in adolescence.

Idiopathic generalized epilepsy with generalized and other seizures in adolescence.

Panel Discussion 1

Panel Discussion 1

Glioneuronal tumors and medically intractable epilepsy: a clinical study with long-term follow-up of seizure outcome after surgery

The present study intends to identify factors that predict postoperative clinical outcome in patients with gangliogliomas (GG) and dysembryoplastic neuroepithelial tumors (DNT). We evaluated the medical records of 45 patients with GG and 13 patients with DNT, treated surgically between 1985 and 1995. We assessed several clinical and histopathological features and analyzed the data statistically. At 5 years postoperatively, 63% of patients with GG and 58% of patients with DNT were seizure-free (Engel's class I). Younger age at surgery ( P<0.01 for GG and P<0.05 for DNT), total resection ( P<0.01 for GG), shorter duration of epilepsy ( P<0.01), absence of generalized seizures ( P<0.01 for GG; P<0.05 for DNT) and absence of epileptiform discharge in the post-operative EEG ( P<0.01 for GG; P=0.01 for DNT) predicted a better postoperative seizure outcome. Tumor recurrence with malignant progression occurred in eight histologically benign GG and two anaplastic GG and was associated which older age at surgery ( P=0.01) and subtotal resection of the tumor ( P<0.01). Our results indicate that a prompt diagnosis, relatively soon after seizure onset, followed by complete resection of glioneuronal tumors provides the best chance for curing epilepsy and preventing their malignant transformation.

Chromosome abnormalities and epilepsy.

Chromosome abnormalities are often associated with central nervous system (CNS) malformations and with other neurologic dysfunctions. In particular, patients with chromosomal abnormalities can have mental retardation (MR) and have a higher risk for seizures than that found in the general population (1). Genetic tools such as karyotyping, high-resolution chromosome banding, fluorescent in situ hybridization (FISH), and other molecular genetics techniques have increased the number of chromosome abnormalities detected in subjects with MR or seizures. However, the majority of studies and reports published have usually considered sporadic cases or very small groups of patients with chromosome abnormalities. Furthermore, the characteristics of seizures and EEGs have been described in detail on very few occasions, to define the electroclinical phenotype, and eventually to classify the epilepsy. In recent years, a few identified chromosome abnormality syndromes seem to show a particular clinical and EEG picture; some of them are relatively common, such as Angelman’s syndrome, the fragile-X (fra-X) syndrome, the Miller‐Dieker syndrome; and others are more rare, such as trisomy 12p syndrome, the Wolf‐ Hirschhorn syndrome, and ring 20 syndrome. We review some clinical and neurophysiologic aspects of these syndromes that can support the neurologist in choosing the genetic analysis to be carried out, and help to identify specific genes influencing epileptogenesis. ANGELMAN’S SYNDROME

Treatment of typical absence seizures and related epileptic syndromes.

Typical absences are brief (seconds) generalised seizures of sudden onset and termination. They have 2 essential components: clinically, the impairment of consciousness (absence) and, generalised 3 to 4Hz spike/polyspike and slow wave discharges on electroencephalogram (EEG). They differ fundamentally from other seizures and are pharmacologically unique. Their clinical and EEG manifestations are syndrome-related. Impairment of consciousness may be severe, moderate, mild or inconspicuous. This is often associated with motor manifestations, automatisms and autonomic disturbances. Clonic, tonic and atonic components alone or in combination are motor symptoms; myoclonia, mainly of facial muscles, is the most common. The ictal EEG discharge may be consistently brief (2 to 5 seconds) or long (15 to 30 seconds), continuous or fragmented, with single or multiple spikes associated with the slow wave. The intradischarge frequency may be constant or may vary (2.5 to 5Hz). Typical absences are easily precipitated by hyperventilation in about 90% of untreated patients. They are usually spontaneous, but can be triggered by photic, pattern, video games stimuli, and mental or emotional factors. Typical absences usually start in childhood or adolescence. They occur in around 10 to 15% of adults with epilepsies, often combined with other generalised seizures. They may remit with age or be lifelong. Syndromic diagnosis is important for treatment strategies and prognosis. Absences may be severe and the only seizure type, as in childhood absence epilepsy. They may predominate in other syndromes or be mild and nonpredominant in syndromes such as juvenile myoclonic epilepsy where myoclonic jerks and generalised tonic clonic seizures are the main concern. Typical absence status epilepticus occurs in about 30% of patients and is more common in certain syndromes, e.g. idiopathic generalised epilepsy with perioral myoclonia or phantom absences. Typical absence seizures are often easy to diagnose and treat. Valproic acid, ethosuximide and lamotrigine, alone or in combination, are first-line therapy. Valproic acid controls absences in 75% of patients and also GTCS (70%) and myoclonic jerks (75%); however, it may be undesirable for some women. Similarly, lamotrigine may control absences and GTCS in possibly 50 to 60% of patients, but may worsen myoclonic jerks; skin rashes are common. Ethosuximide controls 70% of absences, but it is unsuitable as monotherapy if other generalised seizures coexist. A combination of any of these 3 drugs may be needed for resistant cases. Low dosages of lamotrigine added to valproic acid may have a dramatic beneficial effect. Clonazepam, particularly in absences with myoclonic components, and acetazolamide may be useful adjunctive drugs.

Frontal Nonconvulsive Status Epilepticus Associated with High‐Dose Tiagabine Therapy in a Child with Familial Bilateral Perisylvian Polymicrogyria

Antiepileptic drugs are known to exacerbate absence and myoclonic seizures, especially in patients with idiopathic generalized epilepsies. Exacerbation of nonconvulsive generalized seizures in patients with partial epilepsy is less common. Recently, however, a number of cases of putative generalized nonconvulsive status epilepticus (NCSE) or NCSE without further specification have been reported in patients with chronic partial epilepsy treated with the gamma-aminobutyric acid reuptake inhibitor tiagabine. Although complex partial status epilepticus during tiagabine therapy has also been reported, possible precipitation of NCSE specifically associated with frontal lobe discharges does not appear to have been recognized. In this communication, we describe the case of a boy with familial bilateral perisylvian polymicrogyria who developed frontal NCSE after being stabilized on high-dose tiagabine A 12-year-old boy with familial bilateral perisylvian polymicrogyria, mental retardation, and refractory partial seizures was administered tiagabine in addition to sodium valproate. The tiagabine dosage was increased gradually up to 10 mg t.i.d. (1 mg/kg per day), resulting in complete seizure control. After 1 week on maintenance treatment, seizures were completely controlled, but the child developed hypoactivity, decreased reactivity, and affective detachment. An EEG recording revealed subcontinuous sharp-wave discharges with irregular runs of atypical spike-wave complexes over the anterior regions of both hemispheres, consistent with a diagnosis of frontal NCSE. A reduction in tiagabine dosage to 15 mg/day led to complete regression of the behavioral and affective changes and to disappearance of the subcontinuous EEG discharges. Although tiagabine-induced NCSE has been described previously, particularly in patients with preexisting spike-wave abnormalities, this is the first report that identifies its potential role in the precipitation of frontal NCSE.

Myoclonic seizures combined with partial seizures and probable pathophysiology of secondary bilateral synchrony

Objective: We report on a patient who showed an unusual transition from complex partial seizures to a combination of myoclonic seizures and partial seizures, and then to isolated myoclonic seizures. The pathophysiological mechanism of the myoclonic seizures in this uncommon condition was studied.Methods: The interhemispheric small time differences were estimated in the ictal EEG discharges of myoclonic seizures for differentiation between primary and secondary bilateral synchrony. The estimation was performed by coherence and phase analysis based on the two-dimensional autoregressive model.Results: The estimated interhemispheric time differences were at most 27.4 ms. The ictal activity of the myoclonic seizures was suggested to originate from a cortical focus in the right hemisphere, which was also the origin of the partial seizures.Conclusion: The patient was considered to have an unusual type of myoclonic seizures with a probable pathophysiological mechanism of secondary bilateral synchrony.

Duration of rhythmic EEG patterns in neonates: new evidence for clinical and prognostic significance of brief rhythmic discharges

Objective: This study aimed at identifying the characteristics – especially the duration – of rhythmic discharges in neonatal EEG, and their association with clinical neonatal problems. Specifically, we aimed at testing the diagnostic and prognostic validity of using 10 s as minimal duration for defining electroencephalographic seizures. Design and methods: The polysomnographies of 340 neonates were reviewed, and episodes of rhythmic discharges were identified, analyzed, and quantified. The study sample was divided into 3 groups: one in which the maximal duration of rhythmic discharges was shorter than 10 s (brief rhythmic discharges, BRD), a second one in which there were rhythmic discharges longer than 10 s (long rhythmic discharges, LRD), and finally a group in which no rhythmic discharge was found (No-RD). These 3 groups of subjects were compared for the baseline and outcome clinical data. Results: From the 340 neonates studied, 210 did not present any form of rhythmic discharge, 67 (19.7%) had only BRD episodes, and 63 (18.5%) had at least one LRD episode. Prevalence of rhythmic discharges was low among healthy full term newborns, and was significantly higher among preterm and high-risk newborns. Electrophysiological characteristics of rhythmic discharges did not differ between healthy neonates and high-risk ones. Accompanying clinical manifestations were present in 26.3% of the LRD group, but also in 15.9% of the BRD group. The presence of BRD was significantly associated with leukomalacia and with hypoglycemia in the cross-sectional analysis of baseline data, and with an increased risk for abnormal neurodevelopmental outcome after a mean follow-up period of 47 months (adjusted relative risk=4.90, P<0.01). Conclusions: The present data demonstrate an association between BRD and clinical history of hypoxic-ischemic encephalopathy, especially when complicated by leukomalacia, and also with a prognosis of increased risk for abnormal neurodevelopmental outcome. The clinical and prognostic significance of isolated BRD justifies the need to include these brief episodes in future studies of neonatal seizures.

REVIEW ARTICLE Acute and Chronic Electrical Stimulation of the Centromedian Thalamic Nucleus: Modulation of Reticulo-Cortical Systems and Predictor Factors for Generalized Seizure Control

The present report recapitulates the clinical and electrophysiologic studies we have performed on patients with certain forms of medically intractable epilepsy to investigate the basic mechanisms and predictor factors for seizure control of the electrical stimulation of the thalamic centromedian nucleus (CM) procedure. Acute electrical stimulation of CM reveals that in humans, as in other animals, CM represents a thalamic relay of a reticulo-cortical system that participates crucially in wakefulness and attentive processes and in regulation of cortical excitability, as well as in the physiopathology of genuine generalized epileptic seizures. For example, unilateral, threshold, low-frequency (6/sec) stimulation of CM produced electrocortical incremental responses, while high-frequency (60/sec) stimulation of CM produced electroencephalogram (EEG) desynchronization and electronegative DC shifts with no behavioral counterparts. In contrast, combined suprathreshold low-frequency (3/sec) stimulation of CM on one side and of mesencephalic reticular stimulation on the other produced generalized spike-wave complex discharges accompanied by the symptoms of a typical absence attack, including motionless stare, eye blinking, and unresponsiveness of patients to a series of flashes under a simple response task. Chronic bilateral, threshold, high-frequency (60/sec) stimulation of CM significantly decreased the number of primary and secondary generalized tonic-clonic seizures and atypical absence attacks and the amount of interictal generalized EEG discharges in both. In addition, it improved the psychological performance of patients and normalized the EEG by increasing the frequency of background EEG activity. In contrast, chronic stimulation of CM reduced neither the number of complex partial seizures nor the epileptic EEG activities localized in the temporal region. Good outcomes of the chronic CM stimulation procedure were achieved depending on correct selection of patients and accuracy of ventriculographic stereotactic targets, as well as on periodic clinical and EEG evaluation and electrophysiologic monitoring of CM electrical stimulation reliability. However, the presence of 3- to 6-month long-lasting effects of CM stimulation made statistical evaluation of ON-OFF effects of CM stimulation under placebo, double-masked randomized experiments difficult.

The EEG evaluation of single photon emission computed tomography abnormalities in epilepsy.

Single photon emission computed tomography (SPECT) has increasingly been used as a diagnostic procedure for localizing epileptic seizure foci and as a research tool for investigating the physiologic mechanisms underlying seizure activity. With increasing use of SPECT in localizing the seizure focus for epilepsy surgery, there arises a need to critically assess its current role in the evaluation of patients for epilepsy surgery, especially as it relates to other clinical and laboratory data used in presurgical evaluation. Ictal EEG discharge has traditionally been used as the "gold standard" against which SPECT studies are compared in assessing the latter's localizing value. However, this practice presents a major challenge because SPECT studies are often reserved for patients with nonlocalizing EEG or magnetic resonance imaging findings. Nonetheless, SPECT studies in evaluation for epilepsy surgery should always be performed with the knowledge of the patient's EEG activity preceding, during, and after the injection of the radiotracer. The advent of techniques such as subtraction SPECT with co-registration on magnetic resonance imaging (SISCOM) and computer image-guided surgery has great potential in enhancing the clinical electrophysiologic evaluation of SPECT-detected abnormalities in epilepsy. These techniques permit accurate spatial correlation between intracranial EEG activity and SPECT perfusion patterns. The techniques can also be used to evaluate the effect of the extent of EEG focus resection compared with that of SISCOM focus resection to determine which has more prognostic importance in postsurgical control of seizures. Both animal and human studies are warranted to advance our knowledge of the electrophysiology associated with the various SPECT perfusion patterns.

Localization of the epileptic focus by low-resolution electromagnetic tomography in patients with a lesion demonstrated by MRI.

Patients with medically intractable partial epilepsy and well-defined symptomatic MRI lesions were studied using phase-encoded frequency spectral analysis (PEFSA) combined with low-resolution electromagnetic tomography (LORETA). Ten patients admitted to the epilepsy monitoring unit with MRI-identified lesions and intractable partial epilepsy were studied using 31-electrode scalp EEG. The scalp electrodes were located in three-dimensional space using a magnetic digitizer and coregistered with the patient's MRI. PEFSA was used to obtain a phase-encoded scalp map for the ictal frequencies. The ictal generators were obtained from the scalp map using LORETA. In addition, the generators of interictal epileptogenic spikes were identified using time-domain LORETA. The LORETA generators were rostral to the MRI lesion in 87% (7/8) of patients with temporal lobe lesions, but all were located in the mesial temporal lobe in concordance with the patients' MRI lesions. In patients with frontal lobe epilepsy, the ictal generators at the time that the spectral power was maximal localized to the MRI lesions. Eight of 10 patients had interictal spikes, of which 4 were bilateral independent temporal lobe spikes. Only generators of the interictal spikes that were ipsilateral to seizure onset correlated with the ictal generators. LORETA combined with PEFSA of the ictal discharge can localize ictal EEG discharges accurately and improve correlation with brain anatomy by allowing coregistration of the ictal generator with the MRI. Analysis of interictal spikes was less useful than analysis of the ictal discharge.

Cognitive and behavioural concerns in epileptic children.

Cognitive performance in an epileptic child has been a difficult issue to predict in day-to-day clinical practice. Several observations made in early and later part of this century do not provide uniform and convincing answer to this issue. Recent trends in research however, have identified certain variables that are shown to be associated with cognitive decline in epileptic children. Together with associated behavioural problems, the resultant school difficulty is the essence of this concern for the parents. The variables related to cognitive deterioration as identified by several studies include underlying brain pathology (symptomatic epilepsy), early age of onset of seizure, severity and intractability of seizure, repeated head trauma, an episode of status epilepticus, presence of interictal subclinical EEG discharge, adverse psychosocial factor and antiepileptic drug (AED). Association of these variables in a given case cannot only predict adverse cognition outcome but also a preventive management package can be planned aiming at avoiding or minimizing these high risk variables.

EEG-triggered functional MRI of interictal epileptiform activity in patients with partial seizures.

EEG-triggered functional MRI (fMRI) offers the potential to localize the generators of scalp EEG events, such as interictal epileptiform discharges, using a biological measurement as opposed to relying solely on modelling techniques. Although recent studies have demonstrated these possibilities in a small number of patients, wider application has been limited by concerns about patient safety, severe problems due to pulse-related artefact obscuring the EEG trace, and lack of reproducibility data. We have systematically studied and resolved the issues of patient safety and pulse artefact and now report the application of the technique in 24 experiments in 10 consecutive patients with localization-related epilepsy and frequent interictal epileptiform discharges (spikes or spike wave). At least two experiments were performed for each patient. In each experiment, 10- or 20-slice snapshot gradient-echo planar images were acquired approximately 3.5 s after a single typical epileptiform discharge (activation image) and in the absence of discharges (control image). Between 21 and 50 epileptiform discharges were sampled in each experiment. The significance of functional activation was tested using the t test at 95% confidence on a pixel-by-pixel basis. Six of the 10 patients showed reproducible focal changes of the blood oxygen level-dependent (BOLD) signal, which occurred in close spatial relationship to the maximum of the epileptiform discharges in the concurrent EEG. No reproducible focal BOLD signal changes were observed in the remaining four patients. In conclusion, EEG-triggered fMRI is now a sufficiently developed technique to be more widely used in clinical studies, demonstrating that it can reproducibly localize the brain areas involved in the generation of spikes and spike wave in epilepsy patients with frequent interictal discharges.

Electrophysiologic analysis of a chronic seizure model after unilateral hippocampal KA injection.

Unilateral intrahippocampal injections of kainic acid (KA) in rats produce spontaneous recurrent limbic seizures and morphologic changes in hippocampus that resemble hippocampal sclerosis in patients with medically refractory mesial temporal lobe epilepsy (MTLE), that form of temporal lobe epilepsy (TLE) associated with hippocampal sclerosis. Interictal in vivo electrophysiologic studies have revealed high-frequency (250-500 Hz) oscillations, termed fast ripples (FRs). These oscillations may uniquely occur in or adjacent to the site of hippocampal KA injection, in areas that generate spontaneous seizures. Similar field potentials also have been demonstrated in the epileptogenic region of patients with TLE. We have now characterized ictal electrographic patterns in this rat model for comparison with those in human TLE and begun to evaluate the role of FRs in the transition to ictus in the KA-treated rat. Rats received unilateral intrahippocampal injections of KA and, after the development of spontaneous seizures, were implanted with multiple fixed and moveable microelectrodes for single unit, field potential, and EEG recording. They were then monitored by using video-EEG telemetry for several weeks to capture and evaluate electrographic and behavioral seizure types. Results were correlated with Timm's stain demonstration of mossy fiber sprouting. Low-voltage fast (LVF) and hypersynchronous electrographic ictal-onset patterns were seen in the KA-treated rat that resembled similar ictal-onset patterns in patients with TLE. Hypersynchronous, but not LVF, ictal discharges were associated with recurrent FRs. As in the human, hypersynchronous ictal onsets originated predominantly in hippocampus, whereas LVF ictal onsets more often involved extrahippocampal structures. LVF ictal onsets occurred during wakefulness or paradoxical sleep and were usually associated with motor behavior, whereas hypersynchronous ictal onsets occurred during slow-wave sleep or periods of immobility and were not associated with motor behavior unless there was transition to another ictal electrographic pattern. Mossy fiber sprouting did not correlate with the frequency of ictal EEG discharges exhibited by each rat but was greater in those rats that demonstrated frequent behavioral seizures. The electrographic features of spontaneous seizures in the KA-treated rat resemble those of patients with medically refractory TLE with respect to EEG pattern and localization. Our data suggest that hypersynchronous ictal onsets represent epileptogenic disturbances in hippocampal circuits, whereas LVF ictal onsets may involve extrahippocampal areas having more direct connections to the motor system. Hypersynchronous seizures may involve the same neuronal mechanisms that generate interictal FRs.

Generation of scalp discharges in temporal lobe epilepsy as suggested by intraoperative electrocorticographic recordings

OBJECTIVESTo study the variability, topography, polarity, duration, and incidence of interictal epileptiform discharges (EDs) in the scalp EEG and electrocorticogram (ECoG) from 16 patients with temporal lobe epilepsy who underwent...