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PubMed1991

The phenotype: seizures and epilepsy syndromes.

The coincidence of recent advances in human genetics and the development of an international classification system in the field of epilepsy, mostly for practical reasons, has resulted in unexpected progress in syndrome-related epilepsy genetics. This review of the International Classification of Epileptic Seizures as well as of Epilepsies and Epilepsy Syndromes, in addition to presenting up-to-date clinical views on epilepsy classification, tries to draw special attention to problematic areas of the classification and its underlying concepts, particularly to those to which genetic studies could be expected to contribute. These questions include, amongst others: are there genetically different non-specific basic mechanisms for the generation of focal epileptic discharge on one hand, and ambincipient or generalized discharge on the other?; are absence epilepsies, juvenile myoclonic epilepsy, and grand mal on awakening genetically separate or identical disorders?; how do genetically determined precipitating factors such as photosensitivity and, perhaps, pattern and eye closure sensitivity, interact with other genetic factors?; what is the place of idiopathic localization-related epilepsies in relation to idiopathic generalized epilepsies?; and what is the possible role of age-related, regional or diffuse gene action? Further areas of investigation may include the study of regional distributions of 'generalized' spike wave discharge as a possible indicator of subsets of this genetically determined trait; the search for a possible relation of West syndrome to chromosome 21; and the collection of precise data on the phenotype of the occasional later remanifestations in syndromes with age-related offset.

Epilepsy↗
PubMed1994

Progress in mapping human epilepsy genes.

The chromosomal loci for seven epilepsy genes have been identified in chromosomes 1q, 6p, 8q, 16p, 20q, 21q, and 22q. In 1987, the first epilepsy locus was mapped in a common benign idiopathic generalized epilepsy syndrome, juvenile myoclonic epilepsy (JME). Properdin factor or Bf, human leukocyte antigen (HLA), and DNA markers in the HLA-DQ region were genetically linked to JME and the locus, named EJM1, was assigned to the short arm of chromosome 6. Our latest studies, as well as those by Whitehouse et al., show that not all families with JME have their genetic locus in chromosome 6p, and that childhood absence epilepsy does not map to the same EJM1 locus. Recent results, therefore, favor genetic heterogeneity for JME and for the common idiopathic generalized epilepsies. Heterogeneity also exists in benign familial neonatal convulsions, a rare form of idiopathic generalized epilepsy. Two loci are now recognized; one in chromosome 20q (EBN1) and another in chromosome 8q. Heterogeneity also exists for the broad group of debilitating and often fatal progressive myoclonus epilepsies (PME). The gene locus (EPM1) for both the Baltic and Mediterranean types of PME or Unverricht-Lundborg disease is the same and is located in the long arm of chromosome 21. Lafora type of PME does not map to the same EPM1 locus in chromosome 21. PME can be caused by the juvenile type of Gaucher's disease, which maps to chromosome 1q, by the juvenile type of neuronal ceroid lipofuscinoses (CLN3), which maps to chromosome 16p, and by the "cherry-red-spot-myoclonus" syndrome of Guazzi or sialidosis type I, which has been localized to chromosome 10. A point mutation in the mitochondrial tRNA(Lys) coding gene can also cause PME in children and adults (MERFF).

Chromosome Mapping↗
PubMed1991

Binding of Ro 5-4864 to brain membranes of rats with and without absence-like phenomena.

Spontaneously occurring spike-wave discharges (SWD) in rats are used as a model for absence epilepsy in humans. In vitro, the binding parameters of 3H-Ro 5-4864, a ligand labelling the peripheral benzodiazepine receptor, were determined for brain membranes of WAG/Rij rats, an inbred strain showing SWD, and for ACI rats, an inbred strain showing no SWD. No difference in the Kd but a small difference in the Bmax values between the strains were found. Recently, other investigators reported a correlation between a decrease in affinity for 3H-Ro 5-4864 and the occurrence of SWD. Our results suggest however that it is doubtful that a change in Kd of the peripheral benzodiazepine receptor is causal in the etio-pathology of the spontaneous absence like phenomena in rats.

Animals↗
PubMed2005

Genetics of idiopathic generalized epilepsies.

The idiopathic generalized epilepsies (IGEs) are considered to be primarily genetic in origin. They encompass a number of rare mendelian or monogenic epilepsies and more common forms which are familial but manifest as complex, non-mendelian traits. Recent advances have demonstrated that many monogenic IGEs are ion channelopathies. These include benign familial neonatal convulsions due to mutations in KCNQ2 or KCNQ3, generalized epilepsy with febrile seizures plus due to mutations in SCN1A, SCN2A, SCN1B, and GABRG2, autosomal-dominant juvenile myoclonic epilepsy (JME) due to a mutation in GABRA1 and mutations in CLCN2 associated with several IGE sub-types. There has also been progress in understanding the non-mendelian IGEs. A haplotype in the Malic Enzyme 2 gene, ME2, increases the risk for IGE in the homozygous state. Five missense mutations have been identified in EFHC1 in 6 of 44 families with JME. Rare sequence variants have been identified in CACNA1H in sporadic patients with childhood absence epilepsy in the Chinese Han population. These advances should lead to new approaches to diagnosis and treatment.

Epilepsy, Generalized↗
PubMed1999

[Idiopathic epilepsy in the child].

Study of idiopathic epilepsy in childhood can distinguish various syndromes on the basis of clinical and electroencephalographic criteria. There is much overlapping between the syndromes described. The aim of the classification is to define precisely the prognosis of each disorder and to approach treatment effectively and safely, avoiding aggravation of a condition by poorly adapted prescription. The main distinction is between partial seizures, among which the principal is centro-temporal with spikes, and generalised seizures of which the most common are absence epilepsy and juvenile myoclonic epilepsy. Since the phenotypes are well defined, molecular genetic studies should lead to better knowledge of the complex biochemical mechanisms of idiopathic epilepsy. Seizures that occur without lesions are well managed by treatment in most cases and have a good psychosocial prognosis. The possibility of acquiring autonomy, familial overprotection, restrictions and interdictions must all be kept in mind in the psychological, social and educational handling of persons with epilepsy, most of which are benign cases.

Anticonvulsants↗
PubMed2001

Effects of adenosine administration on spike-wave discharge frequency in genetically epileptic rats.

1. In the present study, the effects of the administration of adenosine on absence seizures were investigated in the Wistar Albino Glaxo/Rijswijk (WAG/Rij) strain of rats, which are an adequate model for human absence epilepsy. 2. After baseline electroencephalogram (EEG) recording, adenosine was injected intraperitoneally (i.p.) at doses of 6, 30 and 120 mg/kg and EEG recordings were continued for 1 h postinjection. In addition, to enable evaluation of the contribution of peripheral factors to the occurrence of spike-wave discharges (SWD) after adenosine injection, arterial blood pressure and rectal temperature were also recorded. 3. Injection of adenosine induced a dose-dependent increase in the appearance of SWD. The number and total duration of SWD were found to be significantly increased after 30 and 120 mg/kg adenosine (P < 0.05). Adenosine also induced a fall in both blood pressure and body temperature in all experimental groups. 4. These results show that peripheral administration of adenosine promotes absence seizures. It is likely that the lowering of blood pressure and body temperature and the activation of sensory afferents after adenosine injection may contribute to the facilitation of SWD observed in the present study.

Adenosine↗
PubMed1999

Visual field constriction is not limited to children treated with vigabatrin.

Vigabatrin (GVG) is widely used in the treatment of complex partial seizures and infantile spasms. Persistent visual field constriction associated with GVG therapy in adults was reported as a rare but serious side-effect. Visual field examination in children is more difficult because of a lack of cooperation among very young or mentally handicapped patients. We performed Goldmann perimetry in 12 of 153 patients treated with GVG as mono- or as add-on therapy. The others would not cooperate, and two adolescents refused the examination. For comparison, we examined 12 age-matched patients with complex partial or generalized epilepsy who had never taken GVG. In five of 12 GVG-treated patients, and in one of the control group, we found a concentric visual field constriction. All patients were subjectively asymptomatic. The GVG-treated patients had taken the drug in combination with valproic acid (VPA) or oxcarbazepine (OCB). In four patients, GVG treatment was already stopped at the time of the ophthalmologic examination. Three patients had intracerebral lesions that could not account for the pathologic perimetric findings. The single patient from the control group with concentric visual field constriction had an absence epilepsy, treatment being performed with VPA and lamotrigine (LTG). In conclusion, GVG has a causal but not unique connection with visual field constriction in pediatric patients.

Adolescent↗
PubMed1999

Evaluation of a putative major susceptibility locus for juvenile myoclonic epilepsy on chromosome 15q14.

Juvenile myoclonic epilepsy (JME) is a genetically determined common subtype of idiopathic generalized epilepsy (IGE). Significant evidence for linkage has been reported for a susceptibility locus for JME in the chromosomal region 15q14 that harbors the gene encoding the alpha7 subunit of the neuronal nicotinic acetylcholine receptor (CHRNA7). The present study was designed to test the earlier linkage finding and to explore whether this susceptibility locus is involved in the epileptogenesis of a broader spectrum of IGE syndromes. Multipoint parametric and nonparametric linkage analyses with seven microsatellite polymorphisms encompassing the region of the CHRNA7 gene were performed using two diagnostic schemes of JME-related traits in two groups of multiplex families ascertained through probands with either JME (n = 27) or idiopathic absence epilepsy (n = 30). The present linkage study failed to replicate evidence for a major susceptibility locus for JME in the region encompassing the CHRNA7 gene. In addition, we found no hint in favor of linkage to 15q14 under the broad diagnostic scheme in any of the sets of families. If genetic variation in this region confers susceptibility to JME, then its effect size might be too small or its occurrence too rare to be detected in the investigated families.

Adolescent↗
PubMedDate not supplied

Riluzole enhances the anti-seizure action of conventional antiepileptic drugs against pentetrazole-induced convulsions in mice.

Riluzole, a pre- and postsynaptic modulator of glutamate transmission, administered alone at doses of 5 and 10 mg/kg did not affect pentetrazole-evoked seizures in mice. However, it enhanced the anti-seizure action of valproate, phenobarbital, ethosuximide, although not that of clonazepam, in this model of experimental epilepsy. Keeping in mind that riluzole did not change plasma levels of antiepileptic drugs, a pharmacokinetic interaction, at least in terms of free plasma levels, does not seem probable. Regarding undesired effects, riluzole (5 mg/kg) and its combination with valproate did not produce any motor or long-term memory impairment. In contrast, the concomitant treatment of riluzole (5 mg/kg) with valproate (144 mg/kg), phenobarbital (4.9 mg/kg), or ethosuximide (90 mg/kg), resulted in a moderate motor deficit, but not long-term memory impairment in the tested mice. In conclusion, the results of the present study suggest that riluzole might occur effective as an additive drug in the treatment of myoclonic or absence epilepsy in humans.

Animals↗
PubMed2005

Sleep, epilepsy and thalamic reticular inhibitory neurons.

Thalamic reticular neurons release the potent inhibitory neurotransmitter GABA and their main targets are thalamocortical neurons in the dorsal thalamus. This article focuses on two topics: (i) the role of thalamic reticular neurons in the initiation of spindles, a hallmark oscillation during early sleep stages; and (ii) the reticular-induced inhibition of thalamocortical neurons during cortically generated spike-wave seizures. Although hotly debated during the past decade, the idea of spindle generation by a network of GABAergic reticular neurons was recently supported by in vivo and in computo studies demonstrating interactions between inhibitory reticular neurons that lead to spindle sequences. During spike-wave seizures and electrical paroxysms of the Lennox-Gastaut type, which arise in the neocortex, reticular neurons are powerfully excited through corticofugal projections and they produce prolonged inhibitory postsynaptic potentials in thalamocortical neurons. Thus, GABAergic reticular neurons are crucial in the generation of some sleep rhythms, which produce synaptic plasticity, and in inhibiting external signals through thalamocortical neurons, which leads to unconsciousness during absence epilepsy.

Action Potentials↗
PubMed2005

Activity profile of pregabalin in rodent models of epilepsy and ataxia.

Pregabalin (Lyrica) is a novel amino acid compound that binds with high affinity to the alpha2-delta (alpha2-delta) auxiliary protein of voltage-gated calcium channels. In vivo, it potently prevents seizures, pain-related behaviors and has anxiolytic-like activity in rodent models. The present studies were performed to determine the profile of pregabalin anticonvulsant activity in a variety of mouse and rat models. In the high-intensity electroshock test, pregabalin potently inhibited tonic extensor seizures in rats (ED50 = 1.8 mg/kg, PO), and low-intensity electroshock seizures in mice. It prevented tonic extensor seizures in the DBA/2 audiogenic mouse model (ED50 = 2.7 mg/kg, PO). Its time course of action against electroshock induced seizures in rats roughly followed the pharmacokinetics of radiolabeled drug in the brain compartment. At higher dosages (ED50 1= 31 mg/kg, PO), pregabalin prevented clonic seizures from pentylenetetrazole in mice. In a kindled rat model of partial seizures, pregabalin prevented stages 4-5 behavioral seizures (lowest effective dose = 10 mg/kg, IP), and also reduced the duration of electrographic seizures. Pregabalin was not active to prevent spontaneous absence-like seizures in the Genetic Absence Epilepsy in Rats from Strasbourg (GAERS) inbred Wistar rat strain. Pregabalin caused ataxia and decreased spontaneous locomotor activity at dosages 10-30-fold higher than those active to prevent seizures. These findings suggest that pregabalin has an anticonvulsant mechanism different from the prototype antiepileptic drugs and similar to that of gabapentin except with increased potency and bioavailability. In summary, our results show that pregabalin has several properties that favor treatment of partial seizures in humans.

Animals↗
PubMed1993

Developmental analysis of hippocampal mossy fiber outgrowth in a mutant mouse with inherited spike-wave seizures.

Neural firing patterns are an essential determinant of normal axon terminal growth and synaptic connectivity in developing afferent pathways, but the trophic role of synchronous activity in associative neural networks is less well defined. We examined the ontogeny of inherited synchronous hippocampal network discharges and mossy fiber innervation patterns at sequential stages of development in the stargazer (stg) mutant, a single-locus mouse mutation expressing generalized spike-wave epilepsy. Brief bursts of 6/sec repetitive discharges arise spontaneously on postnatal days 17-18 and persistently activate neocortical and hippocampal networks throughout adulthood. We found a striking pattern of mossy fiber recurrent axon collateral sprouting in the inner molecular layer of dentate gyrus in the adult stg hippocampus. Sprouting is not apparent until 4-6 weeks following seizure onset, but then steadily intensifies with continued synchronous activation. In the adult mutant, axon outgrowth is accompanied by a mild selective loss of hilar interneurons without gliosis. These data indicate that hypersynchronous stimulation during late postnatal brain development is linked, following a prolonged latent period, to significant fiber outgrowth and synaptic reorganization within the hippocampal formation. Since the pattern of synchronous activation in the stg mutant strongly resembles that seen in human spike-wave absence epilepsy, the synaptic plasticity described in this model has important implications for normal brain development in this common disorder.

Aging↗
PubMed1997

Early discontinuation of treatment in children with uncomplicated epilepsy: a prospective study with a model for prediction of outcome.

PURPOSE: The main purpose of the present study was to identify predictor variables with significant influence on seizure outcome after discontinuation of treatment in children with uncomplicated epilepsy and to analyze whether these variables, included in a prognostic model could identify children in whom 1-year treatment would be sufficient. METHODS: Before initiation of treatment in children aged 2-16 years with uncomplicated epilepsy, the duration of treatment was randomized to 1 year (group I) or 3 years (group II). At the end of the allotted period, treatment was discontinued in 161 children who had been seizure fre during the previous 6 months. The mean follow-up period after treatment was 5.8 years. Twenty-three predictor variables were analyzed by survival methods regarding their influences on the outcome. RESULTS: At the latest follow-up check, 60 children (37%) had relapsed. The following predictor variables were selected by multiple regression analysis and constituted a model with a simple scoring system: age at seizure onset; seizure type; generalized, irregular spike-wave activity on EEG after 1 year of treatment; and persistent 3-Hz spike-wave activity after 6 months of treatment in children with absence epilepsy. In group I, the remission rate was 73% in children with high prognostic scores, 10% in children with low scores, and 40% in those with intermediate scores (log-rank test, p = 0.0001). CONCLUSIONS: After 1 year of treatment, our prognostic model identified children in whom treatment could be withdrawn at that time. Our model should be easily applicable in clinical practices and may be of clinical importance in determining the duration of treatment in children with uncomplicated epilepsy.

Adolescent↗
PubMedDate not supplied

[Angelman syndrome: physical characteristics and behavioural phenotype in 37 patients with confirmed genetic diagnosis].

INTRODUCTION: Angelman syndrome (AS) is characterised by mental retardation, ataxic gait, epilepsy, absence of language and a special series of physical traits behavioural phenotype. Its incidence is estimated as one in every 20,000 individuals. On the basis of discoveries made in molecular biology, patients can be classified as belonging to five types: deletion, paternal uniparental disomy (UPD), imprinting defects, mutation of the UBE3A ubiquitin protein ligase gene and unidentified mechanism (15% 20% of patients). Some studies report significant correlations between the phenotype and the genetic cause. PATIENTS AND METHODS: We reviewed, retrospectively, 37 patients suffering from AS with a positive genetic study and who had been controlled for at least two years in the Neurological Service at the Hospital Sant Joan de D u. Data was collected on physical characteristics, behavioural phenotype, type of communication, sleep disorders and the medication they needed, as well as epilepsy, start age, types of seizures, medication, schooling and social integration. RESULTS: 87% of cases were due to de novo deletion, 8% were caused by UPD, and 5% had their origins in imprinting defects. The average age of diagnosis was 6.5 years. The sleep disorders present in 48% of the patients required medication in 67% of cases, and 95% presented epilepsy. The most frequent seizures were myoclonic, tonic clonic and atonic. The electroencephalogram (EEG) was the characteristic found in the AS in 68%. The most effective treatment was afforded by valproate and clonazepam. CONCLUSIONS: As regards the phenotype, no differences were found according to the genetic alteration. The most effective treatment for the sleep disorders was melatonin. Epilepsy was an almost constant finding in our series, as was cognitive affectation. Lastly, it must be pointed out that educational and socio occupational integration is difficult for patients suffering from AS.

Adolescent↗
PubMed2006

Intracellular activity of cortical and thalamic neurones during high-voltage rhythmic spike discharge in Long-Evans rats in vivo.

Spontaneous high-voltage rhythmic spike (HVRS) discharges at 6-12 Hz have been widely described in the electrocorticogram (EcoG) of Long-Evans rats. These ECoG oscillations have been proposed to reflect a state of attentive immobility allowing the optimization of sensory integration within the corticothalamic pathway. This hypothesis has been challenged by recent studies emphasizing similarities between HVRS discharges and spike-and-wave discharges (SWDs) in well-established rat genetic models of absence epilepsy. Here, we made in vivo intracellular recordings to determine, for the first time, the cellular mechanisms responsible for the synchronized oscillations in the corticothalamic loop during HVRS discharges in the Long-Evans rats. We show that HVRS discharges are associated in corticothalamic neurones with rhythmic suprathreshold synaptic depolarizations superimposed on a tonic hyperpolarization, likely due to a process of synaptic disfacilitation. Simultaneously, thalamocortical neurones exhibit a large-amplitude 'croissant'-shaped membrane hyperpolarization with a voltage sensitivity suggesting a potassium-dependent mechanism. This thalamic hyperpolarizing envelope was associated with a membrane oscillation resulting from interactions between excitatory synaptic inputs, a chloride-dependent inhibitory conductance and voltage-gated intrinsic currents. These cortical and thalamic cellular mechanisms underlying HVRS activity in Long-Evans rats are remarkably similar to those previously described in the thalamocortical networks during SWDs. Thus, the present study provides an additional support to the hypothesis that HVRS activity in Long-Evans rats is an absence-like seizure activity.

Animals↗
PubMed1990

[Discontinuation of antiepileptic drug treatment in controlled seizure patients].

Studies on discontinuing medication in epileptic patients who have been maintaining favorable progress and who have remained free of epileptic seizures for a long period have only been reported in comparatively small numbers and the conditions necessary to evaluate such patients as well as the methods used to enable the discontinuation of antiepileptic drug treatment to be decided have not yet been established. With the recent rapid advances in the treatment of epilepsy, any long-term treatment should be designed to include the possibility that the discontinuation of medication may be possible and this possibility should be understood from the start of treatment planning. In this study, the author has attempted to gradually or completely withdraw medication from epileptic patients who maintain favorable progress, using specific criteria and methods established by the author. The criteria used were: (1) patients should have been free of epileptic seizures for three years or more, (2) no epileptic discharge had appeared on the EEG within the previous 2-3 years (recorded during sleep as well as when awake) and (3) the patient's consent should have been obtained regarding the gradual or complete withdrawal of medication. The subjects were 40 patients (23 males and 17 females) with a mean age of 32.2 years. Seizures were primary generalized tonic/clonic in type (P-GTC) in 4 patients, complex partial seizures (CPS) in 22 and generalized sleep convulsions (GC(S)) in 14. In this study, patients with absence epilepsy taking a favorable course and those with benign childhood epilepsy showing epileptic discharges in the temporal to central region (rolandic seizure) or in the occipital region were not included. If epileptic discharges appeared on EEG recordings in the course of this study during the process of gradual drug withdrawal aiming toward complete drug withdrawal, attempts to completely withdraw medication were suspended. In this study, therefore, the period before the process in which the cessation of attempts at complete withdrawal of medication was involved due to the EEG showing epileptic discharges was taken as 'the former period' and the period in which the above process was involved was taken as 'the latter period'.(ABSTRACT TRUNCATED AT 400 WORDS)

Anticonvulsants↗
PubMed2004

The multiple effects of ketamine on electroencephalographic activity and behavior in WAG/Rij rats.

The effects of ketamine, a noncompetitive antagonist at the NMDA receptor, were studied on the EEG and in the open field in a genetic animal model of generalized absence epilepsy--the WAG/Rij rat strain. Animals of this strain display spontaneous occurring generalized spike-wave discharges (SWDs) in the EEG. Ketamine was systemically administered in a dose range from 3 to 30 mg/kg. Biphasic effects of ketamine were observed in the EEG. The first phase was a dose-dependent suppression of SWDs, followed by a second phase characterized by the facilitation of SWDs. This increase was expressed first as an increased number of SWDs, and later on as a significant prolongation of individual discharges and decrease in frequency of SWDs. An obvious amplitude modulation of the discharges was also found. During the period of suppression of SWDs, a new phenomenon was observed: quasi-periodic groups of spikes or wave spikes, with an internal frequency of 4-5 Hz and a periodicity of about 5 s. That quasi-periodic activity vanished a few minutes prior to the recovery of the classical SWDs. However, a specific 5-s amplitude modulation of SWDs remained present in the recovery period. The propensity of that specific ketamine-induced activity was found to be correlated with propensity of SWDs in background EEGs of drug-free animals. Ketamine also produced a dose-related initial behavioral excitation, a decrease of muscle tone in hind quarters, followed by front quarters and head, and an absence of locomotor activity. However, the time course of the behavioral changes cannot explain the effects on the EEG. It can be concluded that ketamine has more effects on the EEG than previously assumed which cannot be explained by a simple blockade of the NMDA receptor. It is proposed that the obtained specific dynamics of SWDs' frequency may be caused by changes in the activity of the thalamo-cortical pacemaker that is generating SWDs.

Anesthetics, Dissociative↗
PubMed1997

Design and construction of a long-term continuous video-EEG monitoring unit for simultaneous recording of multiple small animals.

In recent years several new rat models of human limbic/mesial temporal lobe epilepsy have been described [1,2,4-7,11,15-17]. Unlike earlier models such as kindling in which the seizures are induced by an exogenous stimulus, these new models are characterized by seizures that occur spontaneously at random intervals. Although the spontaneity of the seizures makes these models more like human epilepsy, documentation of these seizures by direct observation is highly inefficient, and sub-behavioral electrographic seizures could be missed. Continuous paper EEG and video recording have been used [5-7,15], but these techniques are resource intensive. The slow paper speed required by long-term paper recordings limits the ability to differentiate between true seizure activity and electrical artifact. Subtle behavioral seizures are likely to be missed during rapid review of video recordings alone [16]. Ambulatory cassette EEG recordings have been used [3], but the systems require expensive proprietary hardware, and the systems have limited channels for recording (8-16). To improve the utility of the models, we developed a long-term EEG/video monitoring system to detect the electrographic seizures and document their behavioral accompaniment. The system is based on commercially available components, including a computerized EEG seizure detection system that was initially developed for human seizure monitoring [8,9,13]. Seizures are reliably detected and the data are reduced so that 24 h of recording can be reviewed in 30-90 min. Although the computer program is accurate, special care must be taken in system design and construction to reduce sources of electrical artifact that can cause false detections when multiple animals are recorded simultaneously on a single EEG machine. During data review it is necessary to differentiate between electrical artifact induced by animal activity from true seizure activity by key EEG patterns. Certain seizure patterns (less than 3 hz. low amplitude) will not be detected by the seizure detection program, but the system is highly effective for typical limbic seizures and may be useful for the animal models of absence epilepsy [12,14]. It can also be used as a continuous or intermittent EEG/physiological recording device for experiments that examine animals' spontaneous behavior and the EEG correlate (e.g. sleep/wake cycles, learning and memory tasks).

Animals↗