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PubMed2004

Role of immediate postictal diffusion-weighted MRI in localizing epileptogenic foci of mesial temporal lobe epilepsy and non-lesional neocortical epilepsy.

OBJECTIVE: To determine whether meaningful changes in signal intensity or in the apparent diffusion coefficient of water (ADC) in the ictal onset zone can be detected through immediate postictal and interictal diffusion-weighted magnetic resonance imaging (DWMRI) in patients with localization-related epilepsy. METHOD: In randomly selected 10 medial and lateral temporal lobe epilepsy (TLE) and four extratemporal epilepsy patients, DWMRI was performed immediately after a seizure and during the interictal period. All 14 patients were non-lesional except for hippocampal sclerosis detected on MRI. The mean time interval from seizure onset to postictal DWMRI was 81 min. Regions of interest (ROI) were selected in both the cortex, which was believed to be the ictal onset zone, and the corresponding anatomical region of the contralateral hemisphere in the postictal and interictal DWMRI. The mean ADC measured from all ROIs was compared. Ictal onset zones were determined by ictal electroencephalography (EEG) and seizure semiology. RESULTS: On visual inspection of postictal and interictal DWMRI, signal changes in the ictal onset zone could be identified in only one patient with medial TLE. The mean ADC values from the ictal onset zones were not significantly different from those of the corresponding contralateral regions of the cortices in both postictal and interictal DWMRI. However, the postictal ADC values of the epileptogenic foci of neocortical epilepsy or neocortical temporal portion of TLE without hippocampal sclerosis were decreased compared with interictal ones in whom both interictal and postictal DWMRIs were obtained (P = 0.028). CONCLUSION: Our results demonstrate that water diffusion can change even after a single seizure in non-lesional neocortical epilepsy.

Adolescent↗
PubMed2006

Cognitive problems related to epilepsy syndromes, especially malignant epilepsies.

Neurocognitive impairment is frequent in epilepsy patients. Causes are multiple, and may be influenced by several factors including the epilepsy syndrome. Most cognitive complaints in adult patients are mental slowness, memory difficulties and attention deficits. In children, cognitive problems are more diffuse, responsible for language troubles, learning difficulties, poor academic outcome, behavior problems and finally unfortunate socio-professional prognosis. The most devastating epilepsy syndromes such as epileptic encephalopathies are nearly exclusively described in infancy and childhood. This paper will review the major cognitive complaints in relation to the epilepsy syndrome, with a more detailed interest for the malignant epilepsies in infancy and childhood such as Ohtahara and West syndrome, Lennox-Gastaut syndrome and epileptic encephalopathis with continuous spike-and-wase during slow wave sleep. The impact of surgery on cognition will be briefly discussed in adults and youger patients.

Cognition Disorders↗
PubMed2005

SCN1A mutation analysis in myoclonic astatic epilepsy and severe idiopathic generalized epilepsy of infancy with generalized tonic-clonic seizures.

Severe myoclonic epilepsy in infancy (SMEI), severe idiopathic generalized epilepsy of infancy (SIGEI) with generalized tonic clonic seizures (GTCS), and myoclonic astatic epilepsy (MAE) may show semiological overlaps. In GEFS+ families, all three phenotypes were found associated with mutations in the SCN1A gene. We analyzed the SCN1A gene in 20 patients with non-familial myoclonic astatic epilepsy -- including 12 probands of the original cohort used by Doose et al. in 1970 to delineate MAE. In addition, 18 patients with sporadic SIGEI -- mostly without myoclonic-astatic seizures -- were analyzed. Novel SCN1A mutations were found in 3 individuals. A frame shift resulting in an early premature stop codon in a now 35-year-old woman with a borderline phenotype of MAE and SIGEI (L433fsX449) was identified. A splice site variant (IVS18 + 5 G --> C) and a missense mutation in the conserved pore region (40736 C --> A; R946 S) were detected each in a child with SIGEI. We conclude that, independent of precise syndromic delineation, myoclonic-astatic seizures are not predictive of SCN1A mutations in sporadic myoclonic epilepsies of infancy and early childhood.

Child↗
PubMed2001

A novel SCN1A mutation associated with generalized epilepsy with febrile seizures plus--and prevalence of variants in patients with epilepsy.

We recently described mutations of the neuronal sodium-channel alpha-subunit gene, SCN1A, on chromosome 2q24 in two families with generalized epilepsy with febrile seizures plus (GEFS+) type 2. To assess the contribution that SCN1A makes to other types of epilepsy, 226 patients with either juvenile myoclonic epilepsy, absence epilepsy, or febrile convulsions were screened by conformation-sensitive gel electrophoresis and manual sequencing of variants; the sample included 165 probands from multiplex families and 61 sporadic cases. The novel mutation W1204R was identified in a family with GEFS+. Seven other coding changes were observed; three of these are potential disease-causing mutations. Two common haplotypes, with frequencies of .67 and .33, were defined by five single-nucleotide polymorphisms (SNPs) spanning a 14-kb region of linkage disequilibrium. An SNP located 18 bp upstream of the splice-acceptor site for exon 3 was observed in 7 of the 226 patients but was not present in 185 controls, suggesting possible association with a disease mutation. This work has confirmed the role of SCN1A in GEFS+, by identification of a novel mutation in a previously undescribed family. Although a few candidate disease alleles were identified, the patient survey suggests that SCN1A is not a major contributor to idiopathic generalized epilepsy. The SCN1A haplotypes and SNPs identified here will be useful in future association and linkage studies.

Amino Acid Sequence↗
PubMed2006

The spectrum of idiopathic Rolandic epilepsy syndromes and idiopathic occipital epilepsies: from the benign to the disabling.

Benign childhood epilepsy with centrotemporal spikes (BCECTS) is an idiopathic focal epilepsy syndrome, the benign characteristics of which are debated; in fact, stable or intermittent specific neuropsychological deficits are frequent and may affect scholastic or adaptive abilities. Cognitive dysfunction may be related to a marked increment of the interictal epileptic discharges in NREM sleep: different degrees of neuropsychological deficits depend on the extent of awake and sleep activity and the predominant discharge localization. The age of onset and duration of atypical sleep EEG patterns may correlate with permanent cognitive impairments. These atypical clinical and EEG evolutions have been reported in the literature as different syndromes that constitute the spectrum of idiopathic rolandic epilepsy. Moreover, a clinical link between BCECTS and early-onset benign childhood occipital epilepsy has been demonstrated. According to the neurobiological approach, the spectrum of Idiopathic Rolandic Epilepsy is based on an age-dependent, idiopathic predisposition to focal seizures and sharp-wave discharges, as an expression of nonlesional cortical excitability. The involvement of a given area of the cerebral cortex may depend on the brain maturational stage.

Age Factors↗
PubMedDate not supplied

Generalized epilepsy with febrile seizures plus and severe myoclonic epilepsy in infancy: a case report of two Italian families.

"Generalized epilepsy with febrile seizures plus" (GEFS+) syndrome has been recently described. This term defines a heterogeneous group of generalized epilepsies observed in several members of large pedigree studies. The syndrome spectrum has been widened by including others forms of generalized epilepsy. We report two Italian families in which the fathers showed febrile seizure plus (FS+), and two sons had severe myoclonic epilepsy of infancy (SMEI). The clinical setting of each epileptic member of the family will be discussed, focusing on the relationship with the GEFS+ group, confirming its wide clinical spectrum. In fact, GEFS+ is different from most other epilepsy syndromes as it is defined not by a set of associated symptoms but by the genetic transmission of a predisposition to febrile convulsions and other seizures, with a variable expression in several members of the same pedigree, perhaps due to ionic channel dysfunction. SMEI could represent the most severe end of the spectrum.

Adult↗
PubMed1995

Impact of epilepsy on employment status: findings from a UK study of people with well-controlled epilepsy.

This paper examines the current employment status and recent employment history of 494 individuals with epilepsy whose seizures were well-controlled or in remission. Information about employment status and history was obtained by means of self-completion questionnaires, sent to eligible subjects by post. The sampling frame from which subjects were recruited were neurology out-patient departments across the UK. The majority of subjects had epilepsy in remission: only 15% had had a seizure in the last year and only 25% reported one in the last two years. A high proportion of respondents were currently in employment. Of those who were not, few attributed this to their epilepsy; nor did epilepsy seem to have a significant impact on recent employment history. In spite of the lack of evidence of any actual discrimination, a third of respondents nevertheless felt their condition affected their ability to obtain employment. The findings from earlier studies of high unemployment rates partly reflect bias in the samples studied. Our data provide evidence that where seizures are well-controlled and uncomplicated by other handicap, people with epilepsy do not generally experience problems with employment.

Age Distribution↗
PubMed2005

Autoimmune epilepsy: distinct subpopulations of epilepsy patients harbor serum autoantibodies to either glutamate/AMPA receptor GluR3, glutamate/NMDA receptor subunit NR2A or double-stranded DNA.

We studied 82 patients with different types of epilepsy and 49 neurologically intact non-epileptic controls, and identified three different subpopulations of epilepsy patients bearing significantly elevated levels of autoantibodies to either GluR3B-peptide of glutamate/AMPA receptor subtype 3 (17/82; 21% of patients), or to a peptide of NR2A subunit of glutamate/NMDA receptors (15/82; 18%), or to double-stranded (ds) DNA, the hallmark of systemic lupus erythematosus (13/80; 16%). Most patients had only one antibody type, arguing against cross-reactivity. Nearly all anti-dsDNA Ab-positive patients did not harbor anti-nuclear autoantibodies. Most patients had no history of brain damage, febrile convulsions, early onset epilepsy, acute epilepsy or intractable seizures. We suggest to measure the 'autoimmune-fingerprints' of epilepsy patients for diagnostic and therapeutic purposes.

Adolescent↗
PubMed2006

The multidrug transporter hypothesis of drug resistance in epilepsy: Proof-of-principle in a rat model of temporal lobe epilepsy.

Resistance to drug treatment is an important hurdle in the therapy of many diseases, including cancer, infectious diseases and brain disorders such as epilepsy. A phenotype that is referred to as multidrug resistance was first described for chemotherapy-resistant cancer cells that overexpressed the drug efflux transporter P-glycoprotein (P-gp). More recently, overexpression of P-gp has been found in capillary endothelial cells of epileptogenic brain tissue from patients with medically intractable epilepsy. Such regionally restricted P-gp overexpression in the blood-brain barrier is likely to reduce the concentration of antiepileptic drugs at epileptic neurons, which would be a plausible explanation for multidrug resistance in epilepsy. However, a definite proof-of-principle for this hypothesis is lacking. In the present study, we used a rat model of temporal lobe epilepsy that allows selecting drug-resistant and drug-responsive subgroups of epileptic rats by prolonged treatment with the antiepileptic drug phenobarbital at maximum tolerated doses. We have shown recently that drug-resistant rats selected from this model exhibit a marked overexpression of P-gp in the hippocampus and other limbic brain regions. This model is thus ideally suited to prove the multidrug transporter hypothesis of drug resistance. For this purpose, we selected a group of phenobarbital-resistant rats, which was subsequently treated by combinations of phenobarbital with the selective P-gp inhibitor tariquidar. Coadministration of tariquidar (15-20 mg/kg) fully restored the anticonvulsant activity of phenobarbital without altering plasma pharmacokinetics or neurotoxicity of the antiepileptic drug. These data demonstrate that inhibiting P-gp in epileptic rats with proven drug resistance counteracts resistance, providing the first proof-of-principle of the multidrug transporter hypothesis of medically refractory epilepsy.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2006

Reproductive endocrine function in women with epilepsy: the role of epilepsy type and medication.

The purpose of the analysis described here was to assess reproductive endocrine disorders in 148 women with epilepsy (WWE) by epilepsy type and antiepileptic drug use. Women with idiopathic generalized epilepsy had a higher prevalence of reproductive endocrine disorders than control subjects. In addition, hyperandrogenism, polycystic ovaries, and polycystic ovary syndrome were more prevalent in WWE on valproate than in WWE taking other drugs or control women. The use of VPA was a predictor of the development of polycystic ovaries and polycystic ovary syndrome, and the use of valproate and younger age predicted the development of hyperandrogenism. In conclusion, both idiopathic generalized epilepsy and valproate were associated with an increased risk of reproductive endocrine disorders in WWE in this post hoc reanalysis of data on a large number of WWE. This was especially evident if the epilepsy was active and required treatment early in life.

Adolescent↗
PubMed1993

The development of a questionnaire to assess knowledge of epilepsy: 1--General knowledge of epilepsy.

It is well documented that knowledge is a vital factor in the ability to cope successfully with epilepsy. Misconceptions and deficits in knowledge have implications not only for psychosocial well-being but also for medical compliance. However, at present there is no commonly accepted objective measure of knowledge of epilepsy. The development of the Epilepsy Knowledge Profile--General (E.K.P.--G) is presented in this paper. Fifty-five true/false items (34 medical knowledge items, 21 social knowledge items) were selected by a range of experts in the field of epilepsy. A clinical trial of the questionnaire was then completed by 82 people with epilepsy attending a city centre outpatient clinic. Results indicated that the scale has both good internal reliability and test-retest reliability. Also the range of scores indicates that it is sensitive to differences in knowledge. Potential uses of the questionnaire are discussed.

Adaptation, Psychological↗
PubMed1998

Childhood epilepsy with neuropsychological regression and continuous spike waves during sleep: epilepsy surgery in a young adult.

We describe the case of a man with a history of complex partial seizures and severe language, cognitive and behavioural regression during early childhood (3.5 years), who underwent epilepsy surgery at the age of 25 years. His early epilepsy had clinical and electroencephalogram features of the syndromes of epilepsy with continuous spike waves during sleep and acquired epileptic aphasia (Landau-Kleffner syndrome), which we considered initially to be of idiopathic origin. Seizures recurred at 19 years and presurgical investigations at 25 years showed a lateral frontal epileptic focus with spread to Broca's area and the frontal orbital regions. Histopathology revealed a focal cortical dysplasia, not visible on magnetic resonance imaging. The prolonged but reversible early regression and the residual neuropsychological disorders during adulthood were probably the result of an active left frontal epilepsy, which interfered with language and behaviour during development. Our findings raise the question of the role of focal cortical dysplasia as an aetiology in the syndromes of epilepsy with continuous spike waves during sleep and acquired epileptic aphasia.

Adult↗
PubMed1996

George A. Savoy, visionary benefactor of Canadians with epilepsy, and the history of the Savoy Foundation for Epilepsy.

George A. Savoy was born in Cohoes, New York, in 1873. He left the U.S.A. in 1921 to manage the Canadian branch of a large manufacturer of ledgers and looseleaf registers. This company was asked to supply Professor Jasper's laboratory with rolls of plain unlined paper and it was George Savoy who later developed fanfolded and lined EEG paper, which was first used at the Montreal Neurological Institute. He also had personal contacts with Wilder Penfield concerning their mutual interest in the needs of patients with epilepsy. He was a successful industrialist involved with several charitable organizations funding programmes for people with epilepsy. He was opposed to the sectarianism then prevalent in Quebec, which was unfamiliar to him, and in reaction built his own institution, Dieppe House, a home for people with epilepsy, later renamed < >. It was to operate without regard to race, language or religion. In 1971, his son Harold and other generous donors decided to create a foundation to support research in epilepsy. The Foyer Savoy was sold in 1988 and the proceeds used to increase the endowment of the foundation. His grandson George M. Savoy is the current president. The fourth generation is also represented by Caroline Savoy, daughter of the president, who joined the board of directors in 1992. The foundation will distribute from $300,000 to $400,000 yearly to researchers from many different countries working in the field of epilepsy in universities and hospitals throughout Canada.

Canada↗
PubMed2003

Epilepsy and comorbidity: infections and antimicrobials usage in relation to epilepsy management.

Infections are probably the most common preventable cause of epilepsy worldwide. There are concerns that endemic infections and infestations, such as malaria and neurocysticercosis, could be responsible for the increased incidence of epilepsy in the developing world. Cases of epilepsy associated with neurocysticercosis are also being seen increasingly in developed countries due to migration from, and travel to, endemic areas. When prescribing antimicrobial agents in patients with epilepsy a number of issues need to be considered, such as potential adverse effects on seizure control and interactions with concomitant antiepileptic drugs (AEDs). Some antimicrobial agents, including penicillins, cephalosporins, carbapenems, quinolones and antimalarials, can have proconvulsant activity and may precipitate seizures, even in patients who do not have epilepsy. Moreover, many antimicrobials increase or decrease the plasma levels of AEDs, whereas some AEDs may adversely affect the efficacy of antimicrobials.

Anti-Bacterial Agents↗
PubMed1999

Quality of epilepsy treatment and services: the views of women with epilepsy.

In three focus group discussions, 18 women with epilepsy were asked about their experiences of and satisfaction with care and treatment at both primary and secondary care, and for views on how epilepsy services might be improved. A fourth focus group was held with six epilepsy nurse specialists to seek their opinions on the service needs of women with epilepsy. Criticisms of services identified by both the women and nurses typically concerned four areas of care; organisation of services, technical competence, information provision and interpersonal skills, and health outcomes. Specific criticisms in each area included: lack of continuity of care and shared care; poor provision of information about side-effects of antiepileptic drugs (AEDs) and their effect on the contraceptive pill; and apparently haphazard prescribing of AEDs with consequent serious side-effects. Recommendations for improvements in services and treatment for people with epilepsy are suggested.

Adult↗
PubMed2002

Amygdala pathology in psychosis of epilepsy: A magnetic resonance imaging study in patients with temporal lobe epilepsy.

Psychosis of epilepsy (POE) has been recognized as a severe complication of chronic intractable epilepsy for more than a century. Most of the clinical symptoms of POE are reminiscent of schizophrenia. Nevertheless, there is general agreement that the phenomenology of POE differs from classical schizophrenia. The temporal lobe hypothesis of schizophrenia put forward in the 1960s notes that episodes with paranoid psychoses are more prevalent in temporal lobe epilepsy (TLE). However, the aetiology and pathogenesis of POE are poorly understood. One of the strongest biological findings in schizophrenia is volume loss of temporal lobe structures and the hippocampus in particular. In order to test the hypothesis that atrophy of the hippocampus and the amygdala is found in patients with TLE and POE, we performed a retrospective study of all patients with TLE who were admitted to the assessment unit of the Chalfont Centre for Epilepsy from 1995 until 1999. Twenty-six (2.6%) of these 1008 patients fulfilled inclusion criteria and were compared with 24 patients with TLE without psychopathology and 20 healthy volunteers. All patients underwent extensive MRI investigations, including volumetric data sets and quantitative T(2 )relaxometry. We found that patients with TLE and POE differed from patients with TLE alone and healthy volunteers in that the total brain volumes were significantly smaller. While there were no differences in hippocampal volumes between the three study groups, there was a significant 16-18% enlargement of the amygdala on both sides in patients with POE. Our findings support the notion that POE is a distinct nosologic entity differing from schizophrenia not only in clinical details but also in neurobiological aspects. The finding of amygdala enlargement agrees with the observation of an association between dysphoric disorders of epilepsy and POE described nearly 100 years ago.

Amygdala↗
PubMed1999

The misdiagnosis of epilepsy and the management of refractory epilepsy in a specialist clinic.

We assessed the frequency, causes and consequences of erroneous diagnosis of epilepsy, and the outcome of patients referred with 'refractory epilepsy', by retrospective analysis of the case records of 324 patients. The sample was divided into those exposed to anti-epileptic drugs (n = 184), of whom 92 were said to have refractory seizures, and those who had not received treatment (n = 140). The latter group is reported elsewhere. The overall misdiagnosis rate was 26.1% (46/184), with incomplete history-taking and misinterpretation of the EEG equally responsible. Side-effects were reported by 19/40, while unnecessary driving restrictions and employment difficulties were encountered by 12/33 and 5/33, respectively. Of those labelled 'refractory epilepsy', 12 did not have epilepsy. Sixteen were rendered seizure-free and 25 significantly improved by the optimal use of anti-epileptic drugs or surgery. Diagnostic and management services for patients with suspected and established epilepsy are suboptimal, with psychological and socio-economic consequences for individual patients. The resulting economic burden on the health and welfare services is probably substantial.

Ambulatory Care↗
PubMedDate not supplied

Previous experiences with epilepsy and effectiveness of information to change public perception of epilepsy.

Differences with regard to the effectiveness of health information and attitude change are suggested between people with direct, behavioral experiences with a health topic and people with indirect, nonbehavioral experiences. The effects of three different methods of health education about epilepsy, frequently used in health education practice, are assessed in a pretest posttest design with control groups, controlling for experiences with epilepsy. Subjects were 132 students from teacher-training colleges. After all treatments, attitudes, and knowledge about epilepsy were changed in a positive way. Treatments were found to be equally effective. Before treatment, direct behavioral experiences were related to knowledge and a more positive attitude towards epilepsy. After treatment, subjects with direct behavioral experiences with epilepsy showed less change of attitude and knowledge as compared with subjects with indirect experiences. Direct experiences appear to restrain the processing of new information and attitude change.

Adult↗