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PubMed1983

Febrile convulsions and later development of epilepsy.

A group of 172 epileptic children who had had prior febrile convulsions was compared with a group of 674 who had not. Children with epilepsy and prior febrile convulsions were similar in some respects (sex ratio, positive family history for seizures) to children with pure febrile convulsions and in most respects (type of epilepsy, mental status, initial EEG, and two- and four-year remission rates in the long-term outcome) to epileptic children without prior febrile convulsions. Our data do not support the current view that febrile convulsions, per se, are the main cause of mesial temporal sclerosis, le, temporal lobe epilepsy. Thus, our clinical findings support previously expressed doubts on the role of febrile seizures in temporal lobe epilepsy that were based on pathohistologic findings.

Child, Preschool↗
PubMed1984

Cognitive-behavioral treatment of depressed affect among epileptics: preliminary findings.

Controlled study showed skills training for the management of depression in an epilepsy population to be effective. Cognitive-behavioral methods were utilized in a structured learning format with 13 clinically depressed epileptic "students." Significantly greater reductions in dysphoria/depression as measured by the Depression Adjective Checklist and the Generalized Contentment Scale occurred among Ss in the treatment group than among control group Ss. Significant decreases in anger and anxiety/stress and increases in social activities were noted on the Community Adjustment Questionnaire (CAQ). Similar trends were evident on the Beck Depression Inventory and the CAQ depression scale.

Adult↗
PubMed1983

Intelligence in epilepsy: a prospective study in children.

A prospective study tested the stability of the IQ in children with seizure disorders. Seventy-two children with epilepsy underwent psychological evaluations within two weeks of initial diagnosis and yearly thereafter for an average of 4 years. Forty-five of the patients also had a nonepileptic sib evaluated in parallel. The mean IQ for all the children with epilepsy was 99.7 (+/- 20.2, standard deviation) at the time of the initial test, not significantly different from the siblings. This score did not change appreciably with time. Eight of the 72 epileptic patients (11.1%), however, had a persistent decrease in IQ of 10 points or more. These patients had a higher incidence of drug levels in the toxic range (p less than 0.001), their epilepsy was more difficult to control (p less 0.005), and their seizures began at an earlier age (p less than 0.05). Discriminant analysis is revealed that the number of drugs to which the patient became toxic and the age at seizure onset were the two best predictors of ultimate IQ. These two predictors correctly classified 71% of all patients as to whether their IQ would drop by 10 or more points during the test period, remain within 10 points of the initial test score, or increase by more than 10 points. Total number of seizures and seizure control were less good predictors, according to this method of analysis. The findings suggest that, in younger children in particular, total seizure control should not be achieved at the price of repeated episodes of drug toxicity.

Adolescent↗
PubMed1984

The search for epilepsies ideal for clinical and molecular genetic studies.

The first step in localizing the chromosomal site of specific epilepsies is to define their pattern of inheritance. This determination is now being carried out for benign juvenile myoclonic epilepsy; fifty multigenerational families are being studied in three separate epilepsy programs in Los Angeles, Winston-Salem, NC, and Berlin. Concurrent with these studies, investigators are combining the principles of classic linkage analysis, using 30 protein markers, with the use of restriction-fragment-length polymorphisms to determine the chromosomal location of juvenile myoclonic epilepsy. Two problems appear formidable, however. First, since the chromosomal location of specific epilepsies is unknown, the entire human genome must be screened. Second, once the location of a specific epilepsy gene is narrowed down to a region of 10(6) base pairs, the problem of identifying the actual molecular defect is difficult, especially if we have no assay or method to show that a given gene is culpable for producing epilepsy. An approach more likely to succeed is to use as markers the DNA fragments of proteins that are suspected to cause the disease in experimental models of genetic epilepsies; for example, the gamma-aminobutyric acid receptor genes, which are suspected to cause myoclonic epilepsy in experimental animals, can be tested in benign juvenile myoclonic epilepsy. At the same time, other marker proteins could be used to locate the chromosomal site of other specific epilepsies. Once the chromosomal site is determined, recombinant DNA technology will permit the measurement of the precise arrangement of the genes for these restriction-fragment-length polymorphisms and protein markers at a given locus of a chromosome.

Chromosome Mapping↗
PubMed1992

Computer model of ethosuximide's effect on a thalamic neuron.

Ethosuximide appears to have a specific effect on the low-threshold calcium current in thalamic cells. This may be related to its efficacy in the treatment of absence epilepsy. We used a computer model of an individual thalamocortical neuron to better understand the alteration in the low-threshold calcium current under voltage clamp and to predict response to current injection in the presence of ethosuximide. The full model included nine voltage-sensitive ionic channels and a realistic dendritic morphology. The model reproduced the two major responses seen in tissue slices: repetitive spiking with depolarization and the low-threshold calcium spike elicited on release from hyperpolarization. The alteration in low-threshold calcium current with ethosuximide can be explained by a 10-mV depolarizing shift in the steady-state activation curve for this channel with a 10% reduction in maximum channel permeability. Simulations of current injection showed that ethosuximide diminished the low-threshold calcium spike while leaving the tonic firing pattern unaffected. Our results support the hypothesis that ethosuximide's effects on low-threshold calcium current might selectively alter the dynamics of slow bursting in thalamic cells.

Action Potentials↗
PubMed2006

Genes and loci involved in febrile seizures and related epilepsy syndromes.

Epilepsy is a paroxysmal disorder with a cumulative incidence of about 3%. About 13% of patients with epilepsy have a history of febrile seizures (FS). Generalized epilepsy with FS plus (GEFS+) is a familial epilepsy syndrome in which patients can have classic FS, FS that persist beyond the age of 5 years (i.e., FS+), and/or epilepsy. Both genetic and environmental factors have been shown to contribute to the pathogenesis of FS and GEFS+. During the past 10 years, molecular genetic studies have contributed a great deal to the identification of genetic factors involved in FS and GEFS+. In this study we aimed to provide a comprehensive review of currently known genes for FS and GEFS+, and the methods and approaches used to identify them. We also discuss the knowledge we currently have and hypotheses regarding the effect of the mutations on their respective protein functions.

Epilepsy, Absence↗
PubMed1976

Computer analysis of the telemetered EEG in the study of epilepsy and schizophrenia.

Computation of power spectra from averaged brief epochs of spike free scalp EEG coincident with the subcortical spike has revealed a distinctive spectral configuration characterized by smooth monotonic decline in power from lowest to highest frequencies. Nine out of 10 patients with epilepsy display similar patterns preceeding long latency responses to a verbal motor reaction time task. Although subcortical spike activity has been recorded from the parasental region of patients with schizophrenia by several investigators half of our patients with schizophrenia displayed a different pattern which resembles a "white noise" spectrum during the delayed reaction time of incorrect response trials. Power spectra derived from 24-hour telemetered scalp EEGs from patients with epilepsy and schizophrenia are also sharply differentiated by similar criteria. These non-invasive methods for analysis of the scalp EEG in relation to careful and controlled behaviour observations may give useful information regarding subcortical activity when intracranial electrodes cannot be utilized.

Adult↗
PubMed1990

Positron emission tomography findings relevant to neurosurgery for epilepsy.

Using the 2-[F-18]fluorodeoxyglucose method, 213 positron emission tomographic (PET) studies of local brain glucose metabolism (CMRglu) were performed in 124 patients with various forms of epilepsy. Interictal PET scans of primary epileptics typically showed some global metabolic depression and decreased functional activity of insular, basal and anterior temporal cortex. Epilepsia partialis continua Kozevnikov was characterized by hypo- or hyper-metabolism of perirolandic cortex. Tuberous sclerosis was distinguished by neocortical foci of significantly decreased glucose consumption. Even in the interictal resting state, with regard to sensitivity (greater than 90%) and accuracy of focus localization. PET was superior to other diagnostic methods in typical temporal lobe epilepsy. Averaging 23% below normal CMRglu, the majority of hypometabolic foci were found in mesial temporal structures. Improved distinction between the epileptogenic area and the surrounding tissue showing comparatively normal functional responsiveness, was achieved by psychophysical activation using emotional speech or continuous visual recognition during PET scanning. In patients who had undergone total cerebral hemispherectomy because of uncontrolled epilepsy, remarkable recruitment of association areas was observed on both motor and speech activation.

Blood Glucose↗