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PubMed2001

Penetrance and expressivity of genes involved in the development of epilepsy in the genetically epilepsy-prone rat (GEPR).

In order to understand the level of complexity of the epileptic phenotype in the two strains of Genetically Epilepsy-Prone Rats (GEPRs), we determined two important measures of genetic complexity, penetrance and expressivity. Penetrance is the percentage of animals of a specific genotype who express the phenotype associated with that underlying genotype. Expressivity refers to the degree that a particular genotype is expressed as a phenotype within an individual. Incomplete penetrance and variable expressivity are caused by genetic and environmental variation. In this paper we have studied the epileptic phenotype for 20,373 rats. Animals were tested on three occasions for audiogenic seizure and given an audiogenic response score (on a scale of 0-9, 0 being no seizure and 9 being the most severe). The GEPR-3 and GEPR-9 animals both show incomplete penetrance and variable expressivity of the underlying genetic predisposition. The GEPR-9 strain has more animals that have variable levels of seizure predisposition (as measured by a scoring system that denotes the severity of generalized tonic/clonic seizures) and a greater percentage of animals that exhibit no susceptibility to such seizures induced by sound. Both strains have a number of animals that are not susceptible to sound-induced GTCSs and that exhibit some variability in seizure severity. The GEPR-9 males show greater differences in expressivity and penetrance compared to GEPR-9 females. The GEPR-3 animals also show sex-associated variable penetrance and expressivity of the epileptic phenotype, although the differences are much smaller. These findings are the first step toward the mapping of the underlying quantitative trait loci (QTL) for seizure in these animals.

Animals↗
PubMed2003

Therapeutics in pediatric epilepsy, Part 2: Epilepsy surgery and vagus nerve stimulation.

When antiepileptic drugs fail to relieve seizures adequately in children and adolescents, more invasive therapies such as epilepsy surgery and an implanted device to stimulate the vagus nerve should be considered. Temporal lobectomy is an effective treatment of complex partial and secondarily generalized tonic-clonic seizures arising in the mesial structures or lateral temporal neocortex. Excellent outcomes (seizure free or rare, nondisabling seizures) are achieved in at least 70% of children. The most common adverse effect is a superior quadrant field cut that is usually asymptomatic. Transient and more long-lasting language difficulties have been reported when the surgery involves the dominant temporal lobe. The excellent outcome rate for extratemporal surgery ranges from approximately 20% to 80%, with better results seen in patients with an identifiable lesion. Potential morbidity is related to the region of resected neocortex. Corpus callosotomy is an excellent procedure for palliation but is not a cure for seizures that cause falls, with substantial improvement seen in more than 80% of patients. Potential adverse effects include more intense focal seizures and dysphasia, depending on the developmental level of the individual. Hemispherectomy provides seizure relief in 60% to 80% of patients with hemispherical pathologies such as Sturge-Weber or Rasmussen syndromes. Operative mortality has been reported in the range of 0% to 6%; other morbidities include infection and hydrocephalus. Stimulation of the vagus nerve has reduced partial seizures by 50% or more in approximately one third of patients. No adverse cognitive or systemic effects are associated with use of the implanted vagus nerve stimulator.

Child↗
PubMed1998

[The relations between electrical synapse and the mechanism of epilepsy in genetical epilepsy-prone rat].

OBJECTIVE: To investigate the role of gap junction protein Cx32 formed electrical synapses in the pathogenesis of epilepsy. METHODS: Antisense oligodeoxynucleotides (ODN) techniques, intracerebroventricular injection, neuronal discharges in temporal cortex slices, in situ hybridization and immunohistochemistry were used. RESULTS: An antisense ODN for Cx32 100 micrograms was intracerebroventricularly injected once daily, for 3 days to P77PMC rat. The audiogenic seizure scores were significantly lowered as compared with the corresponding sense ODN (or PBS) treated control groups. Moreover, in the enterhinal cortex of the temporal cortex slice of antisense ODN treated P77PMC rat, the typical seizure like events and the late recurrent discharges were not induced by lower Mg2+ solution. The frequency and amplitude of neuronal discharges were decreased as compared with the control group. In situ hybridization and immunohistochemistry studies confirmed that Cx32 mRNA expression and Cx32 synthesis were also inhibited by Cx32 antisense ODN in P77PMC rat brain. CONCLUSION: Our results confirmed that gap junction formed electrical synapse between neurons plays an important role in the development of synchronization of neuronal discharges in vivo and in vitro.

Animals↗
PubMed2000

Rolandic epilepsy: neuropsychology of the active epilepsy phase.

This paper reviews the main studies which have evaluated precisely cognitive functions in rolandic epilepsy. There are very few longitudinal data on the cognitive evolution of these children, particularly in relationship to the paroxysmal electroencephalographic activity. The difficulty to demonstrate direct effects of the epileptic EEG discharges on some cognitive functions and on learning, as occurs in some cases, is discussed.

Age Factors↗
PubMed2001

[Psychopathology in children with epilepsy. Specific information about epilepsy].

Childhood epilepsy is frequently concomitant with emotional and psychopathological difficulties. A specific prevention workout of the psychosocial risks is always necessary and should be considered as a major task by the treating physician. Quality of the information provided by the physician and listening to the parents and the child are important factors that will influence the follow-up.

Adaptation, Psychological↗
PubMed1991

[The factors influencing posttraumatic epilepsy; multicentric cooperative study. Japan Follow-up Group for Posttraumatic Epilepsy].

A multicentric cooperative study was performed to investigate the factors influencing posttraumatic epilepsy. The patients with fresh head injury from 1983 through 1990 were entered in this study. The cases were divided into two groups and followed-up for five years; the patients with severe head injury and who satisfied the criteria belonged to group I. Those with mild head injury were classified into group II. The criteria for group I was that the patients had one or more of the following risks; disturbance of consciousness, bloody cerebrospinal fluid, focal neurological sign, depressed fracture or basal fracture, abnormal CT, dural tear, early convulsion and/or linear fracture. After drop-out cases were excluded, 191 cases out of 241 were analyzed. The number of cases was 126 (66.0%) for group I and 65 (34.0%) for group II. Sixteen patients (12.7%) of group I developed seizure, whereas nobody of group II experienced seizure. The difference between the patients with and without seizures was analyzed. The statistical significant difference was discovered in the following factors; disturbance of consciousness (GCS and the duration), focal and generalized neurological sign, abnormal CT, multiple risks, intracerebral hematoma, surgery, alcohol drinking and abnormal EEG a month after the injury. The relative risk rates were calculated. The highest risk for posttraumatic seizure was disturbance of consciousness extending over more than one month. This was followed by five other indicators of risk; abnormal EEG at one month, surgery, focal neurological sign, alcohol drinking, generalized neurological sign, and intracerebral hematoma.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1979

Clinical biochemistry of epilepsy. I. Nature of the disease and a review of the chemical findings in epilepsy.

In idiopathic or generalized epilepsy, serum glucose and cholesterol concentrations tend to be low, especially just before the seizure. Glucose tolerance curves are abnormal and variable. The electrolyte balance is disturbed, and epileptics tend to go readily into alkalosis. Serum [Na+] is usually unaffected, but [K+] is normal to low between attacks and increases during and after the seizure. Serum [Cl-] is usually high just before the seizure. Epileptics are generally mildly hypocalcemic, especially in the period before the seizure. Serum urea and nonprotein nitrogen values are low between paroxysms but increase after the seizure. Serum protein concentration is usually normal. Stress, which releases epinephrine and corticotropin, results in high serum citrate concentration, which probably contributes to decreased serum [Ca2+] just before a seizure. In the healthy individual, any increase in serum citrate is accompanied by increasing [Ca2+]. In the rabbit, convulsions can be induced with corticotropin, a result of increased serum citrate concentration coupled with a decrease in [Ca2+]. The net result is severe hypo-ionic-calcemia. A similar phenomenon has been reported in a few humans. Administration of insulin causes serum citrate concentrations to decrease. Apparently, the dynamic system that controls glucose and lipid metabolism, and thus electrolyte balance, through the hormones epinephrine, corticotropin, insulin, glucagon, calcitonin, and parathormone, is abnormal in the epileptic.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

[Usefulness of ambulatory EEG in detecting critical and intercritical events in patients with epilepsy or with suspected epilepsy].

Ambulatory EEGs (EEGAs) were recorded in 251 patients. In 91 of these patients there was a suspicion of having epileptic seizures, in 117 a diagnosis of epilepsy was already established, in 43 the withdrawal of antiepileptic drugs was envisaged being apparently free from seizures for years. The EEGA showed epileptogenic abnormalities in 31% of patients of the first group. This percentage was not far from the one obtained with standard EEG (EEGS) recordings. In the second group, a divergence was found, as for the classification of seizures, between the ictal events actually recorded on the EEGA and the definition of seizures based on clinical information. Furthermore ictal events recorded by the EEGA were less frequent than one would have anticipated according to the seizure frequency asserted by the patients. In the third group the EEGA disclosed the persistence of epileptic seizures, mostly represented by diffuse spike and wave discharges, in about 30% of the patients. Finally, comparison of the results obtained by the EEGA with those obtained by the EEGS in all patients suggested that the two recording techniques are complementary.

Adolescent↗
PubMedDate not supplied

[Evaluation of the secretory activity of the adrenal cortex and gonads in women with epilepsy. I. Urinary excretion of metabolites of adrenal cortex hormones in women with epilepsy during the 2 days preceding menstrual bleeding].

In 32 women with seizures occurring mainly in the premenstrual phase and during bleeding, (group A) and in 31 women with epilepsy without this relationship of the seizures to the menstrual cycle (group B) the metabolites of adrenocortical hormones (17-ketosteroids and 17-hydroxycorticosteroids) were determined in 24-hour urine. The investigations were done during 2 days preceding menstrual bleeding, in most cases during three menstrual cycles. A significant reduction of the excretion of 17-ketosteroids and total 17-hydroxycorticosteroids was found in both groups as compared to the accepted normal value (p less than 0.01). However, no significant difference was observed in the excretion of these hormones between these groups of patients, although in group A he values of 17-ketosteroids were lower than in group B. On the basis of these results it is suggested that deficiency of androgenic hormones may contribute to the occurrence of seizures on the days before the onset of menstrual bleeding, and the effect of anticonvulsant treatment on the decreased excretion of these hormones is discussed.

17-Hydroxycorticosteroids↗
PubMed1979

[Prognosis in epilepsy and tactics to be applied in terminating anti-epilepsy therapy].

This paper compares basic concepts published by eminent epileptologists, supplementing them by a specific analysis of 350 case records. The author, on the basis of data reported in the literature and the results of his own investigations, makes concrete recommendations for the discontinuation of anticonvulsives in the treatment of epilepsy.

Anticonvulsants↗
PubMed1997

[Neuromechanisms for intractable epilepsy: a review of the studies on the kindling model of epilepsy].

Recent advances in kindling studies were reviewed to search a neurobiological mechanism of the epileptogenesis in intractable epilepsy. Consistent findings that indicate the following three issues were available. First, a long-lasting epileptogenesis can develop acquisitively by the repetition of self-sustained epileptic discharges, which may be produced by recurrent changes in the excitatory amino acid system (EAA) via NMDA receptors. Another brief seizure-induced cascading change that occurs in the third and fourth messenger systems through the metabolic EAA receptor may be critical for the persistence of acquired epileptogenesis. Secondly, an unstable balance between the altered EAAergic facilitatory system and insufficient GABAergic inhibitory system may exist in interictal epileptic disorder. The GABAergic inhibition failure as well as excessive EAA transmission may cause the emergence of epileptic seizures. Thirdly, neuronal sprouting in the mossy fiber of the dentate gyrus and a decrease in the neuronal density in the hilar region seem not to be an essential change for induction of the kindling effect. The clinical validity of these histological changes should be further examined in an over-kindling model sufficient to produce spontaneous seizures.

Animals↗
PubMed1998

[Comparison of the multifactorial model as a hereditary mechanism of non-myoclonic generalized idiopathic epilepsy and partial idiopathic epilepsy].

OBJECTIVE AND METHODS: An experimental study about the predictions from the multifactorial threshold model created by Falconer is presented, assuming that this model may explain the genetic mechanisms underlying the family aggregation of idiopathic epilepsies. RESULTS: We failed to confirm the following predictions from the falconer model: decreased prevalence of disease in relatives, proportional to decreased family links, and the order of birth effect. An heredity greater than 100% was calculated which is concordant with the presence of at least a locus with a major gen affect. CONCLUSION: Our results reject the multifactorial threshold effect and suggest the presence of a major gen or Mendelian effect. An analysis of complex segregation is suggested for future studies.

Adolescent↗