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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We classified epileptic patients with frontal-dominant rhythmic slow-wave bursts into a FIRDA group with frequencies of 1.5 to 2.5 Hz and a 3 Hz group with a frequency of 3 Hz. We compared the two groups in clinical background and EEG findings. The patients in the FIRDA group were older, and partial epilepsy was more common. In the 3 Hz group, idiopathic generalized epilepsy was more common. All of the partial epilepsy in the patients in the FIRDA group was symptomatic, and organic brain damage such as sequelae of brain tumor surgery, or cerebrovascular disorders, etc., were the most common primary diseases. There was no difference between the two groups in frequency of seizures, and VPA was the drug most often used to treat the patients in the 3 Hz group. No morphological differences between the two group, except the difference in frequency, were observed among the EEG findings. Accompaniment by localized spike waves or sharp waves was more common in the FIRDA group. When epilepsy was accompanied by rhythmic slow-wave bursts in the frontal area, its clinical significance depended on whether its frequency was 2.5 Hz or less or 3 Hz. When it was 2.5 Hz or less, symptomatic partial epilepsy was more common, suggesting the presence of large, prominent organic brain damage, such as sequelae of brain tumor surgery or cerebrovascular disorders. Idiopathic generalized epilepsy, on the other hand, was shown to be more common when the frequency was 3 Hz.
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PMID:Study on FIRDA and 3 Hz rhythmic slow wave bursts occurring in the frontal area of epileptic patients. 913 75

Idiopathic generalized epilepsy (IGE) comprises several subsyndromes. These are principally: benign neonatal familial convulsions, benign neonatal convulsions, benign myoclonic epilepsy in infancy, childhood absence epilepsy, juvenile absence epilepsy, juvenile myoclonic epilepsy, epilepsy with generalised tonic-clonic seizures on awakening. In addition, there are less well-recognized syndromes, such as eyelid myoclonia with absences. The pathophysiology of the IGE syndromes is not fully understood; it is evident that typical absences are the result of abnormal oscillations between the thalamus and cerebral cortex. Genetic studies are in progress to elucidate the biochemical defects underlying the conditions. The clinical and electroencephalographic features of the individual subsyndromes are distinct, but some patients may be difficult to classify into a particular subgroup. A correct syndromic diagnosis is important, as treatment strategies differ for patients with the different forms of IGE, and it is necessary for genetic research.
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PMID:Idiopathic generalized epilepsies with typical absences. 926 57

Impaired reproductive function is thought to frequently affect women with epilepsy, mainly when seizures originate in the temporal lobe. In this study, we evaluated menstrual cycle features and assessed ovulation by determining luteal progesterone (Pg) levels in 101 consecutive women with epilepsy (36 with idiopathic generalized epilepsy -IGE; 65 with partial epilepsy -PE), aged between 16 and 50 years, treated with various antiepileptic drugs (AED). PE originated in the temporal lobe (TLE) in 40 subjects, in the frontal lobe in 13, in the parietal lobe in 2, while the origin of focal seizures remained undetermined in 10 patients. In all patients, menstrual and reproductive history, body mass index, hair distribution and hormonal pattern were assessed. Suprapubic ovary ultrasound (US) examination was carried out in 83 patients (28 with IGE, 55 with PE). Three patients with IGE and one with PE were amenorrheic. Oligomenorrhea occurred in 16 patients, polymenorrhea in 2. Changes in menstrual cyclicity were independent from epilepsy type (19.4% in IGE; 23.1% in PE) and from origin of focal discharges (22.5% of patients with TLE; 20.0% with origin in other brain areas). Luteal Pg levels remained below 2 ng/ml in 30 patients independently of epilepsy type. Corpus luteum dysfunction was combined with hyperandrogenism in 15 of these patients. In the other cases different alterations of hypothalamus-pituitary-ovary axis were observed. Valproic acid blunted luteal Pg surge more frequently than other AED. Polycystic ovaries (PCO) were observed in 14 (16.9%) patients (21.0% with IGE: 14.5% with PE). These prevalences are not higher than those reported in the general population. Among PE patients, PCO was found in 1 case with undetermined focal origin and in 7 TLE cases, who also had ovary volume significantly larger than patients with seizures originating from the frontal or parietal lobe. Epileptic women exhibited an increased occurrence of multifollicular ovaries (MFO) found in 12 cases (14.4% vs 5% in the general population). However, no defined hormonal or clinical pictures were associated with this US alteration in most patients. These findings reappraise the impact of ovary alterations in women mainly affected by mild to moderate epilepsy, on differing AED regimens, with the exception of more frequent ovulatory dysfunction and PCO occurrence in patients taking VPA.
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PMID:Menstrual cycle and ovary alterations in women with epilepsy on antiepileptic therapy. 941 5

Most idiopathic generalized epilepsies have an onset in childhood or adolescence, with a moderate second incidence peak in the presenium predominantly in women. This study addressed the question of a later onset. The available literature and the records of four personal data sets (two prospective incidence surveys of epileptic seizures, one prevalence study of epilepsy, and one clinical series of individuals with epilepsy) were screened for patients who had experienced a first generalized convulsive seizure with bilateral spike-wave complexes on EEG after 60 years of age. Reports of first idiopathic generalized tonic-clonic seizures occurring after age 60 were extremely rare and none was found in our four cohorts regardless of the methodology involved. Only five case reports were found, all involving a woman. Two had a family history of seizure disorders and two had had at least one seizure earlier in life. Idiopathic generalized epilepsy of late onset, if this condition actually exists, is likely to be the consequence of a genetic predisposition triggered by acquired epileptogenic factors.
Seizure 1998 Dec
PMID:Idiopathic generalized epilepsy of late onset. 988 93

Several PET receptor ligands have been used to investigate the neurochemical basis of the epilepsies. 11C-Flumazenil binds to the central benzodiazepine receptor (cBZR)-gamma-aminobutyric acid (GABA) A receptor complex; 11C-diprenorphine, 18F-cyclofoxy, and 11C-carfentanil to opiate receptors; and 11C-Deprenyl to monoamine oxidase B. These studies should be considered alongside high-quality magnetic resonance imaging that demonstrates the structural basis of the condition. The results should be correlated with those of quantitative in vitro neuropathologic and autoradiographic studies. Idiopathic generalized epilepsy has been studied with 11C-flumazenil and 11C-diprenorphine. There is no evidence of any interictal overall abnormality of opioid receptors in idiopathic generalized epilepsy, but typical absences have been found to displace 11C-diprenorphine from the association areas of the neocortex. This finding implies that release of endogenous opioids has a role in the pathophysiologic mechanisms of typical absences in humans. In contrast, binding of 11C-flumazenil to cBZRs has been shown not to be affected by serial absences. Studies of interictal 11C-flumazenil binding in idiopathic generalized epilepsy have not given uniform results. In one investigation a slight reduction was reported in the neocortex of patients with idiopathic generalized epilepsy in comparison with patients with partial seizures. Also observed was increased benzodiazepine receptor density in the cerebellar nuclei and decreased density in the thalamus. Widespread increases in cBZRs also have been reported in cerebral neocortex, thalamus, and cerebellar cortex. In unilateral hippocampal sclerosis, reduction of binding of 11C-flumazenil has been shown to be confined to the hippocampus and to be over and above that caused by neuron loss and hippocampal atrophy. In malformations of cortical development, abnormalities of cBZRs, as demonstrated with 11C-flumazenil PET, are more extensive than the structural abnormality revealed with magnetic resonance imaging. There often are areas of increased cBZRs, a pattern that appears unique to malformations of cortical development and that may reflect both functional and structural anomalies. In patients with mesial temporal lobe epilepsy, upregulation of mu opioid receptors has been found in lateral neocortex without an overall increase of opioid receptor binding. The pathophysiologic explanation for this finding is not clear. Possibilities include up-regulation of mu receptors in response to epileptic activity and down-regulation or occupation of kappa opioid receptors. Important future developments in this field that will increase understanding of the processes that underlie the epilepsies will come from the development of further ligands, particularly tracers that are specific for excitatory amino acid receptors, the subtypes of the opioid receptors, and the GABAB receptor.
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PMID:Positron emission tomography receptor studies. 1051 72

Idiopathic generalized epilepsy (IGE) is a common, complex disease with an almost exclusively genetic etiology but with variable phenotypes. Clinically, IGE can be divided into different syndromes. Varying lines of evidence point to the involvement of several interacting genes in the etiology of IGE. We performed a genome scan in 91 families ascertained through a proband with adolescent-onset IGE. The IGEs included juvenile myoclonic epilepsy (JME), juvenile absence epilepsy (JAE), and epilepsy with generalized tonic clonic seizures (EGTCS). Our linkage results support an oligogenic model for IGE, with strong evidence for a locus common to most IGEs on chromosome 18 (lod score 4.4/5.2 multipoint/two-point) and other loci that may influence specific seizure phenotypes for different IGEs: a previously identified locus on chromosome 6 for JME (lod score 2.5/4.2), a locus on chromosome 8 influencing non-JME forms of IGE (lod score 3.8/2.5), and, more tentatively, two newly discovered loci for absence seizures on chromosome 5 (lod scores 3.8/2.8 and 3.4/1.9). Our data also suggest that the genetic classification of different forms of IGE is likely to cut across the clinical classification of these subforms of IGE. We hypothesize that interactions of different combinations of these loci produce the related heterogeneous phenotypes seen in IGE families.
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PMID:Genome scan of idiopathic generalized epilepsy: evidence for major susceptibility gene and modifying genes influencing the seizure type. 1126 7

Idiopathic generalized epilepsy (IGE) is often not recognized with serious consequences on the sufferers. We examined factors contributing to the missed diagnosis of IGE in 41 adults attending our epilepsy clinic with diagnosis of partial epilepsy who had semiology or EEG findings suggesting a possible differential diagnosis. After careful re-evaluation, the diagnosis of IGE was established in 25 patients: 22 (88%) with JME, one with juvenile absence, one with perioral myoclonia with absences, one with eyelid myoclonia with typical absences. Myoclonic jerks, the hallmark of the JME and other IGE, were not usually reported by patients or misdiagnosed as focal motor seizures. Brief and infrequent absence seizures and focal EEG abnormalities were other factors contributing to not recognizing JME. All 25 patients did not achieve seizure control before re-evaluation of diagnosis. After appropriate diagnosis of IGE and change of AED to valproate or valproic acid, 19 (76%) became seizure free and six (24%) had a significant improvement on seizure control. Association with lamotrigine provided further improvement in three of these patients. An appropriate questioning to identify myoclonic and absence seizures and a proper interpretation in the context of whole clinical constellation are essential for a correct seizure classification and diagnosis of IGE in adults.
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PMID:[Idiopathic generalized epilepsies misdiagnosed as partial epilepsies]. 1236 50

Successful treatment of idiopathic generalized epilepsy begins with accurate seizure classification. Seizure types, such as absence, myoclonic, and primary generalized tonic-clonic seizures (PGTCS), often can be classified based on a detailed history and inter-ictal electroencephalogram (EEG). Ideally, patients can be classified into specific epilepsy syndromes, such as childhood absence epilepsy, juvenile myoclonic epilepsy (JME), or generalized tonic-clonic seizures on awakening. Idiopathic generalized epilepsy should be distinguished from focal epilepsy with rapid secondary generalization. If this distinction is not clear after history, physical examination, and routine inter-ictal EEG, then ambulatory EEG, video EEG monitoring, or neuroimaging studies may be needed. Ethosuximide, valproate, or lamotrigine are all appropriate first-line choices in the treatment of childhood absence epilepsy. The specific medication should be chosen based on the side effect profiles, dosing formulations, and titration schedules of the medications. The available evidence best supports valproate as the first-line choice in the treatment of JME, although lamotrigine and topiramate may be appropriate choices in this setting. More data specific to JME are needed to clarify the role of medications such as levetiracetam and zonisamide in the treatment of JME. The available evidence to guide the treatment of PGTCS is limited, because most trials did not rigorously exclude patients with focal epilepsy with rapid secondary generalization. Available evidence suggests that valproate is an appropriate first-line choice for PGTCE. Lamotrigine or topiramate also may be appropriate choices. More data are needed to clarify the role of levetiracetam and zonisamide in the treatment of PGCTS. If it is unclear whether a patient has idiopathic generalized epilepsy or focal epilepsy with secondary generalization, then a broad-spectrum anticonvulsant, including valproate, lamotrigine, or topiramate, should be considered. More data are needed to support the broad-spectrum efficacy of levetiracetam and zonisamide.
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PMID:Idiopathic Generalized Epilepsy. 1504 6

Idiopathic generalized epilepsy (IGE) syndromes are diseases that are characterized by absence, myoclonic, and/or primary generalized tonic-clonic seizures in the absence of structural brain abnormalities. Although it was long hypothesized that IGE had a genetic basis, only recently have causative genes been identified. Here we review mutations in the GABA(A) receptor alpha1, gamma2, and delta subunits that have been associated with different IGE syndromes. These mutations affect GABA(A) receptor gating, expression, and/or trafficking of the receptor to the cell surface, all pathophysiological mechanisms that result in neuronal disinhibition and thus predispose affected patients to seizures.
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PMID:GABA(A) receptor epilepsy mutations. 1717 14

Idiopathic generalized epilepsy (IGE) is a class of genetically determined, phenotypically related epilepsy syndromes. Linkage analysis identified a chromosome 18 locus predisposing to a number of adolescent-onset IGEs. We report a single-nucleotide polymorphism (SNP) association analysis of the region around the marker locus with the high LOD score. This analysis, which used both case-control and family-based association methods, yielded strong evidence that malic enzyme 2 (ME2) is the gene predisposing to IGE. We also observed association among subgroups of IGE syndromes. An ME2-centered nine-SNP haplotype, when present homozygously, increases the risk for IGE (odds ratio 6.1; 95% confidence interval 2.9-12.7) compared with any other genotype. Both the linkage analysis and the association analysis support recessive inheritance for the locus, which is compatible with the fact that ME2 is an enzyme. ME2 is a genome-coded mitochondrial enzyme that converts malate to pyruvate and is involved in neuronal synthesis of the neurotransmitter gamma-aminobutyric acid (GABA). The results suggest that GABA synthesis disruption predisposes to common IGE and that clinical seizures are triggered when mutations at other genes, or perhaps other insults, are present.
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PMID:Malic enzyme 2 may underlie susceptibility to adolescent-onset idiopathic generalized epilepsy. 1553 13


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