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PubMed1994

Propranolol Action in Chronically Unstable Generalized Epilepsy.

Chronically unstable generalized epilepsy (CUGE) is a disabling disease usually treated by ineffective association of drugs. Authors have devoted attention to calcium-dependent mechanisms of seizures. Calcium channel blockers have been used with success in the control of both experimental and clinical epilepsy. beta-Adrenergic blockers, such as propranolol hydrochloride (PR), had been described to be experimentally effective in the control of epilepsy in rats and chicks, due to its receptor-dependent calcium channel blocking and membrane-stabilizing actions. We used PR in this crossover, placebo-controlled, randomized trial. Twelve patients with CUGE were enrolled and treated for 15 days with treatment A (20--40 mg PR bid) and treatment B (20--40 mg placebo); the difference in the total number of seizures in the two periods of treatment was compared. Patients treated with PR showed a 32.9% reduction (p < 0.05) in epileptic manifestations. The authors concluded that PR may be an effective adjunct therapy in CUGE and other forms of generalized epilepsy.

Journal Article↗
PubMed1989

Juvenile myoclonic epilepsy: characteristics of a primary generalized epilepsy.

Juvenile myoclonic epilepsy (JME) is a primary generalized epilepsy that affects approximately 7% of adolescent and adult epilepsy patients. JME is characterized by myoclonic seizures alone or combined with generalized tonic-clonic seizures or absence seizures. Seizures are precipitated by sudden awakening, sleep deprivation, photic stimulation, and alcohol consumption. The ictal electroencephalogram (EEG) shows a typical 4- to 6-Hz polyspike and wave pattern; the interictal EEG may be normal. Valproate controls seizures in approximately 80% of JME patients and is recommended for successful management of this disorder.

Anticonvulsants↗
PubMed2006

Exploration of the genetic architecture of idiopathic generalized epilepsies.

PURPOSE: Idiopathic generalized epilepsy (IGE) accounts for approximately 20% of all epilepsies and affects about 0.2% of the general population. The etiology of IGE is genetically determined, but the complex pattern of inheritance suggests an involvement of a large number of susceptibility genes. The objective of the present study was to explore the genetic architecture of common IGE syndromes and to dissect out susceptibility loci predisposing to absence or myoclonic seizures. METHODS: Genome-wide linkage scans were performed in 126 IGE-multiplex families of European origin ascertained through a proband with idiopathic absence epilepsy or juvenile myoclonic epilepsy. Each family had at least two siblings affected by IGE. To search for seizure type-related susceptibility loci, linkage analyses were carried out in family subgroups segregating either typical absence seizures or myoclonic and generalized tonic-clonic seizures on awakening. RESULTS: Nonparametric linkage scans revealed evidence for complex and heterogeneous genetic architectures involving linkage signals at 5q34, 6p12, 11q13, 13q22-q31, and 19q13. The signal patterns differed in their composition, depending on the predominant seizure type in the families. CONCLUSIONS: Our results are consistent with heterogeneous configurations of susceptibility loci associated with different IGE subtypes. Genetic determinants on 11q13 and 13q22-q31 seem to predispose preferentially to absence seizures, whereas loci on 5q34, 6p12, and 19q13 confer susceptibility to myoclonic and generalized tonic-clonic seizures on awakening.

Chromosome Mapping↗
PubMed2005

Practical management issues for idiopathic generalized epilepsies.

The idiopathic generalized epilepsies (IGE) are a group of epilepsies that are genetically determined, have no structural or anatomic cause, and usually begin early in life. Neurologic examination, intelligence, and imaging studies are normal, and EEG shows only epileptiform abnormalities (i.e., no abnormal slow activity or evidence for diffuse encephalopathy). In some IGE, the genetic substrate has been identified, whereas in most, it remains unknown. Depending on the age at onset and predominant seizure type, individual subtypes of IGE (syndromes) are defined. However, overall, there are more similarities than there are differences among the various subtypes, and the IGE are best viewed as a spectrum or continuum of conditions. In general, IGE respond to treatment, with 80-90% becoming fully controlled. However, not all antiepileptic drugs (AED) are equally effective in IGE. Some AED are ill advised because they either do not work or exacerbate seizure types other than generalized tonic-clonic (GTC) seizures, that is, absence and myoclonic seizures. These include carbamazepine, oxcarbazepine, phenytoin, gabapentin, and tiagabine. Their use is the main cause of "pseudo-intractability," and at least in the United States where PHT and CBZ are the most commonly used AEDs, patients with IGE are often on inadequate medications. For patients with clear IGE, the drug of choice is generally valproic acid because it effectively controls absence myoclonic seizures and GTC seizures. Second-line drugs (when first-line drugs fail or are not tolerated) may include benzodiazepines, but the use of second-line drugs is evolving rapidly. Some of the newer AEDs are considered broad spectrum, meaning that they work in IGE and focal epilepsies, although the evidence is largely preliminary at this point. These newer AEDs include lamotrigine, topiramate, levetiracetam, and zonisamide.

Age Factors↗
PubMed1998

Severe idiopathic generalized epilepsy of infancy with generalized tonic-clonic seizures.

PURPOSE: While the literature on infantile epilepsies with minor and major seizures is extensive, little consideration has been given to infantile epilepsy with generalized tonic-clonic seizures (GTCS) alone. The aim of the present study was to analyze the data of a large group of patients and their families to obtain further insight into the clinical picture and pathogenesis of this type of epilepsy. METHODS: The 101 children (58 boys, 43 girls) met the following inclusion criteria: onset of the epilepsy with febrile or afebrile GTCS in the first 5 years of life, absence of primary organic brain lesion or progressive brain disease, severe course with frequent febrile and/or afebrile GTCS, failure of conventional anticonvulsive therapy. RESULTS: The epilepsy predominantly afflicts normally developed infants, boys and girls being about equally affected. The epilepsy begins with frequent febrile or afebrile GTCS, characteristically of long duration and often with alternating lateralization. In half of the cases additional myoclonic or myoclonic astatic seizures and/or absences occur. The initial GTCS phase is the same in epilepsies with and without minor seizures. Erratic myoclonias are especially characteristic. With advancing age, the symptomatology becomes increasingly polymorphic due to the occurrence of additional simple and complex focal and tonic seizures. Severe impairment of mental development soon after onset is a leading symptom. The overall death rate was 9%. Only 11% of the patients had been seizure-free for at least two years at final examination. The EEG was initially normal and subsequently exhibited diffuse 4-7/s rhythms, and only later spikes and waves of irregular shape (87%). Focal sharp waves occurred transiently in 26%. The family history and EEG of probands and relatives showed the pathogenesis to be decisively determined by genetic factors. CONCLUSION: Early infantile GTCS epilepsy represents a genetically determined (idiopathic) epileptic encephalopathy. It overlaps with other forms of early childhood epilepsy such as severe myoclonic epilepsy, severe type of myoclonic astatic epilepsy, as well as early childhood absence epilepsy with GTCS.

Age of Onset↗
PubMedDate not supplied

[Possible late-onset secondary generalized epilepsy. contribution of computed tomography (author's transl)].

Generalized tonic-clonic epileptic seizures appearing in elderly subjects have been recognized for a long time. The E.E.G. was able to distinguish two types: primary generalized epilepsy, and a secondary type of late onset which can be definitely separated from the group of partial epilepsies with generalized secondary fits by means of scanography. In fact, 60% of generalized attacks in the elderly are due to cerebral involution only. The authors suggest, therefore, that the group of secondary generalized epilepsies be enlarged to include this variety of late-onset generalized epilepsy, which appears to be related to the existence of diffuse cerebral lesions as shown by the cerebral atrophy demonstrated by the use of C.T. scan.

Aged↗
PubMed2002

Focal features in patients with idiopathic generalized epilepsy.

PURPOSE: The stringent dichotomy between focal and generalized epilepsies has become a contentious issue, since neuropathological studies as well as structural and functional imaging data hypothesized the existence of focal brain abnormalities in patients with well-documented idiopathic generalized epilepsy. The aim of our study was to investigate whether clinical and EEG features generally considered typical for a focal seizure disorder also occur in patients with generalized epilepsies to further support the hypothesis of a more continuous transition between focal and generalized epilepsies in contrast to the present concept of a stringent pathophysiologic dichotomy. METHODS: We retrospectively studied 20 consecutive patients with idiopathic generalized epilepsy who underwent video EEG monitoring either because of uncertainty of their epilepsy syndrome or because of a difficult to treat epilepsy. We determined the incidence of (a) focal interictal epileptiform discharges (IEDs), (b) intermittent temporal slow waves, and (c) clinical signs that are widely accepted as typical for a focal seizure onset, i.e. version, tonic/dystonic unilateral posturing, postictal hemiparesis, postictal nose wiping and figure of 4. RESULTS: Focal IEDs occurred in seven patients (35.0%), intermittent temporal slow waves in six (30%), and clinical signs pointing towards a focal seizure onset were found in seven patients (35%). CONCLUSION: Our study of EEG and clinical data supports the more sophisticated previous investigations in which structural and functional imaging as well as histopathological data suggested the presence of focal brain abnormalities in patients with 'generalized' epilepsies. Furthermore we emphasize the cautious use of isolated focal EEG abnormalities and certain clinical signs to prevent a premature diagnosis of focal epilepsy in patients who may indeed suffer from a generalized seizure disorder.

Age of Onset↗
PubMed2004

Idiopathic Generalized Epilepsy.

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.

Journal Article↗
PubMed2005

Idiopathic generalized epilepsies imitating focal epilepsies.

Classification of epileptic seizures and epilepsy syndromes as either focal or generalized is a fundamental and early part in the diagnostic process and is generally fairly easily accomplished. However, in patients with idiopathic generalized epilepsies, seizure and EEG features may suggest, particularly to the unwary, the occurrence of focal rather than generalized seizures. Misinterpretation of typical absence seizures as focal seizures, especially as temporal lobe seizures and of myoclonic seizures as focal clonic seizures, is a relatively common error and focal features during generalized tonic-clonic seizures may also be quite common. Sequences of seizures in idiopathic generalized epilepsies (such as absences or jerks followed by generalized tonic-clonic seizures) may also cause confusion. Versive and circling seizures are seizure types whose ictal semiology is clearly focal; nevertheless such seizures are described in idiopathic generalized epilepsies accompanied by generalized EEG discharges. The occurrence of focal EEG abnormalities in certain idiopathic generalized epilepsy syndromes is common. This is best known in juvenile myoclonic epilepsy.

Diagnosis, Differential↗
PubMed2004

Semiquantitative analysis of interictal glucose metabolism between generalized epilepsy and localization related epilepsy.

Positron emission tomography (PET) with [18F]fluoro-D-deoxyglucose (FDG) has been used to detect seizure foci and evaluate surgical resection with localization related epilepsies. However, few investigations have focused on generalized epilepsy in children. To reveal the pathophysiology of generalized epilepsy, we studied 11 patients with generalized epilepsy except West syndrome, and 11 patients with localization related epilepsy without organic disease. The FDG PET was performed by simultaneous emission and transmission scanning. We placed regions of interest (ROI) on bilateral frontal lobe, parietal lobe, occipital lobe, temporal lobe, basal ganglia, thalamus and cerebellum. Standardized uptake value (SUV) was measured and normalized to SUV of ipsilateral cerebellum. Then, we compared the data of generalized epilepsy to those of localization related epilepsy. FDG PET revealed significant interictal glucose hypometabolism in bilateral basal ganglia in generalized epilepsy compared to that in localization related epilepsy (right side: p = 0.0095, left side: p = 0.0256, Mann-Whitney test). No other region showed any significant difference (p > 0.05) between the two groups. These findings indicate that the basal ganglia is involved in the outbreak of generalized seizures or is affected secondarily by the epileptogenicity itself.

Adolescent↗
PubMed1996

Complex segregation analysis of non-myoclonic idiopathic generalized epilepsy in families ascertained from probands affected with idiopathic epilepsy with tonic-clonic seizures in Antioquia, Colombia.

In an attempt to identify the possible role of major genes, multifactorial inheritance, and cohort effects in the susceptibility to idiopathic epilepsy with generalized tonic-clonic seizures of the awakening type (GTCS), complex segregation analysis was performed in 196 nuclear families ascertained through affected probands with idiopathic epilepsy with GTCS belonging to the Paisa community of Antioquia (Colombia). Models postulating no transmission, single major locus (dominant and recessive) only, and multifactorial component only, were rejected. Since the codominant single major locus model could not be rejected and models that assign no major locus to transmission, no polygenic component to transmission, and no transmission of the major effect were rejected, complex segregation analysis suggested that a major autosomal codominant allele together with a multifactorial component (mixed model) best explained clustering of idiopathic epilepsy with GTCS in families of the Paisa community. The deficit of transmission of heterozygotes (0.17) is compatible with the existence of epistasis acting on a major gene whose frequency was estimated to be 0.0211. Its transmission variance accounts for 81% of the susceptibility to idiopathic epilepsy with GTCS. The complementary variance (19%) is due to the polygenic component.

Alleles↗
PubMed2004

Ictal head version in generalized epilepsy.

Focal physical signs may occur with generalized seizures. The authors retrospectively reviewed video-EEG studies of 20 patients with apparent primary generalized epilepsy to assess the frequency of head version during generalized tonic-clonic seizures. Five patients (25%) demonstrated forced head version, including two with turning to the right and left on consecutive seizures. Forced head turning can occur in generalized epilepsy and may not necessarily indicate focal seizure origin.

Adolescent↗
PubMed1998

Idiopathic generalized epilepsy of late onset.

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.

Age of Onset↗
PubMed2001

[Are idiopathic generalized epilepsies of childhood really benign?].

Most of the idiopathic generalized epilepsies are considered as benign in childhood. Using literature data and some personal investigations, we screened the cognitive impairment and school difficulties observed in children with idiopathic generalized epilepsies, especially absence epilepsies, myoclonic epilepsies considered as non-severe, and generalized epilepsies with tonico-clonic seizures. In a controlled study concerning typical absence epilepsy, we have shown a lack of high or moderately elevated level of non-verbal and total IQ scores on Wechsler's tests (WISC III); we also observed a significant impairment of memory, a lengthening of school realisations, concerning motor skills and alertness and also hyperactivity and/or attention disorders, concerning 35 to 50% of cases. Most of these children present with school difficulties, of variable degree. These results show that the term "benign" is not appropriate in many cases of so-called benign idiopathic generalized epilepsies.

Adolescent↗
PubMed2005

Brain imaging in idiopathic generalized epilepsies.

While it is generally accepted that there is no neuroimaging abnormality in idiopathic generalized epilepsy (IGE), image processing and quantitative magnetic resonance imaging (MRI) studies suggest that there may be subtle structural abnormalities. Magnetic resonance spectroscopy indicates neuronal dysfunction with differing abnormalities in the IGE subsyndromes, and high concentrations of glutamate and glutamine have been inferred in the frontal lobes, and low gamma-aminobutyric acid levels in the occipital lobe. Studies of cerebral blood distribution at the time of absences have given complex results. The general consensus is of an increase in the thalamus and broad decreases in the neocortex, reflecting a suppression of neuronal activity, but with some increases, that may indicate focal areas of activation. Positron emission tomography (PET) ligand studies with an opioid tracer have inferred neocortical release of endogenous opioids at the time of serial absences. In combination with neurophysiological methods, PET studies with specific ligands have the potential to clarify the functional anatomy and neurochemical circuits that underlie IGE.

Brain↗
PubMed1997

Idiopathic generalized epilepsies with typical absences.

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.

Adolescent↗