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PubMedDate not supplied

Primary generalized seizure disorder: correlation of epileptiform discharges with seizure frequency.

The role of routine follow-up EEG in assessment of severity of a seizure disorder is not known. This retrospective chart review study of patients with primary generalized seizure disorders explored the relation between parameters of epileptiform discharge bursts on EEG and number of seizures experienced in the preceding months. Eighty-seven such patients were found, each with one to seven EEGs and corresponding clinical records, comprising a total of 201 clinicoelectrographic epochs. The 56 chronically attending patients (more than two attendances) differed from the 31 nonchronic attenders in receiving more antiepileptic drugs (AEDs) and having fewer EEG polyspikes; otherwise, the two groups were similar and were analyzed together. We noted a strong relation between number and maximum length of epileptiform bursts in the resting EEG record and number of absence seizures reported in the months preceding the EEG. Age did not affect this relation. After stepdown regression analysis, only the maximum length of epileptiform bursts remained significantly related to the reported number of absence seizures. These findings may prove useful in assessing clinical progress, e.g., in patients whose ability to estimate numbers of attacks is suspect. Neither number nor maximum length of epileptiform bursts in the resting EEG record had a significant relation with the number of generalized tonic-clonic seizures. Presence of polyspikes on resting or "activated" EEG had no added predictive value. The presence of epileptiform bursts after activation by sleep, hyperventilation, or photic stimulation was not associated with an increased likelihood of having had seizures.

Adolescent↗
PubMed1994

[Absence seizures in adulthood: four cases].

We present four patients between 40 and 60 years of age with irregular control of seizures in adulthood, with a mean duration of history of 44 years and the following characteristics in common; a) history of childhood absence seizures beginning between age 4 and 7; b) appearance of generalized tonic-clonic seizures during adolescence; and c) persistence of typical absence seizures upon awakening during adulthood, manifested as "clumsiness during the first half hour after awakening". Waking and sleeping EEG polygraphs were done on all patients, including the first half hour after awakening, confirming the presence of generalized polyspike/wave during non-REM sleep and generalized spike/wave periods accompanied by simultaneous loss of consciousness, or intermittent slow generalized polyspike/wave accompanied by bradypsychia. We comment on the usefulness of valproic acid alone or in combination with ethosuximide in the treatment of these patients.

Adult↗
PubMed1996

Basic mechanisms of seizure expression.

While there are many types of seizures, our understanding of their pathophysiology is limited to a few types. On the basis of the behavior of neurons during a seizure, two fundamental types of paroxysms are recognized--spike-wave electrographic seizures and tonic-clonic electrographic seizures. When the former type of paroxysm takes place throughout the forebrain, an absence seizure ensues. When the latter type of paroxysm takes place within a limited set of neurons, a simple partial or complex partial seizure takes place, depending on the functional anatomy. When the latter type of paroxysm takes place throughout the forebrain, a generalized convulsion takes place. The basic cellular and synaptic processes that underlie electrographic spike-wave and tonic-clonic paroxysms are complex and dissimilar between the two types of discharges. This paper reviews these multiple processes. The diverse pathophysiological mechanisms presented provide a theoretical substrate for rational polypharmacy directed to seizure suppression.

Animals↗
PubMed1980

Clinical efficacy and long-term effects of valproic acid therapy on spike-and-wave discharges.

Twenty-two patients with absence seizures and other seizure types were treated with valproic acid and followed up for 1 year. Results were excellent with more than 75% improvement in 80% of patients with absence seizures, in 40% of those with tonic-clonic seizures, in all of those with myoclonic seizures, and in 43% of those with partial seizures. Fifty-seven percent of the patients had more than a 75% reduction in the total number of paroxysmal spike-wave discharges, and 62% had more than a 75% reduction in the number of spike-wave discharges lasting longer than 3 seconds. Photosensitivity and activation by hyperventilation decreased. More patients achieved good EEG control in 1 year than in 10 weeks.

Clinical Trials as Topic↗
PubMed1987

Serum valproate concentrations in epileptic children with favourable responses.

The lower limits of the "therapeutic range" for serum levels of sodium valproate (VPA) were evaluated in epileptic children showing a benign clinical course. Twenty-five outpatients, aged 5 to 16 years, whose seizures were well controlled over three years with VPA alone, were studied. Venous blood was taken 1.1 to 5 hrs after the morning dose. Serum VPA concentrations at steady-state after receiving the maintenance doses to control seizures were determined by enzyme immunoassay. The patients were divided into three groups according to the seizure type and the age at onset; A and B: patients with tonic and/or clonic seizures, aged below 3 yrs (n = 11) and 3 to 11 yrs (n = 6), respectively, C: those with absence seizures, aged 4 to 11 yrs (n = 8). The serum concentrations in A (47.8 +/- 21.6 micrograms/ml, mean +/- SD) were significantly (p less than 0.02) lower than those in groups B and C (85.2 +/- 14.0 and 73.0 +/- 17.4 micrograms/ml, respectively). VPA concentrations below 50 micrograms/ml were seen in 6 patients (55%) in group A. It was concluded that many epileptic children, whose ages at onset were below 3 yrs, with tonic and/or clonic seizures could be controlled even with low initial serum concentrations below the "therapeutic range".

Adolescent↗
PubMed1999

[A successful treatment with intravenous lidocaine followed by oral mexiletine in a patient with Lennox-Gastaut syndrome].

Clusters of atypical absence, myoclonic seizures and tonic seizures developed in a thirteen-year-old boy with Lennox-Gastaut syndrome. As conventional antiepileptic drugs failed to eliminate the seizures, we treated the patient with continuous intravenous lidocaine (4 mg/kg/hr). The treatment reduced the duration of paroxysmal discharges (spike-wave complexes and rapid rhythm) from 3 sec/min to 0.7 sec/min, monitored by EEG. Oral mexiletine (5.4 mg/kg/day) following the lidocaine treatment has maintained good seizure control for two years with no adverse effects, and improved his behavioral problem. The treatment with lidocaine followed by mexiletine was useful for controlling clusters of intractable seizures.

Administration, Oral↗
PubMed1976

Clonazepam. A review of a new anticonvulsant drug.

Clonazepam is a new benzodiazepine anticonvulsant recently approved by the Food and Drug Administration for the treatment of typical absence, infantile myoclonic, atypical absence, myoclonic, and akinetic seizures. It is rapidly absorbed by the oral route and appears to pass quickly from blood to brain. Preliminary results indicate a biological half-life of 22 to 32 hours and a therapeutic serum concentration of 5 to 50 ng/ml. Many studies report tolerance to the anticonvulsant effects with chronic administration. Major side effects of the drug are drowsiness, ataxia, and behavior changes. They tend to be dose related, occur early in the course of therapy, and may subside with chronic administration. Accordingly, the dosage is begun at a low level and increased slowly.

Adult↗
PubMed1980

Uncontrollable cases of absence.

Forty-three cases of absence seizure were studied from the viewpoint of prognosis. thirty-three had been seizure-free for at least one year until the time of follow-up. The remaining 10 cases were uncontrollable and their plasma levels of the drugs were measured. The following characteristics were more significantly found in the uncontrollable group: (1) late onset (14 years old or later) (2) preceding grand mal seizures (3) accompanying automatisms. The above three factors were found to be interrelated. (4) concomitant grand mal seizures of sleep or diffuse (other than awakening) type (5) psychological disturbances (low intelligence, circuitous character) and (6) chronological shift to the Lennox-Gastaut syndrome.

Adolescent↗
PubMed2002

Lack of neuronal damage in atypical absence status epilepticus.

PURPOSE: Whether status epilepticus of nonconvulsive epileptic seizures is harmful still remains controversial. To investigate this, the presence and/or extent of neuronal damage in patients with absence status epilepticus (ASE) and patients with complex partial status epilepticus (CPSE) was examined and compared. METHODS: Neuron-specific enolase (NSE) in CSF was examined in the patients with ASE and compared with that of the patients having CPSE. Clinical aspects of these patients also were investigated. RESULTS: CSF NSE levels in ASE patients were lower than those of CPSE patients and were considered as the normal values. No clinical symptoms indicated neuronal damage in the ASE patients. CONCLUSIONS: This study suggests that ASE does not induce neuronal damage. Serum NSE is not always correlated to CSF NSE, and determination of serum NSE levels may be an inappropriate method of estimating neuronal damage in some cases of ASE.

Adolescent↗
PubMed2001

Frontal absences in children.

In a cohort of 59 consecutive children referred for staring spells, we analysed clinical and electroencephalogram (EEG) characteristics in 23 children with both a history of absence seizures and a generalized spike and wave pattern during long-term video EEG monitoring. In 10 children, a frontal spike preceded the generalized spike and wave pattern. In the remaining 13 children, primary generalized spikes and waves were found. The frontal onset absences were clinically not different from primary generalized absences. The most striking difference between the two groups was the difficulty in controlling the absences in the frontal onset group and the high incidence of learning and behavioural problems in that group. The EEG analysis showed interictal, isolated epileptic discharges in 80% of the children with frontal onset absences. We believe that frontal onset absences should be considered as a secondarily generalized epilepsy syndrome, originating in the frontal regions.

Child↗
PubMed2004

Laforin preferentially binds the neurotoxic starch-like polyglucosans, which form in its absence in progressive myoclonus epilepsy.

Lafora disease (LD) is a fatal and the most common form of adolescent-onset progressive epilepsy. Fulminant endoplasmic reticulum (ER)-associated depositions of starch-like long-stranded, poorly branched glycogen molecules [known as polyglucosans, which accumulate to form Lafora bodies (LBs)] are seen in neuronal perikarya and dendrites, liver, skeletal muscle and heart. The disease is caused by loss of function of the laforin dual-specificity phosphatase or the malin E3 ubiquitin ligase. Towards understanding the pathogenesis of polyglucosans in LD, we generated a transgenic mouse overexpressing inactivated laforin to trap normal laforin's unknown substrate. The trap was successful and LBs formed in liver, muscle, neuronal perikarya and dendrites. Using immunogold electron microscopy, we show that laforin is found in close proximity to the ER surrounding the polyglucosan accumulations. In neurons, it compartmentalizes to perikaryon and dendrites and not to axons. Importantly, it binds polyglucosans, establishing for the first time a direct association between the disease-defining storage product and disease protein. It preferentially binds polyglucosans over glycogen in vivo and starch over glycogen in vitro, suggesting that laforin's role begins after the appearance of polyglucosans and that the laforin pathway is involved in monitoring for and then preventing the formation of polyglucosans. In addition, we show that the laforin interacting protein, EPM2AIP1, also localizes on the polyglucosan masses, and we confirm laforin's intense binding to LBs in human LD biopsy material.

Actins↗
PubMedDate not supplied

Absence of temporal lobe epilepsy pathology in dogs with medically intractable epilepsy.

Epilepsy is a common neurological problem in dogs. In some dogs, seizures cannot be controlled adequately with anticonvulsant medication. Temporal lobe epilepsy is the most common type of epilepsy in adult humans, it is frequently resistant to anticonvulsant therapy, and it is commonly associated with characteristic neuropathological abnormalities in the hippocampal dentate gyrus. We sought to test the hypothesis that dogs with medically intractable epilepsy have temporal lobe epilepsy. The hippocampi of 6 dogs that were euthanized because of chronic, recurrent seizures were compared with those of 8 nonepileptic controls. In control and epileptic dogs, stereological cell counting showed similar numbers of neurons in the hilus of the dentate gyrus, somatostatin immunoreactivity identified numerous immunopositive neurons in the hilus, and Timm staining showed the normal pattern of granule cell axon projections. These findings demonstrate a lack of hilar neuron loss and granule cell axon reorganization, suggesting that temporal lobe epilepsy is not a common cause of medically intractable epilepsy in dogs.

Animals↗
PubMed1978

Valproic acid (Depakene). A new anticonvulsant agent.

Valproic acid, a new anticonvulsant, is most effective in absence seizures (simple and complex), but it has produced improvement in tonicclonic seizures, mixed absence with tonic-clonic seizures, and myoclonic epilepsy. It is useful alone or as an adjunct to other anticonvulsants and may allow the dosage of the latter to be reduced. Some patients who are refractory to other anticonvulsants may respond to valproic acid. Adverse reactions occur in about 20% of patients. Gastrointestinal disturbances and drowsiness (usually noted when valproic acid is given with other anticonvulsants) are the most common reactions; hair loss is observed less frequently. Untoward effects are usually transient and do not require discontinuation of use of the drug.

Animals↗