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PubMedDate not supplied

[Generalized epilepsy disclosing medium-chain-acyl-CoA dehydrogenase deficiency].

BACKGROUND: Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency is the most common inherited defect of fatty acid beta-oxidation. As it causes life-threatening symptoms, it is mandatory to diagnose deficiencies of this enzyme in families. CASE REPORT: A boy was admitted at the age of 3 months because of a recent attack of generalized seizures. His parents were second cousins and one of his 2 sisters, 6 years old, suffered from epilepsy. At admission, the patient had moderate hepatomegaly; he was given clonazepam and phenytoin because of persistent status epilepticus. He developed a fever (temp.: 39 degrees) and a rash 24 hours later. A viral etiology was suggested by CSF contents of 104 cells/mm3 and 1 g/l protein. The patient was given aciclovir. Blood glucose, transaminases, ammonia, lactate, pyruvate and amino acids levels were normal. Analysis of urine by GC-MS revealed a large lactate peak and dicarboxylic acids, unsaturated dicarboxylic acids, hydroxyhexanoate, 7-hydroxyoctanoate, hexanoylglycine and suberylglycine. This profile indicated a MCAD deficiency. The plasma contained partially oxidized medium-chain fatty acids, such as octanoic acid and especially 4-decenoic acid. the diagnosis was confirmed by a phenylpropionate loading test and specific enzyme assay in fibroblasts. Molecular studies identified a G 985 mutation in the patient and revealed that the parents were heterozygotes for the mutation. The condition of the patient at the age of 18 months is excellent; he has a regular, adequate caloric intake and avoids fasting. He has not taken anti-epileptic drugs for the past 6 months. CONCLUSION: There is no typical clinical presentation of MCAD-deficiency; the most frequent features are vomiting and lethargy. Episodic hypoglycemia has been reported, but hypoglycemia was not found in our patient. Molecular studies will allow neonatal diagnosis of the next affected siblings.

Acyl-CoA Dehydrogenase↗
PubMed1981

Anticonvulsant properties of two new 3,3-diethyl-2,4-pyridinedione derivatives. I. Effects in two experimental models of generalized epilepsy in cats.

The anticonvulsant properties of two N-aminomethyl derivatives of 3,3-diethyl-2,4-pyridinedione (persedon) are studied on two experimental models of generalized (pentylenetetrazol and penicillin) epilepsy in cats. N-aminomethylmorpholine 3,3-diethyl-2,4-pyridinedione (DKMM) applied in doses of 100 mg/ng i. v. in cases of pentylenetetrazol epilepsy leads to a rise in the convulsive thresholds (n, N) by 1.5 and two times, respectively. Administration of the drug in the same dose on developed penicillin epilepsy in cats reveals slight to moderate suppression of the generalized paroxysms, lasting until the 90th-120th min. N-aminomethylpiperazine 3,3-diethyl-2,4-pyridinedione (DKMP), injected in a dose of 100 mg/kg i. v., raises the pentylenetetrazol threshold ("n") 3.5 to 4 times and 8-10 times the N-threshold, approaching the effect of diazepam (10 mg/kg i. v.). On the background of injected DKMP it is difficult to attain epileptic status, and in the case of developed epileptic status DKMP in a dose of 50 mg/kg suppresses completely the seizure manifestations. Injection of DKMP in the cases of developed penicillin epilepsy results in complete suppression of the generalized paroxysmal activity, lasting until the 100th-120th min.

Animals↗
PubMed2000

Primary Generalized Epilepsies.

For pure childhood absence epilepsy (CAE), ethosuximide (ESM) remains the drug of first choice. Although valproic acid (VPA) is of equal efficacy, it is more toxic, and is reserved for those patients with accompanying convulsions. Lamotrigine (LTG) is effective as both add-on and monotherapy for CAE. If any of these three drugs fails, one of the other two can be used as monotherapy. Rarely, when ESM, VPA, or LTG does not effectively control CAE, phenytoin (PHT), primidone (PRM), and phenobarbital (PB) may be partially effective, although carbamazepine (CBZ) may worsen absence seizures. Experience is limited with the newer AEDs. Tiagabine (TGB) may induce absence status epilepticus in PGE. Oxcarbazepine (OXC) and vigabatrin (VGB) may worsen absence seizures. Felbamate (FBM) is probably effective, but is potentially fatal. Lifelong therapy is not anticipated. For juvenile absence epilepsy (JAE), VPA is the drug of first choice. LTG is also of proven efficacy. The risks of VPA-induced teratogenicity (possibly lessened by the concurrent use of folic acid) and weight gain are potentially unacceptable in young women of childbearing age. Not enough data exists on the safety of LTG in pregnancy. A combination of VPA and LTG can be used if either drug alone is unsuccessful. For juvenile myoclonic epilepsy (JME), VPA is the traditional drug of first choice in most patients. As in JAE, side effects may make VPA an unacceptable choice in many patients, especially young women. In clinical practice, TPM is being increasingly used as monotherapy for JME. Many patients appreciate the accompanying weight loss seen with TPM, but it has potentially troubling side effects, has not been well studied as monotherapy for JME, and its safety in pregnancy has yet to be confirmed. PHT and CBZ may worsen myoclonus when used alone, but they may have a role as add-on treatment to VPA, LTG, or TPM, especially when generalized tonic-clonic seizures (GTCSs) are not controlled. PB and PRM may also be useful as add-on treatment, but often have unacceptable side effects. Clonazepam may be useful as adjunctive treatment for resistant myoclonic jerks. OXC and VGB both worsen myoclonic seizures. GBP is not useful in JME and can make seizures worse. The efficacy of FBM and TGB in JME is largely unknown. Lifelong AED therapy is necessary. In epilepsy with generalized tonic-clonic seizure (GTCS) on awakening (EGA), VPA is the drug of choice, especially if other seizure types (absence and myoclonic) are present. If only GTCSs are present, then PB, PHT, and CBZ may be as effective as VPA; however, the use of PHT and CBZ may "unearth" other seizure types (absence and myoclonic) in those patients with EGA, although PB is poorly tolerated. As for JME, LTG, and TPM may both be effective monotherapy for EGA, although the use of other AEDs in EGA has not been well studied. Lifelong AED treatment is necessary.

Journal Article↗
PubMed1990

Sleep and sleep deprived EEG in partial and generalized epilepsy.

Sleep and sleep deprivation are often used for EEG activation in epilepsy. We compared postprandial naps and day-long sleep deprived EEGs in 36 patients with generalized seizures, 57 complex partial seizure patients, and 7 individuals with mixed seizure disorders. Ten of 36 generalized seizure patients had normal sleep and sleep deprived EEGs, while both were normal in 16 of 57 partial seizure patients. Both were abnormal in 18 of 36 generalized and 22 of 57 partial epileptics. Seven generalized seizure patients had epileptiform discharges or seizures during afternoon naps but normal sleep deprived EEGs. No partial seizure patients had normal sleep deprived EEGs and abnormal nap, but 29 of 57 had abnormalities or seizures only with sleep deprivation. All 7 mixed seizure patients had abnormal sleep and sleep deprived studies, and 6 had seizures, 4 on both studies. Natural sleep may facilitate the appearance of generalized seizures or epilepti-form discharges, while sleep deprivation may accentuate the yield of EEG abnormality in partial epilepsy. Either is likely to be abnormal in patients with mixed seizures and encephalopathy. Natural sleep and sleep deprived EEGs are an appropriate combination in the evaluation of refractory seizures.

Adolescent↗
PubMed1989

[Spectrum analysis of the EEG in children and adolescents with epilepsy: general characteristics and pathophysiological interpretation of the data].

Spectral EEG analysis (fast Fourier transform) was performed in 48 patients with epilepsy, 4 patients after one epileptic seizure, 12 sibs of epileptic patients, 18 children with febrile convulsions, 18 patients with vasoautonomic dystonia, and 23 normal children. Means, standard deviations, standard errors of the means were calculated for the spectra. A distinct EEG type was found characteristic of the epileptic patients: power increase by the factor of 5 to 10 as compared to normals, predominantly in theta band. This EEG type was shared by epileptic patients and their sibs. Both had peculiar patterns on hyperventilation.

Adolescent↗
PubMed1979

Carbamazepine vs phenytoin. A controlled clinical trial in focal motor and generalized epilepsy.

The antiepileptic effects of carbamazepine and phenytoin were compared in a double-blind crossover trial studying patients with primary and secondary generalized seizures and partial seizures with motor symptoms. Each treatment period lasted ten weeks. The patients were seen every two weeks, and doses were adjusted according to plasma levels. It was attempted to keep levels in the optimal plasma range, ie, 10 to 20 and 4 to 10 mg/liter for phenytoin and carbamazepine, respectively. Twenty-three patients entered and 19 completed the study. No statistically significant differences were found between carbamazepine and phenytoin with regard to seizure control and acute side effects.

Adolescent↗
PubMed1988

Generalized epilepsy in childhood: some notes from a developmental perspective.

Efforts to establish more detailed classification of childhood epilepsy have increased our knowledge in this field, but have also led to a tendency of excessive subdivision, especially in generalized forms. This paper emphasizes the need for the reconsideration of a number of basic factors that favour a more unitary physiopathogenetic and clinical interpretation: 1) the electroclinical pattern is age-related; 2) the electroclinical paroxysmal expressiveness is greatest in childhood; 3) two types of manifestations can be distinguished in the process of spread and generalization (a benzodiazepine-sensitive complex associated with a more regular and organized EEG pattern, and a corticotropin-sensitive complex associated with an irregular, unorganized EEG pattern).

Brain↗
PubMed1982

"Central" commissurotomy for intractable generalized epilepsy: series two.

A second consecutive series of 12 patients underwent microsurgical "central" commissurotomy (division of the entire corpus callosum and hippocampal commissure) for the relief of previously intractable generalized seizures. This modified operation was found to be safer than the multiple commissurotomies performed in the first series of eight patients and was equally effective. Central commissurotomy was modified further by being performed in two stages, which reduced the length and severity of the "acute disconnection syndrome," a common cause of morbidity in the early postoperative phase. Best results were obtained in patients who were not severely retarded, had signs of unilateral cerebral damage, and included akinetic spells as a prominent form of their generalized seizures. EEG showed that bilateral symmetric discharge became either unilateral or asymmetric after surgery, which emphasized the important role played by the corpus callosum in conducting seizure discharges from one hemisphere to the other.

Adolescent↗
PubMed1988

Interictal temporal lobe epileptiform discharges and their relationship to secondarily generalized epilepsy.

In a previous study of epileptic phenomena in 19 patients with partial complex seizures, it was noted that seizures of left temporal lobe origin had a higher incidence of secondary generalization. To evaluate this observation further, we retrospectively reviewed reports of EEGs for evidence of focal interictal epileptiform discharges (FIED) of temporal lobe origin and correlated this finding with seizure type. Of 3,276 EEG reports reviewed, 195 showed FIED. The medical records of these patients were reviewed and 79 had sufficient information therein to enable seizure classification. Of 79 patients, 61 had secondary generalized seizures, 45 with left temporal FIED, 16 with right FIED. Of 79 patients, 18 had partial seizures, 13 with right temporal FIED, 5 with left FIED (p less than 0.001). These findings suggest that seizures of left temporal lobe origin may have a higher incidence of secondary generalization. The significance of this observation and its relevance to medical and surgical treatment of complex partial seizures is discussed.

Adolescent↗
PubMedDate not supplied

Orienting reaction in therapy-resistant generalized epilepsy.

A polygraphic study of the somatic, autonomic and EEG components of the orienting reaction elicited by an auditory stimulus was performed in 39 epileptics with therapy-resistant generalized seizures (TRGS) and in 119 matched subjects in two control groups. The study showed a significant interictal hyperresponsivity in epileptics with TRGS vs. the normal subjects of control group I, which consisted in a marked increase of the intensity of the orienting reaction components. This hyperresponsivity was also more marked than that noted in epileptics with therapy-controlled generalized seizures of control group II. The correlation analysis of data showed that the severity of these responsiveness disturbances in epileptics with TRGS depended on the patients' age, type of electroclinical seizures, pretrial seizure frequency, type of resting EEG, administered treatment (no. of administered antiepileptic drugs/patient), daily dose, as well as on the serum level of these drugs. The multivariate regression analysis showed that the most significant predictive variables for the responsiveness disturbances were the pretrial seizure frequency, type of electroclinical seizures, daily dose of administered antiepileptic drugs and their serum level. The data also evidenced that the antiepileptic treatment improves the interictal responsiveness disturbances, the effect being the more marked as the treatment was more sustained. The above-mentioned responsiveness changes in epileptics with TRGS should be ascribed to some disturbances in nervous excitability.

Adolescent↗
PubMed1983

Generalized epilepsy evoked by freeze lesions in the mesencephalon of the cat.

Epilepsy was induced by making freeze lesions bilaterally in the mesencephalic reticular formation of cats. The convulsive activity was an equivalent of the generalized status epilepticus, devaloping 15-20 min after the freeze lesions had been made. The animals died in this state 16-20 h after it had developed. The generalized seizure activity may have spread to rostra1 structures from the lesioned mesencephalic reticular formation generalizing instantenously, or have been triggered and maintained by a local irritative zone, surrounding the necrotized tissue caused by freezing. The cooling of the same cryoprobes, by which the freeze lesions had been made, had no effect on the status epilepticus, probably because only the necrotized tissue was cooled. The cooling of the inferior thalamic peduncles changed the pattern of epileptic discharges, indicating that thalamocortical structures played a role in sustaining it.

Animals↗
PubMed1984

Generalized epilepsy induced by kainic acid and anticonvulsant effect of N-aminomethylpiperazine-3,3-diethyl-2,4-pyridinedione.

Systemic administration of kainic acid in rats (30 mg/kg s.c.) and cats (5 mg/kg i.p.) produced after a definite period (30 to 60 min) secondary generalized seizures occurring first in the limbic structures (amygdala and hippocampus). The effect of N-aminomethylpiperazine-3,3-diethyl-2,4-pyridinedione (DKMP) at a dose of 100 mg/kg i.v. was evaluated on the background of developed kainic epilepsy. In rats, DKMP inhibited kainic clonic and tonic seizures and 100% of the animals survived. The drug was ineffective against limbic seizures. In cats, DKMP strongly suppressed the cortical EEG paroxysmal activity and slightly influenced the limbic one. The present data contribute to the knowledge of the anticonvulsive activity of DKMP, showing it to be a promising antiepileptic drug with mainly cortical action.

Animals↗
PubMed1981

Effects of PTZ-induced generalized epilepsy on intestinal activity in cats.

Simultaneous recordings of the EEG, the electromyogram of the small intestine, the electrocardiogram, and femoral arterial pressure were monitored in 24 cats anesthetized with halothane, immobilized with gallamine, and artificially respirated. During pentylenetetrazol-induced generalized seizures, intestinal activity was blocked, as demonstrated by the disappearance of spikes from the EMG. This block was abolished by spinal cord section at C1-C2 level and partially abolished by bilateral adrenalectomy. These results demonstrate the existence of inhibitory sympathetic mechanisms during generalized experimental seizures.

Adrenalectomy↗
PubMed1994

Dexmedetomidine decreases seizure threshold in a rat model of experimental generalized epilepsy.

BACKGROUND: Dexmedetomidine (DEX) is a highly selective alpha 2 agonist with marked sedative and analgesic properties thought to be mediated via reduction of central noradrenergic transmission. Because an anticonvulsant effect is associated with increased noradrenergic activity, we investigated the possible proconvulsant effects of DEX in an experimental model of generalized seizures. METHODS: Male rats (n = 82) were administered 0.9% saline as placebo (n = 18) or pretreatment drug(s) before initiation of an infusion of pentylenetetrazol (PTZ) at 5.5 mg.kg-1.min-1. The total dose of PTZ required to elicit electroencephalographic (EEG) and behavioral seizure activity was assessed. Blood samples were obtained 15 min after initiation of infusion (82.5 mg/kg) for determination of serum PTZ concentrations by gas chromatography. Pretreatment drug groups included DEX (20 micrograms/kg [n = 11], 100 micrograms/kg [n = 14], and 500 micrograms/kg [n = 10]); L-medetomidine (500 micrograms/kg [n = 7]); the alpha 2 antagonist atipamezole (500 micrograms/kg [n = 9]); and atipamezole (500 micrograms/kg) before DEX (100 micrograms/kg [n = 7] and 500 micrograms/kg [n = 6]). RESULTS: In control animals, PTZ 25-35 mg/kg induced EEG evidence of epileptiform activity. The mean dose to EEG epileptiform activity and clonic convulsions was 30 +/- 5.8 (SE) and 59 +/- 3.2 mg/kg, respectively. Infusion of DEX at 100 and 500 micrograms/kg resulted in a marked sedative response and reduced the EEG seizure threshold of PTZ to 18 +/- 1.5 and 7 +/- 1.8 mg/kg, respectively (P < 0.05 at both doses). The clonic convulsant threshold also was significantly decreased in both groups, to 37 +/- 3.2 and 28 +/- 2.3 mg/kg (P < 0.01 at each dose). Before clonic convulsion, a significantly greater number of motor seizure manifestations were scored in the DEX-treated animals at all three dose levels compared with the number scored in control animals. The proconvulsant action of DEX was not a result of alteration of PTZ kinetics, because serum concentrations did not differ between control and DEX-treated animals. Animals treated with L-medetomidine demonstrated more paroxysmal motor phenomena before clonic seizures than controls (P < 0.01) although the clonic seizure threshold was not altered. Atipamezole alone did not alter background EEG, nor did it affect the clonic convulsant threshold. Atipamezole did, however, block the proconvulsant behavioral action at both doses of DEX, raising clonic seizure threshold from 37 +/- 3.2 to 59 +/- 5.8 mg/kg (100 micrograms/kg DEX, P < 0.05) and from 28 +/- 2.3 to 59 +/- 6.9 mg/kg (500 micrograms/kg DEX, P < 0.01). CONCLUSIONS: DEX exerted a significant proconvulsant action in the PTZ experimental seizure model. The pharmacodynamic effect was dose-dependent and stereospecific and was blocked by the selective alpha 2-receptor antagonist atipamezole. These data are consistent with previous data demonstrating that inhibition of central noradrenergic transmission facilitates seizure expression. Further evaluation of DEX for possible clinical proconvulsant effects may be warranted.

Adrenergic alpha-Agonists↗