Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this report 52 patients meeting the criteria of centrencephalic myoclonic-astatic petit mal (10) at the beginning of petit mal are included. The results of clinical and encephalographic follow-up examinations are as follows: 1) The type reported here apparently has a petit mal course with peculiar characteristics, it therefore must be separated from Lennox syndrome: centrencephalic myoclonicastatic petit mal, pyknolepsia, bilateral myoclonus (impulsive petit mal). It should file under generalized primary petit mal epilepsy. 2) It is primarily defined by its EEG marker: "centrencephalic" EEG pattern (irregular and/or regular spike-wave groups, photosensibility and abnormal theta- and/or delta-rhythm). Rarely (33%) minor cerebral organic lesions as additional pathogenetic factors are uncovered by clinical and electroencephalographic examinations. 3) The clinical picture is characterized, aside from myoclonic and/or astatic seizures, by frequent absences (80%), rare tonic seizures (6%), petit mal status (25%) and mostly generalized grand mal seizures (62%). 4) There are changes of the course of the disease to Lennox syndrome (N = 6) in in children suffering from marked cerebral organic lesions at the onset of petit mal and in development of severe epilepsy. 5) Least favorite markers with respect to prognosis are concomitant grand mal seizures (p = 0,05), petit mal status (p = 0.008), additional 2/sec spike wave-pattern (spike wave Variant) in the EEG (p = 0.002) and previous seizures with focal signs. Favourite outcome of epilepsy are frequently connected to missing cerebral organic lesions (p = 0.05).
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PMID:[Centrencephalic myoclonic-astatic petit mal. Clinical and electroencephalographic long-term follow-up study in 52 patients (author's transl)]. 9 76

The mechanisms of petit mal epilepsy remain a mystery despite successful therapy. Previous workers have proposed that paroxysmal activity of cortical inhibitory systems plays a role in absence seizures. In this study, we have compared the effects of bicuculline, a potent convulsive agent and GABA antagonist, with ethosuximide, a drug used to treat petit mal epilepsy, on the thalamocortical motor system of the cat. Under chloralose anesthesia, sequential pairs of pulses were delivered to ventrolateral thalamus (VL) varying either pulse amplitude or interval. The evoked responses were recorded from sensorimotor cortex, analyzed on-line by computer, and plotted as an excitability curve (mean response amplitude as a function of pulse interval), or a family of threshold curves (mean response amplitude as a function of stimulus amplitude at various fixed intervals). Administration of each drug resulted in increased thalamocortical excitability and decreased threshold to stimulation for short pulse-pair intervals, with diminished duration of the excitability curve. Increased alertness was produced by both drugs. Studies with grand mal anticonvulsants demonstrated entirely different effects. Because GABA is thought to be the primary inhibitory transmitter in VL and cerebral cortex, bicuculline would be expected to result in disinhibition. The similarity of the data for ethosuximide suggests that ethosuximide also suppresses inhibition in the thalamocortical motor system and adds further to the accumulating evidence of the role of inhibitory system in petit mal epilepsy.
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PMID:Ethosuximide and bicuculline inhibition in petit mal epilepsy. 9 76

Dipropylacetate (DPA) was used in the treatment of different types of epilepsy in 112 children aged 1--20 years, with a mean age of 9.2 years, for a period of 19.8 months, ranging from 1 to 49 months. Of this group, 64 children were therapy-resistant to other antiepileptic medications prior to the introduction of DPA; 31 were treated for the first time with an antiepileptic drug, which was DPA; 44 were treated with DPA alone; and 68 had one or more additional antiepileptic medication. The following results were found while DPA was administered in a relatively high dosage with a mean of 48 mg/kg body weight/day and ranging from 7 to 125 mg/kg/day. 1. Statistically, the results are significantly better in primary generalized epilepsy than in partial or in secondary generalized epilepsy. 2. Ninety-two percent of 51 patients who had absences were treated successfully. The same applies to 87% of 30 patients with primary generalized grand mal with spike wave, to all four patients who had impulsive petit mal, and to 47% of the 15 patients who had centrencephalic myoclonic-astatic petit mal. 3. Positive effect of DPA in partial epilepsy and secondary generalized epilepsy was seen only if the EEG pattern was 'centrencephalic' besides focal changes. During therapy with DPA, five patients with pure focal EEG showed an increase in seizure frequency, which demonstrated complete therapeutic failure. 4. Centrencephalic seizure activity (irregular spike wave, 3/s spike wave, and more than 3.5/s spike wave) were treated successfully (P less than 0.001). Focal changes or focal sharp wave with tendency to spread or generalization were treated unsucessfully.
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PMID:Treatment of childhood epilepsy with dipropylacetic acid (DPA). 10 Nov 86

Monkeys were treated intravenously with various anticonvulsant drugs before and after the intravenous administration of gamma hydroxybutyrate (GHB). Continuous electroencephalographic (EEG) and temperature monitoring was performed throughout all experiments. The GHB-induced EEG changes were abolished by ethosuximide and clonazepam, marginally improved by diazepam, and unaffected by phenobarbital. The GHB-induced myoclonic jerks were abolished by ethosuximide, significantly improved by diazepam, and worsened by clonazepam. Phenobarbital was effective in diminishing the frequency of GHB-induced myoclonic jerks only when given prior to administration of GHB. The GHB-induced stupor was improved only by ethosuximide. The GHB model of petit mal seizures is quite specific for drugs used in this disorder. GHB may play a role in the pathogenesis of absence seizures in children.
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PMID:Gamma hydroxybutyrate in the monkey. III. Effect of intravenous anticonvulsant drugs. 10 97

The electrical seizure activity and trancelike state induced in the rhesus monkey by gamma-hydroxybutyrate (GHB) were abolished by dextroamphetamine. Dextroamphetamine blockade of this neurophysiologic effect was overcome with chlorpromazine, a dopamine receptor blocker. These results suggest that the electroencephalographic (EEG) and behavioral effects of GHB are related to effects on dopaminergic systems. Such a relationship, if substantiated by further studies, might indicate that anticonvulsant drugs used to treat petit mal epilepsy have a dopaminergic mode of action.
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PMID:Gamma hydroxybutyrate in the monkey. IV. Dopaminergic mechanisms. 10 98

Of thirty-five patients with various types of epilepsy treated with sodium valproate, 15 achieved complete seizure control on that drug alone, 12 other patients benefited and eight failed to improve on the drug. Excellent results were more likely in those with petit mal epilepsy and in those whose epilepsy was controlled with other drugs at the expense of side effects. Three patients were unable to tolerate valproate, but in general few patients experienced side effects and several patients felt much better on valproate than on their previous drugs. A twice daily dosage regime was satisfactory. Plasma valproate levels at the final dose covered a wide range, 0.21 - 1.2mmol/l (34 to 190 microgram/ml) and did not correlate with response, lack of response or side effects.
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PMID:Sodium valproate (Epilim) in epilepsy: a trial. 10 32

The evoked potential has been useful in studying characteristics of the epileptic nervous system. To investigate whether an alteration in sensory processing is possibly related to behavioral unresponsiveness observed to precede spike and wave bursts, average visual evoked potentials (VEPs) were studied during a 4.0 sec preburst interval in 6 patients with petit mal epilepsy. Individual responses, evoked by photic flashes, were averaged as a function of flash-to-burst interval. In 3 subjects with classical bursts of spike and wave, the average VEP was degraded 0.5 sec or less before burst onset. In 3 subjects with atypical electroencephalographic seizure discharge, VEP degradation was not seen. Some possible interpretations concerning the significance of the VEP alterations were discussed.
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PMID:Evoked potential studies in petit mal epilepsy. Visual information processing in relation to spike and wave discharges. 10 74

Two patients, aged 23 and 74 years, manifested prolonged episodes of mildly impaired consciousness in conjunction with rhythmical spike waves or spikes (mostly 3/s). This paroxysmal EEG activity was consistently accentuated unilaterally over the superior frontal regions. The first patient showed ictal aphasia and occasional right hemiparesis during these episodes, and partial left frontal lobectomy resulted in temporary freedom from seizures. The classification of these ictal episodes is difficult. They apparently fall into the category of absence status (petit mal status), but the focal neurological signs do not fit the presently valid definitions of absence status, nor does the lack of symmetrical bilateral-synchronous paroxysmal discharges. Perhaps a special category of status epilepticus should be established.
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PMID:Absence status (petit mal status) with focal characteristics. 11 Feb 95

1. Selective deprivation of slow-wave and paradoxical sleep was performed in 10 children with pycnoleptic attacks (8 of them before anticonvulsive treatment, 2 of them while under medication). The frequency and duration of petit mal attacks were intraindividually compared during night sleep and after waking for a 5-h period. 2. After deprivation of slow-wave sleep with reduction of EEG stages 3 and 4 to about one-third of the baseline but normal duration of sleep, petit mal attacks are more frequent and long-lasting than after normal sleep or selective deprivation of REM sleep. 3. Although total sleep time is significantly diminished after selective deprivation of paradoxical sleep the frequency of attacks during the waking state was lower than after normal sleep and deprivation of slow wave sleep. This observation shows a clear i nfluence of the quality of sleep on the frequency of epileptic attacks. 4. During sleep petit mal seizures were mainly found during stages 2 and paradoxical sleep. Single spike and irregular spike were discharges, however, occurred more frequently during slow-wave sleep. Their frequency was not significantly different in the deprivation conditions. 5. In contrast to experimental data in animals, REM deprivation is less provoking to epileptic attacks outside sleep than deprivation of stages 3 and 4 sleep. Therefore a sufficient amount of slow-wave should be preserved for pycnoleptic children.
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PMID:Selective deprivation of sleep in pycnoleptic children. Effects of deprivation of slow-wave and REM sleep on the frequency and duration of petit mal attacks. 19 Sep 77

79 patients with primary generalized epilepsies have been treated with DPA in a medium dosage of 51 mg/kg bodyweight/day, range 14 to 125 mg/kg/day, for a medium time of 22 months, range 2 to 49 months. 51 children out of this group had been treated previously and were therapy resistant to other medications. 27 children got DPA for their first medication. 34 patients were treated with DPA as a single drug, 45 were treated in combination with other medications. Therapeutic success was found to be remarkable good in impulsive petit mal (n = 4, all patients without any more seizures), in absences (n = 52, complete success in 84%), and in primary generalized grand mal seizures with spike-waves in the EEG alone or in combination with petit mal (n = 30, 87% success). However, centrencephalic myoclonic-astatic seizures (n = 17, no more seizures in 35%) were influenced significantly less. Side effects were rarely seen, mostly they could be observed in those patients treated with DPA and another medication. Side effects never induced interruption of treatment with DPA.
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PMID:[The treatment of primary generalized epilepsies with dipropyl acetate (DPA)]. 40 14


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