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

Pupillary hippus was observed and recorded in a man of 44 years, who had epileptic seizures, chronic alcoholism with liver disease and Primidon intoxication, during a period of unconsciousness of 24 h. During this time the simultaneous records of the EEG and pupillogram over a long period of time revealed that the basic EEG rhythm and hippus had the same frequency. Both recordings were temporarily in phase, time-locked, and could be blocked by painful and acoustic stimuli. The etiology and interpretation of hippus are discussed.
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PMID:Simultaneous recording of pupillary hippus and EEG. Report of a case. 7 57

Serotonin was determined in platelets of 140 patients with idiopathic mal seizures. According to anticonvulsive therapy these patients were divided into the following five groups: no medication, Diphenylhydantoin, Diphenylhydantoin calcium, Primidon, and combination of various of the anticonvulsants mentioned. The results obtained in the entire group of patients as well as in the various subgroups were compared with those of a group of healthy persons without therapy. In addition the various subgroups were compared to each other. There were significantly reduced serotonin values in the patients with idiopathic grand mal seizures as well as in each of its various groups as compared with the values obtained in healthy persons. Furthermore, significantly higher values were observed in the patients receiving primidone as compared with those receiving no anticonvulsants, Diphenylhydantoin, and a combination of various anticonvulsants. Our results taken together with those reported in the literature point to the possibility that a special imbalance in the cerebral neurotransmitter system, including a deficiency of serotonin, may represent a pathogenetic factor for idiopathic grand mal seizures. In addition, this investigation indicates that primidone elevates serotonin in platelets of patients with grand mal seizures.
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PMID:Serotonin metabolism with idiopathic grand mal seizures. 8 62

Primidone is an effective anticonvulsant against seizures induced in epileptic fowl by exposure to intermittent photic stimulation. Epileptic fowl metabolize primidone to phenobarbital. Pretreatment of epileptic fowl with SKF 525A to prevent the metabolism of primidone to phenobarbital indicated that primidone itself had anticonvulsant activity. Phenylethylmalonamide, a second metabolite of primidone, did not have anticonvulsant activity when administered at the same dose as primidone.
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PMID:Epileptiform seizures in domestic fowl. VIII. Anticonvulsant activity of primidone and its metabolites, phenobarbital and phenylethylmalonamide. 68 87

Barbiturates retain an important place in clinical neurological practice. They are used as both diagnostic and therapeutic drugs, their most common uses being as anticonvulsant and anaesthetic agents. This article explores the current theories explaining the mechanism of action of the barbiturates, with special emphasis on their anaesthetic and anticonvulsant effects. The primary mechanism of action of barbiturates is to increase inhibition through the gamma-aminobutyric acid (GABA) system. Anaesthetic barbiturates also decrease excitation via a decrease in calcium conductance. Phenobarbital (phenobarbitone), the primary anticonvulsant barbiturate, is effective for partial, complex partial and secondarily generalised seizures. While no longer the drug of choice for all these seizure types, it remains an important and useful agent. Mysoline has been shown to be useful in the treatment of essential tremor and several other movement disorders, and as an anticonvulsant. Barbiturates are also used for their sedative-hypnotic properties. A relatively new use is in the evaluation of patients with medically intractable seizure disorders for possible surgical therapy. The roles of methohexital and amobarbital (amylobarbitone) are discussed in the section on barbiturates used as diagnostic agents. The experimental use of barbiturates is also commented on; the most important of these is perhaps the use of barbiturates in cerebral resuscitation.
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PMID:The clinical use of barbiturates in neurological disorders. 172 Mar 79

The heterogenous psychoses in epilepsies, caused by well known conditions, are not rare but associated with regularly a few of seizure-types not with the nature and development of attacks. Polar transitional ranks and converging courses of schizophrenic (accentuated) syndromes in epilepsies and idiopathic schizophrenias are rather frequent. Also (sub-)acute schizophrenic psychoses are corresponding to the complete palette of first and second rank symptoms (K. Schneider) of idiopathic schizophrenias. After manifestations of epilepsy these syndromes can appear at any time. It is given a profile of risks. Progressive avoidance of a. phenylaceturea, b. mixtures of antiepileptics did not put an end to psychotic syndromes: Long-term therapies with 1. Polytherapy, 2. Primidone and Phenytoin (dosedependant) as well as 3. Ethosuximide (-monotherapy) cause a disorder of feed back mechanisms, especially a disturbed regulation of vigilance and sleeping-waking-cycle and their psychological correlates. Carbamazepine and Sodium Valproate are, plasma-level-controlled of preventive antipsychotic effect. Selected neuroleptics of rather slight epileptogenic potency are of going down importance. Benzodiazepines are required mostly in prepsychotic syndromes, Lithium compounds in selected cases. There is no more alternative seizures or psychosis.
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PMID:[Psychoses in epilepsy]. 198 Oct 95

Primidone can be used for seizures refractory to standard antiepileptic drugs. We administered primidone, 25 mg/kg/day in 3 divided doses, to 10 patients and obtained serum levels of primidone, phenobarbital, and phenylethylmalonic acid at 1, 2, 4, 6, and 8 hours on day 1, alternate days until discharge, and after 6 weeks. Other antiepileptic drugs were discontinued in 8 of 10 patients with refractory seizures. Mean primidone levels were 10.6 +/- 4.4 micrograms/ml by day 3 and remained stable until discharge. Phenylethylmalonic acid was detected by 6 hours and increased to 11.1 +/- 4.0 micrograms/ml by day 7. Phenobarbital levels in 3 of 10 patients not previously treated with phenobarbital ranged from 0.6-3.4 micrograms/ml by day 5. The mean initial phenobarbital level was 30.1 +/- 10.5 micrograms/ml and had decreased to less than 15 micrograms/ml by day 7. Seizure control occurred within 5 days in 8 of 10 patients and was achieved by day 3 in 6 of 8 patients, coinciding with primidone levels greater than 10 micrograms/ml. No toxic effects of primidone were observed. All levels decreased during subsequent examinations suggesting auto-induction of metabolic systems. Our data indicate that seizure control is best correlated with primidone and phenylethylmalonic acid levels and unrelated to phenobarbital levels in this age group.
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PMID:Efficacy of primidone for seizure control in neonates and young infants. 324 32

Premedication with PCPA antagonized in rats the anticonvulsant activity of Primidone and of other drugs against seizures evoked by electroshock. Only in the case of Primidone, however, the anticonvulsant activity could not be re-established by increasing the dosage. Our investigations have shown that PCPA caused a strong inhibition of the conversion of Primidone to phenobarbital, both in vivo and in vitro.
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PMID:On P-chlorphenylalanine interference with phenobarbital formation from primidone. 621 36

Benzobarbital, primidone, phenobarbital, phynytoin and trimethadionum (in order of decreasing activity) were moderately effective against DL-kynurenine (50 micrograms, i. c. v.)-induced seizures in SHR albino male mice. Diazepam was ineffective even in doses of 15 and 25 mg/kg. Against seizures induced by quinolinic acid (5 micrograms, i. c. v.) anticonvulsants, particularly primidone and phenytoin, were more effective than against kynurenine-induced seizures. Diazepam was slightly effective in high doses of 7-15 mg/kg. Primidone and benzobarbital in doses used (10-50 mg/kg) were ineffective against strychnine and pentylenetetrazol. Selective efficacy of primidone and benzobarbital in this model of seizures suggests that kynurenine and quinolinic acid could be involved in the grand mal fits in epileptic patients.
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PMID:[Effect of anticonvulsants on convulsions induced by kynurenine, quinolinic acid, strychnine and corazole]. 645 7

Neurotoxicity and protection against maximal electroshock and Metrazol seizures from primidone (PRM), phenobarbital (PB), and phenylethylmalonamide (PEMA) were determined in mice for each drug separately and expressed in terms of brain concentrations. Compared with PB, PEMA was 16 times less potent against electroshock and Metrazol seizures but only 8 times less toxic. Primidone was markedly less neurotoxic than PB and equally potent against electroshock, but PRM had no effect against Metrazol or bicuculline. PRM is a relatively nontoxic anticonvulsant with a different action than PB, and PEMA is both a weak and a relatively toxic anticonvulsant.
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PMID:Primidone, phenobarbital, and PEMA: I. Seizure protection, neurotoxicity, and therapeutic index of individual compounds in mice. 668 71

The brain stem auditory evoked potential (BSAEP) was recorded in 32 normal control subjects and 81 epileptic patients. Statistically significant differences in regard to sex and laterality of ear stimulated were found to exist in both groups. The epileptic patients also had significantly longer latencies for all wave components and interwaves I-III as well as I-IV than the normal controls. There were no differences in regard to interwave latency III-V. Clinically significant latency prolongations (more than three standard deviations from the norm) were encountered especially in regard to waves I and III. Correlations of wave and interwave latencies with a large variety of clinical variables showed that statistically significant relationships existed mainly in regard to presence or absence of brain damage and the severity of the seizure disorder, as expressed by the number of different seizure types to which a given patient was subject. Waves II and III showed the most consistent latency prolongations for these variables. Anticonvulsant medication levels did affect wave latencies, but apart from Primidone, it involved waves IV through VII rather than II and III. Carbamazepine levels were related to prolongation of I-III interwave latency. It is concluded that severely brain-damaged epileptic patients have demonstrable brain stem dysfunction affecting mainly the medullo-pontine rather than midbrain or thalamic structures.
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PMID:Brainstem auditory evoked potential recording in patients with epilepsy. 712 49


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