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)

Investigations were performed on 13 cats with epileptogenic focus developed after sectioning the optic chiasm and corpus callosum. Learning was begun 3 months after producing the epileptogenic focus by the aluminium method when it was bioelectrically active. Additionally in 6 cats DPH in daily doses of 10--15 mg/kg was given 3 months after development of the focus. Learning of these animals was begun 1--2 months after the beginning of DPH administration which was continued throughout the whole period of learning during a 3-month pause in learning, as well as at the time of memory testing. In all animals the time of conditioned reflex development and differentiation was delayed. Learning was more difficult in animals with epileptogenic focus receiving DPH than in the animals with the epileptogenic focus not receiving DPH. Learning was slightly worse in the hemisphere with the focus than in that without the focus. Presence of clinical epileptic seizures was without any significant effect on the time of learning with the exception of days on which clinical seizures occurred (the percent of responses was then lower). Disturbances of memory of acquired conditioned reflexes were found only in animals with clinical seizures.
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PMID:[Effect of epileptagenic focus on the process of learning and memory in cats]. 126 40

A total of 40 cases of neonatal convulsions of different nonmetabolic aetiological factors were studied. Patients with kernicterus were included in the study. Peak plasma phenobarbital concentrations after incremental loading doses of phenobarbital i.e. 10 mg/kg, 15 mg/kg, and 20 mg/kg were determined. Diphenylhydantoin was added if phenobarbital alone was unable to control seizures. In three patients, a combination of phenobarbital and diphenylhydantoin was used as the initial loading therapy. Increase in the loading dose of phenobarbital was associated with an increase in its peak plasma concentration. Despite increase in the plasma phenobarbital concentration beyond the 'therapeutic' levels suggested by the Western studies, doses of 15 mg/kg and 20 mg/kg of phenobarbital were unable to score over the traditional regimen of 10 mg/kg. Convulsions were controlled in 50% of the patients with any of these three regimens, irrespective of the aetiology. Convulsions were controlled in 7 out of the 9 cases where diphenylhydantoin was added, because of the failure of phenobarbital in controlling the convulsions as a single drug. Convulsions of all the three patients, in whom a combination of phenobarbital and diphenylhydantoin was used by random selection as the initial bolus, were controlled. Seizure effects were difficult to distinguish from drug effects but major side effects were not encountered despite the fluctuating drug levels in the sick neonate.
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PMID:A study of phenobarbital and dilantin in neonatal seizures. 134 Aug 62

The anticonvulsant actions of lamotrigine and phenytoin against pentylenetetrazol-induced seizures were compared in laboratory rats during ontogenesis. Both drugs (lamotrigine in doses of 2.5, 5, 10, and 20 mg/kg and phenytoin in doses of 5, 10, 30 and 60 mg/kg) were injected intraperitoneally 30 min before pentylenetetrazol. Phenytoin and lamotrigine did not affect the incidence or latency of minimal (i.e., predominantly clonic, nongeneralized) seizures, although pretreatment with phenytoin changed the pattern of this phenomenon from short (10-30-s) seizures to long-lasting 'status of minimal seizures'. Both drugs abolished selectively the tonic phase of major, i.e., generalized tonic-clonic seizures, usually without any influence on the clonic phase of these seizures. Only the highest dose of phenytoin in adult animals suppressed the generalized tonic-clonic seizures as a whole. The study did not reveal any change of action of lamotrigine or phenytoin against pentylenetetrazol-induced motor seizures throughout development.
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PMID:Anticonvulsant action of lamotrigine during ontogenesis in rats. 147 94

Various anticonvulsant drugs were evaluated for their ability to protect against clonic seizures induced in mice by intraventricular injection of the K+ channel blocking peptide dendrotoxin (DTX). Phenytoin, the phenytoin-like anticonvulsant carbamazepine and the broad spectrum drug valproate were effective in this model, whereas the GABA-enhancers diazepam and tiagabine, the NMDA antagonists (+/-)-CPP and (+)-MK-801, the AMPA antagonist NBQX, the antiabsence drug ethosuximide and the Ca2+ channel antagonist nimodipine were inactive. In contrast to the lack of activity of other NMDA antagonists, phencyclidine and ADCI [(+/-)-aminocarbonyl-10,11-dihydro-5H-dibenzo [a,d]cyclohepten-5,10-imine] were potent antagonists of DTX-induced seizures.
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PMID:Protection against dendrotoxin-induced clonic seizures in mice by anticonvulsant drugs. 150 73

This study reports results from experiments designed to test common, clinically useful anti-convulsants for their effectiveness, if any, against the high pressure nervous syndrome (HPNS) in rats. Phenytoin, carbamazepine, phenobarbitone, or diazepam were administered orally to rats before compression. Endpoints used to assess the progression of the HPNS were T1, T3, and T5 (onset of, continuous, and severe tremor), myoclonus, and seizures. Of the four drugs tested, only phenobarbitone increased the onset pressure for tremor and seizures by: T1 33%; T3 11%; T5 14%; seizures 10%. Neither phenytoin, carbamazepine, nor diazepam had any significant effect on any of the endpoints studied. High dose chronic pretreatment with phenytoin also had no effect on the HPNS. These data suggest that conventional anticonvulsant treatment would be of limited value for HPNS in man, and the lack of effect also suggests that HPNS seizures are of an unusual type.
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PMID:Effects of four common anticonvulsants on the high pressure nervous syndrome in the rat. 153 60

This prospective study followed the pregnancy course of epileptic women at the Motherisk Program of The Hospital for Sick Children, Toronto. We compared fetal outcome of women treated with carbamazepine (CBZ), those treated with diphenylhydantoin (phenytoin, DPH), and a drug-free control group. Seizures were reported in 15 pregnancies; in a subgroup of 9 women without change in drug or schedule, an increase in seizure frequency was evident in 6, a decrease in 1, and no change in 2, regardless of the drug taken. Of 23 children exposed to CBZ in utero, one was born with a lumbar myelomeningocele and multiple congenital anomalies. Of 21 children exposed to DPH, there was one case of severe developmental delay and four with minor features of fetal hydantoin syndromes (FHS). The three groups did not differ in birth weights or gestational ages of the babies. Although much more experience is needed, as a result of this study and other similar reports, Motherisk now offers women treated with CBZ diagnostic tests to detect neural tube defects during the second trimester of pregnancy.
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PMID:Course of pregnancy and fetal outcome following maternal exposure to carbamazepine and phenytoin: a prospective study. 159 83

Complex partial seizures comprise the major uncontrolled seizure type in adult patients with epilepsy. Any improvement of our understanding of the mechanisms through which these seizures are often refractory to antiepileptic drugs is therefore of considerable importance. By examining the effects of the anti-epileptic drug phenytoin in a large group of kindled rats, a widely used model of complex partial seizures, animals with different sensitivity to this drug were selected. Using determination of the focal seizure threshold for evaluation of phenytoin's anticonvulsant effect, most animals (about 60%) showed variable effects in response to phenytoin. However, about 20% of the animals ("phenytoin nonresponders") showed no increase in their focal seizure threshold at repeated test trials with phenytoin, and 20% ("phenytoin responders") exhibited reproducible increases in focal seizure threshold after injection of phenytoin. Phenytoin responders and nonresponders thus selected were used for subsequent experiments. The different response of focal seizures to phenytoin was not related to differences in pharmacokinetics or location of the stimulating electrode. Although phenytoin reproducibly increased the threshold for induction of afterdischarges in responders, it did not alter severity or duration of the elicited seizure response. In contrast to phenytoin, carbamazepine induced increases in focal seizure threshold in all kindled rats. Duration of seizures and afterdischarges were significantly reduced by carbamazepine in phenytoin responders, but not in nonresponders, although plasma levels of carbamazepine were the same in both groups. The difference in response of kindled rats to phenytoin was restricted to kindled seizures, because phenytoin induced the same anticonvulsant effect on the threshold for generalized tonic electroconvulsions (determined via transauricular electrodes) in both groups of kindled rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Kindling as a model of drug-resistant partial epilepsy: selection of phenytoin-resistant and nonresistant rats. 165 Aug 29

Partially purified (Na+,K+)-ATPase (E.C. 3.6.1.3.) was investigated in the epileptic cortex of audiogenic DBA/2 mice and in the primary and secondary foci of cats with acute or chronic freeze lesions. No differences in specific activities measured at 3 mM K+ were observed between epileptic and control cortex, except an increase of enzymic activities in the primary focus of acutely lesioned cats. The (Na+,K+)-ATPase catalytic subunits were resolved by SDS-gel electrophoresis and their phosphorylation levels were measured in presence of K+ ions and phenytoin. K+ was more effective in inducing maximal dephosphorylation of (Na+,K+)-ATPase in C57/BL, with identical affinity in the two strains. Phenytoin decreased the net phosphorylation level of (Na+,K+)-ATPase by about 50% in C57/BL mice, but only by 20% in DBA/2 mice. Both K+ and phenytoin dephosphorylating influences were decreased in primary and secondary foci of acutely lesioned cats. Those changes were limited to the alpha(-) subunit. In chronic cats, the dephosphorylating step of the (Na+,K+)-ATPase catalytic subunit recovered a normal affinity to K+, but its sensitivity to phenytoin remained decreased. Those differences in K+ and phenytoin influences on brain (Na+,K+)-ATPases between control and epileptic cortex might be responsible for the ictal transformation and seizure spread. In cats, the alteration of the alpha(-) isoform could mainly affect the glial cells.
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PMID:Phosphorylation of brain (Na+,K+)-ATPase alpha catalytic subunits in normal and epileptic cerebral cortex: I. The audiogenic mice and the cat with a freeze lesion. 165 58

Diphenylhydantoin-induced hepatitis and mononucleosis are uncommon in children. The occurrence of these two diseases in the same individual, with progression to hepatic failure is rare and has not been reported in infants. This report represents a 6-month-old male infant who developed an infectious mononucleosis-like syndrome and hepatic failure 16 days after diphenylhydantoin administration. He took this anticonvulsant for controlling seizures after a head injury. Fever, skin rash, hepatosplenomegaly, lymphadenopathy, and atypical lymphocytosis led to the initial diagnosis of infectious mononucleosis. However, negative heterophil antibody did not support the diagnosis. Jaundice ensued in the following course and became more and more profound. Meanwhile, physical examination showed shrinking in liver size. Negative virology studies, including Epstein-Barr virus, cytomegalovirus, and hepatitis B virus, excluded them as causative agents. The patient lapsed into a stage I hepatic coma, but gradually recovered clinically and biochemically after eight successive exchange transfusions and supportive care. Two liver biopsies were performed 20 and 50 days after the onset of disease, respectively. Remarkable hepatic parenchymal loss, cholestasis, and fatty change were found on histologic examination of the first biopsy specimen, and portal fibrosis was noted on the second.
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PMID:Mononucleosis and hepatic failure associated with diphenylhydantoin treatment in an infant. 167 17

The concentrations of central neuropeptides, somatostatin (SS) and substance-P (SP), were determined in the different brain regions of young-aged male rats after a long-term administration of anticonvulsants Qingyangshen (QYS), Diphenylhydantoin (DPH), and Carbamazepine (CBZ). The results were compared with Pentylenetetrazol (PTZ)-induced seizure model and normal saline-treated controls. No effects of QYS on the concentrations of SS and SP were found in the rats of four-week or eight-week group. Both of DPH and PTZ increased the SS levels in the midbrain of rats in four-week group. DPH, CBZ, and PTZ also increased the SP levels in the cerebral cortex, striatum, and brain stem of rats in eight-week group. Our present data indicated that the central neuropeptides SS and SP were involved in the processes of epilepsy and antiepilepsy. Since QYS did not influence the contents of SS and SP after a long-term administration, it suggested that the anticonvulsant mechanism of QYS may be different from those of DPH and CBZ, i.e. it may be not due to its effect on the central neuropeptide pathway.
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PMID:The investigation of antiepileptic action of qingyangshen (QYS)--effect of QYS on the concentrations of neuropeptides in rat brain. 171 32


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