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)

We reported a case with sequelae of SMON and painful tonic seizure (PTS). The patient was a 50-year-old woman. Onset of SMON was when she was 28 years old. She has been suffering from decreased sensation and dysesthesia below C8 cord level to a severe degree, gait disturbance to a moderate degree and visual disturbance to a slight degree. Since January 1990, she experienced stereotyped tonic seizures of all extremities and trunk without consciousness disturbance, preceded by tingling sensation ascending from bilateral distal legs, several times a day. During hospitalization, epilepsy, tetany and multiple sclerosis were ruled out and its seizures were completely depressed by oral administration of a small amount of carbamazepine. PTS which is said to be characteristic of multiple sclerosis is seldom found in SMON patients. This is a very important and interesting case to suggest a certain relation between the mechanism of PTS and the cord lesions of SMON.
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PMID:[A case report of a patient with sequelae of SMON and painful tonic seizure]. 176 54

A seizure model involving slow i.v. infusion of the excitatory amino acid N-methyl-DL-aspartate (NMDLA) in the mouse is described. It allows determination of the threshold doses of NMDLA required to elicit clonic and tonic seizures in individual mice. The NMDA receptor antagonists MK-801, CPP, ifenprodil and 7-chlorokynurenic acid (7-CLK), and diazepam dose-dependently increased the dose of NMDLA required to elicit a tonic seizure. CPP, 7-CLK and diazepam also increased the dose of NMDLA inducing clonic seizures. In contrast, ifenprodil at doses which antagonised tonic seizures had no effect on clonic seizures. The glycine and polyamine modulatory site agonists, D-serine and spermidine respectively, dose-dependently reduced the dose of NMDLA required to induce clonic and tonic seizures. The NMDLA infusion model appears to be more sensitive than the classical bolus injection test and can detect both anticonvulsant and proconvulsant actions mediated by the NMDA receptor complex.
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PMID:A slow intravenous infusion of N-methyl-DL-aspartate as a seizure model in the mouse. 183 93

Infusions of an excitant amino acid, N-methyl-D-aspartate (NMDA) into the inferior colliculus (IC) render normal rats susceptible to audiogenic seizures (AGS) and/or spontaneous audiogenic-like seizures without tonic components. The excess excitant amino acid in the IC and the anticonvulsant effects of NMDA antagonists in genetically epilepsy-prone rats (GEPRs), along with innate norepinephrine (NE) deficits and anticonvulsant effects of NE agonists in these animals suggest a mutual role of excitant amino acids and NE in regulating AGS in GEPRs. Saline or 6-hydroxydopamine (6-OHDA, 4 micrograms/side in 2 microliters) was infused bilaterally into the locus coeruleus (LC) of normal male rats and guide cannulas were implanted into the IC. Two weeks later, NMDA was infused bilaterally into the IC (0.5 microliters; 10 nmol/side) and 10 min later the rats were subjected to an electric bell (110 db, 60 s) unless preceded by spontaneous tonic seizures. Tonic seizures were not observed in male rats following NMDA infusions in rats with LC infusions of saline. However, a marked increase in the incidence of tonic seizures was observed in the 6-OHDA-treated rats which were markedly depleted of brain NE as determined by HPLC. These findings indicate that a NE deficit greatly enhances the incidence of tonic convulsions and support the hypothesis that an excitant amino acid excess in the GEPR IC may act to initiate AGS, whereas the NE deficit may allow expression of the tonic components of AGS seen in some GEPRs.
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PMID:Effect of norepinephrine depletion on audiogenic-like seizures elicited by microinfusion of an excitant amino acid into the inferior colliculus of normal rats. 190 10

Although seizure models using systemic administration of the chemoconvulsant pentylenetetrazol (PTZ) for induction of generalized clonic seizures in rodents are widely employed to identify potential anticonvulsants, the important role of diverse technical, biological and pharmacological factors in interpretation of results obtained with these models is often not recognized. The aim of this study was to delineate factors other than sex, age, diet, climate, and circadian rhythms, which are generally known. For this purpose, experiments with 8 clinically established antiepileptic drugs were undertaken in the following PTZ models: (1) the threshold for different types of PTZ seizures, i.e., initial myoclonic twitch, generalized clonus with loss of righting reflexes, and tonic backward extension of forelimbs (forelimb tonus), in mice; (2) the traditional PTZ seizure test with s.c. injection of the CD97 for generalized clonic seizures in mice; and (3) the s.c. PTZ seizure test in rats. In rats, in addition to evaluating drug effects on generalized clonic seizures, a ranking system was used to determine drug effects on other seizure types. When drugs were dissolved in vehicles which themselves did not exert effects on seizure susceptibility, the most important factors which influenced drug potencies were: (1) bishaped dose-response curves, i.e., a decline in anticonvulsant dose-response at high doses of some drugs, leading to misinterpretations of drug efficacy if only a single high drug dosage is tested; (2) effects of route of PTZ administration (i.v. infusion vs. s.c. injection) on estimation of anticonvulsant potency; (3) species differences in drug metabolism; (4) differences in drug potencies calculated on the basis of administered doses compared to potency calculations based on 'active' drug concentrations in plasma; (5) qualitative and quantitative species differences in drug actions; (6) endpoints used for PTZ tests; (7) misleading predictions from PTZ seizure models. Analysis of anticonvulsant drug actions indicated that myoclonic or clonic seizures induced by i.v. or s.c. PTZ might be suitable for predicting efficacy against myoclonic petit mal seizures in humans, but certainly not to predict efficacy against absence seizures. Tonic seizures induced by PTZ were blocked by drugs, such as ethosuximide, which exert no effect on tonic seizures in humans. In order to reduce the variability among estimates of anticonvulsant activity in PTZ seizure models, the various factors delineated in this study should be rigidly controlled in experimental situations involving assay of anticonvulsant agents.
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PMID:The role of technical, biological and pharmacological factors in the laboratory evaluation of anticonvulsant drugs. III. Pentylenetetrazole seizure models. 190 9

In a retrospective study, records of 46 patients (24 women and 22 men aged 17-51 years; mean 29.2 years), who had been treated with ethotoin (EHN) as adjunctive therapy for control of intractable seizures were reviewed. Overall, approximately 51% of this highly selected patient population had a reduction greater than 50% in overall seizure frequency 1 month after initiation of treatment. This was reduced to approximately 25% for the last 3 months of follow-up (mean follow-up period 10.6 months). Tonic seizure frequency was reduced most dramatically, by greater than 50%, in 60% of patients at 1 month and in 35% of patients for the last 3 months of follow-up. This study suggests that prospective controlled trials of EHN, especially for tonic seizures, are needed.
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PMID:Adjunctive therapy for intractable epilepsy with ethotoin. 197 83

DL-beta-N-methylamino-alanine (DL-BMAA; 1-10 mumol i.c.v.) in mice induced a syndrome of: ataxia, ptosis, scratching, jumping, myoclonic jerks, clonic muscle spasms and tonic seizure, which was unaffected by pretreatment with D(-)-4-(3-phosphonoprop-2-enyl)-piperazine-2-carboxylate (D(-)-CPPene; i.p.), or by co-administration of gamma-D-glutamylamino-methylsulphonate (gamma-D-GAMS with DL-BMAA; i.c.v.). Pretreatment with 1-(aminophenyl)-4-methyl-7,8-methylendioxy-5H-2,3-benzodiazepine (GYKI 52466; i.v.) decreased the incidence of clonic seizures for DL-BMAA, kainic acid and RS-alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (RS-AMPA; i.c.v.). These results suggest an involvement of the AMPA/quisqualate subtype of excitatory amino acid receptors in acute BMAA toxicity.
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PMID:Receptor site specificity for the acute effects of beta-N-methylamino-alanine in mice. 198 Feb 47

We investigated time-dependent changes in low magnesium-induced epileptiform activity in combined rat entorhinal cortex/hippocampal slices with extracellular recording techniques. While in area CA3 short interictal discharges are generated without any major changes in activity during prolonged recording periods, initial tonic clonic ictaform events in the entorhinal cortex may change with time. We observed often a transition into a state of recurrent tonic activity without any clonic afterdischarges. Alternatively, seizures could stay in the clonic discharge mode for the rest of the experiment. These different seizure states were not equally affected by the anticonvulsant valproic acid. While the early clonic tonic discharges in the entorhinal cortex and the interictal like activity in area CA3 were effectively suppressed by valproic acid (VPA) the late recurrent tonic seizure discharge state was unaffected by the drug. It was, however, still sensitive to the N-methyl-D-aspartate (NMDA) receptor antagonist 2-aminophosphonovalerate. These findings point to seizure-induced changes in neuronal interaction in rat entorhinal cortex.
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PMID:Late low magnesium-induced epileptiform activity in rat entorhinal cortex slices becomes insensitive to the anticonvulsant valproic acid. 198 61

The present work deals with an EEG and behavioral study on the effects of the calcium antagonist flunarizine against the convulsions due to pentylenetetrazole in rats. Flunarizine (1.5-18 mg/kg, i.p.) has a dose-dependent protective effect against pentylenetetrazole-induced seizures (50 mg/kg, i.p.). Tonic seizures were primarily affected by flunarizine. N6-L-phenylisopropyl-adenosine (an A1 adenosine receptor agonist) potentiated the anticonvulsant effects of flunarizine at the dose of 0.05 mg/kg, i.p. Conversely, caffeine (10 and 50 mg/kg, i.p.) reverted the antiepileptic activity of flunarizine in a dose-related way. These results confirm some previous reports on the anticonvulsant effects of flunarizine in various experimental models. They also suggest that some interesting interactions may exist between flunarizine and the adenosine system.
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PMID:Possible involvement of the adenosinergic system in flunarizine anticonvulsant activity in rats. 207 48

The effect of i.c.v. administration of dodecasodium and dicalcium inositolhexakisphosphate (Na12IP6 and Ca2IP6, respectively) to mice and rats was studied. In mice, Na12IP6 (1-300 nmol) or Ca2IP6 (10-500 nmol) induced: ataxia, ground-hugging, tremor (often continuous), scratching, hyperlocomotion, wild running, myoclonic jerks, jumping, clonic muscle spasms, tonic seizure, followed by death or full recovery. The CD50 values for clonic seizures for Na12IP6 and Ca2IP6 were 16 and 49 nmol, respectively. The convulsant effect of Na12IP6 (15 nmol i.c.v.) was not blocked by pretreatment with D(-)-4-(3-phosphonoprop-2-enyl)-piperazine-2-carboxylate, but was dose dependently reduced by pretreatment with CaCl2 (30-60 nmol i.c.v.) and abolished by coadministration of CaCl2 (30 nmol) with Na12IP6 (i.c.v.). In rats, Na12IP6 (50 nmol i.c.v.) induced severe electroencephalographic seizures in the hippocampus and cortex. The potent convulsant effect of IP6 (administered i.c.v.) depends at least in part on a calcium-chelating action.
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PMID:Inositolhexakisphosphate is convulsant in mice and rats in the nanomolar range. 208 46

Spontaneously epileptic rats (SER) are a double mutant (zi/zi, tm/tm) spontaneously exhibiting both tonic and absence-like seizures. We examined the long-term effects of continual intake of phenobarbital (PB) on SER as a method of assessing long-term evaluation of antiepileptic drugs (AEDs). Food pellets containing 0.1% PB were given ad libitum from 7 weeks of age. Plasma PB level was maintained at 30-70 micrograms/ml after age 11 weeks. Tonic seizures were inhibited markedly in rats that received PB until age 15-16 weeks, but thereafter the inhibitory effects of PB gradually decreased. An increase of body weight and prolongation of survival were also noted in SER that received PB. Cortical and hippocampal EEG of SER were recorded with chronically implanted electrodes from 11 weeks of age pre-PB and 3, 7, and 14 days post-PB intake. These animals exhibit absence-like seizures characterized by sudden appearance of 5-7-Hz spike-wave-like complexes on EEG concomitant with immobility and staring. The seizures were not affected until age 13 weeks (2 weeks after intake of PB), although tonic seizures were inhibited. SER are considered a useful model for evaluating the long-term effects of AEDs.
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PMID:Long-term effects of continual intake of phenobarbital on the spontaneously epileptic rat. 210 80


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