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)

A 18 year-old boy, without a previous history, presented with psychomotor seizures and, 4 months after, mental deterioration. EEG showed focal epileptic abnormalities characterized by high amplitude spike waves in the left temporal region. Periodic complexes appeared after administration of Diazepam. CT scan showed mild cortical atrophy in the left temporal region. Measles virus HI antibody titers were 1/2048 in the serum and 1/64 in the CSF. The patient died one year after the first complex partial seizures.
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PMID:[Complex partial epileptic seizures as the initial symptom of subacute sclerosing panencephalitis]. 356 39

Status Epilepticus (SE) is defined as an epileptic seizure which is so frequently repeated or so prolonged as to create a fixed and lasting epileptic condition. SE is observed in all age groups, but its frequency increases among younger children. Etiological factors vary with age. During infancy acute encephalopathies (infectious, anoxic-ischaemic, metabolic, etc.) are prevalent, while later non progressive encephalopathies are more frequent. Cryptogenic cases are present in all age groups, but "febrile" cases are observed before two years of age. Generalized forms are rare. The most frequent SE is Unilateral non alternating, which is observed exclusively among children. The semeiological diagnosis of SE with the help of EEG monitoring can be useful, since some forms of SE have constant etiological factors and prognosis. Since the condition of SE may cause brain damage or even endanger patient's life, immediate and adequate treatment is necessary. Diazepam and Phenytoin are particularly effective for stopping the seizures. A practical scheme for treatment is presented.
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PMID:[Status epilepticus in childhood]. 360 9

When fully amygdala-kindled rats are electrically stimulated in grouped trials with intertrial stimulation intervals of less than 60 min, significant residual inhibition can be demonstrated. When these grouped trials of stimulation are repeated daily, additional cumulative inhibition is seen. The present study examined the effect of daily pretreatment with three doses of pentylenetetrazol (5, 10, and 20 mg/kg) and two doses of diazepam (0.5 and 2 mg/kg) on daily, grouped trial electrical stimulations of fully amygdala-kindled rats. Little or no reduction was seen in postictal inhibition by pentylenetetrazol pretreatment including the highest dose tested in which prestimulation bursts of spiking were associated with short episodes of forelimb clonus. Pretreatment with the benzodiazepine receptor agonist, diazepam, resulted in a dose-dependent reduction in the first elicited seizure response each day compared with control trials. Subsequent daily seizure trials of diazepam-treated animals demonstrated a relatively constant degree of dose-dependent seizure suppression without evidence of further postictal inhibition. The neural substrate that governs grouped trial postictal inhibition of amygdala-kindled seizures appears to be resistent to modification by near-convulsant doses of pentylenetetrazol, an agent with a presumed GABA-mediated mechanism of action. Diazepam, an anticonvulsant with a presumed GABA-related or associated mechanism of action, suppressed seizures in a dose-dependent manner nearly equally across all trials.
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PMID:Modification of amygdala-kindled postictal inhibition by pentylenetetrazol and diazepam. 362 15

The effect of clobazam, a 1,5-benzodiazepine, on kindling seizures was compared with the effects of 1,4-benzodiazepines, diazepam and bromazepam, in amygdaloid and hippocampal kindled rats. After kindled seizures were established (stage 5 seizure), the test drugs were administered intraperitoneally. In amygdaloid kindled rats, clobazam significantly suppressed the motor seizures (MS) at doses of 20 and 50 mg/kg and significantly shortened the duration of after-discharge (AD) at doses of 10 to 50 mg/kg. Diazepam at doses of 2 to 10 mg/kg and bromazepam at 1 to 5 mg/kg also significantly suppressed the MS and significantly shortened the duration of AD. Similar suppressive effects by these three benzodiazepines were observed in hippocampal kindled rats. From these results, clobazam was found to have a qualitatively similar but weaker anticonvulsive effect than those of 1,4-benzodiazepines.
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PMID:Effects of clobazam on amygdaloid and hippocampal kindled seizures in rats. 362 52

This report concerns three patients in whom continuous intravenous infusion of Diazemuls (diazepam dissolved in soya bean oil and emulsified) diluted in 5.5% glucose was used for the controlling of epileptic seizures (status). Diazemuls infusion was effective in one patient with complex partial status epilepticus; in another patient with convulsion secondary to a brain stem infarct, the convulsions were abolished; while only reduced jerking was achieved in the third patient suffering from myoclonic jerks caused by anoxic brain damage. Infusion time ranged from 15 to 33 h. The serum concentrations of diazepam obtained during the infusions were higher than recommended in the literature for treatment of status epilepticus, but could not be correlated to either clinical efficacy or infusion rate.
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PMID:Intravenous infusion of Diazemuls in the control of status-like epileptic seizures of different etiology. 363 May 96

A strain of Wistar rats was inbred in our laboratory for its susceptibility to sound. The seizures are characterized by one or two wild running fits which terminate in a tonic dorsiflexion with open mouth, followed by a catatonic state. During the tonic phase of the seizure, the cortical EEG is flattened for 2 to 3 s. Then, a slow and regular low-voltage (9-12 c/s) activity is observed during 40 to 60 s. When these animals are submitted to daily sound-stimulations, the behavioral as well as the EEG manifestations of the audiogenic seizures change progressively. After 5 to 30 exposures, the wild running becomes disorganized by occurrence of myoclonic jerks of the limbs and the body. In some animals, the tonic extension disappears and a myoclonic seizure develops progressively with facial and forelimb clonus, rearing and falling. In other animals, the tonic phase still occurs and is followed by a generalized clonic phase. During both the myoclonic and the tonicoclonic seizures, rhythmic spikes, polyspikes and spike and waves of high amplitude (1-10 c/s) during 40 to 120 s are observed on EEG recordings. These EEG modifications often outlast the sound stimulation. The pharmacological reactivity in rats exposed to single or repeated audiogenic seizures is similar: phenytoin and carbamazepine suppress both kinds of seizures at low doses whereas ethosuximide is efficacious only at high doses. In order to know whether the repeated exposure to sound or the repetition of seizures are responsible of the observed changes in audiogenic seizures, animals susceptible to sound were exposed daily to the seizure-inducing sound after previous injection of Diazepam, which prevented them from convulsing. On the other hand, sound susceptible animals were injected daily with a dose of PTZ inducing one or several convulsions without exposure to sound. None of these treatments ever facilitated the development of kindled audiogenic seizures. The progressive modification of behavioral and EEG modifications occurring when audiogenic seizures are repeated suggests that kindling has developed, the seizure extending from the brainstem to forebrain structures.
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PMID:Kindling of audiogenic seizures in the rat. 366 6

Diazepam's impact on kainic acid seizure-induced local cerebral glucose utilization (LCGU) was assessed by a quantitative [14C]2-deoxyglucose method. Male rats were injected i.p. with either kainic acid (12 mg/kg) or its vehicle, 3 or 48 h before LCGU determination. Diazepam (3.2 mg/kg) or its vehicle were injected i.m. 15 min before, 1 and 2.5 h after kainic acid. Diazepam blocked kainic acid-induced overt convulsions, attenuated LCGU increases at 3 h and prevented 48 h LCGU decreases in piriform cortex and amygdala. LCGU in (% of vehicle): CA3 (438%), CA4 (537%) and CA1-ventral (340%) of hippocampus, interpeduncular nucleus (200%) and lateral lemniscus (213%) were still significantly above vehicle levels in the 3 h diazepam-kainic acid group. These results suggest that diazepam suppresses the spread of kainic acid-induced seizure activity from the proposed CA3 epileptogenic focus. In addition, diazepam reduces, but does not abolish, hypermetabolic activity at the foci itself.
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PMID:Attenuation of cerebral glucose use in kainic acid-treated rats by diazepam. 369 39

Intravenous access for the administration of antiepileptic drugs can be both time-consuming and difficult in an actively seizing infant. We conducted a study to examine the intraosseous route as an alternate means of vascular access for the administration of diazepam in a pentylenetetrazol-seizure model in pigs. Epileptogenic activity was induced with pentylenetetrazol 100 mg/kg in 15 domestic swine that had undergone craniotomies for electrocortical recording. Diazepam (0.1 mg/kg) was administered IV (n = 5) or intraosseously (n = 5); control animals received no drug (n = 5). Epileptogenic activity was suppressed below control levels within one minute in the IV group and within two minutes in the intraosseous group. A two-way analysis of variance did not show a significant difference between the IV and intraosseous routes; however, both were significantly different when compared to the control. There also was no significant difference in plasma diazepam levels between the two groups at one, two, five, ten, 15, and 20 minutes. Our study demonstrated that the intraosseous route is a rapid and effective alternative for diazepam administration.
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PMID:Intraosseous diazepam suppression of pentylenetetrazol-induced epileptogenic activity in pigs. 380 88

Morphological analysis of brains from rats receiving a convulsant dose of the muscarinic cholinergic agonist, pilocarpine hydrochloride (380 mg/kg), revealed a widespread damage to the forebrain as assessed by light microscopy 5-7 days after seizures. The substantia nigra, olfactory cortex, amygdala, hippocampus, septum, temporal cortex and thalamus underwent prominent morphological injury and cell loss. A concurrent assessment of the activity of L-glutamate decarboxylase (GAD), the gamma-aminobutyrate (GABA) synthesizing enzyme, demonstrated marked deficits in GAD activity in the brain regions undergoing morphological insult. Diazepam, 10 mg/kg, and scopolamine hydrochloride, 10 mg/kg, administered 30 min prior to the injection of pilocarpine, 380 mg/kg, prevented acute behavioral and electrographic, and long-term morphological and biochemical sequelae of seizures. These findings suggest that the muscarinic antagonist, scopolamine, and the anticonvulsant benzodiazepine, diazepam, may aid in preventing extensive brain damage related to pathological muscarinic cholinergic overactivity. The similarity of the topography of the damage and deficits in the GAD activity in brains of rats treated with pilocarpine indicates that GABAergic neurons are lost in the subregions of the brain preferentially sensitive to the convulsant action of pilocarpine.
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PMID:Seizures produced by pilocarpine: neuropathological sequelae and activity of glutamate decarboxylase in the rat forebrain. 380 99

The main objective of this study was to determine whether the excitotoxic cholinesterase inhibitor soman increases the catabolism of phospholipids in rat brain. Injections of soman (70 micrograms/kg, s.c.), at a dose that produced toxic effects, increased the levels of both free fatty acids (175-250% of control) and free choline (250% of control) in rat cerebrum 1 h after administration. All fatty acids contained in brain phosphatidylcholine were elevated significantly including palmitic (16:0), stearic (18:0), oleic (18:1), arachidonic (20:4), and docosahexaenoic (22:6) acids. The changes observed were consistent with those reported to occur following ischemia and the administration of other convulsants. Pretreatment of rats with the anticonvulsant diazepam (4 mg/kg, i.p.) prevented both the signs of soman toxicity and the soman-induced increase of choline and free fatty acids. Diazepam alone did not affect the levels of choline or free fatty acids, cholinesterase activity, or soman-induced cholinesterase inhibition, suggesting that soman toxicity involves a convulsant-mediated increase in phosphatidylcholine catabolism. In addition, administration of the convulsant bicuculline, at a dose that produces seizures and increases the levels of free fatty acids in brain, significantly increased the levels of choline. Results suggest that excitotoxic events enhance the hydrolysis of phosphatidylcholine in brain as evidenced by a concomitant increase in the levels of choline and free fatty acids.
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PMID:Concomitant increases in the levels of choline and free fatty acids in rat brain: evidence supporting the seizure-induced hydrolysis of phosphatidylcholine. 381 25


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