Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The treatment of status epilepticus can be improved by using recent developments in the pharmacokinetics and method of intravenous (IV) administration of phenytoin sodium. While diazepam, administered IV, remains the drug of choice for the short-term control of seizures associated with compromised respiratory exchange, phenytoin is effective in preventing recurrence of such seizures and in treating most other forms of status epilepticus. A loading dose of 18 mg/kg given by IV infusion in either 0.45% or 0.9% sodium chloride at a rate no greater than 50 mg/min results in therapeutic serum levels for up to 24 hours in most patients. Maintenance therapy with phenytoin should start at 4 to 7 mg/kg/day and be adjusted to both clinical response and serum levels.
JAMA 1980 Sep 26
PMID:Status epilepticus. The role of intravenous phenytoin. 742 Jun 42

Complex partial status epilepticus developed in two patients following myelography with metrizamide. The status epilepticus was manifested by confusion and complex motor symptoms, and electroencephalograms (EEGs) showed ictal activity alternating independently over both hemisphere. Immediate clinical improvement occurred with antiepileptic treatment, and to date no sequelae have been observed. Neither patient had a previous history of epileptic seizures, but both had preexisting EEG abnormalities.
Ann Neurol 1980 Sep
PMID:Complex partial status epilepticus following myelography with metrizamide. 743 76

In a four-and-a-half year period, 19 patients with focal neurological deficits accompanied by a focal electrographic status epilepticus were encountered. Sixteen of these patients showed clouding of consciousness or confusion. Computed tomography of the brain revealed focal lesions in 15 patients. In 7 patients the lesions were the result of a recent cerebral event and in 8 patients they were long-standing. All patients were treated with anti-epileptic drugs. Ten of the 12 patients without an acute lesion showed a complete recovery in a few days. In these patients the symptoms may have been caused by the continuous seizure activity, classifying them as cases of non-convulsive focal status epilepticus. Only 2 of the 7 patients with an acute lesion had a full recovery. In patients with an acute lesion the part played by the electrographic status epilepticus in the acquired deficits is unclear. Continuous or frequent intermittent focal epileptic discharges on the EEG may warrant treatment with anti-epileptic drugs in patients with focal neurological deficits, even when one of the hallmarks of epilepsy, clonic movements, is absent.
Acta Neurol Scand 1995 Sep
PMID:Non-convulsive status epilepticus as cause for focal neurological deficit. 748 71

Clusterin is a protein that has been implicated in cell death and remodelling in a number of different tissues. To further investigate the role of clusterin in nerve cell death its expression was measured in the rat brain at various times after status epilepticus (SE) induced by 1 h of hippocampal stimulation, by using in situ hybridization, immunocytochemistry, and immunoblotting. SE lead to a dramatic time-dependent increase in clusterin mRNA in non-nerve cells resembling astrocytes in the hippocampus beginning after 24 h. There was also an earlier induction of clusterin mRNA in dentate granule cells, that survive SE. Only a low mRNA signal was observed over the CA1 pyramidal cells, which die after SE. In contrast to these mRNA results, massive clusterin-like immunoreactivity was observed in CA1 pyramidal cells and dentate hilar neurons (and both of these neuronal populations die after SE), but not in dentate granule cells. We speculate that astrocytes produce clusterin after SE and that the clusterin is then secreted and taken up by hippocampal neurons destined to die. Thus, the role of clusterin in nerve cell death/ regeneration warrants further investigation.
Brain Res Mol Brain Res 1995 Sep
PMID:Clusterin accumulates in dying neurons following status epilepticus. 750 Aug 39

The etiology of cerebral abnormalities after focal status epilepticus (SE) is unknown. Possible causes include hypoxia and the excessive release of excitatory amino acids. Magnetic resonance imaging (MRI) of a 21-year-old patient with "cryptogenic" continuous motor seizures showed swelling and signal hyperintensity of the contralateral parietotemporal cortex, the thalamus, and the ipsilateral cerebellum on T2-weighted images. These regions are connected by glutamatergic pathways. Proton magnetic resonance spectroscopy (MRS) of the cortical lesion yielded a signal peak at the resonance frequency of 2.29 ppm, suggesting a focal increase of glutamate or its degradation product glutamine. At 3-month follow-up, structural alterations had disappeared, but the N-acetyl-aspartate/choline ratio was still reduced in the previously abnormal area. These findings are the first to demonstrate the contribution of MRS to pathophysiologic studies of focal SE in humans and, in combination with the pattern of imaging abnormalities, support a major role of glutamate for seizure-related brain damage.
Epilepsia 1995 Sep
PMID:Magnetic resonance imaging and spectroscopy findings after focal status epilepticus. 764 36

During status epilepticus provoked by an intra-amygdala injection of kainic acid, the severity of seizures and of consequent neuronal damage was considerably increased in rats treated with L-NOARG, at a dose which completely inhibited NO synthesis. We propose that the effects of L-NOARG could be related to the loss of a retrograde inhibition exerted by NO on NMDA receptors. The complete suppression of NO formation in the brain finally facilitated the development and the generalization of seizures and their neurotoxic consequences.
Neuroreport 1993 Sep 03
PMID:L-nitroarginine, an inhibitor of NO synthase, dramatically worsens limbic epilepsy in rats. 769 12

Much remains to be learned about mechanisms underlying entry into, and temporal progression of, status epilepticus (SE). This report describes a non-pharmacologic model of generalized convulsive SE in rat. Pulsed trains of suprathreshold electric current, were administered bilaterally to either of four rostral forebrain sites: orbital cortex, medial precentral cortex, deep prepiriform cortex, or rostral caudate-putamen (n = 8 per site). This induction method resulted in 30/32 animals attaining limb-clonic convulsive SE within a mean of 30-35 min for each forebrain site, with no differences between sites. Subsequent SE proceeded without further interventions, permitting observation of the natural course of progression. A stereotyped behavioral/electrographic sequence occurred, characterized by devolution. Behaviorally, animals progressed from predominantly limb clonus to head clonus, then to subtle twitching, and finally to electrical SE before cessation of spikes. The corresponding electrographic progression was from fast and slow spiking to periodic epileptiform discharges (PEDs). In 20 animals surviving to 48 h, pathologic damage affected mainly limbic sites; damage was related to total convulsive time rather than to clonic activity. High-dose phenobarbital but not phenytoin suppressed SE when given during orbital cortex-induced limb-clonic SE. These findings are compatible with human observations and indicate that this model will enable investigations of generalized SE mechanisms and evaluation of new therapeutic agents for refractory SE.
Epilepsy Res 1994 Sep
PMID:A new, non-pharmacologic model of convulsive status epilepticus induced by electrical stimulation: behavioral/electroencephalographic observations and response to phenytoin and phenobarbital. 781 10

We studied the amount of dopamine on the substantia nigra-ventral tegmental area during status epilepticus of male Wistar rats induced by coriaria lactone with fluorescence histochemical technique and autoexposuremeter of microscope. The intensity of dopamine fluorescence in the climax epileptic seizure group (10 rats) and postepileptic seizure group (8 rats) decreased significantly as compared with the control (10 rats), but the intensity of dopamine fluorescence in the pre-eileptic seizure group (10 rats) was not significantly different from that of the control group. The result indicated that epileptic seizure induces a decrease of the inhibitory neurotransmitter-dopamine. Therefore dopamine plays an important role in regulating the epileptic seizures.
Hua Xi Yi Ke Da Xue Xue Bao 1994 Sep
PMID:[Histochemical study of dopamine on rat substantia nigra--ventral tegmental area during status epilepticus]. 789 43

The mentally retarded often need concomitant antiepileptic and neuroleptic drug treatment. High doses of neuroleptic drugs may provoke seizures. Antiepileptic drugs may aggravate behavioural problems. The mutual influence of neuroleptic and antiepileptic drug treatment and the effect of seizure control were studied in 20 mentally retarded patients between 1980 and 1989. The treatment was tailored individually, aiming at the lowest effective dose. Carbamazepine was preferred to phenobarbital and phenytoin. The mean defined daily dose (DDD) of neuroleptics and antiepileptics was reduced by 64% and 5%, respectively. Changing the mean DDD of neuroleptics neither correlated significantly with seizure activity nor with the change of the mean DDD of the antiepileptics. Evidently, seizure control may be improved by small neuroleptic doses in some patients. In one patient, however, a non-convulsive status epilepticus was associated with the introduction of neuroleptics. The assumption that carbamazepine has a beneficial effect on behavioural problems was not supported. Apparently, changing the regime of antiepileptics contributed to less neuroleptic requirements, possibly through reduced side-effects and/or improved seizure control. When combining neuroleptics and antiepileptics, interactions should always be considered. The epileptogenic effect of small to standard doses of neuroleptic drugs should, however, not be overemphasized.
Seizure 1993 Sep
PMID:Neuroleptic and antiepileptic treatment in the mentally retarded. 790 68

The effects of two protein synthesis inhibitors, cycloheximide and anisomycin, were tested on seizures induced by coadministration of lithium and pilocarpine to rats. Systemic cycloheximide (2 mg/kg, s.c.) and centrally administered anisomycin (300 micrograms/10 microliters, i.c.v.) doubled the latency to initiation of seizures and to status epilepticus, while peripherally administered anisomycin (50 mg/kg, s.c.) completely blocked lithium-pilocarpine seizures. These results indicate that protein synthesis is required for initiation of seizures.
Exp Neurol 1994 Sep
PMID:Protein synthesis inhibitors attenuate seizures induced in rats by lithium plus pilocarpine. 792 39


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