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)

Changing attitudes towards the use of antiepileptic drugs have led to an emphasis on monotherapy with serum concentration measurement coupled with standard, weight-adjusted starting and maintenance regimens to guide initial therapy and subsequent dosage titration. Currently, the established anticonvulsants are carbamazepine, valproic acid (sodium valproate) and phenytoin. Phenobarbital is now less commonly prescribed due to its propensity to produce sedation and impair cognitive function. The value of pharmacokinetic optimisation with valproic acid is limited by its wide therapeutic index, large fluctuations in the concentration-time profile and concentration-dependent protein binding. Thus, although serum concentrations are often measured, they are rarely subjected to pharmacokinetic interpretation. Carbamazepine has a flatter concentration-time profile than valproic acid. Its target range is more clearly defined and it undergoes autoinduction of metabolism and interacts with other drugs. Pharmacokinetic principles can, therefore, be more readily applied to carbamazepine, although, in general, a simple clinical approach to its use is usually satisfactory. Phenytoin has required the greatest pharmacokinetic input due to its nonlinear pharmacokinetics and narrow target range. Many different graphical methods, equations and computer programs have been reported, some of which demand 2 steady-state, dose-concentration pairs; others function satisfactorily with only 1. Recent attempts have been made to interpret non-steady-state data. In addition, a number of workers have demonstrated the value of altering the population parameter estimates to account for ethnic differences. A pharmacokinetic approach can also be used to tailor the use of phenytoin in the treatment of status epilepticus. Dosage alterations may be needed for specific patient groups. In particular, children generally require higher dosages on a weight-for-weight basis than adults, while equivalently lower dosages should be given to neonates. Most anticonvulsants are principally cleared by hepatic mechanisms, so dosage adjustment is not usually required in renal disease, although care must be taken in interpreting serum concentrations because of changes in protein binding. Close monitoring is required in the elderly and patients with hepatic impairment, while increased dosages may be needed in critically ill patients and during pregnancy. Pharmacokinetic principles can be used in the treatment of treat self-poisoning with anticonvulsants. There are few data available on the pharmacokinetics of vigabatrin, lamotrigine, oxcarbazepine and gabapentin in patients. Due to its mode of action in binding irreversibly to its target enzyme, serum concentration monitoring of vigabatrin plays no role in optimising therapy. The value of applying pharmacokinetic principles with the other 3 drugs remains to be investigated.(ABSTRACT TRUNCATED AT 400 WORDS)
Clin Pharmacokinet 1992 Sep
PMID:Pharmacokinetic optimisation of anticonvulsant therapy. 151 37

In conscious rats, continuous i.v. infusion of cocaine (2 mg/kg/min) produced a marked increase in blood pressure, an initial moderate increase followed by a decrease in heart rate, tonic-clonic convulsions and, finally, a lethal episode of status epilepticus. No change in rectal temperature was observed. Infusion of cocaine methiodide (2 mg/kg/min), a quaternary derivative of cocaine, also produced a lethal episode of status epilepticus, but it was 6 times less potent than cocaine on a molar basis. In pentobarbital-anesthetized, spontaneously breathing rats, cocaine produced death by respiratory failure. Artificial ventilation of pentobarbital-anesthetized rats elevated the lethal dose of cocaine by 15-fold and these animals died of marked hypotension. In conscious rats, pretreatment with dl-, d- or l-propranolol or the alpha 2-selective adrenoceptor antagonist yohimbine enhanced the convulsive and lethal effects of cocaine. In contrast, the alpha 2-selective adrenoceptor agonist clonidine or the alpha 1-selective adrenoceptor antagonist prazosin attenuated these effects. Yohimbine antagonized the protective effect of clonidine. The nonselective alpha adrenoceptor antagonist phentolamine, the autonomic ganglionic blocker chlorisondamine and various calcium channel blockers had no effect on the convulsive or lethal doses of cocaine. The pressor response to cocaine was attenuated by calcium channel blockers, clonidine, phentolamine and dl- or l-propranolol, but not by d-propranolol. The pressor response to cocaine was abolished by chlorisondamine, reversed to a depressor response by prazosin and enhanced by yohimbine. The initial tachycardiac response to cocaine was reversed to bradycardia by dl- and l-propranolol, prazosin, yohimbine or high doses of the calcium channel blockers, but was unaffected by phentolamine, d-propranolol, clonidine or chlorisondamine. These results indicate that in spontaneously breathing animals, acute i.v. infusions of lethal doses of cocaine produce death primarily by central effects, namely by status epilepticus in conscious rats and by respiratory arrest in pentobarbital-anesthetized rats. In artificially ventilated, pentobarbital-anesthetized rats, however, cocaine produces death by effects on the cardiovascular system. In conscious rats, endogenous alpha 1 adrenoceptors exert a deleterious influence on cocaine-induced convulsive and lethal effects, whereas alpha 2 adrenoceptors provide protective influence. Propranolol appears to enhance cocaine-induced acute lethality through a mechanism independent of beta adrenoceptors. Calcium channel blockers appear ineffective in antagonizing cocaine's lethality.
J Pharmacol Exp Ther 1992 Sep
PMID:Pathophysiological and pharmacological mechanisms of acute cocaine toxicity in conscious rats. 152 34

We report ictal phenomena in two patients with the 4p- syndrome captured on simultaneous video-EEG monitor. One patient, diagnosed as having partial epilepsy, had complex partial seizures and hemiconvulsive status epilepticus. This was associated with more severe mental retardation. The second patient was diagnosed as having the West syndrome and exhibited tonic spasms with a cluster formation. We conclude that various types of epileptic seizures may occur in patients with the 4p- syndrome, including grand mal and myoclonic seizures.
Jpn J Psychiatry Neurol 1991 Sep
PMID:Epileptic seizures in the 4p- syndrome: report of two cases. 180 Aug 12

Status epilepticus, especially the convulsive type, is a medical emergency. Initial treatments include clearing the airway and giving diazepam intravenously (preferably) or rectally. Clonazepam is equally effective. A loading dose of phenytoin should be given to maintain seizure control.
Aust Fam Physician 1991 Sep
PMID:Status epilepticus. 195 68

Cyclosporine is a potent immunosuppressant that is more and more widely used, particularly after organ transplantations. Many neurological side effects, including convulsions, that could be related to this drug, have been previously observed, most often with high blood concentrations. We report, for the first time, a case of prolonged confusion where a non convulsive status epilepticus may be discussed. It occurred in a 64-year-old woman, 17 days after a liver transplantation. The whole blood cyclosporine value was 230 micrograms/l (normal range: 100-200 micrograms/l) at the beginning of the status epilepticus. The cyclosporine imputability and the part of other factors that could have facilite are discussed.
Neurophysiol Clin 1990 Sep
PMID:[Prolonged confusion syndrome in the course of cyclosporine treatment: a state of confusion?]. 223 52

Significant neurotoxicity including seizures, encephalopathy and coma may complicate the use of cyclosporin A (CyA). Two patients are described, receiving CyA, who presented with abnormal behaviour, stupor, focal motor activity and were shown to be in complex partial status epilepticus (CPSE). Abnormalities of behaviour and/or stupor in patients receiving CyA may be a manifestation of CPSE. Patients receiving CyA who develop an encephalopathy should have electroencephalography performed at the time of the abnormal behaviour.
J Neurol Neurosurg Psychiatry 1989 Sep
PMID:Complex partial status epilepticus associated with cyclosporin A therapy. 250 48

We measured the effects of four weeks of dietary lithium treatment and of status epilepticus induced by administration of pilocarpine to lithium-treated rats on the concentrations of amino acids in four regions of rat brain: cerebral cortex, hippocampus, striatum, and substantia nigra. To ensure accurate quantitation of the amino acids, animals were sacrificed by focussed beam microwave irradiation and amino acids were measured using a fully validated triple-column ion-exchanged amino acid analyzer with post-column o-phthalaldehyde derivatization and fluorometric detection. The concentrations of four amino acids, threonine, methionine, lysine and tyrosine, were increased significantly in two to four brain regions by chronic lithium treatment. Their concentrations remained elevated, or were further increased, during status epilepticus. The concentrations of eight amino acids and ammonia were not altered by lithium treatment but increased in concentration during status epilepticus in some brain regions. Glycine, serine, arginine and citrulline were decreased by chronic lithium treatment. Status epilepticus increased the concentrations of these four amino acids above that found in the lithium-treated samples in some of the brain regions that were examined. Six amino acids and glutathione were generally unaltered by both treatments. These results are related to the effects of lithium treatment and are compared with changes reported by others following treatment with a variety of convulsive stimuli.
Neurochem Res 1989 Sep
PMID:Chronic lithium treatment and status epilepticus induced by lithium and pilocarpine cause selective changes of amino acid concentrations in rat brain regions. 259 48

The authors studied the availability of parenteral solutions of diazepam in glass bottles or polyethylene (PE) containers during infusion through polyvinyl chloride (PVC) administration sets. Diazepam solutions in concentration of 1000 mg/500 ml in 0.9% sodium chloride (NS) and 5% glucose (G5W) injection were infused at a flow rate of 30 ml/h, and samples were taken from the bottle and at the end of the administration set, till 12 hours of infusion. The samples were tested in triplicate using ultraviolet spectrophotometry. The greatest loss of diazepam was observed in all solutions at 30 minutes of infusion (63.5% G5W glass, 60.5% NS glass, 55% G5W PE and 58% NS PE from the original concentration of 200 micrograms/ml). The diazepam concentrations in the containers did not significantly changed. The loss of diazepam from solutions infused through PVC administration sets should be kept in mind in severe clinical situations as status epilepticus, tetanus and eclampsia.
Arq Neuropsiquiatr 1989 Sep
PMID:Factors affecting diazepam availability from intravenous admixture solutions. 261 6

Limbic status epilepticus was induced by means of a KA microinjection into unilateral amygdala, and the focus extirpation (amygdalotomy) was made in order to examine whether the status was suppressed or not. The amygdalotomy was effective when the status was mild and the focus was circumscribed to the amygdala. However, the surgery was no more effective when a severe limbic status was induced and a secondary epileptogenic focus was established. Within 8 hours after induction of the limbic status, neuronal cell damage was observed in the pyramidal cell layer of the hippocampus.
Jpn J Psychiatry Neurol 1989 Sep
PMID:Surgical treatment of experimental limbic status epilepticus. 262 91

We report an infant with Shaken Baby syndrome (SBS) who presented with status epilepticus. The initial evaluation with computerized axial tomography (CAT scan) of the head was normal, and there was no history or physical finding consistent with physical abuse or shaking. This prompted an extensive evaluation to determine the etiology of the seizures. An ophthalmology consultation revealed the presence of severe bilateral retinal hemorrhages, which raised the possibility of SBS. Magnetic resonance imaging (MRI) showed cerebral hemorrhages, hemorrhagic contusions, and bilateral subtemporal subdural hematomas. This is the first reported case of SBS diagnosed by magnetic resonance imaging following a normal initial CAT scan. MRI may be a valuable tool in the diagnosis of brain injury in SBS and may be particularly valuable when the CAT scan of the head is normal, the etiology of neurologic injury is unclear, and the presence of retinal hemorrhages raises the suspicion of SBS.
Pediatr Emerg Care 1989 Sep
PMID:Shaken baby syndrome diagnosed by magnetic resonance imaging. 269 92


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