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)

Benzodiazepines (BDZ) interact with components of neuronal membranes to modify excitability in three different ways. Action at a high affinity central receptor (dissociation constant, KD, of 3 nM) linked to the GABAA recognition site enhances the inhibitory action of GABA by increasing the number of openings of Cl- channels produced by a given concentration of GABA. This effect correlates with anticonvulsant activity as evaluated in the antipentylenetetrazol test in animals and with antimyoclonic activity in human beings. It also correlates with anxiolytic activity. Action at a lower affinity membrane site (KD 100 nM to 1 microM) limits repetitive firing as observed in isolated neurons (in a manner similar to the action of phenytoin or carbamazepine). This does not depend primarily on neurotransmitter mechanisms, but probably involves an increase in the population of sodium channels in the inactive state. Action at a lower affinity site (KD 45 microM) in presynaptic terminals decreases voltage sensitive Ca++ conductance and, by limiting Ca++ entry, decreases neurotransmitter release. The two lower affinity BDZ systems may be responsible for therapeutic action in status epilepticus and for sedative side-effects. The high affinity central benzodiazepine binding sites can be differentiated into BZ1 and BZ2 receptors by ligands (such as triazolopyridazines and Quazepam) that preferentially act on BZ1 sites. There are regional differences in the density of the two receptor subtypes, but these have not yet been correlated with specific actions of benzodiazepines. Differences between various 1,4- and 1,5-benzodiazepines in terms of therapeutic action in epilepsy and neurologic side-effects can probably be explained on the basis of variation in full or partial agonist action at the high affinity central receptor, or differing relative action at the high and low affinity receptors.
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PMID:Benzodiazepine receptors and their relationship to the treatment of epilepsy. 301 90

Five patients with severe hyponatraemia and epileptiform seizures were given 50 ml of 29.2% saline (250 mmol) through a central venous catheter over 10 minutes to control seizures rapidly, reduce cerebral oedema, and diminish the incidence of permanent neuronal damage. The saline controlled seizures in all patients, increasing the mean serum sodium concentration by 7.4 (SD 1.14) mmol(mEq)/l and decreasing the mean serum potassium concentration by 0.62 (0.5) mmol(mEq)/l. Further saline and frusemide were then administered over 10 (2) hours, raising the serum sodium concentration by 2.14 (0.49) mmol/l/h until it reached 133 (2.35) mmol/l. A total of 790 (139) mmol saline was infused and a negative fluid balance of 3.34 (0.75) litres achieved. Four patients survived without neurological abnormality. One patient, who was not treated immediately and suffered a prolonged episode of status epilepticus, was left with a permanent neurological defect.
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PMID:Treatment of hyponatraemic seizures with intravenous 29.2% saline. 308 Jan 18

The usefulness of the anticonvulsant drugs is determined by the mechanisms by which the agent acts and its pharmacokinetics. The general mechanisms of action of these agents include (1) effects on neurotransmitter action, (2) effects on repetitive neuronal firing mechanisms, (3) effects on neuronal networks, and (4) effects on neuronal ionic transport. Ethosuximide, valproic acid and clonazepam are used primarily in absence epilepsy. Valproic acid is also effective against generalized tonic-clonic epilepsy. Diazepam is used primarily in status epilepticus. Valproic acid enhances gamma aminobutyric acid (GABA)-mediated inhibition, reduces repetitive firing, and reduces both inhibition and excitation in neuronal networks. Clonazepam and diazepam enhance the inhibitory action of GABA, decrease inhibition in neuronal networks and affect calcium ion transport with lesser effects on repetitive firing. Ethosuximide reduces inhibition in neuronal networks, may interact with dopamine, and possibly affects sodium and potassium ion transport. Further work is needed to assess the degree of involvement of these effects in the anticonvulsant action versus the adverse effects of these agents.
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PMID:Mechanisms of anticonvulsant drug action. II. Drugs primarily used for absence epilepsy. 310 94

A 5 years old girl with status epilepticus refractory to treatment with Diphenylhydantoin at a dose of 30 mg/kg/day and Thiopental in continuous IV perfusion at a dose of 4 mg/kg/h is presented. Control of status was achieved by continuous IV perfusion of Chlormethiazole at a dose of 10 mg/kg/h which also caused respiratory depression. Seizure activity reappeared after IV perfusion of Chlormethiazole was retired, and could be controlled only with Sodium Valproate. Mechanisms of action of Chlormethiazole and its effectiveness in treatment of refractory status epilepticus are revised.
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PMID:[Treatment of refractory status convulsivus with chlormethiazole]. 314 89

The muscarinic cholinergic agonist pilocarpine induces in rats seizures and status epilepticus followed by widespread damage to the forebrain. The present study was designed to investigate the effect of 5 non-steroidal anti-inflammatory drugs, sodium salicylate, phenylbutazone, indomethacin, ibuprofen and mefenamic acid, on seizures produced by pilocarpine. Pretreatment of rats with sodium salicylate, ED50 103 mg/kg (60-174), and phenylbutazone, 59 mg/kg (50-70) converted the non-convulsant dose of pilocarpine, 200 mg/kg, to a convulsant one. Indomethacin, 1-10 mg/kg, and ibuprofen, 10-100 mg/kg, failed to modulate seizures produced by pilocarpine. Mefenamic acid, 26 (22-30) mg/kg, prevented seizures and protected rats from seizure-related brain damage induced by pilocarpine, 380 mg/kg. These results indicate that non-steroidal anti-inflammatory drugs differentially modulate the threshold for pilocarpine-induced seizures.
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PMID:Differential effects of non-steroidal anti-inflammatory drugs on seizures produced by pilocarpine in rats. 319 89

The results of the multiple-modality treatment of epilepsy in 56 children of different age with the use of thiopental-sodium are presented. It has been shown that its early administration to children with a true status epilepticus makes it possible to faster bring the patient out of the pathologic condition as compared to the conventional methods of treatment. In patients with a symptomatic epistatus and in children with marked residual-organic cerebral insufficiency associated with the development of convulsions anticonvulsive therapy should be combined with the treatment of the underlying disease aimed at the correction of extra- and intracranial homeostasis.
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PMID:[Treatment of status epilepticus in children with short-acting barbiturates]. 330 47

The ability of various drugs to prevent the onset of status epilepticus induced by administration of the muscarinic agonist, pilocarpine, to lithium-pretreated rats was determined. Motor limbic seizures and status epilepticus occurred in 100% of rats administered pilocarpine (30 mg/kg, s.c.) 20 h after pretreatment with lithium (3 meq/kg, i.p.). The latency to spike activity and to status epilepticus was 20 +/- 1 min and 24 +/- 1 min, respectively. Atropine, diazepam, phenytoin, carbamazepine, phenobarbital, paraldehyde, and L-phenylisopropyladenosine (L-PIA) prevented all phases of seizure activity induced by lithium/pilocarpine treatment. The initiation of status epilepticus was significantly prolonged by pretreatment with sodium valproate. These findings indicate that the seizures induced by administration of lithium and pilocarpine accurately model generalized tonic-clonic epilepsy. The anticonvulsant activity of L-PIA was prevented by prior treatment with the adenosine antagonist, theophylline. The latency to spike and seizure activity was decreased by theophylline, indicating that endogenous adenosine may have a tonic inhibitory influence on cholinergic neurons. Atropine, diazepam, phenobarbital, phenytoin, sodium valproate, L-PIA, and carbamazepine did not interrupt seizure activity when administered 60 min after pilocarpine (approximately 35 min after initiation of status epilepticus). When rats were administered paraldehyde at this time, status epilepticus was rapidly terminated and all rats survived. Thus, status epilepticus induced by lithium and pilocarpine provides a seizure model that is not responsive to conventional anticonvulsants.
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PMID:Effects of drugs on the initiation and maintenance of status epilepticus induced by administration of pilocarpine to lithium-pretreated rats. 358 62

Single doses of phenytoin (500 and 1.000 mg), carbamazepine 400 and 1.00 mg) and sodium valproate (600 mg) were given orally to 5 healthy young volunteers and serum concentrations determined between 1-8h after administration. The design was double-blind and placebo-controlled. Serum concentrations considered "therapeutic" were obtained after sodium valproate and the 100 mg dose of carbamazepine. The results suggest the loading-doses of phenytoin (1500-2000 mg) and carbamazepine (800 mg) are useful in the subacute control of frequent epileptic seizures on an out-patient basis, and that carbamazepine may be used for lasting control of seizures of status epilepticus treated initially with diazepam or other rapidly-acting preparation.
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PMID:[Efficient serum concentrations after single doses of antiepileptic drugs: concept of loading-dose]. 392 29

Poisoning is an uncommon manifestation of child abuse. The intentional administration of water to a child as a form of punishment has rarely been reported as the responsible substance among children who have been poisoned. We describe a case of a 5-year-old girl presenting with severe hyponatremia due to acute water intoxication. The patient was brought to the emergency room in status epilepticus. A history was obtained from the child's mother stating that the patient had been playing outside when she collapsed. She had had no known prior illnesses. Laboratory evaluation included a hemoglobin of 10.1 mg%, glucose of 60 mg%, serum sodium of 107 mEq/l, potassium of 3.2 mEq/l and chloride of 71 mEq/l. A CAT scan obtained approximately 1 h after admission revealed generalized cerebral edema. Careful examination of the skin revealed multiple linear ecchymosis of varying ages on the back and thighs and a hand print on the right flank. In addition, the child demonstrated severe failure to thrive with height, weight and bone age compatible with a 2.5-year-old girl. Appropriate therapy for severe hyponatremia was successfully instituted. For the next 12 h she was deeply somnolent, but the following morning was alert and conversant. She stated that she "would be good if she didn't have to drink any more water". The child's mother subsequently admitted that she frequently used water ingestion as a form of punishment. The child stabilized metabolically and demonstrated rapid in-hospital weight gain. She was placed in foster care at discharge and has had no further hyponatremia or seizures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyponatremic seizures as a presenting symptom of child abuse. 395 93

Pharmacokinetics as the basis for dosage calculation for acute and subacute treatment of status epilepticus have been discussed. Bolus injection and intravenous infusion are the most common forms of drug administration in these cases. Rectal administration may be a good alternative in certain conditions. Intravenous diazepam and phenytoin are the first-line drugs against status epilepticus. Diazepam and sodium valproate have been reported to be effective by the rectal route. Depending on its pharmacokinetic parameters, each drug effect has a different onset, intensity, and time course.
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PMID:Clinical pharmacokinetics of drugs used in the treatment of status epilepticus. 640 95


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