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)

Frequent epileptic seizures in children are often related to delayed psychomotor development, and status epilepticus is always a neurological emergency. In both situations barbiturate anaesthesia has been used for status epilepticus since the 1960s, and for intractable seizures in children since the 1980s. However, the clinical results on the effectiveness of barbiturate anaesthesia in children with chronic epileptic disorders remain contradictory. Between 1986 and 1991 in Tampere University Hospital in Finland long barbiturate anaesthesia was introduced--using thiopentone sodium--to eight children with very severe epilepsy. Children were 10 months to 7 years 11 months of age and the mean time from the onset of seizures to the introduction of BA was 2 years 8 months. Effects upon seizure frequency, antiepileptic medication and/or psychomotor development were clearly positive in three patients, slightly positive in one patient and in four patients there was no effect. Good effect seemed to be associated with an anaesthesia which is deep and long enough to produce loss of consciousness and spontaneous reactions, and an electroencephalographic pattern of burst-suppression. Positive results were also more often achieved when the treatment lag was less than 12 months. Physical and neurophysiological properties of barbiturates make their effectiveness as anticonvulsants understandable, but there is only little evidence to explain the mechanism of this action.
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PMID:Effects of long barbiturate anaesthesia on eight children with severe epilepsy. 830 18

A 78-year-old woman was admitted to our hospital because of disorientation and fever on January 21, 1992. Two days before admission she experienced vomiting, anorexia and general malaise. Laboratory examinations on admission disclosed a hemoglobin level of 11.1 g/dl and a platelet count of 8,000/microliters. The peripheral blood smear revealed anisocytosis with numerous schistocytes and poikilocytes. Polychromatophilic and nucleated red blood cells were also seen, and the reticulocyte count was 38/1000. Her serum lactate dehydrogenase (LDH) value was 2,977 WU and the total serum bilirubin level was 3.5 mg/dl with 2.7 mg/dl indirect reacting fraction. Serum creatinine was 4.7 mg/dl. Her consciousness became semicomatose after a systemic seizure which lasted approximately 15 seconds and her hemoglobin level decreased to 8.5 g/dl on hospital day 2. Therefore, we diagnosed her as having thrombotic thrombocytopenic purpura (TTP) because of the presence of all 5 features, that is, thrombocytopenia, microangiopathic hemolytic anemia, fluctuating neurologic abnormalities, renal dysfunction and fever. A plasmapheresis with fresh frozen plasma (FFP) replacement was begun on that day. She was also treated with anti-platelet agents, 80 mg/day aspirin, and 300 mg/day dipyridamole. Moreover, packed red blood cells (PRC) were infused. While also receiving diphenylhydantoin and phenobarbital to prevent convulsions, status epilepticus developed on day 3. Because of inhibited spontaneous respiration which was an adverse effect derived from diazepam and sodium thiamylal administered intravenously to treat the status epilepticus, an artificial respiration was initiated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An elderly case of thrombotic thrombocytopenic purpura]. 848 87

We studied causes of new-onset seizures in 55 patients admitted to medical and surgical intensive care units between 1981 and 1991. In one-third of the patients, sudden withdrawal of narcotic agents was associated with tonic-clonic seizures. In another third, acute metabolic changes, predominantly severe hyponatremia (sodium < or = 125 mEq/l), accounted for new-onset seizures. In eight patients, drug toxicity (antibiotics and antiarrhythmic agents) predisposed to seizures. Only five patients had previously unrecognized structural CNS abnormalities that were manifested by focal or generalized tonic-clonic seizures. In six patients, the cause remained unknown. Twenty-four patients had recurrent seizures despite treatment with standard antiepileptic drugs. Status epilepticus occurred in four patients. Outcome was poor in only 34% of the patients, particularly in those with metabolic causes. Sudden withdrawal of narcotic drugs may be a significant cause of new-onset seizures in patients with life-threatening disorders.
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PMID:New-onset seizures in critically ill patients. 849 24

Administration of subconvulsive dose of pilocarpine (30 mg/kg s.c.) to rats pretreated with lithium chloride (3 meq/kg i.p.) produced a state of status epilepticus in animals. The animals showed characteristic symptoms of generalized convulsions, wet dog shakes (WDS), forelimb clonus and falling back. The symptoms of status epilepticus (SE) developed within 26.8 +/- 3.6 min after administering pilocarpine and these symptoms continued uninterrupted. The phenomenon was totally reproducible, with a consistent latency of onset of seizures and a high mortality rate. The symptoms were blocked by atropine, scopolamine and the GABAergic agents GABA, sodium valproate, (+)-baclofen and clonazepam when given prior to pilocarpine, but not when administered 30 min after pilocarpine administration.
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PMID:Protective effects of GABAergic drugs and other anticonvulsants in lithium-pilocarpine-induced status epilepticus. 881 69

Fosphenytoin sodium is reviewed, and its safety is compared with that of phenytoin. After i.v. or i.m. injection, fosphenytoin, a phenytoin prodrug, is rapidly hydrolyzed to phenytoin. Free-phenytoin concentrations equivalent to those obtained with i.v. phenytoin can be achieved with fosphenytoin given at equimolar loading doses by selecting the appropriate rate of fosphenytoin administration. Fosphenytoin can be expected to interact with the same drugs that interact with phenytoin. The dosage is expressed as phenytoin sodium equivalents (PE). The standard loading dose for adults with status epilepticus is 15-20 mg PE/kg i.v. infused at 100-150 mg/min; i.m. administration is not recommended for this condition. For nonemergency situations, a 10- to 20-mg PE/kg loading dose can be given i.v. or i.m. Fosphenytoin has advantages over phenytoin injection that are related to its greater aqueous solubility, which obviates the extreme alkalinity, propylene glycol, and ethanol needed in the injectable phenytoin formulation. Intravenous fosphenytoin has been associated with less soft-tissue injury and fewer adverse effects in general than phenytoin. Fosphenytoin, when administered i.m., is completely absorbed, is relatively well tolerated, and provides more predictable serum drug concentrations than i.m. phenytoin. Fosphenytoin offers practical and clinical advantages over i.v. phenytoin.
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PMID:Safety of fosphenytoin sodium. 904 73

Fosphenytoin is a phosphate ester prodrug of phenytoin developed as a replacement for standard injectable sodium phenytoin. After absorption, phenytoin is cleaved (conversion half-life 8-15 min) from fosphenytoin. Unlike phenytoin, fosphenytoin is freely soluble in aqueous solutions (including standard intravenous solutions) and rapidly absorbed by the intramuscular route. Fosphenytoin has been tested successfully for three indications in humans: intramuscular maintenance dosing, intramuscular loading dose administration, and intravenous treatment of status epilepticus. Local toxicity (pain, burning, itching) is less by the intramuscular or intravenous route for fosphenytoin than for standard injectable sodium phenytoin. Systemic toxicity is similar with both preparations except that hypotension is less common and paresthesias are more common with fosphenytoin.
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PMID:Fosphenytoin (Cerebyx). 903 68

A case of adult Reye's syndrome is described. A previously healthy 17-year-old man developed convulsions 2 days after resolution of an upper respiratory infection with parainfluenza virus type 3. During the preceding infection, he took aspirin. On admission, he was drowsy. There was no focal signs. Cranial CT scan was unremarkable. A lumbar puncture revealed an opening pressure of 180 mm H2O; the cerebrospinal fluid was acellular with normal protein level. Serum chemistry showed elevated transaminase activities and normal bilirubin level. Blood ammonia level was high; urea and citrulline levels were abnormally low. These abnormalities disappeared later, suggesting transient cysfunction of mitochondrial urea-cycle enzymes. Free and acyl carnitine levels were unremarkable. Both metabolic acidosis and ketonuria were absent. Thus, a variety of aminoacidurias and organic acidemias are unlikely. All these findings meet diagnostic criteria for Rye's syndrome proposed by the CDC of the USA. Status epilepticus was treated with intravenous infusion of thiamylal sodium. He was treated with hypertonic glucose solution and osmotic diuretic. Three months after the onset of the illness, his convulsions were controlled only with zonisamide, clonazepam, and carbamazepine. He had motor dysfunctions. This case is unique in that a patient with adult Reye's syndrome and status epilepticus favorably recovered.
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PMID:[A case of adult Reye's syndrome with favorable outcome despite status epilepticus]. 904 59

Mechanisms of brain damage subserving chronic impairment of recent memory and a rationale for terminating convulsive status epilepticus within 60 minutes is discussed. Available first agent regimens (diazepam plus phenytoin, lorazepam alone, barbiturates alone, and phenytoin alone) and the properties of the ideal drug for status epilepticus will be reviewed. A new updated protocol is presented considering the type of status and EEG characteristics. Primary tonic-clonic or clonic-tonic-clonic status, with 8 Hz diffuse sharp rhythms or 2-5 Hz spike or multispike wave complexes and secondary tonic-clonic status with focal 12-18 Hz spikes spreading diffusely can receive intravenous lorazepam as the first agent. Complex partial status and absence status can also receive lorazepam as the first agent. Tonic status and atypical absence status can be treated with phenytoin infusion or rectal sodium valproate. Convulsive status which do not respond to available first agent regimens should be terminated by barbiturate of fluothane general anesthesia.
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PMID:Status epilepticus: recent trends and prospects. 947 Apr 39

The pool of zinc present in excitatory synaptic terminals in normal and pathological conditions (for instance the status epilepticus induced by kainic acid) can be stained by a silver sulphide method followed by physical development of the insoluble zinc-sulphide complexes. In this study we applied a previously described simple and rapid developing procedure that reveals synaptic zinc, to the study of normal and pathological hippocampi and combined it with pre and postembedding immunocytochemical methods to detect different antigens. Normal and kainic acid-treated rats were perfused with fixative solutions containing sodium sulphide and 50 microm-thick vibratome sections of the hippocampi were incubated in a commercial developing solution (IntenSE M, Amersham). The developed vibratome sections were then (1) mounted for light microscopy or osmicated and epon-embedded for electron microscopy; or (2) processed for the preembedding immunoenzymatic detection of various antigens (GABA, parvalbumin, calbindin) with light and electron microscopy. Thin sections from epon-embedded samples were also processed for the postembedding immunogold localization of glutamate. This very simple and rapid procedure gives rise to zinc-specific staining, comparable to that obtained with classical developing methods and good preservation of both antigenicity and ultrastructure. It is therefore possible to detect, in the same thick or thin section, zinc reaction product and different antigens.
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PMID:A simplified procedure for the physical development of the sulphide silver method to reveal synaptic zinc in combination with immunocytochemistry at light and electron microscopy. 953 64

The mechanisms by which neurons die after stroke and status epilepticus and related neuropathological conditions are unclear, but may involve voltage-dependent Na+ channels, glutamate receptors, and nitric oxide (NO.). These questions were investigated using an in vitro primary cell culture model in which hippocampal pyramidal neurons undergo a gradual and delayed neurodegeneration induced by enhanced excitatory neurotransmission. When cells were treated with Mg2+-free, glycine-supplemented medium for a brief period (15 min) and examined 24 h later, approximately 30-40% of the neurons had died. Cell death could be inhibited by blockers of voltage-sensitive Na+ channels and by N-methyl-D-aspartate receptor antagonists. Application of either the endogenous antioxidant melatonin (EC50: 19.2+/-2.8 microM) or the NO. synthase inhibitor Nomega-nitro-L-arginine after, but not during, Mg2+-free exposure protected against delayed neuronal death; significant neuroprotection was observed when the addition was delayed for up to 4 h. This operational time window suggests that an enduring production of NO. and reactive oxygen species from neuronal sources is responsible for delayed cell death. A role for reactive oxygen species in this injury process was strengthened by the finding that, whereas neurons cocultured with astroglia were more resistant to killing, agents capable of lowering intracellular glutathione negated this protection. Because secretion levels of melatonin are decreased with aging, reductions in this pineal hormone may place neurons at a heightened risk for damage by excitatory synaptic transmission.
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PMID:Melatonin prevents the delayed death of hippocampal neurons induced by enhanced excitatory neurotransmission and the nitridergic pathway. 961 51


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