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)

Propofol (2, 6-diisopropylphenol) is a potent intravenous hypnotic agent which is widely used for the induction and maintenance of anesthesia and for sedation in the intensive care unit. Propofol is an oil at room temperature and insoluble in aqueous solution. Present formulations consists of 1% or 2% (w/v) propofol, 10% soybean oil, 2.25% glycerol, and 1.2% egg phosphatide. Disodium edetate (EDTA) or metabisulfite is added to retard bacterial and fungal growth. Propofol is a global central nervous system depressant. It directly activates GABA(A) receptors. In addition, propofol inhibits the NMDA receptor and modulates calcium influx through slow calcium ion channels. Propofol has a rapid onset of action with a dose-related hypnotic effect. Recovery is rapid even after prolonged use. Propofol decreases cerebral oxygen consumption, reduces intracranial pressure and has potent anti-convulsant properties. It is a potent antioxidant, has anti-inflammatory properties and is a bronchodilator. As a consequence of these properties propofol is being increasingly used in the management of traumatic head injury, status epilepticus, delirium tremens, status asthmaticus and in critically ill septic patients. Propofol has a remarkable safety profile. Dose dependent hypotension is the commonest complication; particularly in volume depleted patients. Hypertriglyceridemia and pancreatitis are uncommon complications. Allergic complications, which may include bronchospasm, have been reported with the formulation containing metabisulfite. In addition, this formulation has been demonstrated to result in the generation of oxygen free radicals. High dose propofol infusions have been associated with the "propofol syndrome"; this is a potentially fatal complication characterized by severe metabolic acidosis and circulatory collapse. This is a rare complication first reported in pediatric patients and believed to be due to decreased transmembrane electrical potential and alteration of electron transport across the inner mitochondrial membrane.
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PMID:Propofol: therapeutic indications and side-effects. 1557 60

A 40-year-old woman was diagnosed with iron deficiency anemia (hemoglobin 3.5 g/dl) induced by uterine myomas, and admitted to the Department of Gynecology of our hospital. During admission, she underwent the daily intravenous administration of saccharated ferric oxide for 3 weeks, and monthly GnRH analogue administration was started. Her hemoglobin level acutely increased to 9.3 g/dl over the next 18 days with normal blood pressure. Thirteen days after the 3rd administration of the GnRH analogue, she suddenly developed marked headache. Just before the onset, she had been driving a car, and spun the steering wheel to avoid a traffic accident on a busy street. This headache was so severe that she was brought to our hospital by ambulance. During transport to the hospital, her blood pressure was normal. Soon after arriving, she developed generalized convulsions, followed by status epilepticus. A brain MRI showed vasogenic edema in the posterior and parietal cortices including white matter bilaterally, and minimum subarachnoid hemorrhage was indicated in the bilateral frontal lobe and right temporal lobe. CSF analysis was unremarkable. Anticonvulsants, one course of steroid pulse therapy and glycerol were started, and status epilepticus disappeared on the same day. Abnormal areas on MRI decreased gradually. However, hyperintensity on T1- and FLAIR images remained in the right parietal lobe and bilateral occipital lobe white matter at 15 months after the onset Judging from the clinical and radiological findings, this patient was diagnosed as reversible posterior leukoencephalopathy syndrome (RPLS) accompanied with subarachnoid hemorrhage. This case suggests that an unexpected prompt physical activity or astonishment would induce RPLS in a patient treated with GnRH analogue.
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PMID:[Acutely developed reversible posterior leukoencephalopathy syndrome following a prompt physical activity to avoid a traffic accident: a case report]. 1992 86

We report a case of a 56-year-old woman admitted to our hospital for status epilepticus. Three months before hospitalization, the patient underwent gross total removal of a glioblastoma with BCNU wafer implantation in the left parietal lobe. The cavity was subsequently lined with five BCNU wafers. After admission, magnetic resonance imaging(MRI)showed cyst formation accompanied by strong edema, with no recurrence of glioblastoma. She was initially administered antiepileptic drugs and glycerol with betamethasone, after which her seizures stopped but recurred one month later due to a decrease in betamethasone. The BCNU wafers were removed four months after the initial surgery, after which the seizures completely stopped. Histopathological examination of the cavity indicated the presence of inflamed tissue and no recurrence of glioblastoma. Neurosurgeons should be aware of the possibility of cyst formation after BCNU wafer implantation for malignant gliomas. In this manuscript, we provide a case presentation and a review of the literature.
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PMID:[A Case of Symptomatic Cyst Formation after BCNU Wafer Implantation for Glioblastoma]. 2622 70

The lithium-pilocarpine model of status epilepticus is a well-known animal model of temporal lobe epilepsy. We combined this model with in vivo microdialysis to investigate energy metabolites and acute cellular membrane damage during seizure development. Rats were implanted with dialysis probes and pretreated with lithium chloride (127 mg/kg i.p.). Twenty-four hours later, they received pilocarpine (30 mg/kg s.c.) which initiated seizures within 30 min. In the dialysate from rat hippocampus, we observed a transient increase in glucose and a prominent, five-fold increase in lactate during seizures. Lactate release was because of neuronal activation as it was strongly reduced by infusion of tetrodotoxin, administration of atropine or when seizures were terminated by diazepam or ketamine. In ex vivo assays, mitochondrial function as measured by respirometry was not affected by 90 min of seizures. Extracellular levels of choline, however, increased two-fold and glycerol levels 10-fold, which indicate cellular phospholipid breakdown during seizures. Within 60 min of pilocarpine administration, hydroxylation of salicylate increased two-fold and formation of isoprostanes 20-fold, revealing significant oxidative stress in hippocampal tissue. Increases in lactate, glycerol and isoprostanes were abrogated, and increases in choline were completely prevented, when hippocampal probes were perfused with calcium-free solution. Similarly, administration of pregabalin (100 mg/kg i.p.), a calcium channel ligand, 15 min prior to pilocarpine strongly attenuated parameters of membrane damage and oxidative stress. We conclude that seizure development in a rat model of status epilepticus is accompanied by increases in extracellular lactate, choline and glycerol, and by oxidative stress, while mitochondrial function remains intact for at least 90 min. Membrane damage depends on calcium influx and can be prevented by treatment with pregabalin. Status epilepticus (SE) was induced in rats by lithium-pilocarpine ('Pilo') administration, and extracellular metabolites were measured by microdialysis. Seizures caused several-fold increases in lactate levels which were attenuated by diazepam ('Diaz'), ketamine, atropine and tetrodotoxin (TTX). Indicators of oxidative stress and membrane damage were also increased during seizures. Omission of calcium and pregabalin, a calcium channel blocker, reduced cellular damage induced by SE.
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PMID:Early metabolic responses to lithium/pilocarpine-induced status epilepticus in rat brain. 2636 76