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)

A silver method is proposed for the selective, well-contrasted and reproducible demonstration of "dark" neurons in frozen, vibratome and paraffin sections cut at a thickness of 5 to 200 microns from aldehyde-fixed brains. The Golgi-like staining of the dendrites enables assorting of "dark" neurons according to characteristic neuron classifications. The staining procedure includes an esterification with 1-propanol, a treatment with diluted acetic acid and development. The esterification strongly increases the argyrophilia of both "dark" neurons and mitochondria. Unwanted co-staining of mitochondria is suppressed by the acetic acid treatment, while a special developer is used to render the staining controllable. The applicability of the method to experimental neuropathology is demonstrated by Golgi-like staining of "dark" neurons in rat brains exposed, before transcardial perfusion-fixation and delayed autopsy, to various pathological conditions including ischemia, hypoglycemia, trauma, status epilepticus, deafferentation and poisoning with kainic acid, colchicine and sodium azide, respectively.
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PMID:Golgi-like demonstration of "dark" neurons with an argyrophil III method for experimental neuropathology. 169 82

The pharmacokinetic parameters controlling paraldehyde elimination were determined in nine infants infused with paraldehyde at the rate of 150 mg/kg/hr in a 5% solution in 5% dextrose for the treatment of status epilepticus. The mean +/- SEM values for the observed parameters were as follows: rate constant for the disposition of paraldehyde 0.0680 +/- 0.0071 hr,-1 half-life 10.2 +/- 1.0 hr; volume of distribution 1.73 +/- 0.20 L/kg; clearance 0.121 +/- 0.023 L/hr/kg. Phenobarbital administration prior to or within 24 hours of the cessation of paraldehyde infusion decreased both paraldehyde clearance and volume of distribution in a manner linearly related to the logarithm of the phenobarbital dose. The rate constant for paraldehyde elimination was decreased as a linear function of the logarithm of the combined dose of administered phenobarbital and phenytoin. No acetaldehyde was detected in any blood samples. Paraldehyde administration was not correlated with any adverse reactions or toxicities.
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PMID:Pharmacokinetics of paraldehyde disposition in the neonate. 669 30

Felbamate demonstrates a unique therapeutic profile and often results in seizure control when other agents fail. Its use has been associated with risks for aplastic anaemia and hepatic failure. A number of confounding factors makes the actual incidence rate for each adverse effect difficult to determine. However, certain risk factors are common in reported cases. In order to minimise the risk, at the present time, it is necessary to rely on the clinical profile of the patients reporting these adverse effects. The patient reporting aplastic anaemia is usually female, Caucasian, and an adult. The dose did not appear to be a factor and the time to onset of aplastic anaemia was less than 1 year for all patients. Concomitant medications and diseases may play an important role. Patients with reported aplastic anaemia generally had a history of a serious allergy or toxicity to other anticonvulsants and/or a background of having had a cytopenia due to other anticonvulsants, and a diagnosis or serological evidence of concomitant immune disorder. The demographics associated with hepatic failure are less well defined. Patients were also predominantly female, were equally divided among adult and paediatric patients, and had a broad range of time to presentation of hepatotoxicity following felbamate therapy. Concomitant medications again play an important role with, in this case, valproic acid (sodium valproate), phenytoin and carbamazepine being the most frequent. In 50% of the population, hepatic failure was not felt to be due to felbamate but associated with confounding factors including status epilepticus, paracetamol (acetaminophen) toxicity, hepatitis and shock liver. Initial research has failed to provide a diagnostic indicator. However, work on a potential intermediate felbamate metabolite has suggested the formation of a reactive aldehyde whose end products have been detected in the urine of felbamate treated patients. Until these data are confirmed, the medical history, clinical picture, and laboratory testing, should be used to identify patients at risk. The risks for toxicity with felbamate should be evaluated before starting treatment. In addition, liver function tests and complete blood count (CBC) prior to therapy and at clinically rational intervals should be conducted. Patients must be educated in the likely prodromal symptoms of potential marrow/liver toxicity. Felbamate is too valuable an anticonvulsant to be relegated to the therapeutic scrap heap. With monitoring, patient education, and continued research to further elucidate risk factors, felbamate can be a viable therapeutic agent for patients with epilepsy.
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PMID:Felbamate in epilepsy therapy: evaluating the risks. 1048 99