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)

An elderly man had focal motor status epilepticus secondary to a frontal lobe hematoma. Phenytoin, phenobarbital, and diazepam did not stop the seizures. Intravenous lidocaine by bolus injection and continuous infusion rapidly controlled the seizures.
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PMID:Lidocaine: a neglected anticonvulsant? 11 54

Drug treatment of status epilepticus is reviewed. Tonic-clonic, focal motor, complex partial and absence status epilepticus are discussed. In managing tonic-clonic status epilepticus one should: (1) maintain vital functions at all times, (2) identify and treat precipitating factors and (3) administer an intravenous loading dose of phenytoin sodium or phenobarbital sodium. Careful use of i.v. diazepam sometimes helps to achieve these objectives. Intravenous phenytoin sodium and phenobarbital sodium provide definitive, long-term control of tonic-clonic seizures but must be administered slowly and require time to reach peak brain concentrations. Intravenous diazepam appears to enter and exit from the brain rapidly and may control seizures while therapeutic brain concentrations of long-acting drugs are being achieved. Phenytoin, phenobarbital and diazepam should not be administered intramuscularly in treating status epilepticus. Treatment of focal motor and complex partial status epilepticus is similar to that of tonic-clonic status epilepticus, but i.v. diazepam is required less frequently and loading doses of phenytoin and phenobarbital sometimes can be given more slowly. Status epilepticus of the absence type is managed with i.v. acetazolamide sodium or diazepam. Paraldehyde, muscle relaxants, general anesthesia and lidocaine may be tried when conventional therapies fail.
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PMID:Drug therapy reviews: drug therapy of status epilepticus. 15 Feb 28

A 71-year-old man had status epilepticus and was treated with phenytoin (Dilantin) sodium. Subsequently, an absolute eosinophilia developed, which increased and reached its zenith immediately before the patient died. At autopsy, anasarca and an interstitial nephritis characterized predominantly by eosinophils and occasional focal necrotizing arteriolar glomerular lesions were found. Portal areas also contained an eosinophilic infiltrate. It has been previously stressed that exfoliative dermatitis is often the initiating sign of an allergic hypersensitivity reaction with phenytoin therapy. In view of this, we would suggest that a potential first sign of such an underlying reaction may be the development of an otherwise unexplained absolute eosinophilia.
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PMID:Fatal benign phenytoin lymphadenopathy. 42 84

Alumina cream epileptic focus was established in the right sensorimotor cortex in 20 split-brain cats (partial or complete). EEG and behavioral observations were made in a period ranging from 24 to 836 days. Four types of EEG changes after alumina cream injection were differentiated. These types could be related to the direct effects of brain damage and to development of epilepsy. Spikes and sharp waves and paroxysmal discharges (focal and multifocal) were observed in about 60% of the cats. Clinical seizures developed in about the same percentage of the animals. These values are below those reported for cats with intact interhemispheric commissures. Diphenylhydantoin (DPH) was given orally in a daily dose of up to 15 mg/kg body weight in 9 animals with developed epileptic EEG activity. Five of them had epileptic seizures. DPH was introduced not earlier than 1.5 months after intracortical alumina cream injection. The plasma level of DPH varied between 7-20 mug/ml. This dose produced chronic symptoms of intoxication. Neither EEG changes nor clinical seizures were entirely controlled by this drug. Additional doses of Relanium (diazepam), and phenobarbital were necessary to stop generalized seizures or status epilepticus.
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PMID:EEG and clinical studies of the development of alumina cream epileptic focus in split-brain cats. 97 16

The absorption of phenytoin was studied in man. It is concluded that phenytoin absorbed from the intestine is recirculated via the bile, so that blood levels do not accurately reflect absorption. Phenytoin is loosely bound to serum proteins and is found in red cells in concentrations similar to those in plasma. It is rapidly lost from the blood stream after intravenous administration, which is an important factor to be considered in the treatment of status epilepticus.
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PMID:Studies in man of phenytoin absorption and its implications. 115 2

The purpose of this work was to assess the effects of DPH on a developed epileptogenic focus in cats with split cerebral hemispheres. The investigations were carried out on 12 cats with a chronic epileptogenic focus produced by means of aluminum method in the right motor area. In all cats the epileptogenic focus was found in EEG. All animals received DPH in daily doses of 8-15 mg/kg. In 2 cats they appeared before beginning of treatment. One of these cats died after 3 days from status epilepticus, the other survived status epilepticus and died after 42 days of DPH administration with signs of intoxication. In 3 cats clinical seizures developed during DPH treatment after 30.84 and 210 days. DPH was given during from 171 to 314 days. Clinical seizures appeared in these cats only sporadically and the animals were sacrificed after completion of investigations. In 7 out of 12 cats clinical seizures failed to develop despite presence of bioelectrically active epileptogenic seizures in the right motor area. Administration of DPH in cats with developed epileptogenic focus failed to prevent clinical seizures. In cats with seizures their control was limited by drug toxicity. In all animals toxic effects were observed although the serum DPH level was in the range 8-20 mug/ml.
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PMID:[Effect of diphenylhydantoin on a developed epileptogenic focus in cats with split cerebral hemispheres]. 126 39

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)
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PMID:Pharmacokinetic optimisation of anticonvulsant therapy. 151 37

Phenytoin (PHT) is considered a first or second choice in the treatment of status epilepticus that is refractory to benzodiazepines. The use of an intravenous bolus injection of PHT is hazardous due to the risk of cardiac conduction disturbances, dose-dependent side effects in general, as well as the possibility of severe necrotic lesions in case of extravasation. We compared the number and intensity of side effects and serum level profiles of a highly concentrated, non-dilutable bolus (46 mg/ml) of PHT [Fenytoin, DAK] with a dilutable standard solution (1.5 mg/ml) [Phenhydan] administered intravenously in 500 ml saline. Six healthy volunteers received both regiments (9.1 mg/kg). The diluted solution showed a curvilinear saturation curve with a lower concentration maximum (C-max) than the concentrated solution. Lower toxicity of the diluted solution was indicated by a clinical rating of side effects. Based on a higher incidence and degree of side effects following administration of the more concentrated formulation of PHT, compared with the more diluted preparation, we recommend the use of the less concentrated formulation.
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PMID:Phenytoin-loading: pharmacokinetic comparison between an intravenous bolus injection and a diluted standard solution. 157 98

Status epilepticus (SE) evolves through several stages when untreated. The later stages of SE are less responsive to standard anticonvulsants and may require general anesthesia to suppress seizures. Antagonists acting at the N-methyl-D-aspartate (NMDA) subclass of glutamate (excitatory) receptors have been demonstrated to exert antiepileptic activity in some seizure models. We report experiments performed to determine if NMDA receptor antagonists are effective in stopping seizures in the late stages of SE. A model of limbic SE induced by 90 min of 'continuous' electrical stimulation of the hippocampus in rats was employed. Three NMDA receptor antagonists, one 'competitive' (CPP) and two 'non-competitive' (ketamine and MK-801), were compared to 3 standard antiepileptic drugs (diazepam, phenobarbital, and phenytoin) for their ability to suppress seizures at a physiologically defined stage of SE. All NMDA receptor antagonists, diazepam and phenobarbital were effective in suppressing behavioral and electrographic seizures for varying periods of time. Phenytoin had no effect on SE. Ketamine and MK-801 induced a paradoxical enhancement of electrographic seizures that preceded SE suppression. We believe that NMDA-receptor antagonists offer a novel approach for treating the late stages of SE.
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PMID:NMDA receptor antagonists and limbic status epilepticus: a comparison with standard anticonvulsants. 216 58

Among 630 patients with human immunodeficiency virus infection, 70 patients with new-onset seizures were studied. Generalized seizures occurred in 66 patients (94%): they occurred as the initial seizure in 56 patients (80%) and during follow-up in another 10 patients (14%). Partial seizures (18 patients), status epilepticus (10 patients), and recurrent seizures (38 patients) were also noted. Identified processes included cerebral toxoplasmosis in 11 patients, cerebral lymphoma in 8, metabolic derangement in 8, cryptococcal meningitis in 7, and vascular infarction in 4. In 32 patients (46%) seizures were not associated with identifiable brain lesions and were believed to result from human immunodeficiency virus cerebral infection. Phenytoin treatment was associated with adverse drug reactions in 16 of 62 patients who received it. Our results suggest that the majority of patients with human immunodeficiency virus and seizures do not have secondary focal brain lesions as the cause of the seizures and that human immunodeficiency virus infection alone can, and often does, cause seizures.
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PMID:Seizures in human immunodeficiency virus infection. 234 90


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