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)

EEG is a major tool in convulsive status epilepticus. Several techniques may be used, including conventional or digitized EEG using 4, 8, 10 or 16 channels, continuous monitoring with or without simultaneous video recording, and cerebral function monitor. During the first phase, in the emergency ward, EEG may be useful in severe convulsive status epilepticus to assess further evolution and/or prognosis. However, rapid control of seizure at this phase is the primary goal, and optimization of EEG availabilities may lead to more systematic indications. After adequate control of seizures, EEG is mandatory in the following situations: i) a difficult-to-control convulsive status epilepticus, with a high risk of subsequent evolution towards subtle status epilepticus; ii) a resistant status epilepticus which needed high dose of sedatives drugs and/or curarization, to evaluate the level of anaesthesia and to watch for recurrence of epileptiform abnormalities; iii) a permanent, unexplained impairment of consciousness which followed an apparently successful treatment, to detect non convulsive status epilepticus; 4. a doubtful clinical diagnosis, to confirm pseudo-status epilepticus.
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PMID:[Status epilepticus: indications for emergency EEG]. 948 Apr 6

The pharmacologic management of major motor status epilepticus is summarized. When general anesthesia is required, the electroencephalogram (EEG) is used for monitoring the adequacy of treatment. The EEG findings may also be important in recognizing status epilepticus and monitoring its response to treatment when this is clinically difficult, as when it occurs in comatose or pharmacologically paralyzed patients or in the context of severe brain damage. Finally, the EEG helps to clarify the nature of motor activities of uncertain basis in patients in the intensive care unit and has indicated that non-convulsive seizures or status are more common than clinically suspected in such patients.
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PMID:Management of status epilepticus. 953 89

We retrospectively reviewed the clinical course of 66 patients treated for generalized tonic-clonic status epilepticus at the Ege University neurological intensive care unit from 1988 to 1997. Seventy-two per cent of the study group had a pre-existing seizure disorder, and antiepileptic drug withdrawal was the most prominent cause of status epilepticus. The other causes included drug toxicity, central nervous system infection, cerebrovascular disease, tumour and trauma. Seventy-three per cent of all patients responded to the first-line therapy (diazepam and/or phenytoin), and the remainder were considered to have refractory status epilepticus and required pentobarbital anaesthesia. Overall case fatality was 21%, but death could be attributed directly to status epilepticus and/or treatment complication in 10% of the study group. Major determinants of fatal outcomes were: increasing age, longer duration of status epilepticus before initiation of therapy and central nervous system infection as a causal factor.
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PMID:Generalized tonic-clonic status epilepticus: causes, treatment, complications and predictors of case fatality. 977 62

This is a case study in managing refractory status epilepticus under long-term usage of secobarbital (SB). The patient is a 26-year-old woman with viral encephalitis. Fifteen days after the onset of the disease, status epilepticus with complex partial seizures began. The seizures were so refractory to conventional anti-epileptic drugs, such as valproate, carbamazepine, phenytoin, phenobarbital, clonazepam, lorazepam and lidocaine, that we had to put her on anesthesia with SB for approximately 10 months. Finally, we stopped the administration of SB and support for ventilation; we reduced the dose of SB extremely slowly, using zonisamide at the same time. After trial and error, we found that a reduction of the dosage after long-term anesthesia with high-dose administrations of barbiturate should be made very slowly.
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PMID:[Experience in managing refractory status epilepticus caused by viral encephalitis under long-term anesthesia with barbiturate: a case report]. 980

We have compared the effect of clinical doses of propofol with thiopental on epileptiform activity in the electrocorticograms (ECoG) of 20 epileptic patients undergoing temporal lobe resection. After baseline ECoG had been obtained, with inspired concentrations of 0.5-1% isoflurane and 70% nitrous oxide to provide background anaesthesia, subjects were allocated randomly to receive boluses of either thiopental 25 mg or propofol 20 mg i.v. every 30 s to a maximum of 5 mg kg-1 or until burst suppression was seen. The ECoG was recorded throughout administration and for 10 min thereafter. After return of baseline ECoG tracings, the alternate agent was administered. The amount of epileptiform activity was recorded on an ordinal rating scale, an increase being indicated by either a rise of at least one category on the scale or discharges occurring at a minimum of one new site. Activation occurred more frequently with thiopental but the difference was not significant. This study suggests that propofol has no greater proconvulsive effect than thiopental, a drug commonly used in managing status epilepticus.
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PMID:Effect of propofol on the electrocorticogram in epileptic patients undergoing cortical resection. 1036 87

In several experimental models, status epilepticus (SE) leads to secondary brain hyperexcitability and epileptogenesis. In humans, such phenomena have been rarely demonstrated, particularly in cases of SE involving the neocortical structures. We report a 36 year old woman that presented partial SE in May 1991 involving the right cerebral hemisphere. The patient was then treated in the intensive care unit with artificial ventilation and anesthesia by pentobarbital and clometiazole. MRI showed transient right parietal and temporal posterior cortical hyperintensity. The cause of SE was not determined. Three months later, the patient developed partial complex seizures with aura characterized by vertigo, nausea and auditory hallucination. Ictal video/EEG recording showed a clear right temporal posterior onset of the discharges. We speculate that status epilepticus created the lesions which subsequently caused the focal chronic epilepsy.
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PMID:Development of focal chronic epilepsy following focal status epilepticus in adult patients. 1043 Dec 92

Postoperative epileptic seizures are recognised but rare. Psychogenic seizures and pseudostatus epilepticus are relatively common, particularly in the peri-operative period. Our series of five cases of postoperative pseudostatus epilepticus demonstrates that the failure to recognise the psychogenic nature of this condition may cause anaesthetists to give inappropriate and potentially harmful treatment. Psychogenic 'status' is easy to diagnose once it has been considered. Convulsive episodes lasting longer than 90 s, closed eyes during a 'tonic-clonic' attack, retained pupillary response and resistance to eye opening are useful signs. Often there is a history of multiple admissions with 'status epilepticus' and of previous postoperative 'status'.
Anaesthesia 2000 Jan
PMID:Postoperative pseudostatus: not everything that shakes is epilepsy. 1086 41

If continuous seizure activity lasts longer than 5 minutes generalized tonic-clonic seizures require prompt treatment, if significant morbidity and mortality are to be avoided. The mortality varies (mean: 20%) depending on patient age and etiology. Control of status epilepticus is achieved by benzodiazepines in about 80% of cases: Lorazepam is recommended due to its longer-acting effects on the central nervous system. To maintain the anticonvulsive effect phenytoin is usually administered intravenously. Fosphenytoin (not approved in Germany) has advantages over phenytoin, because it can be given three times more rapidly and produces fewer side effects. The IV use of valproic acid in status epilepticus seems to be promising, but needs further evaluation. There is no generally accepted treatment protocol for the therapy of persistent seizure activity lasting more than 60 minutes (i.e., refractory status epilepticus). Usually phenobarbital, or general anesthesia with thiopental or pentobarbital are treatment recommendations. In recent reports, the administration of midazolam or propofol proved to be effective and well-tolerated.
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PMID:[Therapy of generalized tonic-clonic status epilepticus in adulthood]. 1070 6

The authors report a patient with partial and secondarily generalized status epilepticus who required 70 days of general anesthesia for seizure control. Although antiepileptic medications failed to control the seizures, they resolved with plasma exchange. The patient's serum reacted with rat cerebral cortex, hippocampus, and cerebellum, but not with cells expressing the glutamate receptor GluR3. These findings suggest an immune response against neuronal antigens other than GluR3.
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PMID:Status epilepticus with neuron-reactive serum antibodies: response to plasma exchange. 1109 54

Aspirin (acetylsalicylic acid), and its main metabolite sodium salicylate, have been shown to protect neurons from excitotoxic cell death in vitro. The objective of our study was to investigate the possible neuroprotective effects of sodium salicylate in vivo in rats with kainic acid-induced seizures, a model for temporal lobe epilepsy in human patients. Male Sprague-Dawley rats received intraperitoneal injections of kainic acid either alone, or with sodium salicylate given before and for 40h after kainic acid injections. The control group received either phosphate-buffered saline or sodium salicylate without co-administration of kainic acid. Animals developed status epilepticus, which was aborted 1.5-2h later with diazepam. On day 3 following kainic acid-induced seizures, animals received bromodeoxyuridine to measure cellular proliferation, and were killed under anesthesia 24h later. Brains were removed, sectioned, and analysed for gross histological changes, evidence of hemorrhage, DNA fragmentation, cellular proliferation, and microglial immunohistochemistry. We report that sodium salicylate did not protect neurons from seizure-induced cell death, and to the contrary, it caused focal hemorrhage and cell death in the hippocampal formation and the entorhinal/piriform cortex of rats with kainic acid-induced seizures. Hemorrhage was never observed in animals that received vehicle, kainic acid or sodium salicylate only, which indicated that sodium salicylate exerted its effect only in animals with seizures, and was confined to select regions of the brain that undergo seizure activity. Large numbers of cells displaying DNA fragmentation were detected in the hippocampal formation, entorhinal/piriform cortex and the dorsomedial thalamic nucleus of rats that received kainic acid or kainic acid in combination with sodium salicylate. Bromodeoxyuridine immunohistochemistry revealed large numbers of proliferating cells in and around the areas with most severe neural injury induced by kainic acid or kainic acid co-administered with sodium salicylate. These same brain regions displayed intense staining with a microglia-specific marker, an indication of microglial activation in response to brain damage. In all cases, the degree of cell death, cell proliferation and microglia staining was more severe in animals that received the combination of kainic acid and sodium salicylate when compared to animals that received kainic acid alone. We hypothesize that our findings are attributable to sodium salicylate-induced blockade of cellular mechanisms that protect cells from calcium-mediated injury. These initial observations may have important clinical implications for patients with epilepsy who take aspirin while affected by these conditions, and should promote further investigation of this relationship.
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PMID:The aspirin metabolite sodium salicylate causes focal cerebral hemorrhage and cell death in rats with kainic acid-induced seizures. 1092 56


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