Disease relevance of Status Epilepticus

• There were only 5 epilepsy-related deaths (1 each of sudden unexpected death in epilepsy, status epilepticus, burns, drowning, and cervical fracture), suggesting that death directly due to epileptic seizures is uncommon in a population-based cohort with epilepsy [1].
• A 20-year-old woman with psychomotor seizures developed prolonged unilateral status epilepticus followed by coma, right hemiparesis, fever, liver failure, and eventually death [2].
• Pharmacological studies with agonists and antagonists of these receptors suggest that they may mediate the neurodegenerative consequences of Huntington's disease, status epilepticus, and hypoxemia, and that glutamate receptor antagonists have clinical potential as anticonvulsants, analgesics, and neuroprotective agents [3].
• However, it may be that following an initial insult (such as febrile convulsions, status epilepticus or head injury) secondary processes occur both of an anticonvulsant nature in an attempt to compensate for seizure activity, and in a kindling type of fashion, resulting in an increased susceptibility to seizures, leading to future seizures [4].
• Secondary hyperparathyroidism manifesting as acute pancreatitis and status epilepticus [5].

Psychiatry related information on Status Epilepticus

• The acute confusional state following metrizamide myelography is briefly reviewed and compared with the confusional state resulting from adult-onset absence status [6].
• BACKGROUND: Initiating a course of electroconvulsive therapy (ECT) in patients taking theophylline has been associated with status epilepticus and consequent brain damage or even death [7].
• Traumatic brain injury (TBI) was the cause of cortical damage in two patients, cerebral ischemia in two patients and carbon monoxide (CO) poisoning, status epilepticus and Alzheimer's Disease (AD) each in three separate patients [8].
• Ictal simple and complex sexual manifestations during partial seizures in focal epilepsy are rare, but, to our knowledge, our report of this sexual automatism during absence status in generalized epilepsy is unique [9].
• Three patients with EEG documented ictal catatonia, a nonconvulsive status epilepticus, who responded dramatically to intravenous phenytoin are described [10].

High impact information on Status Epilepticus

• A comparison of lorazepam, diazepam, and placebo for the treatment of out-of-hospital status epilepticus [11].
• After adjustment for covariates, the odds ratio for termination of status epilepticus by the time of arrival in the lorazepam group as compared with the placebo group was 4.8 (95 percent confidence interval, 1.9 to 13.0) [11].
• Patients were classified as having either overt generalized status epilepticus (defined as easily visible generalized convulsions) or subtle status epilepticus (indicated by coma and ictal discharges on the electroencephalogram, with or without subtle convulsive movements such as rhythmic muscle twitches or tonic eye deviation) [12].
• The occurrence of seizure activity in human temporal lobe epilepsy or status epilepticus is often associated with a characteristic pattern of cell loss in the hippocampus [13].
• Status epilepticus. The role of intravenous phenytoin [14].

Chemical compound and disease context of Status Epilepticus

• The treatment of status epilepticus can be improved by using recent developments in the pharmacokinetics and method of intravenous (IV) administration of phenytoin sodium [14].
• Phencyclidine hydrochloride abuse has become increasingly common and should be considered in patients with unexplained acute psychosis, dystonic reactions, status epilepticus, or coma [15].
• Rectal valproate in intractable status epilepticus [16].
• Propofol infusion for the treatment of status epilepticus [17].
• Status epilepticus complicating intrathecal baclofen overdose [18].

Biological context of Status Epilepticus

• Lorazepam in childhood status epilepticus and serial seizures: effectiveness and tachyphylaxis [19].
• We studied semaphorin gene expression, as assessed by in situ hybridization, using riboprobes generated from rat cDNA in an adult model of synaptic reorganization, kainic acid (KA)-induced status epilepticus (SE) [20].
• Intravenous phenytoin loading in patients after neurosurgery and in status epilepticus. A population pharmacokinetic study [21].
• Changes in phosphorylation of the NMDA receptor in the rat hippocampus induced by status epilepticus [22].
• The data suggest that inhibition of microsomal Mg(2+)/Ca(2+) ATPase Ca(2+) uptake is involved in NMDA-dependent deregulation of cytosolic Ca(2+) homeostasis associated with status epilepticus [23].

Anatomical context of Status Epilepticus

• Systemic administration of kainic acid, a cyclic analogue of glutamate, produces many of the clinical features of human temporal lobe epilepsy and status epilepticus in rats, including the induction of motor convulsions and the degeneration of neurons in the hippocampus and piriform cortex [24].
• To study this phenomenon, we evoked status epilepticus in rats with systemic kainic acid (KA), and 2 weeks later assessed granule cell inhibition with paired-pulse stimulation of the perforant path (PP) in vitro [25].
• In pup and adult rats, status epilepticus induced a reduction in expression of mGluR2 mRNA in granule cells of the dentate gyrus [26].
• The embryonic form of neural cell surface molecule (E-NCAM) in the rat hippocampus and its reexpression on glial cells following kainic acid-induced status epilepticus [27].
• The substantia nigra pars reticulata (SNPR) has previously been shown to undergo tissue necrosis following status epilepticus induced by flurothyl in the rat [28].

Gene context of Status Epilepticus

• Recent evidence suggests that substance P (SP), a peptide that has been implicated in cardiovascular function, inflammatory responses, and nociception, also contributes to hippocampal excitability and status epilepticus, in part by enhancing glutamate release [29].
• These findings indicate that status epilepticus affects mGluR expression in a gene- and cell-specific manner, and that these changes vary with the developmental stage [26].
• Our data suggest that BDNF signaling may partly mediate the development of epilepsy and propose that regrowth or repair processes initiated by status epilepticus and promoted by BDNF signaling may not be as advantageous as previously thought [30].
• Expression of multidrug transporters MRP1, MRP2, and BCRP shortly after status epilepticus, during the latent period, and in chronic epileptic rats [31].
• Spatiotemporal distribution of gp130 cytokines and their receptors after status epilepticus: comparison with neuronal degeneration and microglial activation [32].

Analytical, diagnostic and therapeutic context of Status Epilepticus

• Double-blind study of lorazepam and diazepam in status epilepticus [33].
• These include spontaneously seizing models with status epilepticus as the initial precipitating injury (including the kainate, pilocarpine, and electrical stimulation models), kindling, and models of drug refractoriness [34].
• Galanin modulation of seizures and seizure modulation of hippocampal galanin in animal models of status epilepticus [35].
• The functional anatomy of limbic status epilepticus in the rat. I. Patterns of 14C-2-deoxyglucose uptake and Fos immunocytochemistry [36].
• Another report of nonconvulsive status epilepticus after metrizamide myelography [37].

References