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)

Seventy-two patients with postischemic seizures were evaluated with electroencephalography (EEG), computerized tomography (CT) and neurosonography. There were 24% early-onset and 76% late-onset initial seizures. Early-onset seizure was more likely to be simple partial (53%), whereas late-onset seizure was more likely to be primarily generalized (56%). 76% early-onset and 80% late-onset seizures were single. Status epilepticus was more frequent in early-onset that late-onset seizures (p = 0.023). The possibility of recurrence was greater in late-onset than early-onset seizures (p < 0.001). 88% patients had EEG abnormalities, and the most common finding was focal slowing. 75% patients had cerebral infarctions on CT scan, and the majority of them involved cortex. 89% postischemic seizures had carotid lesions which mostly were carotid plaques < 50%. We failed to find these data to be useful in predicting the time of onset of initial seizures after acute ischemic stroke and recurrence.
J Neurol Sci 1995 Sep
PMID:EEG, CT and neurosonographic findings in patients with postischemic seizures. 852 31

We report 5 pediatric patients (2 male, 3 female; age range: 4-8 years) with complex partial status epilepticus (CPSE). Four patients had previous illnesses and mild motor or mental retardation. In 2 patients, CPSE was induced by inappropriate management or selection of antiepileptic drugs. Clinical features varied and automatisms were observed in 3 patients. In 1 patient, decreased physical tone with syncope and impaired consciousness with amaurosis were observed. The episodes of CPSE were continuous in 3 patients and recurrent in 2 patients. In 4 patients, ictal electroencephalographic (EEG) findings, including video-EEG analyses of 3 patients, demonstrated persistent focal epileptic features. Intravenous diazepam abolished CPSE in 3 patients with brief periods of definite EEG localizations remaining. In 4 patients, seizure prognoses were favorable after appropriate treatments; in 1 patient, seizures were intractable even after antiepileptic drug administration.
Pediatr Neurol 1995 Sep
PMID:Complex partial status epilepticus in childhood. 853 78

Three children with refractory status epilepticus, unresponsive to intravenous administration of diazepam, phenytoin, and lidocaine, received pentobarbital therapy and were monitored by electroencephalography (EEG). They required mechanical ventilation and vasopressor therapy. Intravenous pentobarbital therapy was successful and without distinct sequelae in all 3 patients, and could be incrementally discontinued without breakthrough seizures after 12-65 hours of a burst-suppression or complete suppression pattern on EEG. Obtaining a suppression pattern was important for controlling status epilepticus in children as well as adults. We suggest that 12 hours after a burst-suppression pattern is obtained, tapering of pentobarbital should be attempted to avoid serious complications of extended pentobarbital anesthesia (e.g., respiratory depression, hypotension, pneumonia).
Pediatr Neurol 1995 Sep
PMID:Pentobarbital therapy for status epilepticus in children: timing of tapering. 853 84

A 6-year-old boy developed rhabdomyolysis following hyperthermia and status epilepticus with a diagnosis of severe myoclonic epilepsy of infancy. At 2 and 3 years of age, he had similar episodes. Each time he recovered completely in 3-4 weeks with conservative management, in spite of renal insufficiency and marked liver dysfunction. Several cases of recurrent myoglobinuria after intense exercise of generalized tonic-clonic convulsions were reported to have genetic errors of carbohydrate or lipid metabolism of muscle. In our patient, however, the activity of these enzymes was found to be normal. This indicates that status epilepticus may cause recurrent rhabdomyolysis in subjects with normal glycolytic and lipolytic enzyme activity.
Acta Paediatr 1995 Sep
PMID:Recurrent reversible rhabdomyolysis associated with hyperthermia and status epilepticus. 865 66

The present study evaluated the neurotoxic potential of phospholipase A2 (PLA2) in in vitro (primary neuronal cultures) and in vivo (EEG and behavior) rat models of CNS excitability. In vitro, PLA2 (0.0038-5.8 nM) or melittin (a potent activator of endogenous PLA2; 100-5000 nM), were highly neurotoxic, causing approximately 500 units/ml LDH release. The neurotoxic EC50s for PLA2 and melittin were 1.8 (1.4-2.3) and 848 (501-1280) nM, respectively. Neurotoxic concentrations of PLA2 stimulated neuronal release of [3H]AA. Preliminary in vitro experiments evaluating changes in neuronal calcium flux indicated that PLA2 caused transient, and melittin sustained, increases in [Ca2+]i. In vivo, PLA2 (0.5-5 micrograms i.c.v.) or melittin (2.5-20 micrograms i.c.v.) produced nonconvulsive EEG seizures, which generalized to status epilepticus. While the onset of seizure development was markedly delayed for PLA2 (1.5-4.5 h), the seizure inducing effects of melittin were evident within 3.5 +/- 0.2 min and more severe. Both PLA2 and melittin were lethal, exhibiting LD50s of 0.62 micrograms and 8.4 micrograms, respectively. Pretreatment with (+)-MK801 (5 micrograms, i.c.v.) significantly attenuated melittin, but not PLA2, in vivo neurotoxicity. PLA2 induced neuropathology in surviving rats revealed extensive cortical and subcortical injury to forebrain neurons and fibre pathways. Collectively, these results demonstrate the potent neurotoxic potential of PLA2, the delayed clinical nature of its in vivo neurotoxicity and the applicability of these model systems to future studies on mechanisms of PLA2 neurotoxicity and the development of potential PLA2 antagonists.
Brain Res 1995 Sep 25
PMID:Phospholipase A2-induced neurotoxicity in vitro and in vivo in rats. 865 97

Kainic acid (KA)-induced convulsions are accompanied by histopathological changes that are most prominent in the temporal lobe structures. In the present study, we investigated whether a selective alpha2-adrenoceptor agonist, dexmedetomidine could attenuate KA-induced epileptic convulsions and subsequent neuronal damage in the rat hippocampus. Rats were pretreated 30 min before KA injection (9 mg/kg, i.p.) with dexmedetomidine (3 micrograms/kg, s.c.). The behavior of animals was observed for at least 3 h. Dexmedetomidine suppressed the development (p < 0.001), generalization (p < 0.05) and severity (p < 0.01) of convulsions. In addition, histological analysis revealed that dexmedetomidine-treated animals without convulsions or with only partial convulsions had no neuronal damage in the principal cell layers of the hippocampus. A selective alpha2-antagonist, atipamezole (1 mg/kg, s.c.) potentiated KA-induced convulsions and increased the mortality in status epilepticus. In conclusion, the present study demonstrated that dexmedetomidine, in addition to possessing anticonvulsant properties, has a neuroprotective effect in the KA model of status epilepticus.
Brain Res 1995 Sep 25
PMID:Alpha 2-adrenoceptor agonist, dexmedetomidine, protects against kainic acid-induced convulsions and neuronal damage. 865 12

Aberrant neural sprouting of mossy fiber terminals in the supragranular layer of dentate gyrus is consistently observed following seizures in an animal model of epilepsy. It is also observed in hippocampi taken from epileptic patients with hippocampal sclerosis. The aberrant neural sprouting with synaptic reorganization is one of the proposed cellular mechanisms underlying epileptogenesis. It is not known whether aberrant synaptogenesis can be induced in the cortex, as in hippocampus, by seizure activity. In this study, synaptic terminals in the cortex were measured after focal cortical seizures by a semiquantitative image analysis of synaptophysin immunoreactivity. Brief intracortical perfusion of kainic acid induced focal status epilepticus and destructive cortical lesions. Synaptophysin immunoreactivity was significantly increased in the area where kainic acid was perfused. The increase of synaptophysin immunoreactivity, indicating an increase of synaptogenesis, was observed at 2 and 4 weeks after focal cortical seizures. This result suggests that kainic acid-induced seizure activity is associated with long-lasting synaptogenesis in the cortex. Studies centering on the physiological consequences of aberrant synaptogenesis may lead to additional understanding of the mechanisms underlying cortical epileptogenesis.
Exp Neurol 1996 Sep
PMID:Kainic acid-induced focal cortical seizure is associated with an increase of synaptophysin immunoreactivity in the cortex. 879 64

Rats treated systemically with kainate develop stereotyped epileptic seizures involving mainly limbic structures that may last for hours. This model of limbic status epilepticus has been widely studied using classical neuropathological techniques. We used in situ nick translation histochemistry to examine patterns of DNA fragmentation in this model. We found a stereotyped and reproducible pattern of neuronal populations that demonstrate evidence of DNA fragmentation from 24 h to one week after kainate treatment. Neither blockade of new protein synthesis nor blockade of the N-methyl-D-aspartate-type glutamate receptors significantly altered this response. Moreover, we saw no evidence of the regular internucleosomal cleavage of DNA that produces a characteristic laddered appearance of 180-200 bp DNA fragments after gel electrophoresis in samples obtained from microdissected affected regions. These studies suggest that DNA fragmentation after systemic kainate-induced seizures is not the result of programmed cell death. This assay may be useful for quantitative testing of both neuroprotective agents and mechanistic hypotheses.
Neuroscience 1996 Sep
PMID:Anatomical studies of DNA fragmentation in rat brain after systemic kainate administration. 886 4

With the introduction of several new anticonvulsant drugs into clinical practice in recent years, renewed attention has been paid to treatment-emergent effects, especially behavioural syndromes. In this review, the more severe psychiatric syndromes that may be associated with anticonvulsants are discussed, especially personality disorders, affective syndromes and psychoses. The important concept of forced normalisation is discussed, and its clinical counterpart, alternative psychosis. Affective disorders and psychoses have been described as associated with most of the new anticonvulsant agents, and they are often seen in a setting in which previously intractable patients suddenly become seizure free. Other cases may relate to intoxication, the precipitation of a status epilepticus, or ensue as part of the background frequency of those syndromes that are seen in epilepsy irrespective of medication.
Drug Saf 1996 Sep
PMID:Anticonvulsant-induced psychiatric disorders. The role of forced normalisation. 887 70

An afebrile child with focal status epilepticus and an altered mental status presents a diagnostic and therapeutic challenge. Traditional morphological neuroimaging may be of limited value in the evaluation of such patients, and one may have to rely more upon functional neuroimaging studies. Recent advances in the understanding of the pathogenesis and the role of functional neuroimaging studies in the evaluation of focal status epilepticus are discussed.
Semin Pediatr Neurol 1996 Sep
PMID:Focal status epilepticus and hemiparesis in an 8-year-old boy. 888 56


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