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 case of hypothermia and metabolic derangement in a 60-year-old man following a period of status epilepticus is reported. A CT head scan performed subsequently demonstrated agenesis of the corpus callosum. Hypercalcaemia which has not been reported before was a prominent abnormality in the metabolic profile.
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PMID:Status epilepticus, hypothermia and metabolic chaos in a man with agenesis of the corpus callosum. 399 55

Three pediatric patients with generalized status epilepticus unresponsive to therapy with conventional anticonvulsants were successfully treated with moderate hypothermia (30 degrees to 31 degrees C) and barbiturate coma with thiopental. All 3 patients were treated with thiopental at doses producing burst suppression or an isoelectric tracing on the EEG and thiopental and barbiturate levels were followed sequentially in the plasma. Continuous thiopental infusion rates of 5 to 55 mg/kg X h maintained burst suppression and correlated with plasma thiopental levels of 25 to 40 mg/dl. Total doses of thiopental used to obtain and maintain burst suppression ranged from 15 to 50 g over 48 to 120 h. In all 3 patients, control of the status epilepticus was obtained. Moderate hypothermia and thiopental barbiturate coma are indicated in patients with generalized tonic-clonic status epilepticus which cannot be controlled with standard anticonvulsant drug therapy. This regimen has the advantage that the patient can be managed in an ICU without the need for general anesthesia with volatile anesthetic agents.
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PMID:Hypothermia and barbiturate coma for refractory status epilepticus. 670 45

The influence of hyperthermia and hypothermia on epileptic brain damage was studied in rats, in which status epilepticus was induced by flurothyl. Histopathological changes were examined by light microscopy after 1 or 7 days of recovery. Two series of animals were studied. In the first, short periods of seizures (20 and 25 min) were employed to examine whether moderate hyperthermia (39.5 degrees C) would aggravate epileptic brain damage, and a longer period (45 min) was used to investigate whether moderate hypothermia (32.5 degrees C) would ameliorate the damage. The second series investigated whether brief periods of status epilepticus (10 min) would cause brain damage if hyperthermia were high or excessive. For this series, animals with body temperatures of 37.0, 39.0, and 41.0 degrees C were studied. Data from normothermic animals (37.5 degrees C) confirmed previously described neuronal damage. Although hyperthermic animals failed to show increased damage in the CA1 sector, or in the hilar region of the dentate gyrus, they showed enhanced damage in the neocortex and globus pallidus (GP). In substantia nigra pars reticulata (SNPR) four out of five hyperthermic animals had bilateral infarcts after 20 min of status epilepticus, whereas no normothermic animal showed such damage. Hypothermia seemed to ameliorate epileptic brain damage in the neocortex (n.s.) and GP (P < 0.05) following status epilepticus for 45 min. Three out of seven hypothermic animals had mild SNPR involvement compared to severe infarction of the nucleus in five out of six normothermic animals (P < 0.05). Thus, hyperthermia aggravated and hypothermia ameliorated epileptic brain damage both in regions showing selective neuronal necrosis (neocortex) and in regions developing pan-necrosis (GP and SNPR). The second series displayed an unexpected result of excessive hyperthermia. Animals subjected to only 10 min of status epilepticus at a temperature of 41 degrees C showed not only neocortical lesions, but also moderate to extensive damage to the hippocampus (CA1, subiculum, and dentate gyrus). It is concluded that at high body and brain temperature, brief periods of status epilepticus can yield extensive brain damage, primarily affecting the hippocampus.
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PMID:Hyperthermia aggravates and hypothermia ameliorates epileptic brain damage. 792 95

The present study investigates some neuropharmacological effects of an ethanolic extract of the leaves of Trema guineensis (Ulmaceae), a medicinal plant of central Africa. Intraperitoneal administration of the extract induced hypothermia. In addition, the extract significantly shortened the latency to sleep and prolonged the duration of sleeping time induced by sodium pentobarbital in mice. Moreover, T. guineensis significantly delayed the onset of clonic seizures induced by pentylenetetrazole in mice. In contrast, T. guineensis did not affect convulsions induced by maximal electroshock and picrotoxin in mice nor status epilepticus produced by pilocarpine and kainic acid in rats.
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PMID:Some pharmacological effects of an ethanolic extract of Trema guineensis on the central nervous system in rodents. 793 62

The ethanolic extract of the leaves of Maprounea africana (Euphorbiaceae), a medicinal plant in the Congolese traditional medicine, induced hypothermia and reduced the latency to the loss of the righting reflex and prolonged the sleeping time induced by pentobarbital in mice. It also significantly delayed the onset of clonic convulsions induced by pentylenetetrazole in mice. However, the extract did not affect either generalized convulsions induced by maximal electroshock and picrotoxin or limbic status epilepticus produced by pilocarpine and kainic acid.
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PMID:Some neuropharmacological effects of an ethanolic extract of Maprounea africana in rodents. 799 Apr 88

The effects of body temperature on kainic acid-induced seizures and seizure-related brain damage were examined in rats. In rats with status epilepticus induced by intraperitoneal injection of 12 mg/kg of kainic acid (KA), ictal discharges were decreased by 50% when body temperature was lowered to 28 degrees C and nearly abolished when body temperature was lowered to 23 degrees C. In rats with mild hypothermia (28 degrees C), the duration of ictal discharges following KA injection was significantly lower than in rats with normal body temperature. No detectable hippocampal cell loss was observed in rats with hypothermia to 28 degrees C whereas gross cell loss in the hippocampus was observed in all rats with KA injection at normal body temperature. In contract to hypothermia, hyperthermia markedly aggravated the seizures and hippocampal damage induced by KA. Following elevation of body temperature to 42 degrees C KA (12 mg/kg) resulted in severe seizures and all rats died of tonic seizures within 2 h. Furthermore, 6 mg/kg of KA administered to rats with a body temperature of 41-42 degrees C, resulted in up to 4 h of continuous ictal discharges whereas no continuous ictal discharges were observed after the same injections in rats with normal body temperature. Histological examination in rats receiving 6 mg/kg of KA revealed severe cell loss in the hippocampus in rats with hyperthermia but not in rats with normal temperature. These results demonstrate that body temperature plays an important role in the control of epileptic seizures and seizure-related brain damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of temperature on kainic acid-induced seizures. 829 96

This study investigates some pharmacological effects of the ethanolic extract of the leaves of Desmodium adscendens (Papillionaceae), a medicinal plant in the African traditional medicine, on the central nervous system. The plant extract induced hypothermia and had analgesic effect in mice. D. adscendens suppressed the tonic phase of convulsion and mortality induced by pentylenetetrazole (PTZ) in mice. In addition, the plant extract delayed the onset of PTZ forelimb clonus, and generalized limbic seizures induced by kainic acid. In contrast, the plant extract did not affect either tonic convulsion induced by maximal electroshock in mice or the progression of limbic seizures towards the status epilepticus in rats.
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PMID:Effects of an ethanolic extract of Desmodium adscendens on central nervous system in rodents. 873 51

Induced hypothermia has improved neurological outcome after cardiac arrest. Even though anoxic insults to the brain often provoke epileptic activity, it is unclear whether EEG monitoring is necessary in these patients. We report the case of a 53-year-old female who suffered cardiac arrest. During induced hypothermia extensive shivering was managed by sedation and curare. After their discontinuation convulsions appeared and status epilepticus was disclosed on EEG recording, and was treated by thiopental infusion for 10 days. The patient recovered slowly and has now regained independent living (CPC 1). In induced hypothermia several factors including the use of curare, may conceal clinical signs of epileptic activity. We therefore suggest a broader use of EEG in these patients.
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PMID:EEG should be performed during induced hypothermia. 1675 80

We report the case of a 30-year-old woman with severe, prolonged refractory status epilepticus requiring more than 6 months of iatrogenic coma. Opinions on prognosis and clinical management were solicited from a number of experienced neurointensivists and epileptologists at multiple time-points during the clinical course. The ensuing discussion, annotated with references, is presented here. Several experts commented on isolated cases of young patients with encephalitis requiring up to 2-3 months of iatrogenic coma, yet still having good outcomes. Treatments discussed include ketamine, gammaglobulin, plasmapheresis, steroids, adrenocorticotropic hormone, very high-dose phenobarbital, isoflurane, lidocaine, electroconvulsive therapy, ketogenic diet, hypothermia, magnesium, transcranial magnetic stimulation, vagus nerve stimulation, deep brain stimulation, and neurosurgery. The patient eventually suffered a cardiac arrest but was resuscitated as requested by the family. Seizures then stopped, and the patient has remained in a persistent vegetative state since.
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PMID:Literature review, case report, and expert discussion of prolonged refractory status epilepticus. 1649 94

A 50-year-old patient had status epilepticus and no adequate reactions nine days after prolonged out-of-hospital cardiac arrest. The cause of the arrest was acute myocardial infarction which was treated successfully with percutaneous cardiac intervention (PCI) and a stent placement. He was treated with therapeutic hypothermia (33 degrees C) for 24h and in intensive care with respiratory support for 42 days. One year later he has fully recovered and is back to normal life and academic work. The previously reported 100% prognosis of a poor neurological outcome in the presence of seizures 72 h post arrest may need to be re-examined after introduction of therapeutic hypothermia.
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PMID:Determination of prognosis after cardiac arrest may be more difficult after introduction of therapeutic hypothermia. 1651 42


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