Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats were exposed for 24 min to bilateral clamping of the common carotid arteries (BCCA) in pentobarbital anaesthesia. The GABA content was measured 24 hours, 48 hours, 4 days, 14 days and 3 months after BCCA. In other groups of rats seizures were elicited by i.p. injection of (+)-bicuculline (3 mg/kg) 24 hours, 48 hours, 4 days, 14 days and 3 months after BCCA. Analysis of the GABA content revealed significant increase compared with controls in the hippocampus, frontal cortex and substantia nigra from 24 hours up to 3 months. Bicuculline treatment induced tonic/clonic seizures and status epilepticus in sham operated animals; these effects were drastically diminished at various time points after BCCA. The present results suggest that BCCA produces a longlasting increase in GABA content and as a consequence protection from bicuculline-induced seizures.
J Neural Transm Gen Sect 1992
PMID:Transient reduction of cerebral blood flow leads to longlasting increase in GABA content in vulnerable structures and decreased susceptibility to bicuculline induced seizures. 163 44

Rats were exposed for 24 min to bilateral clamping of the common carotid arteries (BCCA) in pentobarbital anaesthesia. 14 days later the animals were subjected to subcutaneous injection of (+)-bicuculline (3 or 4 mg/kg). A significantly decreased susceptibility to bicuculline-induced seizures could be observed in BCCA treated rats compared with sham operated controls. It is suggested that BCCA treatment protects animals against status epilepticus and lethal toxicity produced by bicuculline. Electrographic recordings of the BCCA animals revealed no ictal activity within 1 h after bicuculline injection. An analysis of the GABA content showed a significant increase in the hippocampus (HPC), frontal cortex (FCX), parietal cortex and substantia nigra in BCCA animals compared with controls. It is therefore possible that an increase in GABA content postsynaptically counteracts the GABAA antagonistic effect of bicuculline in BCCA animals thus preventing the normal seizure inducing effect of this substance.
J Neural Transm Gen Sect 1991
PMID:Decreased susceptibility to seizures induced by bicuculline after transient bilateral clamping of the carotid arteries in rats. 185 Feb 83

A middle-aged man, who presented to the emergency room because of bizarre outbursts of laughter, was found to be in partial complex status epilepticus. His seizure disorder had been misdiagnosed, at various times, as a variety of "functional" psychiatric disorders. Despite proper diagnosis and aggressive treatment, management was difficult, being complicated by postictal agitation and confusion, postictal psychosis, and interictal compulsive and paranoid personality features. This case is described, and issues of diagnosis and management in partial complex epilepsy are briefly discussed. The importance of not overlooking organic and especially epileptic factors, despite the presence of prior psychiatric illness, psychologic contributors, and environmental stressors, is emphasized.
Gen Hosp Psychiatry 1986 Jan
PMID:Complex partial status epilepticus presenting as gelastic seizures: a case report. 394 17

1. The premorbid behaviors produced by the administration of cocaine, ethanol, their combination, as well as a metabolite produced by their co-administration, viz. cocaethylene, were defined, determined and quantified in the HS strain of mice. 2. The LD50 for ethanol was 9.71 g/kg in males and 9.45 g/kg in females, whereas the LD50 values in male and female mice for cocaine were 101.55 and 90.00 mg/kg, respectively. 3. The data indicate that clonic-tonic seizures continued into status epilepticus after cocaine administration and prior to cocaine-induced lethality. In contrast, administration of the cocaine-ethanol metabolite cocaethylene produced status epilepticus without producing clonic-tonic seizures yet still resulted in lethality. 4. Thus, both cocaine and cocaethylene may produce their lethal effects in mice through neuro-regulatory mechanisms mediating protracted seizure induction.
Gen Pharmacol 1995 Jan
PMID:Premorbid behaviors produced by cocaine, ethanol and cocaethylene in the mouse. 771 72

1. Rats with spontaneous recurrent seizures (SRS) were obtained by injection of kainic acid (KA; 10 mg/kg SC) to drug-naive rats that regularly developed wet-dog shakes followed by complex partial seizures and status epilepticus. Three to five weeks later, the rats with manifest SRS were selected. 2. The SRS rats were challenged with KA (10 mg/kg SC). The seizures induced in SRS rats by KA were similar to SRS regarding their clinical stage and duration (mean duration of seizures: 44 sec and 43 sec, respectively). The frequency of seizures was, however, increased compared with the frequency of SRS in control, vehicle-treated SRS rats (mean frequency of seizures: 12.9 and 0.4 per 3 hr, respectively). The KA-induced seizures in SRS rats differ behaviorally from KA-induced seizures in naive rats-namely, neither wet-dog shakes nor the status epilepticus could be induced. 3. Repeated injection of an equal dose of KA, applied to the SRS rats 1 day after the previous KA challenge, did not induce seizures. The loss of seizure susceptibility to KA was only temporary, as shown after a 7-day drug-free period, when the repeated injection of KA regained its seizure-triggering capacity. 4. The results indicate that reactivity to the seizure-inducing agent kainic acid changes in rats with spontaneous recurrent seizures.
Gen Pharmacol 1998 Sep
PMID:The effects of kainic acid in rats with spontaneous recurrent seizures. 970 17

Diligence in the interpretation of results is essential as information gained from the psychiatric patient's history might often be restricted. Nonobservance of established guidelines may lead to a wrong diagnosis, induce a false therapy and result in life-threatening situations. Communication errors between hospitals and doctors and uncritical acceptance of prior diagnoses add substantially to this problem. We present a patient with alcohol-related dementia who received anti-retroviral therapy that promoted a non-convulsive status epilepticus. HIV serodeconversion was considered after our laboratory result yielded a HIV-negative status. Critical review of previous diagnostic investigations revealed several errors in the diagnosis of HIV infection leading to a "pseudo-serodeconversion." Finally, anti-retroviral therapy could be discontinued.
Gen Hosp Psychiatry
PMID:Anti-retroviral therapy-induced status epilepticus in "pseudo-HIV serodeconversion". 2085 Dec 80

Status epilepticus (SE) is a prolonged seizure activity associated with mortality and morbidity. SE is characterized by changes in neurotransmitter systems and oxidative stress that facilitate cellular damage. These alterations represent the neurochemical mechanisms underlying the initiation and progression of seizure activity and co-existing morbidity. In the present study, amino acid levels (glutamine, glutamate, GABA, aspartate, glycine and taurine) and oxidative stress parameters malondialdehyde (MDA), reduced glutathione (GSH) and nitric oxide NO) were determined in the cerebral cortex during SE induced by pilocarpine in rats. The study has also evaluated the effects of hypothermia, as a physical non-invasive tool, on neurotransmitters and oxidative stress alterations. The results obtained revealed that there are significant increases in glutamate, GABA, glycine and taurine and NO in the cortex of pilocarpinzed rats. Hypothermia pretreatment mitigated most of the alterations induced by pilocarpine and significantly decreased GABA concentration. These findings emphasize the involvement of extrahippocampal amino acid neurotransmitters in pilocarpine-induced SE and the ameliorative role played by hypothermia.
Gen Physiol Biophys 2015 Oct
PMID:Hypothermia mitigates neurochemical alterations in rat's cerebral cortex during status epilepticus induced by pilocarpine. 2622 43