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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovascular complications frequently occur during status epilepticus. To determine the changes in systemic and pulmonary arterial pressure, cardi output, and left ventricular contractility during seizures, 1-week-old pigs were intubated, paralyzed, mechanicall entilated, and catheterized with a Swan-Ganz catheter. Seizures were induced with intravenous bicuculline. Early changes consisted of significant systemic and pulmonary arterial hypertension. After 2 hours of seizures, the animals developed progressive systemic hypotension and decreased cardiac output. M-mode echocardiography disclosed a decrease in left ventricular contractility. Cardiac tissue frozen in situ showed a significant increase in lactate and reductions in glucose, triglyceride, and adenosine triphosphate levels. Prolonged seizures in the neonatal pig result in cardiac dysfunction, which may play a role in the development of epileptic brain damage.
Ann Neurol 1985 Sep
PMID:Cardiac dysfunction during status epilepticus in the neonatal pig. 405 58

1. DL-C-Allyglycine, 4-deoxypyridoxine hydrochloride and 3-mercaptopropionic acid have been studied with reference to their convulsant effects in mice and in baboons (Papio papio) with photosensitive epilepsy, and their action on the cerebral enzyme synthesizing gamma-aminobutyric acid (L-glutamate-1-carboxy-lyase).2. In mice, the ED(50) values for seizures following intraperitoneal injection were allylglycine 1.0 mmol/kg body weight, 4-deoxypyridoxine 1.1 mmol/kg and 3-mercaptopropionic acid 0.27 mmol/kg. Latency to seizure onset was longest after allylglycine (44-240 min), intermediate after 4-deoxypyridoxine (9-114 min) and shortest after 3-mercaptopropionic acid (2.5-8 min).3. In Papio papio intravenous administration of subconvulsant doses of allylglycine (0.87-3.1 mmol/kg), or of 4-deoxypyridoxine (0.21-0.53 mmol/kg) enhanced the occurrence and persistence of myoclonic responses to intermittent photic stimulation, and augmented the associated electroencephalographic abnormalities, without modifying their character or distribution. Higher doses produced brief seizures recurring at regular intervals, between 2-14 h after allylglycine (4.0-4.3 mmol/kg) or 1-4 h after 4-deoxypyridoxine (0.53-0.87 mmol/kg). Electroencephalographically these seizures originated unilaterally in the occipital or posterior parietal cortex.4. In Papio papio photically-induced epileptic responses were enhanced 5-10 min after the intravenous injection of 3-mercaptopropionic acid (0.09-0.28 mmol/kg). A sequence of brief generalized seizures followed by complete recovery occurred 4-17 min after the injection of 3-mercaptopropionic acid (0.28-0.38 mmol/kg). Fatal status epilepticus followed the injection of 3-mercaptopropionic acid (0.57-0.75 mmol/kg). E.E.G. records showed generalized cortical involvement at the onset of the seizures.5. L-Glutamate 1-carboxy-lyase (GAD) activity was determined in whole brain homogenates from mice killed at various intervals after receiving i.p. a convulsant dose of one of the compounds. Inhibition of GAD activity was evident 30-60 min before seizure onset following allylglycine or 4-deoxypyridoxine administration, and was maximal (40-60%) just before or during seizure activity. Addition of pyridoxal phosphate to the brain homogenate relieved inhibition produced by 4-deoxypyridoxine but not that produced by allylglycine. Inhibition of GAD activity in brain homogenates from animals killed 2 or 4 min after injection of a convulsant dose of 3-mercaptopropionic acid varied from 0-49% depending on the dose of 3-mercaptopropionic acid and the concentration of substrate in the assay system.6. Kinetic analysis of the inhibition of GAD activity following direct addition of the compounds to mouse brain homogenates indicated that 3-mercaptopropionic acid (0.01-0.5 mM) was competitive with respect to the substrate. A comparable percentage inhibition of GAD activity was obtained only with much higher concentrations of 4-deoxypyridoxne, i.e. 10-50 mM. Allylglycine in vitro was a very weak inhibitor of GAD activity.7. Three biochemically different mechanisms underlie the inhibition of cerebral GAD activity that precedes seizures induced by ailylglycine, 4-deoxypyridoxine and 3-mercaptopropionic acid. The data are consistent with a critical reduction in the rate of synthesis of gamma-aminobutyric acid being responsible for the onset of seizures.
Br J Pharmacol 1973 Sep
PMID:Seizures induced by allylglycine, 3-mercaptopropionic acid and 4-deoxypyridoxine in mice and photosensitive baboons, and different modes of inhibition of cerebral glutamic acid decarboxylase. 420 45

Electrographic and clinical observations were made after the injection of kainic acid into the unilateral hippocampus of freely moving cats. Vehicle solution (phosphate buffer solution) for control study and kainic acid(1, 4 and 12 micrograms) were administered via a chronically implanted cannula. The control group showed no modification during the observation period. After the injection of 1 microgram of kainic acid, focal status epilepticus was observed for 2-3 days and then cats became normal afterwards. In the group of 4 micrograms kainic acid infection, cats demonstrated limbic status for 3 days, and persistent inter-ictal discharges continued during the observation period. Independent amygdaloid seizures and secondary generalized convulsions developed in the cats administered 12 micrograms of kainic acid. The cats died in the status epilepticus. The dose-dependent and substantial effect of KA without the influences of anesthesia and surgery was demonstrated. The results were discussed in relation to the human medial temporal sclerosis and the effects on the emotional mechanism of the limbic system. We suggest this model to be useful in the study of various types of temporal lobe epilepsy and the emotional mechanisms of the limbic system.
Electroencephalogr Clin Neurophysiol 1982 Sep
PMID:Electroclinical features of kainic acid-induced status epilepticus in freely moving cats. Microinjection into the dorsal hippocampus. 617 56

In dogs the development of tolerance to the anticonvulsant effect of diazepam was followed by weekly determinations of the convulsive threshold for pentetrazole, 10-15 min after intravenous (i.v.) injection of 0.25 or 0.5 mg/kg diazepam. As soon as after 1 week of oral treatment with diazepam, 0.25 or 0.5 mg/kg three times daily (t.i.d.), the pentetrazole threshold showed a decline or even a fall to the control level in spite of unaltered or rising concentrations of diazepam and its active metabolites. Tolerance also developed when the dogs were treated with chlorazepate, 2 mg/kg t.i.d., between the weekly diazepam injections for threshold determination. The results favor a functional type of tolerance since there was no indication of a more rapid inactivation of diazepam. Treatment with desmethyldiazepam (2 mg/kg i.v. for threshold determination and oral treatment with the desmethyldiazepam precursor chlorazepate, 2 mg/kg t.i.d.) did not produce tolerance. In further experiments in dogs anesthetized, relaxed with suxamethonium and ventilated, a spike-wave activity in the EEG was induced and maintained by an injection and subsequent infusion of pentetrazole. Out of 6 dogs, receiving 4-5 i.v. injections of 0.25-0.5 mg/kg diazepam, 2 showed the phenomenon of acute tolerance, i.e. the effect of the drug on the spiking activity in the EEG became less from one injection to the next, and thus paralleled a situation which may be observed during treatment of clinical status epilepticus. No acute tolerance was observed in corresponding experiments with desmethyldiazepam.
Eur J Pharmacol 1984 Sep 03
PMID:Development of tolerance to the anticonvulsant effect of diazepam in dogs. 643 48

The occurrence of status epilepticus during a course of modified unilateral nondominant electroconvulsive therapy (ECT) in a patient with chronic schizophrenia is described. ECT was continued in this case with no further complication.
J Clin Psychiatry 1984 Sep
PMID:Status epilepticus with unilateral ECT: case report. 646 28

We describe two patients in whom clonazepam withdrawal status epilepticus occurred in spite of therapeutic levels of carbamazepine in plasma and cerebrospinal fluid. The failure of carbamazepine to prevent clonazepam withdrawal status epilepticus is discussed.
Ital J Neurol Sci 1984 Sep
PMID:Failure of carbamazepine to prevent clonazepam withdrawal status epilepticus. 650 Sep 1

Status epilepticus is a medical emergency. Recent experimental studies have shown that permanent brain damage can occur after only 60 minutes of uncontrolled seizure activity. Cardiac arrhythmias are a common cause of death. Other complications include rhabdomyolysis, acute tubular necrosis and neurogenic pulmonary edema. Management is divided into three phases: stabilization of the patient, termination of the seizures and diagnostic evaluation.
Am Fam Physician 1983 Sep
PMID:Status epilepticus. 661 91

Behavioural, electroencephalographic and neuropathological responses to increasing doses of pilocarpine (100-400 mg/kg) administered intraperitoneally to rats were studied. At the dose of 400 mg/kg pilocarpine produced a sequence of behavioural alterations including staring spells, olfactory and gustatory automatisms and motor limbic seizures that developed over 1-2 h and built up progressively into limbic status epilepticus. Smaller doses showed different threshold for these behavioural phenomena but a similar time course of development. The earliest electrographic alterations occurred in the hippocampus and then epileptiform activity propagated to amygdala and cortex. Subsequently electrographic seizures appeared in both limbic and cortical leads. The ictal periods recurred each 5-15 min and were followed by variable periods of depression of the electrographic activity. The sequence of electrographic changes correlated well with the development of behavioural phenomena. Histological examination of frontal forebrain sections revealed disseminated, apparently seizure-mediated pattern of brain damage. Neuropathological alterations were observed in the olfactory cortex, amygdaloid complex, thalamus, neocortex, hippocampal formation and substantia nigra. Pretreatment of animals with scopolamine (20 mg/kg) and diazepam (10 mg/kg) prevented the development of convulsive activity and brain damage. These results show that systemic pilocarpine in rats selectively elaborates epileptiform activity in the limbic structures accompanied by motor limbic seizures, limbic status epilepticus and widespread brain damage. It is suggested that a causative relationship between excessive stimulation of cholinergic receptors in the brain and epileptic brain damage may exist.
Behav Brain Res 1983 Sep
PMID:Limbic seizures produced by pilocarpine in rats: behavioural, electroencephalographic and neuropathological study. 663 40

Cerebral oxygenation initially increases and later decreases in rats subjected to experimental status epilepticus. In this study, we have compared cerebral oxygen supply and vascular changes during paroxysmal events of different durations and at different time intervals to test the hypothesis that oxygen insufficiency is associated more readily with paroxysmal events of greater intensity. Continuous measurements were made of local changes in cortical blood volume, redox levels of cytochrome a, a3, cortical Po2, and systemic arterial blood pressure during recurrent seizures induced by pentylenetetrazol or bicuculline. In contrast to expectations, systemic and cerebral vascular responses and associated increases in cerebral oxygenation were better maintained during long-duration ictal episodes than during short-duration ictal bursts, interictal spikes, or evoked potentials. Short-duration paroxysmal events were often accompanied by decreases in cerebral oxygenation, whereas long-duration events were still accompanied by increases in oxygenation. Ictal bursts occurring with short interburst intervals caused a more rapid failure of vascular responsiveness than those occurring at longer intervals. These relationships of intensity and frequency of repetition of seizures to changes in vascular responses indicate progressive dissociation of the normally tight couple between neuronal activity, energy demand, and cerebral blood flow during status epilepticus.
J Cereb Blood Flow Metab 1983 Sep
PMID:Importance of vascular responses in determining cortical oxygenation during recurrent paroxysmal events of varying duration and frequency of repetition. 687 42

The author describes an occurrence of ECT-induced status epilepticus in a patient who was psychotically depressed and unresponsive to tricyclic and neuroleptic medication. After an extensive evaluation and further unsuccessful use of treatment alternatives the patient then received a course of specially modified ECT; he had no further sequelae and had a good clinical response.
Am J Psychiatry 1981 Sep
PMID:ECT-induced status epilepticus and further ECT: a case report. 727 Jul 32


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