Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intraperitoneal injection of ethanol (1-2 g/kg) and chlordiazepoxide (2-16 mg/kg) suppressed susceptibility to audiogenically induced, clonic-tonic seizures and antagonized forelimb tremor in rats undergoing ethanol withdrawal, 30 min after treatment. However, a smaller dose of ethanol (0.5 g/kg) actually increased clonic seizure frequency, suggesting that ethanol exerts a biphasic proconvulsant/anticonvulsant action. Direct activation of gamma-aminobutyric acid (GABA) receptors by intracisternal administration of GABA (100-1000 micrograms), muscimol (0.3-1.0 micrograms) or 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) (0.3-3.0 micrograms) 5 to 10 min before testing also reduced susceptibility to audiogenic clonic-tonic seizures. In sharp contrast to these anticonvulsant actions, GABA, muscimol and THIP had no effect on withdrawal-induced forelimb tremors. Blockade of GABA uptake with 1-2,4-diaminobutyric acid (300 and 600 mg/kg i.p.) and inhibition of GABA transaminase with aminooxyacetic acid (12.5 and 25.0 mg/kg i.p.) both reduced susceptibility to seizures. However, anticonvulsant doses of these two drugs, unlike GABA, muscimol and THIP, also reduced forelimb tremor. Three other GABA transaminase inhibitors, gamma-vinyl GABA (450 and 900 mg/kg i.p.), gamma-acetylenic GABA (50-150 mg/kg i.p.) and ethanolamine-O-sulfate (250-750 mg/kg i.p.), were inactive against ethanol withdrawal audiogenic seizures and forelimb tremors. These results indicate that direct GABA receptor activation can selectively suppress one type of ethanol withdrawal response (i.e., audiogenic seizure susceptibility) while failing to influence another (forelimb tremors).
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PMID:Differential sensitivity of ethanol withdrawal signs in the rat to gamma-aminobutyric acid (GABA)mimetics: blockade of audiogenic seizures but not forelimb tremors. 631 80

The effects of several doses of intracerebroventricularly injected cholecystokinin octapeptide sulfate ester (CCK-8-SE) and nonsulfated scholecystokinin octapeptide (CCK-8-NS) were studied on electroconvulsive shock (ECS)-induced retrograde amnesia, as measured in a one-trial step-through passive avoidance paradigm. Both CCK-8-SE and CCK-8-NS were able to attenuate amnesia slightly when they were injected into rats 10 min prior to ECS treatment, possibly by reducing the severity of the ECS-induced seizures. Of the treatments carried out immediately after ECS, only the 0.8 pmole dose of CCK-8-NS could significantly restore retrograde amnesia. After treatment 20 min prior to testing 24-hr retention, no effect of the peptides was observed. The lack of a dose-dependency and of any effect on retrieval raises the possibility that the CCK octapeptides influence memory processes by an indirect mechanism.
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PMID:The effects of sulfated and nonsulfated cholecystokinin octapeptides on electroconvulsive shock-induced retrograde amnesia after intracerebroventricular administration in rats. 632 92

The effects of repeated infusion of small, initially subconvulsive amounts of beta-endorphin, met-enkephalin or morphine sulfate into the amygdala and hippocampus were investigated. beta-endorphin and met-enkephalin evoked epileptiform spiking when infused into the posterior amygdala or ventral hippocampus. Morphine evoked epileptiform spiking when infused into the anterior amygdala. Naloxone blocked or terminated the spiking. Repetition of the infusions led to the gradual development of bilateral generalized convulsions by beta-endorphin and met-enkephalin and to the development of tolerance to morphine. An unexpected observation was that handling, immobilization or conspecific threat potentiated the epileptiform effects of beta-endorphin and morphine in many cases. These results suggest that endogenous opiate mechanisms might play a role in convulsive seizures and that stressful stimuli can exacerbate opiate seizures.
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PMID:Intracerebral beta-endorphin, met-enkephalin and morphine: kindling of seizures and handling-induced potentiation of epileptiform effects. 632 69

The anticonvulsant effect of inhibitors of GABA-T (R/S-gamma-vinyl-GABA, ethanolamine-O-sulfate, gabaculine, aminooxyacetic acid) was enhanced by 10 mmol/kg glycine in animal seizure models which are based on a functional GABA deficit. Similar to glycine in their action, although less effective, were its close structural analogues (sarcosine, N,N-dimethylglycine) and homologous omega-aminoacids (beta-alanine, taurine, gamma-aminobutyric acid, delta-aminovaleric acid). It is assumed that glycine and its structural analogues act on supraspinal glycine receptors as glycine agonists. Our observation is the first example of the synergistic interaction of two inhibitory neuronal systems resulting in the amplification of the anticonvulsant effect. Combined treatment with GABA-T inhibitors and glycine may turn out to be of practical importance in the therapy of seizure disorders and other diseases, for which treatment with GABA-T inhibitors is considered a potentially useful therapeutic approach.
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PMID:Synergistic anticonvulsant effects of GABA-T inhibitors and glycine. 647 85

A study was undertaken of 27 patients with severe preeclampsia who had hemolysis, liver enzyme elevation, and thrombocytopenia as described by Weinstein. In addition to this triad, all patients exhibited the symptoms and signs of pregnancy-induced hypertension by which the diagnosis is usually established. These patients were admitted to the hospital for strict bed rest. Patients who showed evidence of rapid maternal or fetal deterioration were delivered promptly. The remainder were managed without immediate delivery and with the institution of magnesium sulfate to prevent eclamptic seizures. Patients were monitored closely, and amniocentesis was performed to ascertain fetal lung status. If the lungs were mature, the infant was delivered. Attempting to delay delivery until a lecithin: sphingomyelin (L:S) ratio was mature resulted in only two infants developing respiratory distress syndrome (RDS); both had L:S ratios of less than 1.5 and were delivered for maternal indications. Maternal condition rapidly improved within 72 hours of delivery, and there was no persistence of thrombocytopenia or elevation of liver enzymes. Immediate delivery of preeclamptic patients who have thrombocytopenia and elevated liver enzymes may not be warranted. These findings suggest that the syndrome of hemolysis, elevated liver enzymes, and low platelets is not a separate entity, but merely a cluster of signs seen in some patients with hypertensive disorders in pregnancy.
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PMID:Preeclampsia associated with hemolysis, elevated liver enzymes, and low platelets--an obstetric emergency? 663 2

Anesthesia was induced in six patients scheduled for elective aortocoronary bypass (ACB) surgery with intravenous fentanyl, either 50 (n = 2) or 150 micrograms/kg (n = 4) over 20 or 60 sec, respectively. Patients had been given their usual antianginal medications before surgery and were premedicated with morphine sulfate. Arterial plasma fentanyl levels were measured repetitively at frequent intervals, and eight leads of the cortical electroencephalogram (EEG) were recorded continuously. Peak plasma fentanyl concentrations exceeded 1750 ng/ml at the end of the injection of 150 micrograms/kg and then decreased by more than 75% within 3 min. In an additional two patients, incremental doses of fentanyl (25, 25, 50, 50 micrograms/kg; total 150 micrograms/Kg) maintained fentanyl concentrations between 30 and 650 ng/ml for the entire 15 min of the study. In all cases, diffuse slow-wave EEG activity, characteristic of fentanyl anesthesia, was seen. Motor activity, including wrist flexion and ocular movements, was observed during the onset of fentanyl-induced truncal rigidity, but no seizure-like activity was found in the EEG.
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PMID:Absence of seizures during induction of anesthesia with high-dose fentanyl. 671 43

Electroencephalograms (EEGs) were recorded in 36 eclamptic, 14 preeclamptic, and 13 normotensive control patients. In the eclamptic group, EEGs were recorded while patients were receiving intravenous magnesium sulfate (MgSO4) with serum magnesium (Mg) levels of 4.5 to 11 mg/dL, and recorded again after MgSO4 was discontinued (serum Mg levels 1.8 to 2.5 mg/dL). In preeclamptic patients, EEGs were recorded before starting MgSO4, during administration of the loading dose (serum Mg levels 6 to 10 mg/dL), and eight hours through the maintenance dose (serum Mg levels 3.6 to 6.2 mg/dL). Twenty-seven (75%) eclamptic patients had abnormal EEGs, four patients showed paroxysmal spike activity, and the others showed focal or diffuse slowing (delta waves). Seven (50%) preeclamptic women had abnormal EEGs (all had generalized slowing). In preeclamptic-eclamptic patients who had serial EEG recordings, the gross EEG findings obtained during MgSO4 infusion and in the absence of MgSO4 were similar. In addition, the abnormal EEG findings were frequent despite the serum Mg levels considered therapeutic in the clinical management of these patients. Two eclamptic patients had seizure activity at serum Mg levels of 9.6 and 11 mg/dL. These findings suggested that abnormal EEGs are frequent in preeclamptic-eclamptic patients. Abnormal EEG findings in such patients are not altered by serum Mg levels achieved in the clinical management of these patients.
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PMID:Effect of magnesium sulfate on electroencephalographic findings in preeclampsia-eclampsia. 673 59

Seizures produced by intracerebral injection of zinc sulfate in rabbits are a new chronic model of experimental epilepsy. The main features of this model are: the animals are easily controlled, the electrocorticogram is conveniently recorded, the endpoints are definite, and the rate of seizure is higher than with other methods. The commonly used antiepileptic drugs, such as phenobarbital (30 mg/kg), diphenylhydantoin (30 mg/kg), nitrazepam (3 mg/kg), and sodium valproate (300 mg/kg), have therapeutic effects in treating this experimental epilepsy, when they are given intravenously. But they can not protect the rabbits from death, except phenobarbital.
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PMID:Zinc-induced seizures: a new experimental model of epilepsy. 683 78

We studied the frequency of oligoclonal immunoglobulin G bands in the cerebrospinal fluid (CSF) of patients with various neurological diseases. We used a micromethod employing sodium dodecyl sulfate polyacrylamide gel electrophoresis that required only 50 microliters of unconcentrated CSF. Oligoclonal bands were detected in the CSF of 95% of the patients with multiple sclerosis, 90% with subacute sclerosing panencephalitis, and 100% with herpes simplex encephalitis, but less frequently in other central nervous system infections. No oligoclonal bands were detected in the CSF of patients with Parkinson, Huntington, Creutzfeldt-Jakob, or herniated disc diseases. Bands were detected in some patients with Alzheimer disease, cerebrovascular accident, idiopathic vertigo, idiopathic seizures, amyotrophic lateral sclerosis, polyneuropathy, and central nervous system glioma. Patients with other conditions infrequently had positive bands. The determination of oligoclonal bands is a useful aid in the diagnosis of multiple sclerosis, subacute sclerosing panencephalitis, and herpes simplex encephalitis. The presence of oligoclonal bands indicates an immunological response but is not diagnostic for a particular condition.
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PMID:Oligoclonal IgG bands in cerebrospinal fluid in various neurological diseases. 683 75

Picolinic, kynurenic, xanthurenic and anthranilic acids are metabolites of L-kynurenine which, when administered intraperitoneally (i.p.) antagonized (in descending order of potency) the seizures induced by intracerebroventricular (i.c.v.) injections of l-kynurenine sulfate in SHR and C57BL/6 mice. Picolinic and anthranilic acids were also effective after oral administration. Picolinic acid completely prevented seizures. Kynurenic acid, when injected i.c.v. prior to l-kynurenine sulfate, appeared to be more effective than after i.p. administration while picolinic and anthranilic acids were less effective. This suggest that the antikynurenine effect of metabolites of kynurenine (kynurenines) is related to different brain structures, i.e. kynurenic acid predominantly affects structures adjacent to ventricles (e.g. hippocampus, caudate nucleus) while picolinic and anthranilic acids act on other brain structures or the periphery. Xanthurenic, kynurenic and picolinic acids merely prolonged the latency of seizures induced by i.c.v. quinolinic acid (another metabolite of kynurenine) or by subcutaneous strychnine sulfate and i.p. pentylenetetrazole, and did not modify seizures induced by i.p. caffeine and thiosemicarbazide. This selective antagonism of the tested kynurenines against kynurenine might be an important anticonvulsant factor in kynurenine-dependent seizures. It is suggested that increased excretion of xanthurenic, kynurenic and picolinic acids in patients with convulsive states may be manifestations of compensatory processes.
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PMID:Antagonism of kynurenine-induced seizures by picolinic, kynurenic and xanthurenic acids. 686 8


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