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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Male Long-Evans rats were stereotaxically implanted bilaterally with bipolar electrodes in the central amygdala. Rats were then kindled once daily for 1 sec until 3 consecutive Stage V [25] kindled seizures were elicited. On the following day, animals were injected (IP) with either saline, naloxone (10 mg/kg), naltrexone (10mg/kg) or morphine sulfate (10 mg/kg) and again stimulated at the kindling stimulation parameters. Saline injected animals continued to show long bilateral AD's and behaviors (i.e., forelimb clonus, rearing, falling) typical of Stage V kindled animals. In contrast, rats injected with naloxone or naltrexone showed reduced behavioral seizures. Potentiation of post-ictal spiking by morphine in amygdaloid-kindled rats was also observed supporting previous reports [7,21]. In a second experiment, the reduction of kindled seizure serverity by naloxone was systematically replicated. It is concluded that opiates can significantly modify amygdaloid-kindled seizures, and that brain endorphins may play a role in the development or maintenance of an amygdaloid-kindled seizure focus.
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PMID:Opiate modification of amygdaloid-kindled seizures in rats. 708 32

When introduced intracerebroventricularly, quinolinic acid appeared to be the only kynurenine metabolite among those tested (L- and DL-kynurenine sulfate, kynurenic and nicotinic acids, nicotinamide) which induced locomotor excitement and clonic seizures in rats; in high dosage all exhibited convulsant action in mice. L-Kynurenine sulfate (500 micrograms) induced continuous rotation in rats around a longitudinal axis in one or other direction. It also potentiated the convulsant effect of strychnine sulfate and caffeine. Neither the excitatory amino acids, L-glutamic and L-aspartic acids nor the inhibitory amino acids, GABA, glycine and taurine induced excitement or seizures in rats but did in mice. In rats, GABA, glycine and taurine induced sedation, side position and discoordination. The convulsants, strychnine sulfate and pentylenetetrazole, induced seizures both in rats and mice. Differences between species may derive from the better access of intracerebroventricularly administered drugs to mouse hippocampus. Thus mice may be preferable for studies of this type on excitatory amino acids (including kynurenine pathway metabolites) and rats for those on inhibitory amino acids.
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PMID:Excitatory effects of kynurenine and its metabolites, amino acids and convulsants administered into brain ventricles: differences between rats and mice. 713 Sep 75

Quinolinic acid appeared to be the only kynurenine metabolite among tested (L- and DL-kynurenine sulfate, kynurenic and nicotinic acids, nicotinamide) which induced locomotor excitation and clonic seizures in rats whereas all of them exerted convulsant action in mice. Excitatory 1-glutamic and 1-aspartic amino acids and inhibitory amino acids GABA, 1-glycine and taurine did not induce either excitation of seizures in rats but did so in mice. Moreover, GABA, 1-glycine and taurine induced obvious sedation, side position and discoordination in rats. Convulsants strychnine sulfate and pentylenetetrazol induced seizures both in rats and in mice. The differences between mice and rats seem to be due to better availability of hippocampus for the intraventricularly administered drugs in mice. Mice seem to be preferable for studies with intraventricularly administered excitatory amino acids including kynurenines, whereas rats are preferable for inhibitory amino acids.
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PMID:[Stimulatory effects of intraventricular administration of kynurenines, amino acids, and convulsants: differences between rats and mice]. 715 52

Zenker's solution is a tissue fixative containing mercuric chloride, potassium bichromate, sodium sulfate, and glacial acetic acid. In 1956, Anderson and Johnson reported its use in clinical neurosurgery. They applied the solution to the exposed dura after craniectomy. Delayed bone formation was thought to be due to the suppression of the osteoblastic activity of the outer layer of the dura. The fixative has since become a well-accepted adjuvant to the treatment of craniosynostosis. In 1972, Pawl and Sugar reported postoperative seizures in 6 of 34 patients treated with this solution. They assumed that the fixative penetrated the dura and irritated or damaged the cortex. To clarify the effect of Zenker's solution on the underlying brain, we performed bilateral parasagittal craniectomies in a group of kittens and adult cats. Zenker's solution was applied to one side and the other side served as a control. The animals were killed after periods varying from 24 hours to 2 months. We then examined the cortex under the craniectomies. There was immediate breakdown of the blood-brain barrier, as evidenced by the penetration of intravenous Evans blue. In the postoperative period investigated, an inflammatory response in the underlying brain with thickening of the arachnoid occurred. The results and implications of these experiments are presented. (Neurosurgery, 6: 45--48, 1980)
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PMID:Effect of the dural application of Zenker's solution on the feline brain. 735

Three cases of generalized seizures in patients with high cerebrospinal fluid (CSF) concentrations of cefazolin are reported. Patient 1, a 60-year-old woman with impaired renal function and a Klebsiella pneumoniae infection, was treated with 70 mg every eight hours of i.v. gentamicin sulfate and 1.5 g every four hours of i.v. cefazolin sodium. Gentamicin was discontinued on day 11. On day 12, the patient had a generalized tonic-clonic seizure. Serum and CSF concentrations of cefazolin one day later were 470 and 64 micrograms/ml, respectively. Patient 2, a 70-year-old man with impaired renal function, was given i.v. cefazolin, 1 g every 12 hours; the dosage interval was shortened later to every six hours. Two days later, the patient had two tonic-clonic seizures. Serum and CSF concentrations eight hours after the last dose of cefazolin were 360 and 34 micrograms/ml, respectively. Patient 3, a 67-year-old woman with renal vein thrombosis, received 55 mg every eight hours of i.v. gentamicin and 2 g every six hours of i.v. cefazolin. The antibiotics were discontinued after eight days when the patient had two tonic-clonic seizures. Serum and CSF concentrations of cefazolin measured 28 hours later were 1000 and 106 micrograms/ml, respectively. Previous reports of cefazolin-associated seizures are reviewed. In patients with renal failure, cefazolin may obtain high CSF concentrations. To avoid seizures, cefazolin doses should be adjusted in these patients.
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PMID:Seizures associated with high cerebrospinal fluid concentrations of cefazolin. 736 4

Intraventricular injection of DL-kynurenine and L-kynurenine sulfate (40 microgram) into conscious mice potentiated convulsions and lethality produced by strychnine (1 mg/kg) and not by thiosemicarbazide nor pentylenetetrazol. Another metabolite of tryptophan with convulsive effect, quinolinic acid, was ineffective. Intraperitoneal injection of DL-kynurenine sulfate and quinolinic acid (25-100 mg/kg) was associated with prolongation of the latency of strychnine and thiosemicarbazide (only the former drug) seizures. Nicotinic, picolinic, and anthranilic acids (100 and 250 mg/kg) did not modify the action of convulsants. Data and suggestions about probable involvement of brain glycine and gamma-aminobutyric acid receptors in the convulsive action of kynurenines is discussed.
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PMID:Effect of kynurenine and quinolinic acid on the action of convulsants in mice. 740 16

Taurine in doses of 100 and 200 mg/kg (intraperitoneally) and 2.5 micrograms (into brain ventricles) antagonized clonic seizures produced by L-kynurenine sulfate injected into brain ventricles of SHR adult male albino mice. Seizures produced by another metabolite of tryptophan in the kynurenine pathway, quinolinic acid, were intensified. The convulsant effects of strychnine, pentylenetetrazol and thiosemicarbazide was not modified.
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PMID:Taurine selectivity antagonizes L-kynurenine-produced seizures in mice. 742 78

The occurrence of seizures in preeclamptic and eclamptic women is considered very unlikely during treatment with the standard dose of continuous intravenous magnesium sulfate. During a 21-month period, the authors encountered 13 patients who developed seizure activity while receiving intravenous MgSO4. Serum magnesium (Mg) levels at the time of seizure were below the therapeutic range in 11 of the 13 patients, thus prompting a study of serum Mg levels in preeclamptic patients treated with MgSO4. Random serum Mg samples were obtained from 120 patients treated with intravenous MgSO4 for preeclampsia-eclampsia. The samples were collected 2 to 48 hours after the loading dose and while the patients were taking a maintenance dose of either 1, 2, or 3 g/hr. When a maintenance dose of 1 or 2 g/hr was used, 98 and 50% of the respective serum magnesium values were below levels considered therapeutic by several authors. Therapeutic levels were achieved in ll patients receiving a maintenance dose of 3 g/hr. The recommended maintenance dose of MgSO4 of 1 g/hr was found insufficient to prevent the occurrence of eclamptic seizures in some preeclamptic patients.
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PMID:Reassessment of intravenous MgSO4 therapy in preeclampsia-eclampsia. 746 24

We have shown previously that the neurosteroid pregnenolone sulfate acts as a positive allosteric modulator at the N-methyl-D-aspartate (NMDA) receptor while inhibiting the kainate, the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA), the glycine, and the gamma-aminobutyric acid (GABA) responses of chick spinal cord neurons. Here, we report that 3 alpha-hydroxy-5 beta-pregnan-20-one sulfate (5 beta 3 alpha S), a sulfated form of naturally occurring 5 beta 3 alpha, inhibits both the NMDA and the non-NMDA receptor-mediated responses as measured by whole cell voltage clamp recordings. 100 microM 5 beta 3 alpha S rapidly and reversibly inhibits the response to 30 microM NMDA by 66%, 50 microM kainate by 37%, and 25 microM AMPA by 29%. Application of 50 microM nonsulfated 5 beta 3 alpha does not produce any significant effect on the NMDA response, demonstrating that the sulfate moiety is important for the effect of 5 beta 3 alpha S on the NMDA response. The effect of 5 beta 3 alpha S on the NMDA response is concentration dependent, with an EC50 of 62 microM. 5 beta 3 alpha S reduces the maximum NMDA response with little effect on the NMDA EC50, indicating that antagonism of the NMDA response by 5 beta 3 alpha S is noncompetitive. The fact that 5 beta 3 alpha S inhibition of the NMDA response is neither agonist nor voltage dependent demonstrates that 5 beta 3 alpha S does not act as an open channel blocker. Furthermore, inhibition of the NMDA response by 5 beta 3 alpha S is not reduced by the addition of a maximal concentration (10 microM) of glycine, indicating that 5 beta 3 alpha S does not act via the glycine recognition site. The inhibitory action of 5 beta 3 alpha S on the NMDA and non-NMDA receptors may provide a basis for inhibiting glutamate receptor-induced seizures and excitotoxic cell death.
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PMID:3 alpha-Hydroxy-5 beta-pregnan-20-one sulfate: a negative modulator of the NMDA-induced current in cultured neurons. 752 Jan 24

Untreated hyperthyroidism during pregnancy is associated with increased maternal and perinatal morbidity. Some features of this disease simulate preeclampsia, which may encourage delivery of the fetus. We report a case of poorly controlled hyperthyroidism associated with generalized seizures, where patient management was directed at a diagnosis of preeclampsia-eclampsia. Although the presence of eclampsia and marked hyperthyroidism is very rare, this case illustrates the importance of aggressive medical management of hyperthyroidism. A 17-year-old gravida was diagnosed with hyperthyroidism at 15 weeks' gestation. At 26 weeks' gestation, she was admitted to the hospital after noting edema of the upper and lower extremities, nausea, vomiting, shortness of breath, and a cough. At admission, she was hypertensive, tachycardic, and dyspneic. The patient was believed to have preeclampsia with pulmonary edema complicated by hyperthyroidism. We initiated magnesium sulfate therapy and administered several bolus doses of hydralazine, with little effect on blood pressure. Oliguria was noted, and a pulmonary artery catheter was inserted. Hours later, generalized seizure activity occurred, and a decision was made for abdominal delivery. Postoperatively, cardiovascular function stabilized. On postoperative day 3, we received the results of the thyroid function tests obtained at admission, which suggested a markedly hyperthyroid condition. Untreated or poorly treated hyperthyroidism may present a clinical picture similar to preeclampsia. In our case, both disease processes coexisted in their severest forms. It is possible, although completely unproven, that a relationship exists between poorly controlled hyperthyroidism and preeclampsia-eclampsia. More importantly, accurate diagnosis of hyperthyroidism should lead to prompt medical or surgical management, thereby decreasing maternal and perinatal morbidity.
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PMID:Hyperthyroidism and seizures during pregnancy. 761 94


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