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

The effects of acute changes in plasma magnesium concentration on the threshold for lidocaine-induced seizures were evaluated in mechanically ventilated rats receiving 70% nitrous oxide and 30% oxygen. In experiment 1, male rats were intravenously administered either 0.9% sodium chloride (group I) or 5.0% magnesium sulfate to elevate plasma magnesium levels to 5.8 +/- 0.1 (group II) or 10.5 +/- 1.0 mg/dl (group III). In experiment 2, pregnant rats were intravenously administered either 0.9% sodium chloride (normomagnesemia) or magnesium sulfate, resulting in a plasma magnesium concentration of 7.8 +/- 1.4 mg/dl. Thirty minutes later, a continuous intravenous infusion of lidocaine (2.3 mg/kg per minute) was begun in both experiments. Biparietal electroencephalographic activity was monitored continuously. At the onset of electroencephalographic seizure activity, arterial plasma magnesium and lidocaine concentrations were measured. In groups I and III (experiment 1), brain parenchymal magnesium was also assayed. There were no differences in plasma lidocaine concentrations (in experiments 1 or 2) between saline solution and hypermagnesemic groups at onset of seizures. Brain magnesium level was unaltered by magnesium sulfate infusion. We conclude that acute administration of magnesium sulfate alters neither brain magnesium level nor the plasma lidocaine concentration associated with onset of electroencephalographic seizures.
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PMID:Effects of acute hypermagnesemia on the threshold for lidocaine-induced seizures in the rat. 199 23

Pulmonary function was studied in ten preeclamptic women in labor (mean gestational age 38.1 +/- 0.9 weeks measured from the last menstrual period) receiving continuous intravenous (IV) infusions of magnesium sulfate. Baseline maximal inspiratory pressure, maximal expiratory pressure, functional vital capacity, and forced expiratory volume at 1 second were measured immediately before a 6-g IV loading dose of magnesium sulfate and 2 hours after the initiation of a continuous 2-g/hour infusion of magnesium sulfate. Serum magnesium levels were measured at the same time pulmonary function tests were performed. All values are reported as the mean +/- standard deviation. The maximal inspiratory pressure, an indicator of generalized respiratory muscle weakness, decreased from a baseline value of 26.2 +/- 7.7 to 19.4 +/- 6.3 cm H2O (P less than .05). The maximal expiratory pressure, an indicator of expiratory muscle strength, decreased from a baseline value of 30.6 +/- 9.2 to 25.2 +/- 7.1 cm H2O (P less than .005). The functional vital capacity decreased from a baseline value of 3.37 +/- 0.49 to 3.19 +/- 0.73 L, and the forced expiratory volume at 1 second decreased from a baseline value of 2.61 +/- 0.58 to 2.36 +/- 0.68 L at 2 hours (P less than .05). The mean serum magnesium level was 1.7 +/- 0.2 mg/dL before the administration of the IV loading dose and 4.51 +/- 0.67 mg/dL 2 hours after initiation of the continuous infusion. Our results demonstrate a significant decrease in pulmonary function tests in term preeclamptic patients receiving magnesium sulfate for seizure prophylaxis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulmonary function of preeclamptic women receiving intravenous magnesium sulfate seizure prophylaxis. 206 69

Administration of reserpine, trifluperidol, chlorpromazine, haloperidol, spiroperidol, and thioproperazine to adult mice shortened the latency and increased the number of animals with clonic seizures induced by 1-kynurenine sulfate or its metabolite quinolinic acid. Haloperidol dose-dependently intensified kynurenine-induced seizures and did not alter pentylenetetrazole seizures. Dopamine abolished the effect of haloperidol while serotonin was ineffective. Pretreatment with 6-hydroxydopamine potentiated kynurenine-induced seizures, but not quinolinic acid-induced seizures. The seizure thresholds of kynurenine and quinolinic acid were not affected by pretreatments with yohimbine, clonidine, piperoxan, phentolamine and tricyclic antidepressants. Apomorphine and amphetamine (i.p.), noradrenaline and adrenaline (i.c.v.) possess anticonvulsant action against kynurenine and not against quinolinic acid. The data obtained suggest a similarity of kynurenine and known convulsants in the involvement of the catecholaminergic processes in their convulsant action. Quinolinic acid markedly differs from kynurenine in its mechanism of action as indicated by their interactions with numerous endogenous substances.
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PMID:Effect of catecholaminergic drugs on quinolinate- and kynurenine-induced seizures in mice. 214 73

It would appear from the above that Pritchard agrees with the use of some agents other than magnesium sulfate that have known anticonvulsant properties. We believe that the subject at issue is whether magnesium sulfate should be used in treating the seizures of eclampsia. In our "Controversies" article, we do not address the issue of whether magnesium sulfate modifies pathophysiological factors leading to preeclampsia, but restrict ourselves to the treatment of the seizure per se, once seizures supervene, and the avoidance of their recurrence. The pathophysiological mechanisms and optimal treatment of preeclampsia and of eclampsia (excepting seizures) remain to be determined, as does the use of magnesium sulfate in this condition. Eclamptic seizures are clinically and electroencephalographically indistinguishable from generalized tonic-clonic seizures. Whether seizures arise in or out of the setting of preeclampsia, they should be treated as are other seizures, with known anticonvulsants. Controlled clinical trials are needed to address the effectiveness of alternative antiseizure regimens.
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PMID:A continuing controversy: magnesium sulfate in the treatment of eclamptic seizures. 183 Apr 69

In experiments on rats it was shown that i.p. administration of finoptin (verapamil), magnesium sulfate or ryodipine (an 1,4-dihydropyridine) 15 min before each daily injection of pentylenetetrazole (PTZ) in a subconvulsive dose (30 mg/kg i.p.) significantly (for 10-12 days delayed the development of pentylenetetrazole-induced kindling and attenuated kindled seizure reaction as compared with the controls. In animals sensitive to PTZ which were selected on the test of their reaction to previous single PTZ injection in a dose of 40 mg/kg finoptin, magnesium or finoptin + magnesium resulted in suppression of kindling development at late stages (after 2-week administration of drugs together with PTZ). After the withdrawal of the drugs there was a tendency to an increase of seizure reaction to the testing PTZ dose (30 mg/kg). The enhanced seizure susceptibility to test PTZ dose has being persisted during all observation period (8 months). Finoptin administered 15 min prior to PTZ had no effect on the severity of seizure reaction of fully kindled animals which had not received the drugs. The results obtained show that organic Ca-antagonists and magnesium delay the development of kindling induced seizure susceptibility, but cannot completely prevent it. The results also suggest that mechanisms of the chronic epileptogenesis (development of kindling induced seizure susceptibility) and those of the acute convulsive reaction to the epileptogen are not similar.
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PMID:[Effects of organic calcium antagonists and magnesium on the development of corazol kindling]. 227 78

To evaluate the protein-related mechanism for epileptogenesis, we examined protein behavior during cobalt-induced epileptic seizure activity and the effect of injection of cobalt-induced proteins into cerebral cortex on electrocorticographic discharge in rats. Cobalt-induced epileptic seizure activity caused an increase in two proteins that migrated at about 84 kDa (P84) and 70-71 kDa (P70) and a decrease in a protein of about 57 kDa (P57) as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Among these proteins, P70 evoked epileptic discharges on the electroencorticograph and behavioral seizure, when it was intracortically injected into the motor region of the normal rat cerebrum. The data suggest that P70 may be a factor for epileptogenesis.
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PMID:Induction of epileptic seizure activity by a specific protein from cobalt-induced epileptogenic cortex of rats. 230 72

We studied the effects of parenteral magnesium sulfate (MgSO4) administration on electroencephalographic seizures induced by hyperbaric oxygen (HBO) in awake rats. Sixteen rats chronically implanted with electrocorticographic electrodes were preinjected i.p. with either vehicle or 3 mmol/kg MgSO4 (the latter resulted in serum levels of 3.5-5.5 mmol/liter) and then exposed to 6 ATA O2 in a pressure chamber. The time to develop an electric ichtal seizure was measured and compared to that in the same animal receiving the alternate treatment 3 days later. Mean and median times after the magnesium treatment were almost double those of vehicle administration. A central anticonvulsive action of magnesium, which should be investigated over the entire HBO range, is indicated.
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PMID:Magnesium sulfate suppresses electroencephalographic manifestations of CNS oxygen toxicity. 231 59

The specificity of the hypoglycemic response to the intrathecal (i.t.) administration of the naturally occurring (-)-enantiomer of morphine previously reported from our laboratory was studied in mice. (+)-Morphine HBr (50 micrograms) caused a behavioral syndrome (scratching, biting, seizures) comparable to that produced by (-)-morphine sulfate (50 micrograms), but did not cause hypoglycemia. Many opioids, at a dose of 50 micrograms i.t. in nonfasted mice, showed either a saline-like hyperglycemic response or no significant effect on blood glucose. (+)-Morphine, ketocyclazocine, U-50,488, (-)- and (+)-N-allyl-normetazocine, beta-endorphin, (-)- and (+)-naloxone and naltrexone caused hyperglycemia. Significant changes from basal blood glucose were not produced by [D-Pen2, L-Pen5]-enkephalin, [D-Ser2]-Leu-enkephalin-Thr or sufentanil in 50-micrograms doses, or by codeine (300 micrograms), levorphanol (400 micrograms) or methadone (200-400 micrograms). Agonists which produced both hypoglycemic and behavioral effects were, in order of decreasing potency, hydromorphone greater than normorphine greater than morphine greater than 6-acetylmorphine greater than oxymorphone much greater than heroin. Morphine-induced hypoglycemia was partially antagonized by the i.t. coadministration of naloxone methobromide (10 micrograms). Fasting for 24 hr increased the sensitivity to hypoglycemic and lethal effects of morphine. D-Ala2-N-Me-Phe4-Gly5-ol]-enkephalin (5-50 micrograms i.t.) tended to decrease blood glucose in both nonfasted and fasted mice, but these effects were moderate and appeared to be unrelated to dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypoglycemia induced by intrathecal opioids in mice: stereospecificity, drug specificity and effect of fasting. 235 29

A case is presented of a primigravida with transient diabetes insipidus, gestational hypertension, and multiple seizures resistant to magnesium sulfate and diazepam. After addition of phenytoin, no further seizures occurred. Transient diabetes insipidus in pregnancy has been previously associated with hypertension, liver dysfunction, and fetal distress. Considered with previous cases, it is suggested that seizures may frequently be part of this syndrome.
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PMID:Transient diabetes insipidus in pregnancy complicated by hypertension and seizures. 237 40

The normalization of hyperreflexia has been proposed by some authorities as an indicator of adequate seizure prophylaxis in preeclamptic women receiving magnesium sulfate. To test this hypothesis the patellar reflex response was measured with a quantitative technique in 20 preeclamptic patients during their progression from subtherapeutic to therapeutic serum levels of magnesium. Patients meeting selected criteria for hyperreflexia demonstrated a 46% decrease in their reflex response. Those without initial hyperreflexia failed to demonstrate a significant decrease.
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PMID:The patellar reflex in preeclamptic women with subtherapeutic and therapeutic serum magnesium levels. 237 54


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