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

Intracerebroventricular administration of 10--20 microgram of steroid-O-sulfates induced hypermotility, agitation, salivation, EEG abnormalities, stereotypies, wet dog shakes and seizures. Equivalent effects resulted from 30--200 microgram morphine sulfate (H2SO4 salt), 50 microgram EGTA or 300--400 microgram of sodium sulfate or phosphate, but not chloride, nitrate or acetate. Non-steroid sulfates, steroid glucuronides and steroid phosphates were inactive. Naloxone, previously found to antagonize the excitatory effects of androsterone sulfate, failed to antagonize those of cortisol sulfate, sodium sulfate or EGTA. These findings suggest a role for extracellular calcium ions and for sulfate derived from circulating steroids in central responses to opiates.
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PMID:Opiate-like excitatory effects of steroid sulfates and calcium-complexing agents given cerebroventricularly. 21 60

Clinical seizures, or subclinical EEG discharges, were observed in sixteen new-born babies or infants under one year of age admitted to hospital. Clinical observation and initial biological tests showed that: --seizures occurring during rehydration of infants with salt retention are not associated with severe neurological lesions,--in dehydrated babies, a dissociation between electroencephalographic and clinical manifestations (electrical discharges without clinical signs or vice versa) and large abnormalities in the intercritical tracing are bad prognostic elements;--in new-born babies with severe dehydration and meningeal hemorrhage, the occurence of clinical and electroencephalographic seizures does not imply that there will be an unfavourable evolution. The authors discuss the physiopathological correlations arising from the study of this series.
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PMID:[Clinical and electroencephalographaic aspects of seizures due to electrolyte and water disturbances in infants (author's transl)]. 49 17

The results from systematic determinations of the serum level of phenytoin in 121 epileptic children are reported. The range 12-25 mg/l is effective in most of the children, responding at all to phenytoin, and causes few and minimal side effects. Practically all children with pure grand mal epilepsy could be kept seizure-free on an optimal dose of phenytoin alone. Possibly the level aimed at should be higher in severe cases than in mild ones. Our initial dose was 10 mg/kg daily; this dose was adjusted according to the serum level until the desired range was reached. Phenytoin produced a lower serum level than the same dose of its sodium salt. Interaction possibly occurs with carbamazepine, which tended to decrease the level, and with acetazolamide, which tended to increase the level. With the help of serum phenytoin determinations an individual dose can be chosen for each patient and phenytoin therapy be rendered safer and more effective.
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PMID:Systematic determination of the serum phenytoin level as an aid in the management of children with epilepsy. 80 79

A case of giant aneurysm arising from the anterior communicating artery, 24 X 28 X 30 mm in diameter was found in a 30 year old man. About ten years ago he became blind and recently developed right anosmia and diencephalic seizures. No subarachnoid hemorrhage, however, was found. Radiograms and tomograms of the cranium showed a ring-like calcification, but by angiography it couldn't be recognized as a giant aneurysm. The right frontal craniotomy and partial resection, therefore, was performed. A histological study of the resected material revealed that it was a spontaneously thrombosed giant aneurysm. The inner layer of its wall had neither endothelium nor elastic lamina, but had deposits of calcium salt. The outer layer was composed of collagen fibers without cell infiltration. The aneurysm was thrombosed except for its neck but its organization occurred incompletely. We want to emphasize the importance of a correct preoperative diagnosis, as an erroneous operative procedure can result in disaster. Volume, viscosity and tension of flowing blood into the aneurysm as well as the size of its neck and dome regulate dynamic properties. These properties may determine the enlargement rate or growth of the aneurysm. The dynamic characteristics and features of the inner surface of the aneurysmal wall may regulate the formation of thrombosis in the aneurysm. The intraluminal thrombosis and strength of aneurysmal wall, for example, calcium deposits, may prohibit aneurysm from its rupture.
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PMID:[Giant anterior communicating artery aneurysm (author's transl)]. 123 24

Zinc is a potent inducer of the 72 kD heat shock protein (HSP72). In brain, pathological conditions such as ischemia and seizures increase extracellular zinc. The present study examines the effect of zinc on HSP72 expression in rat primary cortical astrocyte culture. Astrocytes were grown to confluence and exposed to zinc chloride in CO2-equilibrated Earle's buffered salt solution. Expression of HSP72 was examined using immunocytochemistry. HSP72 was induced with zinc concentrations of 5 to 100 microM after 4 h exposures, or 200 to 300 microM after 15 min exposures. At the lower concentrations expression occurred in small clusters of contiguous cells. At concentrations high enough to cause cell death, HSP72-positive astrocytes formed a continuous margin around patches of dead cells. These patterns of HSP72 expression are similar to the patterns seen after cerebral ischemia in vivo. Exposure to zinc at 100 microM for 4 h or 400 microM for 15 min caused greater than 90% cell death. Increases in extracellular zinc may contribute to HSP72 induction and astrocyte death under ischemia and other pathological conditions in brain.
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PMID:Zinc toxicity and induction of the 72 kD heat shock protein in primary astrocyte culture. 133 69

Hypernatremia is a common electrolyte disturbance, most often caused by volume depletion. Hypernatremia due to sodium excess occurs less frequently, and fatal hypernatremia solely from ingestion of table salt is rare. We describe a 41-year-old man who had seizures and hypernatremia after ingestion of a supersaturated salt water solution intended for gargling. He had consumed approximately a third cup of table salt (approximately 70 to 90 g of salt or 1,200 to 1,500 meq of sodium). His initial serum sodium concentration was 209 meq/liter. Hypotonic fluid therapy was given to provide free water and to correct the hypernatremia gradually. Our patient, however, failed to recover from the initial insult and died 3 days later. Review of the literature revealed 10 adult and 20 pediatric cases of hypernatremia attributable to exogenous intake of salt. The type of therapy (fluid or peritoneal dialysis), the type of fluid used, and the rate of correction of hypernatremia did not influence survival. The age of the patient and the initial serum sodium concentration were the most important prognostic indicators. Both very young patients and those with lesser degrees of hypernatremia had a better rate of survival than did other patients. In addition, our review illustrates the surprisingly small amount of salt that can cause severe hypernatremia and the danger of using salt or saline as an emetic.
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PMID:Fatal hypernatremia from exogenous salt intake: report of a case and review of the literature. 201 96

Several lines of evidence implicate zinc in the pathogenesis of epileptic seizures, and administration of zinc salts has been shown to affect seizure susceptibility. In the present work, we studied the effects of subcutaneous (s.c.) injections of ZnCl2 on seizures induced by intraperitoneal (i.p.) kainic acid (10 mg/kg) in rats and by noise (80-120 dB) in the DBA/2J mouse. Previous administration of zinc salt (20-200 mg/kg) substantially reduced the frequency of noise-induced running fits, clonic and tonic seizures, and deaths in mice, but had no significant effect on the incidence or severity of kainic acid-induced seizures in rats. Together with findings in the literature, our results suggest that zinc plays multiple, sometimes antagonistic roles in seizure development.
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PMID:Effects of subcutaneous injections of zinc chloride on seizures induced by noise and by kainic acid. 231 67

Amygdala-kindled rats were treated with valproic acid (VPA; administered as its sodium salt) 3 times daily at 200 mg/kg i.p. for 6 weeks, and anticonvulsant and adverse effects during this period were studied. Groups of nonkindled rats were treated in parallel for determination of VPA and its major active metabolites in various brain regions after different durations of treatment. After the first injection of VPA, 200 mg/kg, seizure severity, seizure duration and duration of electrical afterdischarges recorded from the stimulated amygdala were reduced significantly, but only one of nine animals was protected completely from kindled seizures. At day 3 of chronic treatment, the anticonvulsant activity of VPA had increased markedly so that seven of nine animals were totally protected from seizures. However, this potent anticonvulsant effect was only transitory so that after 1 week of treatment the anticonvulsant effect of the medication was similar to that obtained after the first dosing. The effect of VPA remained at this level for the subsequent weeks, but there was a second, more permanent increase in the number of protected animals after 4 to 6 weeks. Plasma and brain levels of VPA and its metabolites remained relatively constant throughout the chronic treatment although there was a moderate accumulation of some metabolites, e.g., trans isomer of 2-propyl-2-pentenoic acid, in specific brain nuclei. The most prominent adverse effects of VPA were ataxia, muscle relaxation, wet-dog shake behavior and an increase in body temperature. Except for body temperature, tolerance developed to these adverse effects, but escape from wet-dog shake behavior occurred much more rapidly than reduction of other adverse effects. Pathohistological examination of liver sections from animals treated with VPA for 6 weeks showed no indication of any hepatotoxic effects. After drug withdrawal, kindled seizure parameters returned toward control values without evidence of significant carry-over effects. Five days after termination of treatment, only minute amounts of VPA and trans isomer of 2-propyl-2-pentenoic acid were determined in some brain regions, indicating that there was no persistence of active drug or metabolite concentrations in the brain.
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PMID:Valproic acid in amygdala-kindled rats: alterations in anticonvulsant efficacy, adverse effects and drug and metabolite levels in various brain regions during chronic treatment. 250 34

The anticonvulsant activity of a salt of valproic acid (VA), magnesium valproate (MgV), was assessed against amygdala-kindled seizures in rats. The anti-epileptic power of MgV was compared with that of sodium valproate (NaV). Kindling was obtained by delivering daily to one of the amygdala a 2 s train of monophasic square-wave pulses (1 ms, 60 c.p.s., 100-130 microA) via chronically implanted electrodes. Magnesium valproate and NaV were tested once kindling was stabilized and the post-kindling threshold for generalized convulsions was determined. The drugs were administered intraperitoneally in doses ranging from 25 to 200 mg/kg. The injection/test interval was 30 min. Each animal received a single dose every 24 h. Magnesium valproate exhibited an anticonvulsant activity qualitatively and quantitatively similar to that of NaV. Statistically significant differences were not found between the two drugs with respect to the reduction of seizure severity and afterdischarge (AD) duration. The calculated ED50's were 94.58 and 97.41 mg/kg for the suppression of generalized seizures, 176.96 and 129.26 mg/kg for the suppression of partial seizures, 275.96 and 224.13 mg/kg for the suppression of the local AD in the MgV and NaV treated groups, respectively.
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PMID:Effect of magnesium valproate on amygdala-kindled seizures in the rat: comparison with sodium valproate. 256 44

Phenytoin (DPH) was delivered to the brain by a dihydropyridine in equilibrium pyridinium salt redox system, which was evaluated for anticonvulsant activity. Following iv injection of the lipophilic delivery system of DPH (2) to rats, concentrations of DPH were lower but sustained and, after 30 min, essentially the same as the levels after equimolar administration of DPH. While 2 delivered the same levels of DPH to the brain as DPH did, it was twice as potent as DPH in rats (ED50 was 7.5 mumol/kg for 2 and 14.2 mumol/kg for DPH) and mice (2: 10.5; DPH: 23.9) against maximal electroshock seizures (MES), and seven times more potent in mice (2: 10.0, DPH: 70.6) against maximal pentylenetetrazole seizures (MPS). Moreover, 2 was active against pentylenetetrazole threshold seizures (PTS) in mice and rats (ED50 = 44.1 and 40.5 mumol/kg, respectively), while DPH was ineffective (up to a dose of 79.2 mumol/kg). After evaluation of acute neurological toxicity in rats, 2 was found to possess 1.5 times higher a protective index (for MES) than DPH. It appeared also that while DPH was 2.9 times less sensitive to MPS than to MES, 2 was equally potent to both types of convulsions. Thus, the data indicate that 2 delivered DPH more efficiently to the brain. The better anticonvulsant activity (quantitatively as well as qualitatively) of 2 can be explained on the basis of an improved distribution in the brain due to its higher lipophilicity, and by favorable regional differences in the rates of conversion of 2 to DPH at the convulsing foci.
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PMID:Improved anticonvulsant activity of phenytoin by a redox brain delivery system. III: Brain uptake and pharmacological effects. 260 Jul 90


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