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)

A comparison of hospitalized epileptic patients with matched normals showed that the mean whole blood manganese (Mn) concentration of the epileptic population was significantly lower than the mean of the normal population. The whole blood Mn concentration in the epileptics did not correlate either with seizure frequency or with anticonvulsant therapy. It was observed, however, that patients whose epilepsy was a result of trauma had significantly higher blood Mn concentrations than patients whose history was negative for trauma.
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PMID:Association of low blood manganese concentrations with epilepsy. 378 72

In the isolated frog spinal cord penicillin or strychnine produced spinal seizures with spontaneous slow paroxysmal ventral root depolarizations (pVRDs) and superimposed motoneuron spikes. Mn2+, tetrodotoxin, mephenesin and low [Na+]o suppressed pVRDs, an indication that paroxysmal activity requires intact excitatory synaptic transmission involving interneurons. Compounds reducing the release of amino acids [-)baclofen) or interfering with the activation of N-methyl-D-aspartic acid (NMDA) receptors (D,L-alpha-aminoadipate, D-2-amino-5-phosphonovalerate, gamma-D-glutamylglycine) eliminated pVRDs. The results suggest that synaptic release of excitatory amino acids (e.g. L-glutamate, L-aspartate) and subsequent activation of specific receptors sensitive to the action of NMDA underlie spinal convulsions.
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PMID:Spinal seizures and excitatory amino acid-mediated synaptic transmission. 632 51

The effect of manganese (Mn2+, 3 mg/ml drinking water) on brain GABA content and electroshock seizure susceptibility in low (10% casein) and normal (21% casein) protein fed rats were investigated. Manganese exposure caused a decrease in the brain GABA content, lowered the seizure threshold and increased the seizure duration. These effects were more marked in the low protein fed rats. Diet rehabilitation caused a recovery in the GABA levels but has only a moderating effect on the seizure susceptibility and duration. An inverse correlation was observed between the brain GABA levels and seizure threshold. Results indicate a lowered GABA-ergic activity and a functional dysbalance between the GABA-ergic-dopaminergic neuronal systems in manganese toxicity.
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PMID:Effect of low protein diet on manganese neurotoxicity: II. Brain GABA and seizure susceptibility. 641 Feb 94

The effects of seizures on the cerebral and peripheral metabolism of essential metals were studied in mice. Acute and chronic seizures were produced either by electroshock (ES) or by a systemic convulsant. Organ and subcellular distribution of 54Mn and 65Zn were determined prior to and at different intervals after seizure cessation. In mice shocked for 21 days, the concentrations of manganese, zinc, magnesium, and copper were determined in selected tissues. Sham-seizured mice served as controls. When 54Mn was injected after a single ES, the isotope's retention increased in the liver by 67% (P less than 0.01) and decreased in the brain and carcass by 53 and 42%, respectively (P less than 0.01). Repeated ES further augmented these effects (P less than 0.01). These changes diminished as a function of time to the animal's recovery from ES. Liver and regional brain fractionations revealed significant perturbation in the intercellular partition of 54Mn, suggesting increased metal utilization. Brain and liver 65Zn were not affected by ES. Manganese content increased in the liver by 67% (P less than 0.01) and decreased in whole brain by 16.5% (P less than 0.01), after chronic ES. Cortical manganese and hypothalamic magnesium were the principal sites of loss. Small (12 to 13%), but significant elevations of magnesium were found in liver and skeletal muscle (P less than 0.05). Copper increased in muscle by 26% (P less than 0.02). Seizures selectively altered the normal brain and extracerebral distribution of essential metals which may lead to regional metal deficiency or excess. These changes were linked to the metabolic consequences of convulsive activity and may be relevant to seizure control and electroshock therapy in man.
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PMID:Generalized seizures alter the cerebral and peripheral metabolism of essential metals in mice. 662 11

Human and experimental animal studies suggest a relationship between low Mn status and seizures. The genetically epilepsy prone rat (GEPR), which has low tissue Mn levels, was studied in the context of Mn supplementation. Manganese was provided at 45 micrograms/g diet (control) or 1000 micrograms/g diet (supplemented) to dams during pregnancy and lactation, then to the offspring after weaning. Offspring were tested for seizure susceptibility as young adults; tissue trace elements, brain monoamines and brain glutamine synthetase activity were measured as endpoint biochemical indices. Supplementation, although developmentally encompassing and highly effective in elevating tissue Mn levels, had no effect on seizure latency or severity. Similarly, brain monoamine concentrations and glutamine synthetase activities were resistant to Mn supplementation. Notably, the GEPR was confirmed to have low whole brain glutamine synthetase activity. These findings suggest that seizure activity in the GEPR does not stem from an increased nutritional/metabolic need for Mn.
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PMID:The influence of manganese supplementation on seizure onset and severity, and brain monoamines in the genetically epilepsy prone rat. 809 51

Low blood manganese (Mn2+) concentration is associated with epilepsy in humans and rats. The low Mn2+ concentration is attributed by some investigators to the seizure activity associated with the epilepsy, whereas others propose that the low Mn2+ concentration may be secondary to genetic mechanisms underlying the epilepsy. To begin to differentiate between these possibilities, Mn(2+)-binding enzymes of liver and brain (i.e., arginase and glutamine synthetase, respectively) were assayed in rats exposed to chronically induced seizures and in genetically epilepsy-prone rats (GEPRs). Chronic seizures caused a decrease in whole blood Mn2+ levels but did not affect brain Mn2+ concentrations. Arginase activity was increased in livers of rats with chronic seizure as compared with controls, but this difference was eliminated when Mn2+ was added to the assay. Brain glutamine synthetase activity was unaffected by chronic seizures, but the activity of this enzyme was significantly lower in GEPR brain than in control brain. Liver arginase activity tended to be lower in GEPRs, although the difference was not statistically significant. These data indicate that seizures affect liver arginase activity through changes in liver Mn2+ concentration, but GEPRs show abnormalities in Mn(2+)-dependent enzymes apparently independent of seizure activity.
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PMID:Manganese and epilepsy: brain glutamine synthetase and liver arginase activities in genetically epilepsy prone and chronically seizured rats. 809 25

In the present study the water and ion (Na+, K+, Ca2+, Fe3+, Se4+, Mg2+, Mn2+, Mn2, Se4+, Cu2+) content in the brain of genetically epilepsy-prone rats (GEPRs) and of 21-, 45-, and 60-day-old DBA/2 mice were determined, and compared with those measured in normal controls (Sprague-Dawley rats and Swiss mice), to verify whether the predisposition to audiogenic seizures (AGS) may be partially related to changes in the cerebral osmotic and ionic state. Our findings clearly evidenziate two points: a) a more complex shift in brain ionic balance (rather than a peculiar modification in the concentration of a single ion) seems very likely involved in AGS susceptibility; (b) brain Ca2+ and Se4+ amounts, together with the water content, appear to be really important factors to which a role in abnormal seizure predisposition may be attributed.
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PMID:Genetically epilepsy-prone rodents show some changes of ion levels in the brain. 827 21

Human epileptics have been reported to have low blood manganese (Mn) concentrations in comparison to nonepileptics, an observation that is important because Mn deficiency can increase seizure susceptibility in experimental animals. Factors that have been suggested to contribute to the low blood Mn levels in epileptics include anticonvulsant use, seizure-induced tissue redistribution of Mn, and genetics; in the present study, the first of these possibilities was tested. Wistar rats were fed semipurified diets containing diphenylhydantoin ([DPH] 3 g/kg diet), phenobarbital ([PB] 2 g/kg diet), or primidone ([PRIM] 3 g/kg diet) for 7 weeks, at which time they were killed and tissues collected and analyzed for Mn, zinc (Zn), copper (Cu), and iron (Fe) concentrations. In comparison to pair-fed rats, DPH- and PRIM-fed rats had significantly elevated liver Mn concentrations, while Mn concentrations in blood, brain, heart, and kidney were unaffected by anticonvulsant exposure. Changes in the concentrations of Zn, Cu, and Fe in specific tissues were also found. Overall, these findings suggest that the anticonvulsants tested do not lead to significant derangements in the metabolism of Mn.
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PMID:Anticonvulsant-induced changes in tissue manganese, zinc, copper, and iron concentrations in Wistar rats. 834 1

Tremor and seizures developed in a 2-year-old girl receiving total parenteral nutrition. T1-weighted images on MRI revealed areas of hyperintensity in the basal ganglia, brainstem and cerebellum. Blood manganese was elevated. The symptoms and MRI abnormalities disappeared after withdrawal of manganese administration. The recommendation of daily parenteral manganese intake was discussed.
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PMID:Tremor and seizures associated with chronic manganese intoxication. 1020 31

In this study, hair magnesium (Mg), zinc (Zn), copper (Cu), and manganese (Mn) levels, and serum Zn and Mg levels were measured by atomic absorption spectrophotometer in patients with epilepsy (n = 33) and healthy subjects (n = 21), and results obtained were statistically compared. The mean hair Cu, Mg, and Zn levels of epileptic patients were significantly lower than the levels of control subjects. There was no significant difference between epileptic patients and control subjects in respect to the mean Mn levels. Mean serum Mg levels in epileptic patients showed significant difference, but serum Zn levels were similar among both groups. When the effects of anticonvulsant therapy on Cu, Zn, Mn, and Mg in the hair, and Mg and Zn in the serum were analyzed in epileptics, there was no significant difference between the patients with or without therapy. Likewise, the mean trace element levels in epileptics showed no significant difference according to the type of antiepileptic drug and seizure, and gender. We suggest that the changed element status (Zn, Mg, and Cu) in hair may play an indicator role in the diagnosis of epileptic patients.
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PMID:Serum and hair trace element levels in patients with epilepsy and healthy subjects: does the antiepileptic therapy affect the element concentrations of hair? 1052 59


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