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

Reports suggesting participation of trace metals in processes of seizure initiation and propagation in humans and experimental animals prompted an investigation of the relationship between copper and zinc status and seizure activity in the Senegalese baboon, Papio papio. An evaluation of serum trace metal concentrations in three species of nonhuman primates revealed the presence of elevated zinc levels in P. papio moderately sensitive to photically induced seizures, compared with mildly seizure-prone and nonseizure-prone P. papio as well as nonseizure-prone primates. Papio cynocephalus and Macaca mulatta. By contrast, copper levels appeared similar in all three species. Chronic oral treatment with D-penicillamine, a chelating agent, resulted in marked protection against photic-induced seizures in the P. papio baboon, as well as changes in the trade metal status of serum and urine. Oral dosages of 30 to 40 mg/kg/day were sufficient to establish anticonvulsant effect over a period of 4 to 9 weeks in all animals tested without signs of toxicity or tolerance. Results suggest that metal chelation treatment may represent a new approach to the management of certain forms of human epilepsy.
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PMID:The influence of D-penicillamine treatment upon seizure activity and trace metal status in the Senegalese baboon, Papio papio. 720 48

A case of diabetic ketoacidosis in a 64-year-old black woman with maturity-onset diabetes receiving phenytoin for a seizure disorder is reported. The woman was admitted to the hospital with a one-day history of polyuria and polydipsia. For the 10 months before admission, her diabetes was controlled with isophane insulin suspension 27 units daily. She also took phenytoin 100 mg orally three times a day. This was prescribed approximately six weeks earlier for right-sided focal seizures that were detected by electroencephalogram during a previous hospitalization for nonketotic hyperosmolar coma. No other medications were taken. The patient was treated with i.v. fluids and intermittent doses of i.v. insulin. Her condition rapidly improved and insulin zinc suspension 35 units daily was prescribed on discharge. Phenytoin was discontinued because the seizure disorder was considered secondary to the previous episode of hyperosmolar coma. A literature review of phenytoin-induced hyperglycemia is presented, including previous case reports, possible mechanisms of action, monitoring guidelines, and potential therapeutic uses. If hyperglycemia occurs in a patient taking phenytoin, especially after starting phenytoin therapy or increasing the dose, drug-induced hyperglycemia should be considered in the differential diagnosis.
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PMID:Phenytoin-induced hyperglycemia. 729 47

The toxicity and efficacy of the acute rodenticide scilliroside was evaluated in the laboratory against the lesser bandicoot rat, Bandicota bengalensis. The acute oral LD50 and LD95 doses for males were 0 . 8 mg/kg and 2 . 5 mg/kg respectively, and for females were 0 . 5 mg/kg and 1 . 6 mg/kg, respectively. When caged bandicoots were given a choice between plain and poison baits, the optimum concentration of scilliroside was found to be 0 . 05%. Symptoms of poisoning appear from 22 to 34 min after feeding starts and the latency pattern indicated an abrupt ceasing to feed at these points. Death occurred from 2 h to as long as 6 days after poisoning, following prolonged convulsive seizures. There appears to be aversion to scilliroside at all concentrations in food baits. Maximum mortality attained on free-choice feeding on scilliroside was 90%. Despite these disadvantages, the material may have merit as an alternative rodenticide to zinc phosphide where acute toxicants are to be used.
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PMID:Laboratory evaluation of scilliroside used as a rodenticide against the lesser bandicoot rat, Bandicota bengalensis. 745 59

Zinc modulates the activity of glutamic acid decarboxylase, the rate limiting enzyme in the synthesis of gamma-aminobutyric acid (GABA), which is a major inhibitory neurotransmitter. Low cerebrospinal fluid GABA values have been reported in association with several seizure disorders, including febrile convulsions. It is also known that fever and/or infections may cause a reduction in serum zinc concentrations. In this study the hypothesis that febrile convulsions are related to low cerebrospinal fluid zinc was tested. Cerebrospinal fluid zinc concentrations were measured in 66 febrile children: 32 with febrile convulsions, 18 with fever but without convulsions, and 16 with aseptic (viral) meningitis. There was no statistically significant difference in the cerebrospinal fluid zinc between the three groups of children, and the mean concentration was 26.2 micrograms/l. No significant relationship was found between either age, gender, maximal temperature, type of infection, or time of performance of the lumbar puncture and cerebrospinal fluid zinc concentration. These results do not support the hypothesis that febrile convulsions are related to reduced cerebrospinal fluid zinc concentrations.
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PMID:Cerebrospinal fluid zinc concentrations in febrile convulsions. 749 99

Chronic alcoholism is associated with hypercortisolemia and low serum zinc (Zn). Hypercortisolemia could be responsible for alcoholic cerebral atrophy and is also associated with enhanced NMDA neurotoxicity. It is hypothesized that low brain Zn, noted in chronic alcoholics, enhances NMDA excitotoxicity and ethanol withdrawal seizure susceptibility. Also, Zn deficiency can produce neuronal damage through increased free radical formation. Clinically, Zn replacement therapy may be a rational approach to the treatment of alcohol withdrawal seizures and alcohol-related brain dysfunction.
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PMID:Zinc deficiency and corticosteroids in the pathogenesis of alcoholic brain dysfunction--a review. 797 2

Tetanus toxin is a potent clostridial neurotoxin responsible for causing spastic paralysis in humans, often accompanied by seizures and death. The tetanic syndrome is believed to originate from a disinhibitory action of the toxin in the CNS. To produce its effects, tetanus toxin undergoes retrograde, intra-axonal transport to the CNS, where it blocks preferentially the release of gamma-aminobutyric acid and glycine, two inhibitory neurotransmitters. These effects stem from the cleavage of synaptobrevin, a constitutive small-vesicle protein, by tetanus toxin, whose zinc-dependent metalloprotease characteristics recently have been recognized. Blockade of inhibitory transmission produces a predominance of excitatory amino acid neurotransmission, which is responsible for the neurodegenerative effect caused by tetanus toxin after intrahippocampal injection in rats. In fact, hippocampal damage can effectively be prevented by reduction of glutamate-mediated excitatory transmission, thus suggesting that unopposed excitation may be the underlying mechanism for neuronal cell death.
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PMID:Tetanus toxin as a neurobiological tool to study mechanisms of neuronal cell death in the mammalian brain. 799 46

A normobar hypoxia (9% oxygen) of 8 h reduces the neurotoxicity of a subcutaneous injection of 10 mg/kg kainic acid given one week later. Both seizures and degenerative changes, including cell death of hippocampal and cortical neurons are markedly decreased by hypoxia. It is also shown that hypoxia also markedly reduced the extensive depletion of zinc from mossy fiber terminals normally induced by kainic acid. This suggests that a protective mechanism induced by hypoxia may affect the glutamatergic transmission in these synapses and prevent excessive synaptic excitation. The possible involvement of adenosine and/or GABA in this protective mechanism is discussed.
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PMID:Hypoxia protects against the neurotoxicity of kainic acid. 805 40

The anticonvulsive activity of three kinds of pyrazolidinones: 5-benzyl-substituted-3-pyrazolidinones; 5-benzyl-1-alkyl substituted and 1-alkyl substituted-3-pyrazolidinones were studied. Fourteen substitutes of these three kinds of pyrazolidinones were found to be potent anticonvulsants. In doses less than TD50, they were found to be able to protect mice and rats from seizures produced by maximal electroshock seizure (MES), such action appeared rapidly and lasted for a short period. II-f was shown to be the most potent anti-MES agent among these three kinds of pyrazolidinones. It also showed therapeutic effect in treating experimental epilepsy produced by intrahippocampal injection of zinc sulfate in rabbits and audiogenic seizures in rats. The third kind of pyrazolidinones also showed anti-metrazol induced seizures in mice.
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PMID:[Studies on the anticonvulsive activity of pyrazolidinones]. 807 46

The c-fos immediate early gene is induced by normal stimuli including light, stress, hyperosmolar solutions, and hormones. Ischemia, hypoxia, seizures, cortical injury, nerve section and other pathological stimuli can also induce c-fos. The induction can occur via increases in intracellular calcium that act through a Ca2+/cAMP element on its promoter, or via trophic and other factors that act through a serum response element (SRE) on its promoter. Several studies show that calcium entry via voltage sensitive calcium channels (VSCCs) is important for inducing c-fos. We have shown that calcium entry via the NMDA receptor is important for induction of c-fos mRNA by glutamate and cAMP in cultured cortical neurons. Moreover, the NMDA receptor appears to regulate translation of c-fos mRNA to Fos protein when cells are stimulated with other types of stimuli including vasoactive intestinal peptide, zinc, and fibroblast growth factor. These results suggest that toxins that elevate intracellular calcium will likely induce the c-fos gene in brain. The heat shock or stress genes are induced by a wide variety of stimuli including heavy metals, heat, oxidative and ischemic stress, prolonged seizures, hypoglycemia, calcium ionophores, and certain toxins. It is believed that denatured proteins stimulate heat shock factors to bind to heat shock elements on the promoters of all heat shock genes to induce gene transcription. We and others have shown that global and focal ischemia induce the hsp70 heat shock gene in brain. Mild ischemia induces hsp70 mRNA and HSP70 protein in neurons only.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alterations in gene expression as an index of neuronal injury: heat shock and the immediate early gene response. 809 Mar 62

Zinc, a trace element, is epileptogenic in rats and rabbits. Its distribution in the CNS is mainly localized in the hippocampus, where kainate (KA) can develop neuronal damage with limbic seizures. We examined the zinc neurotoxicity int he rat brain with KA. The unilateral intracarotid artery infusion of zinc chloride seemed to enhance the specific binding of KA at the ipsilateral hippocampus in the method of receptor-binding autoradiography. Actually, the zinc infusion followed by the intravenous injection of KA 0.5 mg-1 kg-1 body weight induced ipsilateral neuronal damage at the cortex and the CA3-4 of the hippocampus. A potent non-N-methyl-D-aspartate (NMDA) antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) could not change KA binding, but could partially prevent that neuronal damage. According to these results, we consider that zinc administration through intracarotid infusion can enhance the KA neurotoxicity in its binding activities and that CNQX is potent to decrease KA neurotoxicity in the KA insulted area in the rat brain.
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PMID:Zinc enhances kainate neurotoxicity in the rat brain. 809 5


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