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)

Young pigs were fed a diet moderately high or low in manganese (Mn) (0.95 +/- 0.10 mmol Mn/kg, n = 8 or 0.040 +/- 0.003 mmol Mn/kg, n = 6) and deficient in magnesium (Mg) (4.1 mmol Mg/kg) for 5 wk. All eight pigs consuming the high Mn diet died following convulsive seizures, whereas only two of six died in the group fed low Mn. In an attempt to determine the cause of death, a subsequent study examined the interactive effect of deficient dietary Mg and Mn on the tissue distribution of Mg and Mn. Pigs were individually fed, for 5 wk, diets that contained: 4.1 mmol Mg/kg and 36.0 micromol Mn/kg, 4.1 mmol Mg/kg and 0.91 mmol Mn/kg, 4.1 mmol Mg/kg and 0.91 mmol Mn/kg with added ultratrace minerals, or 41.1 mmol Mg/kg and 0. 91 mmol Mn/kg, and ultratrace minerals. Liver and skeletal muscle Mn concentrations were significantly elevated by increased dietary Mn. Increased dietary Mn did not affect heart Mn, but heart Mg concentrations were significantly depressed by high, as compared to low, dietary Mn (38.7 +/- 3.3 vs. 32.7 +/- 2.6 mmol Mg/kg). These data suggest high dietary Mn may exacerbate Mg deficiency in heart muscle and thus may be a complicating factor in the deaths observed in Mg-deficient pigs.
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PMID:High dietary manganese lowers heart magnesium in pigs fed a low-magnesium diet. 1091 21

The objective of this study was to determine the role of mitochondrial superoxide radical-mediated oxidative damage in seizure-induced neuronal death. Using aconitase inactivation as an index of superoxide production, we found that systemic administration of kainate in rats increased mitochondrial superoxide production in the hippocampus at times preceding neuronal death. 8-Hydroxy-2-deoxyguanosine, an oxidative lesion of DNA, was also increased in the rat hippocampus following kainate administration. Manganese(III) tetrakis(4-benzoic acid)porphyrin, a catalytic antioxidant, inhibited kainate-induced mitochondrial superoxide production, 8-hydroxy-2-deoxyguanosine formation and neuronal loss in the rat hippocampus. Kainate-induced increases of mitochondrial superoxide production and hippocampal neuronal loss were attenuated in transgenic mice overexpressing mitochondrial superoxide dismutase-2. We propose that these results demonstrate a role for mitochondrial superoxide production in hippocampal pathology produced by kainate seizures.
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PMID:Mitochondrial superoxide production in kainate-induced hippocampal damage. 1111 5

The most frequently prescribed herb for "devil-sickness" in the vernacular medical books from Anglo-Saxon England, the lupine, is exceptionally high in manganese. Since manganese depletion has been linked with recurring seizures in both clinical and experimental studies, it is possible that lupine administration responded to the particular pathophysiology of epilepsy. Lupine is not prescribed for seizures in classical Mediterranean medical sources, implying that the Northern European peoples (if not the Anglo-Saxons themselves) discovered whatever anticonvulsive properties the herb may exhibit.
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PMID:Lupines, manganese, and devil-sickness: an Anglo-Saxon medical response to epilepsy. 1142 Apr 53

Patients receiving long-term parenteral nutrition (PN) with trace elements (TE) may exhibit T (1) shortening in the anterior pituitary gland and basal ganglia. The purposes of this study were to clarify at what time or from what site the signal change begins in children. Retrospective analysis of magnetic resonance imaging results was performed for 10 pediatric patients aged from 1 to 16 years receiving temporal PN, eight of which received PN with TE for less than two months, and 13 patients with headache or seizures as age-matched controls. Axial and sagittal T (1)-weighted images were obtained to analyze the T (1) shortening in the anterior pituitary gland and globus pallidus. All eight patients receiving PN with TE exhibited T (1) shortening in the anterior pituitary gland (six patients) and/or globus pallidus (five patients). No T (1) shortening was observed in the other two patients without TE, or the 13 age-matched controls. Therefore, the signal change may be associated with TE administration, and begins markedly earlier than previously reported. We discussed the possibility that manganese (Mn) caused the signal change, and proposed that the administration of a lower dose of Mn is recommended, even in the case of temporal PN, to prevent possible Mn toxicity toward both the brain and liver.
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PMID:Temporal parenteral nutrition in children causing t1 shortening in the anterior pituitary gland and globus pallidus. 1297 61

Non-Asian individuals with Down syndrome are much more likely to develop epileptic seizure disorders than individuals without Down syndrome. Examination of nutrient and metabolite levels in patients with these two seemingly disparate disorders reveals numerous similarities. Compared to individuals without these disorders, individuals with Down syndrome and individuals with seizures may have lower levels of vitamin A, vitamin B1, folate, vitamin B12, vitamin C, magnesium, manganese, selenium, zinc, carnitine, carnosine, choline, and possibly serine. Excesses of copper, cysteine, phenylalanine, and superoxide dismutase are also sometimes encountered in both disorders. In addition to common nutritional lower levels and excesses, disorders of metabolism involving vitamin B6, vitamin D, calcium, and tryptophan may play a common role. This paper hypothesizes that nutritional factors may account for the high joint occurrence of these conditions. Further examination of these data may provide insights into nutritional, metabolic and pharmacological treatments for both conditions.
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PMID:Down syndrome and epilepsy: a nutritional connection? 1472 2

Curcumin is a natural antioxidant isolated from the medicinal plant Curcuma longa Linn. We previously reported that manganese complexes of curcumin (Cp-Mn) and diacetylcurcumin (DiAc-Cp-Mn) exhibited potent superoxide dismutase (SOD)-like activity in an in vitro assay. Nitric oxide (NO) is a free radial playing a multifaceted role in the brain and its excessive production is known to induce neurotoxicity. Here, we examined the in vivo effect of Cp-Mn and DiAc-Cp-Mn on NO levels enhanced by kainic acid (KA) and L-arginine (L-Arg) in the hippocampi of awake rats using a microdialysis technique. Injection of KA (10 mg/kg, i.p.) and L-Arg (1000 mg/kg, i.p.) significantly increased the concentration of NO and Cp-Mn and DiAc-Cp-Mn (50 mg/kg, i.p.) significantly reversed the effects of KA and L-Arg without affecting the basal NO concentration. Following KA-induced seizures, severe neuronal cell damage was observed in the CA1 and CA3 subfields of hippocampal 3 days after KA administration. Pretreatment with Cp-Mn and DiAc-Cp-Mn (50 mg/kg, i.p.) significantly attenuated KA-induced neuronal cell death in both CA1 and CA3 regions of rat hippocampus compared with vehicle control, and Cp-Mn and DiAc-Cp-Mn showed more potent neuroprotective effect than their parent compounds, curcumin and diacetylcurcumin. These results suggest that Cp-Mn and DiAc-Cp-Mn protect against KA-induced neuronal cell death by suppression of KA-induced increase in NO levels probably by their NO scavenging activity and antioxidative activity. Cp-Mn and DiAc-Cp-Mn have an advantage to be neuroprotective agents in the treatment of acute brain pathologies associated with NO-induced neurotoxicity and oxidative stress-induced neuronal damage such as epilepsy, stroke and traumatic brain injury.
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PMID:Prevention of kainic acid-induced changes in nitric oxide level and neuronal cell damage in the rat hippocampus by manganese complexes of curcumin and diacetylcurcumin. 1626 25

Neurological complications are common in cirrhotic patients with end-stage liver failure. They comprise a wide array of etiologies, which may originate before, during, or after liver transplantation. The objective of this study was to describe the nature of the main neurological complications in patients with end-stage liver failure. Several toxins including ammonia, manganese, benzodiazepine-like substances, gamma-aminobutyric acid-like substances, and impaired dopaminergic neurotransmission are at the top of the list of candidates for hepatic encephalopathy, subclinical encephalopathy, and extrapyramidal signs before liver transplantation. Central pontine myelinolysis, cerebrovascular autoregulation impairment, and paradoxical cerebral embolism are probably responsible for the neurological complications during liver transplantation. Neurological complications represented by alterations of mental status, seizures, and focal motor deficits have been described after liver transplantation. These complications have been attributed to several pathogenetic factors, such as a poorly functioning graft, an intracranial hemorrhage, a cerebral infarction, an infection, or the toxicity of immunosuppressants.
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PMID:Neurological complications of liver cirrhosis and orthotopic liver transplant. 1664 71

The human IMPA2 gene, which encodes myo-inositol monophosphatase 2 (IMPA2), is mapped onto 18p11.2, a susceptibility region for bipolar disorder. This chromosomal region has also been proposed to include a susceptibility locus for schizophrenia and febrile seizures. Here we report the crystal structures of human IMPA2 and its complex with calcium and phosphate ions. Human IMPA2 comprises an alpha-beta protein with a five-layered sandwich of alpha-helices and beta-sheets (alpha-beta-alpha-beta-alpha). The crystal structure and analytical ultracentrifugation results indicated that IMPA2 exists as a dimer in solution. The overall structure of IMPA2 is similar to that of IMPA1, except for the loop regions. In IMPA1, the loop region (31-43) is located at the entrance of the active site cavity. In the corresponding region (42-54) of IMPA2, the residues are disordered and partially form an alpha-helix. The structural difference in the opening of the active site cavity suggests that the substrate specificity differs between IMPA1 and IMPA2. The widely opened cavity of IMPA2 implies that the physiological substrate may be a larger compound than inositol monophosphate. The structure of IMPA2 complexed with Ca2+ revealed two metals and one phosphate binding sites, which were the same sites as in IMPA1 complexed with Mn2+ and phosphate, suggesting that the mechanism of the enzymatic reaction is similar to that of IMPA1. The crystal structures of human IMPA2 are useful for understanding the effect of nonsynonymous polymorphism reported in IMPA2, and will contribute to further functional analyses of IMPA2 that potentially predisposes to the vulnerabilities of bipolar disorder, schizophrenia, and febrile seizures.
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PMID:Crystal structure of human myo-inositol monophosphatase 2, the product of the putative susceptibility gene for bipolar disorder, schizophrenia, and febrile seizures. 1734 Jun 35

The trace element manganese is usually supplied when total parenteral nutrition is used. However, long-term parenteral administration of manganese, which bypasses the normal regulatory mechanism, may cause hypermanganesemia. Manganese poisoning presents clinically with parkinsonian-like symptoms and psychological changes. Seizures are a rare presentation of this disease. This report describes a 10-year-old female who had received total parenteral nutrition for 3 months because of short bowel syndrome, and presented with tonic-clonic seizure, decreased level of consciousness, and fever. The serum electrolytes, glucose and the cerebrospinal fluid examination were normal. The blood culture grew Pantoea agglomerans. The brain magnetic resonance imaging disclosed no evidence of central nervous system infection. However, symmetric high-intensity signal on T1-weighted images was documented in the basal ganglia, especially in the globus pallidus. Her whole blood manganese level was 3.7 microg/dL, which was significantly higher than the normal range (0.4-1.4 microg/dL). Diagnosis of hypermanganesemia related to total parenteral nutrition was made.
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PMID:Seizure associated with total parenteral nutrition-related hypermanganesemia. 1735 53

This article reviews research on the use of diet, nutritional supplements, and hormones in the treatment of epilepsy. Potentially beneficial dietary interventions include identifying and treating blood glucose dysregulation, identifying and avoiding allergenic foods, and avoiding suspected triggering agents such as alcohol, aspartame, and monosodium glutamate. The ketogenic diet may be considered for severe, treatment-resistant cases. The Atkins diet (very low in carbohydrates) is a less restrictive type of ketogenic diet that may be effective in some cases. Nutrients that may reduce seizure frequency include vitamin B6, magnesium, vitamin E, manganese, taurine, dimethylglycine, and omega-3 fatty acids. Administration of thiamine may improve cognitive function in patients with epilepsy. Supplementation with folic acid, vitamin B6, biotin, vitamin D, and L-carnitine may be needed to prevent or treat deficiencies resulting from the use of anticonvulsant drugs. Vitamin K1 has been recommended near the end of pregnancy for women taking anticonvulsants. Melatonin may reduce seizure frequency in some cases, and progesterone may be useful for women with cyclic exacerbations of seizures. In most cases, nutritional therapy is not a substitute for anticonvulsant medications. However, in selected cases, depending on the effectiveness of the interventions, dosage reductions or discontinuation of medications may be possible.
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PMID:Natural approaches to epilepsy. 1739 65


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