folate/crise epiléptica

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Harmful effect of megadoses of vitamins: electroencephalogram abnormalities and seizures induced by intravenous folate in drug-treated epileptics.

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Folic acid was administered intravenously during constant EEG monitoring to eight epileptic subjects who had received diphenylhydantoin therapy for more than 1 year. Six of the subjects displayed low folate levels by Lactobacillus casei assay in plasma and/or whole blood. Six patients received 75 mg

Serum folate concentrations during pregnancy in women with epilepsy: relation to antiepileptic drug concentrations, number of seizures, and fetal outcome.

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Serum folate concentrations, blood counts, and antiepileptic drug concentrations were measured during 133 pregnancies of 125 women with epilepsy. There was an inverse correlation between serum folate concentrations and concentrations of phenytoin and phenobarbitone. The number of epileptic seizures

Electroencephalographic and seizure manifestations in two patients with folate receptor autoimmune antibody-mediated primary cerebral folate deficiency.

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Seizure semiology and electroencephalographic (EEG) manifestations of autoimmune-mediated cerebral folate deficiency (CFD) before and after therapy have yet to be fully characterized. Here, we report these findings in two such patients. Our first patient presented with the novel manifestation of

Pyridoxal phosphate-responsive seizures in a patient with cerebral folate deficiency (CFD) and congenital deafness with labyrinthine aplasia, microtia and microdontia (LAMM).

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We present an 8-year-old boy with folate receptor alpha (FRα) defect and congenital deafness with labyrinthine aplasia, microtia and microdontia (LAMM syndrome). Both conditions are exceptionally rare autosomal recessive inherited diseases mapped to 11q13. Our patient was found to have novel

Cerebrospinal fluid folate and cobalamin levels in febrile convulsion.

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Folate and cobalamin parameters were studied in the serum and cerebrospinal fluid of 40 febrile paediatric patients. Eighteen of these children were in a state of febrile convulsion while the remaining 22 were non-convulsing. The serum folate concentration of all the patients was higher than that of

Diagnosis and management of cerebral folate deficiency. A form of folinic acid-responsive seizures.

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Folinic acid-responsive seizures (FARS) are a rare treatable cause of neonatal epilepsy. They have characteristic peaks on CSF monoamine metabolite analysis, and have mutations in the ALDH7A1 gene, characteristically found in pyridoxine-dependent epilepsy. There are case reports of patients

Late diagnosis of cerebral folate deficiency: Fewer seizures with folinic acid in adult siblings.

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Cerebral folate deficiency is a genetically heterogeneous condition.(1) Mutations in FOLR1 are responsible for a rare but treatable form of cerebral folate deficiency (OMIM #613068).(1) The gene codes for folate receptor alpha (FRα), a specific CNS folate transporter. Individuals with FOLR1-related

Alterations in hippocampal extracellular amino acids and purine catabolites during limbic seizures induced by folate injections into the rabbit amygdala.

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The effects on hippocampal extra- and intracellular amino acids of focal injection of folic acid into the amygdala in the rabbit were studied with brain dialysis. Folate seizures were accompanied by pronounced elevations of extracellular alanine and phosphoethanolamine. The increase of extracellular

Vitamin B12 Deficiency and Elevated Folate Levels: An Unusual Cause of Generalized Tonic-Clonic Seizure.

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BACKGROUND Vitamin B12 deficiency leads to abnormal myelination or demyelination, resulting in sub-acute combined degeneration, peripheral neuropathy, and psychiatric problems, including delusions, hallucinations, cognitive changes, depression, and dementia. Vitamin B12 deficiency also leads to

Does Folate Supplementation Leads to Better Seizure Control with Antiepileptic Drug Therapy?

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Folate treatment of diphenylhydantoin-induced gingival hyperplasia.

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It has recently been reported that folic acid supplementation reduced DPH-induced gingival hyperplasia in cat and in a pilot study also in man. The present study was performed to further evaluate this therapy in man. Twenty-three children with DPH-treatment for more than 1 yr, and eight children

Interactions between folates and carbamazepine or valproate in the rat.

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Carbamazepine and valproate each afforded protection against seizures induced by electroshock or by inhalation of hexafluorodiethyl ether (HFDE). After injections of either anticonvulsant for 10 days, plasma folate concentration decreased, but brain folate concentration did not change. Folinic acid

Truncal ataxia in chronic anticonvulsant treatment. Association with drug-induced folate deficiency.

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The association of truncal ataxia with a number of different factors has been studied in a group of 95 epileptic outpatients on chronic anticonvulsant treatment. The 28 patients showing truncal ataxia had been epileptic for a longer period of time, received a significantly larger number of drugs,

[Epileptic seizure model utilizing additive effects of excitatory amino acids].

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L-glutamate (GLU) and L-aspartate (ASP), major excitatory amino acids in the brain, are believed to have an important role in the generalization and expression of epileptic seizures. Their analogues such as kainate, folate, ibotenate and quisqualate have been widely used to produce epileptic

The antiepileptic drugs phenobarbital and carbamazepine reduce transport of methotrexate in rat choroid plexus by down-regulation of the reduced folate carrier.

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Intrathecal methotrexate (MTX) has been associated with severe neurotoxicity. Because carrier-associated removal of MTX from the cerebrospinal fluid (CSF) into blood remains undefined, we determined the expression and function of MTX transporters in rat choroid plexus (CP). MTX neurotoxicity usually

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