pyridoxine/seizures

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[Chronological change of EEG findings in a case of pyridoxine dependency seizures].

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A patient of pyridoxine dependent seizures was reported. He was born at 34 weeks' gestation and weighted 2,760 g. Apgar scores were 6 and 9 at 1 and 5 minutes, respectively. He showed the first seizure 2 hours after his birth. Phenobarbital, phenytoin, sodium valproate, diazepam and clonazepam were

Infantile hypophosphatasia secondary to a novel compound heterozygous mutation presenting with pyridoxine-responsive seizures.

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Hypophosphatasia (HPP) is a rare metabolic disease with the hallmark finding of deficient serum tissue nonspecific alkaline phosphatase (TNSALP) activity. TNSALP is primarily known for its role in mineralization; hence, HPP is characterized by defective mineralization of bone and/or teeth. TNSALP is

Transient nonketotic hyperglycinemia in an asphyxiated patient with pyridoxine-dependent seizures.

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An asphyxiated neonate with pyridoxine-dependent seizures and associated transient nonketotic hyperglycinemia is reported. Frequent seizures and their resultant hypoxic-ischemic insult may have led to the elevation of the cerebrospinal fluid glycine level in this patient. Early diagnosis and

Beneficial interaction between clobenpropit and pyridoxine in prevention of electroshock-induced seizures in mice: lack of histaminergic mechanisms.

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Clobenpropit, an H( 3) receptor antagonist, has been reported to modulate both the release of neurotransmitters and also the activity of histidine decarboxylase (HDC). Therefore, a decarboxylase-positive modulator, namely pyridoxine, was taken for interaction studies with clobenpropit in the

A 15-year follow-up of a boy with pyridoxine (vitamin B6)-dependent seizures with autism, breath holding, and severe mental retardation.

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Pyridoxine (vitamin B6) (2q31) dependency is a rare autosomal-recessive disorder that causes a severe seizure disorder of prenatal or neonatal onset. The abnormality appears to inhibit the binding of vitamin B6 to the enzyme glutamic acid decarboxylase-1, which is needed for the biosynthesis of

Pyridoxine-dependent seizures: magnetic resonance spectroscopy findings.

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Pyridoxine-dependent seizures are an extremely rare genetic disorder. Early diagnosis and treatment are important for the prevention of permanent brain damage. Elevated levels of glutamate and decreased levels of gamma-aminobutyric acid (GABA) in the frontal and parietal cortices are among the

Dietary pyridoxine and the susceptibility to limbic motor seizures in rats.

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Dietary pyridoxine (PN) deficiency in adult female rats produced a 32% decrease in hippocampal gamma-aminobutyric acid content, measured by a radioreceptor assay. No spontaneous seizures were observed in pyridoxine-deficient animals, but the seizure latency after a systemic kainic acid challenge

Reduced GABA synthesis in pyridoxine-dependent seizures.

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An abnormality in the pyridoxal-5'-phosphate (PLP) dependent enzyme, glutamic acid decarboxylase (GAD), which synthesizes gamma-aminobutyric acid (GABA), may underlie the epileptic syndrome of pyridoxine-dependent seizures. GABA synthesis by skin fibroblasts from an infant with pyridoxine-dependent

Lack of protection by pyridoxine or hydrazine pretreatment against monosodium L-glutamate-induced seizures.

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Pretreatment of rats with hydrazine (100 mg/kg), a compound which raises brain gamma-aminobutyric acid (GAGA) 175 percent in 12 hr was not able to prevent the occurrence of seizures induced by monosodium L-glutamate (MSG). Pyridoxine (50 mg/kg) the cofactor essential in the conversion of glutamate

A controlled trial of pyridoxine supplementation in children with febrile convulsions.

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A total of 107 children who had been hospitalized following a febrile convulsion were enrolled into the trial. By random allocation, 55 children were treated with pyridoxine hydrochloride (20 mgs twice daily) and the remaining 52 children were treated with a placebo until there had been either a

[Pyridoxine for severe metabolic acidosis and seizures due to isoniazid overdose].

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A 15-year-old girl took 3 g of isoniazid (15 tablets) in a suicide attempt and was brought unconscious to the emergency room. She was in respiratory failure, with seizures that could not be stopped with diazepam. Severe metabolic acidosis with normal serum lactate developed (pH 6.85), but did not

Alterations in seizure mechanisms caused by oxygen high pressure, 1,1-dimethylhydrazine, and pyridoxine.

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High pressure oxygen (HBO) and 1,1-dimethylhydrazine (UDMH) both cause grand mal seizures, brain glycogen degradation, and inhibition of glutamic acid decarboxylase (GAD). Brain glycogen degradation is a sudden process that is perhaps initiated by convulsions in the case of UDMH-poisoning, but a

A 9-year follow-up of a girl with pyridoxine (vitamin B6)-dependent seizures: magnetic resonance spectroscopy findings.

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Being an extremely rare condition makes the diagnosis of pyridoxine-dependent seizures (PDS) difficult. Early diagnosis of PDS is very important to prevent unwanted clinical outcomes. Elevated levels of glutamate and decreased levels of y-aminobutyric acid (GABA) in the frontal and parietal cortices

CSF glutamate/GABA concentrations in pyridoxine-dependent seizures: etiology of pyridoxine-dependent seizures and the mechanisms of pyridoxine action in seizure control.

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Several lines of evidence suggest that the binding affinity of glutamate decarboxylase (GAD) to the active form of pyridoxine is low in cases of pyridoxine-dependent seizures (PDS) and that a quantitative imbalance between excitatory (i.e. glutamate) and inhibitory (i.e. gamma-aminobutyric acid,

Pyridoxine as therapy in theophylline-induced seizures.

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Theophylline-induced seizures have significant morbidity and mortality and are difficult to treat. Theophylline therapy for asthma has been observed to depress plasma pyridoxal 5'-phosphate (PLP) levels which may decrease gamma-aminobutyric acid (GABA) synthesis and thereby contribute to seizures.

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