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Stimulational seizures without pseudopregnancy in white rats.

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Pyridoxine-dependent seizures associated with white matter abnormalities.

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Pyridoxine-dependent seizures are a disorder of GABA metabolism probably due to a defective binding of pyridoxal phosphate coenzyme (PALP) with glutamate decarboxylase (GAD), the rate-limiting enzyme in GABA synthesis. The resulting GABA deficiency causes severe epilepsy in infancy. We report on a

Reflex anoxic seizures ('white breath-holding'): nonepileptic vagal attacks.

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From clinical history 58 children were diagnosed as having reflex anoxic seizures secondary to provoked cardioinhibition (also known as white breath-holding attacks). Before referral, these seizures were commonly misdiagnosed as epileptic either because the provocation was ignored, not recognised,

HEXAFLUORODIETHYL ETHER (INDOKLON) CONVULSIONS IN CORPUS-CALLOTOMIZED WHITE RATS.

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[Electroencephalogram of the white rat subjected to audiogenic seizure].

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Long-term white matter tract reorganization following prolonged febrile seizures.

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Diffusion magnetic resonance imaging (MRI) studies have demonstrated acute white matter changes following prolonged febrile seizures (PFS), but their longer-term evolution is unknown. We investigated a population-based cohort to determine white matter diffusion properties 8 years after PFS. We used

Prolonged febrile seizures cause reversible reductions in white matter integrity.

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Prolonged febrile seizures (PFS) are the commonest cause of childhood status epilepticus and are believed to carry a risk of neuronal damage, in particular to the mesial temporal lobe. This study was designed to determine: i) the effect of prolonged febrile seizures on white matter and ii) the

Oligodendrocytes control potassium accumulation in white matter and seizure susceptibility.

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The inwardly rectifying K+ channel Kir4.1 is broadly expressed by CNS glia and deficits in Kir4.1 lead to seizures and myelin vacuolization. However, the role of oligodendrocyte Kir4.1 channels in controlling myelination and K+ clearance in white matter has not been defined. Here, we show that

Vanishing white matter disease associated with ptosis and myoclonic seizures.

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A 5-year-old boy who presented with progressive ataxia, neuroregression, and worsening with febrile illnesses is described. He also had myoclonic jerks and ptosis. His elder sister had died of a similar illness. Serial magnetic resonance imaging of the brain demonstrated extensive abnormality of the

White matter and neurite morphology differ in psychogenic nonepileptic seizures

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Objective: To further evaluate the relationship between the clinical profiles and limbic and motor brain regions and their connecting pathways in psychogenic nonepileptic seizures (PNES). Neurite Orientation Dispersion and Density Indices

Seizures in Children With Cerebral Palsy and White Matter Injury.

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OBJECTIVE The goal of this study was to describe the prevalence, syndromes, and evolution of seizure disorders in children with cerebral palsy (CP) due to white matter injury (WMI). METHODS For this population-based cohort study, brain MRI scans and medical records were reviewed in children in the

Natural History of Vanishing White Matter.

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OBJECTIVE To comprehensively describe the natural history of vanishing white matter (VWM), aiming at improving counseling of patients/families and providing natural history data for future therapeutic trials. METHODS We performed a longitudinal multicenter study among 296 genetically confirmed VWM

Wolff-Parkinson-White syndrome in a child with recurrent seizures.

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White matter diffusion abnormalities in patients with psychogenic non-epileptic seizures.

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The purpose of this study was to conduct a preliminary investigation of the white matter characteristics in patients with psychogenic non-epileptic seizures (PNES). Diffusion Tensor Imaging (DTI) data were collected at 3T in 16 patients with PNES and 16 age- and sex-matched healthy controls (HC).

Sensing limbic seizures within the fornical white matter: A technical report.

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