phosphofructokinase/epileptische aanval

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Muscle phosphofructokinase deficiency with neonatal seizures and nonprogressive course.

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Muscle phosphofructokinase deficiency is known to cause childhood-onset exercise intolerance, muscle cramps, and myoglobinuria. Rarely, phosphofructokinase deficiency manifests in infancy as congenital myopathy and arthrogryposis with fatal outcome. Here, the authors report the case of a 2-year-old

Muscle phosphofructokinase deficiency (Tarui's disease): report of a case.

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A 14-year-old girl had an acute episode of rhabdomyolysis after vigorous exercise and seizures. Laboratory studies revealed elevated creatine phosphokinase (CPK) activity and myoglobinuria without acute renal failure, as well as mild indirect hyperbilirubinemia, and hyperuricemia. The elevated CPK

Impaired hippocampal glucose metabolism during and after flurothyl-induced seizures in mice: Reduced phosphorylation coincides with reduced activity of pyruvate dehydrogenase.

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To determine changes in glucose metabolism and the enzymes involved in the hippocampus ictally and postictally in the acute mouse flurothyl seizure model. [U-13 C]-Glucose was injected (i.p.) prior to, or following a 5 min flurothyl-induced seizure. Fifteen minutes later, mice were killed and the

Fatal infantile form of muscle phosphofructokinase deficiency.

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We studied a girl with an infantile syndrome of limb weakness, seizures, cortical blindness, and corneal opacifications; she died at age 7 months of respiratory failure. There was no consanguinity or family history of neuromuscular diseases. Histochemical and biochemical studies of muscle showed

Starvation and seizures. Observation on the electroconvulsive threshold and cerebral metabolism of the starved adult rat.

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Acute starvation of adult rats resulted in a rise in the electroconvulsive threshold at 48 hours (P less than .10) and at 72 hours (P less than .01), but not at 24 hours. Biochemical correlates included (1) ketonemia and mild hypoglycemia in the blood; (2) a significant rise in the brain cytoplasmic

Neurologic and cardiac progression of glycogenosis type VII over an eight-year period.

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Little is known about the progression of phosphofructokinase deficiency (glycogenosis type VII, Tarui's disease). We describe a 66-year-old woman who had this disease diagnosed in 1997. Initial manifestations had included simple partial seizures since 1977, anginal chest pain since 1982, and muscle

Developmental impairments of select neurotransmitter systems in brains of Cln3(Deltaex7/8) knock-in mice, an animal model of juvenile neuronal ceroid lipofuscinosis.

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The neuronal ceroidlipofuscinoses (NCL) are a group of neurodegenerative disorders and are the most common lysosomal storage diseases of infancy and childhood. Juvenile NCL is caused by CLN3 mutation, producing retinal degeneration, uncontrollable seizures, cognitive and motor decline, and early

Glycogen synthesis and immunocytochemical study of fructose-1,6-biphosphatase in methionine sulfoximine epileptogenic rodent brain.

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The effects of the convulsant methionine sulfoximine (MSO) on the glucose pathway have been investigated in mouse and rat brain. The key gluconeogenic enzyme fructose-1,6-biphosphatase (FBPase) (EC 3.1.3.11) was immunostained by rat anti-FBPase antibody. The rat cortex slices were very lightly

Alterations in Cytosolic and Mitochondrial [U-13C]Glucose Metabolism in a Chronic Epilepsy Mouse Model.

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Temporal lobe epilepsy is a common form of adult epilepsy and shows high resistance to treatment. Increasing evidence has suggested that metabolic dysfunction contributes to the development of seizures, with previous studies indicating impairments in brain glucose metabolism. Here we aim to

Alterations of hippocampal glucose metabolism by even versus uneven medium chain triglycerides.

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Medium chain triglycerides (MCTs) are used to treat neurologic disorders with metabolic impairments, including childhood epilepsy and early Alzheimer's disease. However, the metabolic effects of MCTs in the brain are still unclear. Here, we studied the effects of feeding even and uneven MCTs on

Lactic acidosis in the brain: occurrence, triggering mechanisms and pathophysiological importance.

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Brain cells are better protected against systemic acidosis (and alkalosis) than most other cells since they are surrounded by an extracellular fluid which is, in itself, subjected to pH regulation. For all practical purposes, therefore, cerebral intracellular acidosis is endogenous and arises when

Neurologic manifestations of diabetic comas: correlation with biochemical alterations in the brain.

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Coma and other neurologic abnormalities are present in patients with either diabetic ketoacidosis (DKA) or nonketotic coma (NKC), and the cause of such phenomena are not known. Patients with NKC also manifest seizures and focal neurologic changes. Treatment of diabetic coma with insulin may induce

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