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Query: UMLS:C0009952 (febrile convulsions)
 1,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcium and magnesium have been measured in cerebrospinal fluid by atomic absorption spectrophotometry in children. The normal values on 194 C.S.F., obtaining for the calcium x: 5.24 mg. % and s: +/- 0.378 mg. % [50--56 % lower than serum values] and for magnesium x: 2.64 mg. % and s: +/- 0.155 mg. % [19--33 % higher than serum values] are found. Higher values of calcium at birth and on the first year of life and no differences with magnesium are noted. Applying the t-test, between normal values obtained and the different pathological entities, authors find singificant differences on the level of calcium, finding higher values on the following diseases: dehydration by diarrhoea, poliomyelitis, anoxy, tumours, bacterial meningitis. Magnesium showed values significantly higher in dehydration by diarrhoea and epilepsy, and values significantly lower on febrile convulsions and virical and bacterial meningitis.
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PMID:[Study of calcium and magnesium in cerebrospinal fluid and its' relation to different neurological diseases (author's transl)]. 72 8

Levels of calcium, magnesium, and glucose were measured in the blood and cerebrospinal fluid (CSF) of children with febrile convulsions. Calcium and magnesium levels were within the normal range and the blood: CSF ratios were similar to those of normal subjects. Hyperglycaemia was a frequent finding and was reflected in raised CSF glucose levels. Blood glucose levels were only transiently raised and none of the children had diabetes mellitus.
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PMID:Calcium, magnesium, and glucose levels in blood and CSF of children with febrile convulsions. 125 60

Current knowledge suggests integration of cerebral perfusion and metabolism as enabling normal neuronal function, and their pertubations explaining the brain damage of hypoxia, hypoglycaemia, hypoperfusion and status epilepticus. Similar mechanisms appear operative in the viral encephalopathies and cause psychomotor dysfunction and epilepsy. A transient inhibition of plasma membrane glucose transport is central to the understanding of the metabolic abnormalities of these encephalopathies, the ensuing cell energy crisis resulting from neuroglycopoenia being evidenced by electroencephalographic changes, lactic and ketoacidosis, hyperuricaemia and ionic aberrations. Failure of Na+ and Ca2+ pumps cause cerebral oedema and neuronal death respectively, the selective nature of the latter being due to alpha-adrenergic vasoconstriction. Management with hyperglycaemia-producing infusions and the judicious use of lactate and steroids can overcome the transport dysfunction and enable complete recovery. The temporal profile of the metabolic aberrations of febrile convulsions, which are the result of adaptation, provide a template supporting this mode of management of the severe encephalopathies.
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PMID:The probable mechanisms of brain damage and epilepsy in febrile convulsions, Singapore syndrome and Reye's syndrome. 250 20

Though children with febrile convulsions only have seizures in the early stage of a febrile illness and not later, these seizures have been attributed to the fever. We studied the serum electrolyte and metabolite profiles in the later stage to see if there were fuel responses resulting in electrophysiological changes which prevented further seizure activity. On admission there was intracellular glucose starvation, as evidenced by increased ketones and lactate, and the possibility of the failure of some electrolyte pumps, as suggested by hyperuricaemia (energy crisis) and decreased serum Na+, Cl- and Ca2+. However, there was adaptive hyperglycemia and decreased serum K+. It seems likely that the hyperglycemia, induced the uptake of K+ by neurones, enabling their repolarization and hyperpolarization, which prevented further seizure activity, while Cl- influx short-circuited depolarizing currents produced by Na+ influx. Studies during recovery showed a gradual return of the metabolic and electrolyte aberrations to normality, suggesting that the provision of energy through adaptation to the stress, enabled recovery of the aforementioned pumps.
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PMID:Hyperpolarization and short-circuiting as mechanisms of seizure prevention following febrile convulsions. 277 93

We studied 153 children who experienced convulsions associated with shigellosis. The male-female ratio was 1.2:1.0. Thirty-six children had a previous history of febrile convulsions, and 31 children had a family history of convulsive disorder. Most of the children were 0.5 to 3 years of age, although 49 (32%) were older than 3 years of age and 20 (13.1%) were older than 5 years of age. All children were febrile; in 75% of the children, the temperature was over 39 degrees C. The majority of the children had generalized, self-limited convulsions, which lasted less than ten minutes. In 30 children the seizures were categorized as complex; ten of them had recurrent episodes, although none had any residual neurologic deficit. The total leukocyte count was usually within normal limits, but the differential count characteristically showed a marked increase in the number of band forms. Hypocalcemia (blood calcium level, less than 9.01 mg/dL [less than 2.25 mmol/L]) was observed in four patients; hyponatremia (blood sodium level, 130 mEq/L [130 mmol/L]), in 11 patients; and hypernatremia (blood sodium level, 157 mEq/L [157 mmol/L]), in one patient. Electroencephalographic (EEG) studies were performed in ten children, and lumbar punctures were performed in 34 children; both procedures usually yielded normal results. Shigella sonnei was isolated from 69% of the children; Shigella flexneri from 25%; Shigella boydii from 5%; and Shigella dysenteriae from 1%. Due to the benign and self-limited nature of most of the convulsions, neither diagnostic procedures, nor drug therapy, are usually necessary. These measures should, however, be considered in complicated cases characterized by focal or prolonged seizures.
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PMID:Convulsions in childhood shigellosis. Clinical and laboratory features in 153 children. 354 8

The authors valued some metabolic parameters (sodium, potassium, calcium, blood levels of glucose, proteins, nitrogen, creatinine) in 159 children with febrile convulsions and compared the results with those of a group of children with fever (50 subjects) and of a group of health, fever free children (50 subjects). In the patients with febrile convulsions serum levels of sodium, calcium and osmolarity resulted significantly lower than those obtained in both control groups. The electrolytic modification (overall hyponatremia, probably due to a SIADH) may have a role in short-term relapses of febrile convulsions. Hyponatremia is present also in some children with high fever, without seizures; it may be that hyponatremia, in predisposed subjects, lower the threshold of neuromuscular excitability.
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PMID:[Electrolytic changes in febrile convulsions]. 409 12

Febrile seizures are a common pediatric problem, yet there is a great deal of disagreement about the appropriate diagnostic evaluation of a child with this disorder. We reviewed the routine diagnostic tests performed on 100 consecutive children admitted with their first "simple" febrile seizure. The studies performed included lumbar puncture, measurement of blood glucose, serum calcium, serum electrolytes, and BUN levels, blood cell count, urinalysis, skull roentgenograms, and EEG. Though resulting in a significant expense, these routine investigations proved to be of little diagnostic value. Based on this experience and a review of the current literature, we concluded that diagnostic procedures should be performed only when specifically called for by the patient's condition or medical history.
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PMID:The child with a 'simple' febrile seizure. Appropriate diagnostic evaluation. 723 69

Specific defects in neuronal ion channel proteins have recently been identified in some forms of hereditary epilepsy. A deletion of 300 amino acids from the COOH terminal of the K+ channel reduces the electrical stability of the neuron in subjects with benign familial neonatal seizures. Defects in the protein subunits of the Na+ channel may prolong neuronal depolarization in children with generalized epilepsy with febrile convulsions. A point mutation in one of the ACh receptor subunits may reduce the function of inhibitory interneurons in subjects with autosomal dominant nocturnal frontal lobe epilepsy. Finally, several different defects in the Ca2+ channel amino acid sequence have been identified in various types of epilepsy in mice in which symptoms and EEG show similarities to those in human petit mal. This remarkable progress in the precise localization of ion channel defects in epilepsy provides a novel basis for the development of more differentiated diagnosis and pharmacological therapy.
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PMID:[Molecular defects may cause epilepsy. New discoveries can provide better possibilities for directional diagnostics and treatment]. 1111 87

Genetic defects have been recently identified in certain inherited epilepsy syndromes in which the phenotypes are similar to common idiopathic epilepsies. Mutations in the neuronal nicotinic acetylcholine receptor 4 and 2 subunit genes have been detected in families with autosomal dominant nocturnal frontal lobe epilepsy. Both receptors are components of neuronal acetylcholine receptor, a ligand-gated ion channel in the brain. Furthermore, mutations of two K+-channel genes were also identified as the underlying genetic abnormalities of benign familial neonatal convulsions. Mutations in the voltage-gated Na+-channel 1, 2 and 1 and the gamma aminobutyric acid (GABAA) receptor 2 subunit genes were found as a cause of generalized epilepsy with febrile seizures plus, a clinical subset of febrile convulsions. Na+-channels, GABAA receptor and their auxiliaries may be involved in the pathogenesis of this subtype and even in simple febrile convulsions. Mutation of a voltage-gated K+-channel gene can cause partial seizures associated with periodic ataxia type 1 and some forms of juvenile myoclonic epilepsy and idiopathic generalized epilepsy can result from mutations of a Ca2+-channel. This line of evidence suggests the involvement of channels expressed in the brain in the pathogenesis of certain types of epilepsy. Our working hypothesis is to view certain idiopathic epilepsies as disorders of ion channels, i.e. 'channelopathies'. Such hypothesis should provide a new insight to our understanding of the genetic background of epilepsy.
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PMID:Genetic abnormalities underlying familial epilepsy syndromes. 1201 63

Genetic defects have been recently identified in certain inherited epilepsy syndromes in which the phenotypes are similar to those of common idiopathic epilepsies. Mutations in the neuronal nicotinic acetylcholine receptor alpha4 and beta2 subunit genes have been detected in families with autosomal dominant nocturnal frontal lobe epilepsy. Both receptors are components of neuronal acetylcholine receptor, a ligand-gated ion channel in the brain. Furthermore, mutations of two K+ channel genes also were identified as the underlying genetic abnormalities of benign familial neonatal convulsions. Mutations in the voltage-gated Na+-channel alpha1 and beta1 subunit genes were found as the cause of generalized epilepsy with febrile seizures plus, a clinical subset of febrile convulsions. Mutation of a voltage-gated K+-channel gene can cause partial seizures associated with periodic ataxia type 1 and some forms of juvenile myoclonic epilepsy can result from mutations of a Ca2+ channel. This line of evidence suggests the involvement of channels expressed in the brain in the pathogenesis of certain types of epilepsy. Our working hypothesis is to view certain idiopathic epilepsies as disorders of ion channels (i.e., "channelopathies"). Such a hypothesis should provide a new insight into our understanding of the genetic background of epilepsy.
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PMID:Molecular genetics of human familial epilepsy syndromes. 1238 75


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