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

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

Since glucose transport appears to be inhibited in viral infections, we looked for inhibitors in cerebrospinal fluid (CSF) and serum of children with febrile convulsions (FC) and Singapore syndrome (SS). When incubated with rat and human adipocytes both fluids from FCs inhibited the utilization of glucose supplied in the medium as exhibited by decreased synthesis of triglycerides. Sera in the acute stage of the illness were more inhibitory than those from convalescents. There was competition between 3-0 methyl glucose and the CSF factors suggesting competitive inhibition at the plasma membrane. This may be due to anti-idiotypic antibodies. The likelihood of a second inhibitor is suggested by (1) the inhibitory activity of the larger of two fractions (about 80,000 molecular weight, corresponding to albumin) obtained in gel filtration chromatography of pooled CSF and (2) failure to observe a decrease in inhibitory activity with recovery from SS following management with hyperglycaemia-producing infusions. These observations are consistent with glycated albumin as a possible factor. Further characterization is called for to ascertain the genesis of viral encephalopathies.
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PMID:Factors in serum and cerebrospinal fluid from children with viral encephalopathies impair glucose transport. 228 25

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

Simultaneous blood and CSF glucose levels were investigated in 143 febrile children without cerebromeningeal illness, who were evaluated due to fever in the first 2 months of life or febrile convulsions. There was a significant decrease (P less than 0.001) in the mean CSF-blood glucose ratio from 0.67 +/- 0.13 in the first 2 weeks of life to 0.56 +/- 0.11, 0.57 +/- 0.8 and 0.58 +/- 0.11 at the ages 2-4, 5-6 and 6-8 weeks, respectively. The mean CSF and blood glucose levels did not change significantly in this period. After the 2nd month of life there was a significant rise P less than 0.01 in the mean CSF-blood glucose ratio to 0.72 +/- 0.11, the customary normal value in children. This was associated with a significant rise in CSF glucose levels as compared to the first 8 weeks as a whole. Our study suggests age-related changes in CSF blood-glucose ratios during the first weeks of life which are important when evaluating infants for the possibility of meningitis.
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PMID:CSF glucose levels in febrile infants. 339 97

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

A prospective epidemiological study of the incidence of simple febrile convulsions (FC) was performed in a northern Swedish county. The yearly incidence was 700/100 000. The children with FC were re-examined three years later. The pre- and perinatal complications were significantly more common in the group of children with FC than in a randomly collected group of controls. The value of an extensive investigation program is discussed. Between six months and five years of age the children with FC can be separated from those with other cerebral diseases causing epileptic seizures by recording a thorough history followed by a somatic and neurological physical examination and a determination of acute blood glucose. In children less than six months of age and in children in which meningitis or encephalitis cannot be ruled out, a lumbar puncture and a blood culture should be performed. If the onset of the convulsion has been after five years of age, if the seizures are partial or have a duration of more than 30 minutes, or if signs of cerebral disease are found, the examination should be supplemented with EEG and relevant investigations. There is no need for an extensive routine program of investigations in the care of children with FC.
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PMID:Simple febrile convulsions. A prospective incidence study and an evaluation of investigations initially needed. 689 23

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

Cerebrospinal fluid (CSF) examinations of 212 children aged two to 24 months with idiopathic nonfebrile seizures, complex febrile seizures, or status epilepticus, who had a lumbar puncture within 24 hours of the convulsion, were reviewed to determine whether an idiopathic convulsion can result in CSF abnormalities. Children with complex febrile seizures had a median CSF white blood cell count of 1 cell/mm3 (range 0-19 cells/mm3) and a median CSF polymorphonuclear (PMN) cell count of 0 cells/mm3 (range 0-8 cells/mm3). The CSF white blood cell (WBC) count was elevated above the upper limit of normal of 5 cells/mm3 in 9.8% and the absolute number of polymorphonuclear cells was more than 0 cells/mm3 in 26.2% of the complex febrile seizure subjects. Values at the 95th percentile were calculated; a total of 8 WBC/mm,3 4 PMN/mm,3 protein of 73 mg/dl and glucose of 119 mg/dl determined the 95th percentile CSF values for the patients with complex febrile seizures. Patients with nonfebrile seizures or with status epilepticus had similar findings. We conclude that complex febrile, idiopathic nonfebrile convulsions or status epilepticus may affect CSF findings in children: CSF with > 20 WBC/mm3 or > 10 PMN/mm3 should not be attributed to seizures.
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PMID:Cerebrospinal fluid analysis in children with seizures. 853 68

In febrile convulsions glucose concentrations are known to increase both in the blood and cerebrospinal fluid (CSF). The reason behind this increase is, however, incompletely understood. We have studied the effects of convulsion and fever on the CSF and blood glucose concentrations in four different groups of children: febrile and non-febrile children, with and without convulsions. The concentration of glucose in the CSF was significantly higher in febrile children with (4.4 +/- 0.1 mmol/l, mean +/- SEM n = 35, p < 0.01. ANOVA, Duncan's test) and without convulsions (3.9 +/- 0.2 mmol/l, n = 22, p < 0.05) than in non-febrile, non-convulsive children (3.3 +/- 0.1 mmol/l, n = 21). In non-febrile convulsive children, the CSF glucose concentration was 3.7 +/- 0.2 mmol/l (n = 10). Both fever and seizures increased the CSF glucose levels (p < 0.0001) and p = 0.028, respectively, analysis of covariance). There was a linear correlation between the body temperature and concentration of glucose in the CSF (r = 0.454, p < 0.0001, n = 88, Pearson's correlation analysis). The changes in blood glucose concentrations between the groups paralleled those found in the CSF. Our results show that hyperglycaemia and an increase in the CSF glucose concentration in febrile convulsions is not explained just by a stress reaction, evoked by the seizure, as has been hypothesized earlier, but by the influence of increased body temperature as well.
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PMID:The role of fever on cerebrospinal fluid glucose concentration of children with and without convulsions. 858 Jun 26


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