Febrile Seizure Group Research Articles

Influence of nitric oxide on heme oxygenase/carbon monoxide system in hippocampus of febrile seizures rats

Febrile seizures (FS) are the most common type of seizure disorders. Studies have found that there have respective changes of heme oxygenase (HO)/CO system and nitric oxide synthase (NOS)/NO system during FS. The present study was to explore the influence on expression of HO-1 mRNA and protein and content of CO after recurrent FS by NOS inhibitor N(omega)-nitro-L-arginine Methyl ester (L-NAME), in order to demonstrate a regulating role in HO/CO system by NO. Forty-eight SD rats were randomly divided into 3 equal groups: FS group, undergoing intraperitoneal injection of normal saline (NS) and then bath in 45.2 degrees C hot water for 5 minutes every other day for 10 times, FS + L-NAME group, undergoing intraperitoneal injection of NOS inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) and then FS for 10 times, and control group, undergoing intraperitoneal injection of NS and then bath in 37.0 degrees C water. Twenty-four hours after the last bath blood was collected from the abdominal cardinal vein to measure the concentrations of plasma nitric oxide and carbon monoxide with spectrophotometer. The brains were taken out to be made into frozen slices to undergo HO-1 in situ hybridization to measure the mRNA expression of HO-1. The hippocampus was taken out to undergo Western blotting to measure the expression of HO-1 protein. The plasma CO concentration was higher by 94.5% in the FS group in comparison with that in the control group (P < 0.01). The plasma CO concentration of the FS + L-NAME group was higher by 63.18% than that of the control group (P < 0.05) and lower by 16.14% than in the FS group (P < 0.05). The HO-1 mRNA expression was significantly higher in the FS group than in the control group. The HO-1 mRNA expression of the in hippocampal neurons of the L-NAME was lower than that of the FS group, however, still higher than that of the control group. Western blotting showed that HO-1 protein was expressed in all 3 groups; the HO-1 protein expression of the FS group was higher by 208% than that of the control group; and the HO-1 protein expression of the FS + L-NAME group was higher by 115% than that of the control group (P < 0.01) and lower by 30.19% than that of the FS group (P < 0.01).

Hydrogen sulfide may improve the hippocampal damage induced by recurrent febrile seizures in rats

The aim of the present study was to investigate the possible role of hydrogen sulfide (H 2S) in the pathogenesis of recurrent febrile seizures (FS) in rats. On a rat model of recurrent FS, the ultrastructure of hippocampal neurons, the plasma level of H 2S, the expressions of cystathionine b-synthase (CBS) and c-fos, and the development of mossy fiber sprouting (MFS) in hippocampus were examined after treatment with NaHS, a donor of H 2S, or hydroxylamine (HA), an inhibitor of CBS. We found that the plasma level of H 2S increased significantly, the expressions of CBS and c-fos increased markedly, and MFS was evident in hippocampus in FS group. NaHS alleviated the neuronal damage of recurrent FS rats, decreased the expression of c-fos, and inhibited MFS obviously. HA aggravated the neuronal damage of recurrent FS rats, further increased the expression of c-fos, and enhanced the mossy fiber outgrowth. The results showed that endogenous H 2S system was involved in the development of FS. Exogenous H 2S may exert beneficial effect on the pathogenesis of FS-related brain damage.

Association of the nicotinic receptor beta 2 subunit and febrile seizures

The nicotinic acetylcholine receptors are members of a superfamily of ligand-gated ion channels that mediate fast signal transmission at synapses. Mutations in neuronal nicotinic acetylcholine receptor beta 2 subunit have been associated with autosomal dominant nocturnal frontal lobe epilepsies. A major challenge is to establish whether the monogenic epilepsy gene also contributes to the common epilepsies. Because febrile seizures represent the majority of childhood seizures, and a genetic predisposition, we investigated the possibility that the nicotinic acetylcholine receptor beta 2 subunit might be involved in the etiology of febrile seizures. Children were divided into two groups: those with febrile seizures (group 1; n = 104) and control patients (group 2; n = 83). Polymerase chain reaction was used to identify the G/C and T/C polymorphisms of the nicotinic acetylcholine receptor beta 2 subunit gene, which is mapped on chromosome 1. Genotypes and allelic frequencies for nicotinic acetylcholine receptor beta 2 subunit gene polymorphisms in both groups were compared. The results indicated that genotypes and allelic frequencies in both groups were not significantly different. These data suggest that nicotinic acetylcholine receptor beta 2 subunit polymorphisms are not a useful marker for prediction of the susceptibility to febrile seizures.

Possible contribution of interferon-α to febrile seizures in influenza

The systemic symptoms associated with influenza infection are mainly attributable to cytokines. To elucidate whether the high incidence of creatine kinase elevation and febrile seizures in influenza infection could be related to cytokines, we examined the serum levels of creatine kinase and cytokines (interferon-α, interleukin-6, and tumor necrosis factor-α) in patients with influenza and other febrile illness. Among those in the influenza group, 12 of 43 patients demonstrated elevated levels of creatine kinase (more than 200 IU/L), whereas in the control group two of 14 patients demonstrated elevated creatine kinase levels. When age was limited to under 7 years, seven of 32 patients (21.9%) in the influenza group had febrile seizures, whereas one of seven patients (14.3%) had a seizure in the control group. The influenza group demonstrated significantly high levels of interferon-α and interleukin-6. There was no correlation between cytokine levels and duration of fever or serum creatine kinase levels. The number of patients with high levels of interferon-α (>400 pg/mL) was significantly larger in the febrile seizure group than in the control group (six of seven patients in the febrile seizure group, 16 of 36 in the control group; P < 0.05). The present findings suggest the possible contribution of interferon-α in the pathogenesis of febrile seizures.

Cerebrospinal fluid somatostatin levels in febrile seizures and epilepsy in children

We analysed the level of cerebrospinal fluid (CSF) somatostatin in children with febrile seizures and epilepsy. In the febrile seizure group (n = 23), the somatostatin level was 83.9 ± 11.2 pg/ml, which was significantly higher than that of age-matched controls. CSF samples obtained within 3 h of the last seizure had higher somatostatin levels (106.1 ± 12.4 pg/ml;n = 14) than did the CSF obtained after 3 h (49.4 ± 15.6 pg/ml;n = 9). The mean somatostatin level in the epilepsy group was 35.3 ± 4.3 pg/ml (n = 34), and was distributed as follows: 27.6 ± 3.6 pg/ml in the idiopathic generalized epilepsy group (n = 16), 44.0 ± 9.4 pg/ml in the symptomatic generalized epilepsy group (n = 13), and 37.2 ± 10.1 pg/ml in the partial epilepsy group (n = 5). The levels in each group were significantly higher than those in age-matched controls. Somatostatin is a hypothalamic tetradecapeptide with excitatory effects on neurons in children with febrile seizures and epilepsy. The finding that patients with convulsive disease had elevated levels of CSF somatostatin suggests that somatostatin release is somehow related to seizure activity. It remains to be determined whether this is due to increased release from over-active excitatory neurons or leakage from damaged or anoxic neurons, secondary to seizure activity.

Pathogenetic role of monoamine metabolism in complex febrile seizures

To investigate the pathogenetic role of monoamine metabolism for febrile seizures, concentrations of homovanillic acid and 5-hydroxyindoleacetic acid were evaluated in the lumbar cerebrospinal fluid of affected children. This series included children who underwent lumbar puncture within 4 hours after seizures, at which time the lumbar cerebrospinal fluid is presumed to represent a ventricular source of cerebrospinal fluid, without the consequence of a seizure. The subjects were 21 patients with simple febrile seizures, eight with complex febrile seizures, and eight control patients. The complex febrile seizure group had lower homovanillic acid and 5-hydroxyindoleacetic acid levels than the control group, whereas the simple febrile seizure group and control group did not have a significant difference. Although statistically not significant, the complex febrile seizure group was inclined toward lower homovanillic acid and 5-hydroxyindoleacetic acid levels than the simple febrile seizure group. These results implied that abnormal monoamine metabolism contributes to seizure susceptibility in the complex febrile seizure group. The simple febrile seizure group may be heterogeneous, and abnormal monoamine metabolism can play a role in seizure development for some children of this group

Bilateral reductions in hippocampal volume in adults with epilepsy and a history of febrile seizures

OBJECTIVESTo examine the degree and frequency of reductions in hippocampal volume in patients with temporal lobe epilepsy with and without a history of febrile seizures.METHODSIn vivo measures of hippocampal volume...

Interleukin-1β levels in serum and cerebrospinal fluid of children with febrile seizures

We compared interleukin-1β (IL-1β) levels in peripheral blood and cerebrospinal fluid (CSF) of children with febrile seizures with those of children with febrile illnesses without seizures (control). Twenty patients were included in the study, 10 with febrile seizures and 10 with febrile illness not complicated by seizures (control). Blood and CSF were obtained after the patients' admission to the hospital. IL-1β levels were measured by a specific radioimmunoassay method. No significant differences were observed between mean IL-1β levels in CSF (4.15 ± 1.5 pg/ml) and blood (2.92 ± 2.6 pg/ml) of the patients with febrile seizures group as compared with those in CSF (3.2 ± 3.2 pg/ml) and blood (3.44 ± 3.16 pg/ml) in the control group. These results do not support the hypothesis that increased production of IL-1β or increased diffusion of IL-1β through the blood-brain barrier is involved in the pathogenesis of febrile seizures in children.

Does Iron Deficiency Raise the Seizure Threshold?

To determine the effect of iron status on the seizure threshold, measures of iron sufficiency were prospectively evaluated in 51 children presenting to a pediatric emergency department with a febrile illness with (26) or without (25) an associated febrile seizure. A higher proportion of children from the febrile seizure group had a family history of mental retardation (5/26 versus 0/25, P = .02) or of previous febrile seizures (10/26 versus 2/23, P = .01). The two groups were otherwise comparable for age, sex, race, family history of afebrile seizures, temperature at presentation, white blood cell count, differential, and vitamin and antibiotic use. Patients with febrile seizures were less frequently iron deficient as defined by a free erythrocyte protoporphyrin level above 0.80 ng/L (2/23 versus 10/25, P < .01), hemoglobin concentration less than 110 g/L (1/26 versus 6/25, P < .03), hematocrit less than 0.30 L/L (0/22 versus 4/25, P < .02), mean corpuscular hemoglobin less than 20 pg (0/25 versus 3/24, P < .04), mean corpuscular volume less than 65 fL (0/26 versus 4/24, P < .02), and platelet count higher than 550 x 10(9)/L (0/26 versus 3/25, P < .04). This association was even stronger when adjusted for differences in family history. None of the patients in the febrile seizure group was being treated for iron deficiency at presentation, whereas three of 25 controls used an iron supplement (P < .04). Iron deficiency may protect against the development of febrile seizures.