Disease relevance of FEB1

• RESULTS: We report the exclusion of the FC trait in our families to FEB1 on 8q13-21 and to a second febrile convulsion locus on 19p13 [1].
• We report a clinical and genetic study of a French family among whom febrile convulsions (FC) are associated with subsequent temporal lobe epilepsy (TLE) in the same individual, without magnetic resonance imaging-identifiable hippocampal abnormalities [2].
• A 10-year-old boy developed febrile convulsions at age 2 years, and multiple types of nonfebrile generalized seizures over the ensuing months and years [3].
• The association between complex febrile convulsions and partial seizures, on the other hand, may reflect either a causal association or the presence of preexisting brain disease that is responsible for both the complex febrile seizures and later partial seizures [4].
• 10 of these 24 children had temperatures in excess of 38 degrees C and 5 were greater than 40 degrees C. There was a transition in age at presentation between the two groups, with most cot deaths occurring before six months of age and febrile convulsions after that age [5].

Psychiatry related information on FEB1

• BACKGROUND: Hospital-based studies have reported that children with febrile convulsions have subsequent mental retardation and behavior problems [6].
• Even among patients with treatment-refractory temporal lobe epilepsy, a specific subgroup of patients, characterized by bitemporal seizure foci, an absence of febrile convulsions, and a history of clustering of seizures, appears to be particularly prone to develop psychotic disorders [7].
• Psychometric tests were performed on 50 children with a history of febrile convulsions [8].
• Prevalence rates for simple febrile convulsions and minimal brain dysfunction were similarly calculated [9].
• The neuropsychological test results did not demonstrate significant differences between the children with febrile convulsions and the healthy controls [10].

High impact information on FEB1

• Two putative loci have been mapped (FEB1 and FEB2), but specific genes have not yet been identified [11].
• After excluding 16 children who had neurodevelopmental problems before their first febrile convulsion and 1 child whose case was atypical, we studied 381 children, 287 with simple febrile convulsions and 94 with complex febrile convulsions [6].
• This is the case for the influence of vasopressin on social communication, temperature regulation, epilepsy, and barrel rotation which may be an animal model of febrile convulsions, and some aspects of the central regulation of the cardiovascular system and for oxytocin on sexual behavior, social communication, and grooming [12].
• However, the possibility that the aseptic meningitis induced by vaccination was largely asymptomatic and a chance laboratory finding in children investigated for other clinical conditions, particularly febrile convulsions, could not be excluded [13].
• Phenobarbitone in the prophylaxis of febrile convulsions [14].

Chemical compound and disease context of FEB1

• The effectiveness and toxicity of phenobarbital (PB), primidone (PRM), and sodium valproate (VPA), used exclusively in monotherapy, were compared in 95 children affected with febrile convulsions [15].
• In 47 children followed for 1 year after the first "simple" febrile convulsion, dipropylacetate (Depakine, 20 mg/kg) was as effective in preventing new febrile convulsions (a single recurrence in 4% of 47 children) as was phenobarbital (5 mg/kg) or primidone (25 mg/kg) (a single recurrence in 4% of 47 children), and there were no side effects [16].
• Effectiveness and toxicity of phenobarbital, primidone, and sodium valproate in the prevention of febrile convulsions, controlled by plasma levels [15].
• METHODS: A novel model of FCs was used, in which lipopolysaccharide (LPS, Escherichia coli), in combination with a subconvulsant dose of kainic acid, caused FCs in 50% of 14-day-old male rats [17].
• Children with febrile convulsions [103 (range: 63-170) pmol/ml] and acute meningitis [105 (range: 65-171) pmol/ml] had significantly decreased CSF GABA concentrations (P less than 0.001 and P less than 0.02 compared with controls) [18].

Biological context of FEB1

• Two putative FS loci, FEB1 (chromosome 8q13-q21) and FEB2 (chromosome 19p13.3) have been mapped [19].
• METHODS: Members of the two families were genotyped with microsatellite markers linked to the previously identified febrile convulsion loci, FEB1, FEB2, and GEFS+, and we performed two-point linkage analyses by assuming an autosomal dominant mode of inheritance [1].
• Evidence favoring genetic heterogeneity for febrile convulsions [1].
• In families of probands with multiple febrile convulsions, an autosomal dominant inheritance with reduced penetrance is suspected [20].
• However, metoprolol produced small declines of 14% in the forced expiratory volume in 1 sec (FEB1) and 21% in the forced expiratory flow rate between 25% and 75% of the forced vital capacity (FVC) (FEF25-75) [21].

Anatomical context of FEB1

• Evidence for digenic inheritance in a family with both febrile convulsions and temporal lobe epilepsy implicating chromosomes 18qter and 1q25-q31 [2].
• Homovanillic acid and 5-hydroxyindoleacetic acid in lumbar cerebrospinal fluid in children with afebrile and febrile convulsions [22].
• The putamen and thalamus seemed to be affected predominantly in patients with a history of febrile convulsions, whereas patients without febrile convulsions had smaller caudate nuclei bilaterally [23].
• Association of human herpesvirus 6 infection of the central nervous system with recurrence of febrile convulsions [24].
• Our results indicate that FCs affected local circuits in the amygdala and possibly in the hippocampus but not circuits responsible for seizure generalization [17].

Associations of FEB1 with chemical compounds

• Placebo-controlled study of phenobarbitone and phenytoin in the prophylaxis of febrile convulsions [25].
• The results indicated that the CSF GABA level may not be abnormal in patients with first-time febrile convulsions [26].
• Plasma melatonin was measured in 118 infants and children (39 controls, 28 with epileptic convulsions, and 51 with febrile convulsions) [27].
• Effective short-term diazepam prophylaxis in febrile convulsions [28].
• The behavior of the free fraction of valproic acid (VPA) was evaluated during long-term treatment of 24 children (9-18 months of age) with febrile convulsions [29].

Physical interactions of FEB1

• Clinical features and surgical outcome of medial temporal lobe epilepsy with a history of complex febrile convulsions [30].

Regulatory relationships of FEB1

• Familial antecedents for epilepsy and/or febrile convulsions influenced the presence of epilepsy in patients with posterior fossa malformations (P < .01) [31].

Other interactions of FEB1

• PURPOSE: Two large Canadian kindreds appearing to segregate febrile convulsions as an autosomal dominant trait were evaluated for linkage to three known FC loci, as well as other epilepsy loci [1].
• The lack of association between febrile convulsions and polymorphisms in SCN1A [32].
• All patients were ASA grade III/IV and the mean FEB1/FVC was 0.52 (range, 0.4-0.68), due to chronic asthma (two cases) and COPD (four cases) [33].
• The voltage-gated potassium channel KCNQ2 in Taiwanese children with febrile convulsions [34].
• The IL-1 beta exon 5 gene polymorphisms are not a useful marker for predicting the susceptibility to febrile convulsions [35].

Analytical, diagnostic and therapeutic context of FEB1

• Completion of vaccination by 4 months instead of 10 months after the change in the UK to an accelerated immunisation schedule may have resulted in a 4-fold decrease in febrile convulsions attributable to DTP vaccine [36].
• Lumbar puncture and febrile convulsions [37].
• Poor seizure control was related to an early age of seizure onset, a history of febrile convulsions, and epileptiform discharges on the EEG [38].
• Epidemiologic studies have changed our approach to febrile convulsions [39].
• Twin study: The pairwise concordance rate for FC was 56% (10/18 pairs) in monozygotic and 14% (2/14 pairs) in dizygotic twins (P less than 0.05) [40].

References