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1  2008-2009 with at least 1 diagnosis code of febrile convulsions.
2 .3 implicated in a familial form of juvenile febrile convulsions.
3 nt view of the 'benign' nature of early-life febrile convulsions.
4 95% CI 2.4-4.7; p<0.0001), family history of febrile convulsions (14.6, 6.3-34.1; p<0.0001), history
5  is a positional candidate gene for familial febrile convulsion and Cayman type cerebellar ataxia.
6 re no deaths in children following prolonged febrile convulsions and idiopathic convulsive status epi
7 udies reported progressive volume loss after febrile convulsions and in active epilepsy.
8 ) for seizures, 1.11 (95% CI, 1.06-1.17) for febrile convulsions, and 1.04 (95% CI, 0.97-1.13) for ep
9 30 days after vaccination, mainly pneumonia, febrile convulsions, and salmonella sepsis.
10                                              Febrile convulsions are a common form of childhood seizu
11 ral sclerosis often have histories of severe febrile convulsions as infants.
12 hat between 2 and 5% of children will have a febrile convulsion before the age of 5.
13 ce imaging (MRI) was performed after complex febrile convulsions (CFCs) in 27 infants.
14 study of 4 nested algorithms for identifying febrile convulsions from the administrative databases of
15  children aged 2-8 years (10 postvaccination febrile convulsions +/- gastroenteritis and 7 fever and/
16 ted linkage of a putative autosomal dominant febrile convulsion gene to chromosome 8q13-21.
17 naffected family members indicates that this febrile convulsion gene, which we call FEB2 , can be loc
18 onsistently prognostic across meta-analyses: febrile convulsions, hippocampal sclerosis, focal abnorm
19                              Postvaccination febrile convulsions in young children were rare but not
20    We report here another autosomal dominant febrile convulsion locus on chromosome 19p.
21 nance imaging have shown that very prolonged febrile convulsions may produce hippocampal injury and t
22 ysgenesis may play a role in the etiology of febrile convulsions, mesial temporal sclerosis, and temp
23  were increased with a family history of non-febrile convulsions (odds ratio 3.3, 95% CI 2.4-4.7; p<0
24                                Two had short febrile convulsions, one had PFC and one had non-febrile
25 s and the duration of epilepsy, a history of febrile convulsions or of generalized seizures.
26  the skeleton (OR, 0.27; 95% CI, 0.11-0.60), febrile convulsions (OR, 0.39; 95% CI, 0.21-0.67), viral
27 atients with MTS have a history of prolonged febrile convulsion (PFC) in childhood.
28 us, including 21 with a history of prolonged febrile convulsion (PFC), underwent qualitative and quan
29                           A prior history of febrile convulsions was obtained in 13 HTS patients (81.
30 ile myoclonic epilepsy, absence epilepsy, or febrile convulsions were screened by conformation-sensit