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• W1978586780 abstract "Febrile seizures (FS) are a common disorder affecting approximately 2–5% of children, mostly between 3 months and 6 years of age (Hauser & Kurland, 1975). It is usually a benign self-limited disorder. In the recently proposed diagnostic scheme of the International League Against Epilepsy (ILAE), FS are classified as a condition with epileptic seizures that does not require a diagnosis of epilepsy (Engel, 2001). However, FS are associated with an increased risk of later epilepsy, estimated at 7% by age 25 years (Annegers et al., 1987). Risk factors that predict a greater likelihood of later epilepsy include preexisting neurodevelopmental abnormalities; complex features of FS (prolonged duration, focal features, and multiple FS in 1 day); family history of epilepsy; and recurrent FS (Annegers et al., 1987). It has been debated whether FS are a nonspecific marker of a lower seizure threshold for patients who later develop epilepsy. In favor of this hypothesis is that several forms of epilepsy can be preceded by FS, and FS were a risk factor for complex partial, absence, and generalized tonic–clonic seizures (Rocca et al., 1987a,b,c). Evidence counter to this hypothesis is the association between specific epileptic syndromes, particularly temporal lobe epilepsy (TLE), and antecedent FS (Hamati-Haddad & Abou-Khalil, 1998), as well as the association between specific FS risk factors and specific forms of epilepsy later in life (Annegers et al., 1987). Later partial epilepsy was related to complex features, whereas later generalized epilepsy was related to a high number of FS and family history of unprovoked seizures. A high incidence of antecedent FS, particularly prolonged FS, has been observed repeatedly in surgical series of patients with TLE (Falconer et al., 1964; Abou-Khalil et al., 1993). The incidence is greatest in a pure mesial TLE population with hippocampal sclerosis (HS) (French et al., 1993). The association of HS and antecedent FS was also noted in pathologic (Sagar & Oxbury, 1987) and imaging (Cendes et al., 1993; Theodore et al., 1999) studies. However, the association of TLE with antecedent FS was not clearly noted in population-based studies. In one pediatric study of 489 patients with epilepsy, 14.9% of patients had at least one febrile seizure before the first afebrile seizure, but prior FS were more likely in children with generalized tonic–clonic seizures (22%) than in those with complex partial seizures (13%) or partial seizures becoming generalized tonic–clonic (14%). A hospital-based study of 1,005 mostly adult patients with proven epilepsy, found that partial epilepsy was not more likely than generalized epilepsy to be associated with FS. However, when localization was taken into consideration, TLE was more likely to be preceded by FS than extratemporal epilepsy or generalized epilepsy (25.2% vs. 5.6%, p < 0.00001, vs. 11%, p < 0.001) (Hamati-Haddad & Abou-Khalil, 1998). Patients with TLE were more likely to have had complex FS than were patients with generalized epilepsy (81% vs. 31%, p < 0.00001). However, this observation could not be confirmed in a community-based study of 524 children that failed to show a specific association between FS and TLE (Berg et al., 1999). One possible explanation for the discrepancy could be that pediatric studies may fail to capture patients who develop TLE after puberty. Studies of individual families and identical twins suggested that development of TLE was more likely after prolonged FS (Maher & McLachlan, 1995; Jackson et al., 1998). Definitive evidence that complex FS can cause HS came from a study of 27 infants who received magnetic resonance imaging (MRI) scans after complex FS (VanLandingham et al., 1998). Some infants with prolonged and focal complex FS had acute hippocampal swelling and delayed development of HS on one side. However, there is also evidence that subtle preexisting hippocampal malformation may facilitate FS and contribute to the development of HS and TLE (Fernandez et al., 1998; Depondt et al., 2002). To complicate matters, studies of familial mesial TLE have demonstrated that HS may be present in the absence of FS and even in family members who never had FS or TLE (Kobayashi et al., 2002, 2003). It seemed that one or more genes predisposed both to the clinical features of mesial TLE and to the development of HS. Therefore, FS, TLE, and HS can all exist independently as well as overlap with each other. A genetic component has long been recognized for FS, and the concordance is high in monozygotic twins (Berkovic et al., 1994). There are also genetic epilepsies that include antecedent FS and others that do not. Patients with epilepsy and antecedent FS were more likely to have a family history of FS than patients without antecedent FS, whereas the two groups did not differ with respect to family history of epilepsy (Abou-Khalil et al., 2007), suggesting that the antecedent FS may have a genetic component that is distinct from the epilepsy. There have been a number of major gene loci identified for familial febrile convulsions (Wallace et al., 1996; Johnson et al., 1998; Peiffer et al., 1999; Nabbout et al., 2002; Hedera et al., 2006). Some of these families had pure FS, whereas others included epilepsy. A digenic inheritance was suggested in some families with FS and epilepsy (Baulac et al., 2001; Nabbout et al., 2007). A very notable syndrome with FS is generalized epilepsy with FS plus (GEFS+). In this autosomal dominant syndrome, there is a heterogeneous clinical phenotype that could include FS, FS continuing beyond age 6 or intermingled with afebrile tonic–clonic seizures, as well as other seizure types (Singh et al., 1999). TLE is rarely a phenotype of GEFS+ (Abou-Khalil et al., 2001; Scheffer et al., 2007). In conclusion, most children with simple FS and the majority of those with complex FS do not develop epilepsy. However, for those who develop epilepsy, FS often are not just a nonspecific marker of a lowered seizure threshold, as specific epilepsies are characterized by antecedent FS. Febrile status epilepticus, particularly with focal features, may injure the hippocampus and produce HS in some patients, but a preexisting hippocampal malformation and preexisting genetic profile may predispose to FS and HS. Some genetic mutations are associated with FS only and others with both FS and subsequent epilepsy. Progress in the genetics of FS and associated epileptic syndromes may help identify children with FS at risk of developing epilepsy. The author has no conflicts of interest to disclose." @default.
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• W1978586780 title "The relationship between febrile seizures and epilepsy" @default.
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