Key result
Homozygous or compound heterozygous SCN1A variants cause autosomal recessive epilepsies with phenotypes ranging from GEFS+ to Dravet syndrome, similar to dominant heterozygous variants.
Why the study?
Dominant pathogenic SCN1A variants cause various neurodevelopmental disorders, but few cases with homozygous or compound heterozygous variants have been published.
Case Report (n=12)
This study expands the genetic spectrum of SCN1A-related epilepsies by highlighting that certain hypomorphic variants can cause disease through an autosomal recessive inheritance pattern.
Answers are grounded in this paper and cite their sources.
Supports recessive SCN1A testing in unexplained epilepsies; leaves open validation in larger cohorts.
Dominant pathogenic variations in the SCN1A gene are associated with several neuro developmental disorders with or without epilepsy, including Dravet syndrome (DS). Conversely, there are few published cases with homozygous or compound heterozygous variations in the SCN1A gene. Here, we describe two siblings from a consanguineous pedigree with epilepsy phenotype compatible with genetic epilepsy with febrile seizures plus (GEFS+) associated with the homozygous likely pathogenic variant (NM_001165963.1): c.4513A > C (p.Lys1505Gln). Clinical and genetic data were compared to those of other 10 previously published patients with epilepsy and variants in compound heterozygosity or homozygosity in the SCN1A gene. Most patients (11/12) had missense variants. Patients in whom the variants were located at the cytoplasmic or the extracellular domains frequently presented a less severe phenotype than those in whom they are located at the pore-forming domains. Five of the patients (41.7%) meet clinical criteria for Dravet syndrome (DS), one of them associated acute encephalopathy. Other five patients (41.7%) had a phenotype of epilepsy with febrile seizures plus familial origin, while the two remaining (17%) presented focal epileptic seizures. SCN1A-related epilepsies present in most cases an autosomal dominant inheritance; however, there is growing evidence that some genetic variants only manifest clinical symptoms when they are present in both alleles, following an autosomal recessive inheritance.
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Hernández et al. (2021) conducted a case report in SCN1A-related epilepsy (n=12). Homozygous or compound heterozygous SCN1A variants was evaluated on Clinical phenotype and genotype-phenotype correlation. Homozygous or compound heterozygous SCN1A variants cause autosomal recessive epilepsies with phenotypes ranging from GEFS+ to Dravet syndrome, similar to dominant heterozygous variants.
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