Key result
SCN1A mutations occur in ~83% of Dravet syndrome cases but not in other severe epilepsies.
Why the study?
The genetic mutations underlying Dravet syndrome in Chinese children, including SCN1A-negative cases, were not fully characterized.
Cross-Sectional (n=100)
Yes
Absolute Event Rate: 83% vs 0%
A high prevalence of SCN1A mutations was found in Chinese children with Dravet syndrome, with specific mutation types linked to more severe intellectual disability.
May support SCN1A testing in suspected Dravet syndrome; extends prevalence data to Chinese children but leaves broader adoption open.
BACKGROUND: Dravet syndrome is a severe form of epilepsy. Majority of patients have a mutation in SCN1A gene, which encodes a voltage-gated sodium channel. A recent study has demonstrated that 16% of SCN1A-negative patients have a mutation in PCDH19, the gene encoding protocadherin-19. Mutations in other genes account for only a very small proportion of families. TSPYL4 is a novel candidate gene within the locus 6q16.3-q22.31 identified by linkage study. OBJECTIVE: The present study examined the mutations in epileptic Chinese children with emphasis on Dravet syndrome. METHODS: A hundred children with severe epilepsy were divided into Dravet syndrome and non-Dravet syndrome groups and screened for SCN1A mutations by direct sequencing. SCN1A-negative Dravet syndrome patients and patients with phenotypes resembling Dravet syndrome were checked for PCDH19 and TSPYL4 mutations. RESULTS: Eighteen patients (9 males, 9 females) were diagnosed to have Dravet syndrome. Among them, 83% (15/18) had SCN1A mutations including truncating (7), splice site (2) and missense mutations (6). The truncating/splice site mutations were associated with moderate to severe degree of intellectual disability (p<0.05). During the progression of disease, 73% (11/15) had features fitting into the diagnostic criteria of autism spectrum disorder and 53% (8/15) had history of vaccination-induced seizures. A novel PCDH19 p.D377N mutation was identified in one SCN1A-negative female patient with Dravet syndrome and a known PCDH19 p.N340S mutation in a female non-Dravet syndrome patient. The former also inherited a TSPYL4 p.G60R variant. CONCLUSION: A high percentage of SCN1A mutations was identified in our Chinese cohort of Dravet syndrome patients but none in the rest of patients. We demonstrated that truncating/splice site mutations were linked to moderate to severe intellectual disability in these patients. A de novo PCDH19 missense mutation together with an inherited TSPYL4 missense variant were identified in a patient with Dravet syndrome.
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Kwong et al. (2012) conducted a cross-sectional in Dravet syndrome and severe epilepsy (n=100). SCN1A, PCDH19, and TSPYL4 mutations vs. Patients without mutations / non-Dravet syndrome patients was evaluated on Frequency of SCN1A mutations. SCN1A mutations were identified in 83% of Chinese children with Dravet syndrome, whereas no SCN1A mutations were found in children with other severe epilepsies.
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