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  1. Siti Aishah Abdul Wahab, Yusnita Yakob, Khoo,Teik-Beng, Sangita Dharshini Terumalay, Vigneswari Ganesan, Teh,Chee-Ming, et al.
    Neurology Asia, 2017;22(2):99-111.
    MyJurnal
    Background & Objective: SCN1A gene which encodes for sodium channel alpha 1 subunit has been
    found to be the most common mutated gene in patients with epilepsy. This study aims to characterize the
    SCN1A mutations as well as to describe genotype and phenotype association in children with SCN1Arelated
    infantile-onset epileptic encephalopathies in Malaysia.

    Methods: Children with infantile-onset
    epileptic encephalopathy mostly suspected to have Dravet syndrome who had mutational analysis for
    SCN1A gene from hospitals all over Malaysia were included in the study. Their epilepsy syndrome
    diagnosis was classified into severe myoclonic epilepsy in infancy and its variants. Polymerase chain
    reaction and bidirectional sequencing were used to identify SCN1A mutations.

    Results: A total of 38
    children with heterozygous mutations were analysed, 22 (57.9%) of which were novel mutations.
    Truncated mutations were the most common mutation type (19, 50%). Other mutation types were
    missense mutations (14, 36.8%), splice site mutations (4, 10.5%) and in-frame deletion (1, 2.6%). The
    mean age of seizure onset was 4.7 months. Seizure following vaccination was observed in 26.3% of
    the children. All of them had drug resistant epilepsy. There was no significant association between
    the type of mutation with the syndromic diagnosis, age of seizure onset, tendency of the seizures to
    cluster or having status epilepticus, mean age when developmental delay was observed and response
    to various antiepileptic drugs.

    Conclusion: This study expands the spectrum of SCN1A mutations and proves the importance of
    SCN1A gene testing in diagnosing infantile-onset epileptic encephalopathies patients. Although, our
    study does not support any clinically meaningful genotype-phenotype association for SCN1A-related
    infantile-onset epileptic encephalopathies, the clinical characteristics of our cohort are similar to those
    that have been described in previous studies.
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