speech impairment
Here we demonstrate that about 20% of cases of LKS, CSWSS and electroclinically atypical rolandic epilepsy often associated with speech impairment can have a genetic origin sustained by de novo or inherited mutations in the GRIN2A gene (encoding the N-methyl-D-aspartate (NMDA) glutamate receptor ?2 subunit, GluN2A).
Here we demonstrate that about 20% of cases of <span class="gene" id="23933820-4-47-50">LKS</span>, CSWSS and electroclinically atypical rolandic epilepsy often associated with <span class="disease" id="23933820-4-129-146">speech impairment</span> can have a genetic origin sustained by de novo or inherited mutations in the <span class="gene" id="23933820-4-224-230">GRIN2A</span> gene (encoding the N-methyl-D-aspartate (NMDA) glutamate receptor &alpha;2 subunit, <span class="gene" id="23933820-4-309-315">GluN2A</span>).