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1 lamotrigine in children with newly diagnosed childhood absence epilepsy.
2 fective than lamotrigine in the treatment of childhood absence epilepsy.
3 .2 channels were discovered in patients with childhood absence epilepsy.
4 nit mutation, G32R, has been associated with childhood absence epilepsy.
7 le myoclonic epilepsy, 10 patients each with childhood absence epilepsy and juvenile absence epilepsy
8 s in the I-II loop (the region in which most childhood absence epilepsy-associated mutations are foun
10 than 30 mutations apparently predisposing to childhood absence epilepsy (CAE) and other idiopathic ge
14 e that may contribute to the pathogenesis of childhood absence epilepsy (CAE), but the molecular basi
15 ed with genetic epilepsy syndromes including childhood absence epilepsy (CAE), juvenile myoclonic epi
19 our groups: (i) classic JME (72%), (ii) CAE (childhood absence epilepsy) evolving to JME (18%), (iii)
20 clonic epilepsy, one out of 10 patients with childhood absence epilepsy, four out of 10 patients with
21 d with genetic epilepsy syndromes, including childhood absence epilepsy, generalized epilepsy with fe
22 ed with several epilepsy syndromes including childhood absence epilepsy, generalized tonic clonic sei
24 autosomal dominant mutation associated with childhood absence epilepsy that generates a PTC in exon
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