ライフサイエンスコーパス: childhood absence epilepsy

1 nit mutation, G32R, has been associated with childhood absence epilepsy.

2 lamotrigine in children with newly diagnosed childhood absence epilepsy.

3 fective than lamotrigine in the treatment of childhood absence epilepsy.

4 .2 channels were discovered in patients with childhood absence epilepsy.

5 s relatively mild epilepsy syndromes such as childhood absence epilepsy.

6 was identified in an Australian family with childhood absence epilepsy and febrile seizures.

7 autosomal dominant mutation associated with childhood absence epilepsy and febrile seizures.

8 le myoclonic epilepsy, 10 patients each with childhood absence epilepsy and juvenile absence epilepsy

9 s in the I-II loop (the region in which most childhood absence epilepsy-associated mutations are foun

10 nd lifelong neurological deficits, including childhood absence epilepsy, ataxia and dystonia.

11 orders, including myoclonic atonic epilepsy, childhood absence epilepsy, autism, and intellectual dis

12 Childhood absence epilepsy (CAE) accounts for 10% to 12%

13 than 30 mutations apparently predisposing to childhood absence epilepsy (CAE) and other idiopathic ge

14 Childhood absence epilepsy (CAE) is the most common paed

15 polymorphisms (SNPs) that were found only in childhood absence epilepsy (CAE) patients.

16 Childhood absence epilepsy (CAE), a common form of idiop

17 e that may contribute to the pathogenesis of childhood absence epilepsy (CAE), but the molecular basi

18 ed with genetic epilepsy syndromes including childhood absence epilepsy (CAE), juvenile myoclonic epi

19 Moreover, human childhood absence epilepsy (CAE)-linked hCaV3.2(C456S) m

20 h differential short-term seizure outcome in childhood absence epilepsy (CAE).

21 tion Cacna1h gene variants reported in human childhood absence epilepsy cases.

22 ABSTRACT: In childhood absence epilepsy, cortical seizures are brief

23 our groups: (i) classic JME (72%), (ii) CAE (childhood absence epilepsy) evolving to JME (18%), (iii)

24 clonic epilepsy, one out of 10 patients with childhood absence epilepsy, four out of 10 patients with

25 d with genetic epilepsy syndromes, including childhood absence epilepsy, generalized epilepsy with fe

26 ed with several epilepsy syndromes including childhood absence epilepsy, generalized tonic clonic sei

27 which encodes Ca(v)3.2) are associated with childhood absence epilepsy in a Chinese population.

28 These four GGE syndromes are childhood absence epilepsy, juvenile absence epilepsy, j

29 f thalamic reticular nucleus-enriched, human childhood absence epilepsy-linked gene Cacna1h in iKOp/q

30 autosomal dominant mutation associated with childhood absence epilepsy that generates a PTC in exon

31 Childhood absence epilepsy, the most common pediatric ep