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1 lonic encephalopathy, Ohtahara syndrome, and infantile spasms.
2 gnature in patients with a recent history of infantile spasms.
3 the hypsarrhythmia pattern characteristic of infantile spasms.
4 c-clonic, complex partial, focal clonic, and infantile spasms.
5 in early infancy and subsequently developed infantile spasms.
6 he treatment of TSC brain disease, including infantile spasms.
7 er cortical layers and a positive history of infantile spasms.
8 olone and tetracosactide in the treatment of infantile spasms.
9 n the first 3 years of life and a history of infantile spasms.
10 These patients did not have a history of infantile spasms.
11 base enrolling infants with new diagnosis of infantile spasms.
13 lled infants who had a clinical diagnosis of infantile spasms and a hypsarrhythmic (or similar) EEG n
14 Our findings indicate that patients with infantile spasms and bitemporal glucose hypometabolism o
16 A tract (Arx(E)), a mutation associated with infantile spasms and intellectual disabilities in humans
20 rase (GABA-AT) inactivator, is used to treat infantile spasms and refractory complex partial seizures
21 frequency of ARX mutations in patients with infantile spasms and related disorders, our data unveil
22 , loss of communication and motor skills and infantile spasms and seizures in predominantly females.
24 ton disease, adrenocorticotropic hormone for infantile spasms, and enzyme replacement therapy with al
25 ly and electroencephalographically resembles infantile spasms, and show evolution through development
28 ilepsy, with some characteristics resembling infantile spasms, caused by mutations in a known infanti
31 nt screening of 47 patients with unexplained infantile spasms did not reveal additional de novo mutat
32 troencephalogram results correspond to human infantile spasms: electrodecrement or afterdischarges we
33 ocal cortical abnormalities in patients with infantile spasms even when the computed tomographic (CT)
35 , our new model correlates well with current infantile spasm hypotheses and opens an opportunity for
38 hould be considered as initial treatment for infantile spasms, including those with impaired developm
39 bility, cataracts, severe epilepsy including infantile spasms, irritability, failure to thrive, and s
45 erhaps even as first-line therapy, including infantile spasms, myoclonic-astatic epilepsy (Doose synd
46 al 5'-phosphate (n = 6); (ii) a patient with infantile spasms (onset 5 months) responsive to pyridoxa
47 is necessary for the GABAB R agonist-induced infantile spasms phenotype in the Ts mouse and may repre
48 in Ts brain upon the GABAB R agonist-induced infantile spasms phenotype in the Ts mouse model of DS.
51 syndrome (DS) is exquisitely sensitive to an infantile spasms phenotype induced by gamma-aminobutyric
58 12 consanguineous families of children with infantile spasms were analysed for linkage to the phosph
60 ildren with ISOD; however, to our knowledge, infantile spasms with a corresponding hypsarrhythmia pat
61 hat presented with cranial asymmetry, severe infantile spasms with hypsarrhythmia, and dysproportiona
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