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1 abnormalities, recurrent fever episodes, and infantile spasms .
2 base enrolling infants with new diagnosis of infantile spasms.
3 lonic encephalopathy, Ohtahara syndrome, and infantile spasms.
4 gnature in patients with a recent history of infantile spasms.
5 the hypsarrhythmia pattern characteristic of infantile spasms.
6 c-clonic, complex partial, focal clonic, and infantile spasms.
7  in early infancy and subsequently developed infantile spasms.
8 he treatment of TSC brain disease, including infantile spasms.
9 er cortical layers and a positive history of infantile spasms.
10 olone and tetracosactide in the treatment of infantile spasms.
11 n the first 3 years of life and a history of infantile spasms.
12     These patients did not have a history of infantile spasms.
13 rticosteroids for treating relapses of MS or infantile spasms.
14 h later time to onset and lower incidence of infantile spasms.
15 late key symptoms of the disorder, including infantile spasms.
16 et inclusion criteria; of those, 11 involved infantile spasms, 10 involved multiple sclerosis (MS), 1
17                         For the treatment of infantile spasms, 8 controlled studies were identified (
18                                              Infantile spasms (a catastrophic epileptic syndrome of c
19 -of-function (LoF) patients typically having infantile spasms after 6 months of age.
20 severe neurodevelopmental disorder marked by infantile spasms, an early symptom that typically subsid
21 lled infants who had a clinical diagnosis of infantile spasms and a hypsarrhythmic (or similar) EEG n
22     Our findings indicate that patients with infantile spasms and bitemporal glucose hypometabolism o
23 iated with infant-onset developmental delay, infantile spasms and features of ASD.
24 ely to initially reduce seizure frequency in infantile spasms and focal seizures compared to other tr
25 irst case of a child with ISOD who developed infantile spasms and hyperekplexia.
26 A tract (Arx(E)), a mutation associated with infantile spasms and intellectual disabilities in humans
27 nderlying the pathogenesis of the associated infantile spasms and mental retardation.
28 been identified in a subset of patients with infantile spasms and mental retardation.
29 that p.Glu200Ala, previously associated with infantile spasms and microcephaly, is also pathogenic.
30 vidence was most robust for the treatment of infantile spasms and MS.
31  approved drug (Sabril) for the treatment of infantile spasms and refractory adult epilepsy.
32 rase (GABA-AT) inactivator, is used to treat infantile spasms and refractory complex partial seizures
33  frequency of ARX mutations in patients with infantile spasms and related disorders, our data unveil
34 cellular, and circuit disruptions that cause infantile spasms and seizures are largely unknown, but i
35 , loss of communication and motor skills and infantile spasms and seizures in predominantly females.
36 are associated with intellectual disability, infantile spasms and seizures.
37 es including hypsarrhythmia (associated with infantile spasms) and burst suppression.
38 ton disease, adrenocorticotropic hormone for infantile spasms, and enzyme replacement therapy with al
39 ly and electroencephalographically resembles infantile spasms, and show evolution through development
40                                              Infantile spasms are seizures associated with a severe e
41             Epileptic seizures, particularly infantile spasms, are often seen in infants with tuberou
42  in STXBP1 (n = 39) were more likely to have infantile spasms between 5 and 6 months followed by seiz
43 seizure types, with 90% cumulative onset for infantile spasms by 6 months and focal-onset seizures by
44 ilepsy, with some characteristics resembling infantile spasms, caused by mutations in a known infanti
45 lipoma-predominant TSC (cluster 1), TSC with infantile spasms (cluster 2), neuropsychiatric TSC (clus
46                  The prospective US National Infantile Spasms Consortium database includes children w
47                                 The National Infantile Spasms Consortium established a multicenter, p
48                                              Infantile spasms constitutes a severe infantile epilepsy
49 nt screening of 47 patients with unexplained infantile spasms did not reveal additional de novo mutat
50 troencephalogram results correspond to human infantile spasms: electrodecrement or afterdischarges we
51 ocal cortical abnormalities in patients with infantile spasms even when the computed tomographic (CT)
52 ntile spasms, caused by mutations in a known infantile spasms gene.
53 , our new model correlates well with current infantile spasm hypotheses and opens an opportunity for
54 cephalopathies in 58% of the cohort and with infantile spasms in 62%; 63% of developmental epileptic
55 ovel therapeutic target for the treatment of infantile spasms in DS.
56  an autism plus developmental syndrome after infantile spasms in others.
57 hould be considered as initial treatment for infantile spasms, including those with impaired developm
58 bility, cataracts, severe epilepsy including infantile spasms, irritability, failure to thrive, and s
59                                              Infantile spasms is a severe infantile seizure disorder
60                                              Infantile spasms (IS) and Lennox-Gastaut syndrome (LGS)
61                                              Infantile spasms (IS) is an early-onset epileptic enceph
62 her selection of treatment for children with infantile spasms (IS) varies by race/ethnicity.
63 thies (EEs) Lennox-Gastaut syndrome (LGS) or infantile spasms (IS).
64                                              Infantile spasms, mental retardation, autism, and dyston
65 erhaps even as first-line therapy, including infantile spasms, myoclonic-astatic epilepsy (Doose synd
66 al 5'-phosphate (n = 6); (ii) a patient with infantile spasms (onset 5 months) responsive to pyridoxa
67 sistant epilepsy (OR = 0.23, p = 0.022), and infantile spasms (OR = 0, p < 0.001).
68 preceding spasms, which was also observed in infantile spasm patients.
69     Comparisons were made to recordings from infantile spasm patients.
70 is necessary for the GABAB R agonist-induced infantile spasms phenotype in the Ts mouse and may repre
71 in Ts brain upon the GABAB R agonist-induced infantile spasms phenotype in the Ts mouse model of DS.
72 n-Q also rescued the GABAB R agonist-induced infantile spasms phenotype in Ts mutants.
73 is necessary for the GABAB R agonist-induced infantile spasms phenotype in Ts.
74 syndrome (DS) is exquisitely sensitive to an infantile spasms phenotype induced by gamma-aminobutyric
75  Ts mice rescued the GABAB R agonist-induced infantile spasms phenotype.
76 2 gene are associated with schizophrenia and infantile spasms, respectively.
77       Infants enrolled in the United Kingdom Infantile Spasms Study (UKISS) were randomly assigned ho
78                           The United Kingdom Infantile Spasms Study assessed these treatments in a mu
79                                              Infantile spasms syndrome (ISS) is a catastrophic pediat
80  is significantly more effective at stopping infantile spasms than hormonal therapy alone.
81  is significantly more effective at stopping infantile spasms than hormonal therapy alone.
82                                 Incidence of infantile spasms was lower and time to spasms after rand
83  12 consanguineous families of children with infantile spasms were analysed for linkage to the phosph
84                                              Infantile spasms, which comprise a severe infantile seiz
85 ildren with ISOD; however, to our knowledge, infantile spasms with a corresponding hypsarrhythmia pat
86 hat presented with cranial asymmetry, severe infantile spasms with hypsarrhythmia, and dysproportiona
87 Lennox-Gastaut syndrome, Dravet syndrome and infantile spasms with intellectual disability as well as