ライフサイエンスコーパス: absence seizure

1 l role for GABAB antagonists in treatment of absence seizures.

2 ctively suppresses MLT bursting and prevents absence seizures.

3 n whether SWD/immobility is a valid model of absence seizures.

4 indle oscillations and primarily generalized absence seizures.

5 eurons of the intralaminar nuclei to provoke absence seizures.

6 c resonance imaging characteristics of human absence seizures.

7 the DLSC exerts anti-seizure effects against absence seizures.

8 scillatory activity of the TC network during absence seizures.

9 thalamus (MLT) neurons effectively prevents absence seizures.

10 lated to spike-wave discharges (SWDs) during absence seizures.

11 chronized bursting during the ictal phase of absence seizures.

12 ng thalamocortical phasic firing would treat absence seizures.

13 tico-thalamo-cortical rhythms that result in absence seizures.

14 rcuits are traditionally thought to underlie absence seizures.

15 ctal cerebral perfusion in IGE patients with absence seizures.

16 s oscillations that manifest behaviorally as absence seizures.

17 otective brakes might be restored to prevent absence seizures.

18 d to epileptic activity in IGE patients with absence seizures.

19 uts to the cortex advance the termination of absence seizures.

20 the BG are essential for the maintenance of absence seizures.

21 uts to the cortex advance the termination of absence seizures.

22 changes and altered consciousness than other absence seizures.

23 thalamic nuclei, is effective in controlling absence seizures.

24 nd-wave discharges (GSWDs) characteristic of absence seizures.

25 orticothalamic networks to the generation of absence seizures.

26 nance imaging that have been associated with absence seizures.

27 jects (44 seizures) with untreated childhood absence seizures.

28 mma-butyrolacetone-treated mice experiencing absence seizures.

29 c strain may contribute to the generation of absence seizures.

30 spike-wave discharges (SWDs) associated with absence seizures.

31 iverse genetic and pharmacological models of absence seizures.

32 in the network hypersynchrony that underlies absence seizures.

33 ferent behavioral states, and predisposes to absence seizures.

34 s at similar frequencies, as observed during absence seizures.

35 eneration of thalamocortical SWs in atypical absence seizures.

36 rious thalamocortical oscillations including absence seizures.

37 alized tonic-clonic, and in 30% of patients, absence seizures.

38 Absence seizures (3-4 Hz) and sleep spindles (6-14 Hz) o

39 at SWD/immobility in rats does not represent absence seizures, although they appear to have many simi

40 A total of 21 IGE patients with absence seizures and 24 healthy control subjects were en

41 properties of GHB, and its ability to elicit absence seizures and an increase in sleep stages 3 and 4

42 y contribute to the behavioral phenotypes of absence seizures and ataxia seen in stargazer mice and i

43 These mice exhibit absence seizures and deficiencies in motor control and o

44 adigm-shifting views of our understanding of absence seizures and demand careful choice of initial mo

45 encing nigrotegmental terminals reduced only absence seizures and exacerbated seizures evoked by PTZ.

46 halamus plays a crucial role in experimental absence seizures and has been attributed, on the basis o

47 hyperexcitability and effectively mitigates absence seizures and locomotor deficits in mice.

48 ch likely contributes to the pathogenesis of absence seizures and paroxysmal dyskinesia.

49 nterpretation of these results is that human absence seizures and perhaps CPSs could permit a far gre

50 Females with both absence seizures and stress-related precipitants constit

51 nd widespread cortical networks during human absence seizures and suggest reductions in cortical bloo

52 novel therapeutic targets for treating both absence seizures and their comorbidities.

53 If SWDs model mild absence seizures and/or complex partial seizures in huma

54 p microsatellites, and only individuals with absence seizures and/or electroencephalogram 3-4-Hz spik

55 cortical phasic firing state is required for absence seizures, and switching to tonic firing rapidly

56 s in thalamocortical network activity during absence seizures, and their potential therapeutic benefi

57 Absence seizures are 5-10 s episodes of impaired conscio

58 Absence seizures are a leading form of childhood epileps

59 Absence seizures are brief episodes of impaired consciou

60 Absence seizures are characterized by brief interruption

61 Absence seizures are characterized by brief interruption

62 Absence seizures are characterized by brief periods of u

63 Absence seizures are characterized by spike-and-wave dis

64 Slow-wave sleep as well as generalized absence seizures are characterized by the occurrence of

65 del of absence epilepsy, we demonstrate that absence seizures are highly sensitive to arterial carbon

66 ies, however, show that 30% of children with absence seizures are pharmaco-resistant and 60% are affe

67 nisms responsible for generalized spike-wave absence seizures are poorly understood.

68 wave discharges (SWD), the hallmark of human absence seizures, are generated in thalamocortical netwo

69 more, within the corticothalamic loop, where absence seizures arise, CACNG4 expression is restricted

70 nal amplitude and frequency in children with absence seizures can be detected in specific cortical ne

71 hat activity-dependent myelination driven by absence seizures contributes to epilepsy progression; ma

72 rcuits are traditionally thought to underlie absence seizures, converging experimental evidence suppo

73 aves similar to those occurring during human absence seizure discharges.

74 e, pharmacologically induced thalamocortical absence seizures displayed a reduction in length and pow

75 inctive phenotype including ataxia, frequent absence seizure episodes, and head elevation.

76 partial seizures evoked from the forebrain, absence seizures evoked by gamma-butyrolactone (GBL), an

77 t, open-loop optogenetic silencing increased absence seizure expression and facilitated SE onset but

78 attenuates burst firing, leading to reduced absence seizure frequency and increased vigilance.

79 imultaneous EEG-fMRI in 88 typical childhood absence seizures from nine pediatric patients.

80 able hyperventilation to powerfully activate absence seizure-generating circuits remain entirely unkn

81 ate intellectual disability, frequently with absence seizures); Group 5, unclassifiable epilepsy (n =

82 larities to spike-wave-discharges (SWDs) and absence seizures, have been proposed to represent noncon

83 Absence seizures in children and teenagers are generally

84 e generation of paroxysmal events resembling absence seizures in children.

85 magnetic resonance imaging (fMRI) changes in absence seizures in relation to EEG and behavior is not

86 res in another form of epilepsy, generalized absence seizures, in both clinical and experimental sett

87 essential role for basal ganglia networks in absence seizures, in particular the ictal increase in fi

88 (generalized tonic-clonic, complex partial, absence seizures), including refractory (or pharmacoresi

89 del confirmed that CBZ treatment exacerbates absence seizures, increasing both seizure frequency and

90 T-type calcium channel, are associated with absence seizures, intellectual disability, and schizophr

91 en reported, and the presence of HFOs during absence seizures is a novel finding.

92 Impaired consciousness in absence seizures is related to the intensity of physiolo

93 Generalized epilepsy with absence seizures is the main epilepsy phenotype of loss-

94 insic firing patterns of neurons involved in absence seizures, it was suggested that these SNPs might

95 hypothesized that, if SWD/immobility models absence seizures, it would not exist in wild-caught rats

96 state might exist at the initiation of some absence seizures leading them to have more severe physio

97 n created by selectively inbreeding rats for absence seizure-like events with similar electrical and

98 e tentatively, two newly discovered loci for absence seizures on chromosome 5 (lod scores 3.8/2.8 and

99 ral interruption classically associated with absence seizures or CPSs in humans.

100 t always associated with classically defined absence seizures or CPSs.

101 only, this was associated with experiencing absence seizures (OR = 2.0, p < 0.001).

102 catamenial seizures (OR = 14.7, p = 0.001), absence seizures (OR = 6.0, p < 0.001) and stress-precip

103 that display a robust spontaneous spike-wave absence seizure phenotype accompanied by behavioral arre

104 d or even suppressed by the occurrence of an absence seizure, potentially contributing to decreased r

105 nd genetic mechanisms underlying generalized absence seizures, primarily through the study of animal

106 ng in ataxia, motor seizures, and behavioral absence seizures resembling petit mal epilepsy in humans

107 thalamocortical neurons launched and aborted absence seizures, respectively.

108 Absence seizures result from 3 to 5 Hz generalized thala

109 Stargazer (stg) mice have prominent absence seizures resulting from a mutant form of the AMP

110 Absence seizures significantly predicted drug resistance

111 in Purkinje cells and the separation of the absence seizures (spike/wave type discharges) from the p

112 and resistant to GABA(B) receptor-dependent absence seizures, suggesting roles for alpha(1g) and rel

113 mouse appeared normal with no ataxic gait or absence seizures, suggesting that other members of the g

114 The stargazer mouse mutation causes absence seizures that are more prolonged and frequent th

115 arently common cellular pathology in typical absence seizures that may have epileptogenic importance

116 tes from a well-established genetic model of absence seizures, the genetic absence epilepsy rats from

117 ver, in some children and animal models with absence seizures, the ictal increase in thalamic inhibit

118 ecause SWDs have features similar to genetic absence seizures, these results challenge the hypothesis

119 ated beta 3 subunit protein could thus cause absence seizures through a gain in glycosylation of muta

120 uncover a mechanism by which CBZ exacerbates absence seizures through selective inhibition of RT neur

121 observed bidirectional communications during absence seizures through top-down cortical excitation an

122 le severity of behavioural deficits from one absence seizure to the next are not well understood.

123 regulate thalamocortical network activity in absence seizures, to investigate whether CBZ alters thei

124 k in two models of generalized epilepsy with absence seizures (Wag/Rij rats and Scn8a(+/mut) mice), e

125 Absence seizures were more common in family members of C

126 Absence seizures were observed in combination with the s

127 Two unrelated mouse models of generalized absence seizures were used: the natural mutant tottering

128 epresentative of slow-wave sleep, as well as absence seizures, were demonstrated to cease spontaneous

129 and long-lasting sequence of fMRI changes in absence seizures, which are not detectable by convention

130 The cellular mechanisms underlying typical absence seizures, which characterize various idiopathic

131 ctivity-dependent myelination resulting from absence seizures, which manifest as frequent behavioral

132 and electroencephalography (EEG) changes in absence seizures with impaired task performance compared

133 The inbred mouse strain C3H/HeJ is prone to absence seizures, with a major susceptibility locus, spk

134 phenotypes, featuring early-onset ataxia and absence seizure without significant alterations in the b