ライフサイエンスコーパス: absence seizure

1 ng thalamocortical phasic firing would treat absence seizures.

2 rcuits are traditionally thought to underlie absence seizures.

3 ctal cerebral perfusion in IGE patients with absence seizures.

4 s oscillations that manifest behaviorally as absence seizures.

5 otective brakes might be restored to prevent absence seizures.

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

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

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

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

10 changes and altered consciousness than other absence seizures.

11 thalamic nuclei, is effective in controlling absence seizures.

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

13 orticothalamic networks to the generation of absence seizures.

14 nance imaging that have been associated with absence seizures.

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

16 mma-butyrolacetone-treated mice experiencing absence seizures.

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

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

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

20 iverse genetic and pharmacological models of absence seizures.

21 in the network hypersynchrony that underlies absence seizures.

22 ferent behavioral states, and predisposes to absence seizures.

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

24 eneration of thalamocortical SWs in atypical absence seizures.

25 rious thalamocortical oscillations including absence seizures.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 Absence seizures are a leading form of childhood epileps

42 Absence seizures are characterized by brief interruption

43 Absence seizures are characterized by brief interruption

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 thalamocortical neurons launched and aborted absence seizures, respectively.

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

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

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

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

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

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

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

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

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

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

78 Absence seizures were more common in family members of C

79 Absence seizures were observed in combination with the s

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

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

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

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

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

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

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