ライフサイエンスコーパス: epileptiform discharge

1 ossy fiber boutons, reduced the magnitude of epileptiform discharge.

2 new in vitro synaptic-independent model for epileptiform discharge.

3 itute a trigger for pathological synchronous epileptiform discharge.

4 he emergence of network activities including epileptiform discharges.

5 ed slowing to bilateral periodic lateralized epileptiform discharges.

6 activity that precedes and is necessary for epileptiform discharges.

7 to the occurrence of spontaneous, recurrent epileptiform discharges.

8 of seconds to minutes as the consequence of epileptiform discharges.

9 2+) conditions induced unremitting recurrent epileptiform discharges.

10 the mouse dorsal hippocampus rapidly caused epileptiform discharges.

11 ruitment of group I mGluR-mediated prolonged epileptiform discharges.

12 uit deficient in rhythmogenesis and prone to epileptiform discharges.

13 Cre; Clock(flox/flox) mouse have spontaneous epileptiform discharges.

14 ity with frequent generalized and multifocal epileptiform discharges.

15 ning (BBBD) leads to the occurrence of acute epileptiform discharges.

16 ield potential amplitudes and produces focal epileptiform discharges.

17 scale events were associated with interictal epileptiform discharges.

18 sociated with group I mGluR agonist-elicited epileptiform discharges.

19 orms normal neuronal activity into prolonged epileptiform discharges.

20 ls were preceded by spontaneous granule cell epileptiform discharges.

21 ictal semiology in localizing the source of epileptiform discharges.

22 background slowing and generalized and focal epileptiform discharges.

23 ); (3) prior seizure (1 point); (4) sporadic epileptiform discharges (1 point); (5) frequency greater

24 d approximately 3.5 s after a single typical epileptiform discharge (activation image) and in the abs

25 apses, effective in eliciting mGluR-mediated epileptiform discharges, also induced long-lasting I(mGl

26 In these patients, interictal epileptiform discharges, also termed spikes, are seen ro

27 stimulation for 3 hours evoked granule cell epileptiform discharges and convulsive status epilepticu

28 re present and associated with temporal lobe epileptiform discharges and early-onset, persistent spas

29 Several models that develop epileptiform discharges and epilepsy have been associate

30 intra- and inter-hemispheric propagation of epileptiform discharges and highlight possible neurophys

31 relationship to the occurrence of interictal epileptiform discharges and may vary in relation to the

32 ith a cerebral infarct developed spontaneous epileptiform discharges and recurrent seizures (100%); i

33 stimulation of the fornix reduces interictal epileptiform discharges and seizures in patients with in

34 equency stimulation is tolerable and reduces epileptiform discharges and seizures in patients with in

35 expression of convulsive and non-convulsive epileptiform discharges and seizures.

36 long been recognized to influence interictal epileptiform discharges and seizures.

37 inase inhibitor, suppressed the DHPG-induced epileptiform discharges and the ERK1/2 activation in the

38 lved in generation of the wave of spike-wave epileptiform discharges, are mediated by the GABAB recep

39 nt patterns of neuronal circuit activity and epileptiform discharges at the network level.

40 tisol was positively related to incidence of epileptiform discharges (beta = 0.26, P = 0.002) in peop

41 ta receptor antagonist, were investigated on epileptiform discharges, brain inflammation, and BBB dam

42 mmonly associated with widespread interictal epileptiform discharges but not with locally generated '

43 sm of NMDA receptors reduced the duration of epileptiform discharge, but increased the amplitude of p

44 uction of long-lasting spontaneous recurrent epileptiform discharges, but not the Mg2+-induced spike

45 lso prevented the induction of the prolonged epileptiform discharges by DHPG.

46 used with Mg(2+)-free medium, which leads to epileptiform discharges caused by a relief of voltage-de

47 Experimental conditions that shortened the epileptiform discharge correlated with more rapid intrac

48 activity was increased and the frequency of epileptiform discharges could be greatly reduced by inhi

49 relationship between cortisol levels and the epileptiform discharges distinguishing persons with from

50 EG of Emx-Cre; Clock(flox/flox) mice reveals epileptiform discharges during sleep and also seizures a

51 In two patients, local interictal epileptiform discharge frequencies correlated precisely

52 in vitro SE model and suggest that prolonged epileptiform discharges give rise to abnormal sustained

53 ars, 6 males) with known frequent interictal epileptiform discharges had an [(18)F]GE-179 PET scan, i

54 pectomy (ATL), but the utility of interictal epileptiform discharge (IED) identification and its role

55 he seizure onset zone and surface interictal epileptiform discharges (IED).

56 Interictal epileptiform discharges (IEDs) identify epileptic brain

57 lation activity characteristic of interictal epileptiform discharges (IEDs) to more prolonged epochs

58 Interictal epileptiform discharges (IEDs) were identified on intra-

59 sociated with (i) isoelectricity or periodic epileptiform discharges; (ii) prolonged depression of sp

60 was a significant decrease in the number of epileptiform discharges immediately after (p = 0.01) and

61 Furthermore, mutant LGI1 promoted epileptiform discharge in vitro and kindling epileptogen

62 trode by measuring the magnetic signature of epileptiform discharges in a rat model of epilepsy.

63 ATPA also specifically activates epileptiform discharges in BLA slices in vitro via GluK1

64 24 hours, which evoked population spikes and epileptiform discharges in both dentate granule cells an

65 hold electrical stimulation is used to evoke epileptiform discharges in brain slices, a latent period

66 Here, we show that prolonged high-frequency epileptiform discharges in cultured hippocampal neurons

67 exin36 is not critical for the generation of epileptiform discharges in GABAergic networks and that t

68 endent kinase activity on the development of epileptiform discharges in hippocampal neurons in cultur

69 eptors (mGluRs) induces persistent prolonged epileptiform discharges in hippocampal slices via a prot

70 ng neurons manifested spontaneous, recurrent epileptiform discharges in neural networks, characterize

71 cortisol levels and incidence of interictal epileptiform discharges in people with stress-sensitive

72 by using voltage imaging techniques to study epileptiform discharges in rat piriform cortex slices.

73 an abnormally high resistance to generating epileptiform discharges in response to afferent stimulat

74 rhythmic single cell bursts and synchronized epileptiform discharges in the CA3 region of the hippoca

75 e spatial relationship to the maximum of the epileptiform discharges in the concurrent EEG.

76 The number of epileptiform discharges in the electroencephalogram and

77 is necessary for the induction of prolonged epileptiform discharges in the hippocampus.

78 reases cortical excitability, culminating in epileptiform discharges in vitro and spontaneous seizure

79 Moreover, the speed of propagation of epileptiform discharges in vivo and in vitro can vary ov

80 recordings in hAPP mice revealed spontaneous epileptiform discharges, indicating network hypersynchro

81 the effects of such repetitive activation on epileptiform discharges induced by 4-aminopyridine.

82 Conducting polymer electrodes recorded epileptiform discharges induced in mouse hippocampal pre

83 These results suggest that: (i) interictal epileptiform discharges may originate from a complex int

84 d not prevent the generation of DHPG-induced epileptiform discharges, nor did they suppress the activ

85 Epileptiform discharges not accompanied by obvious clini

86 activity including evidence of temporal lobe epileptiform discharges on EEG, the age to onset of seiz

87 GLUT-1+/- mice have epileptiform discharges on electroencephalography (EEG),

88 te analysis showed that localized interictal epileptiform discharges on scalp EEGs were associated wi

89 We measured the number of seconds of epileptiform discharges or seizure activity in every 10-

90 seizures (100%); in contrast, no spontaneous epileptiform discharges or seizures were detected with c

91 c currents with strikingly long duration and epileptiform discharge patterns, similar to waveforms ob

92 The conversion is long lasting in that epileptiform discharges persist after washout of the ind

93 Similar to group I mGluR-mediated prolonged epileptiform discharges, persistent I(mGluR(V)) was no l

94 e rats but had surprisingly little effect on epileptiform discharges produced by disinhibition of sli

95 ng process underlying the induction of these epileptiform discharges remains unknown.

96 tically released glutamate induced prolonged epileptiform discharges resulting from enhanced group I

97 ntorhinal cortical slices (HEC), spontaneous epileptiform discharges (SEDs) were induced using 0 Mg t

98 ion-related epilepsy and frequent interictal epileptiform discharges (spikes or spike wave).

99 exclusively connected to brief intervals at epileptiform discharges, strengthening the association b

100 brile, often focal seizure types, multifocal epileptiform discharges strongly activated by sleep, mil

101 scharges (also known as periodic lateralized epileptiform discharges), subjects with focal nonrhythmi

102 of the GABA(A) receptors transforms GDPs to epileptiform discharges suggesting dual, both excitatory

103 s, and were longer when preceded by periodic epileptiform discharges than by continuous delta (0.5-4.

104 nges identifying prolonged bursts of complex epileptiform discharges that became more prevalent 7 hr

105 wn of stx1b showed seizure-like behavior and epileptiform discharges that were highly sensitive to in

106 BDNF exposure led to spontaneous epileptiform discharges that were larger in amplitude an

107 Paired-pulse suppression and epileptiform discharge thresholds increased gradually af

108 odel of in vitro SE that produces continuous epileptiform discharges to study spatial and dynamic cha

109 We test this in the 0 Mg(2+) model of epileptiform discharges using slices from healthy and ch

110 tors of scalp EEG events, such as interictal epileptiform discharges, using a biological measurement

111 Induction of DHPG-mediated epileptiform discharges was also suppressed by 4-amino-5

112 ion with Mg(2+)-free ACSF, an enhancement of epileptiform discharges was found in the EC of slices fr

113 ion of the group I mGluR-mediated, prolonged epileptiform discharges was inhibited in preparations th

114 The relationship between cortisol and epileptiform discharges was positively associated only w

115 s Blue we found that, at time of BBB-induced epileptiform discharges, WBCs populated the perivascular

116 In both cases, prolonged epileptiform discharges were blocked by group I mGluR an

117 ticipants (54% female, median age 24 years), epileptiform discharges were detected on 14% of SBS2 and

118 Interictal epileptiform discharges were determined in the same time

119 Spontaneous epileptiform discharges were induced in vitro in the CA3

120 Spontaneous epileptiform discharges were initially lateralized to ip

121 In vitro, spontaneous epileptiform discharges were not observed in hippocampal

122 Increased neuronal excitability and frank epileptiform discharges were observed after a significan

123 In addition, interictal epileptiform discharges were recorded in 15 (88.2%) of t

124 Epileptiform discharges were recorded in layer V-VI pyra

125 Granule cell epileptiform discharges were recruited during 11% of spo

126 Between 21 and 50 epileptiform discharges were sampled in each experiment.

127 observed in 0 Mg pre-treated slices while no epileptiform discharges were seen in control slices.

128 ir implications in pharmacologically-induced epileptiform discharges were studied in the same slices.

129 rs and tetrodotoxin (blockers), DHPG-induced epileptiform discharges were suppressed, whereas ERK1/2

130 glutamatergic neurons resulted in recurrent epileptiform discharge, which provoked cognitive dysfunc

131 94.8% specificity (95% CI 90.0%, 97.7%) for epileptiform discharges with positive and negative predi

132 sure, synaptic stimulation induced prolonged epileptiform discharges with properties similar to those