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 ital was effective at reducing or preventing epileptiform discharges.

5 ictal semiology in localizing the source of epileptiform discharges.

6 background slowing and generalized and focal epileptiform discharges.

7 he emergence of network activities including epileptiform discharges.

8 activity that precedes and is necessary for epileptiform discharges.

9 to the occurrence of spontaneous, recurrent epileptiform discharges.

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

11 An electroencephalogram showed no epileptiform discharges.

12 y (EEG) revealed frequent bilateral parietal epileptiform discharges.

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

14 antly increased in seizures and coupled with epileptiform discharges.

15 derlying physiological drivers of rhythms of epileptiform discharges.

16 ed) nuclei immediately suppressed interictal epileptiform discharges.

17 is essential to prevent subicular-originated epileptiform discharges.

18 s later (median: 42 months) with generalized epileptiform discharges.

19 a combination of these signals together with epileptiform discharges.

20 xplain most of the observed distributions of epileptiform discharges.

21 the hippocampus and cortex during interictal epileptiform discharges.

22 ed slowing to bilateral periodic lateralized epileptiform discharges.

23 2+) conditions induced unremitting recurrent epileptiform discharges.

24 the mouse dorsal hippocampus rapidly caused epileptiform discharges.

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

26 uit deficient in rhythmogenesis and prone to epileptiform discharges.

27 focal cortical malformation with spontaneous epileptiform discharges.

28 ity with frequent generalized and multifocal epileptiform discharges.

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

30 recorded from intracranial electrodes during epileptiform discharges.

31 ield potential amplitudes and produces focal epileptiform discharges.

32 scale events were associated with interictal epileptiform discharges.

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

34 orms normal neuronal activity into prolonged epileptiform discharges.

35 ls were preceded by spontaneous granule cell epileptiform discharges.

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

37 brain atrophy (27/182; 14.8%), and periodic epileptiform discharges (11/151; 7.3%) were exclusively

38 Moreover, flicker decreased interictal epileptiform discharges, a pathological biomarker of epi

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

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

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

42 Both genders had delayed weight gain, epileptiform discharges and altered power spectral distr

43 athy, children exhibit sleep-activated focal epileptiform discharges and cognitive difficulties durin

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

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

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

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

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

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

50 es, in addition to the changes in interictal epileptiform discharges and ripples during the stimulati

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

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

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

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

55 tivated bursts of generalized and multifocal epileptiform discharges and slowing was observed in two

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

57 Interictal epileptiform discharges are associated with higher risk

58 be challenging when seizures and interictal epileptiform discharges are infrequent or discordant, an

59 l optical GABA sensor, showing that periodic epileptiform discharges are preceded by transient, regio

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

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

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

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

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

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

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

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

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

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

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

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

72 , hippocampal ripple activity and interictal epileptiform discharges during an associative memory tas

73 Interictal epileptiform discharges during encoding were associated

74 Hippocampal interictal epileptiform discharges during retrieval predicted 25% d

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

76 pairment arises from pathological interictal epileptiform discharge events competing with physiologic

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

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

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

80 Interictal epileptiform discharges have been shown to propagate fro

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

82 on a unique dataset of long-term inter-ictal epileptiform discharge (IED) rates from human hippocampu

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

84 d spatiotemporal distribution of inter-ictal epileptiform discharges (IEDs) across different sleep st

85 l percentage of routine EEGs show interictal epileptiform discharges (IEDs) and overall misdiagnosis

86 Interictal epileptiform discharges (IEDs) are a widely used biomark

87 Interictal epileptiform discharges (IEDs) are abnormal electrical p

88 Interictal epileptiform discharges (IEDs) are an electrographic man

89 Interictal epileptiform discharges (IEDs) are expressed in epilepti

90 lography recordings, we show that interictal epileptiform discharges (IEDs) are significantly coupled

91 processes.SIGNIFICANCE STATEMENT Interictal epileptiform discharges (IEDs) are thought to be a cause

92 Interictal epileptiform discharges (IEDs) are transient abnormal el

93 l field potential (LFP) power and interictal epileptiform discharges (IEDs) as primary and secondary

94 Interictal epileptiform discharges (IEDs) identify epileptic brain

95 dynamics of abGCs and mGCs during interictal epileptiform discharges (IEDs) in mice with TLE as well

96 nce that K448 had on intracranial interictal epileptiform discharges (IEDs) in sixteen subjects under

97 ist that markedly attenuated interictal-like epileptiform discharges (IEDs) in TLE patient-derived hi

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

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

100 deep or weak (low SNR) sources of interictal epileptiform discharges (IEDs), along with three childre

101 Interictal epileptiform discharges (IEDs), also known as interictal

102 mited by coarse spatial sampling, interictal epileptiform discharges (IEDs), and a lack of consensus

103 has important influences on focal interictal epileptiform discharges (IEDs), and the rates and spatia

104 heterogeneous factors, including interictal epileptiform discharges (IEDs), antiseizure medications

105 aditional SoZ biomarkers, such as interictal epileptiform discharges (IEDs), high-frequency oscillati

106 used to detect and localize focal interictal epileptiform discharges (IEDs).

107 ished by spontaneous seizures and interictal epileptiform discharges (IEDs).

108 the interictal EEG commonly shows interictal epileptiform discharges (IEDs).

109 f a homeostatic relationship with interictal epileptiform discharges (IEDs): exhibiting progressive a

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

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

112 We hypothesize that interictal epileptiform discharges impair associative memory in a r

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

114 revealed frequent sleep-activated multifocal epileptiform discharges in 8 of 11 (73%).

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

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

117 24 hours, which evoked population spikes and epileptiform discharges in both dentate granule cells an

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

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

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

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

122 ocal NMDA stimulation to elicit reproducible epileptiform discharges in hippocampal organotypic brain

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

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

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

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

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

128 umped magnetometers helped detect interictal epileptiform discharges in school-aged children with epi

129 IGE and brain areas activated by generalized epileptiform discharges in simultaneous electroencephalo

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

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

132 The number of epileptiform discharges in the electroencephalogram and

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

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

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

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

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

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

139 al electrodes on average during at least 120 epileptiform discharges lasting less than one second, pe

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

141 halography showed sleep-activated multifocal epileptiform discharges (n = 4) and hippocampal sclerosi

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

143 Epileptiform discharges not accompanied by obvious clini

144 mbering were reduced by 25-52% if interictal epileptiform discharges occurred during the 500-2000 ms

145 The presence of interictal epileptiform discharges on EEG may indicate increased ep

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

147 Epileptiform discharges on electroencephalogram (EEG) we

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

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

150 freedom, and the proportions with interictal epileptiform discharges on the diagnostic EEG; overall q

151 two subgroups with distinct distributions of epileptiform discharges: one with highest incidence duri

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

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

154 Cases showed predominance of right temporal epileptiform discharges (OR = 4.87, p = 0.007).

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

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

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

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

159 Mechanisms that entrain and pace rhythmic epileptiform discharges remain debated.

160 ms that determine these rhythmic patterns of epileptiform discharges remains an open question.

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

162 eting with physiological ripples, interictal epileptiform discharges represent a promising therapeuti

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

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

165 tages of focal cooling are trifold: stopping epileptiform discharges, seizures, and status epilepticu

166 demonstrated that ripples co-occurring with epileptiform discharges ('spike ripple events') are easi

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

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

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

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

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

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

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

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

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

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

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

178 e, we investigate the dynamics of interictal epileptiform discharges using a combination of quantitat

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

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

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

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

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

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

185 ivity, and electroencephalographic posterior epileptiform discharges) was described for variants in t

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

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

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

189 Interictal epileptiform discharges were detected using custom softw

190 Interictal epileptiform discharges were determined in the same time

191 coding and retrieval, hippocampal interictal epileptiform discharges were followed by a transient dec

192 Spontaneous epileptiform discharges were induced in vitro in the CA3

193 Spontaneous epileptiform discharges were initially lateralized to ip

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

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

196 Polyspike epileptiform discharges were observed in rats with kaini

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

198 Epileptiform discharges were recorded in layer V-VI pyra

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

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

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

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

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

204 es (median age of onset: 4 months) and focal epileptiform discharges, whereas the onset of seizures i

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

206 94.8% specificity (95% CI 90.0%, 97.7%) for epileptiform discharges with positive and negative predi

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

208 egions often preceding irregular generalized epileptiform discharges, with frontal predominance.