ライフサイエンスコーパス: epileptiform

1 Smartphone Brain Scanner-2 (SBS2), to detect epileptiform abnormalities compared to standard clinical

2 between cortisol levels and the incidence of epileptiform abnormalities in the electroencephalogram o

3 a viable supportive test for the capture of epileptiform abnormalities, and extend EEG access to new

4 izures before remission, focal seizures, and epileptiform abnormality on EEG before withdrawal.

5 epilepsy syndrome, developmental delay, and epileptiform abnormality on electroencephalogram (EEG) b

6 8, 1.05-1.11), electroencephalogram results (epileptiform abnormality vs normal, 1.26, 1.07-1.50), se

7 somatostatin-expressing interneurons during epileptiform activation.

8 t to inhibit action potential generation and epileptiform activities in vitro.

9 ivity of Pv interneurons enhances or opposes epileptiform activities.

10 rcuits govern generation and spread of focal epileptiform activities.

11 tivity is a condition in which lights induce epileptiform activities.

12 myoclonus, less frequently in myoclonus with epileptiform activity (2% vs 15%; p < 0.001).

13 ound activity (unsynchronized oscillations), epileptiform activity (highly synchronized oscillations)

14 all patients, the device recorded interictal epileptiform activity (IEA; >=6 months of continuous hou

15 ersistent increases in spontaneous bursts of epileptiform activity (spike-wave discharges) that occur

16 Patients with AD who had subclinical epileptiform activity also had an early onset of cogniti

17 omes, usually in patients without associated epileptiform activity and after prolonged hospitalizatio

18 ital malformations, intellectual impairment, epileptiform activity and autism spectrum disorder.

19 hat VU0422465 is an agonist PAM that induces epileptiform activity and behavioral convulsions in rode

20 associated with significant improvements in epileptiform activity and cross-frequency coupling measu

21 ive seizure/nonconvulsive status epilepticus/epileptiform activity and odds ratio of detecting outcom

22 c levels can significantly attenuate ongoing epileptiform activity and prophylactically dampen subseq

23 electrographic biomarkers in the absence of epileptiform activity and provide a potential network co

24 R-related models, Depdc5cc+ mice had minimal epileptiform activity and rare seizures prior to seizure

25 K(+)-ATPase alpha3 isoform in the control of epileptiform activity and seizure behavior.

26 he band heterotopia in generating interictal epileptiform activity and seizures in brains with SBH.

27 rious neurological disorders associated with epileptiform activity and seizures.

28 ippocampal infusion of Zn(2+) elicited rapid epileptiform activity and significantly blocked the anti

29 of synaptic conductances from neurons during epileptiform activity and then replayed them in pharmaco

30 The hippocampal epileptiform activity appears unusually susceptible to d

31 ung adult male rats and mice, we report that epileptiform activity at CA3-CA1 synapses, generated by

32 s supported by our finding that synaptic and epileptiform activity at SynII(-) and wild-type synapses

33 and a reduced threshold for the induction of epileptiform activity by 4-aminopyridine (4-AP).

34 ansitions in the pattern of locally recorded epileptiform activity can be indicative of a shift in th

35 These signature features of local epileptiform activity can provide useful insight into th

36 strong activation of GABAergic inputs during epileptiform activity can switch GABA(A) receptor (GABA(

37 At the time of monitoring, AD patients with epileptiform activity did not differ clinically from tho

38 followed by prolonged suppression of ongoing epileptiform activity during light exposure.

39 dazolam or normocapnia, the risk of inducing epileptiform activity during spontaneous respiration is

40 iseizure efficacy and conversely exacerbates epileptiform activity during this stage of status epilep

41 Epileptiform activity evoked by zero Mg(2+) incubation d

42 followed by local inflammatory response and epileptiform activity ex vivo.

43 The avalanches collected during interictal epileptiform activity had not only a stereotypical size

44 Inhibition of epileptiform activity has been demonstrated in hippocamp

45 e upon loss of the eyelash reflex to prevent epileptiform activity has not been shown to reduce the r

46 oencephalography demonstrated myoclonus with epileptiform activity in 209 of 374 (55%), including sta

47 ut electroencephalography demonstrated ictal epileptiform activity in 7 patients (24%).

48 us epilepticus-like state, actually enhanced epileptiform activity in a GABAAR dependent manner.

49 Extended monitoring detects subclinical epileptiform activity in a substantial proportion of pat

50 Here, we sought to identify the origin of epileptiform activity in a targeted genetic model of SBH

51 However, the incidence of subclinical epileptiform activity in AD and its consequences are unk

52 ed higher than expected rates of subclinical epileptiform activity in AD with deleterious effects on

53 Kbeta4 was sufficient to normalize excessive epileptiform activity in an in vitro model of seizure ac

54 cally, it has also been reported to increase epileptiform activity in clinical and experimental studi

55 xacerbated behavioral deficits and increased epileptiform activity in hAPP mice.

56 regulating synaptic strengthening following epileptiform activity in hippocampal slices.

57 togenetics and study their impact on ongoing epileptiform activity in mouse acute hippocampal slices.

58 und that tau reduction prevented spontaneous epileptiform activity in multiple lines of hAPP mice.

59 d molecules in the dentate gyrus and CA1 and epileptiform activity in parietal cortex.

60 Some evidence indicates that subclinical epileptiform activity in patients with Alzheimer's disea

61 izure onset zone, suggesting that interictal epileptiform activity in patients with epilepsy is not a

62 lar mechanism, has been reported to increase epileptiform activity in several clinical and experiment

63 minant-negative SNARE domain in mice reduced epileptiform activity in situ, delayed seizure onset aft

64 mes inhibitory with maturation and can block epileptiform activity in the adult brain.

65 alpha(2) adrenergic receptors (ARs) inhibits epileptiform activity in the hippocampal CA3 region.

66 y associated with synaptic transmission, but epileptiform activity in the hippocampus can propagate w

67 (LFS) is an alternative tool for controlling epileptiform activity in these patients.

68 stitute a primary origin for interictal-like epileptiform activity in vitro and is dispensable for ge

69 Here, we have taken advantage of a model of epileptiform activity in vitro to quantify the charge tr

70 ited, are sufficient to initiate synchronous epileptiform activity in vitro.

71 Epileptiform activity induced by high potassium and low

72 and chronically epileptic rats and find that epileptiform activity is associated with increased synap

73 Hippocampal epileptiform activity is promoted by 4-aminopyridine and

74 In the zero-Mg(2+) model, the earliest epileptiform activity is restricted to neocortical and e

75 Because mounting evidence suggests that epileptiform activity may play an important role in the

76 inhibition suppresses action potentials and epileptiform activity more robustly than perisomatic inh

77 olazine was able to significantly reduce the epileptiform activity of the neuronal cultures, suggesti

78 acterised by several seizure types, frequent epileptiform activity on EEG, and developmental slowing

79 cycle and were not correlated with increased epileptiform activity or seizure frequency.

80 evidence argues against the hypothesis that epileptiform activity per se contributes to focal brain

81 robust release of glutamate during sustained epileptiform activity requires that neurons be provided

82 These abnormalities resemble the epileptiform activity seen in children with Batten disea

83 However, patients with subclinical epileptiform activity showed faster declines in global c

84 the TGF-beta pathway by TGF-beta1 results in epileptiform activity similar to that after exposure to

85 port key features of AD-related seizures and epileptiform activity that are instructive for clinical

86 tical territories differ both in the type of epileptiform activity they can sustain and in their susc

87 l lobes or the effects of the propagation of epileptiform activity through the network of brain regio

88 nanolone reverted the threshold for inducing epileptiform activity to virgin levels.

89 inhibitory effect of EPI on hippocampal CA3 epileptiform activity uses an alpha(2A)AR/Galpha(o) prot

90 xamination (3.9 points/year in patients with epileptiform activity vs 1.6 points/year in patients wit

91 Subclinical epileptiform activity was assessed, blinded to diagnosis

92 where the occurrence of interictal and ictal epileptiform activity was confirmed by either stereo-ele

93 Subclinical epileptiform activity was detected in 42.4% of AD patien

94 Epileptiform activity was induced by arterial perfusion

95 The inhibition of epileptiform activity was less pronounced if only parval

96 Consistent with this, epileptiform activity was observed in hippocampal and co

97 orders characterized by seizures, interictal epileptiform activity with a disorganized electroencepha

98 The algorithm identified epileptiform activity with high fidelity compared to vis

99 od for quantification of multiple classes of epileptiform activity within the murine EEG and is tunab

100 At low levels of KA, generating epileptiform activity without seizures, we indeed found

101 rger doses and sevoflurane appear to support epileptiform activity, although the clinical significanc

102 ng Mg2+ ions leads to an evolving pattern of epileptiform activity, and eventually to a persistent st

103 titative electrographic biomarkers free from epileptiform activity, and provide a potential network c

104 The devices detect normal physiologic and epileptiform activity, both in acute and chronic recordi

105 frequency of cardiac events correlated with epileptiform activity, circadian (light/dark) cycle, the

106 bility that, rather than being initiators of epileptiform activity, fast ripples may be markers of a

107 GABA delivery stopped epileptiform activity, recorded simultaneously and coloc

108 gies as well as beta-amyloid (Abeta)-induced epileptiform activity, some of the mechanisms that event

109 By contrast, we detected no epileptiform activity, spontaneous behavioral seizures,

110 igate this paradox during realistic neuronal epileptiform activity, we developed a method, activity c

111 Using in vitro and in vivo models of epileptiform activity, we show that acutely increasing O

112 stered before a chemoconvulsant, exacerbates epileptiform activity, whereas a P2Y(1) agonist (MRS2365

113 astrocytes are observed to alkalinize during epileptiform activity, whereas neurons are observed to a

114 hibit distinct pH dynamics during periods of epileptiform activity, which has relevance to multiple p

115 that Sema4D rapidly and dramatically alters epileptiform activity, which is consistent with a Sema4D

116 hysiological oscillations in addition to the epileptiform activity.

117 cute ex vivo rat hippocampal slice models of epileptiform activity.

118 r avalanches, particularly during interictal epileptiform activity.

119 brain dynamics, particularly during abnormal epileptiform activity.

120 pe-specific rules, are sufficient to promote epileptiform activity.

121 ions at the transition from resting-state to epileptiform activity.

122 ors almost completely abolished this form of epileptiform activity.

123 circuit dynamics underlie this phase of the epileptiform activity.

124 hood substantially delayed the appearance of epileptiform activity.

125 ty and changes in GABAergic signaling during epileptiform activity.

126 information about interictal or sub-clinical epileptiform activity.

127 EEG at detecting interictal and subclinical epileptiform activity.

128 he thalamocortical seizure network modulates epileptiform activity.

129 ed a burst-suppression pattern or multifocal epileptiform activity.

130 h neurotransmitter glutamate during enhanced epileptiform activity.

131 used voltage-clamp waveforms that replicated epileptiform activity.

132 nhanced excitatory synaptic connectivity and epileptiform activity.

133 d sterotypical patterns of acutely evolving, epileptiform activity.

134 onal changes and prevented the generation of epileptiform activity.

135 e of synaptic responses and plasticity after epileptiform activity.

136 citatory circuits are sufficient to generate epileptiform activity.

137 ly propagating activity, including spreading epileptiform activity.

138 auing or regression associated with frequent epileptiform activity.

139 the second action potential in each burst of epileptiform activity.

140 nation for the paradoxical effects of CBZ on epileptiform activity.SIGNIFICANCE STATEMENT The effects

141 mGlu1 ago-PAMs/PAMs do not possess the same epileptiform adverse effect liability as mGlu5 ago-PAMs/

142 nule cell paired-pulse inhibition, decreased epileptiform afterdischarge durations during 8 hours of

143 knock-out (KO) for Ophn1 display hippocampal epileptiform alterations, which are associated with chan

144 eals a clinically underappreciated burden of epileptiform and epileptic activity in patients with pri

145 the direction of pH change, the kinetics of epileptiform-associated intracellular pH transients are

146 hich blocks inhibitory GABA(A) receptors, an epileptiform burst consisting of a series of PSs was evo

147 Taken together, our data suggest that epileptiform burst firing generated in the CA3 region by

148 itical role in the generation of spontaneous epileptiform burst firing in cornu ammonis (CA) 3 pyrami

149 with long-form Homers enhanced mGluR-induced epileptiform burst firing in wild-type (WT) animals, rep

150 arizing plateau potential that underlies the epileptiform burst firing induced by metabotropic glutam

151 were classified as isoelectric, low voltage, epileptiform, burst-suppression, diffusely slowed, or no

152 mice, and contributes to the development of epileptiform bursting activity in the TSC2(+/-) CA3 regi

153 that TRPC1/4 double-knockout (DKO) mice lack epileptiform bursting in lateral septal neurons and exhi

154 dependence to LTD, and significantly reduces epileptiform bursting in TSC2(+/-) hippocampal slices.

155 Interestingly, epileptiform bursting induced by agonists for metabotrop

156 2DG (10mM) reduced interictal epileptiform bursts induced by 7.5mM [K(+)](o), 4-aminop

157 onged activation of GABA(A) receptors during epileptiform bursts may even initiate a shift in GABAerg

158 dback inhibition promote the transmission of epileptiform bursts to hippocampal projection areas.SIGN

159 Epileptiform bursts with an underlying plateau potential

160 se using recordings of mouse hippocampal CA3 epileptiform bursts.

161 also reduced the EPI-mediated inhibition of epileptiform bursts.

162 of epilepsy in vitro by comparing GABAergic epileptiform currents and their sensitivity to gap junct

163 d amplitude, frequency and half-width of the epileptiform currents both in wild-type and in knockout

164 Furthermore, epileptiform currents propagated similarly across hippoc

165 leculare interneurons from knockout animals, epileptiform currents were not eliminated.

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

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

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

169 itute a trigger for pathological synchronous epileptiform discharge.

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

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

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

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

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

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

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

177 Interictal epileptiform discharges (IEDs) identify epileptic brain

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

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

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

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

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

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

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

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

186 Interictal epileptiform discharges are associated with higher risk

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

214 Interictal epileptiform discharges were determined in the same time

215 Spontaneous epileptiform discharges were initially lateralized to ip

216 Epileptiform discharges were recorded in layer V-VI pyra

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

218 94.8% specificity (95% CI 90.0%, 97.7%) for epileptiform discharges with positive and negative predi

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

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

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

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

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

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

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

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

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

228 ed slowing to bilateral periodic lateralized epileptiform discharges.

229 2+) conditions induced unremitting recurrent epileptiform discharges.

230 focal cortical malformation with spontaneous epileptiform discharges.

231 the mouse dorsal hippocampus rapidly caused epileptiform discharges.

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

233 uit deficient in rhythmogenesis and prone to epileptiform discharges.

234 recorded from intracranial electrodes during epileptiform discharges.

235 ity with frequent generalized and multifocal epileptiform discharges.

236 ital was effective at reducing or preventing epileptiform discharges.

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

238 ield potential amplitudes and produces focal epileptiform discharges.

239 scale events were associated with interictal epileptiform discharges.

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

241 orms normal neuronal activity into prolonged epileptiform discharges.

242 a combination of these signals together with epileptiform discharges.

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

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

245 ures on CEEG decays to <5% by 24 hours if no epileptiform EEG abnormalities emerge, independent of in

246 In 54 subjects, epileptiform EEG abnormalities were identified before se

247 In the absence of epileptiform EEG abnormalities, the duration of monitori

248 rtex or hippocampus reversibly can attenuate epileptiform EEG activity and seizures, but engineering

249 ic or clinical seizure, or preventively when epileptiform EEG activity before seizures was detected.

250 clinical seizures; more commonly, it causes epileptiform EEG activity that only weakly portends seiz

251 ion of the seizure network to the forebrain, epileptiform electrocorticographic activity, and prolong

252 based on the clinical practice of observing epileptiform electrocorticography and simultaneous ictal

253 rief (<2 s) focal, recurrent and spontaneous epileptiform electrocorticography events (EEEs) that are

254 taxia accompanied by epilepsy and/or clearly epileptiform electroencephalograms (EEGs).

255 s among the pharmacokinetics of sevoflurane, epileptiform electroencephalographic (EEG) activity and

256 Ictal epileptiform electroencephalographic changes were presen

257 Bicuculline evoked high-amplitude rhythmic epileptiform events at the site of injection which resem

258 campal slices showed no Mg(2+)/NMDA-mediated epileptiform events in knockouts.

259 etween injection and the occurrence of first epileptiform events were 3.93 +/- 2.76 (+/-STD) min for

260 ry required to capture these very infrequent epileptiform events.

261 could exercise voluntary control over these epileptiform events.

262 alography variables (reactivity, continuity, epileptiform features, and prespecified "benign" or "hig

263 Spontaneous and evoked epileptiform field potentials occurred at multiple sites

264 If epileptiform findings developed, the seizure incidence w

265 If there were no epileptiform findings on EEG, the risk of seizures withi

266 and optical recordings showed glutamatergic epileptiform hyperexcitability that spread into adjacent

267 ar release of tRNA fragments was lower after epileptiform-like activity in hippocampal neurons.

268 There was a decreased threshold to induce epileptiform local field potentials in slices from pregn

269 orn (abGC) and mature (mGC) granule cells to epileptiform network events remains unknown.

270 ve rates for mortality were less than 5% for epileptiform or nonreactive early electroencephalography

271 are unknown and unexpected because thalamic epileptiform oscillatory activity requires AMPARs.

272 standard EEG for the epileptiform versus non-epileptiform outcome was kappa = 0.40 (95% CI 0.25, 0.55

273 EEG risk state is defined by emergence of epileptiform patterns.

274 ony can limit information coding and lead to epileptiform responses.

275 on of focal brain lesions or the presence of epileptiform rhythms, do not necessarily predict the bes

276 al inhibitory feedback is necessary to avoid epileptiform runaway activity (an "inhibition-stabilized

277 s in hippocampal circuitries can manifest in epileptiform seizures, and impact specific behavioral tr

278 dent neuroprotection from chemically induced epileptiform seizures.

279 We noninvasively detected epileptiform signals unaveraged in a pediatric patient w

280 However, quantitative analyses of epileptiform spatial dynamics with cellular resolution h

281 ature dependence and frequency of interictal epileptiform spike activity.

282 ocal field potential dynamics and interictal epileptiform spike generation.

283 Interictal epileptiform spike rate correlated with spectral band po

284 re was a significant reduction in interictal epileptiform spike rate in the amygdala, hippocampus, an

285 redicted significant reduction in interictal epileptiform spike rate.

286 nd age dependence of seizures and interictal epileptiform spike-and-wave activity in mSMEI.

287 We conclude that interictal epileptiform spikes are modulated by the patterns of net

288 d clinically silent hippocampal seizures and epileptiform spikes during sleep, a period when these ab

289 ous recurrent convulsive seizures in 45% and epileptiform spikes in 100%, of the rats.

290 synchronization 200 ms before the interictal epileptiform spikes that arose during this period of enc

291 Interictal epileptiform spikes were manually marked and their rate

292 During the latent pre-seizure period, epileptiform spikes were more frequent in epileptic comp

293 e examined, in addition to the daily rate of epileptiform spikes, the relative power of five frequenc

294 ss, its degree of functional activity during epileptiform synchronization has not been thoroughly inv

295 ge but also to control excitation to prevent epileptiform synchronization.

296 tion in the recurrent CA3 network preventing epileptiform synchronization.

297 tex in the in vitro 4-aminopyridine model of epileptiform synchronization.

298 Although the temporal dynamics of epileptiform synchronizations are well described at the

299 a) for the SBS2 EEG and standard EEG for the epileptiform versus non-epileptiform outcome was kappa =

300 Mild sleep abnormalities and abnormal epileptiform waveforms were found in the electroencephal