ライフサイエンスコーパス: seizure

1 esion (53.5%, 396 of 740 free from disabling seizures).

2 s and consecutive paroxysmal cycles within a seizure.

3 but not the initiation or maintenance of the seizure.

4 rienced a witnessed generalized tonic-clonic seizure.

5 le tone, and one of them developed recurrent seizure.

6 l output neurons, Purkinje cells, attenuated seizures.

7 d with memory impairment after temporal lobe seizures.

8 ed sensitivity to pentylenetetrazole-induced seizures.

9 l excitation robustly attenuated hippocampal seizures.

10 of life in individuals who suffer prolonged seizures.

11 estwick Chemical Library that could suppress seizures.

12 sed molecular markers of epileptogenesis and seizures.

13 s as a driver of undesirable consequences of seizures.

14 al disorder defined by recurrent, unprovoked seizures.

15 d to pentylenetetrazole induced tonic-clonic seizures.

16 highly effective at attenuating hippocampal seizures.

17 ontaneous subclinical and evoked generalized seizures.

18 resent a novel approach to classification of seizures.

19 ic plasticity are impaired following kindled seizures.

20 s and results in neurologic deficits such as seizures.

21 ression from hyperexcitability to convulsive seizures.

22 d mesial temporal lobe during rhythmic onset seizures.

23 ch is tested on street samples from forensic seizures.

24 oped behavioral expression of electrographic seizures.

25 susceptible to chemically induced convulsive seizures.

26 rmal sensors found during sleep, stress, and seizures.

27 with developmental delay, cerebral palsy or seizures.

28 lepsy, that were tracked throughout multiple seizures.

29 n of freely moving mice undergoing epileptic seizures.

30 of memantine and cDCS suppressed KA-induced seizures.

31 ve to other behaviors, including jumping and seizures.

32 of the EP2-related negative consequences of seizures.

33 ity, as well as of how pathology can lead to seizures.

34 into the ictal activity during the course of seizures.

35 e tendency of a region to become involved in seizures.

36 ies for approved compounds that can suppress seizures.

37 autistic-like behaviors and protect against seizures.

38 , we analyzed a total of 1,027 spikes and 86 seizures.

39 ssential, and reuptake failure worsens human seizures.

40 y as one-third of patients with uncontrolled seizures.

41 hronizes the activity of neurons, leading to seizures.

42 r IPSCs, which may underlie the induction of seizures.

43 rogressive loss of nodal Na(+) channels, and seizures.

44 eral to the seizure focus is able to inhibit seizures.

45 sorders characterised by recurrent epileptic seizures.

46 y offers better opportunity to control these seizures.

47 l loss and developed more severe spontaneous seizures.

48 epsy is usually restricted to the control of seizures.

49 de age >=65 years, fever, GCS score <13, and seizures.

50 he differences between generalized and focal seizures.

51 mmon overall (6.9%), with a low incidence of seizures (1.1%), ischemic stroke (1.9%), intracranial he

52 After their first seizure, 56 children were followed prospectively over 12

53 ion from quiescent adult ECs leads to severe seizures, accompanied by neuronal loss and CNS inflammat

54 Complex patterns of seizure activity and bi-stable seizure end-points arise

55 The propagation of epileptic seizure activity in the brain is a widespread pathophysi

56 y dysfunctional neuronal subtypes underlying seizure activity in the human brain, we have performed s

57 e administration of fasudil had no impact on seizure activity, seven weeks of treatment in adulthood

58 the transition from loss of SV2A function to seizure activity.

59 the transition from loss of SV2A function to seizure activity.SIGNIFICANCE STATEMENT SV2A is a synapt

60 g data, are associated with the emergence of seizures after TBI.

61 ver, Glasgow Coma Scale (GCS) score <13, and seizures (all P values <=0.01).

62 Additionally, to characterize electrographic seizure and hyperexcitable pattern predictors in each gr

63 adverse events occurred in two patients (one seizure and one haemoptysis).

64 to a high lysine/low PN diet led to vigorous seizures and a quick death in KO mice.

65 o somnolence, obtundation, and in some cases seizures and cerebral edema.

66 neurons are sparsely recruited to successive seizures and consecutive paroxysmal cycles within a seiz

67 ifting views of our understanding of absence seizures and demand careful choice of initial monotherap

68 rders characterized by intractable epileptic seizures and developmental delay.

69 It is characterized by elevation of glycine, seizures and failure to thrive, but glycine reduction of

70 Treatment with PN controlled seizures and improved survival of high-lysine/low PN fed

71 Traumatic brain injury (TBI) causes early seizures and is the leading cause of post-traumatic epil

72 nting with initial learning difficulties and seizures and later psychiatric symptoms, cerebellar atax

73 tly presented with continuous simple partial seizures and occasional breakthrough complex partial sei

74 phalopathy suspected of having nonconvulsive seizures and physicians evaluating these patients.

75 presented in infancy with intractable focal seizures and severe developmental delay.

76 toantibody target in patients with recurrent seizures and suspected encephalitis as leading symptoms.

77 nt resistance to electrically-induced limbic seizures and to pentylenetetrazole induced tonic-clonic

78 , which are characterized by abrupt onset of seizures and/or movement and psychiatric symptoms.

79 We characterized ictal (during a seizure) and interictal (between seizure) cardiac arrhyt

80 other (52.3%, 212 of 405 free from disabling seizures), and for those with no histopathological lesio

81 1%) ischemic stroke, 6% (95% CI, 0.01-0.16%) seizures, and 4% (95% CI, 0.01-0.1%) intracerebral hemor

82 ich is characterized by developmental delay, seizures, and a lack of sweat and tears.

83 logical symptoms such as mental retardation, seizures, and epilepsy.

84 ockade of glial xCT activity inhibited later seizures, and genomic reduction of host brain excitabili

85 recordings of spontaneously occurring human seizures, and here report two dichotomous activity patte

86 rocephaly with brachycephaly, optic atrophy, seizures, and hypertonia with hyperreflexia.

87 d VII are implicated in neuronal excitation, seizures, and neuropathic pain (NP).

88 -specific paresis and paralysis, tremors and seizures, and other clinical signs, along with separate

89 EA) content was downregulated after repeated seizures, and pharmacological enhancement of AEA signali

90 e signs, the radiologic approach to managing seizures, and the differences between generalized and fo

91 x (OI), the tendency of a region to generate seizures; and Participation Index (PI), the tendency of

92 Focal to bilateral tonic-clonic seizures are associated with lower quality of life, high

93 These seizures are blocked in the presence of nest-like levels

94 Electrographic seizures are frequent in lobar intraparenchymal hemorrha

95 While epileptic seizures are known to often manifest also with autonomic

96 he epilepsy diagnosis, may persist even when seizures are pharmacologically controlled and are aggrav

97 aracterized by mild intellectual disability, seizures, behavioral abnormalities, and various skeletal

98 ntagonists was correlated with a decrease in seizure burden.

99 eiving intense local synaptic drive from the seizure but without neuronal evidence of local seizure i

100 ts significantly delayed the onset of lethal seizures but did not prevent them.

101 ll homozygotes exhibited lethal tonic-clonic seizures by mid-third week.

102 n the current study, we determined whether a seizure can activate nociceptive pathways that carry pai

103 An epileptic seizure can trigger a headache during (ictal) or after (

104 Because seizures can significantly impact the quality of life of

105 l (during a seizure) and interictal (between seizure) cardiac arrhythmogenesis following SE using con

106 We found that repeated seizures cause an allostatic maladaptation of AEA signal

107 n-Tr20 expression also modulated seizures caused by an epilepsy-linked mutation in Gabrg2

108 Seizure cessation was achieved at multiple stimulation f

109 ty comprising of four major disease domains (seizure, cognitive failure, muscular and motor control a

110 SRS include osteoporosis, hypotonic stature, seizures, cognitive impairment, and developmental delay.

111 Long before seizures, coincident with loss of inhibitory cells and t

112 ifted towards more closed-loop therapies for seizure control, and on-demand optogenetic modulation of

113 (VPA) is a drug commonly used for epileptic seizure control.

114 ectrodes during ictal discharges in both the seizure core and penumbra (spatial seizure domains defin

115 bility that were tested on subsequent unseen seizure data and evaluated against surrogate time-series

116 Seizures, defined as abnormal transient discharges of ne

117 medial entorhinal area (MEA) that underlies seizure development.

118 children that showed features of early-onset seizures, developmental delay, microcephaly, sensorineur

119 v7/KCNQ channels are linked to a spectrum of seizure disorders.

120 both the seizure core and penumbra (spatial seizure domains defined by multiunit activity patterns).

121 epilepsy (TLE) is characterized by recurrent seizures driven by synchronous neuronal activity.

122 on of the fastigial nucleus had no effect on seizure duration.

123 in ictal events is pivotal to understanding seizure dynamics and in defining clinical localization o

124 n keeping with the "dual territory" model of seizure dynamics.

125 in epilepsy of infancy with migrating focal seizures (EIMFS) and several other forms of epilepsy ass

126 Current explanatory concepts suggest seizures emerge from ongoing dynamics of brain networks.

127 ral/peripheral hyperexcitabability including seizures, encephalopathy, myoclonus, tremor and spastici

128 x patterns of seizure activity and bi-stable seizure end-points arise when stochastic noise is includ

129 ired around day 14 post-injury, detection of seizure events occurred early (within 1 week) and late (

130 duced by chemoconvulsants, we examined acute seizures evoked by intraperitoneal injections of kainic

131 t different timescales, shape within-patient seizure evolutions, leading to variable seizure pathways

132 rons, though the latter is not essential for seizure expression.

133 s either ipsilateral or contralateral to the seizure focus is able to inhibit seizures.

134 encies, regardless of laterality relative to seizure focus, and even with single light pulses.

135 vation of CA1 pyramidal neurons during brief seizures, followed by a short period of reduced activity

136 ated with autism-like symptoms and epileptic seizures for further proof of pathogenicity.

137 027 of 1325) of patients free from disabling seizures for LEAT, 74.0% (328 of 443) for vascular malfo

138 ptic brain tissue and may also be useful for seizure forecasting.

139 t multidien IEA cycles alone generated daily seizure forecasts for the next calendar day with IoC in

140 hus new, more effective therapies to achieve seizure freedom are needed.

141 in tissue is the most important predictor of seizure freedom following surgery for cortical dysplasia

142 nd dramatic seizure reduction with months of seizure freedom.

143 with epilepsy, studies regarding changes in seizure frequency during pregnancy have been limited by

144 oup to provide data on the natural course of seizure frequency in both groups.

145 ive cenobamate reduced focal (partial)-onset seizure frequency, in a dose-related fashion.

146 ntravenous immunoglobulin (IVIG) in reducing seizure frequency.

147 ht to forecast 24-hour risk of self-reported seizure from e-diaries.

148 cephalographic (iEEG) recordings of over 500 seizures from 31 patients with focal epilepsy (mean 16.5

149 sticity plays a role in sustaining seizures, seizure generalization, and mortality observed during fo

150 o-convulsive stimulus successfully prevented seizure generalization.

151 nding network properties would cast light on seizure-generating mechanisms and allow to quantify to w

152 ted background show substantially diminished seizure generation.

153 ree individuals have cerebral malformations, seizures, global developmental delay or intellectual dis

154 of controlled trials, treatment of neonatal seizures has changed minimally despite poor drug efficac

155 e mechanisms by which the cerebellum impacts seizures, however, are unknown.

156 0011172; p = 2.1 x 10(-5)) and "focal clonic seizures" (HP: 0002266; p = 8.9 x 10(-6)), STXBP1 with "

157 associations of SCN1A with "complex febrile seizures" (HP: 0011172; p = 2.1 x 10(-5)) and "focal clo

158 played susceptibility to induced generalized seizures, hyperactivity, repetitive and reduced anxiety

159 sion identified predictors of electrographic seizures, hyperexcitable patterns, and poor outcomes (sc

160 ctual disability, motor delay, speech delay, seizures, hypotonia, and behavioral problems.

161 chronization may contribute to transition to seizure in Dravet syndrome.

162 creased spontaneous generalized tonic-clonic seizures in a model of temporal lobe epilepsy, and rescu

163 of the cerebellum does not alter hippocampal seizures in a mouse model of temporal lobe epilepsy.

164 n almost complete suppression of spontaneous seizures in both hippocampi.

165 o the ictal state during temperature-induced seizures in Dravet syndrome.SIGNIFICANCE STATEMENT Epile

166 of these three microRNAs reduced spontaneous seizures in epileptic mice.

167 ging in neocortex during temperature-induced seizures in male and female Dravet syndrome (Scn1a+/-) m

168 , Orai1, in the brain show markedly stronger seizures in response to the chemoconvulsants, kainic aci

169 f PNs and parvalbumin-expressing INs, during seizures IN responses were reduced and less synchronized

170 zon of 1 h, possible only for electrographic seizures in the development cohort, showed IoC in all 18

171 ide added to phenobarbital to treat neonatal seizures in the first trial to include a standard-therap

172 jor infection at 1 year in one and new-onset seizures in the other.

173 Seizure incidence prior to the baseline visit was highes

174 histories of focal to bilateral tonic-clonic seizures, including both remote (none for >1 year) and c

175 Although FVB/N mice can have seizures, increases in seizure severity and death of C9

176 logical enhancement of AEA signaling rescued seizure-induced anxiety by restoring the tonic control o

177 nvolved in the initiation and maintenance of seizure-induced headache, and that their activation patt

178 Little is known about the pathophysiology of seizure-induced headaches.

179 However, basic mechanisms of seizure initiation and propagation remain poorly underst

180 ed immediately (1 min) or up to 90 min after seizure initiation, and lasted as short as 10 min or as

181 The mechanistic basis of seizure initiation, and the contribution of defined neur

182 amplitude are neuron-intrinsic hallmarks of seizure invasion that impede traditional spike sorting a

183 izure but without neuronal evidence of local seizure invasion) showed stable waveforms.

184 of high frequency LFP before and after local seizure invasion.

185 isms and allow to quantify to which extent a seizure is focal or generalised.

186 tter understanding of the early detection of seizures is highly desirable as identification of an imp

187 Analyzing neuronal activity during human seizures is pivotal to understanding mechanisms of seizu

188 ition characterised by spontaneous recurrent seizures, is common in older adults (aged >65 years) and

189 ility to spreading depolarizations (SDs) and seizures, known agents of clinical worsening after TBI.

190 d using a computer model and used to predict seizure likelihood and onset patterns.

191 more broadly distributed and less useful for seizure localization.

192 desirable as identification of an impending seizure may afford improved treatments, such as antiepil

193 t alteration of eCB signaling after repeated seizures may contribute to the development of epilepsy-r

194 in silico testbed for future explorations of seizure mechanisms and clinical therapies.

195 Seizures, memory impairment, and increased protein conte

196 cortex (S1), and in a mouse kainic acid (KA)-seizure model.

197 d derepressed TGF-beta signaling as a shared seizure-modifying mechanism.

198 We quantitatively compared within-patient seizure network evolutions using intracranial electroenc

199 containing key parts of the thalamocortical seizure network modulates epileptiform activity.

200 During a seizure, neural activity will deviate from its current d

201 In cortex that is recruited to the seizure, neuronal firing rates increase and waveforms be

202 Myoclonic seizures occurred at behavioral-state transitions both i

203 le DS mice and persisted only if spontaneous seizures occurred.

204 rformance, taking into account the number of seizures occurring during the consolidation period and o

205 hmic delta activity predicted electrographic seizures (odds ratio, 6.24; CI, 1.49-26.08; p = 0.012);

206 ad been treated for a generalised convulsive seizure of longer than 5 min duration with adequate dose

207 Seizures often herald the clinical appearance of gliomas

208 toxin) to determine the effects of epileptic seizure on the activity of trigeminovascular Adelta-, C-

209 or each patient and the effects of sleep and seizures on these dynamics were evaluated.

210 le tone, and one of them developed recurrent seizure.On physical examination, the child showed marked

211 mentally observed spatiotemporal patterns of seizure onset and even less so for the properties of the

212 ion of Scn8a transcript by 25 to 50% delayed seizure onset and lethality in mouse models of SCN8A enc

213 for the spatiotemporal patterns observed at seizure onset and may ultimately contribute to a more pe

214 es is pivotal to understanding mechanisms of seizure onset and propagation.

215 anterior, intermediate, and posterior insula seizure onset group.

216 ider three different patterns of domino-like seizure onset in Idiopathic Generalized Epilepsy (IGE) a

217 Seizure onset patterns were heterogeneous; the seizure o

218 izure onset patterns were heterogeneous; the seizure onset zone was focal.

219 ibits decreased synchrony immediately before seizure onset.

220 caused by abnormal neuronal firing during a seizure onset.

221 activity in a distinct sub-network prior to seizure onset.

222 ighest OI and PI corresponded to the side of seizure onset.

223 In conclusion, spikes localize seizure onset.

224 , using invasive brain voltage recordings at seizure onset.

225 (C(c)), the ability of a network to generate seizures; Onset Index (OI), the tendency of a region to

226 e the association between histopathology and seizure outcome and drug freedom up to 5 years after epi

227 tion, and hippocampal sclerosis had the best seizure outcome at 2 years after surgery, with 77.5% (10

228 associated with reduced chance of favourable seizure outcomes and drug freedom.

229 The worst seizure outcomes at 2 years were seen for patients with

230 g-free; temporal lobe surgeries had the best seizure outcomes; and a longer duration of epilepsy was

231 sented with altered mental status (p<.0001), seizures (p=.0005), elevated intracranial opening pressu

232 contribution of defined neuronal subtypes to seizure pathophysiology, remains poorly understood.

233 r in time, and a simple model suggested that seizure pathways change on circadian and/or slower times

234 ient seizure evolutions, leading to variable seizure pathways that may require tailored treatment app

235 m 31 patients with focal epilepsy (mean 16.5 seizures per patient).

236 severe postictal hypoperfusion/hypoxia, not seizures per se, are associated with memory impairment a

237 PR2-IgG-seropositive adult patients with >=2 seizures per week.

238 rthermore, our method observes potential pre-seizure phenomena in some cases.

239 echniques and an established animal model of seizure (picrotoxin) to determine the effects of epilept

240 third of patients continue to have disabling seizures postoperatively.

241 lvement, hematoma volume, and electrographic seizures predicted poor outcome in lobar intraparenchyma

242 chymal hemorrhage volume, and electrographic seizures predicted poor outcome.

243 head circumference, higher weight, and lower seizure prevalence relative to the other gene group.

244 This study shows that seizure probability can be forecasted days in advance by

245 G data (both cohorts) generated forecasts of seizure probability that were tested on subsequent unsee

246 otics after resuscitation, postresuscitation seizure prophylaxis and treatment, and neuroprognosticat

247 Seizure protein 6 (SEZ6) is required for the development

248 (R = -0.59, p < 0.0001) and time to a second seizure (R = -0.64, 95% confidence interval [CI] = -0.77

249 ne monocytes.SIGNIFICANCE STATEMENT Unabated seizures reduce quality of life, promote the development

250 Recent clinical evaluation of everolimus for seizure reduction in patients with tuberous sclerosis co

251 ient 3 experienced an immediate and dramatic seizure reduction with months of seizure freedom.

252 d with lower quality of life, higher risk of seizure-related injuries, increased chance of sudden une

253 of dynamic network communities during human seizures remains poorly understood.

254 coronavirus disease 2019 who presented with seizure, right hemiparesis, and dysarthria with positive

255 a cohort of children with a first unprovoked seizure, ripples predict the development of epilepsy bet

256 Seizure risk was associated with a combination of these

257 ttern predictors in each group and determine seizure risk with thalamic involvement.

258 ceptor plasticity plays a role in sustaining seizures, seizure generalization, and mortality observed

259 rtex that was temporally correlated with pre-seizure self-reported dissociation, and local brief elec

260 Seizure semiology, cognitive and mood phenotypes, alongs

261 h FVB/N mice can have seizures, increases in seizure severity and death of C9 and NT animals, which m

262 s should include a control group and balance seizure severity.

263 ime-domain differences to spatial domains of seizures, showing that penumbral discharges are more bro

264 f developmental delay and medical refractory seizures since birth most recently presented with contin

265 l spikes in the hippocampus during sleep and seizures specifically impair long-term memory consolidat

266 ractory status epilepticus to achieve either seizure suppression or burst suppression on continuous E

267 ted by serotonin/dopamine signaling, causing seizure suppression.

268 This seizure-suppressive action during daily stimulation rema

269 Using statistical testing with seizure surrogate data and a unique dataset of continuou

270 ling augmented both network excitability and seizure susceptibility in uninjured controls.

271 removal of the GluA1 subunit did not affect seizure susceptibility; however, it reduced susceptibili

272 at, in this cohort, immunotherapy-responsive seizure syndromes with autoantibodies largely fall under

273 s returned to their preictal waveforms after seizure termination.

274 PDE is characterized by recurrent seizures that are resistant to conventional anticonvulsa

275 to other Dup15q models, these flies develop seizures that worsen with age.

276 ly extended the neural mass model of partial seizures, the Epileptor, by including two neuron subpopu

277 some children and animal models with absence seizures, the ictal increase in thalamic inhibition is e

278 During onset of seizures, the recruitment dynamics markedly differed bet

279 pment (50.0%, 213 of 426 free from disabling seizures), those with malformation of cortical developme

280 learning and of pathways that link cortical seizures to other regions required for animal survival.

281 de clinical guidance in support of epileptic seizure treatments in practice.

282 e personalized approach to classification of seizure types in clinical practice.

283 ients exhibit a wide spectrum of intractable seizure types, severe developmental delay, movement diso

284 dynamic community organization during human seizures, using invasive brain voltage recordings at sei

285 singly little is known about whether and how seizures vary in the same patient.

286 The time to the first clinical seizure was significantly longer with preventive than co

287 When the number of seizures was below 5, spike frequency during sleep highe

288 sion tree analysis showed that the number of seizures was the first factor that impaired the verbal m

289 epilepsy (9.9 +/- 5.8 years; 27 females; 161 seizures) we investigated differences between inter- and

290 Both spikes and seizures were associated with intense synchronized activ

291 KO mice lacked epileptic seizures when fed a low lysine/high PN diet.

292 by eliminating a secondary phase of intense seizures, which was evident in littermate controls.

293 e six times as likely to have electrographic seizures, which were associated with 5.47 higher odds of

294 mplitude as the neurons are recruited to the seizure, while penumbral tissue shows stable action pote

295 ice, are also informative about an impending seizure with statistically significant sensitivity and s

296 or the detection and prediction of epileptic seizures with electroencephalogram (EEG).

297 and occasional breakthrough complex partial seizures with postictal migraines.

298 sights into the pathophysiology of epileptic seizures with respect to ANS function, and, while furthe

299 Seizures with similar pathways tended to occur closer to

300 mino acid transporter cause microcephaly and seizures, yet the mechanisms responsible for these pheno