ライフサイエンスコーパス: seizure

1 al model with 3 states (entry, EEG risk, and seizure).

2 l risk factors) and 36% (coma and history of seizures).

3 l risk factors) and 64% (coma and history of seizures).

4 ross interneuron subtypes or evolve during a seizure.

5 and remission, and those who had relentless seizures.

6 owers the threshold for triggering epileptic seizures.

7 higher in CD rats that developed spontaneous seizures.

8 icits in conditions accompanied by recurrent seizures.

9 oupling to local field potential even before seizures.

10 es, implicating this miR in the avoidance of seizures.

11 neurodevelopmental disorders with or without seizures.

12 hesis, exaggerated mGluR-LTD, and audiogenic seizures.

13 mocortical phasic firing would treat absence seizures.

14 l neuronal injury during prolonged epileptic seizures.

15 ng sleep disorders, motor hyperactivity, and seizures.

16 mice but induced neither acute nor recurrent seizures.

17 atterns were reproducible across consecutive seizures.

18 disease, manifested in unprovoked recurrent seizures.

19 nterneurons ultimately help maintain ongoing seizures.

20 e with no seizures and those with continuing seizures.

21 intellectual disability, hyperactivity, and seizures.

22 imulation-induced patterns, and the risk for seizures.

23 thought to be crucial for the generation of seizures.

24 Scn1a (+/-) mice and suppressed spontaneous seizures.

25 as no significant reduction in nonconvulsive seizures.

26 clinical sequela of brain injury: edema and seizures.

27 tients with stroke, and 50% in patients with seizures.

28 anxiety-like behaviour and susceptibility to seizures.

29 metabolic conditions that could explain the seizures.

30 taxia, myokymia, and increased prevalence of seizures.

31 er (ASD), developmental delay, and infantile seizures.

32 ent periodic discharges (1 point); (3) prior seizure (1 point); (4) sporadic epileptiform discharges

33 was lower in patients with prolonged febrile seizures (14.3%, 6.3-29.4) and survivors of acute sympto

34 Serious adverse events included seizure (18 [5%] vs 22 [6%]) and brain oedema (seven [2%

35 video-monitored for spontaneous, convulsive seizures 9 hr/day every day for 24-36 days.

36 lectrocorticography-documented nonconvulsive seizures, accompanied by forebrain accumulation of the c

37 the SCN1A homologue recapitulate spontaneous seizure activity and mimic the convulsive behavioural mo

38 ere (1) pediatric seizure onset with ongoing seizure activity in adulthood, (2) intellectual disabili

39 also more likely to provoke seizures or pre-seizure activity in patients with photosensitive epileps

40 for 6 weeks and has the potential to control seizure activity up to 4 months (longest periods examine

41 these same mice, an 84% to 88% reduction in seizure activity was observed between 180 and 210 DAT.

42 Seizure activity, in particular status epilepticus, incr

43 and [Cl(-)]i in response to hypercapnia and seizure activity.

44 r fMRI responses are much less predictive of seizure activity.

45 D98 amino acid transporters was performed in seizure-affected cortex (n = 2) and compared with glioma

46 or spontaneous and pharmacologically induced seizures alongside changes in the cholinergic pathway ge

47 ntal delay, intellectual disability, ataxia, seizures and a happy affect.

48 ssue obtained from 20 patients with frequent seizures and a long history of drug-resistant focal epil

49 a significantly higher rate of freedom from seizures and better scores with respect to behavior and

50 ptic encephalopathy (EIEE) experience severe seizures and cognitive impairment and are at increased r

51 f a new class of drugs for treatment of both seizures and comorbid memory impairments associated with

52 ction) versus generalized (gain-of-function) seizures and corresponding epileptic discharges with pro

53 In parallel, it reduced the incidence of seizures and delayed their occurrence.

54 llectual disability syndrome associated with seizures and dysmorphic features.

55 impairment, as well as generalized and focal seizures and EEG abnormalities for patients with gain- a

56 ost presented in the first week of life with seizures and encephalopathy.

57 These individuals are prone to seizures and have high brain levels of the inflammatory

58 fects of toxic exposure in these animals are seizures and hippocampal damage, and they have been prop

59 In animal studies, both seizures and interictal spikes induce synaptic potentiat

60 s and calcium sensitive exocytosis underlies seizures and large body size associated with 16p11.2 hom

61 ften accompanied by intellectual disability, seizures and other features is a severe, clinically and

62 g countries, where it is a frequent cause of seizures and other neurological disease.

63 to consider redefining the continuum between seizures and PDs, suggesting that additional damage afte

64 d onset epilepsies with medication-resistant seizures and poor developmental outcomes.

65 res on CEEG is dependent on history of prior seizures and presence of coma.

66 thological phenotypes, including spontaneous seizures and sudden death.

67 those experiencing auras only, those with no seizures and those with continuing seizures.

68 r progression corresponded with the onset of seizures and tumor invasion.

69 atency period (and thus predict the onset of seizures) and with the power change of the high-gamma rh

70 ecorded: heart failure, neurological deficit/seizure, and hemorrhage.

71 ech, a history of febrile and/or non-febrile seizures, and a wide-based, spastic, and/or stiff-legged

72 inhibition of mGluR5 corrects hyperactivity, seizures, and elevated de novo synaptic protein synthesi

73 , number of seizures before remission, focal seizures, and epileptiform abnormality on EEG before wit

74 TATION: Underlying pathology, repeated focal seizures, and global insults each contribute to atrophy

75 her incidence of pharmacoresistant epileptic seizures, and more severe neuropsychiatric disorders.

76 ts, a more severe phenotype with intractable seizures, and the potential for sudden unexpected death

77 epileptic mice correlated with frequency of seizures, and the set of genes differentially RNA-edited

78 Because recurrent intractable seizures are a common feature of FCDs, epileptogenic ele

79 Focal seizures are assumed to arise from a hypersynchronous ac

80 Focal seizures are episodes of pathological brain activity tha

81 ctivity patterns associated with spontaneous seizures are not fully understood.

82 While daily seizures are uncommon in Rett syndrome, prolonged remiss

83 resenting in infancy with pharmaco-resistant seizures; are often accompanied by debilitating neuropsy

84 nical or electroencephalographic evidence of seizure around the time of the event.

85 These effects were not caused by seizures as indicated by EEG recordings.

86 e UBE3A gene, with behavioral phenotypes and seizures as key features.

87 epsy, history of febrile seizures, number of seizures before remission, absence of a self-limiting ep

88 e sex, family history of epilepsy, number of seizures before remission, focal seizures, and epileptif

89 to the severity of hippocampal sclerosis and seizure burden in chronic epilepsy.

90 ABAergic interneurons play critical roles in seizures, but it remains unknown whether these vary acro

91 brain amino acid metabolism during epileptic seizures by (18)F-FET PET and to elucidate the pathophys

92 iece of evidence to the proposal that limbic seizures can be supported by GABAergic hyperactivity.

93 Kainate seizures cause an immediate, but transient, vacuolizatio

94 Recurrent high-frequency epileptic seizures cause progressive hippocampal sclerosis, which

95 e identified that, similar to electrographic seizures, cause brain tissue hypoxia, a measure of ongoi

96 developmental delay, hypotonia, early-onset seizures, cerebellar atrophy, and osteopenia.

97 Similar to seizures, cerebral blood flow increases in patients with

98 last year of follow-up, suggesting enduring seizure control was not regained by this timepoint.

99 denosine levels, which might have effects on seizure control.

100 for SRSE requiring pharmacological coma for seizure control.

101 o been proposed as models of complex partial seizures (CPSs) following traumatic brain injury (post-t

102 d access to high-quality, expertly annotated seizure data from prolonged recordings.

103 geons using simulated and recorded epileptic seizure data to demonstrate our system's effectiveness.

104 We combined human encephalographic seizure data with data of a computational model of seizu

105 ompetition to crowdsource the development of seizure detection algorithms using intracranial electroe

106 eveloping accurate, validated algorithms for seizure detection is limited access to high-quality, exp

107 Affected individuals suffer from refractory seizures, developmental delay, cognitive disability, and

108 s a promising target for further research on seizure disorder therapeutics.

109 luding low birth weight, maternal education, seizure disorder, kidney disease duration, and genetical

110 could be a novel therapeutic target to treat seizure disorders and epilepsy.SIGNIFICANCE STATEMENT We

111 nts (1 day-25 years), 13 children with other seizure disorders receiving B6 supplementation (1 month-

112 any other neurological impairments including seizures, disrupted cortical lamination, and widespread

113 is one mechanism through which intermittent seizures drive persistent cognitive deficits in conditio

114 43 expression by shRNA significantly reduced seizure duration and severity in CD rats after acute sei

115 ed at 5 months without modifying the average seizure duration or the incidence of epilepsy in animals

116 months, most TBI mice exhibited spontaneous seizures during a 7 d video-EEG recording period.

117 campus, we control the risk of temporal lobe seizures during a specific time period.

118 iate early gene induced by electroconvulsive seizures (ECS), blocks its antidepressant efficacy.

119 s ratio [OR] = 1.8, p < 0.01) and history of seizures, either remotely or related to acute illness (3

120 in deaths (23.5%), 85 stroke (19.9%), and 60 seizure events (14.1%).

121 is study aimed to clarify how DHA suppresses seizures, focusing on the regulation of 17beta-estradiol

122 lformations (CCMs) are a cause of stroke and seizure for which no effective medical therapies yet exi

123 e proportion of patients remaining free from seizures for 6 consecutive months after stabilisation at

124 -loop TES in rats can consistently interrupt seizures for 6 weeks and has the potential to control se

125 n withdrawal of medications in those who are seizure free is propitious.

126 Stg/+ mice are seizure free with normal baseline beta/gamma power and n

127 obe epilepsy will not be rendered completely seizure-free after temporal lobe surgery.

128 n cohorts of patients with epilepsy who were seizure-free and had started withdrawal of antiepileptic

129 completed 6 months of treatment and remained seizure-free entered a 6-month maintenance period on the

130 Patients who were entirely seizure-free for 1, 2 and 3 years had COSY of 4.9%, 3.5%

131 ewly diagnosed epilepsy cases fail to become seizure-free in response to antiseizure drugs.

132 nce were epilepsy duration before remission, seizure-free interval before antiepileptic drug withdraw

133 -up were epilepsy duration before remission, seizure-free interval before antiepileptic drug withdraw

134 The percentage of patients who became seizure-free was 5% with cannabidiol and 0% with placebo

135 ent and a consistent definition of long-term seizure freedom.

136 changes in the dentate gyrus correlate with seizure frequency and help prioritize potential mechanis

137 hermia-induced seizures, reduced spontaneous seizure frequency and prolonged survival in the Scn1a (+

138 n hyperthermia-induced seizures, spontaneous seizure frequency and survival.

139 imary end point was the change in convulsive-seizure frequency over a 14-week treatment period, as co

140 Seizure frequency ranged from an average of one every 3.

141 Seizure frequency significantly correlated with the loss

142 o had at least a 50% reduction in convulsive-seizure frequency was 43% with cannabidiol and 27% with

143 patients who were seropositive, reduction in seizure frequency was associated with use of immunomodul

144 iol group and the placebo group in change in seizure frequency, -22.8 percentage points; 95% confiden

145 GABA-mediated inhibition, reduce spontaneous seizure frequency, and rescue behavioral deficits in a c

146 d eight multiscale recordings of spontaneous seizures from four patients with epilepsy.

147 mulation did not show an additional risk for seizures from the underlying pattern risk (P > .10).

148 an epilepsy GWAS meta-analysis and a febrile seizures (FS) GWAS are significantly more enriched with

149 d to intellectual disability with or without seizures, gait abnormalities, problems of social behavio

150 ed in human visual cortex may play a role in seizure generation [1,2].

151 tive contribution of regions of the brain to seizure generation and consequently which brain regions

152 epilepsy, including "neuron projection" and "seizures." Genes with differential RNA editing were pref

153 nt (2.9%, 0.5-14.5) in the prolonged febrile seizures group developed temporal lobe epilepsy with mes

154 thy, encephalitis, meningitis, myelitis, and seizures have also been reported.

155 tive problems.SIGNIFICANCE STATEMENT Whereas seizures have been the central focus of epilepsy researc

156 osahexaenoic acid (DHA) attenuates epileptic seizures; however, the molecular mechanism by which it a

157 To calculate the chance of a seizure in the next year (COSY) for seizures with impair

158 nderwent epilepsy surgery for drug-resistant seizures in 36 centers from 12 European countries over 2

159 ptin, produces a dose-dependent reduction in seizures in a mouse model of pharmacoresistant epilepsy.

160 tment with ethosuximide significantly blocks seizures in both genotypes, but the abnormal phase-ampli

161 Neurosurgical treatment may improve seizures in children and adolescents with drug-resistant

162 tool to aid clinical judgment of the risk of seizures in critically ill patients.

163 lence was associated with increased risk for seizures in LPDs and GPDs.

164 Treatment of clinical seizures in patients with Alzheimer's disease with selec

165 We propose that a risk factor for seizures in patients with photosensitive epilepsy is eng

166 into the causes of persistent postoperative seizures in patients with temporal lobe epilepsy.

167 We pharmacologically induced focal seizures in primary visual cortex (V1) of awake mice, an

168 y that viewing particular images can trigger seizures in some individuals.

169 ade, a treatment that paradoxically enhances seizures in stg/stg mice.

170 Seizures in temporal lobe epilepsy (TLE) disturb brain n

171 generation and propagation of temporal lobe seizures in temporal lobe epilepsy, using diffusion tens

172 ith the frequency of secondarily generalized seizures in the 3-5 days preceding the recordings.

173 metanide reduced rMF sprouting and recurrent seizures in the chronic epileptic phase.

174 nabidiol for the treatment of drug-resistant seizures in the Dravet syndrome.

175 Independent predictors of seizures in the last year of follow-up were epilepsy dur

176 9%) of 1455 for whom data were available had seizures in their last year of follow-up, suggesting end

177 Recurrent seizures in TLE are associated with disturbances in ARAS

178 If epileptiform findings developed, the seizure incidence was between 18% (no clinical risk fact

179 dation versus synthetic CB agonist on limbic seizures induced by maximal dentate activation (MDA) acu

180 cts in normal conditions, while it prevented seizure-induced alterations of both STP and LTP.

181 have clinical implications for mechanisms of seizure-induced astrocyte injury and potential therapeut

182 ng the mTOR pathway is involved in mediating seizure-induced astrocyte injury.

183 Our data also indicate a seizure-induced upregulation of neuronal, endothelial, a

184 e memory, the mechanisms by which early-life seizures influence them, and the means to abrogate the e

185 Neuronal spiking activity at seizure initiation was highly heterogeneous and not hype

186 We show that during seizure large-scale neural populations spanning centimet

187 Distinctive seizure-like events (SLEs) are induced in the olfactory

188 nel blocker 4-aminopyridine reliably induces seizure-like events in temporal lobe structures.

189 vity consistently preceded the initiation of seizure-like events.

190 brain reproduces many neuropathological and seizure-like hallmarks characteristic of epilepsy.

191 acterized by periodic dynamics that increase seizure likelihood at certain times of day, and which ar

192 reating this disease remains a challenge, as seizures manifest through mechanisms and features that s

193 tically reduced the frequency of spontaneous seizures measured at 5 months without modifying the aver

194 by forebrain accumulation of the convulsive seizures mediating miR-134.

195 Complete remission off anti-seizure medications is possible, but future efforts shou

196 veness in two of the most widely used animal seizure models, namely, the maximal electroshock (MES) t

197 (MES) test and the psychomotor 6 Hz (32 mA) seizure models.

198 ute encephalopathy syndromes, simple febrile seizures (n = 14), other seizures (n = 16), acute ataxia

199 mes, simple febrile seizures (n = 14), other seizures (n = 16), acute ataxia (n = 4), and other subac

200 [5%]), brain oedema (eight [2%] vs 11 [3%]), seizure (nine [2%] vs eight [2%]), and headache (six [2%

201 no evidence of transient ischemic attack or seizure, no acute lesion on diffusion-weighted imaging,

202 age at onset of epilepsy, history of febrile seizures, number of seizures before remission, absence o

203 Febrile seizures occurred after dose 1 of MMR vaccine at a known

204 The onset of seizures occurred before 18 years of age in 75.9% of pat

205 patients in the placebo group (P=0.001), and seizures occurred in 0.7% and 0.1%, respectively (P=0.00

206 greatest predictive value were coma (31% had seizures; odds ratio [OR] = 1.8, p < 0.01) and history o

207 The frequency of total seizures of all types was significantly reduced with can

208 INTERPRETATION: The initial risk of seizures on CEEG is dependent on history of prior seizur

209 acute structural effects of kainate-induced seizures on cortical astrocytes.

210 cids rather than ketones are likely to block seizure onset and raise seizure threshold.

211 dinal course of epilepsy nor the patterns of seizure onset and remission have been described in Rett

212 gest that network mechanisms responsible for seizure onset can be region specific.

213 were compared at 3 weeks of age, the time of seizure onset for homozygous mice.

214 ozygotes, consistent with the earlier age of seizure onset in homozygotes.

215 le mechanisms underlying the different focal seizure onset patterns in the model.

216 The inclusion criteria were (1) pediatric seizure onset with ongoing seizure activity in adulthood

217 al distribution of spikes in relation to the seizure onset zone as well as anatomical regions of the

218 rlap with those identified clinically as the seizure onset zone.

219 esia, scoliosis, gastrostomy feeding, age of seizure onset, and late age of diagnosis were independen

220 g stimulation of hyperperfused areas outside seizure onset, positive significant correlations between

221 associated with classically defined absence seizures or CPSs.

222 visual cortex is also more likely to provoke seizures or pre-seizure activity in patients with photos

223 Ten patients with 11 episodes of serial seizures or status epilepticus, who underwent MRI and (1

224 of 70 to 84 and either GMFCS level 2, active seizures, or hearing with amplification.

225 often arise before the onset of spontaneous seizures, or independent from them, yet the mechanisms i

226 emotely or related to acute illness (34% had seizures; OR = 3.0, p < 0.001).

227 e, lamotrigine, and valproate had short-term seizure outcome determined.

228 We audited seizure outcome of 693 adults who had resective epilepsy

229 ng the International League Against Epilepsy seizure outcome scale.

230 re Ab positive were more likely to have good seizure outcome than were patients with epilepsy of unkn

231 peratively identifiable risk factors of poor seizure outcome.

232 edictors of seizure recurrence and long-term seizure outcomes and to produce nomograms for estimation

233 nor allele frequency >/= 15%) in 4 genes and seizure outcomes were assessed.

234 ct of depression on the risk of epilepsy and seizure outcomes.

235 The novel seizure pattern here described is not observed in other

236 s.SIGNIFICANCE STATEMENT We describe a novel seizure pattern peculiar of the olfactory cortex that re

237 Seizure patterns identified in focal epilepsies caused b

238 The median frequency of convulsive seizures per month decreased from 12.4 to 5.9 with canna

239 ated cells mediate epileptogenesis, but that seizures per se are initiated elsewhere in the circuit.

240 During the latent pre-seizure period, epileptiform spikes were more frequent i

241 Following this common beginning, however, seizures persist and propagate both locally and into hom

242 By contrast, lamotrigine exacerbated the seizure phenotype.

243 VGSC gene, Scn8a, contribute to two distinct seizure phenotypes: (1) hypoexcitation of cortical circu

244 Epileptic seizures potently modulate hippocampal adult neurogenesi

245 The ability to improve seizure prediction algorithms through straightforward, p

246 For all subjects, clinically relevant seizure prediction results were significant, and the add

247 es of Dravet syndrome, including spontaneous seizures, premature death and seizures triggered by hype

248 Three distinct patterns of seizure prevalence emerged in classic Rett syndrome, inc

249 ere not significantly associated with either seizure prevalence or seizure severity.

250 many clinical features were associated with seizure prevalence; frequency of hospitalizations, inabi

251 Thus, while their roles may evolve during seizures, PV+ and SOM+ interneurons ultimately help main

252 of our study were to identify predictors of seizure recurrence and long-term seizure outcomes and to

253 Independent predictors of seizure recurrence were epilepsy duration before remissi

254 The risk with this action, however, is seizure recurrence.

255 es also had to contain information regarding seizure recurrences during and after withdrawal.

256 tment protected against hyperthermia-induced seizures, reduced spontaneous seizure frequency and prol

257 the pathophysiology of epileptic disorders, seizures remain poorly controlled in approximately one-t

258 Surgical treatment can bring seizure remission in people with focal epilepsy but requ

259 Epileptic seizures represent altered neuronal network dynamics, bu

260 n of cortical circuits leading to convulsive seizure resistance, and (2) hyperexcitation of thalamoco

261 It is characterised by seizures resulting from aberrant hypersynchronous neural

262 ce of LPDs and GPDs also conferred increased seizure risk (37% frequent vs 45% abundant/continuous, O

263 owever, specific features that confer higher seizure risk remain unclear.

264 sk factors and guide clinicians in assessing seizure risk.

265 rface and cortical thickening that result in seizures, severe neurological impairment and development

266 rgery with respect to the score on the Hague Seizure Severity scale (difference, 19.4; 95% confidence

267 condary outcomes were the score on the Hague Seizure Severity scale, the Binet-Kamat intelligence quo

268 associated with either seizure prevalence or seizure severity.

269 e to predict the future onset of spontaneous seizures.SIGNIFICANCE STATEMENT Postinjury epilepsy is a

270 effect of treatment on hyperthermia-induced seizures, spontaneous seizure frequency and survival.

271 mouse visual areas to demonstrate that these seizures start as local synchronous activation and then

272 tability and is associated with pathological seizure states.

273 no common polymorphisms were associated with seizure status.

274 eurologic injury was defined as brain death, seizures, stroke, and intracranial hemorrhage occurring

275 ot, however, cause an immediate reduction in seizures, suggesting that peri-insult generated cells me

276 IL-1Ra treatment reduced seizure susceptibility 2 weeks after TBI compared with v

277 pairments, the degree of neuropathology, and seizure susceptibility, after pediatric brain injury in

278 stored normal synaptic responses and reduced seizure susceptibility.

279 neurons, which could explain how AE3 reduces seizure susceptibility.

280 mediator of post-traumatic astrogliosis and seizure susceptibility.SIGNIFICANCE STATEMENT Epilepsy i

281 ate the neuronal network dynamics underlying seizure termination and the postictal generalized EEG su

282 applications, such as preventing audiogenic seizures that originate in the auditory midbrain.

283 t-unilateral, and frontomedial) and magnetic seizure therapy (MST) with cap coil on vertex.

284 These findings may guide the development of seizure therapy dosing paradigms with improved risk/bene

285 itude titrations of motor threshold (MT) and seizure threshold (ST) in four nonhuman primates (NHPs)

286 Here we show that SZT2 (seizure threshold 2), a metazoan-specific protein mutate

287 V-containing neurons transiently reduced the seizure threshold of the mice but induced neither acute

288 are likely to block seizure onset and raise seizure threshold.

289 t syndrome, including those who did not have seizures throughout the study, those who had frequent re

290 e data with data of a computational model of seizures to elucidate the neuronal network dynamics unde

291 ng spontaneous seizures, premature death and seizures triggered by hyperthermia.

292 onset epileptic encephalopathy with multiple seizure types that are often refractory to conventional

293 Seizure was the most common symptom, but almost 30% of e

294 The induced seizures were qualitatively and quantitatively indisting

295 characterized by brief (seconds) spontaneous seizures, which involve spike-wave discharges (SWDs) in

296 nce of a seizure in the next year (COSY) for seizures with impaired awareness in those experiencing a

297 of the olfactory cortex that resembles focal seizures with low-voltage fast activity at onset observe

298 duration and severity in CD rats after acute seizures with subsequent reduction in interictal spiking

299 no epileptiform findings on EEG, the risk of seizures within 72 hours was between 9% (no clinical ris

300 es, featuring early-onset ataxia and absence seizure without significant alterations in the basic pro