ライフサイエンスコーパス: convulsive

1 en appeared to have bilateral onset and were convulsive.

2 Folates have been shown to be neurotoxic and convulsive.

3 n of thalamocortical circuits leading to non-convulsive absence epilepsy.

4 acid (GABA) systems have been implicated in convulsive activity and have been proposed to underlie t

5 lent to 0.9 LD50) or saline and observed for convulsive activity.

6 chemotype fills a gap in a comparison set of convulsive and neurotrophic sesquiterpenes, which we hyp

7 with improved efficacy for the treatment of convulsive and non-convulsive epilepsy that expert group

8 ributions of astrocytes to the expression of convulsive and non-convulsive epileptiform discharges an

9 rats video-EEG analysis over 9 days revealed convulsive and non-convulsive seizure activity in rats i

10 complex seizure disorder that includes both convulsive and non-convulsive seizures, and is dependent

11 bility of CA3 pyramidal neurons and elicited convulsive and non-convulsive spontaneous epileptic seiz

12 f electrographically recorded seizures (both convulsive and nonconvulsive) was analyzed quantitativel

13 In spite of their potentially pro-convulsive arrangement with granule cells, mossy cells h

14 the premotor interneurons in regulating the convulsive behavior caused by a gain-of-function mutatio

15 k undergo a dominance shift as each specific convulsive behavior of AGS is elaborated.

16 sent study examined DLSC neuronal firing and convulsive behavior simultaneously in freely-moving gene

17 h in generation of this AGS kindling-induced convulsive behavior.

18 play a direct role in the generation of this convulsive behavior.

19 ellular single neuron firing and concomitant convulsive behaviors associated with 14 repetitive AGS w

20 increases of seizure duration and additional convulsive behaviors.

21 e spontaneous seizure activity and mimic the convulsive behavioural movements observed in Dravet synd

22 -approved compound (clemizole) that inhibits convulsive behaviours and electrographic seizures.

23 l electrographic activity, hyperactivity and convulsive behaviours.

24 red early in the management of patients with convulsive blackouts.

25 s particularly promising because of its anti-convulsive capabilities.

26 s the leading cause of acquired epilepsy and convulsive conditions worldwide.

27 Consequently, the convulsive dose of PTZ caused more significant molecular

28 sess this, rats were injected with a single, convulsive dose of soman (77.7 micrograms/kg, i.m.).

29 ntervals between 1 hour and 24 hours after a convulsive dose of soman.

30 motor response to pentylenetetrazole, a pro-convulsive drug, consistent with impaired neurodevelopme

31 levated in specific rat brain regions by the convulsive drug, pentylenetetrazole, as well as by the a

32 Recently, we identified anti-convulsive effects of naltrexone, a mu-opioid receptor (

33 Adjusted odds of active convulsive epilepsy for all individuals were increased w

34 gap in, and possible risk factors for active convulsive epilepsy in Kenyan people aged 6 years or old

35 ost studies in Africa have focused on active convulsive epilepsy in rural areas, but there are few da

36 heterogeneity exists in prevalence of active convulsive epilepsy in this rural area in Kenya.

37 cacy for the treatment of convulsive and non-convulsive epilepsy that expert groups have recognized a

38 Overall prevalence of active convulsive epilepsy was 2.9 per 1000 (95% CI 2.6-3.2); a

39 8.7 cases per 1000 people (8.0-9.6), and non-convulsive epilepsy was 3.2 cases per 1000 people (2.7-3

40 .9 cases per 1000 people (95% CI 11.0-12.8), convulsive epilepsy was 8.7 cases per 1000 people (8.0-9

41 defined as the proportion of cases of active convulsive epilepsy without detectable amounts of antiep

42 .4-11.0; p<0.0001) raised the odds of active convulsive epilepsy.

43 omyography (EMG) for differentiation between convulsive epileptic and psychogenic nonepileptic seizur

44 ytes to the expression of convulsive and non-convulsive epileptiform discharges and seizures.

45 epression, suicidal behavior, psychosis, and convulsive episodes.

46 Forty-four consecutive episodes with convulsive events were automatically analyzed with the a

47 of clinical history (loss of consciousness, convulsive fits) and neurological signs (face, arm, or l

48 ntrasted with fast polyspike activity during convulsive generalized seizures.

49 s to anomalous brain activity (increased non-convulsive hyperactivity) but is not a risk factor for t

50 Status epilepticus was convulsive in 124 (70.1%) and nonconvulsive in 53 (29.9%

51 Status epilepticus was convulsive in 132 cases (92%).

52 ude-titrated seizure threshold (ST) by a non-convulsive measurement of motor threshold (MT) using sin

53 nstem AGS network nuclei responsible for the convulsive motor behaviors of ETX seizures.

54 electroencephalogram, with or without subtle convulsive movements such as rhythmic muscle twitches or

55 Also, branched networks undergo rare convulsive movements, "avalanches," that release strain

56 dered relatively benign because of their non-convulsive nature and the large incidence of remittance

57 genously administered morphine can have both convulsive or anticonvulsive effects, depending on the d

58 tatus epilepticus was defined as generalized convulsive or nonconvulsive status epilepticus (SE) that

59 th complex partial compared with generalized convulsive or nonconvulsive status epilepticus in coma.

60 was first identified based on its ataxic and convulsive phenotype.

61 (GTCSs) from 11 patients, and 19 episodes of convulsive PNES from 13 patients.

62 nd 5 Hz consistently showed evidence of anti-convulsive properties in their iEEG-based seizure profil

63 s might affect the mechanisms underlying the convulsive properties of nicotine.

64 erval between MS and the first appearance of convulsive response (2 weeks) was characterized by deep

65 o sequential morphological stages preceded a convulsive rupture of membranes and rapid radial dischar

66 ssation of SE within 1 hour (for generalized convulsive SE [GCSE]) and 12 hours (for non-GCSE) of ini

67 ysis over 9 days revealed convulsive and non-convulsive seizure activity in rats infused with LGI1-mA

68 eatment was initiated after observation of a convulsive seizure and repeated at 4 to 6 week intervals

69 essive increase in the number and density of convulsive seizure clusters.

70 rvation period to establish baseline monthly convulsive seizure frequency (MCSF; convulsive seizures

71 provided significantly greater reduction in convulsive seizure frequency compared with placebo and w

72 Together with solitary living and convulsive seizure frequency, peri-ictal apnoea (>14 s f

73 or older, had been treated for a generalised convulsive seizure of longer than 5 min duration with ad

74 poexcitation of cortical circuits leading to convulsive seizure resistance, and (2) hyperexcitation o

75 Focal and convulsive seizure thresholds were evaluated 10-12 min p

76 A brief convulsive seizure was associated with marked changes in

77 The primary end point was the change in convulsive-seizure frequency over a 14-week treatment pe

78 nnabidiol resulted in a greater reduction in convulsive-seizure frequency than placebo and was associ

79 patients who had at least a 50% reduction in convulsive-seizure frequency was 43% with cannabidiol an

80 rosis), a history of secondarily generalised convulsive seizures (2.3; 95% CI 1.7 to 3.0 for these se

81 (SUDEP) that exhibit audiogenic generalized convulsive seizures (GCS), ending in death due to respir

82 ere we found that both focal and generalized convulsive seizures (GCSs) in epilepsy patients caused a

83 all animals as did the total duration of non-convulsive seizures (NCS) in the alpha-chloralose-anesth

84 ce (n = 9) had increased numbers of observed convulsive seizures (P = 0.004), a higher total seizure

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

86 se is a strain that is highly susceptible to convulsive seizures after repeated sensory stimulation.

87 ed per 100 000 person-years) for generalised convulsive seizures and intussusception were similar bet

88 tion of p.Arg1872Trp by EIIa-Cre resulted in convulsive seizures and lethality at 2 weeks of age.

89 e detect ictal discharges that coincide with convulsive seizures and myoclonic jerks.

90 ctal arrhythmias were mostly found following convulsive seizures and often associated with (near) SUD

91 ication which may be impaired in autism, non-convulsive seizures and other conditions.

92 eizure phenotype associated with spontaneous convulsive seizures and profound deficits in hippocampus

93 esults suggest that local anesthetic-induced convulsive seizures are mediated by excitatory glutamate

94 Lethal convulsive seizures are observed beginning at postnatal

95 h sexes, two models of SUDEP, and found that convulsive seizures caused a postictal decrease in venti

96 milial Alzheimer's disease transgene-induced convulsive seizures did not occur in mice lacking PrP(C)

97 Convulsive seizures during ethanol withdrawal (ETX) in r

98 was the change in mean monthly frequency of convulsive seizures during the treatment period compared

99 that were validated in EEG recordings of 48 convulsive seizures from 48 subjects with refractory foc

100 se models of SUDEP we found that generalized convulsive seizures impaired CO(2) chemoreception, and i

101 Certain anti-convulsant drugs, as well as convulsive seizures impede recovery when administered du

102 l symptoms, as well as spontaneous recurrent convulsive seizures in 45% and epileptiform spikes in 10

103 umented to exert a protective action against convulsive seizures in animal models, when administered

104 in the mouse hippocampal CA1 reliably evoked convulsive seizures in awake mice.

105 potential as an acute abortive treatment for convulsive seizures in emergency situations.

106 ic activities and neural dynamics leading to convulsive seizures in patients and mouse models of Drav

107 5% CI 3.94-14.71), three or more generalised convulsive seizures in the previous year (3.1, 1.64-5.87

108 5-year seizure freedom (eg, a normal MRI and convulsive seizures in the previous year has a probabili

109 Generalized convulsive seizures increase glucose utilization within

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

111 was to elucidate the effects of generalized convulsive seizures on distinct and separate corticotrop

112 The median frequency of convulsive seizures per month decreased from 12.4 to 5.9

113 e minutes or more) or repetitive generalized convulsive seizures received intravenous diazepam (5 mg)

114 FPI-treated rats developed nonconvulsive or convulsive seizures that could be distinguished electrog

115 monthly convulsive seizure frequency (MCSF; convulsive seizures were defined as hemiclonic, tonic, c

116 1) a strong IEGP response to kainate-induced convulsive seizures, (2) no IEGP response after prolonga

117 e hypersynchronization and nonconvulsive and convulsive seizures, accompanied by expression changes i

118 on of consciousness occurs after generalized convulsive seizures, and includes analgesia, lasting for

119 sorder that includes both convulsive and non-convulsive seizures, and is dependent upon Celf4 gene do

120 seizures (lightning-like jerks), generalized convulsive seizures, and varying degrees of neurological

121 o the bilateral motor cortex, which mediates convulsive seizures, have not been delineated.

122 spinal cord in several forms of generalized convulsive seizures, including audiogenic seizures (AGS)

123 Generalised-particularly nocturnal-convulsive seizures, longstanding epilepsy, and solitary

124 es, with or without progression to bilateral convulsive seizures, was the most common seizure type.

125 acute group I mGluR-dependent propensity for convulsive seizures.

126 gy through blood-brain barrier breakdown and convulsive seizures.

127 lsant pentylenetetrazole-induced generalized convulsive seizures.

128 ucible progression from hyperexcitability to convulsive seizures.

129 ns ranging from mild cognitive impairment to convulsive seizures.

130 (AD)-generating stimulations and individual convulsive seizures.

131 were hypersusceptible to chemically induced convulsive seizures.

132 inguishing between epileptic and psychogenic convulsive seizures.

133 ng of treatment relative to the cessation of convulsive seizures.

134 One serious adverse effect of these drugs is convulsive seizures; however, the mechanisms underlying

135 idal neurons and elicited convulsive and non-convulsive spontaneous epileptic seizures in mice and ra

136 critical period delayed recovery, while non-convulsive Stage 0 seizures were neutral.

137 Specifically, convulsive Stage 1 seizures evoked ipsilateral to the le

138 ulsions into a prolonged (> 8 min) postictal convulsive state expressed mainly by continuous partial

139 he corresponding prevalence was high in post convulsive status epilepticus (33.5%, 20.2%, and 32.9%),

140 stematic review on the outcome of paediatric convulsive status epilepticus (CSE) and investigated the

141 Episodes of childhood convulsive status epilepticus (CSE) commonly start in th

142 The prognosis of convulsive status epilepticus (CSE), a common childhood

143 dren died within 30 days of their episode of convulsive status epilepticus and 16 during follow-up.

144 ediatric data will help inform management of convulsive status epilepticus and appropriate allocation

145 y the 518 patients with verified generalized convulsive status epilepticus as well as with data on al

146 of death within 8 years following childhood convulsive status epilepticus but most deaths are not se

147 al experiments suggest that treatment of non-convulsive status epilepticus following specific insults

148 This study reviews protocols for treating convulsive status epilepticus from 33 emergency medical

149 %, 6-18) of children with first ever febrile convulsive status epilepticus had acute bacterial mening

150 -term mortality and its predictors following convulsive status epilepticus in childhood are uncertain

151 Convulsive status epilepticus in childhood is more commo

152 .98 years) were included in the North London Convulsive Status Epilepticus in Childhood Surveillance

153 S): a prospective, population-based study of convulsive status epilepticus in childhood, to obtain a

154 y ascertained during a surveillance study of convulsive status epilepticus in childhood.

155 s anticonvulsant for treatment of paediatric convulsive status epilepticus in the UK; however, some e

156 Generalized convulsive status epilepticus is a life-threatening emer

157 Although generalized convulsive status epilepticus is a life-threatening emer

158 Generalized convulsive status epilepticus is a neurological emergenc

159 icate that hippocampal epileptogenesis after convulsive status epilepticus is an immediate network de

160 Generalized convulsive status epilepticus is associated with a rapid

161 Generalized convulsive status epilepticus is associated with high mo

162 A common form of generalized convulsive status epilepticus is of focal onset.

163 e human condition remains uncertain, but non-convulsive status epilepticus is probably an under-recog

164 cant neurological impairments at the time of convulsive status epilepticus is the main risk factor fo

165 Convulsive status epilepticus is the most common childho

166 Convulsive status epilepticus is the most common neurolo

167 Convulsive status epilepticus is the most serious manife

168 Convulsive status epilepticus often results in permanent

169 The attributable role of convulsive status epilepticus on mortality remains uncer

170 aged 3 months to younger than 18 years with convulsive status epilepticus presenting to 1 of 11 US a

171 ith epilepsy, its frequency in patients with convulsive status epilepticus remains unknown.

172 ipants aged 6 months to under 18 years, with convulsive status epilepticus requiring second-line trea

173 Non-convulsive status epilepticus should be considered in an

174 hort from north London, UK (the north London convulsive status epilepticus surveillance study cohort;

175 d demographic data for episodes of childhood convulsive status epilepticus that took place in north L

176 and valproate - in children and adults with convulsive status epilepticus that was unresponsive to t

177 servative estimation of 1-year recurrence of convulsive status epilepticus was 16% (10-24%).

178 dian time from randomisation to cessation of convulsive status epilepticus was 35 min (IQR 20 to not

179 Convulsive status epilepticus was terminated in 106 (70%

180 ignificant neurological impairments prior to convulsive status epilepticus was the only independent r

181 pairment who survived their acute episode of convulsive status epilepticus were not at a significantl

182 ly assigned 270 critically ill patients with convulsive status epilepticus who were receiving mechani

183 ked granule cell epileptiform discharges and convulsive status epilepticus with minimal lethality.

184 was time from randomisation to cessation of convulsive status epilepticus, analysed in the modified

185 mortality within 8 years after an episode of convulsive status epilepticus, and investigate its predi

186 up were associated with intractable seizures/convulsive status epilepticus, and the rest died as a co

187 Prevalence was particularly high in post convulsive status epilepticus, CNS infection, and post c

188 isoning or infection, seizures including non-convulsive status epilepticus, endocrinopathy, or thiami

189 The latter led to the hypothesis that convulsive status epilepticus, including PFC, can cause

190 intravenous treatment for overt generalized convulsive status epilepticus, lorazepam is more effecti

191 h a verified diagnosis of subtle generalized convulsive status epilepticus, no significant difference

192 naesthetic agents for refractory generalised convulsive status epilepticus, rather than additional tr

193 In the context of benzodiazepine-refractory convulsive status epilepticus, the anticonvulsant drugs

194 successfully modeled experimentally because convulsive status epilepticus, the insult most commonly

195 Among pediatric patients with convulsive status epilepticus, treatment with lorazepam

196 ork, we identify three phases of generalised convulsive status epilepticus, which we call impending,

197 urs of subsequent stimulation, and prevented convulsive status epilepticus.

198 pal excitation in awake rats without causing convulsive status epilepticus.

199 en enrolled, 176 had a first ever episode of convulsive status epilepticus.

200 ad a verified diagnosis of overt generalized convulsive status epilepticus.

201 tam for second-line management of paediatric convulsive status epilepticus.

202 al diseases, hepatic encephalopathy, and non-convulsive status epilepticus.

203 re used identify subclinical seizures or non-convulsive status epilepticus.

204 rmia on neurologic outcomes in patients with convulsive status epilepticus.

205 es than standard care alone in patients with convulsive status epilepticus.

206 myopathy in patients admitted to the ICU for convulsive status epilepticus.

207 s common in patients admitted to the ICU for convulsive status epilepticus.

208 nticonvulsant in the treatment of paediatric convulsive status epilepticus.

209 irments when they had their acute episode of convulsive status epilepticus.

210 prolonged febrile convulsions and idiopathic convulsive status epilepticus.

211 ting of benzodiazepine-resistant established convulsive status epilepticus: the EcLiPSE and ConSEPT s

212 Furthermore, LFS for 30 min before a pro-convulsive stimulus successfully prevented seizure gener

213 he value of cardiovascular tests to diagnose convulsive syncope in patients with apparent treatment-r

214 involves a variety of methods, from electro-convulsive therapy to inter-personal psychotherapy.

215 generally been limited to 1 to 2.5 times the convulsive threshold and the antidepressant efficacy has