ライフサイエンスコーパス: convulsive

1 Folates have been shown to be neurotoxic and convulsive.

2 en appeared to have bilateral onset and were 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 complex seizure disorder that includes both convulsive and non-convulsive seizures, and is dependent

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

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

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

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

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

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

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

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

18 increases of seizure duration and additional convulsive behaviors.

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

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

21 l electrographic activity, hyperactivity and convulsive behaviours.

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

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

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

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

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

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

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

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

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

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

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

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

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

35 .4-11.0; p<0.0001) raised the odds of active convulsive epilepsy.

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

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

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

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

40 ntrasted with fast polyspike activity during convulsive generalized seizures.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

58 A brief convulsive seizure was associated with marked changes in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

73 Convulsive seizures during ethanol withdrawal (ETX) in r

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

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

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

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

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

79 5-year seizure freedom (eg, a normal MRI and convulsive seizures in the previous year has a probabili

80 Generalized convulsive seizures increase glucose utilization within

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

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

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

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

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

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

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

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

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

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

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

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

93 inguishing between epileptic and psychogenic convulsive seizures.

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

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

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

97 lsant pentylenetetrazole-induced generalized convulsive seizures.

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

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

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

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

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

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

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

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

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

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

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

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

110 %, 6-18) of children with first ever febrile convulsive status epilepticus had acute bacterial mening

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

112 Convulsive status epilepticus in childhood is more commo

113 .98 years) were included in the North London Convulsive Status Epilepticus in Childhood Surveillance

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

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

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

117 Generalized convulsive status epilepticus is a neurological emergenc

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

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

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

121 Convulsive status epilepticus is the most common childho

122 Convulsive status epilepticus is the most common neurolo

123 Convulsive status epilepticus often results in permanent

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

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

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

127 Non-convulsive status epilepticus should be considered in an

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

151 prolonged febrile convulsions and idiopathic convulsive status epilepticus.

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

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

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

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

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

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