ライフサイエンスコーパス: epileptic seizure

1 ity, neurodegeneration and susceptibility to epileptic seizure.

2 thology and die 30-60 days postnatal from an epileptic seizure.

3 out (AE3(-/-) ) mice are more susceptible to epileptic seizure.

4 with impaired consciousness with or without epileptic seizure.

5 in mice lowers the threshold for triggering epileptic seizures.

6 dence implicates glutamatergic mechanisms in epileptic seizures.

7 attention for their potential involvement in epileptic seizures.

8 temporally correlates with the emergence of epileptic seizures.

9 s such as ischemic stroke, brain trauma, and epileptic seizures.

10 ted in ERK activation and caused spontaneous epileptic seizures.

11 he feedback control of neuronal circuits and epileptic seizures.

12 KO) mice exhibit brain enlargement and fatal epileptic seizures.

13 n parameters, and long-term effect of DBS on epileptic seizures.

14 ion and to the development and expression of epileptic seizures.

15 both control conditions and during prolonged epileptic seizures.

16 ippocampus in the occurrence and severity of epileptic seizures.

17 le after 30 min of experimental induction of epileptic seizures.

18 e imbalance as a molecular rationale for the epileptic seizures.

19 EEG abnormalities and dose-dependent risk of epileptic seizures.

20 ng the evaluation of gustatory and olfactory epileptic seizures.

21 ppocampal excitability and predisposition to epileptic seizures.

22 nt neural activity typically associated with epileptic seizures.

23 ous insults, including cerebral ischemia and epileptic seizures.

24 onized rhythmic oscillations of sleep and of epileptic seizures.

25 psy but there was no other family history of epileptic seizures.

26 and type 1 InsP3R mutants display ataxia and epileptic seizures.

27 erative conditions such as stroke and severe epileptic seizures.

28 cation, and thereby reduce susceptibility to epileptic seizures.

29 uronal death induced by proneurotrophins and epileptic seizures.

30 column (DCS) of the spinal cord to suppress epileptic seizures.

31 central to the initiation and progression of epileptic seizures.

32 (median follow-up 23.6 years) had unprovoked epileptic seizures.

33 , a disrupted blood-brain barrier (BBB), and epileptic seizures.

34 ting, on-demand CN stimulation could disrupt epileptic seizures.

35 enetic activation has been reported to block epileptic seizures.

36 is that astrogliosis is sufficient to induce epileptic seizures.

37 convulsant drug is used for the treatment of epileptic seizures.

38 hippocampal neuronal injury during prolonged epileptic seizures.

39 is can cause hippocampal neuronal loss after epileptic seizures.

40 iched in the hippocampus, often the focus of epileptic seizures.

41 nsidered during the evaluation of vestibular epileptic seizures.

42 hat appears to be related to the presence of epileptic seizures.

43 Traumatic brain injury often leads to epileptic seizures.

44 to sensory stimuli, and a high incidence of epileptic seizures.

45 the effect of the ketogenic diet in reducing epileptic seizures.

46 re classified at 6 months as having definite epileptic seizures, 228 as having possible epileptic sei

47 and the lack of nElavl leads to spontaneous epileptic seizure activity.

48 neocortex on the development of neocortical epileptic seizures after head injury in the rat.

49 nd persistent prevention and modification of epileptic seizures after head injury with a cooling prot

50 nd persistent prevention and modification of epileptic seizures after head injury with a cooling prot

51 Epileptic seizures also repress Cbln1 and are found to e

52 monstrate the spontaneous transition between epileptic seizure and spreading depression states as the

53 fast hemodynamic changes during inter-ictal epileptic seizures and 2) temperature variations during

54 e epileptic seizures, 228 as having possible epileptic seizures and 220 as having febrile seizures.

55 AC in cortical gray matter may contribute to epileptic seizures and cell death in diverse diseases of

56 e treatment of patients with psychogenic non-epileptic seizures and generates ideas for future resear

57 s, which possibly leads to the initiation of epileptic seizures and ictal events.

58 ypes including resistance to kainite-induced epileptic seizures and neuronal toxicity.

59 w-carbohydrate (ketogenic) diet might reduce epileptic seizures and offer neuroprotection in part bec

60 t clinically lie in the "borderland" between epileptic seizures and physiological deja vu.

61 Spontaneous epileptic seizures and the integrity of the blood-brain

62 gy and explosive dynamical transitions as in epileptic seizures and their propagations in the brain.

63 tor cells causes mice to develop progressive epileptic seizure, and dramatically reduces basal synapt

64 tributes to the variability in occurrence of epileptic seizures, and (4) the window for antiepileptog

65 ary studies of patients with focal dystonia, epileptic seizures, and auditory hallucinations indicate

66 pilocarpine-treated animals began to display epileptic seizures, and CB(1) receptor expression was ch

67 FGF22-deficient mice are resistant to epileptic seizures, and FGF7-deficient mice are prone to

68 pomas, higher incidence of pharmacoresistant epileptic seizures, and more severe neuropsychiatric dis

69 fected tissues, and in plasma in response to epileptic seizures, and point to it as biomarker of hipp

70 system are involved in learning and memory, epileptic seizures, and processing the amyloid precursor

71 Epileptic seizures are a common and poorly understood co

72 Epileptic seizures are associated with increases in hipp

73 Epileptic seizures are characterized by periods of hyper

74 Epileptic seizures are characterized by periods of recur

75 Epileptic seizures are generally unpredictable and arise

76 r ex vivo and in vivo data, we conclude that epileptic seizures are manifested as the first symptom w

77 Epileptic seizures are traditionally characterized as th

78 vioral domains, as well as hyperactivity and epileptic seizures, as have been reported in humans with

79 s (RE), a childhood disease characterized by epileptic seizures associated with progressive destructi

80 isoaspartate and typically succumb to fatal epileptic seizures at 4-10 weeks of age.

81 1970s engineers designed systems to predict epileptic seizures based upon quantitative changes in th

82 lmost 40 years, neuroscientists thought that epileptic seizures began abruptly, just a few seconds be

83 re of these syndromes is a predisposition to epileptic seizures but each is associated with different

84 ing to severe neurological symptoms, such as epileptic seizures, but no specific treatment is availab

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

86 Recurrent high-frequency epileptic seizures cause progressive hippocampal scleros

87 e and fertile, and they did not manifest the epileptic seizures characteristic of the Alpl(-/-) model

88 In epileptic seizures consciousness is often transiently lo

89 patterns and an increased susceptibility to epileptic seizures consistent with an impairment of cort

90 id 10 significantly reduced the incidence of epileptic seizures, cortical amyloid burden, and neuroin

91 ural circuitry that address the question "Do epileptic seizures damage the brain?"

92 d neurosurgeons using simulated and recorded epileptic seizure data to demonstrate our system's effec

93 Understanding how epileptic seizures develop or identifying diagnostic ind

94 trophies), strokes and stroke-like episodes, epileptic seizures, developmental delay, and demyelinati

95 e behavioural testing have shed light on how epileptic seizures disrupt the consciousness system.

96 ce display frequent myoclonus and occasional epileptic seizures, documented by electroencephalographi

97 deo-telemetry database who had 30 documented epileptic seizures during video-EEG recording and who la

98 Epileptic seizure emergencies are life-threatening condi

99 in the development of hyperexcitability and epileptic seizures following traumatic brain injury (TBI

100 ewly diagnosed, previously untreated partial epileptic seizures from 44 European centres and randomly

101 e regions and networks involved during focal epileptic seizure generation in humans.

102 he galanin neuropeptide in the regulation of epileptic seizures has been established in animal models

103 RY ON THIS ARTICLE : Accurate forecasting of epileptic seizures has the potential to transform clinic

104 e the diagnostic features of psychogenic non-epileptic seizures have been better characterized in rec

105 Patients with partial epileptic seizures have focal regions that periodically

106 By observing the march of epileptic seizures he developed the idea of somatotopic

107 At high levels, generating sustained epileptic seizures, however, we find that rNSCs divide s

108 n that docosahexaenoic acid (DHA) attenuates epileptic seizures; however, the molecular mechanism by

109 by 0.5 to 2 degrees C inhibited the onset of epileptic seizures in a dose-dependent fashion.

110 molecular model explaining the occurrence of epileptic seizures in association with malignant gliomas

111 providing a noninvasive tool for localizing epileptic seizures in humans because of its high spatial

112 have been identified as a likely trigger of epileptic seizures in mesial temporal lobe epilepsy (MTL

113 ave been identified in which mutations cause epileptic seizures in mice.

114 integrins, and have been thought to underlie epileptic seizures in patients with cortical malformatio

115 Pilocarpine injection induces epileptic seizures in rodents, an experimental paradigm

116 oscopic lights or repeated sounds can induce epileptic seizures in susceptible individuals.

117 tant in the development and/or generation of epileptic seizures in this mouse strain and may be a sig

118 ults of radiofrequency surgery indicate that epileptic seizures in this syndrome originate and propag

119 ncy treatment of acute febrile and afebrile (epileptic) seizures in children.

120 The identification of epileptic seizure-induced alterations on the brain relat

121 nd collaborators show the key role of Bim in epileptic seizure-induced neuronal injury and identify t

122 An epileptic seizure is frequently the presenting sign of i

123 onal processes implicated in the etiology of epileptic seizures, learning, and memory (see the relate

124 ibe a novel method of adaptively controlling epileptic seizure-like events in hippocampal brain slice

125 rom a small number of patients, suggest that epileptic seizures may begin as a cascade of electrophys

126 Tissue acidosis following ischaemia and epileptic seizures may contribute to neuronal damage, wh

127 logical syndrome of infancy characterized by epileptic seizures of cerebellar origin.

128 e comprising severe retardation, early onset epileptic seizures, optic nerve/cerebellar atrophy, peda

129 whose absence or modification either causes epileptic seizures or, conversely, limits epileptogenesi

130 In patients with impaired consciousness, epileptic seizure, or temporal lobe symptoms of new onse

131 Brain injuries by physical trauma, epileptic seizures, or microbial infection upset the osm

132 Epileptic seizures, particularly infantile spasms, are o

133 Some evidence suggests that psychogenic non-epileptic seizures (PNES) are associated with increased

134 Psychogenic non-epileptic seizures (PNES) are classified with other func

135 60 consecutive patients with psychogenic non-epileptic seizures (PNES), 5-10 years after diagnosis.

136 dies of long-term outcome in psychogenic non-epileptic seizures (PNES), and none of long-term healthc

137 Epileptic seizures potently modulate hippocampal adult n

138 ntral nervous system characterized by severe epileptic seizures, progressive degeneration of a single

139 the entire network, which is reminiscent of epileptic seizure propagation in the brain.

140 Epileptic seizures reflect a pathological brain state ch

141 Epileptic seizures represent altered neuronal network dy

142 Epileptic seizures represent dysfunctional neural networ

143 ue plasminogen activator, and so explain the epileptic seizures seen in individuals with more severe

144 neurodevelopmental disorder characterized by epileptic seizures, severe intellectual disability, and

145 ies of epilepsy action mechanisms underlying epileptic seizures should be lightened.

146 In contrast, regions associated with epileptic seizures, such as the hippocampus, did not exh

147 among the females, were prone to spontaneous epileptic seizures, suggesting that USF is important in

148 pared with 30 matching live controls with 92 epileptic seizures taken from the same database.

149 ulti-unit computational neural mass model of epileptic seizure termination and postictal recovery was

150 vances in the understanding and treatment of epileptic seizures that derive from a non-neurocentric v

151 r focal neurological deficits (not including epileptic seizure) that were definitely or possibly rela

152 citation may constitute a mechanism by which epileptic seizures trigger compensatory interictal netwo

153 nd manifests in an altered susceptibility to epileptic seizures, underscoring the importance of FGF-d

154 euronal death induced by proneurotrophins or epileptic seizures was assessed and compared with respon

155 eurons caused by focal cerebral ischemia and epileptic seizures was exacerbated in TNFR-KO mice, indi

156 ited at the time of their first diagnosis of epileptic seizures was undertaken; in those classified 6

157 data to diagnose epilepsy following a single epileptic seizure; we find that a prediction model expla

158 ailable antagonist, JNJ-47965567, suppressed epileptic seizures well beyond the time of treatment and

159 Epileptic seizures were assessed by 5-electrode video-el

160 e a possible mechanism for the recurrence of epileptic seizures, which are known to be the results of

161 nized activities, including those underlying epileptic seizures, which often appear as a transformati

162 evelopment of epilepsy and the generation of epileptic seizures will require delineation of the aberr

163 evelopment of epilepsy and the generation of epileptic seizures will undoubtedly benefit from researc

164 e frequently implicated in the generation of epileptic seizures, with temporal lobe epilepsy constitu

165 eased GABAergic inhibition, and can generate epileptic seizures within 1 month of lesioning.