ライフサイエンスコーパス: loss of consciousness

1 ally defined functional networks despite the loss of consciousness.

2 a-rhythm at dose levels sufficient to induce loss of consciousness.

3 yncope is only 1 of many causes of transient loss of consciousness.

4 l energy consumption with anesthesia-induced loss of consciousness.

5 cause impaired cerebral functions, including loss of consciousness.

6 produce analgesia but do not induce complete loss of consciousness.

7 K(+) channels (TREK-1) and reversibly induce loss of consciousness.

8 anaesthetic levels known to induce profound loss of consciousness.

9 the terminal), including 99 with documented loss of consciousness.

10 ovement that can lead to physical injury and loss of consciousness.

11 ting in the common end point of sedation and loss of consciousness.

12 riencing unresponsiveness, such as transient loss of consciousness.

13 improvement of swallowing, eight years after loss of consciousness.

14 , and pharmacologically-induced (anesthesia) loss of consciousness.

15 s sensory and cognitive processes to achieve loss of consciousness.

16 ated headache, seizures, vomiting, fever, or loss of consciousness.

17 halography (TMS-EEG), breaks down during the loss of consciousness.

18 ia, chorea or a combination thereof, without loss of consciousness.

19 e of these neurons during anesthetic-induced loss of consciousness.

20 sequence different from that observed during loss of consciousness.

21 nsiveness, which is commonly associated with loss of consciousness.

22 o-cortical hypoconnectivity, apparent during loss of consciousness.

23 ions and help to understand propofol-induced loss of consciousness.

24 fulness, propofol-induced mild sedation, and loss of consciousness.

25 rk changes that occurred simultaneously with loss of consciousness.

26 lta to alpha range) rises selectively during loss of consciousness.

27 h marked topological alterations observed in loss of consciousness.

28 ility, which did not further increase during loss of consciousness.

29 thalamo-cortical transmission characterizing loss of consciousness.

30 in by dampening brain activity and promoting loss-of-consciousness.

31 soldiers, 124 (4.9%) reported injuries with loss of consciousness, 260 (10.3%) reported injuries wit

32 re dyspnea (53.0%), diaphoresis (48.5%), and loss of consciousness (40.7%).

33 Of those reporting loss of consciousness, 43.9% met criteria for post-traum

34 ncluding a significantly higher frequency of loss of consciousness (58.3% [14 of 24] vs 34.3% [37 of

35 If so, the loss of consciousness, a feature of sleep, would be the

36 s with behavioral arrest, moderate-to-severe loss of consciousness (absence), and distinct spike-wave

37 al anesthesia is characterized by reversible loss of consciousness accompanied by transient amnesia.

38 Head injury with loss of consciousness, although uncommon in this sample,

39 experienced an MMTBI (blunt head trauma with loss of consciousness, amnesia, or disorientation and a

40 ile anesthetics (VAs) produce their effects (loss of consciousness, analgesia, amnesia, and immobilit

41 ead impacts that showed clear video signs of loss of consciousness and 21 showing clear abnormal post

42 We found that single mTBI causes a brief loss of consciousness and a transient reduction in dendr

43 sorders, and the presence of clinical signs (loss of consciousness and amnesia) were the factors asso

44 .47 [95% CI, 1.62-3.78]) and clinical signs (loss of consciousness and amnesia; AOR, 1.90 [95% CI, 1.

45 To understand the mechanisms underlying loss of consciousness and analgesia induced by general a

46 ause transient neurological events including loss of consciousness and dystonic posturing.

47 s states, but which is diminished during the loss of consciousness and enhanced during psychedelic st

48 ose lesions are likely to be associated with loss of consciousness and fatal hyperthermia in humans.

49 memory loss, dizziness, ataxia, hemiparesis, loss of consciousness and hemisensory symptoms, in the h

50 This strong correlation between loss of consciousness and high amplitude delta oscillati

51 d neurological effects, including reversible loss of consciousness and immobility.

52 We quantified clinical signs of loss of consciousness and intracranial EEG activity duri

53 ingestion of raw seafood, he showed wheals, loss of consciousness and low blood pressure.

54 brain displacement has been associated with loss of consciousness and poor outcome in a range of acu

55 Syncope is a sudden transient loss of consciousness and postural tone with spontaneous

56 ized by severe hypoglycemia that may lead to loss of consciousness and seizures.

57 When symptomatic, it may result in loss of consciousness and thus cause injury.

58 xpansion foam to quantify the time to induce loss of consciousness and ultimately brain death.

59 developed an acute-onset severe headache and loss of consciousness and was diagnosed with a Hunt and

60 Results demonstrated that the presence of loss of consciousness and/or post-traumatic amnesia was

61 tion to the cerebral cortex (for amnesia and loss of consciousness) and to the spinal cord (for atoni

62 of factors that constitute consciousness and loss of consciousness, and aspects of neurovascular cont

63 ndex, history of traumatic brain injury with loss of consciousness, and family history of PD.

64 g wakefulness, propofol-induced sedation and loss of consciousness, and the recovery of wakefulness.

65 isability (age, admission neurologic status, loss of consciousness, aneurysm size, intraventricular h

66 Although wheezes, dyspnea or loss of consciousness are known to occur with severe all

67 l mechanisms by which anesthetic drugs cause loss of consciousness are poorly understood.

68 ow that while clustering is increased during loss of consciousness, as recently suggested, it also re

69 However, when a contemporary estimate for loss of consciousness associated with an ICD shock of 14

70 The likelihood of loss of consciousness associated with an ICD shock was e

71 this study was to analyze in detail cases of loss of consciousness associated with ECD deployment.

72 Transient loss of consciousness associated with focal temporal lob

73 clinical grade, intraventricular hemorrhage, loss of consciousness at ictus, global cerebral edema, a

74 Loss of consciousness at onset was identified by structu

75 Loss of consciousness at symptom onset is an important m

76 ted incident and 63.0% (515 of 817) reported loss of consciousness at the time of injury.

77 nlike during focal impaired awareness, early loss of consciousness before generalization was accompan

78 ggest differences in the mechanisms of ictal loss of consciousness between focal impaired awareness a

79 results show that in head impacts producing loss of consciousness, brain deformation is disproportio

80 gesia (loss of pain) independent of inducing loss of consciousness, but the underlying mechanisms rem

81 ted that anesthetics such as propofol induce loss of consciousness by acting primarily at histaminerg

82 h mortality included fire as a source of CO, loss of consciousness, carboxyhemoglobin level, arterial

83 Loss of consciousness caused by positional changes of th

84 Thus, loss of consciousness coincides with a breakdown of info

85 Impacts leading to loss of consciousness compared to controls produced high

86 The relatively rapid loss of consciousness compared to other methods limits t

87 vidence for different neural dynamics during loss of consciousness compared with loss of arousability

88 Those who reported >=1 hit followed by loss of consciousness, compared to those who did not, al

89 brain networks involved in motor control and loss of consciousness consistent with generalized seizur

90 onstructed on the basis of clinical history (loss of consciousness, convulsive fits) and neurological

91 al discharges, during the post-ictal period, loss of consciousness, decreased responsiveness or other

92 ng upright is the largest of all animals yet loss of consciousness does not occur.

93 We find that loss of consciousness due to general anaesthesia or diso

94 and (iii) provide insight into mechanisms of loss of consciousness during certain seizures.

95 ile cortical sleep-like activities accompany loss of consciousness during focal impaired awareness se

96 impaired awareness, the neural signatures of loss of consciousness during focal to bilateral tonic-cl

97 paired awareness seizures, the mechanisms of loss of consciousness during focal to bilateral tonic-cl

98 nus syndrome have similar rates of witnessed loss of consciousness during laboratory testing regardle

99 rict seizure propagation might contribute to loss of consciousness during larger seizures.

100 cortical networks are especially affected by loss of consciousness during temporal states of high int

101 was admitted to the hospital with transient loss of consciousness, effort-associated vertigo, upper

102 in bidirectional GC in most subjects during loss-of-consciousness, especially in the beta and gamma

103 clonic seizures were characterized by deeper loss of consciousness, even before generalization occurr

104 sia lasting less than 30 minutes), moderate (loss of consciousness for 30 minutes to 24 hours or a sk

105 y informants reported prior head injury with loss of consciousness for 32 of 349 patients with probab

106 except frontal, no loss of consciousness or loss of consciousness for less than 5 s, non-severe inju

107 Traditionally, loss of consciousness has been a prerequisite for the de

108 for PCS was increased in older children with loss of consciousness, headache, and/or nausea/vomiting.

109 of the central thalamus, we investigate how loss of consciousness impacts distributed patterns of st

110 s been suggested as the mechanism underlying loss of consciousness in anesthesia.

111 cortical arousal is a critical mechanism for loss of consciousness in focal temporal lobe seizures.

112 The inherent problems in studying loss of consciousness in humans are legion.

113 The loss of consciousness in non-REM (NREM) sleep or to GAs

114 the main impairing factor, often leading to loss-of-consciousness, in people with epilepsy.

115 uman neural spiking activity recorded during loss of consciousness induced by the anesthetic propofol

116 te changes can be catastrophic, resulting in loss of consciousness, injury and even death.

117 Loss of consciousness is a hallmark of many epileptic se

118 Prior concussion that results in loss of consciousness is a risk factor for increased hip

119 support of the theory that propofol-induced loss of consciousness is associated with disrupted thala

120 Blast-related injury and loss of consciousness is common in military TBI.

121 respond meaningfully to stimuli, whereas the loss of consciousness is defined by unresponsiveness.

122 These findings suggest that propofol-induced loss of consciousness is mainly tied to cortico-cortical

123 How general anesthetics cause loss of consciousness is unknown.

124 Individuals with SRC who reported loss of consciousness (LOC) (33% of SRC cases) had highe

125 and cellular effects, how anesthesia induces loss of consciousness (LOC) and affects sensory processi

126 behavioral transition from full alertness to loss of consciousness (LOC) and on through a deeper anes

127 sed on reported lifetime history of TBI with loss of consciousness (LOC) but no chronic deficits occu

128 rading criteria with emphasis on the role of loss of consciousness (LOC) in the diagnostic rubric.

129 cortical effective connectivity may underlie loss of consciousness (LOC) induced by pharmacologic age

130 ensory and frontal premotor area) during the loss of consciousness (LOC) induced by propofol in nonhu

131 Loss of consciousness (LOC) is a common presenting sympt

132 While loss of consciousness (LOC) is a key factor in assessing

133 A history of loss of consciousness (LOC) is frequently a driving fact

134 A history of traumatic brain injury with loss of consciousness (LOC) was reported in one CTE and

135 ical neuronal dynamics during transitions of loss of consciousness (LOC) with the alpha2-adrenergic a

136 he specific association of TBI, even without loss of consciousness (LOC), with pathologic findings th

137 oddballs before and after propofol-mediated loss of consciousness (LOC).

138 atified by TBI severity (no TBI, TBI without loss of consciousness [LOC], and TBI with LOC).

139 a greater frequency of respiratory failure, loss of consciousness, lower body mass index, hemoglobin

140 appears significantly increased only during loss of consciousness, marking a decrease of global info

141 ns is a neural correlate of propofol-induced loss of consciousness, marking a shift to cortical dynam

142 al presentation are unknown, but amnesia for loss of consciousness may be the underlying cause.

143 2 years and older (normal mental status, no loss of consciousness, no vomiting, non-severe injury me

144 neuron-level mechanisms responsible for the loss of consciousness occurring in NREM sleep.

145 Syncope is a symptom in which transient loss of consciousness occurs as a consequence of a self-

146 When a likelihood of loss of consciousness of 32% associated with an ICD shoc

147 mination of cardiac activity associated with loss of consciousness, of spontaneous breathing, and of

148 t a dose that produced mild sedation without loss of consciousness, on spontaneous cerebral activity

149 a (three), rash (two), hyperglycaemia (one), loss of consciousness (one), sepsis (one), and vomiting

150 rimotor and cognitive processing, as well as loss-of-consciousness, one of the main impairing aspects

151 atic brain injury, defined as an injury with loss of consciousness or altered mental status (e.g., da

152 (defined as an injury during deployment with loss of consciousness or altered mental status) and time

153 to 24 hours or a skull fracture), or severe (loss of consciousness or amnesia for more than 24 hours,

154 sion with subdural hematoma, skull fracture, loss of consciousness or amnesia for more than one day,

155 Injuries were classified as mild (loss of consciousness or amnesia lasting less than 30 mi

156 ive to baseline in concussed athletes with a loss of consciousness or amnesia.

157 and interviewed regarding head injuries with loss of consciousness or concussion prior to Parkinson's

158 specially when the patient has no history of loss of consciousness or direct head trauma.

159 MHI was defined as either a documented loss of consciousness or evidence of posttraumatic amnes

160 tatus, no scalp haematoma except frontal, no loss of consciousness or loss of consciousness for less

161 nal measures of TBI severity (e.g. length of loss of consciousness or period of posttraumatic amnesia

162 it with reduced or no blink reflex following loss of consciousness or receiving sedatives.

163 or older, neck pain or stiffness, witnessed loss of consciousness, or onset during exertion had 98.5

164 to assess unexplained altered mental status, loss of consciousness, or poor arousal and responsivenes

165 In contrast, loss of consciousness per se was accompanied by a decrea

166 Phase 3, the loss of consciousness phase, lasted on average for 8.9 +

167 eers during wakefulness and propofol-induced loss of consciousness (PI-LOC).

168 ith traumatic brain injury (characterized by loss of consciousness, post-traumatic amnesia, or skull

169 sional American football impacts that led to loss of consciousness, posturing or no neurological sign

170 the speed at which water-based foam induces loss of consciousness prior to death, a major welfare co

171 The mechanisms underlying anesthesia-induced loss of consciousness remain a matter of debate.

172 hich volatile anesthetics produce reversible loss of consciousness remains a mystery.

173 How general anesthesia (GA) induces loss of consciousness remains unclear, and whether diver

174 el explanation for how these changes lead to loss of consciousness remains unclear.

175 Similar to loss of consciousness, return of consciousness was ident

176 impairment does not explain the amnesia for loss of consciousness seen in fallers with carotid sinus

177 d that results in cognitive deficits without loss of consciousness, seizures, or gross or microscopic

178 Loss of consciousness, status epilepticus classification

179 generalization, when all patients displayed loss of consciousness, stronger increases in slow-wave a

180 The relationship between brief loss of consciousness, subsequent cognitive and emotiona

181 of consciousness is not simply an inverse of loss of consciousness, suggesting a unique process.

182 orrelation) and are more impacted during the loss of consciousness than integrative neurons.

183 n our understanding of the various causes of loss of consciousness thanks to the publication of sever

184 f particular interest to neuroscience is the loss of consciousness that accompanies both states.

185 rousal, suggesting that head impacts produce loss of consciousness through a biomechanical effect on

186 sessions, as compared to a rather consistent loss of consciousness time.

187 Transient loss of consciousness (TLoC) is common and often leads t

188 Loss of consciousness was also associated with more preh

189 A prior head injury with amnesia or loss of consciousness was associated with an increased r

190 Loss of consciousness was associated with poor clinical

191 Loss of consciousness was marked simultaneously by an in

192 5.4 s; p = 0.42), but witnessed amnesia for loss of consciousness was more frequent in fallers than

193 Loss of consciousness was specifically associated with h

194 Eight cases of TASER X26 ECD-induced loss of consciousness were studied.

195 Falls (without loss of consciousness) were reduced by two-thirds: contr

196 umatic brain injury, primarily those who had loss of consciousness, were significantly more likely to

197 flex syncope is the major cause of transient loss of consciousness, which affects one-third of the po

198 ese patients, 7547 (57%) experienced initial loss of consciousness, which persisted to rehabilitation

199 by transient, spontaneously self-terminating loss of consciousness with complete and prompt recovery;

200 n may represent a generalisable biomarker of loss of consciousness, with potential relevance for clin

201 No loss of consciousness, withdrawal symptoms, or increased

202 with the highest biomechanical forces, that loss of consciousness would be associated with high forc

203 tested the hypotheses that impacts producing loss of consciousness would be associated with the highe