ライフサイエンスコーパス: loss of consciousness

1 sequence different from that observed during loss of consciousness.

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

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

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

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

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

7 rk changes that occurred simultaneously with loss of consciousness.

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

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

10 thalamo-cortical transmission characterizing loss of consciousness.

11 ally defined functional networks despite the loss of consciousness.

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

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

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

15 cause impaired cerebral functions, including loss of consciousness.

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

17 anaesthetic levels known to induce profound loss of consciousness.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

42 Transient loss of consciousness associated with focal temporal lob

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

44 Loss of consciousness at onset was identified by structu

45 Loss of consciousness at symptom onset is an important m

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

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

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

49 Loss of consciousness caused by positional changes of th

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

69 How general anesthetics cause loss of consciousness is unknown.

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

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

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

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

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

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

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

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

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

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

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

81 2 years and older (normal mental status, no loss of consciousness, no vomiting, non-severe injury me

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

108 Loss of consciousness was also associated with more preh

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

110 Loss of consciousness was associated with poor clinical

111 Loss of consciousness was marked simultaneously by an in

112 5.4 s; p = 0.42), but witnessed amnesia for loss of consciousness was more frequent in fallers than

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

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

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

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