ライフサイエンスコーパス: unconsciousness

1 electroencephalogram during propofol-induced unconsciousness.

2 n before LOC to only tactile modality during unconsciousness.

3 ess (94.9%) reported less than 30 minutes of unconsciousness.

4 ave been suggested as a primary mechanism of unconsciousness.

5 tional connectivity is sufficient to produce unconsciousness.

6 ocessing efficiency uniquely associated with unconsciousness.

7 ng-distance connections is characteristic to unconsciousness.

8 ing cells in the brain at doses that produce unconsciousness.

9 r neural activity during the transition into unconsciousness.

10 ferior parietal cortices upon awakening from unconsciousness.

11 ate that shifted to the frontal leads during unconsciousness.

12 -cortical transmission with the induction of unconsciousness.

13 propofol accomplishes its effects, including unconsciousness.

14 wakefulness, disconnected consciousness, and unconsciousness.

15 vity was noted relative to consciousness and unconsciousness, again with increased local efficiency.

16 During profound unconsciousness, alpha amplitudes were maximal at low-fr

17 hereas during the transition into and out of unconsciousness, alpha amplitudes were maximal at low-fr

18 Halothane resulted in unconsciousness and a lack of response to tail clamping,

19 ance our understanding of anesthesia-induced unconsciousness and altered arousal and further establis

20 One state occurs during unconsciousness and may be similar to sleep slow oscilla

21 nance imaging, we studied anesthesia-induced unconsciousness and recovery using the alpha(2)-agonist

22 eases in sedation, sometimes to the point of unconsciousness, but consciousness is maintained if poss

23 euronal dynamics leading to propofol-induced unconsciousness by recording single-neuron activity and

24 During unconsciousness, cerebral metabolic rate of glucose and

25 n before LOC to only tactile modality during unconsciousness, consistent with an inhibition of multis

26 ghts into the mechanisms of propofol-induced unconsciousness, establish EEG signatures of this brain

27 ion is that recovery from anesthesia-induced unconsciousness follows a "boot-up" sequence actively dr

28 The neural mechanism of unconsciousness has been a major unsolved question in ne

29 Syndromes of unconsciousness have established diagnostic criteria, bu

30 Unconsciousness, induced by altered arousal and/or cogni

31 Unconsciousness is a fundamental component of general an

32 s and amnesia, the extent to which it causes unconsciousness is harder to establish.

33 Unconsciousness is likely to ensue when a complex of bra

34 sychologists debate whether consciousness or unconsciousness is most central to human behavior.

35 hat a transitional state from wakefulness to unconsciousness is not a continuous process, but rather

36 A related issue is that unconsciousness is typically the null hypothesis that ev

37 tch the brain from wakefulness to a state of unconsciousness, knowing how and where they work is a po

38 Anesthetic-induced unconsciousness may result from specific interactions of

39 We show that propofol-induced unconsciousness occurs within seconds of the abrupt onse

40 at if a treatment merely preserves permanent unconsciousness or cannot end dependence on intensive me

41 nces for avoiding the indignity of permanent unconsciousness or other gravely debilitated states.

42 vomiting everything, convulsions, lethargy, unconsciousness, or head nodding).

43 Delirium or unconsciousness prompted evacuation to the hospital.

44 tive sedation with the intended end point of unconsciousness (PSU) is a more controversial practice t

45 gh which volatile anesthetics act to produce unconsciousness remain obscure.

46 between consciousness and anesthetic-induced unconsciousness remain unclear.

47 muscimol, and ethanol) produce analgesia and unconsciousness (sedation).

48 The altered states of arousal are sedation-unconsciousness, sedation-analgesia, dissociative anesth

49 ntal power during general anesthesia-induced unconsciousness--termed anteriorization--is well known,

50 During unconsciousness the spectrograms in the frontal leads sh

51 res of transitions between consciousness and unconsciousness under anaesthesia have not yet been iden

52 Sedation and unconsciousness under GA are associated with stereotyped

53 ced state of profound brain inactivation and unconsciousness used to treat refractory intracranial hy

54 Duration of unconsciousness was not associated.

55 Thus, anesthetics seem to cause unconsciousness when they block the brain's ability to i

56 We also show that at deep levels of unconsciousness where movement ceases, coherent thalamoc

57 ction and for sedation, as well as hypnosis (unconsciousness) which is induced by general anesthetics

58 at Thiopental caused a prolonged duration of unconsciousness with a high rate of mortality, that Thio

59 ring gradual induction of and emergence from unconsciousness with propofol.

60 - pathological reports associating permanent unconsciousness with structural damage to these regions.