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1 , immobility, amnesia and lack of awareness (unconsciousness).
2 als between the awake state and anesthetized unconsciousness.
3 itude delta oscillations are an indicator of unconsciousness.
4  reversed the electrophysiologic features of unconsciousness.
5 eural circuits regulating arousal to produce unconsciousness.
6 , have remained enigmatic, especially during unconsciousness.
7  or by injury/disease are reactivated during unconsciousness.
8  typically associated with consciousness and unconsciousness.
9 o execute sensorimotor behaviors even during unconsciousness.
10 upraspinal networks in maturity, even during unconsciousness.
11 euronal basis of anesthetic-induced state of unconsciousness.
12 ntegration with the rest of the brain during unconsciousness.
13 electroencephalogram during propofol-induced unconsciousness.
14 propofol accomplishes its effects, including unconsciousness.
15 wakefulness, disconnected consciousness, and unconsciousness.
16 n before LOC to only tactile modality during unconsciousness.
17 rior cortices in mediating consciousness and unconsciousness.
18 ess (94.9%) reported less than 30 minutes of unconsciousness.
19 ave been suggested as a primary mechanism of unconsciousness.
20 tional connectivity is sufficient to produce unconsciousness.
21 ocessing efficiency uniquely associated with unconsciousness.
22 ng-distance connections is characteristic to unconsciousness.
23 ing cells in the brain at doses that produce unconsciousness.
24 r neural activity during the transition into unconsciousness.
25 lved in the transition from consciousness to unconsciousness.
26 ferior parietal cortices upon awakening from unconsciousness.
27 ate that shifted to the frontal leads during unconsciousness.
28 -cortical transmission with the induction of unconsciousness.
29 y distinguish wakefulness, dissociation, and unconsciousness.
30 nst both isoflurane- and sevoflurane-induced unconsciousness.
31 connect the network, and are associated with unconsciousness.
32 s sensory- and motor-dominant regions during unconsciousness.
33 izures are characterized by brief periods of unconsciousness accompanied by lapses in motor function
34 vity was noted relative to consciousness and unconsciousness, again with increased local efficiency.
35                              During profound unconsciousness, alpha amplitudes were maximal at low-fr
36 hereas during the transition into and out of unconsciousness, alpha amplitudes were maximal at low-fr
37                        Halothane resulted in unconsciousness and a lack of response to tail clamping,
38 ance our understanding of anesthesia-induced unconsciousness and altered arousal and further establis
39     Conservatively, average (+/- SD) time to unconsciousness and brain death was 1 min, 53 s +/- 36 s
40                      One state occurs during unconsciousness and may be similar to sleep slow oscilla
41 nance imaging, we studied anesthesia-induced unconsciousness and recovery using the alpha(2)-agonist
42 tal-to-frontal connectivity between reported unconsciousness and reported consciousness.
43 ery is possible following anesthetic-induced unconsciousness and the intermediate recovery state is n
44 pattern is a signature of anesthetic-induced unconsciousness, and (3) the paradoxical, desynchronized
45 ted with meningismus, transient or prolonged unconsciousness, and focal neurological deficits includi
46 ualizing pharmacological control of amnesia, unconsciousness, and immobility.
47         Outside of these frequent moments of unconsciousness, approximately a third of people living
48              Unresponsiveness rarely denoted unconsciousness, as the majority of the subjects had int
49  states is almost invariably associated with unconsciousness, both in animal models and clinical stud
50 eases in sedation, sometimes to the point of unconsciousness, but consciousness is maintained if poss
51 euronal dynamics leading to propofol-induced unconsciousness by recording single-neuron activity and
52    Understanding how the brain recovers from unconsciousness can inform neurobiological theories of c
53                                       During unconsciousness, cerebral metabolic rate of glucose and
54  that 'unresponsiveness' does not equate to 'unconsciousness' changes how patients should be assessed
55 d that neural dynamics were more unstable in unconsciousness compared with the awake state.
56                                Compared with unconsciousness, conscious experiences during NREM sleep
57  locked to heartbeats were useful to predict unconsciousness/consciousness, but HERs were more accura
58 n before LOC to only tactile modality during unconsciousness, consistent with an inhibition of multis
59 fol to determine whether anaesthetic-induced unconsciousness diminishes the uniqueness of the human b
60 harmacologically induced reversible state of unconsciousness-enables millions of life-saving procedur
61 ghts into the mechanisms of propofol-induced unconsciousness, establish EEG signatures of this brain
62 ion is that recovery from anesthesia-induced unconsciousness follows a "boot-up" sequence actively dr
63 ra-mTL lesions at 3-month MRI, and prolonged unconsciousness (>=60 days).
64                      The neural mechanism of unconsciousness has been a major unsolved question in ne
65                                 Syndromes of unconsciousness have established diagnostic criteria, bu
66  mechanisms through which anesthetics induce unconsciousness have not been completely characterized.
67  clinical parameters such as the duration of unconsciousness, immunotherapy profiles, cytokine/chemok
68 lation of broadband activity, changes during unconsciousness in humans.
69 oral cortices and thalamus while maintaining unconsciousness in non-human primates (NHPs) with the an
70                           Anesthetics induce unconsciousness in part by impinging upon sexually dimor
71 oring and precisely controlling the level of unconsciousness in patients under general anesthesia.
72                                      Whereas unconsciousness increases structure-function coupling ac
73 n by high gamma waves (52-104 Hz); moreover, unconsciousness induced by propofol anesthesia or genera
74                                              Unconsciousness, induced by altered arousal and/or cogni
75 ics during transitions from propofol-induced unconsciousness into consciousness by directly recording
76    Non-random functional connectivity during unconsciousness is a defining feature of supraspinal net
77                                              Unconsciousness is a fundamental component of general an
78  Our results suggest that anesthetic-induced unconsciousness is associated with a topological re-orga
79 alamocortical circuits in anesthesia-induced unconsciousness is difficult due to anatomical and funct
80 s and amnesia, the extent to which it causes unconsciousness is harder to establish.
81                                              Unconsciousness is likely to ensue when a complex of bra
82                                              Unconsciousness is linked to cortical and thalamic slow
83 sychologists debate whether consciousness or unconsciousness is most central to human behavior.
84 hat a transitional state from wakefulness to unconsciousness is not a continuous process, but rather
85                                     Although unconsciousness is typically considered the cardinal fea
86                      A related issue is that unconsciousness is typically the null hypothesis that ev
87 imuli through the nervous system even during unconsciousness, is critical for proper anesthesia care
88 tch the brain from wakefulness to a state of unconsciousness, knowing how and where they work is a po
89                                              Unconsciousness maintained by GABAergic anesthetics, suc
90 rom SDA to burst suppression and back during unconsciousness maintained with propofol or sevoflurane
91                           Anesthetic-induced unconsciousness may result from specific interactions of
92                We show that propofol-induced unconsciousness occurs within seconds of the abrupt onse
93 at if a treatment merely preserves permanent unconsciousness or cannot end dependence on intensive me
94 nces for avoiding the indignity of permanent unconsciousness or other gravely debilitated states.
95 een states of consciousness and drug-induced unconsciousness, or anesthesia.
96  vomiting everything, convulsions, lethargy, unconsciousness, or head nodding).
97                                  Delirium or unconsciousness prompted evacuation to the hospital.
98 le unconsciousness (sleep) vs. non-arousable unconsciousness (propofol-induced general anesthesia).
99 tive sedation with the intended end point of unconsciousness (PSU) is a more controversial practice t
100 gh which volatile anesthetics act to produce unconsciousness remain obscure.
101 tterns that differentiate consciousness from unconsciousness remain unclear.
102 between consciousness and anesthetic-induced unconsciousness remain unclear.
103 esearch, the mechanism of anesthetic-induced unconsciousness remains incompletely understood, with so
104 AP persists in mature spinal networks during unconsciousness remains unclear, and its function(s), if
105 mmunication - and its possible disruption in unconsciousness - remains poorly understood.
106 muscimol, and ethanol) produce analgesia and unconsciousness (sedation).
107   The altered states of arousal are sedation-unconsciousness, sedation-analgesia, dissociative anesth
108                                They generate unconsciousness selectively through alpha2-adrenergic re
109 gional involvement during wake vs. arousable unconsciousness (sleep) vs. non-arousable unconsciousnes
110  and clearance and accelerated recovery from unconsciousness, suggest rescue-like efforts.
111 ntal power during general anesthesia-induced unconsciousness--termed anteriorization--is well known,
112                                       During unconsciousness the spectrograms in the frontal leads sh
113 res of transitions between consciousness and unconsciousness under anaesthesia have not yet been iden
114                     Our results suggest that unconsciousness under anesthesia comprises several disti
115 ars necessary for perception and can reverse unconsciousness under anesthesia.
116 he animal transitioned from consciousness to unconsciousness under different anaesthetics (ketamine a
117                                 Sedation and unconsciousness under GA are associated with stereotyped
118 ced state of profound brain inactivation and unconsciousness used to treat refractory intracranial hy
119                                              Unconsciousness was marked by slow frequency (~1 Hz) osc
120                                  Duration of unconsciousness was not associated.
121 se state transitions between wakefulness and unconsciousness were rapid and unstable.
122              Thus, anesthetics seem to cause unconsciousness when they block the brain's ability to i
123          We also show that at deep levels of unconsciousness where movement ceases, coherent thalamoc
124 ction and for sedation, as well as hypnosis (unconsciousness) which is induced by general anesthetics
125 ntially fatal seizures resulted in prolonged unconsciousness, which also exhibited a circadian rhythm
126  the rapid onset of cognitive impairment and unconsciousness, which frequently accompany an overdose
127 at Thiopental caused a prolonged duration of unconsciousness with a high rate of mortality, that Thio
128 , and dissociation at low doses and profound unconsciousness with antinociception at high doses.
129 ring gradual induction of and emergence from unconsciousness with propofol.
130 - pathological reports associating permanent unconsciousness with structural damage to these regions.
131 antly lower during consciousness compared to unconsciousness, with differences in the clustering coef

 
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