ライフサイエンスコーパス: somatosensory evoked potential

1 s indexed by the early cortical component of somatosensory evoked potentials.

2 matosensory input was monitored by recording somatosensory evoked potentials.

3 alterations at nodes of Ranvier and reduced somatosensory-evoked potentials.

4 (confidence interval 40%-60%) for bilateral somatosensory evoked potential absence, both with a posi

5 reactive late electroencephalography, absent somatosensory-evoked potential, absent pupillary or corn

6 ith cerebral electrophysiology, and cortical somatosensory evoked potential amplitudes were significa

7 group showed significantly higher postinjury somatosensory-evoked potential amplitudes with longer la

8 ature) and other clinical, neurophysiologic (somatosensory-evoked potential), and biochemical prognos

9 etiology, age group, presence or absence of somatosensory evoked potentials, and coma outcomes.

10 (NSE) measurements, brain imaging findings, somatosensory evoked potentials, and electroencephalogra

11 ients, positron emission tomography studies, somatosensory evoked potentials, and jugular venous satu

12 linical examination, electroencephalography, somatosensory-evoked potentials, and serum neuron-specif

13 y reactivity during therapeutic hypothermia, somatosensory-evoked potentials, and serum neuron-specif

14 se higher than 33 mug/L (p = 0.029), but not somatosensory-evoked potentials, as independent predicto

15 ated the changes in single- and double-pulse somatosensory-evoked potentials before and after PAS, wh

16 5% CI, 2.52-18.38), and bilateral absence of somatosensory-evoked potentials between days 1 and 7 (fa

17 We compared the time course of the somatosensory-evoked potentials between the FHD and heal

18 ssant effects of isoflurane on barrel cortex somatosensory-evoked potentials but failed to elicit spe

19 oring modalities such as the wake-up test or somatosensory-evoked potentials can be eliminated.

20 oked potential (P1) at 60 ms, but no further somatosensory evoked potential components.

21 Somatosensory evoked potentials demonstrated central slo

22 ostication of early postanoxic coma, whereas somatosensory-evoked potentials do not add any complemen

23 onstrated rapid ablation of the amplitude of somatosensory evoked potentials during ischemia, with no

24 S significantly attenuated the amplitudes of somatosensory evoked potentials elicited by median nerve

25 In contrast, a decrease in the somatosensory-evoked potential (forepaw-evoked potential

26 methods (cortical stimulation, median nerve somatosensory-evoked potential, functional magnetic reso

27 ulse median nerve stimulation with recording somatosensory evoked potentials in 138 healthy subjects

28 n in the ascending spinal cord pathways with somatosensory-evoked potentials in injured rats.

29 hen produced a dose-dependent suppression of somatosensory-evoked potentials in response to electrica

30 By recording motor- and somatosensory-evoked potentials in the PrG of patients u

31 Under attention, amplitudes of somatosensory evoked potentials increased 50-60 ms after

32 Somatosensory evoked potentials indicated a cortical ori

33 lumbar-to-cerebral peaks on posterior tibial somatosensory evoked potentials (on right side, P=.03, a

34 Ps elicited by BES, (ii) amplitudes of early somatosensory-evoked potentials or (iii) M-responses.

35 res that other monitoring modalities such as somatosensory-evoked potentials or electromyography be u

36 asymmetry of saccadic velocity (P=.03), and somatosensory evoked potentials (P< or =.01); and those

37 A systematic review of somatosensory evoked potentials performed early after on

38 Simple bedside tests and somatosensory-evoked potentials predict poor neurologic

39 e positive/negative (P1/N1) slow wave of the somatosensory evoked potential primarily reflects sequen

40 t preinjury, weekly postinjury (up to 4 wks) somatosensory-evoked potential recordings and standard m

41 Four sessions of somatosensory-evoked potentials recordings were performe

42 At 180 mins of reperfusion, somatosensory evoked potentials recovered to 28 +/- 4% o

43 lue in dogs treated with saline, whereas the somatosensory evoked potentials recovered to 58 +/- 4% o

44 ation of hypoxanthine significantly improved somatosensory evoked potential recovery and preserved ne

45 ventilation on the amplitude of the cortical somatosensory evoked potential response.

46 as the sensitivity and specificity of absent somatosensory evoked potential responses during the firs

47 hypoxic-ischemic encephalopathy with absent somatosensory evoked potential responses have <1% chance

48 lmost two times larger than bilateral absent somatosensory evoked potential responses.

49 For each somatosensory evoked potential result, rates of awakenin

50 Somatosensory evoked potential results predict the likel

51 the primary and secondary components of the somatosensory evoked potential (SEP) before and during m

52 The literature regarding somatosensory evoked potential (SEP) gating is commonly

53 ent age, T2 high signal intensity (HSI), and somatosensory evoked potential (SEP) were analyzed by us

54 g the recovery cycle of the N20 component of somatosensory evoked potentials (SEP) and the area of hi

55 We decomposed somatosensory evoked potentials (SEP) into three major c

56 Total CBF, cerebral oxygen consumption, and somatosensory evoked potentials (SEP) were measured duri

57 tio index (PRI), burst suppression ratio and somatosensory evoked potentials (SEP) were obtained and

58 rosseous muscle (1DI) of the preferred hand, somatosensory evoked potentials (SEP) were recorded from

59 howed that GC microelectrode arrays recorded somatosensory evoked potentials (SEP) with an almost twi

60 Measuring somatosensory evoked potentials (SEP), electroencephalog

61 ompound sensory action potentials (SAPs) and somatosensory evoked potentials (SEPs) (recorded central

62 imulus frequency on the relationship between somatosensory evoked potentials (SEPs) and cerebral bloo

63 l MRI (fMRI) during a passive movement task, somatosensory evoked potentials (SEPs) arising from elec

64 ranscranial magnetic stimulation (MEPs), (2) somatosensory evoked potentials (SEPs) evoked by ulnar n

65 In three experiments we recorded somatosensory evoked potentials (SEPs) from 6.5-, 8-, an

66 microECoG for detailed cortical recording of somatosensory evoked potentials (SEPs) in an ovine model

67 ation level-dependent (BOLD) fMRI signal and somatosensory evoked potentials (SEPs) using short, typi

68 nges of intracranially recorded median-nerve somatosensory-evoked potentials (SEPs) and somatosensory

69 ron-specific enolase (NSE), and median nerve somatosensory-evoked potentials (SEPs) to predict poor o

70 The amplitude of the P25/N33, but not other somatosensory evoked potential (SSEP) components, was re

71 l examination, electroencephalography (EEG), somatosensory evoked potentials (SSEP), and serum neuron

72 tudy aims to develop a novel marker based on somatosensory evoked potentials (SSEPs).

73 of the ulnar nerve at the wrist, we examined somatosensory evoked potentials (SSEPs; P14/N20, N20/P25

74 This study explored the use of steady-state somatosensory evoked potentials (ssSEPs) as a continuous

75 EG-fMRI and used modulations of steady-state somatosensory evoked potentials (SSSEPs) as a measure of

76 ctroencephalography, 2% (one of 49) received somatosensory evoked potential testing, and 71% (35 of 4

77 Addition of somatosensory-evoked potentials to this model did not im

78 However, the recovery of the somatosensory-evoked potential was significantly delayed

79 Somatosensory evoked potentials were categorized as norm

80 blood flow, cerebral oxygen consumption, and somatosensory evoked potentials were measured during 180

81 s, continuous electroencephalogram and daily somatosensory evoked potentials were recorded during the