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

1 aptic currents from the N20 component of the somatosensory evoked potential.

2 s, imaging, cerebrospinal fluid markers, and somatosensory evoked potentials.

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

4 h as CSF examination, MRI, nerve biopsy, and somatosensory evoked potentials.

5 matosensory input was monitored by recording somatosensory evoked potentials.

6 the amplitude of cortical components of the somatosensory-evoked potentials.

7 tability and a reduction in the amplitude of somatosensory-evoked potentials.

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

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

10 er prognostic markers (electroencephalogram, somatosensory evoked potentials, absent pupillary reflex

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

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

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

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

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

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

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

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

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

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

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

22 5% CI, 2.52-18.38), and bilateral absence of somatosensory-evoked potentials between days 1 and 7 (fa

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

24 omotor assessment, whole-body MRI, motor and somatosensory evoked potentials; brain, spinal cord, hin

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

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

27 rebral function, neuromonitoring modalities (somatosensory-evoked potentials, cerebral oximetry, and

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

29 sory evoked potentials, the increment of the somatosensory evoked potential cortical components was o

30 it significantly increased the amplitude of somatosensory evoked potential cortical components, long

31 Somatosensory evoked potentials demonstrated central slo

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

33 sory-motor deficit with absence of motor and somatosensory evoked potentials due to loss of spinal co

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

35 sing this system, we successfully suppressed somatosensory evoked potentials elicited by functional e

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

37 maging, which were favored over median nerve somatosensory evoked potentials for prognostication, alt

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

39 conducted by indirectly recording motor and somatosensory evoked potentials from either muscles or t

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

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

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

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

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

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

46 Somatosensory evoked potentials indicated a cortical ori

47 All participants underwent somatosensory evoked potentials, long-latency reflexes a

48 The N13 component of somatosensory evoked potential (N13 SEP) represents the

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

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

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

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

53 as measured by a multifrequency steady-state somatosensory evoked potential paradigm.

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

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

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

57 and prespecified highly malignant patterns), somatosensory-evoked potentials, quantified pupillometry

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

59 Four sessions of somatosensory-evoked potentials recordings were performe

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

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

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

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

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

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

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

67 For each somatosensory evoked potential result, rates of awakenin

68 Somatosensory evoked potential results predict the likel

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

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

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

72 on, as indicated by the N20 component of the somatosensory evoked potential (SEP), prestimulus alpha

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

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

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

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

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

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

79 Measuring somatosensory evoked potentials (SEP), electroencephalog

80 in early (P50) as well as late (N140, P300) somatosensory-evoked potential (SEP) amplitudes.

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

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

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

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

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

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

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

88 The 4-month-olds' somatosensory evoked potentials (SEPs) were enhanced whe

89 ynaptic currents inferred from short-latency somatosensory evoked potentials (SEPs), (ii) pre-stimulu

90 oup differences in mid-latency components of somatosensory evoked potentials (SEPs).

91 rious neurophysiological measures, including somatosensory evoked potentials (SEPs).

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

93 nt approaches: fMRI, behavioral testing, and somatosensory-evoked potentials (SEPs) at spinal and cor

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

95 Median nerve somatosensory-evoked potentials showed improved activity

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

97 recovery of neurologic function based on the somatosensory evoked potential (SSEP) N20 cortical respo

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

99 ditionally, electroencephalography (EEG) and somatosensory evoked potentials (SSEPs) were used to ass

100 EG background, neurological examination, and somatosensory evoked potentials (SSEPs).

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

102 ultra-high-density EEG system (uHD EEG) and somatosensory evoked potentials (SSEPs).

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

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

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

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

107 ing patients in those with and without giant somatosensory evoked potentials, the increment of the so

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

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

110 Somatosensory evoked potentials were categorized as norm

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

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