ライフサイエンスコーパス: central sensitization

1 ing hypersensitivity of dorsal horn neurons (central sensitization).

2 l sensitization) and spinal cord mechanisms (central sensitization).

3 in the absence, but not in the presence, of central sensitization.

4 a and dorsal horn neurons, thus resulting in central sensitization.

5 the calcium channel alpha2delta-1 subunit in central sensitization.

6 ficient to counteract an already established central sensitization.

7 ed with peripheral sensitization, as well as central sensitization.

8 primary afferent neurons and has been termed central sensitization.

9 in chronic pain by mediating peripheral and central sensitization.

10 rties of other nociceptive neurons and drive central sensitization.

11 to prevent hyperalgesia and formalin-induced central sensitization.

12 heral nociceptors, before the development of central sensitization.

13 tability of central (spinal) neurons, termed central sensitization.

14 dministration, a measure of C fiber-mediated central sensitization.

15 The allodynia reflects a central sensitization.

16 s important in the generation of wind-up and central sensitization.

17 spinal cord, an area critically involved in central sensitization.

18 on producing an increase in excitability and central sensitization.

19 nisms that may be involved in peripheral and central sensitization.

20 se state of chronic pain, which is caused by central sensitization.

21 ttle is known about the mediators that drive central sensitization.

22 iour, suggesting a potential role of SOCs in central sensitization.

23 Several mechanisms contribute to central sensitization.

24 ute to heightened clinical pain, perhaps via central sensitization.

25 ansmitter release within the spinal cord and central sensitization.

26 lity, spinal cord synaptic transmission, and central sensitization.

27 d the development of cutaneous allodynia and central sensitization.

28 ions that we consider indicative of possible central sensitization.

29 n the development of neuronal plasticity and central sensitization.

30 phology parameters without and with signs of central sensitization.

31 ith noncardiac chest pain (NCCP), suggesting central sensitization.

32 S play an important role in pain mediated by central sensitization.

33 ll as in normal subjects during experimental central sensitization.

34 Central sensitization, an activity-dependent increase in

35 nist suppresses behavioral manifestations of central sensitization, an activity-dependent increase in

36 of integration in the brainstem, may lead to central sensitization analogous to that described in som

37 naling could be an effective way to suppress central sensitization and alleviate chronic pain.

38 To date, central sensitization and astrocyte changes have not bee

39 ld provide a neurophysiological mechanism of central sensitization and chronic pain associated with s

40 ation of Nav1.8(+) afferents in vivo induced central sensitization and conditioned place aversion, th

41 lve the processes of amplification including central sensitization and descending facilitation.

42 ms that may be the prepotent contributors to central sensitization and development of secondary hyper

43 spinal nociceptive processing indicative of central sensitization and for adaptive changes in the sp

44 on of the mutual neuron-glia interactions to central sensitization and hyperalgesia prompts new treat

45 our data have demonstrated that PICs induce central sensitization and hyperalgesia via distinct and

46 have an opposite role and even contribute to central sensitization and hyperalgesia.

47 f the spinal circuits involved in triggering central sensitization and hyperalgesia.

48 ce that activation of CB2 receptors inhibits central sensitization and its contribution to the manife

49 underlying the generation and maintenance of central sensitization and LTP indicates that, although t

50 Central sensitization and network hyperexcitability of t

51 trocytes after JNK activation contributes to central sensitization and neuropathic pain facilitation

52 lity in DRG neurons and leads to spinal cord central sensitization and neuropathic pain symptoms.

53 ty in the DRG neurons and led to spinal cord central sensitization and neuropathic pain-like symptoms

54 or (BDNF) signaling appears to contribute to central sensitization and nocifensive behaviors in certa

55 , contributing thereby to activity-dependent central sensitization and pain hypersensitivity.

56 atory synaptogenesis, which together lead to central sensitization and pain state development.

57 erapies may target the peripheral drivers of central sensitization and/or the central consequences.

58 le in spinal cord synaptic plasticity (i.e., central sensitization) and pain hypersensitivity after t

59 ed neuronal excitability in the spinal cord (central sensitization), and a syndrome comprising diffus

60 cornea morphology without and with signs of central sensitization, and a group with abnormal cornea

61 excitability of spinal dorsal horn neurons, central sensitization, and the behavioral correlate, hyp

62 es of these circuits, such as peripheral and central sensitization, and the segmental and descending

63 Nociceptor sensitization and central sensitization are considered to underlie, respec

64 However, synaptic mechanisms underlying central sensitization are incompletely known.

65 rrently available drugs that aim to suppress central sensitization are ineffective, this study stress

66 New findings regarding peripheral and central sensitization are presented in this review.

67 Manifestations of this central sensitization are windup and long-term potentiat

68 on animal studies, it has been proposed that central sensitization associated to nociception (maladap

69 may contribute to nociceptive plasticity and central sensitization associated with chronic inflammato

70 nce of secondary hyperalgesia and underlying central sensitization associated with persistent pain de

71 f several interplaying mechanisms, including central sensitization, blunting of inhibitory pain pathw

72 n can prevent and/or suppress peripheral and central sensitization by using single-unit recording in

73 A similar state of central sensitization can be experimentally produced wit

74 Diagnosing central sensitization can be particularly difficult.

75 of the CCM parameters and sensory tests for central sensitization, (cold pain threshold, mechanical

76 n to peripheral nociceptors, peripheral- and central sensitization contribute to the pathophysiology

77 cent clinical evidence has demonstrated that central sensitization contributes to OA pain.

78 g and inflammation, with both peripheral and central sensitization contributing to joint pain.

79 Nitroglycerin (NTG)-triggered central sensitization (CS) provides a rodent model of mi

80 Central sensitization (CS) refers to an increase in the

81 ence suggests that opioid withdrawal induces central sensitization (CS) that is maintained by suprasp

82 If central sensitization develops, the therapeutic rational

83 Consequently, central sensitization-driven pain hypersensitivity, but

84 tan intervention counteracted two aspects of central sensitization: dural receptive fields, which ini

85 in the dorsal horn and in the generation of central sensitization during chronic pain states.

86 gnal-regulated kinases (ERKs), which mediate central sensitization during inflammatory pain.

87 ly blocked the development of all aspects of central sensitization expected to be induced 2 h after I

88 spinal dorsal horn that functions to prevent central sensitization following brief, mild, noxious sti

89 This central sensitization has been attributed to the enhance

90 dorsal horn neurons and its contribution to central sensitization have been investigated.

91 inal cord dorsal horn neurons, indicative of central sensitization (hyperactivity of dorsal horn neur

92 lar cortex, independently of the presence of central sensitization; (ii) gabapentin reduced the activ

93 the activation in the brainstem, only during central sensitization; (iii) gabapentin suppressed stimu

94 is study reveals that CaMK II contributes to central sensitization in a manner similar to its role in

95 ng the NK1 receptor, shown to be involved in central sensitization in adults, in the negative effects

96 time, the optical control of nociception and central sensitization in behaving mammals and enables se

97 rrent that is believed to be associated with central sensitization in chronic neuropathic pain states

98 ns may contribute to synaptic plasticity and central sensitization in diabetic neuropathic pain.

99 ion of PKC contributes to the development of central sensitization in dorsal horn neurons produced by

100 Central sensitization in inflammatory pain conditions re

101 The results suggest that central sensitization in knee OA is especially apparent

102 e with recent findings regarding the role of central sensitization in pain chronification, especially

103 Evidence for central sensitization in pain processing included increa

104 al medulla (RVM) attenuates hyperalgesia and central sensitization in several models of persistent pa

105 tudy tested the hypothesis that induction of central sensitization in the dorsal horn by an intraderm

106 t the combined effects of afferent input and central sensitization in the dorsal horn.

107 gic system is involved in the development of central sensitization in the pain neuraxis, associated w

108 nce phase of secondary hyperalgesia involved central sensitization in Vc neurons conducted by a delay

109 PGE(2)) is a mediator in both peripheral and central sensitization, in part via the prostaglandin E2

110 er assessed in models presumably mediated by central sensitization, including CFA- and capsaicin-indu

111 Central sensitization, increased sensitivity in spinal c

112 fects of sumatriptan (300 microg/kg i.v.) on central sensitization induced by topical application of

113 Central sensitization is a form of activity-dependent pl

114 Because central sensitization is considered to reflect plasticit

115 Central sensitization is maintained by continuing input

116 ribution of specific classes of afferents to central sensitization is possible.

117 in modulating nociceptive transmission when central sensitization is present.

118 Central sensitization is thought to play a role in chron

119 Primary afferent-evoked central sensitization is, in addition, reduced in B2 rec

120 ensory inputs in the central nervous system (central sensitization) is the mechanism accounting for t

121 hnic afferents results in the development of central sensitization manifested as hyperalgesia and inc

122 ion phase of secondary hyperalgesia involved central sensitization mechanisms in Vc neurons that were

123 europathic pain reflects both peripheral and central sensitization mechanisms.

124 icacy in a rat surrogate model indicative of central sensitization, namely phase 2 response of formal

125 ield size, mechanical and thermal coding and central sensitization of deeper dorsal horn neurons that

126 ms have been implicated in neuropathic pain, central sensitization of dorsal horn spinothalamic tract

127 activation was not required for maintaining central sensitization of itch.

128 similar mechanisms that result in wind-up or central sensitization of spinal cord neurons.

129 Central sensitization of spinothalamic tract (STT) neuro

130 study was designed to examine the effects of central sensitization of spinothalamic tract (STT) neuro

131 enhanced anterior cingulate and PAG reflect central sensitization of the pain matrix, while decrease

132 uch cutaneous allodynia suggests a state of 'central sensitization' of pain transmission pathways and

133 in temporal summation (surrogate measures of central sensitization) on the forearm.

134 For pain, the covered topics are central sensitization, pain-touch and pain-pain interact

135 understanding, at a subject-specific level, central sensitization processes that contribute to chron

136 ation of AMPA receptor GluR1 subunits during central sensitization produced by capsaicin injection.

137 ration of JWH133 attenuated these markers of central sensitization, providing a neurobiological basis

138 Issues related to plasticity, central sensitization, psychological confounds, genetics

139 Central sensitization refers to the increased synaptic e

140 erents could be the signal that produces the central sensitization responsible for the development of

141 le for the initiation and maintenance of the central sensitization seen in neuropathic pain states.

142 Hallmarks of central sensitization, significant spinal astrogliosis a

143 ntervention did not reverse other aspects of central sensitization: spontaneous firing rate and neuro

144 ing of nociceptive information in normal and central sensitization states.

145 ord to promote excitatory synaptogenesis and central sensitization that contribute to neuropathic pai

146 injury may reduce the initial peripheral and central sensitization that occurs after tissue injury.

147 lgesia) and spinal cord hyperexcitability or central sensitization that results in secondary hyperalg

148 nts of dorsal horn neuronal excitability and central sensitization that underlies hypersensitivity af

149 to injury-induced spinal neuroplasticity and central sensitization that underlies neuropathic pain de

150 the important role of these receptors in the central sensitization that underlies the maintenance of

151 rsal horn of the spinal cord is required for central sensitization, the central facilitation of pain

152 stimulus-induced deactivations, only during central sensitization; this effect was more robust than

153 y in vivo evidence that OA pain is caused by central sensitization through communication between peri

154 th PKA and PKC, and that this contributes to central sensitization through post-translational and CRE

155 that PKC is important for the development of central sensitization to peripheral mechanical stimuli.

156 ss of these inhibitory mechanisms that allow central sensitization to proceed.

157 s have demonstrated that both peripheral and central sensitization to pruritogenic stimuli occur duri

158 werful means of preventing the initiation of central sensitization triggered by chemical stimulation

159 Central sensitization was indexed through quantitative s

160 This functions to prevent central sensitization when the noxious stimulus does not

161 The neuropeptide may help maintain central sensitization, which could serve to enhance guar

162 CAPS is a result of central sensitization with disinhibition of pain signals

163 atory response, resulting in "peripheral and central sensitization," with the latter resulting from r