ライフサイエンスコーパス: persistent pain

1 ration causes impaired tactile sensation and persistent pain.

2 ar mechanisms of neuron-glia interactions in persistent pain.

3 ture implicates a role for glia/cytokines in persistent pain.

4 sses of antidepressants in the management of persistent pain.

5 tory conditions can lead to debilitating and persistent pain.

6 nown mechanism underlying the development of persistent pain.

7 effective analgesic agents in many models of persistent pain.

8 effective analgesic agents in many models of persistent pain.

9 lgesic efficacy in the rat formalin model of persistent pain.

10 atment strategies for aging populations with persistent pain.

11 AR-mediated synaptic function and associated persistent pain.

12 administration in mouse models of acute and persistent pain.

13 tial biochemical target for the treatment of persistent pain.

14 ties of dorsal column nucleus neurons during persistent pain.

15 ntially may contribute to the development of persistent pain.

16 lective agents, may be useful analgesics for persistent pain.

17 ts that facilitate transitions from acute to persistent pain.

18 CNS-derived TNFalpha in the pathogenesis of persistent pain.

19 d central sensitization in several models of persistent pain.

20 re is a distinct neurochemistry of acute and persistent pain.

21 nt insight into targets for the treatment of persistent pain.

22 al constriction (writhing) assay, a model of persistent pain.

23 ncer patients using transdermal fentanyl for persistent pain.

24 cal target for the prevention and therapy of persistent pain.

25 stems, and contributes to the maintenance of persistent pain.

26 a key mediator of neuroplasticity underlying persistent pain.

27 r the development of effective therapies for persistent pain.

28 nalgesia in experimental models of acute and persistent pain.

29 of Tmem100-3Q mimics its effect and inhibits persistent pain.

30 dependent analgesia in the formalin model of persistent pain.

31 surgical procedures are used in treatment of persistent pain.

32 the diagnosis, monitoring, and management of persistent pain.

33 tanding of the transition from acute pain to persistent pain.

34 We focus on this plasticity as a cause of persistent pain.

35 analgesics in an in vivo model of tonic and persistent pain.

36 ired decision-making can be a consequence of persistent pain.

37 a useful therapeutic target in some forms of persistent pain.

38 ing to the brain and serve as analgesics for persistent pain.

39 generation and maintenance of injury-induced persistent pain.

40 sensory neuron excitability associated with persistent pain.

41 and age all influence the risk of developing persistent pain.

42 OR 0.43, 95% CI 0.34-0.55; P <.001) (overall persistent pain: 120 in 2,368 vs. 215 in 1,998; OR 0.36,

43 ays in the preceding month, 9% versus 2% had persistent pain, 24% versus 16% had incident pain, and 2

44 Yet how persistent pain affects the key brain area regulating th

45 Purpose Persistent pain after breast cancer surgery is a well-re

46 reen for patients at high risk of developing persistent pain after breast cancer surgery.

47 Finally, the risk for persistent pain after cesarean deliveries may be associa

48 underlying mechanism for the development of persistent pain after injury.

49 esearch in pain epigenetics to patients with persistent pain after thoracic surgery.

50 Persistent pain after thoracotomy is not an acute somati

51 pain facilitation during the development of persistent pain after tissue and nerve injury.

52 Recent studies indicate that persistent pain after tissue or nerve injury is accompan

53 rat model of chronic pain, we determined how persistent pain altered behavioral responses to morphine

54 orn neurons of the spinal cord, resulting in persistent pain, an exacerbated response to noxious stim

55 S) is characterized by altered bowel habits, persistent pain and discomfort, and typically colorectal

56 findings demonstrate: (i) the development of persistent pain and hyperalgesia in 10-day-old rats that

57 steroid, progesterone, in the development of persistent pain and hyperalgesia in lactating ovary-inta

58 ts of sucrose and suckling in a rat model of persistent pain and hyperalgesia that mimics the respons

59 Loss of full strength, persistent pain and need for professional change occurs

60 otective role for AG in processes underlying persistent pain and neuronal injury.

61 differs from primary Raynaud's phenomenon as persistent pain and paresthesia are common in the hands

62 ency in the face of aversive stimuli such as persistent pain and potentially other stressors.

63 These results identify a target for treating persistent pain and suggest that the small population of

64 algesia may be different under conditions of persistent pain and that (2) combining EA with a sub-eff

65 ions and interaction partners in relation to persistent pain and the potential side effects of anti-N

66 pain facilitation during the development of persistent pain, and may not mediate opioid-induced desc

67 rodent models of acute thermal nociception, persistent pain, and neuropathic allodynia.

68 e those individuals prone to a transition to persistent pain, and thus requiring therapeutic strategi

69 Acute neuritis and persistent pain are the most significant clinical manife

70 -mediated selective suppression of second or persistent pain as compared to first pain; and (3) NTB,

71 ei may contribute to thalamic changes during persistent pain as well as to supraspinal centers that m

72 The chronic, persistent pain associated with chronic pancreatitis (CP

73 ral neuronal hyperexcitability contribute to persistent pain associated with temporomandibular disord

74 The outcome variable was moderate to severe persistent pain at 1 year from surgery in the Finnish an

75 However, tissue injury-evoked persistent pain behavior, inflammation of the hindpaw, a

76 drug prescribed for alleviation of severe or persistent pain, both preclinical and clinical studies h

77 xpression have been studied in rat models of persistent pain but have not been characterized in any m

78 ontribute to nociceptive hypersensitivity in persistent pain, but the molecular mechanisms underlying

79 y contribute to spinal hyperexcitability and persistent pain by enhancement of PKC-mediated phosphory

80 ding 5-HT in rat nocifensive behaviors after persistent pain by selectively depleting functional phen

81 Persistent pain can result in sensitization of neurons i

82 II, which has previously been implicated in persistent pain caused by injury.

83 Because persistent pain changes neural response to external stim

84 Because persistent pain changes neural response to external stim

85 ccess of stratified models of care for other persistent pain conditions, dichotomized GCPS status may

86 ous inflammatory mediators may contribute to persistent pain conditions.

87 EREG may be suitable therapeutic targets for persistent pain conditions.

88 dvances in relation to somatic and orofacial persistent pain conditions.

89 thophysiology and management of a variety of persistent pain conditions.

90 the mechanism of pain hypersensitivity under persistent pain conditions.

91 We found that rats with persistent pain consumed a similar amount of daily morph

92 rlying central sensitization associated with persistent pain depend on a transition to supraspinal me

93 tients were referred for ablation because of persistent pain despite use of analgesics, and one patie

94 nervous system (CNS) component underpinning persistent pain disease states.

95 y of the cerebral representation of ongoing, persistent pain due to OA.

96 algesics outweigh the risks in patients with persistent pain due to rheumatoid arthritis?

97 ciation between severe postdelivery pain and persistent pain, early recognition of an increased susce

98 kinase C (PKC) underlie the exaggerated and persistent pain experienced in the inflammatory state.

99 VI), multisymptom illnesses characterized by persistent pain, fatigue, and cognitive symptoms, have b

100 Several risk factors for persistent pain have been recognized, but tools to ident

101 bed therapeutic agent for the alleviation of persistent pain; however, it is becoming increasingly cl

102 (ROS) scavengers have been shown to relieve persistent pain; however, the mechanism is not clearly u

103 ve spinal neurons contributes, therefore, to persistent pain hypersensitivity, possibly via transcrip

104 role in the establishment and maintenance of persistent pain in animal models, the role of glial cell

105 both acute pain during treatment and chronic persistent pain in cancer survivors.

106 ntral nociceptive networks and thereby evoke persistent pain in children following injury.SIGNIFICANC

107 rther demonstrated that IL-17 contributes to persistent pain in EAE and functions as an upstream regu

108 KIIalpha and IL-17 as critical regulators of persistent pain in EAE, which may ultimately offer new t

109 Treatment planning for persistent pain in later life requires a clear understan

110 afferent neurons similar to those that drive persistent pain in mammals, robust changes far from site

111 dogenous inhibitory mechanism for regulating persistent pain in mice.

112 and guidelines relevant to the management of persistent pain in older adults.

113 ttenuated behavioral responses indicative of persistent pain in rodent models of peripheral nerve inj

114 enth postoperative day ( P = .003) predicted persistent pain in the final prediction model, which per

115 odulation of reflex nocifensive responses to persistent pain in the formalin test.

116 cking PSD-93 exhibit blunted NMDAR-dependent persistent pain induced by peripheral nerve injury or in

117 tes to the hyperexcitability associated with persistent pain induced by spinal cord injury (SCI).

118 Persistent pain is a sequela of several neurological con

119 rived sensorimotor cortex, the experience of persistent pain is associated with preserved structure a

120 In animals, persistent pain is characterized by peripheral and spina

121 Persistent pain is highly prevalent, costly, and frequen

122 ve pain is clearly an adaptive alarm system, persistent pain is maladaptive, essentially an ongoing f

123 Persistent pain is measured by means of self-report, the

124 functional relevance of this upregulation to persistent pain is unknown.

125 rs, but how their interaction contributes to persistent pain is unknown.

126 Persistent pain leads to changes in the spinal cord that

127 These results suggest that persistent pain leads to neurochemical changes within th

128 work is topologically reorganized to support persistent pain-like behavior following neuropathic inju

129 s neurotransmitter system is implicated (ie, persistent pain, mood disorders, substance use disorders

130 e common comorbidity with other disorders of persistent pain, mood, and affect, as well as possibly m

131 these neurotransmitters have a role, such as persistent pain, mood, and substance use disorders, and

132 Results Moderate to severe persistent pain occurred in 13.5%, 13.9%, and 20.3% of t

133 R in inflammatory and nerve-injury models of persistent pain, occurring at least in part through the

134 A higher BMI was predictive of persistent pain (odds ratio [OR] 1.14, 95% confidence in

135 Prediction models for persistent pain of moderate to severe intensity at 1 yea

136 ce of radiographic knee OA was predictive of persistent pain (OR 3.70, 95% CI 1.34-10.28; P = 0.012),

137 reported knee injury was predictive of both persistent pain (OR 4.13, 95% CI 1.34-12.66; P = 0.013)

138 of diameter on imaging during the admission, persistent pain, or clinical malperfusion leading to a d

139 s that underlie the development of acute and persistent pain, our laboratory has been studying mice w

140 o the emergency department for evaluation of persistent pain over the volar portion of his right fift

141 ed along with non-cancer pain, chronic pain, persistent pain, pain management, intractable pain, and

142 the dorsal column nuclei can participate in persistent pain processes.

143 How primary sensory neurons contribute to persistent pain remains unclear.

144 Moreover, in the acute versus persistent pain settings, the analgesic actions of the S

145 Persistent pain should be considered a disease state of

146 heral nerve hyperexcitability as a driver of persistent pain signaling after SCI.

147 terations in the spinal cord reflective of a persistent pain state.

148 ammatory cytokines play an important role in persistent pain states and represent potential therapeut

149 Current therapies to treat persistent pain states are limited and often cause major

150 from the dorsal horn, their participation in persistent pain states is relatively unexplored, perhaps

151 cer pain is one of the most difficult of all persistent pain states to fully control.

152 llness (that is, diabetes, heart disease and persistent pain states) in depressed individuals.

153 Here, we show that persistent pain states, but not acute pain behavior, are

154 criptional alterations are characteristic of persistent pain states, but the key regulators remain el

155 ug targets for the treatment of pathological persistent pain states, such as inflammatory and neuropa

156 Na(V)1.8 after nerve injury is essential for persistent pain states.

157 yric acid (GABA) receptors may contribute to persistent pain states.

158 ongoing primary afferent input in acute and persistent pain states.

159 velopment of tissue and nerve injury-induced persistent pain states.

160 tor could therefore ameliorate injury-evoked persistent pain states.

161 as a long-needed potential new drug to stop persistent pain states.

162 ogical route for therapeutic intervention in persistent pain states.

163 a were almost identical in the two models of persistent pain, suggesting that behavioral testing may

164 nd our ability to predict who will develop a persistent pain syndrome is poor at best.

165 ed (for example, mood and anxiety disorders, persistent pain syndromes or even Parkinson disease and

166 or perpetuating pathological states such as persistent pain syndromes, depression, substance use dis

167 of EA anti-hyperalgesia may be different in persistent pain than in health.

168 Bodily injury in mammals often produces persistent pain that is driven at least in part by long-

169 a in the establishment and or maintenance of persistent pain, the present findings offer clinical imp

170 NFalpha) is implicated in the development of persistent pain through its actions in the periphery and

171 toperative pain and drives its transition to persistent pain via persistent neuronal and microglial M

172 e of these factors were present, the risk of persistent pain was increased.

173 acement (OR 1.26, 95% CI 0.76-2.08; P =.36), persistent pain was less common after laparoscopic than

174 way of CREB activation--fear memory, but not persistent pain, was significantly reduced.

175 r neuropathic (spared nerve injury) model of persistent pain, we observed that young adult female mic

176 in severity being the strongest predictor of persistent pain with long-lasting disability.

177 nt a class of antihyperalgesics for treating persistent pain with minimal side effects because of the

178 fficacy in the formalin paw-licking model of persistent pain with no obvious adverse effects on motor

179 al trait: the ability of opioids to suppress persistent pain without preventing response to a new inj