ライフサイエンスコーパス: persistent pain

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

2 generation and maintenance of injury-induced persistent pain.

3 1 function and its contribution to acute and persistent pain.

4 sensory neuron excitability associated with persistent pain.

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

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

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

8 sses of antidepressants in the management of persistent pain.

9 tory conditions can lead to debilitating and persistent pain.

10 nown mechanism underlying the development of persistent pain.

11 effective analgesic agents in many models of persistent pain.

12 effective analgesic agents in many models of persistent pain.

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

14 atment strategies for aging populations with persistent pain.

15 AR-mediated synaptic function and associated persistent pain.

16 administration in mouse models of acute and persistent pain.

17 tial biochemical target for the treatment of persistent pain.

18 ties of dorsal column nucleus neurons during persistent pain.

19 ntially may contribute to the development of persistent pain.

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

21 ts that facilitate transitions from acute to persistent pain.

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

23 d central sensitization in several models of persistent pain.

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

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

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

27 ncer patients using transdermal fentanyl for persistent pain.

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

29 cal role in the emergence and maintenance of persistent pain.

30 flammation, acinar cell death, fibrosis, and persistent pain.

31 terior cingulate cortex in the patients with persistent pain.

32 ted with loss of sensation, paresthesia, and persistent pain.

33 nd insights into new approaches for treating persistent pain.

34 ot reproduce key characteristics of clinical persistent pain.

35 However, these drugs can cause severe and persistent pain.

36 y of the maladaptive changes associated with persistent pain.

37 iceptor sensitization and the development of persistent pain.

38 rane hyperexcitability in Y1-INs, leading to persistent pain.

39 athway has been reported in rodent models of persistent pain.

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

41 the development of effective treatments for persistent pain.

42 1-expressing dorsal horn neurons, leading to persistent pain.

43 e processes could prevent the development of persistent pain.

44 ration causes impaired tactile sensation and persistent pain.

45 ts with resolved pain but none in those with persistent pain.

46 ls globally each year, with <=50% developing persistent pain.

47 ng state without desensitization and induces persistent pain.

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

49 al NSAIDs and intra-articular injections for persistent pain.

50 a key mediator of neuroplasticity underlying persistent pain.

51 r the development of effective therapies for persistent pain.

52 nalgesia in experimental models of acute and persistent pain.

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

54 entral to the development and maintenance of persistent pain.

55 dependent analgesia in the formalin model of persistent pain.

56 surgical procedures are used in treatment of persistent pain.

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

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

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

60 wing the same surgery, some patients develop persistent pain.

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

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

63 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,

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

65 Chronic, or persistent pain affects more than 10% of adults in the g

66 Persistent pain affects one in five people worldwide, of

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

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

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

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

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

72 re (1) ocular pain before surgery predicated persistent pain after surgery (odds ratio [OR], 1.87; 95

73 Factors that predicted persistent pain after surgery in a multivariable analysi

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

75 Persistent pain after thoracotomy is not an acute somati

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

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

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

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

80 diates the progression to and maintenance of persistent pain and comorbid anxiodepressive-like behavi

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

82 modulation of pain, but its specific role in persistent pain and engagement of descending control mec

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

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

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

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

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

88 plans after diagnosis (participants reported persistent pain and other symptoms despite treatment).

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

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

91 e specifically involved in chemically evoked persistent pain and pruritogen-induced itch.

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

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

94 ping the very early trajectory from acute to persistent pain and that targeting these processes could

95 ficacious in the phase II formalin model for persistent pain and the chronic-constriction-injury-indu

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

97 individual valued life goals in the face of persistent pain, and further improvements in pain treatm

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

99 ement cascade leads to chronic inflammation, persistent pain, and neural dysfunction.

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

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

102 New therapeutic approaches to resolve persistent pain are highly needed.

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

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

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

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

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

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

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

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

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

112 mmune interactions are critical mediators of persistent pain, but sex-dependent differences in spinal

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

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

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

116 Persistent pain can result in sensitization of neurons i

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

118 Because persistent pain changes neural response to external stim

119 Because persistent pain changes neural response to external stim

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

121 ous inflammatory mediators may contribute to persistent pain conditions.

122 neuroblastomas could be repurposed to treat persistent pain conditions.

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

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

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

126 the mechanism of pain hypersensitivity under persistent pain conditions.

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

128 gesic effects, requiring dose escalation for persistent pain control and leading to overdose and fata

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

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

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

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

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

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

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

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

137 in Vancouver, Canada, who reported major or persistent pain from June 1, 2014, to December 1, 2017 (

138 more at both time points and constituted the persistent pain group.

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

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

141 erest in medicinal cannabis for treatment of persistent pain; however, the limited superiority of can

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

143 Remarkably, CFA treatment did not induce persistent pain hypersensitivity in male and female mice

144 nstrate that the complement pathway promotes persistent pain hypersensitivity via microglia-mediated

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

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

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

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

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

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

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

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

153 dogenous inhibitory mechanism for regulating persistent pain in mice.

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

155 argeting macrophage signaling might suppress persistent pain in patients with OSA.

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

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

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

159 plantation of the SCD gut microbiome induced persistent pain in wild-type recipients via bilirubin-va

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

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

162 Persistent pain is a common and disabling health problem

163 Persistent pain is a sequela of several neurological con

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

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

166 Persistent pain is highly prevalent, costly, and frequen

167 after 3 months, the trajectory from acute to persistent pain is likely to be determined very early an

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

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

170 ynthesis of eCBs during the initial onset of persistent pain is the critical link leading to depressi

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

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

173 Persistent pain leads to changes in the spinal cord that

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

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

176 ML382 has been shown to effectively inhibit persistent pain, making MRGPRX1 a promising target for n

177 sing neurotrophic activity and potential for persistent pain management.

178 -photon calcium imaging, mouse genetics, and persistent pain models to study how tissue injury alters

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

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

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

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

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

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

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

186 RK, a subset of patients suffers intense and persistent pain, of unknown origin, described by patient

187 In two models of persistent pain, optogenetic activation of LH(PV) neuron

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

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

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

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

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

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

194 sms of how long-term alcohol use can lead to persistent pain pathology are unclear.

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

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

197 who recovered (SBPr) compared to those with persistent pain (SBPp), and predicted changes in pain se

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

199 Persistent pain should be considered a disease state of

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

201 al inhibition to prevent the transition to a persistent pain state span developmental stages.SIGNIFIC

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

203 le of RVM populations in pain modulation and persistent pain states and explores recent advances outl

204 ked to pain, showing altered levels in human persistent pain states and modulation of pain behaviour

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

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

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

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

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

210 in the superficial dorsal horn contribute to persistent pain states, and that the lateral parabrachia

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

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

213 euronal hyperexcitability is a key driver of persistent pain states, including neuropathic pain.

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

215 ogical route for therapeutic intervention in persistent pain states.

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

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

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

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

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

221 have therapeutic potential in management of persistent pain states.

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

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

224 e who undergo surgery for endometriosis have persistent pain, suggesting that other factors besides t

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

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

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

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

229 will be beneficial in the pursuit to target persistent pain that involves both neural and immune com

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

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

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

233 d effectiveness of gallein in the context of persistent pain using a nitroglycerin (NTG)-induced ther

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

235 gate the mechanisms underlying FKBP51-driven persistent pain vulnerability, we analysed male spinal c

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

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

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

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

240 Using a model of persistent pain, we show by quantitative real-time-PCR,

241 a pathway underlying temporal summation and persistent pain, which may be amenable to therapeutic ta

242 ved the way for psychological treatments for persistent pain, which routinely outperform other forms

243 Furthermore, TBS of sensory nerves induced persistent pain, which was maintained by a2d-1-bound NMD

244 Furthermore, TBS of sensory nerves induced persistent pain, which was maintained by alpha2delta-1-b

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

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

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

248 kbp5 reduced stress-induced vulnerability to persistent pain, with a more pronounced protective effec

249 emale mice exhibited behaviors indicative of persistent pain, with biochemical markers in the spinal

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