ライフサイエンスコーパス: neuropathic pain

1 sm (eg, painful cramps, nociceptive pain, or neuropathic pain).

2 expression in the injured DRG and attenuates neuropathic pain.

3 a new role for the RGMa/Neogenin pathway on neuropathic pain.

4 cer pharmacotherapy, leading to debilitating neuropathic pain.

5 contribute to the pathogenesis of orofacial neuropathic pain.

6 y and retraction scars limiting movement) or neuropathic pain.

7 ependent distribution resulting in disabling neuropathic pain.

8 els, expressed by nociceptors, contribute to neuropathic pain.

9 development of more specific treatments for neuropathic pain.

10 ng in rat spared nerve injury (SNI) model of neuropathic pain.

11 that a D1/D5 antagonist transiently inhibits neuropathic pain.

12 e nociceptive system is a basic mechanism of neuropathic pain.

13 ing in small fibre neuropathy and associated neuropathic pain.

14 the somatosensory cortex of a mouse model of neuropathic pain.

15 been suggested to be novel drug targets for neuropathic pain.

16 potentially contributing to the mechanism of neuropathic pain.

17 se and rat peripheral nerve injury models of neuropathic pain.

18 useful in the treatment of inflammatory and neuropathic pain.

19 nal cord persistently attenuated SNL-induced neuropathic pain.

20 ted sodium channel NaV1.7 is dysregulated in neuropathic pain.

21 in microglial activation and pathogenesis of neuropathic pain.

22 mer's disease; and schizophrenia and chronic neuropathic pain.

23 the rat chronic constrictive injury model of neuropathic pain.

24 ity in preclinical models of inflammatory or neuropathic pain.

25 rs including depression, drug addiction, and neuropathic pain.

26 paired heat hyperalgesia in inflammatory and neuropathic pain.

27 bute to hypersensitivity in rodent models of neuropathic pain.

28 potential targets for the pharmacotherapy of neuropathic pain.

29 also inhibited allodynia in a mouse model of neuropathic pain.

30 uent RIM1alpha/CaV2.2 cascade in SNL-induced neuropathic pain.

31 analgesic effect in the treatment of chronic neuropathic pain.

32 hanical hypersensitivity, a major symptom of neuropathic pain.

33 y be a useful analgesic in the management of neuropathic pain.

34 -5p decreased CXCL13 expression, alleviating neuropathic pain.

35 opioid analgesic effects in animal models of neuropathic pain.

36 ipheral nerve injury- and paclitaxel-induced neuropathic pain.

37 ists holds promise as a viable treatment for neuropathic pain.

38 ant role of oligodendrocyte-derived IL-33 in neuropathic pain.

39 ession of MORs in primary sensory neurons in neuropathic pain.

40 activates astrocytes via CXCR5 to facilitate neuropathic pain.

41 as a treatment option for paclitaxel-induced neuropathic pain.

42 ling may be suitable therapeutic targets for neuropathic pain.

43 ain perception and relieves inflammatory and neuropathic pain.

44 he potential of cell-based therapies against neuropathic pain.

45 a crucial contribution to the development of neuropathic pain.

46 on (DRG) and diminishes the opioid effect on neuropathic pain.

47 algesics for the dual treatment of acute and neuropathic pain.

48 ministration of TGF-beta1 potently inhibited neuropathic pain.

49 dations for the pharmacological treatment of neuropathic pain.

50 l nucleus in subjects with chronic orofacial neuropathic pain.

51 timulation, represents a cardinal feature of neuropathic pain.

52 death, axonal retraction, and development of neuropathic pain.

53 calcium channel ligands in the treatment of neuropathic pain.

54 es a substantial unmet need in patients with neuropathic pain.

55 tic silencing as a new treatment modality in neuropathic pain.

56 al disorders, including absence epilepsy and neuropathic pain.

57 method for targeted silencing of A-fibers in neuropathic pain.

58 development and/or maintenance of peripheral neuropathic pain.

59 of chronic constriction injury (CCI)-induced neuropathic pain.

60 ganglion (DRG) in the development of chronic neuropathic pain.

61 G recommendations for the pharmacotherapy of neuropathic pain.

62 represent a novel strategy for management of neuropathic pain.

63 s of the A1R can be effective treatments for neuropathic pain.

64 apses in a rat partial nerve-injury model of neuropathic pain.

65 y targeting the receptor in the treatment of neuropathic pain.

66 h the cognitive and the sensory component of neuropathic pain.

67 ntion of chronic cancer chemotherapy-induced neuropathic pain.

68 the rat chronic constrictive injury model of neuropathic pain.

69 itivity in peripheral nerve injury models of neuropathic pain.

70 odone in pain-free states, and in a model of neuropathic pain.

71 nhibition of Panx1 may be useful in treating neuropathic pain.

72 which may contribute to nerve injury-induced neuropathic pain.

73 n the rat spared nerve injury (SNI) model of neuropathic pain.

74 eurological disorders including epilepsy and neuropathic pain.

75 thus promotes post-traumatic axonal loss and neuropathic pain.

76 stically distinct models of inflammatory and neuropathic pain.

77 and treatment algorithms designed to target neuropathic pain.

78 CXCL12/CXCR4 signaling pathway may alleviate neuropathic pain.

79 ined therapeutic target for inflammatory and neuropathic pain.

80 ovel strategy for preventing and controlling neuropathic pain.

81 nced amygdala activity in an animal model of neuropathic pain.

82 effective in the treatment of some types of neuropathic pain.

83 hanical hypersensitivity, a major symptom of neuropathic pain.

84 nctional role in SNI- and paclitaxel-induced neuropathic pain.

85 c pain, 100% had probable and 95.2% definite neuropathic pain.

86 apeutic target to alleviate inflammatory and neuropathic pain.

87 ent amnesia, dysautonomia, neuromyotonia and neuropathic pain.

88 a cellular target for treating this form of neuropathic pain.

89 ssociation for the Study of Pain grading for neuropathic pain, 100% had probable and 95.2% definite n

90 In addition, the effect on neuropathic pain, a pain type reported by women treated

91 for neuropathic pain.SIGNIFICANCE STATEMENT Neuropathic pain, a type of moderate to severe chronic p

92 al over-expression of Arrb2 reverses chronic neuropathic pain after nerve injury.

93 eripheral monocytes are sufficient in gating neuropathic pain after SNT.

94 peutic target for SCI.SIGNIFICANCE STATEMENT Neuropathic pain after spinal cord injury (SCI) may in p

95 rom segments where patients had a history of neuropathic pain also showed electrophysiological and im

96 of the complement system in inflammatory and neuropathic pain, although the underlying mechanisms are

97 seases, inflammation, neurodegeneration, and neuropathic pain, among others.

98 cal symptoms, such as diarrhea, fatigue, and neuropathic pain, among others.

99 Neuropathic pain and bladder dysfunction represent signi

100 e chronic constriction nerve injury model of neuropathic pain and carrageenan model of inflammatory p

101 ate the effects of EpFAs on diabetes induced neuropathic pain and define a previously unknown mechani

102 lts in prolongation of inflammatory pain and neuropathic pain and enhancement of GluN2B-mediated NMDA

103 this study we investigated the incidence of neuropathic pain and examined the presence of nerve dysf

104 changes that arise during the development of neuropathic pain and identify the activation of specific

105 rtant role in multiple preclinical models of neuropathic pain and in inherited human pain phenotypes,

106 w male-dominant microglial signaling in some neuropathic pain and inflammatory pain states, although

107 of extract from Corydalis yanhusuo alleviate neuropathic pain and levo-tetrahydropalmatine (l-THP) is

108 Beyond impaired motor and sensory function, neuropathic pain and loss of bladder control caused by s

109 first-line treatment in chemotherapy-induced neuropathic pain and may be highly efficacious in neurop

110 pain, including trigeminal hypersensitivity, neuropathic pain and migraine.

111 which are associated with the persistence of neuropathic pain and motor dysfunction.

112 tivated pro-drugs to localize treatments for neuropathic pain and nerve injury to injured nerves.

113 t in biology and therapeutically in treating neuropathic pain and neurological disorders.

114 te that trkB.T1 in astrocytes contributes to neuropathic pain and neurological dysfunction following

115 regulation contributes to the development of neuropathic pain and stimulation of inflammasome signali

116 esic actions in preclinical rodent models of neuropathic pain and that A3AR analgesia is independent

117 berrant afferent input in the maintenance of neuropathic pain and the potential for targeted chemogen

118 , and led to robust motosensory improvement, neuropathic pain and tissue damage mitigation, and myeli

119 ripheral sensory and motorneuronal function, neuropathic pain and tissue necrosis.

120 play a critical role in mPFC deactivation in neuropathic pain and underlie the mPFC-specific cognitiv

121 ials that included 396 patients investigated neuropathic pain, and 12 trials that included 1600 patie

122 ne contribute to the generation of epilepsy, neuropathic pain, and autism spectrum disorders; thus, i

123 atherosclerosis, multiple sclerosis, asthma, neuropathic pain, and diabetic nephropathy, as well as c

124 gies, among which glaucoma, edema, epilepsy, neuropathic pain, and hypoxic tumors.

125 implicated in neurodevelopmental disorders, neuropathic pain, and schizophrenia.

126 I-mtO2(.-)-pCREB-pC/EBPbeta signaling in HIV neuropathic pain, and should help in the development of

127 Use of marijuana for chronic pain, neuropathic pain, and spasticity due to multiple scleros

128 ia, nausea/vomiting related to chemotherapy, neuropathic pain, and spasticity in multiple sclerosis.

129 neurotransmission as a critical mechanism of neuropathic pain, and suggest that targeting insular M2

130 ility-related disorders, including epilepsy, neuropathic pain, and tinnitus.

131 aggravating stroke, temporal lobe epilepsy, neuropathic pain, and various neurodegenerative diseases

132 Here, we show that both basal mechanical and neuropathic pain are controlled by the microRNA-183 (miR

133 ors effectively reduce inflammatory pain and neuropathic pain, arguing against the importance of morp

134 Peripheral neuropathic pain arises as a consequence of injury to se

135 ng an important novel therapeutic avenue for neuropathic pain as a class.

136 eclinical profile in two different models of neuropathic pain as well as in a reserpine model of cent

137 ) recommendations for the pharmacotherapy of neuropathic pain based on the results of a systematic re

138 ensory scores were unchanged and below-level neuropathic pain became prominent.

139 P2, and DPP10 are potential drug targets for neuropathic pain because they form a channel complex wit

140 activity with intrathecal anti-IL10 unmasks neuropathic pain behavior in infant nerve injured mice,

141 plays a critical role in CeA plasticity and neuropathic pain behaviors in the rat spinal nerve ligat

142 Slack opener loxapine ameliorated persisting neuropathic pain behaviors.

143 nal blockade of intracellular mGluR5 reduces neuropathic pain behaviours and signalling molecules, wh

144 In rats with postsurgical or neuropathic pain, blockade of opioid signaling in the ro

145 w-strength evidence that cannabis alleviates neuropathic pain but insufficient evidence in other pain

146 ciception in models of post-surgical and HIV neuropathic pain but only slightly blocked anti-nocicept

147 Alleviation of neuropathic pain by cannabinoids is limited by their cen

148 a proinflammatory cytokine, IFN-gamma drives neuropathic pain by inducing microglial activation in th

149 ndings suggest that DNMT3a may contribute to neuropathic pain by repressing Kcna2 expression in the D

150 recovery ("remission") from inflammatory or neuropathic pain can be reversed by opioid antagonists.

151 Chemotherapy-induced peripheral neuropathic pain (CIPN) is a common and severe debilitat

152 Chemotherapy-induced peripheral neuropathic pain (CIPNP) is a severe dose- and therapy-l

153 e role of pregabalin in CIBP with a clinical neuropathic pain component is unknown.

154 nsmission in the posterior insular cortex in neuropathic pain condition and the involvement of M2 rec

155 mia is thought to play a role in a number of neuropathic pain conditions, and yet the role of hypoxia

156 therapeutic strategies for inflammatory and neuropathic pain conditions.

157 ng is male dominant in some inflammatory and neuropathic pain conditions.

158 f hypoxia has also not been characterized in neuropathic pain conditions.

159 suggesting that adaptive immune responses in neuropathic pain could be sexually dimorphic.

160 molecule-1alpha (RIM1alpha) participates in neuropathic pain development by binding to and upregulat

161 se findings indicate that G9a contributes to neuropathic pain development through epigenetic silencin

162 Spinal plasticity, a key process mediating neuropathic pain development, requires ubiquitination-de

163 onic non-freezing cold injury is a disabling neuropathic pain disorder due to a sensory neuropathy.

164 eund's adjuvant injection and the late phase neuropathic pain following chronic constriction injury (

165 Neuropathic pain following peripheral nerve injury is as

166 use and proposal as first-line treatment in neuropathic pain for tricyclic antidepressants, serotoni

167 Neuropathic pain frequently leads to decisions about usi

168 l new mechanisms and therapeutic targets for neuropathic pain from different origins.

169 Neuropathic pain from injury to the peripheral and CNS r

170 In neuropathic pain, GABAAR-mediated signaling can be furth

171 s critical for DRG neuronal excitability and neuropathic pain genesis.

172 Whether LY2828360 suppresses neuropathic pain has not been reported, and its signalin

173 ng, we found that individuals with orofacial neuropathic pain have increased infra-slow oscillatory a

174 le of the medial prefrontal cortex (mPFC) in neuropathic pain have led to an increased awareness of h

175 Peripheral nerve injury can trigger neuropathic pain in adults but not in infants; indeed, f

176 knowledge of the mechanisms contributing to neuropathic pain in diabetes.

177 Using the spared nerve injury (SNI) model of neuropathic pain in Long-Evans rats and patch-clamp reco

178 or (ST2) signaling in experimental models of neuropathic pain in mice.

179 nic pain, and notably in oxaliplatin-induced neuropathic pain in mice.

180 receptor G2A (GPR132) in oxaliplatin-induced neuropathic pain in mice.

181 ling, and functional profiling can attenuate neuropathic pain in patients carrying the S241T mutation

182 R4) antagonist and has been shown to reverse neuropathic pain in rat studies.

183 dose of RgIA4 prevented chemotherapy-induced neuropathic pain in rats.

184 vidence suggests that cannabis may alleviate neuropathic pain in some patients, but insufficient evid

185 In a mouse model of neuropathic pain, in vivo two-photon imaging and patch c

186 a potential new target for the treatment of neuropathic pain, including chemotherapy (paclitaxel)-in

187 dies of oral and topical pharmacotherapy for neuropathic pain, including studies published in peer-re

188 In this study, we report in individuals with neuropathic pain increased oscillatory neural activity w

189 sults suggest that A3AR-mediated reversal of neuropathic pain increases modulation of GABA inhibitory

190 We show that chronic neuropathic pain increases PACAP expression at multiple

191 Sustained neuropathic pain induced by spinal nerve ligation is acc

192 phrine, TNFalpha, and interleukin-6, and the neuropathic pain induced by the cancer chemotherapy pacl

193 tions, drug discovery, prosthetic design and neuropathic pain investigations.

194 We conclude that development of neuropathic pain involves abnormal homeostatic activity

195 Neuropathic pain involves long-lasting modifications of

196 Chronic, intractable neuropathic pain is a common and debilitating consequenc

197 Neuropathic pain is a complex, chronic pain state that o

198 Neuropathic pain is a debilitating condition for which t

199 Chronic neuropathic pain is a major clinical problem with poorly

200 Neuropathic pain is a major, intractable clinical proble

201 experimental animal investigations show that neuropathic pain is associated with altered infra-slow (

202 ence from human investigations suggests that neuropathic pain is associated with altered thalamic bur

203 Significance statement: Chronic neuropathic pain is associated with altered thalamic fir

204 Neuropathic pain is caused by a primary lesion or dysfun

205 ng the underlying mechanisms responsible for neuropathic pain is critical if we are to develop more e

206 echanisms responsible for the maintenance of neuropathic pain is imperative for the development of mo

207 not in infants; indeed, for unknown reasons, neuropathic pain is rare before adolescence.

208 The data may explain why neuropathic pain is rare in young children and also why

209 a primary dermatological disorder can cause neuropathic pain is still unclear.

210 re severe dry eye symptoms, ocular pain, and neuropathic pain-like ocular symptoms.

211 led to spinal cord central sensitization and neuropathic pain-like symptoms.

212 s in understanding the mechanisms underlying neuropathic pain, limited success in therapeutic approac

213 d non-pharmacological treatment protocol for neuropathic pain management, was reported to selectively

214 ent of cortical hyperexcitability underlying neuropathic pain may involve homeostatic plasticity in r

215 new insights in the understanding of the HIV neuropathic pain mechanisms and treatment.SIGNIFICANCE S

216 Here, we used a neuropathic pain model of perineural HIV envelope glycop

217 In a neuropathic pain model of perineural HIV gp120 applicati

218 lar behavioral and pathological changes in a neuropathic pain model of peripheral nerve injury.

219 In a neuropathic pain model, LC(:SC) activation reduced hind-

220 a L5 spinal nerve ligation (SNL)-induced rat neuropathic pain model.

221 tenance of neuropathic nociception in either neuropathic pain model.

222 nical hypersensitivity produced in different neuropathic pain models in adult mice.

223 fects in myriad preclinical inflammatory and neuropathic pain models.

224 ids alleviated allodynia and hyperalgesia in neuropathic pain models.

225 se, like alpha2delta-1, it is upregulated in neuropathic pain models.

226 ne tolerance, in both acute pain and chronic neuropathic pain models.

227 in the spinal cord in a nerve injury-induced neuropathic pain mouse model.

228 E), we revised the Special Interest Group on Neuropathic Pain (NeuPSIG) recommendations for the pharm

229 between structural changes and magnitude of neuropathic pain (NP) remains incompletely understood.

230 Skin biopsies from patients with neuropathic pain often show changes in epidermal innerva

231 linum toxin A are recommended for peripheral neuropathic pain only.

232 steroidal anti-inflammatory drugs, drugs for neuropathic pain, opioids, and cannabinoids, to physical

233 nged in a sciatic nerve transection model of neuropathic pain or in the Complete Freund's adjuvant mo

234 . x 12 days) suppressed chemotherapy-induced neuropathic pain produced by paclitaxel without producin

235 yer 5 mPFC pyramidal neurons is abolished in neuropathic pain rats due to a severe reduction of a mus

236 Therefore, in neuropathic pain rats, the acetylcholine (ACh)-dependent

237 his single cluster controls more than 80% of neuropathic pain-regulated genes and scales basal mechan

238 e in silencing sensory neurons and reversing neuropathic pain-related hypersensitivity.

239 increased 5-HT2CR in the BLA contributes to neuropathic-pain-related amygdala plasticity by driving

240 e, decreases neuronal activity, and inhibits neuropathic-pain-related behaviors.

241 ategy, 5-HT2CR knockdown in the BLA inhibits neuropathic-pain-related behaviors.SIGNIFICANCE STATEMEN

242 DRGs to elicit neuroprotection and sustained neuropathic pain relief via TGF-beta1 secretion.

243 g the development and maintenance of chronic neuropathic pain remain unclear.

244 progression of spinal plasticity-associated neuropathic pain remains unclear.

245 neurodegenerative diseases, but its role in neuropathic pain remains unclear.

246 ical sensitivity, which resemble features of neuropathic pain reported in humans and other species an

247 of the pain-sensing system, as in chronic or neuropathic pain, represents a major health burden with

248 RGMa antibody also attenuated neuropathic pain responses, which was associated with fe

249 These findings also support the use of neuropathic pain screening tools in these patients and t

250 dynia) is prevalent in many inflammatory and neuropathic pain settings, with little known of the mech

251 questionnaire, and treatment algorithms for neuropathic pain should now be used in the management of

252 y, we report that individuals with orofacial neuropathic pain show altered functional connectivity be

253 adigms in a rat model of oxaliplatin-induced neuropathic pain, showed the better antihypersensitive p

254 subunits could be potential drug targets for neuropathic pain.SIGNIFICANCE STATEMENT Neuropathic pain

255 ic cognitive deficits that are comorbid with neuropathic pain.SIGNIFICANCE STATEMENT The medial prefr

256 including chemotherapy (paclitaxel)-induced neuropathic pain.SIGNIFICANCE STATEMENT This work demons

257 therapeutic target against inflammatory and neuropathic pain.SIGNIFICANCE STATEMENT We demonstrate t

258 Using the Neuropathic Pain Special Interest Group of the Internati

259 ed thalamocortical activity and a persistent neuropathic pain state.

260 triggers pC/EBPbeta in the HIV gp120-induced neuropathic pain state.

261 pathic pain and may be highly efficacious in neuropathic pain states that are refractive to opioid an

262 and dorsal root ganglia that contributes to neuropathic pain states through unknown mechanisms.

263 ck selectively controls the sensory input in neuropathic pain states, suggesting that modulating its

264 ains present in sensory neurons may modulate neuropathic pain states.

265 nges when the injured animals have developed neuropathic pain states.

266 and central sensitization that contribute to neuropathic pain states.

267 Cold allodynia occurs as a major symptom of neuropathic pain states.

268 ons vulnerable to peripheral nerve injury or neuropathic pain stimuli.

269 subscale (d = 0.26; P = .026), the SF-MPQ-2 neuropathic pain subscale (d = 0.24; P = .036), and SF-M

270 5], Ocular Surface Disease Index [OSDI], and Neuropathic Pain Symptom Inventory modified for the eye

271 Neuropathic pain symptoms respond poorly to available th

272 ar puncture alleviates early- and late-phase neuropathic pain symptoms, such as allodynia and hyperal

273 mes where patients are experiencing acquired neuropathic pain symptoms.

274 ads to spinal cord central sensitization and neuropathic pain symptoms.

275 analgesic against thermal, inflammatory, and neuropathic pain that acts independently of 7TM mu-opioi

276 ong-term treatments to ameliorate peripheral neuropathic pain that includes mechanical allodynia are

277 have been implicated in nerve injury-induced neuropathic pain, the manner by which injured sensory ne

278 sic effects in rodent models of experimental neuropathic pain through the A3 adenosine receptor (A3AR

279 1.9 cause severe pain disorders ranging from neuropathic pain to congenital pain insensitivity.

280 In this study we used a mouse model of neuropathic pain to dissociate these factors.

281 tivity in nociceptive neurons and suppresses neuropathic pain transduction in a specific, light-touch

282 gh several efficacious medications exist for neuropathic pain treatment, pain is still underrecognize

283 l for targeted silencing of Abeta-fibers and neuropathic pain treatment.

284 nomimetics could be an effective therapy for neuropathic pain treatment.

285 ng central cholinomimetics could be used for neuropathic pain treatment.

286 aviors in C57BL/6J male mice were induced by neuropathic pain, unpredictable chronic mild stress, and

287 post-traumatic intraneural inflammation and neuropathic pain using the chronic constriction injury (

288 A3AR agonists (IB-MECA and MRS5698) reverse neuropathic pain via a spinal mechanism of action that m

289 d CXCR5 expression in spinal astrocytes, and neuropathic pain was abrogated in Cxcr5-/- mice.

290 igation was to determine whether, in humans, neuropathic pain was also associated with altered infra-

291 Orofacial neuropathic pain was associated with significant regiona

292 Neuropathic pain was induced by cuffing the right sciati

293 Neuropathic pain was induced by partial sciatic nerve li

294 enerated by the spared nerve injury model of neuropathic pain was reversed by ivermectin treatment.

295 m male and female humans with cancer-related neuropathic pain was tested here.

296 ing the spinal nerve ligation (SNL) model of neuropathic pain, we found that CXCL13 was persistently

297 T2 represents a valuable strategy to relieve neuropathic pain, we synthesized novel activators (4a-f)

298 d to increased hypersensitivity in models of neuropathic pain, whereas the behavior in models of infl

299 B1 signaling would suppress inflammatory and neuropathic pain without producing cannabimimetic effect

300 agonist that attenuates chemotherapy-induced neuropathic pain without producing tolerance and may pro