ライフサイエンスコーパス: acute pain

1 16:0, and 9,10-EpOME in oxaliplatin-induced acute pain.

2 iate opioid-induced descending inhibition in acute pain.

3 on approaches to the clinical management of acute pain.

4 ened therapeutic options in the treatment of acute pain.

5 nd well tolerated analgesia to patients with acute pain.

6 S2 are the regions consistently activated in acute pain.

7 history of prodromal pain, or the extent of acute pain.

8 rs sufficient to process reflex responses to acute pain.

9 both chronic pain and recurrent episodes of acute pain.

10 ids are the mainstay of treatment for severe acute pain.

11 eptions resulting in suboptimal treatment of acute pain.

12 opment and improvements in the management of acute pain.

13 display intact nociceptive responsiveness to acute pain.

14 er pain, but many of the principles apply in acute pain.

15 se is characterized by recurrent episodes of acute pain.

16 assay, which is a model of tonic rather than acute pain.

17 el of inflammatory pain and formalin induced acute pain.

18 in nervous tissue during oxaliplatin-induced acute pain.

19 endent analgesic effects in rodent models of acute pain.

20 ing the duration of opioid prescriptions for acute pain.

21 .028 (SE 0.01), p = 0.006) predicted greater acute pain.

22 agation and therefore could be used to treat acute pain.

23 pharmacological agents for the treatment of acute pain.

24 alth benefits and might reduce self-reported acute pain.

25 -7 Hz) reflects pain relief from chronic and acute pain.

26 opioid analgesic to treat moderate to severe acute pain.

27 ic, recurrent, and unpredictable episodes of acute pain.

28 ectional control of the aversive response to acute pain.

29 s effective at alleviating thermally induced acute pain.

30 ronic pain may be distinct from activity for acute pain.

31 oduce an antinociceptive effect in models of acute pain.

32 cit an antinociceptive response in models of acute pain.

33 gic and nonpharmacologic methods of managing acute pain.

34 approach to the assessment and treatment of acute pain.

35 ay provide valuable avenues for treatment of acute pain.

36 rest directed toward peripheral mediators of acute pain.

37 enarios that are associated with significant acute pain.

38 symptomatic treatment of osteoarthritis and acute pain.

39 phine are extremely effective treatments for acute pain.

40 nin is the most potent endogenous inducer of acute pain.

41 wnstream effectors do not play a key role in acute pain.

42 gitation requiring therapeutic intervention, acute pain, accidental disconnection or dysfunction of e

43 s reveal reliable neurobehavioral markers of acute pain across naturalistic contexts, underscoring th

44 4.85-10.65; ARDA = 0.25%); among those with acute pain, adjusted HR = 6.64 (95% CI, 3.31-13.31; ARDA

45 o phase 2 trials involving participants with acute pain after abdominoplasty or bunionectomy.

46 aking on the role of 'rescue analgesics' for acute pain after day-case surgery.

47 e opioid prescriptions for the management of acute pain after minor upper extremity surgeries increas

48 ies have shown that opioid prescriptions for acute pain after surgical procedures are often excessive

49 to develop guidelines for the management of acute pain after tooth extraction.

50 onths), 62 (86%) of the 72 patients (19 with acute pain and 53 with subacute pain) had improvement or

51 characterized by repeated episodes of severe acute pain and acute chest syndrome, and by other compli

52 he mainstays for treating moderate to severe acute pain and alleviating chronic cancer pain.

53 es of tissue injury and inflammation elicits acute pain and alters the sensitivity of nociceptive neu

54 We discuss the pharmacological management of acute pain and anxiety, reviewing invasive and non-invas

55 ious in the management of moderate to severe acute pain and cancer pain, use of oxycodone imposes a r

56 are first-line drugs for moderate to severe acute pain and cancer pain.

57 ribed to ameliorate symptoms associated with acute pain and chronic inflammatory diseases such as art

58 development of oxycodone tolerance, in both acute pain and chronic neuropathic pain models.

59 anism could contribute to paclitaxel-induced acute pain and chronic painful neuropathy.

60 cortex (piDLPFC) in migraine patients during acute pain and cognitive task performance.

61 ty in the tail-flick and hot-plate models of acute pain and for their ability to affect core body tem

62 eptors is essential for normal perception of acute pain and heat hyperalgesia, and that heat and mech

63 e corticolimbic system) in the modulation of acute pain and in the prediction and amplification of ch

64 a mechanonociceptors that mediate both sharp acute pain and inflammatory pain; (2) sanshool inhibits

65 conditions for which it is promoted, such as acute pain and insomnia.

66 e neural activation patterns associated with acute pain and its anticipation.

67 ses both pre and postoperatively may improve acute pain and lessen conversion to chronic pain.

68 This paper describes the process of acute pain and measures to control it with drugs or non-

69 widely used experimentally as an inducer of acute pain and neurogenic inflammation, which are largel

70 Hence, acute pain and other types of pain (cancer-related or ch

71 Consequently, WaTx elicits acute pain and pain hypersensitivity but fails to trigge

72 ically relevant concentrations elicited both acute pain and persistent mechanical hyperalgesia which

73 e understanding of claustrum function during acute pain and provide evidence of a possible circuit me

74 that enrolled children (aged <18 years) with acute pain and randomized them to receive a pharmacologi

75 y regulated TRPV1 and TRPA1 agonist-elicited acute pain and spinal cord synaptic plasticity [spontane

76 expression) play a role in the initiation of acute pain and the maintenance of chronic pain while Iba

77 wide range of clinical situations to prevent acute pain and to stop or ameliorate pain produced by ca

78 ous R24W mice of both sexes are resistant to acute pain and to thermal hypersensitivity in chronic in

79 e influenced their decision-making regarding acute pain and treatment.

80 ifocal neuropathies typically presented with acute pain and weakness, and focal neuropathies often mi

81 thway is a key regulator of both chronic and acute pain, and a novel target for pain relief.

82 When intense, these stimuli generate acute pain, and in the setting of persistent injury, bot

83 etically stimulating this pathway suppresses acute pain, and inhibiting it, in naive animals, evokes

84 he virtual world, increased VR analgesia for acute pain, and reduced accuracy on an attention demandi

85 he discriminative and defensive qualities of acute pain, and these neurons are under the control of a

86 ach thus far has been limited to people with acute pain, and translation to chronic pain must still b

87 dicious prescribing of opioid analgesics for acute pain are needed owing to the risks of diversion, m

88 al practice guidelines for the management of acute pain are not based on randomized clinical trials.

89 Outcomes studied were acute (pain area under the curve (AUC) over POD0-2) and

90 m protecting the organism from injury, while acute pain as failure of avoidant behavior, and a mesoli

91 On acute pain assays, we found that loss of LGI1 resulted i

92 t plasma taken from patients with SCD during acute pain associated with a vaso-occlusive event increa

93 sed DeltaFC across MC and PFC in response to acute pain associated with differences in acute pain per

94 e hind paws of healthy mice evoked both more acute pain behavior and greater enhancement of mechanica

95 we show that persistent pain states, but not acute pain behavior, are substantially alleviated by cen

96 ctivated brain regions commonly observed for acute pain, best exemplified by the insula, which tightl

97 Not only is acute pain better controlled, but the development of chr

98 ntinue to be used as the major treatment for acute pain both before and after surgery.

99 not only to acetaminophen analgesia against acute pain but also against inflammatory pain, and sugge

100 eurons, and mice lacking NCX3 showed normal, acute pain but hypersensitivity to the second phase of t

101 low the force output to be maintained during acute pain but this strategy could lead to increased mus

102 hat Rf inhibits tonic pain without affecting acute pain, but other possibilities exist.

103 mu-opioid receptor are effective at managing acute pain, but their chronic use can lead to tolerance

104 Morphine is effective for treating severe acute pain, but tolerance and hypersensitivity often dev

105 We show here that acute pain can also be reduced by multisensory integrati

106 Even brief intervals of acute pain can induce long-term neuronal remodelling and

107 cs for extended periods, but such persistent acute pain can undergo a transition to an opiate-resista

108 Peripheral mediators of acute pain can vary depending upon the type of injury.

109 al fat necrosis is a rare cause of abdominal acute pain, classified into primary or secondary accordi

110 hy controls; N = 112) with and without CP or acute pain completed clinical assessments and participat

111 rt-term analgesic treatment for a variety of acute pain conditions such as occur following trauma, an

112 Beyond the immediate perioperative period, acute pain contributes to the development of the debilit

113 Although racial disparities in acute pain control are well established, the role of pat

114 Acute pain control has advanced dramatically and is now

115 We found no studies comparing uncomplicated acute pain crises in individuals with SCT and SCD.

116 in, P < .05) and was elevated further during acute pain crisis (crisis: 1.10 [0.78-1.30] vs recovered

117 Remifentanil infusion in acute pain decreases the activation in pain perception r

118 pioids represent the frontline treatment for acute pain, despite their side effects, motivating effor

119 ble for the production of PGE2 that mediates acute pain during an inflammatory response.

120 l cancer chemotherapy and can result in both acute pain during treatment and chronic persistent pain

121 e primary end point for prevention trials of acute pain episodes and highlights the importance of eva

122 Chronic hemolytic anemia and intermittent acute pain episodes are the 2 hallmark characteristics o

123 drug trials in SCD have involved the use of acute pain episodes as the primary clinical end point.

124 Trials to prevent acute pain episodes have largely evaluated those episode

125 no association of PlGF with the frequency of acute pain episodes or history of acute chest syndrome.

126 easures, nor clinical outcomes (specifically acute pain episodes or megaloblastic changes) when indiv

127 A (HbSS or HbSbeta0-thalassemia), history of acute pain episodes, and elevated high-sensitivity C-rea

128 ably predict clinically important effects on acute pain episodes.

129 highlighting the complex pathophysiology of acute pain episodes.

130 he epidemiology and management strategies of acute pain events and we will identify limitations in th

131 Most acute pain events in adults with SCD are managed at home

132 nly improves convenience but also may reduce acute pain, fatigue, and the extent to which patients ar

133 andomized placebo-controlled trials studying acute pain following the surgical extraction of impacted

134 t that ATP was most likely to play a role in acute pain, following its release from damaged or stress

135 harmacologic and pharmacologic management of acute pain from non-low back, musculoskeletal injuries i

136 harmacologic and pharmacologic management of acute pain from non-low back, musculoskeletal injuries i

137 suggest that clinicians treat patients with acute pain from non-low back, musculoskeletal injuries w

138 ecommend that clinicians treat patients with acute pain from non-low back, musculoskeletal injuries w

139 suggest that clinicians treat patients with acute pain from non-low back, musculoskeletal injuries w

140 st against clinicians treating patients with acute pain from non-low back, musculoskeletal injuries w

141 the target patient population is adults with acute pain from non-low back, musculoskeletal injuries.

142 ractive benefit-harm ratio for patients with acute pain from non-low back, musculoskeletal injuries.

143 se from several treatment options to address acute pain from non-low back, musculoskeletal injuries.

144 Management of acute pain from non-low back, musculoskeletal injuries:

145 In contrast, the predominantly acute pain grouping was associated with a mixture of act

146 cognition of an increased susceptibility for acute pain has become particularly relevant.

147 ion of opioid receptors provides relief from acute pain; however, the mechanisms of long-term opioid

148 g that regional anaesthesia might impact the acute pain/hyperalgesia and chronic postsurgical pain, t

149 aviors, characterized by a first phase (i.e. acute pain) immediately following formalin injection, th

150 Additional clinical trials in management of acute pain in children and adults with SCD are critical

151 suzetrigine) has shown efficacy for treating acute pain in clinical trials.

152 man brain as compared with the processing of acute pain in healthy controls.

153 We observed a similar recovery from acute pain in male mice following CCI when p38alphaMAPK

154 Although challenging, acute pain in patients receiving this type of therapy ca

155 -related analgesia has been demonstrated for acute pain in rats.

156 es synaptic protein-protein interactions and acute pain in response to injury.

157 phosphodiesterase (PDE) dramatically reduced acute pain in rodents.

158 Treatment of severe chronic and acute pain in sickle cell disease (SCD) remains challeng

159 The choice of analgesic to treat acute pain in the emergency department (ED) lacks a clea

160 nted to the emergency department with severe acute pain in the right hip and right leg which was aggr

161 This review will summarize the physiology of acute pain in transplant recipients, assess the impact o

162 rts, and facial expression analysis to study acute pain in twelve epilepsy patients under continuous

163 Acute pain indices did not differ in the RIbeta PKA muta

164 Chronic pain, however, altered acute pain intensity representation in the ACC to increa

165 Acute pain is adaptive, but chronic pain is a global cha

166 Acute pain is an unpleasant experience caused by noxious

167 lective inhibitor of Na(V)1.8, on control of acute pain is being studied.

168 The underlying neurophysiology of acute pain is fairly well characterized, whereas the cen

169 While acute pain is initiated by afferent signaling from the p

170 udies have shown that experimentally induced acute pain is processed within at least 2 parallel netwo

171 Acute pain is protective and a cardinal feature of infla

172 Undertreatment of acute pain is suboptimal medical treatment, and patients

173 a 3 days earlier accompanied by an attack of acute pain lasting for 3-4 hours.

174 ilable GH signaling to neurons and prevented acute pain-like behaviors, primary afferent sensitizatio

175 nhibition of neonatal nociceptors to promote acute pain-like behaviors.

176 interplay among addictive disease, OAT, and acute pain management and describes 4 common misconcepti

177 Opioids are a mainstay of acute pain management but can have many adverse effects,

178 ut there is paucity of data when it comes to acute pain management in the elderly, let alone pain res

179 a core component of multimodal analgesia for acute pain management in the emergency department (ED).

180 mediators specific to the injury may improve acute pain management in the future.

181 Adapting CBT to target acute pain management in the post-operative period may i

182 regional anesthetic/analgesic techniques and acute pain management modalities in the elderly and cogn

183 Acute pain management modalities offer the potential of

184 preciated element throughout this process is acute pain management related to the surgical procedure.

185 perioperative cyclooxygenase-2 inhibitors in acute pain management strategies.

186 With a more aggressive acute pain management strategy, the military has decreas

187 cal trial, Black patients received different acute pain management than White patients after patient

188 s have traditionally been the cornerstone of acute pain management, they have potential negative effe

189 id receptor (MOR) agonists are a mainstay in acute pain management.

190 pioids are the gold standard for chronic and acute pain management; however, their consequence on gas

191 ts of health; (6) language and literacy; (7) acute pain-management disparities; (8) quality of care e

192 evidence to show that the use of opioids in acute pain may increase the likelihood of developing opi

193 is postulated that mechanisms implicated in acute pain may not be the same as those that subserve pa

194 of momentary pain as a distinct naturalistic acute pain measure, which can be reliably discriminated

195 of rat CART (55-102) in the modulation of an acute pain model after intrathecal administration.

196 6-Azaindole 18 showed activity in an acute pain model but was inactive in a chronic model.

197 AR pathways both leading to benefit in this acute pain model.

198 -globin gene, resulting in hemolytic anemia, acute pain, multiorgan damage, and early mortality.

199 we have investigated the effect of deqi and acute pain needling sensations upon brain fMRI blood oxy

200 macodynamic effect, such as the treatment of acute pain, obesity, viral infection, and inflammation,

201 nce lifelong struggles with both chronic and acute pain, often requiring medical interventMaion.

202 A 52-year-old male presented with acute pain on the maxillary right second premolar.

203 d CP (15.9-21.1% difference) than those with acute pain only, suggesting specific associations betwee

204 rolled-release opioids for the management of acute pain, opioid-free anesthesia and analgesia, and pr

205 (aged younger than 18 years) and those with acute pain or pain associated with known trauma, surgery

206 However, with persistent acute pain or when pain becomes chronic, these memories

207 ighest dose, but not at lower doses, reduced acute pain over a period of 48 hours after abdominoplast

208 In addition to episodic acute pain, patients with SCD also report chronic pain.

209 to acute pain associated with differences in acute pain perception and fibromyalgia symptoms.

210 opsin enabled light-inducible inhibition of acute pain perception, and reversed mechanical allodynia

211 opsin enabled light-inducible stimulation of acute pain, place aversion and optogenetically mediated

212 operating procedure to monitor and diagnose acute pain post-castration in large-scale systems.

213 in reducing nociception in animal models of acute pain, postoperative pain, and visceral pain.

214 ooxygenase-2 inhibitors in the management of acute pain processes.

215 Acute pain processing, by contrast, is intact in the PKC

216 r inflammatory pain hypersensitivity but not acute pain processing.

217 seeing the body can reduce the experience of acute pain, producing a multisensory analgesia.

218 state laws that restrict or cap opioids for acute pain reduce post-TJR opioid use.

219 cute back pain group, activity diminished in acute pain regions, increased in emotion-related circuit

220 We show here that acute pain-related behavior evoked by elevated ionic str

221 ndogenous kappa-opioid systems, in mediating acute pain-related behavioral depression in rats.

222 conditioned place avoidance without reducing acute pain-related behaviors.

223 Interestingly, STING agonists produce acute pain relief through direct neuronal modulation.

224 as negative in polarity, suggesting that the acute pain relieves the ongoing back pain.

225 relevant timescales, or how this relates to acute pain, remains unclear.

226 , express correct neuropeptides, and mediate acute pain responses normally.

227 Human brain imaging has revealed that acute pain results from activation of a network of brain

228 rded) using the Unesp-Botucatu Pig Composite Acute Pain Scale (UPAPS) in piglets before and after cas

229 The Unesp-Botucatu Pig Composite Acute Pain Scale (UPAPS) was validated to diagnose pain

230 essed using the Unesp-Botucatu pig composite acute pain scale (UPAPS).

231 was determined using the UNESP-Botucatu Goat Acute Pain Scale.

232 TATEMENT Despite their critical role in both acute pain sensation and chronic pain, little is known o

233 redominately deqi sensation grouping and the acute pain sensation grouping (deqi>pain contrast), only

234 i sensations versus those with predominantly acute pain sensations.

235 hen found that PAP knockout mice have normal acute pain sensitivity but enhanced sensitivity in chron

236 In a capsaicin model of acute pain sensitization, the responses of excitatory ne

237 dicated that greater age, rash severity, and acute pain severity are risk factors for prolonged PHN.

238 Advancing age, prodromal symptoms, and acute pain severity at presentation predicted those indi

239 ponent of a multimodal analgesic regimen for acute pain, short-term NSAID administration reduces opio

240 The network structure of patients reporting acute pain showed important differences when compared to

241 re implicated in modes of persistent but not acute pain signaling.

242 In the acute pain state, activation was seen in the ipsilateral

243 be the transmission accounting for different acute pain states and itch transmitted via the transient

244 USP5 is a critical regulator of chronic and acute pain states in humans by acting as a dominant-nega

245 ls of the polyamine spermine in baseline and acute pain states of plasma from patients with SCD, whic

246 be equally important in both sensitized and acute pain states.

247 ls may play a role in mediating responses to acute pain stimuli and/or participate in the central con

248 b in rats increased the aversive response to acute pain stimuli in the opposite limb, as assessed by

249 mma (PKCgamma) displayed normal responses to acute pain stimuli, but they almost completely failed to

250 tional connectivity (FC) response pattern to acute pain stimulus in the motor (MC) and prefrontal (PF

251 antihyperalgesic properties in this study of acute pain suggesting that BCP might be an alternative t

252 f the nervous system, not merely a prolonged acute pain symptom of some other disease conditions.

253 istics and natural history of the paclitaxel-acute pain syndrome (P-APS) and paclitaxel's more chroni

254 nts for peripheral neuropathy and paclitaxel acute pain syndrome remain elusive.

255 ent functional neuroimaging during a thermal acute pain task before and after random assignment to MB

256 In acute pain tests, responses were equivalent in CCR2 knoc

257 in the absence of antinociceptive effects in acute pain tests.

258 highly effective antinociception in several acute pain tests.

259 Unlike investigations of acute pain that are based on the introduction of real-ti

260 fect nociception measured in three assays of acute pain: the acute phase of the formalin test, and th

261 sary for it to become a routine component of acute pain therapy.

262 rent treatments can be effective for mild or acute pain, they are largely inadequate for managing mod

263 normal number of sensory neurons and normal acute pain thresholds.

264 microglia contribute to the transition from acute pain to chronic pain, as inhibition of microglial

265 on the understanding of the transition from acute pain to persistent pain.

266 The adaptive significance of acute pain (to withdraw from tissue-damaging or potentia

267 type mice were indistinguishable in tests of acute pain, transgenic mice exhibited enhanced responsiv

268 Mechanisms of acute pain transition to chronic pain are not fully unde

269 The recent approval of suzetrigine for acute pain treatment highlights both the success of targ

270 Acute pain triggers a robust LC stress response, produci

271 ain exhibit a reciprocal relationship, where acute pain triggers ANS responses, whereas resting ANS a

272 In a second model of acute pain using capsaicin, SP16 significantly reduced p

273 This review describes the pathophysiology of acute pain utilizing three preclinical models: surgery,

274 zation-driven pain hypersensitivity, but not acute pain, was impaired in Tlr3(-/-) mice.

275 Eight of 9 products for acute pain were supported by at least 1 pivotal trial; t

276 hR) agonists is antinociceptive in models of acute pain whereas their intrathecal (i.t.) administrati

277 DKO) mice were indistinguishable in tests of acute pain, whereas behavioral responses to peripheral i

278 pain group is limited to regions involved in acute pain, whereas in the chronic back pain group, acti

279 Unlike acute pain, which carries survival value, chronic pain m

280 inhibiting nociception in an animal model of acute pain while lacking any positive reinforcement.

281 ns for providing analgesia for patients with acute pain who are receiving OAT are presented.

282 We induced acute pain with an infrared laser while human participan

283 r CNS penetration) blocked capsaicin-induced acute pain with the same potency.