ライフサイエンスコーパス: acute pain

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

2 ectional control of the aversive response to acute pain.

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

4 rs sufficient to process reflex responses to acute pain.

5 both chronic pain and recurrent episodes of acute pain.

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

7 eptions resulting in suboptimal treatment of acute pain.

8 opment and improvements in the management of acute pain.

9 display intact nociceptive responsiveness to acute pain.

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

11 se is characterized by recurrent episodes of acute pain.

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

13 s effective at alleviating thermally induced acute pain.

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

15 oduce an antinociceptive effect in models of acute pain.

16 cit an antinociceptive response in models of acute pain.

17 gic and nonpharmacologic methods of managing acute pain.

18 approach to the assessment and treatment of acute pain.

19 ay provide valuable avenues for treatment of acute pain.

20 rest directed toward peripheral mediators of acute pain.

21 enarios that are associated with significant acute pain.

22 symptomatic treatment of osteoarthritis and acute pain.

23 phine are extremely effective treatments for acute pain.

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

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

26 iate opioid-induced descending inhibition in acute pain.

27 on approaches to the clinical management of acute pain.

28 ened therapeutic options in the treatment of acute pain.

29 nd well tolerated analgesia to patients with acute pain.

30 S2 are the regions consistently activated in acute pain.

31 4.85-10.65; ARDA = 0.25%); among those with acute pain, adjusted HR = 6.64 (95% CI, 3.31-13.31; ARDA

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

69 Acute pain control has advanced dramatically and is now

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

96 Acute pain is protective and a cardinal feature of infla

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

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

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

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

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

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

103 Acute pain management modalities offer the potential of

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

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

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

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

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

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

110 6-Azaindole 18 showed activity in an acute pain model but was inactive in a chronic model.

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

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

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

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

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

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

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

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

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

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

121 r inflammatory pain hypersensitivity but not acute pain processing.

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

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

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

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

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

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

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

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

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

131 i sensations versus those with predominantly acute pain sensations.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

148 highly effective antinociception in several acute pain tests.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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