A Longitudinal Study to Evaluate Pregnancy-Induced Endogenous Analgesia and Pain Modulation

Carvalho, Brendan; Granot, Michal; Sultan, Pervez; Wilson, Hilary; Landau, Ruth

doi:10.1097/aap.0000000000000359

Cited by 8 publications

(12 citation statements)

References 24 publications

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“…Temporal summation, another measure of central sensitisation, did not differ in women during the third trimester of pregnancy compared with repeat testing in the postpartum period, although no non-obstetric control was included. 8 Contrary to our hypothesis, capsaicin-evoked sensitisation was not decreased in postpartum women compared with controls. Several interpretations of this lack of difference are possible.…”

Section: Discussioncontrasting

confidence: 84%

“…31e33 We showed no difference between groups in pain ratings across a range of suprathreshold noxious heat stimuli, similar to a lack of difference in threshold to heat pain between women during their third trimester compared with postpartum. 8 The lack of reduction in acute nociception in the postpartum period is consistent with similar intensity of pain in the initial days after Caesarean delivery compared with other surgery. 2 The strength of CPM did not differ between the study groups in the current study, just as it did not differ in women tested at third trimester and postpartum.…”

Section: Discussionsupporting

confidence: 63%

“…A previous study found no difference in the measure of sensitisation (temporal summation) in women during the third trimester and in the postpartum period, but that study did not include a non-obstetric control group. 8 Endogenous pain inhibition can be induced by exposure to noxious conditioning stimuli in what is termed conditioned pain modulation (CPM), and this effect is increased by peripherally administered oxytocin. 9 The strength of preoperative CPM is inversely related to the risk of persistent pain after injury, 10 so oxytocin might speed recovery after surgery by increasing endogenous inhibition.…”

mentioning

confidence: 99%

“…A previous study showed no difference in CPM in women between the postpartum period and during pregnancy, but the method used failed to induce CPM at either time. 8 Oxytocin could also speed recovery from pain by reducing the nociceptor input from the periphery. Peripherally administered oxytocin reduces pain to acute noxious heat stimuli in some studies, 11 but not in others.…”

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confidence: 99%

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Capsaicin-induced pain and sensitisation in the postpartum period

Street

Harris

Curry

et al. 2019

British Journal of Anaesthesia

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Background: Recovery from Caesarean delivery in women and surgical nerve injury in animals after delivery is more rapid than expected, an effect reversed in animals by spinal injection of an oxytocin receptor antagonist. We hypothesised that endogenous modulation of acute pain is altered postpartum. Methods: Endogenous inhibition of acute pain in a conditioned pain modulation paradigm or endogenous sensitisation by topical capsaicin was tested in women who were breastfeeding 10e14 days after Caesarean delivery and age-matched controls (n¼80 total: 20 per group and 20 per test). The study was powered to detect a difference in area of hyperalgesia after capsaicin of 33%. Capsaicin-evoked pain was recorded in women, and capsaicin-evoked mechanical hypersensitivity was measured in rats 48 h after delivery and in age-matched female and male animals. Results: There was no effect of the postpartum period in the endogenous sensitisation assay in women, and the conditioned pain modulation assay failed to produce analgesia in either group. Postpartum women, however, reported less intense pain than controls at the end of topical capsaicin exposure (1.3 [1.4] vs 2.0 [2.0] on 0e10 verbal scale), and acute hypersensitivity after capsaicin was less in postpartum than control rats (withdrawal threshold 25 [15] vs 3.6 [1] g). Conclusions: These results agree with a recent report that oxytocin may desensitise the transient receptor potential for vanilloid-1 channel, although other explanations, including hormone effects, are possible. These results do not, however, support the inhibition of capsaicin-evoked spinal sensitisation in the postpartum period. Clinical trial registration: NCT01843517. Editor's key pointsRecovery from Caesarean delivery in women is more rapid than expected, so the authors hypothesised that endogenous modulation of acute pain is altered postpartum.There was no effect of the postpartum period on endogenous sensitisation, but women reported less intense capsaicin-evoked pain and rats had less acute hypersensitivity after capsaicin. There was no postpartum difference in pain experience to acute phasic heat stimuli and experimentally induced hypersensitivity in new mothers who are breastfeeding, but capsaicin-evoked pain was reduced. The mechanisms of this postpartum analgesic effect are not clear, but may involve oxytocin-induced desensitisation of pain-related ion channels.

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Section: Discussioncontrasting

confidence: 84%

Section: Discussionsupporting

confidence: 63%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Capsaicin-induced pain and sensitisation in the postpartum period

Street

Harris

Curry

et al. 2019

British Journal of Anaesthesia

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“…In addition, many animal studies suggest that pregnancy modulates the endogenous pain control system and decreases pain thresholds 9–11. Some studies report that women experience a progressive increasing heat pain threshold during pregnancy,12 whereas others have not observed this phenomenon 13,14. Pregnancy-induced protection mechanisms against neuropathic pain have not been explored.…”

Section: Introductionmentioning

confidence: 99%

Pregnancy suppresses neuropathic pain induced by chronic constriction injury in rats through the inhibition of TNF-α

Onodera¹,

Kanao-Kanda²,

Kanda³

et al. 2017

JPR

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PurposePregnancy-induced analgesia develops during late pregnancy, but it is unclear whether this analgesia is effective against neuropathic pain. The detailed molecular mechanisms underlying pregnancy-induced analgesia have not been investigated. We examined the antinociceptive effect of pregnancy-induced analgesia in a neuropathic pain model and the expression of tumor necrosis factor (TNF)-α, glial fibrillary acidic protein (GFAP), Iba-1, and c-Fos in the spinal dorsal horn just before parturition.Materials and methodsFemale Sprague Dawley rats (200–250 g) were randomly assigned to one of four groups (pregnant + chronic constriction injury [CCI]; pregnant + sham injury; not pregnant + CCI; and not pregnant + sham injury). Separate groups were used for the behavioral and tissue analyses. CCI of the left sciatic nerve was surgically induced 3 days after confirming pregnancy in the pregnancy group or on day 3 in the not pregnant group. The spinal cord was extracted 18 days after CCI. TNF-α, GFAP, Iba-1, and c-Fos expression levels in the spinal dorsal horn were measured by Western blot analysis. Mechanical threshold was tested using von Frey filaments.ResultsThe lowered mechanical threshold induced by CCI was significantly attenuated within 1 day before parturition and decreased after delivery. TNF-α expression in CCI rats was decreased within 1 day before parturition. Further, GFAP, Iba-1, and c-Fos expression in the spinal dorsal horn was reduced in the pregnant rats. Serum TNF-α in all groups was below measurable limits.ConclusionOur findings indicate that pregnancy-induced analgesia suppresses neuropathic pain through reducing spinal levels of TNF-α, GFAP, Iba-1, and c-Fos in a rat model of CCI.

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Assessment and manifestation of central sensitisation across different chronic pain conditions

Arendt-Nielsen

Morlion

Perrot

et al. 2017

European Journal of Pain

517

494

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Different neuroplastic processes can occur along the nociceptive pathways and may be important in the transition from acute to chronic pain and for diagnosis and development of optimal management strategies. The neuroplastic processes may result in gain (sensitisation) or loss (desensitisation) of function in relation to the incoming nociceptive signals. Such processes play important roles in chronic pain, and although the clinical manifestations differ across condition processes, they share some common mechanistic features. The fundamental understanding and quantitative assessment of particularly some of the central sensitisation mechanisms can be translated from preclinical studies into the clinic. The clinical perspectives are implementation of such novel information into diagnostics, mechanistic phenotyping, prevention, personalised treatment, and drug development. The aims of this paper are to introduce and discuss (1) some common fundamental central pain mechanisms, (2) how they may translate into the clinical signs and symptoms across different chronic pain conditions, (3) how to evaluate gain and loss of function using quantitative pain assessment tools, and (4) the implications for optimising prevention and management of pain. The chronic pain conditions selected for the paper are neuropathic pain in general, musculoskeletal pain (chronic low back pain and osteoarthritic pain in particular), and visceral pain (irritable bowel syndrome in particular). The translational mechanisms addressed are local and widespread sensitisation, central summation, and descending pain modulation. Significance Central sensitisation is an important manifestation involved in many different chronic pain conditions. Central sensitisation can be different to assess and evaluate as the manifestations vary from pain condition to pain condition. Understanding central sensitisation may promote better profiling and diagnosis of pain patients and development of new regimes for mechanism based therapy. Some of the mechanisms underlying central sensitisation can be translated from animals to humans providing new options in development of therapies and profiling drugs under development.

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A Longitudinal Study to Evaluate Pregnancy-Induced Endogenous Analgesia and Pain Modulation

Cited by 8 publications

References 24 publications

Capsaicin-induced pain and sensitisation in the postpartum period

Capsaicin-induced pain and sensitisation in the postpartum period

Pregnancy suppresses neuropathic pain induced by chronic constriction injury in rats through the inhibition of TNF-α

Assessment and manifestation of central sensitisation across different chronic pain conditions

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A Longitudinal Study to Evaluate Pregnancy-Induced Endogenous Analgesia and Pain Modulation

Cited by 8 publications

References 24 publications

Capsaicin-induced pain and sensitisation in the postpartum period

Capsaicin-induced pain and sensitisation in the postpartum period

Pregnancy suppresses neuropathic pain induced by chronic constriction injury in rats through the inhibition of TNF-&alpha;

Assessment and manifestation of central sensitisation across different chronic pain conditions

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Pregnancy suppresses neuropathic pain induced by chronic constriction injury in rats through the inhibition of TNF-α