The Effect of Hydromorphone Therapy on Psychophysical Measurements of the Descending Inhibitory Pain Systems in Patients with Chronic Radicular Pain

Suzan, Erica; Treister, Roi; Pud, Dorit; Haddad, May; Eisenberg, Elon

doi:10.1111/pme.12565

Cited by 24 publications

(37 citation statements)

References 31 publications

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“…This is further supported by studies showing that the administration of ketamine (a N‐methyl‐ d ‐aspartate (NMDA) antagonist) influences CPM, but not offset analgesia (Niesters, Dahan, et al, ) suggesting that CPM is NMDA‐dependent, and offset analgesia is NMDA‐independent. Administration of hydromorphone (an opioid) does not have an effect on CPM or offset analgesia in pain patients (Suzan, Treister, Pud, Haddad, & Eisenberg, ). Administration of remifentanil (an opioid agonist) and naloxone (an opioid antagonist) to healthy subjects does not alter offset analgesia (Martucci, Eisenach, Tong, & Coghill, ), suggesting that offset analgesia is opioid‐independent whereas administration of morphine impairs the CPM in healthy subjects (Martini et al, ), which suggests that CPM is opioid‐dependent.…”

Section: Discussionmentioning

confidence: 99%

Pain inhibitory mechanisms and response to weak analgesics in patients with knee osteoarthritis

Petersen

Simonsen

Olesen

et al. 2019

European Journal of Pain

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Background Conditioned pain modulation (CPM) and offset analgesia are different features of descending pain inhibition. This study investigated CPM, offset analgesia and clinical pain measures in patients with knee osteoarthritis (KOA) before and after treatment with the combination of a non‐steroidal anti‐inflammatory drug (NSAIDs) plus acetaminophen. Methods Forty‐two patients with KOA received Ibuprofen 1.2 g/daily and acetaminophen 3.0 g/daily for three weeks. Before administration, CPM magnitude was assessed as the difference between cuff pain detection (cPDT) with and without a conditioning stimulus (evoked by tourniquet pain). Offset analgesia was assessed as the pain intensities evoked by a constant 46°C for 30‐s stimulus compared to an offset analgesia paradigm of 46°C for 5‐s, 47°C for 5‐s and 46°C for 20‐s. The worst pain within the last 24‐hr and pain during activity were assessed before and after treatment. Results Clinical pain significantly decreased after treatment (p < 0.001) and less efficient CPM before treatment was associated with weaker analgesic effect (R = 0.354, p = 0.043). No significant modulation of CPM or offset analgesia was found for the treatment. Conclusion This study found that less efficient CPM is associated with reduced analgesic effect of NSAIDs plus acetaminophen in patients with KOA whereas the treatment did not modulate CPM nor offset analgesia magnitude. Significance This study demonstrated that conditioned pain modulation is correlated with the response to a standard pharmaceutical interventions treating osteoarthritis pain. Furthermore, we demonstrated that a decrease in clinical pain intensity is not associated with a normalization of conditioned pain modulation or offset analgesia, which questions if restoring these descending pain inhibitory mechanisms are pain intensity driven.

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Section: Discussionmentioning

confidence: 99%

Pain inhibitory mechanisms and response to weak analgesics in patients with knee osteoarthritis

Petersen

Simonsen

Olesen

et al. 2019

European Journal of Pain

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“…The complementary mechanisms behind OA and its pain attenuation still remain unclear, but impaired OA‐effects have been observed in different groups of chronic pain patients. The chronic neuropathic pain patients showed reduced OA‐effect (Niesters et al., ; Suzan et al., ), which could imply that the peripheral pathologies reduce OA and that peripheral mechanisms are involved in OA. In addition, the reduced OA‐effect has also been observed in patients with central sensitization, such as fibromyalgia (Julien et al., ; Oudejans et al., ).…”

Section: Discussionmentioning

confidence: 99%

Offset analgesia: The role of peripheral and central mechanisms

Ligato

Petersen

Mørch

et al. 2017

European Journal of Pain

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Background: Offset Analgesia (OA) can be evoked by a threeheat-stimulus train (T1-T2-T3), with T1 (5 s) and T3 (20 s) having the same temperature (e.g. 48°C) and T2 (5 s) being slightly higher (1-3°C). OA is defined as a disproportional pain reduction caused by the slight temperature decrease from T2 to T3. As the pain modulatory mechanisms behind OA are still poorly understood, the current study aimed to investigate the role of peripheral and central mechanisms by applying heat stimuli to the same location and to different unilateral and bilateral locations. Method: Young healthy volunteers participated in the study. A 'standard-OA' paradigm (48-49-48°C) was applied to the nondominant volar forearm (T1-T2-T3 applied on the same location). 'Unilateral-OA' trials were applied on three different locations of the non-dominant volar forearm (the same dermatome). 'Bilateral-OA' trials were applied by shifting T1-T2-T3 between dominant and nondominant volar forearms. A constant stimulus of 48°C was applied as control for the evoked pain. The pain intensities were continuously recorded using an electronic visual analogue scale. Results: The largest pain intensity reduction was reported for the 'standard-OA' paradigm (p < 0.001) compared with the control stimulus. Both 'Unilateral-OA' and 'Bilateral-OA' trials caused a significant pain reduction (p < 0.05) compared with the control; however, the pain reduction was less than that evoked by 'standard-OA' (p < 0.05). Conclusion: This study showed that OA could be elicited when the stimuli were applied both to the same and to different locations (ipsiand contralateral) indicating that peripheral as well as central mechanisms are involved in mediating OA. Significance: This study investigated offset analgesia by applying thermal painful stimuli to the ipsi-and bilateral forearms in healthy subjects and found that both peripheral and central mechanisms seem to mediate offset analgesia.

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“…Ketamine [76], tapentadol [77], opioid agonists [78], [79], and an opioid antagonist [78] have not shown any modulatory effect.…”

Section: Offset Analgesiamentioning

confidence: 96%

Altered Central Sensitization and Pain Modulation in the CNS in Chronic Joint Pain

Arendt‐Nielsen

Skou

Nielsen

et al. 2015

Curr Osteoporos Rep

142

136

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Musculoskeletal pain disorders are the second largest contributor to global disability underlining the significance of effective treatments. However, treating chronic musculoskeletal pain, and chronic joint pain (osteoarthritis (OA)) in particular, is challenging as the underlying peripheral and central pain mechanisms are not fully understood, and safe and efficient analgesic drugs are not available. The pain associated with joint pain is highly individual, and features from radiological imaging have not demonstrated robust associations with the pain manifestations. In recent years, a variety of human quantitative pain assessment tools (quantitative sensory testing (QST)) have been developed providing new opportunities for profiling patients and reaching a greater understanding of the mechanisms involved in chronic joint pain. As joint pain is a complex interaction between many different pain mechanisms, available tools are important for patent profiling and providing the basic knowledge for development of new drugs and for developing pain management regimes.

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The Effect of Hydromorphone Therapy on Psychophysical Measurements of the Descending Inhibitory Pain Systems in Patients with Chronic Radicular Pain

Abstract: These results suggest that the descending inhibitory pain modulation, as manifested in humans by CPM and OA, is unlikely to be mediated by hydromorphone therapy.

Cited by 24 publications

References 31 publications

Pain inhibitory mechanisms and response to weak analgesics in patients with knee osteoarthritis

Pain inhibitory mechanisms and response to weak analgesics in patients with knee osteoarthritis

Offset analgesia: The role of peripheral and central mechanisms

Altered Central Sensitization and Pain Modulation in the CNS in Chronic Joint Pain

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