Prolonged time of after-sensation after experimental pain stimuli despite efficient conditioned pain modulation in patients with chronic neuropathic pain after traumatic nerve injuries in upper extremity

Miclescu, Adriana; Essemark, Marie; Astermark, Mathias; Gkatziani, Panagiota; Straatmann, Antje; Butler, Stephen; Karlsten, Rolf; Gordh, Torsten

doi:10.1097/pr9.0000000000000908

Cited by 4 publications

(10 citation statements)

References 45 publications

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“…In a previous study, 30 we could not find a statistically significant interaction between the different sexes and chronic pain after traumatic nerve injuries in the upper extremities. In the present study also, contrary to our hypotheses, we did not find consistent differences between subjects with chronic neuropathic pain and neuropathy without pain.…”

Section: Discussioncontrasting

confidence: 67%

“…Patients with peripheral nerve injuries with upper extremity involvement were more likely to be young male subjects in both severe trauma with multiple injuries 22 (78.6%) or localized hand and arm injuries (between 66.5%–74% and 80%). 30 , 41 …”

Section: Discussionmentioning

confidence: 99%

“…According to their answers to the questionnaires, a group of patients with pain and a group of pain-free controls were invited to participate in a follow-up study. 30 The inclusion criteria for the participants were age ≥18 years, a surgical nerve repair after a traumatic nerve lesion in hand and lower arm region, chronic postoperative neuropathic pain with a history of 6 months to 7 years before the screening visit, pain intensity more than 50 mm on a 100-mm visual analogue scale (VAS) for the group of the participants with pain, and intensity of pain <20 mm VAS for the group without pain. The exclusion criteria were evidence or history of any clinically significant neurological disease or other systemic diseases or conditions potentially interfering with study assessments (polyneuropathy, diabetes mellitus, peripheral vascular disease, history of malignant disease, or chronic alcohol consumption).…”

Section: Methodsmentioning

confidence: 99%

“…All the participants were prescreened by the Self-report Leeds Assessment of Neuropathic Signs and Symptoms (S-LANSS questionnaire). 30 The participants with pain and S-LANSS ≥12 (indicating predominantly neuropathic pain) 5 were recruited for the group with neuropathic pain and those with S-LANSS <12 and sensory impairment were recruited for the group with neuropathy without pain.…”

Section: Methodsmentioning

confidence: 99%

“…We have previously demonstrated that CPM cannot be used as a mechanism to differentiate chronic neuropathic pain from neuropathy without pain because the neuropathic pain patients after trauma and surgery had well-functioning CPM, similar to that of patients with the same type of nerve lesions but with no pain. 30 In this follow-up study, we hypothesized that sex differences would be reflected in different endogenous inhibitory systems that would confer risk for or protection against persistent pain. Thus, we intended to find (1) whether men and women with painful vs posttraumatic painless neuropathy are similarly sensitive to experimental stimuli and (2) whether they have similar CPM effects.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Sex-related differences in experimental pain sensitivity in subjects with painful or painless neuropathy after surgical repair of traumatic nerve injuries

Miclescu¹,

Gkatziani²,

Granlund³

et al. 2022

PR9

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Section: Discussioncontrasting

confidence: 67%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Sex-related differences in experimental pain sensitivity in subjects with painful or painless neuropathy after surgical repair of traumatic nerve injuries

Miclescu¹,

Gkatziani²,

Granlund³

et al. 2022

PR9

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Increased risk of persistent neuropathic pain after traumatic nerve injury and surgery for carriers of a human leukocyte antigen haplotype

Miclescu,

Rönngren,

Bengtsson

et al. 2023

Pain

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It is not known why some patients develop persistent pain after nerve trauma while others do not. Among multiple risk factors for the development of persistent posttrauma and postsurgical pain, a neuropathic mechanism due to iatrogenic nerve lesion has been proposed as the major cause of these conditions. Because there is some evidence that the human leukocyte antigen (HLA) system plays a role in persistent postsurgical pain, this study aimed to identify the genetic risk factors, specifically among HLA loci, associated with chronic neuropathic pain after traumatic nerve injuries and surgery in the upper extremities. Blood samples were taken to investigate the contribution of HLA alleles (ie, HLA-A, HLA-B, HLA-DRB1, HLA-DQB1, and HLA-DPB1) in a group of patients with persistent neuropathic pain (n = 70) and a group of patients with neuropathy without pain (n = 61). All subjects had intraoperatively verified nerve damage in the upper extremity. They underwent bedside clinical neurological examination to identify the neuropathic pain component according to the present grading system of neuropathic pain. Statistical analyses on the allele and haplotype were conducted using the BIGDAWG package. We found that the HLA haplotype A*02:01-B*15:01-C*03:04-DRB1*04:01-DQB1*03:02 was associated with an increased risk of developing persistent neuropathic pain in the upper extremity (OR = 9.31 [95% CI 1.28-406.45], P < 0.05). No significant associations were found on an allele level when correcting for multiple testing. Further studies are needed to investigate whether this association is on a haplotypic level or if certain alleles may be causing the association.

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Association between systemic inflammation and experimental pain sensitivity in subjects with pain and painless neuropathy after traumatic nerve injuries

Miclescu

Granlund

Butler

et al. 2022

Scandinavian Journal of Pain

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Objectives Peripheral neuropathies that occur secondary to nerve injuries may be painful or painless, and including a low-grade inflammation and pro-inflammatory cytokines associated with both regeneration and damage of peripheral nerve cells and fibers. Currently, there are no validated methods that can distinguished between neuropathic pain and painless neuropathy. The aim of this study was to search for proinflammatory and anti-inflammatory proteins associated with pain and experimental pain sensitivity in subjects with surgeon-verified nerve injuries in the upper extremities. Methods One hundred and thirty-one subjects [69 with neuropathic pain, NP; 62 with painless neuropathy, nP] underwent a conditioned pain modulation (CPM) test that included a cold pressor task (CPT) conducted with the non-injured hand submerged in cold water (4 °C) until pain was intolerable. CPM was assessed by pain ratings to pressure stimuli before and after applying the CPT. Efficient CPM effect was defined as the ability of the individual’s CS to inhibit at least 29% of pain (eCPM). The subjects were assigned to one of two subgroups: pain sensitive (PS) and pain tolerant (PT) after the time they could tolerate their hand in cold water (PS<40 s and PT=60 s) . Plasma samples were analyzed for 92 proteins incorporated in the inflammation panel using multiplex Protein Extension Array Technology (PEA). Differentially expressed proteins were investigated using both univariate and multivariate analysis (principal component analysis-PCA and orthogonal partial least-squares discriminant analysis-OPLS-DA). Results Significant differences in all protein levels were found between PS and PT subgroups (CV-ANOVA p<0.001), but not between NP and nP groups (p=0.09) or between inefficient CPM (iCPM) and eCPM (p=0.53) subgroups. Several top proteins associated with NP could be detected using multivariate regression analysis such as stromelysin 2 (MMPs), interleukin-2 receptor subunit beta (IL2RB), chemokine (C-X-C motif) ligand 3 (CXCL3), fibroblast growth factor 5 (FGF5), chemokine (C-C motif) ligand 28 (CCL28), CCL25, CCL11, hepatocyte growth factor (HGF), interleukin 4 (IL4), IL13. After adjusting for multiple testing, none of these proteins correlated significantly with pain. Higher levels of CCL20 (p=0.049) and CUB domain-containing protein (CDCP-1; p=0.047) were found to correlate significantly with cold pain sensitivity. CDCP-1 was highly associated with both PS and iCPM (p=0.042). Conclusions No significant alterations in systemic proteins were found comparing subjects with neuropathic pain and painless neuropathy. An expression of predominant proinflammatory proteins was associated with experimental cold pain sensitivity in both subjects with pain and painless neuropathy. One these proteins, CDC-1 acted as “molecular fingerprint” overlapping both CPM and CPT. This observation might have implications for the study of pain in general and should be addressed in more detail in future experiments.

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Prolonged time of after-sensation after experimental pain stimuli despite efficient conditioned pain modulation in patients with chronic neuropathic pain after traumatic nerve injuries in upper extremity

Abstract: Prolonged time of after-sensation after experimental pain stimuli despite efficient conditioned pain modulation was observed in patients with neuropathic pain after traumatic nerve injuries

Cited by 4 publications

References 45 publications

Sex-related differences in experimental pain sensitivity in subjects with painful or painless neuropathy after surgical repair of traumatic nerve injuries

Sex-related differences in experimental pain sensitivity in subjects with painful or painless neuropathy after surgical repair of traumatic nerve injuries

Increased risk of persistent neuropathic pain after traumatic nerve injury and surgery for carriers of a human leukocyte antigen haplotype

Association between systemic inflammation and experimental pain sensitivity in subjects with pain and painless neuropathy after traumatic nerve injuries

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