425 research outputs found

    Temporal Aspects of Endogenous Pain Modulation During a Noxious Stimulus Prolonged for 1 Day

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    Background This study investigated (a) if a prolonged noxious stimulus (24‐hr topical capsaicin) in healthy adults would impair central pain inhibitory and facilitatory systems measured as a reduction in conditioned pain modulation (CPM) and enhancement of temporal summation of pain (TSP) and (b) if acute pain relief or exacerbation (cooling and heating the capsaicin patch) during the prolonged noxious stimulus would affect central pain modulation. Methods Twenty‐eight participants (26.2 ± 1.0 years; 12 women) wore a transdermal 8% capsaicin patch on the forearm for 24 hr. Data were collected at baseline (Day 0), 1 hr, 3 hr, Day 1 (post‐capsaicin application) and Day 3/4 (post‐capsaicin removal) that included capsaicin‐evoked pain intensity, heat pain thresholds (HPTs), TSP (10 painful cuff pressure stimuli on leg) and CPM (cuff pressure pain threshold on the leg prior vs. during painful cuff pressure conditioning on contralateral leg). After 3 hr, cold (12°C) and heat (42°C) stimuli were applied to the capsaicin patch to transiently increase and decrease pain intensity. Results Participants reported moderate pain scores at 1 hr (2.5 ± 2.0), 3 hr (3.7 ± 2.4), and Day 1 (2.4 ± 1.8). CPM decreased 3‐hr post‐capsaicin (p = .001) compared to Day 0 and remained diminished while the capsaicin pain score was reduced (0.4 ± 0.7, p \u3c .001) and increased (6.6 ± 2.2, p \u3c .001) by patch cooling and heating. No significant differences occurred for CPM during patch cooling or heating compared to initial 3HR; however, CPM during patch heating was reduced compared with patch cooling (p = .01). TSP and HPT did not change. Conclusions This prolonged experimental pain model is useful to provide insight into subacute pain conditions and may provide insight into the transition from acute to chronic pain. Significance During the early hours of a prolonged noxious stimulus in healthy adults, CPM efficacy was reduced and did not recover by temporarily removing the ongoing pain indicating a less dynamic neuroplastic process

    Preoperative neuropathic pain like symptoms and central pain mechanisms in knee osteoarthritis predicts poor outcome 6 months after total knee replacement surgery

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    Preoperative pain characteristics in osteoarthritis (OA) patients may explain persistent pain after total knee replacement (TKR). Fifty patients awaiting TKR and 22 asymptomatic controls were recruited to evaluate the degree of neuropathic pain symptoms and pain sensitisation. OA patients were pain phenotyped into two groups based on the PainDETECT questionnaire: High PainDETECT group (scores ≥19) indicating neuropathic pain-like symptoms, Low PainDETECT group (scores 19) indicating nociceptive or mixed pain.Cuff algometry assessing pain detection thresholds (PDT) and pain tolerance (PTT) was conducted on the lower legs. Temporal summation of pain (TSP) was assessed using ten sequential cuff stimulations and a von Frey stimulator. Conditioning pain modulation was assessed by cuff pain conditioning on one leg and parallel assessment of PDT on the contralateral leg. Pressure pain thresholds (PPTs) were recorded by pressure handheld algometry local and distant to the knee. Knee pain intensity (VAS) and pain assessment were collected before and 6 months post-TKR. 30% of patients demonstrated neuropathic pain-like symptoms (High PainDETECT group). Facilitated TSP and reduced PPTs distant to the knee were found in High PainDETECT group compared to Low PainDETECT group and healthy controls groups (

    Brain perfusion patterns are altered in chronic knee pain:a spatial covariance analysis of arterial spin labelling MRI

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    Chronic musculoskeletal pain is a common problem globally. Current evidence suggests that maladapted central pain pathways are associated with pain chronicity, for example, in postoperative pain after knee replacement. Other factors such as low mood, anxiety, and tendency to catastrophize are also important contributors. We aimed to investigate brain imaging features that underpin pain chronicity based on multivariate pattern analysis of cerebral blood flow (CBF), as a marker of maladaptive brain changes. This was achieved by identifying CBF patterns that discriminate chronic pain from pain-free conditions and by exploring their explanatory power for factors thought to drive pain chronification. In 44 chronic knee pain and 29 pain-free participants, we acquired both CBF and T1-weighted data. Participants completed questionnaires related to affective processes and pressure and cuff algometry to assess pain sensitization. Two factor scores were extracted from these scores representing negative affect and pain sensitization. A spatial covariance principal component analysis of CBF identified 5 components that significantly discriminated chronic pain participants from controls, with the unified network achieving 0.83 discriminatory accuracy (area under the curve). In chronic knee pain, significant patterns of relative hypoperfusion were evident in anterior default-mode and salience network hubs, while hyperperfusion was seen in posterior default mode, thalamus, and sensory regions. One component correlated positively with the pain sensitization score (r = 0.43, P = 0.006), suggesting that this CBF pattern reflects neural activity changes encoding pain sensitization. Here, we report a distinct chronic knee pain-related representation of CBF, pointing toward a brain signature underpinning central aspects of pain sensitization
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