European journal of pain : EJP
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Chronic pain is pathological, persisting beyond normal tissue healing time. Previous work has suggested ∼50% variation in chronic pain development is heritable. No data are currently available on the heritability of pain categorized using the Chronic Pain Grade (CPG). ⋯ After adjustment, 'any chronic pain' h(2) = 16% (SE 7%; p = 0.02) and 'severe' chronic pain h(2) = 30% (SE 13%; p = 0.007). Co-heritability of both traits was 11% (SE 76%). This study supports the use of chronic pain as a phenotype in genetic studies, with adequate correction for confounders to specifically identify genetic risk factors for chronic pain.
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Lysophosphatidic acid (LPA), an initiator of neuropathic pain, causes allodynia. However, few studies have evaluated the pharmacological profile of LPA-induced pain. In this study, a LPA-induced pain model was developed and pharmacologically characterized with clinically relevant drugs used for neuropathic pain, including antiepileptics, non-steroidal anti-inflammatory agents, analgesics, local anaesthetics/antiarrhythmics and antidepressants. ⋯ In LPA-injected mice, expression of the α2δ1 subunit of the voltage-gated calcium channel (VGCC) was increased in the dorsal root ganglion (DRG) and spinal dorsal horn. Furthermore, the VGCC current was potentiated in both the DRG from LPA-injected mice and LPA (1 μM)-treated DRG from saline-injected mice, and the potentiated VGCC current was amended by treatment with gabapentin (100 μM). The LPA-induced pain model described here mimics aspects of the neuropathic pain state, including the sensitization of VGCC, and may be useful for the early assessment of drug candidates to treat neuropathic pain.
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Randomized Controlled Trial
Spouse-assisted training in pain coping skills and the outcome of multidisciplinary pain management for chronic low back pain treatment: a 1-year randomized controlled trial.
This study examined the comparative efficacy of three interventions: a spouse-assisted coping skills training protocol for patients undergoing a multidisciplinary pain management programme (SA-MPMP), conventional patient-oriented multidisciplinary pain management programme (P-MPMP) and standard medical care (SMC). Thirty-six chronic low back pain (CLBP) patients and their spouses were randomly assigned to one of the three conditions. The SA-MPMP condition consisted of seven, weekly, 2-h, group sessions of training in dyadic pain coping and couple skills, delivered by a clinical psychologist with support of a multidisciplinary team of specialists, to patients together with their spouses. ⋯ The SMC condition entailed continuation of routine treatment, entailing medical care only. Data analysis revealed that, at the 12-month follow-up time point, patients receiving SA-MPMP had significant improvements in kinesiophobia and rumination about pain compared to those receiving P-MPMP and SMC. In patients suffering from CLBP, an intervention that combines spouse-assisted coping skills training with a multidisciplinary pain management programme can improve fear of movement and rumination about low back pain.
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The COMT enzyme metabolizes catecholamines and thus modulates adrenergic, noradrenergic and dopaminergic signaling. A functional polymorphism in the gene encoding this enzyme, i.e. the COMT Val158Met SNP that reduces enzyme activity, has previously been linked to pain sensitivity. ⋯ We conclude that the functional COMT Val158Met SNP contributes to long lasting low back pain, sciatica and disability after lumbar disc herniation.
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Randomized Controlled Trial
Sex differences in analgesic response to ibuprofen are influenced by expectancy: a randomized, crossover, balanced placebo-designed study.
To determine whether there is a sex difference in placebo and ibuprofen analgesia expectancy. ⋯ We found no sex difference in baseline pain threshold or tolerance levels. When partitioned by sex and expectancy state, analgesia only occurred in males during positive expectancy states at 2, 3 and 4 h post-placebo, and at 1 and 2 h post-ibuprofen. The time course of analgesic action in males was as expected considering the pharmacokinetic profile of ibuprofen. Our study found that dosages of 800 mg of ibuprofen are ineffective in producing analgesia in women regardless of their expectations. We hypothesize that ibuprofen analgesia is produced by a combination of specific pharmacological effects and a non-specific beta endorphin-mediated placebo effect. Whatever the mechanism responsible for the analgesic response seen in males, this research re-emphasizes the importance of psychological factors in determining drug response. It also shows that these factors can differ between men and women, and thus the contribution of psychological factors on analgesia needs to be seriously re-evaluated.