European journal of pain : EJP
-
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.
-
Catastrophizing is a defining factor in the pain experience and strongly contributes to the prediction of various aspects of health. Catastrophizing is not just present in pain patients, but may also be present in people with non-clinical pain. The aim of the present study is to investigate levels of catastrophizing in pain patients and people with pain from the general population. Also, the relationship between catastrophizing and pain intensity, specialist consultation and use of pain medication is studied. ⋯ It can be concluded that pain-related catastrophizing is present in pain patients as well as people with pain from the general population in a dose-response pattern. Catastrophizing seems to be an important factor determining certain aspects of pain-related medical consumption, even in non-clinical pain, and should therefore be a target of the screening procedure and early intervention.
-
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.