European journal of pain : EJP
-
The analgesic properties and mechanisms of loperamide hydrochloride, a peripherally acting opioid receptor agonist, in neuropathic pain warrant further investigation. ⋯ These findings suggest that both systemic and local administration of loperamide induce an opioid receptor-dependent inhibition of heat and mechanical hyperalgesia in nerve-injured rats, but that local paw administration of loperamide also induces thermal and mechanical antinociception.
-
The purpose of this study was to examine differences in heat pain threshold (HPTh) and heat pain tolerance (HPTo) between temporomandibular joint disorder (TMJD) patients and healthy controls. Using suprathreshold heat pain, this study also examined between-group (i.e. TMJD vs. healthy controls) differences in hyperalgesia and temporal summation (TS) of heat pain. ⋯ Data analysis revealed a significant simple mediation effect whereby the presence of TMJD was strongly associated with poorer self-reported sleep quality, which, in turn, was related to enhanced hyperalgesia at 46 °C. These findings support the hypothesis that the thermal hyperalgesia demonstrated by TMJD patients may be related to poor quality of their self-reported sleep. The ability of interventions that improve sleep quality to also affect pain sensitivity is currently the topic of ongoing investigation.
-
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.
-
To clarify the mechanism of tenderness after bone injury, we investigated changes in the withdrawal threshold to mechanical stimuli, nerve distribution and nerve growth factor (NGF)-expression in a rat model of bone injury without immobilization for bone injury healing. Rats were divided into three groups as follows: (1) rats incised in the skin and periosteum, followed by drilling a hole in the tibia [bone lesion group (BLG)]; (2) those incised in the skin and periosteum without bone drilling [periosteum lesion group (PLG)]; and (3) those incised in the skin [skin lesion group (SLG)]. Mechanical hyperalgesia continued for 28 days at a lesion in the BLG, 21 days in PLG and 5 days in SLG after treatments, respectively. ⋯ Anti-NGF and trk inhibitor K252a inhibited hyperalgesia in the different time course. This study shows that localized tenderness coincides with the bone healing and involves NGF expression and nerve sprouting after bone injury. The findings present underlying mechanisms and provide pathophysiological relevance of local tenderness to determination of bone fracture and its healing.