Pain
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Depression and musculoskeletal pain are associated, but long-term follow-up studies are rare. We aimed to examine the relationship of early depressive symptoms with developmental patterns of musculoskeletal pain from adolescence to middle age. Adolescents ending compulsory school (age 16) in Luleå, Northern Sweden, in 1981 (n = 1083) were studied and followed up in 1986, 1995, and 2008 (age 43) for musculoskeletal pain. ⋯ For severe pain, 2 trajectories were found: moderate-increasing (women 19%, men 9%) and low-stable. For each 0.1-point increase in the DSS, the odds ratio of membership in the moderate-increasing trajectory was 1.14 (1.04-1.25) in women and 1.17 (1.04-1.31) in men in the fully adjusted model. Thus, depressive symptoms at baseline are strongly associated with pain trajectory membership.
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Individuals with chronic pain may experience negative responses from spouse, family, and friends. Responses such as overt criticism and hostility may be associated with worsening pain and function for chronic pain sufferers. We used a laboratory procedure to evaluate whether variability in spouse criticism/hostility exhibited toward chronic low back pain (CLBP) patients during a conflictual discussion predicted variability in patient pain and function during a subsequent pain-induction task. ⋯ Results support the hypothesis that spouse criticism and hostility-actually expressed or perceived-may worsen CLBP patient symptoms. Further, women patients and patients high in depressive symptoms appeared most vulnerable to spouse criticism/hostility. Thus, negative marital communication patterns may be appropriate targets for intervention, especially among these 2 at risk groups.
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Heart rate variability (HRV) and baroreflex sensitivity (BRS) are indexes reflecting the ability to maintain cardiovascular homeostasis amidst changing conditions. Evidence primarily from small studies suggests that both HRV and BRS may be reduced in individuals with chronic pain (CP), with potential implications for cardiovascular risk. We compared HRV and BRS between individuals with CP (broadly defined) and pain-free controls in a large unselected population sample. ⋯ Results were somewhat weaker for the post-CPT period. Mediation analyses indicated that for 6 of 7 HRV and BRS measures tested, there were significant indirect (mediated) effects of CP status on the presence of comorbid hypertension via reduced HRV or BRS. Results confirm in the largest and broadest sample tested to date that the presence of CP is linked to impaired cardiovascular regulation and for the first time provide support for the hypothesis that links between CP and comorbid hypertension reported in previous population studies may be due in part to CP-related decrements in cardiovascular regulation.
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Chronic pain conditions are highly comorbid with insufficient sleep. While the mechanistic relationships between the 2 are not understood, chronic insufficient sleep may be 1 pathway through which central pain-modulatory circuits deteriorate, thereby contributing to chronic pain vulnerability over time. To test this hypothesis, an in-laboratory model of 3 weeks of restricted sleep with limited recovery (5 nights of 4-hour sleep per night followed by 2 nights of 8-hour sleep per night) was compared with 3 weeks of 8-hour sleep per night (control protocol). ⋯ These changes may reflect abnormalities in central pain-modulatory processes. Limited recovery sleep did not completely resolve these alterations in pain-modulatory processes, indicating that more extensive recovery sleep is required. Results suggest that exposure to chronic insufficient sleep may increase vulnerability to chronic pain by altering processes of pain habituation and sensitization.
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Pyrethroid insecticides are widely used for pest control in agriculture or in human public health commonly as a topical treatment for scabies and head lice. Exposure to pyrethroids such as permethrin or tetramethrin (TM) causes sensory alterations such as transient pain, burning, stinging sensations, and paraesthesias. Despite the well-known effects of pyrethroids on sodium channels, actions on other channels that control sensory neuron excitability are less studied. ⋯ In TRESK knockout mice, pain-associated behaviors elicited by TM were enhanced, providing further evidence for a role of this channel in preventing excessive neuronal activation. Our results indicate that inhibition of K2P channels facilitates sensory neuron activation and increases their excitability. These effects contribute to the generation of paraesthesias and pain after pyrethroid exposure.