Pain
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The investigation of neurotransmitter systems in placebo and nocebo effects has improved our understanding of these phenomena. Yet, most studies involve healthy participants. Because the pain modulatory system may differ in healthy participants and patients with chronic pain, it is important to investigate the evidence for neurotransmitter involvement in placebo and nocebo effects in each of these populations. ⋯ Overall, research has come a long way in specifying the neurotransmitter systems involved in placebo effects in healthy participants. Yet, evidence for the involvement of neurotransmitter systems in placebo effects in patients with chronic pain and in nocebo effects in healthy participants and patients is scarce. Based on the existing evidence, this systematic review suggests that knowledge obtained in healthy participants may not necessarily be transferred to chronic pain.
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A child maltreatment history is reported more frequently among adults with chronic pain compared with the general population; unfortunately, studies have primarily relied upon retrospective maltreatment reports by adults with chronic pain. This prospective study assessed pain symptoms in a cohort of young adult women with a documented history of child maltreatment, compared with a matched cohort of women who did not experience childhood maltreatment. Young women (N = 477) were recruited between ages 14 to 17 years and followed annually to age 19. ⋯ As adults, women who had experienced child maltreatment reported higher pain intensity, a greater number of pain locations, and were more likely to experience pain in the previous week than nonmaltreated women. Adolescent post-traumatic stress partially explained the effects of maltreatment on pain. Young adult women who experienced child maltreatment are at higher risk of pain, particularly when they also experienced post-traumatic stress as adolescents.
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An imbalance between excitatory and inhibitory neurotransmission has been linked to fibromyalgia (FM). Magnetic resonance spectroscopy has shown increased levels of glutamate in the insula and posterior cingulate cortex in FM as well as reduced insular levels of gamma-aminobutyric acid (GABA). Both of these changes have been associated with increased pain sensitivity. ⋯ The changes were widespread and not restricted to pain-processing regions. These findings suggest that the GABAergic system is altered, possibly indicating an imbalance between excitatory and inhibitory neurotransmission. Future studies should try to understand the nature of the dysregulation of the GABAergic system in FM and in other pain syndromes.
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Postamputation stump and phantom pain are highly prevalent but remain a difficult condition to treat. The underlying mechanisms are not fully clarified, but growing evidence suggests that changes in afferent nerves, including the formation of neuromas, play an important role. The main objective of this cross-sectional study was to investigate whether ultrasound-verified neuroma swellings are more frequent in amputees with postamputation pain than in amputees without pain (primary outcome). ⋯ No difference was found in stump pain intensity (P = 0.42) during the last week or in phantom pain intensity in the last month (P = 0.74) between amputees with and without swollen neuromas. Our findings suggest that it is not the presence of swollen neuromas itself that drives postamputation pain. However, changes in the transected nerve endings may still be crucial for driving postamputation pain because a positive Tinel sign was significantly more frequent in amputees with pain, irrespectively of the degree of neuroma swelling.
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Early life stress (ELS) can significantly influence biological pathways associated with nociception, increasing vulnerability to future heightened pain sensitivity and subsequent risk of pain events. However, very little human research has investigated the association of ELS, measured across multiple domains, with future pain sensitivity. Data from Gen1 and Gen2 of the Raine Study were used to assess the association between a wide range of early life stressors, including antenatally, and pressure and cold pain sensitivity at young adulthood. ⋯ More problematic behaviour at age 2 years was associated with less pressure pain sensitivity at 22 years (13.7 kPa, 95% CI: 1.0-27.0, P = 0.037), with no interaction between problematic behaviour and pain experience at 22 years. For those reporting a moderate/high pain experience at 22 years, poor family functioning increased the odds ratio for high cold pain sensitivity (3.0, 95% CI: 1.6-5.6), but for those reporting no/low pain experience, it did not (OR:1.2, 95% CI: 0.8-1.8). This study provides the most comprehensive investigation of the relationship between ELS and pressure and cold pain sensitivity in young adults supporting early life as a critical period of development influencing future nociceptive processing.