Psychology

Past studies have shown that pain memories are often inaccurate, a phenomenon known as mnemonic pain bias. Pain memories are thought to play an important role on how future pain is felt. Recent evidence from our laboratory suggests that individuals who exaggerate past pain display increased superior temporal gyrus (STG) and parahippocampal gyrus (PHG) activity during the encoding of experimental painful stimulations, suggesting that these brain structures play an important role in pain memories.

Traumatic injury is a major source of chronic pain, particularly for individuals with traumatic fracture of the fibula and/or tibia (lower extremity fracture) [LEFx]. Although several factors (e.g., older age, being female sex, high pain intensity at time of initial injury) have been identified as risk factors for chronic pain associated with LEFx. Comprehensive biopsychosical models to predict the odds of transitioning from acute to chronic pain after LEFx are needed to better understand the underlying processes, predict risk for chronic pain, and develop personalized therapies for individuals at higher risk for developing chronic pain.

Intense or sustained activation of peripheral nociceptors can induce central sensitization. This enhanced responsiveness to nociceptive input of the central nervous system primarily manifests as an increased sensitivity to painful mechanical pinprick stimuli extending beyond the site of injury (secondary mechanical hyperalgesia) and is thought to be a key mechanism in the development of chronic pain, such as persistent post-operative pain. It is increasingly recognized that emotional and cognitive factors can strongly influence the pain experience. Furthermore, through their potential effects on pain modulation circuits including descending pathways to the spinal cord, it has been hypothesized that these emotional and cognitive factors could constitute risk factors for the susceptibility to develop chronic pain. Here, we tested whether, in healthy volunteers, the experimental induction of central sensitization by peripheral nociceptive input can be modulated by selective spatial attention. While participants performed a somatosensory detection task that required focusing attention towards one of the forearms, secondary hyperalgesia was induced at both forearms using bilateral and simultaneous high-frequency electrical stimulation (HFS) of the skin. HFS induced an increased sensitivity to mechanical pinprick stimuli at both forearms, directly (T1) and 20 min (T2) after HFS, confirming the successful induction of secondary hyperalgesia at both forearms. Most importantly, at T2, the HFS-induced increase in pinprick sensitivity as well as the area of secondary hyperalgesia was greater at the attended arm as compared to the non-attended arm. This indicates that top-down attentional factors can modulate the development of central sensitization by peripheral nociceptive input, and that the focus of spatial attention, besides its modulatory effects on perception, can affect activity-dependent neuroplasticity.

There are bidirectional links between sleep quality and pain, with recent research suggesting that sleep impairment more strongly predicts future pain than vice versa. Relatively few studies have examined the relationship between sleep quality and acute pain among chronic pain patients. The purpose of the current study is to investigate relationships among subjective sleep quality and behavioral and physiological responses to a cold pressor pain task (CPT) in chronic pain patients.

To compare the impacts of trigeminal neuralgia (TN) and painful posttraumatic trigeminal neuropathy (PPTTN) on psychologic function and health-related quality of life (HRQoL) using a comprehensive quantitative assessment.

Chronic pain in adults with sickle cell disease (SCD) may be the result of altered processing in the central nervous system as indicated by quantitative sensory testing (QST). Sensory pain quality descriptors on the McGill Pain Questionnaire (MPQ) are indicators of typical or altered pain mechanisms but have not been validated with QST-derived classifications.

This study aims to (1) examine the temporal influence of peer victimization on mood, sleep quality, pain, and activity limitations in clinical and community samples of youth, and (2) test mood and sleep as mediators of peer victimization-pain pathways. One hundred fifty-six adolescents (n=74 chronic pain group) completed a week of online diary monitoring assessing their daily peer victimization experiences, negative mood, sleep quality, pain intensity, and pain-related activity limitations. In multilevel models controlling for group status, person-mean peer victimization (averaged across days) significantly predicted worse mood, pain, and activity limitations (all ps < .01) while daily victimization predicted worse mood (p < .05). Results from within-person mediation indicated a significant indirect effect of daily peer victimization on next-day activity limitations, through daily negative mood. Results from between-person mediation indicated that negative mood significantly mediated the relation between peer victimization and pain and the relation between peer victimization and activity limitations. Peer victimization is associated with negative health indicators in clinical and community samples of youth and may exert its influence on pain and pain-related activity limitations through negative mood. PERSPECTIVE: This article examines the temporal influence of peer victimization on pain in adolescents with and without chronic pain, and examines mood and sleep quality as mechanisms linking victimization to pain. This information may be useful for pain prevention researchers as well as providers who assess and treat pain in childhood.