Psychology

Acupuncture has been shown to be effective for the treatment of chronic musculoskeletal back, neck, and osteoarthritis pain. However, access to acupuncture treatment has been limited in medically underserved and low-income populations.

Conditioned pain modulation (CPM) is a task that involves measuring pain in response to a test stimulus before and during a painful conditioning stimulus (CS). The CS pain typically inhibits pain elicited by the test stimulus; thus, this task is used to assess endogenous pain inhibition. Moreover, less efficient CPM-related inhibition is associated with chronic pain risk. Pain catastrophizing is a cognitive-emotional process associated with negative pain sequelae, and some studies have found that catastrophizing reduces CPM efficiency.

The current study assessed the role of hypervigilance for bodily sensations in the back in long term low back pain (LBP) problems.

It is unclear if anxiety sensitivity may serve as mechanism underlying the relation between posttraumatic stress symptom severity and opioid misuse and dependence among trauma-exposed persons with chronic pain. Therefore, the current study evaluated the explanatory role of anxiety sensitivity in the relations between posttraumatic stress symptom severity and opioid misuse and dependence. Participants included 294 trauma-exposed adults with chronic pain (71.4% female, M = 37.79 years, SD = 10.85, M = 7.32/10) that reported current moderate to severe chronic pain and prescription opioid use. Participants were recruited via an online national survey in the United States of America. There were statistically significant indirect effects of posttraumatic stress symptom severity via anxiety sensitivity in relation to opioid misuse and dependence. The indirect effects of the reverse models for opioid misuse and dependence also were significant and suggest the potential for bi-directional relations; however, the magnitude of the effect was smaller in the tests of specificity than in the original models. The present findings provide initial empirical evidence that greater posttraumatic stress symptom severity is related to anxiety sensitivity, which in turn, is associated with increased opioid misuse and dependence among trauma-exposed individuals with chronic pain.

Previous work suggests that sleep disruption can contribute to poor pain modulation. Here, we used experimental sleep disruption to examine the relationship between sleep disruption-induced pain sensitivity and functional connectivity (FC) of cognitive networks contributing to pain modulation. Nineteen healthy individuals underwent two counterbalanced experimental sleep conditions for one night each: uninterrupted sleep versus sleep disruption. Following each condition, participants completed functional MRI including a simple motor task and a noxious thermal stimulation task. Pain ratings and stimulus temperatures from the latter task were combined to calculate a pain sensitivity change score following sleep disruption. This change score was used as a predictor of simple motor task FC changes using bilateral executive control networks (RECN, LECN) and the default mode network (DMN) masks as seed regions of interest (ROIs). Increased pain sensitivity after sleep disruption was positively associated with increased RECN FC to ROIs within the DMN and LECN (F = 25.28, pFDR = 0.05). However, this pain sensitivity change score did not predict FC changes using LECN and DMN masks as seeds (pFDR > 0.05). Given that only RECN FC was associated with sleep loss-induced hyperalgesia, findings suggest that cognitive networks only partially contribute to the sleep-pain dyad.

Retrospective cohort study OBJECTIVE.: To (1) confirm validity of PROMIS physical function and pain interference computer adaptive tests (CATs) and (2) assess the validity of PROMIS Global Health (GH) and five additional PROMIS CATs: social role satisfaction, fatigue, anxiety, depression, and sleep disturbance in a population of chronic low back pain (cLBP) patients who completed a 3-month Interdisciplinary Pain Program (IPP).

Chronic pain and mood disorders share common neuroanatomical substrates involving disruption of the reward system. Although increase in negative affect (NA) and decrease in positive affect (PA) are well-known factors complicating the clinical presentation of chronic pain patients, our understanding of the mechanisms underlying the interaction between pain and PA/NA remains limited. Here, we used a validated task probing behavioral and neural responses to monetary rewards and losses in conjunction with functional magnetic resonance imaging (fMRI) to test the hypothesis that dysfunction of the striatum, a key mesolimbic structure involved in the encoding of motivational salience, relates to mood alterations comorbid with chronic pain.