Over 100 million Americans suffer from chronic pain (CP), which causes more disability than any other medical condition in the United States at a cost of $560-$635 billion per year (Institute of Medicine, 2011). Opioid analgesics are frequently used to treat CP. However, long term use of opioids can cause brain changes such as opioid-induced hyperalgesia that, over time, increase pain sensation. Also, opioids fail to treat complex psychological factors that worsen pain-related disability, including beliefs about and emotional responses to pain. Cognitive behavioral therapy (CBT) can be efficacious for CP. However, CBT generally does not focus on important factors needed for long-term functional improvement, including attainment of personal goals and the psychological flexibility to choose responses to pain. Acceptance and Commitment Therapy (ACT) has been recognized as an effective, non-pharmacologic treatment for a variety of CP conditions (Gutierrez et al., 2004). However, little is known about the neurologic mechanisms underlying ACT. We conducted an ACT intervention in women ( = 9) with chronic musculoskeletal pain. Functional magnetic resonance imaging (fMRI) data were collected pre- and post-ACT, and changes in functional connectivity (FC) were measured using Network-Based Statistics (NBS). Behavioral outcomes were measured using validated assessments such as the Acceptance and Action Questionnaire (AAQ-II), the Chronic Pain Acceptance Questionnaire (CPAQ), the Center for Epidemiologic Studies Depression Scale (CES-D), and the NIH Toolbox NeuroQoL (Quality of Life in Neurological Disorders) scales. Results suggest that, following the 4-week ACT intervention, participants exhibited reductions in brain activation within and between key networks including self-reflection (default mode, DMN), emotion (salience, SN), and cognitive control (frontal parietal, FPN). These changes in connectivity strength were correlated with changes in behavioral outcomes including decreased depression and pain interference, and increased participation in social roles. This study is one of the first to demonstrate that improved function across the DMN, SN, and FPN may drive the positive outcomes associated with ACT. This study contributes to the emerging evidence supporting the use of neurophysiological indices to characterize treatment effects of alternative and complementary mind-body therapies.
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http://dx.doi.org/10.3389/fnhum.2021.587018 | DOI Listing |
Scand J Pain
January 2025
Department of Clinical Sciences Malmö, Center for Primary Health Care Research, Lund University, Jan Waldenströms Gata 35, 202 13 Malmö, Sweden.
Harm Reduct J
January 2025
Department of Psychology, Memorial University of Newfoundland, St. John's, NL, Canada.
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View Article and Find Full Text PDFBMC Musculoskelet Disord
January 2025
Department of Orthopaedics, Canisius Wilhelmina Ziekenhuis, Nijmegen, The Netherlands.
Background: Patellofemoral pain (PFP) is a common musculoskeletal disorder resulting in anterior knee pain. Physiotherapy is the current standard treatment, while surgical intervention (tibial tubercle transfer [TTT]) is reserved for chronic cases when nonoperative treatment has failed. TTT can result in clinically meaningful improvement in patients with patellofemoral maltracking without instability.
View Article and Find Full Text PDFMed Biol Eng Comput
January 2025
Auckland Bioengineering Institute, The University of Auckland, Auckland, New Zealand.
Lower limb biomechanics of chronic ankle instability (CAI) individuals has been widely investigated, but few have evaluated the internal foot mechanics in CAI. This study evaluated bone and soft tissue stress in CAI contrasted with copers and non-injured participants during a cutting task. Integrating scanned 3D foot shapes and free-form deformation, sixty-six personalized finite element foot models were developed.
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January 2025
Department of Pharmacology, University of Arizona College of Medicine, Tucson, AZ, USA.
Background: Women with endometriosis are more likely to have migraine. The mechanisms underlying this co-morbidity are unknown. Prolactin, a neurohormone secreted and released into circulation from the anterior pituitary, can sensitize sensory neurons from female, but not male, rodents, monkeys and human donors.
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