CHRONIC LIMB PAIN DEVELOPING FROM REDUCED MOBILITY. Roger J. Allen2; Lisa R. Koshi*1,2 1. Physical Therapy, Apple Physical Therapy, Olympia, WA; 2. Physical Therapy, University of Puget Sound, Tacoma, WA THEORY: Excessive restrictions in movement following trauma or surgery may lead to a multifaceted sequence of changes that develops into chronic pain syndromes due to the creation of secondary pain generation sites. PHENOMENON: Operant conditioning quickly teaches patients to restrict movement and functional use of painful limbs. Therapists know well the consequences to both normal motion and functional usage of prolonged restrictions in mobility. What is less understood is how diminished movement may progress into a chronic pain syndrome in a minority of patients. PURPOSE: The purpose of this presentation is to propose a comprehensive model articulating the multiple structural and pathophysiological sequela operating in the development of chronic pain due to excessive reductions in active limb use following trauma or surgery. EVIDENCE: Current literature is in agreement that excessive postural guarding and restrictions in mobility following limb trauma is the primary risk factor in the development of complex regional pain syndrome. Hypothesizing a comprehensive model describing progressive tissue changes capable of generating long standing pain due to prolonged immobilization is now possible by bringing together evidence from a broad range of research areas. Maladaptive changes involve alterations in both tissue structure and regional physiology. Immobility may lead to structural changes such as contracture and adhesions of soft connective tissue and peripheral nerves, and breakdowns in peripheral articular cartilage resulting in painful motion when joint movement enters the premature end range. Regional physiologically changes include diminished rhythmic muscular contraction leading to venous stasis and edema, decreased arterial perfusion, reduced oxygen delivery to local tissue, local acidosis, and fibrotic changes. Skeletal muscle disuse atrophy lowers anaerobic threshold making even minor functional exertion a lactate producing anaerobic exercise, while progressing muscle weakness lowers dynamic joint stabilization transferring excess painful stress to noncontractile connective t issue. Reduced functional limb usage minimizes or eliminates normal tactile contact thus hampering opportunities for exogenous analgesia via large diameter fiber pain inhibition. Exogenous causes of immobilization include splinting, fixation, or neuropat hology. Endogenous factors of maladaptive mobility restrictions include kinesiophobia, postural guarding, fear of reinjury, or socially reinforced inactivity. Early symptomatic warning signs may be evident such as pain persisting after apparent tissue he aling has occurred, pain out of proportion to the initiating trauma, trophic changes to distal tissue, unresolving edema, and sympathetic changes to the affected region. Psychobehavioral signs may include overguarding, disinclination to participate in the rapeutic exercise or functional activities, or evidence of salient secondary gains reinforcing pain behavior or disability. TESTABLE HYPOTHESIS: A range of testable hypotheses arise from the conceptual theory of deactivation pain which may guide a future research agenda exploring the relationship between excessive immobility and the development of chronic pain. These include, but are not limited to the following: 1) Quantifications of limb usage and movement may be associated with the development of chronic limb pain or response to therapy. 2) Early identification of patients behaviorally resisting restoration of normal movement and usage fol lowing trauma or surgery may predict increased risk of developing a chronic limb pain syndrome. 3) Appropriately paced reactivation therapy may arrest the development of chronic pain syndromes if initiated upon early observation of excessive behavioral immobilization. 4) Excessive immobilization may be a precursor of pathophysiological changes in autonomic, vascular, and trophic activity in affected limbs. IMPORTANCE: Although chronic pain syndromes are notoriously difficult to treat once established, early recognition of excessive postural guarding or immobilization may empower therapists to help prevent subacute lesions from developing into chronic pain conditions through early identification of at-risk patients and therapeutic remobilization. FUNDING SOURCE: None KEYWORDS: Complex regional pain syndrome, Immobilization, Deactivation pain, Disuse syndrome, Chronic pain Copyright 2009 by the American Physical Therapy Association. Requests for reprints should be directed to the corresponding author of the article. Educators, students, and other academic customers may receive permission to reprint copyrighted material from Physical Therapy (ISSN 1538-6724) by contacting the Copyright Clearance Center Inc, 222 Rosewood Dr, Danvers, MA 01923. Other types of customers who want permission to reprint should contact the APTA Editorial Office, Attn: Physical Therapy.