RESEARCH REPORT POSTER DISPLAY

DELAYED PAIN REACTIONS DUE TO STRESS IN PATIENTS WITH COMPLEX REGIONAL PAIN SYNDROME. Allen R, Hulten J, Roelofson M, Martin T, McCormack S; University of Puget Sound, Tacoma, WA, USA

PURPOSE: This study’s purpose was to determine the effect of perceived stress on pain intensity, timing of episodic pain increases, and related functional changes in patients with complex regional pain syndrome (CRPS). RELEVANCE: Intensity of pain associated with CRPS varies over time and may be exacerbated by activity, temperature, stress, etc. Episodes of severe pain intensity are often inexplicable, hard to predict, and markedly impact therapy and function. Latent endocrine changes associated with psychogenic stress can increase peripheral nerve excitability long after the initiating event, possibly explaining delayed increases in neuropathic pain intensity. PARTICIPANTS: This was a case study design involving two functionally stable, male volunteers with sympathetically mediated Type I CRPS. Patient 1 was an unemployed 49 year-old, with a six-year CRPS history affecting the right lower extremity. Patient 2 was an employed 31 year-old with an eight-year history of CRPS affecting the left upper extremity. METHODS: To track temporal fluctuations in perceived pain, stress, and function, participants completed a visual analog pain and stress scales, the Daily Stress Index, and the RAND 36-Item Health Survey daily for ten weeks. ANALYSIS: Daily values for all scales were graphed across the ten-week tracking epoch for each participant. Episodic peaks were manifested on days when ratings exceeded 1.5 and 2.5 standard deviations above the participant’s ten-week means for pain and stress, respectively. To analyze temporal relationships between stress and delayed pain flares, serial lag correlations were performed using 0-14 day lags. The same statistical comparisons were made between stress and function. RESULTS: No clear relationship was evident between ratings stress levels and perceived pain intensity occurring on the same day (r = +0.04 & +0.14). However, serial lag correlations revealed strong concordance between days of peak stress and high pain intensity experienced ten days later for both participants (r = +0.49 & +0.52). For each participant, every criterion peak stress day was followed ten days later by a sharp pain intensity increase. Notable reductions in measured function were also reported ten days following each peak stress day. These findings are consistent with timing of the thyroxine axis in the stress response. Once released, thyroxine is bound by serum proteins, whose timed dissociation results in peak effects ten days later. Thyroxine’s relevant effect is increased peripheral nerve excitability, thereby possibly heightening perceived neuropathic pain severity. CONCLUSIONS: Based on findings from two participants measured over ten weeks, these individuals with CRPS experienced delayed increases in pain magnitude and decreased function occurring ten days following stressful episodes. IMPLICATIONS: Patients and therapists are frequently unable to explain debilitating CRPS pain flares. Knowing that stressful episodes may lead to pain flares, and related functional attenuation ten days later, patients could predict the onset of particularly painful days, and better time and plan activity. This may placate some patient fear and anxiety related to latent pain increases. Therapists can use this information to time treatment components and distinguish stress-related pain flares from those induced by activity or treatment intensity. KEYWORDS: Complex Regional Pain Syndrome, Stress, Delayed Pain. FUNDING ACKNOWLEDGEMENTS: This study was supported by a Student Research Award grant from the University Enrichment Committee of the University of Puget Sound, Tacoma, WA, USA. CONTACT: rallen@ups.edu

ETHICS COMMITTEE: Institutional Review Board, University of Puget Sound, Tacoma, WA, USA