Logan T Dowdle1, Jeffrey J Borckardt2, Sudie E Back3, Katherine Morgan4, David Adams4, Alok Madan5, Wendy Balliet6, Colleen A Hanlon7. 1. Department of Psychiatry and Behavioral Sciences, Medical University of South Carolina, Charleston, SC, USA; Department of Neurosciences, Medical University of South Carolina, Charleston, SC, USA. 2. Department of Psychiatry and Behavioral Sciences, Medical University of South Carolina, Charleston, SC, USA; Center for Biomedical Imaging, Medical University of South Carolina, Charleston, SC, USA; Ralph H. Johnson VA Medical Center, Charleston, SC, USA. 3. Department of Psychiatry and Behavioral Sciences, Medical University of South Carolina, Charleston, SC, USA; Ralph H. Johnson VA Medical Center, Charleston, SC, USA. 4. Department of Surgery, Medical University of South Carolina, Charleston, SC, USA. 5. Houston Methodist Behavioral Health, Houston, TX, USA. 6. Department of Psychiatry and Behavioral Sciences, Medical University of South Carolina, Charleston, SC, USA. 7. Department of Psychiatry and Behavioral Sciences, Medical University of South Carolina, Charleston, SC, USA; Department of Neurosciences, Medical University of South Carolina, Charleston, SC, USA; Center for Biomedical Imaging, Medical University of South Carolina, Charleston, SC, USA; Ralph H. Johnson VA Medical Center, Charleston, SC, USA. Electronic address: hanlon@musc.edu.
Abstract
BACKGROUND: Chronic opiate use leads to a sensitized behavioral response to acute pain, which in turn, leads to escalating doses of opiates. This study was designed to test the hypothesis that chronic opiate usage is also associated with a sensitized neurobiological response to acute pain in individuals that have used prescription opiates for 6 or more months. METHODS: Fourteen patients with non-alcoholic chronic pancreatitis that have been taking prescription opiates for 6 or more months and 14 gender matched, non-opiate using controls were enrolled. Functional neuroimaging data was acquired while participants received blocks of thermal stimulation to their wrist (individually-tailored to their pain threshold). RESULTS: Self-reported pain was significantly greater in opiate using patients (3.4 ± 3.4) than controls (0.2 ± 0.8: Brief Pain Inventory p < 0.005), however no significant difference between groups was observed in the individually-tailored pain thresholds. Opiate using patients evidenced a significantly greater response to pain than controls in two established nodes of the "Pain Matrix": somatosensory cortex (pFWE≤0.001) and anterior cingulate cortex (p ≤ 0.01). This response was positively correlated with prescribed morphine equivalent dosages (average: 133.5 ± 94.8 mg/day). CONCLUSION: The findings suggest that in chronic pancreatitis patients, a dose of opiates that normalizes their behavioral response to acute pain is associated with an amplified neural response to acute pain. Further longitudinal studies are needed to determine if this neural sensitization hastens a behavioral tolerance to opiates or the development of an opioid use disorder.
BACKGROUND: Chronic opiate use leads to a sensitized behavioral response to acute pain, which in turn, leads to escalating doses of opiates. This study was designed to test the hypothesis that chronic opiate usage is also associated with a sensitized neurobiological response to acute pain in individuals that have used prescription opiates for 6 or more months. METHODS: Fourteen patients with non-alcoholic chronic pancreatitis that have been taking prescription opiates for 6 or more months and 14 gender matched, non-opiate using controls were enrolled. Functional neuroimaging data was acquired while participants received blocks of thermal stimulation to their wrist (individually-tailored to their pain threshold). RESULTS: Self-reported pain was significantly greater in opiate using patients (3.4 ± 3.4) than controls (0.2 ± 0.8: Brief Pain Inventory p < 0.005), however no significant difference between groups was observed in the individually-tailored pain thresholds. Opiate using patients evidenced a significantly greater response to pain than controls in two established nodes of the "Pain Matrix": somatosensory cortex (pFWE≤0.001) and anterior cingulate cortex (p ≤ 0.01). This response was positively correlated with prescribed morphine equivalent dosages (average: 133.5 ± 94.8 mg/day). CONCLUSION: The findings suggest that in chronic pancreatitispatients, a dose of opiates that normalizes their behavioral response to acute pain is associated with an amplified neural response to acute pain. Further longitudinal studies are needed to determine if this neural sensitization hastens a behavioral tolerance to opiates or the development of an opioid use disorder.
Authors: Ulf Baumgärtner; Hans-Georg Buchholz; Alexander Bellosevich; Walter Magerl; Thomas Siessmeier; Roman Rolke; Sabine Höhnemann; Markus Piel; Frank Rösch; Hans-Jürgen Wester; Gjermund Henriksen; Peter Stoeter; Peter Bartenstein; Rolf-Detlef Treede; Mathias Schreckenberger Journal: Neuroimage Date: 2005-12-07 Impact factor: 6.556
Authors: Kevin E Vowles; Mindy L McEntee; Peter Siyahhan Julnes; Tessa Frohe; John P Ney; David N van der Goes Journal: Pain Date: 2015-04 Impact factor: 6.961
Authors: James J Mahoney; Colleen A Hanlon; Patrick J Marshalek; Ali R Rezai; Lothar Krinke Journal: J Neurol Sci Date: 2020-09-20 Impact factor: 3.181