C. M. Trevino1, S. Chesney2, C. Hillard1, T. DeRoon-Cassini1 1Medical College Of Wisconsin,Surgery Trauma And Acute Care Surgery,Milwaukee, WI, USA 2Marquette University,Milwaukee, WI, USA
Introduction:
Little is known about the progression of acute pain to chronic pain in the traumatically injured population and the risk factors associated with this transition. In addition, there are few reliable or clinically significant biomarkers, for either of these conditions. Preclinical research suggests a role for the endocannabinoid signaling system (ECSS) in pain. Specifically, increased endocannabinoid (EC) signaling that is promoted by tissue injury and contributes at first to reduced pain could also contribute to some forms of pain sensitization and, thus contribute to the development of chronic pain. We hypothesized that EC levels would correlate with pain scores at baseline and 6 months after traumatic injury.
Methods:
A prospective longitudinal cohort study was conducted with participants admitted to an Adult Level I Trauma Center post traumatic injury. Participant demographic and injury-related data, pain scores, pain interference scores, and symptoms of Post-Traumatic Stress Disorder (PTSD) were assessed via measures obtained at the time of hospitalization (baseline) and 6 months following the index traumatic event. Non-fasting whole blood samples measuring ECs [2-arachidonoylglycerol (2AG) and anandamide (AEA)] and EC genetic polymorphisms of fatty acid amide hydrolase (FAAH) expression were drawn at baseline and at 6 month follow up. Pearson correlations and ANOVAs were used to determine relationships.
Results:
280 participants comprised a subset of a population base sample (72.5% Male, 27.5% Female) with 170 participants (61% retention) completing 6-month follow-up. 2AG at baseline was significantly correlated with pain interference at 6 months (r=0.197, p=0.01). AEA at 6 months was significantly correlated with both pain severity (r=0.164, p=0.04) and pain interference (r=0.191, p=0.02) at 6 months. Participants with the rare genetic allele for FAAH had significantly higher 6 month pain severity (likelihood ratio=10.431; p=.034, Cramer’s V=0.175). Pain scores and PTSD here highly correlated both at baseline and at 6 months (r=0.3, p<0.001; r=0.4, p<0.001).
Conclusion:
The ECSS is known to play a role in both the perception of pain and psychological distress. Similar to previous studies, pain and PTSD was highly comorbid in this population. These data suggest higher levels of 2AG and AEA at 6 months may play a role in the development of chronic pain. Those with genetic FAAH over expression, and ultimately higher ECs, can prevent the decrease in AEA. This decrease in AEA overtime is protective in reducing the activation of ascending pain pathways, thereby potentially affecting the negative feedback of AEA in the development of chronic pain. From these data a significant relationship exists between the EC system and chronic pain. Therefore, the EC system may play a pivotal role in the development of chronic pain from acute traumatic injury and is potentially a target for intervention.