BACKGROUND AND AIMS: Globally, chronic low back pain (CLBP) affects 70-80% of adults at some point in their lives and current treatments are widely unsuccessful in relieving pain. Understanding the underlying neurophysiological (e.g., descending pain inhibition) and biobehavioral (e.g., stress) processes contributing to chronic pain in patients with CLBP is needed for the development of novel treatments. Previous studies have shown that acute stress can impact pain sensitivity and that childhood trauma may predispose a person to CLBP, but the mechanisms underlying this impact are unknown. Conditioned Pain Modulation (CPM) is a psychophysical paradigm used in research to assess descending pain modulatory pathways, which are thought to be impaired in patients with CLBP as well as in those with childhood trauma. The overlap of conditions has not been explored. The current study explored the impact of childhood trauma on the CPM response within a sample of patients with CLBP being treated at a tertiary pain clinic. CLBP patients exposed to an acute stress paradigm were expected to shower higher pain sensitivity, with acute stress significantly interacting with a history of childhood trauma as a factor leading to the higher pain sensitivity. METHODS: 46 Participants with CLBP (n=46, mean age=49 years, 55.3% female) recruited from a pain treatment service completed a Quantitative Sensory Testing (QST) and CPM before and after an acute psychological stressor. Participants were randomized to a control (n=25) or an acute-stress (n=21) condition. The acute-stress condition included the Stroop Color Word Task (SCWT) and a mental arithmetic task prior to completing the QST protocol a second time. The control participants did not undergo any additional stressors and completed the QST protocol a second time after a 20-minute break. Participants’ CPM response was measured by the average change in pressure pain threshold (PPT) from baseline to the conditioning stimulus (non-dominant hand in ice-water bath). A “Good CPM response” was defined as a CPM effect above 100, indicating that the pain threshold increased when exposed to the conditioning stimulus. To examine the impact of childhood trauma on pain sensitivity, participants completed a Childhood Traumatic Events Scale (CTES) to assess the presence and severity of six types of trauma (death, parental upheaval, sexual, violence, illness or injury, other upheaval) during childhood. The CTES was scored as a continuous variable by calculating the sum the trauma severity for all six trauma types. RESULTS: A large majority of the sample (94% of participants) showed an increase in pain threshold during hand immersion in ice water, which was contrary to our hypothesis based on prior research done on other chronic pain conditions and CLBP. Participants exposed to an acute stressor had an impaired CPM effect compared to those that were not exposed to an acute stressor, however there was no difference between groups (p=0.277). A history of childhood traumatic events did not correlate significantly with an impaired baseline CPM or a change in CPM effect when exposed to an acute stressor. CONCLUSION: The current study used novel QST modalities, including CPM, to analyze the interaction between acute and chronic stress on pain sensitivity. Ultimately, this study found that exposure to an acute stressor had a negative effect on CPM, indicating that when under experimental stress participants were more sensitive to pain compared to when they were not under stress, although the findings were not statistically significant. These findings should be further investigated to expand the understanding of the neurophysiological mechanisms underlying CLBP and to potentially provide novel treatment modalities for patients with CLBP.