Depression as a mediator of the relationship between temporal summation of second pain and subclinical borderline personality characteristics

Borderline personality (BP) is characterized by affect dysregulation and is positively associated with chronic pain. Previously, our laboratory observed that affect dysregulation was associated with enhanced temporal summation of second pain (TSSP). TSSP refers to the sensitization of pain evoked by repetitive heat pulses applied to the skin, which reflects a summation process of peripheral C-fiber nociceptive inputs and NMDA mediated sensitization of spinal dorsal horn neurons. However, further study is needed to investigate psychological mediators of enhanced pain sensitivity in individuals with BP characteristics. The purpose of this study is to examine whether depression mediates the relationship between affect dysregulation and central sensitization. TSSP was induced by 10 heat pulses in three trials. Before TSSP testing, sensitivity tests were conducted to identify a peak temperature to induce moderate pain (35 to 55 out of a 0-100 scale). While a thermode was applied to the thenar eminence of the non-dominant hand, participants rated their subjective pain after each peak. BP characteristics were assessed by the Personality Assessment Inventory-Borderline scale (PAI-BOR) and depression was assessed by the Center for Epidemiologic Studies Depression Scale in 80 pain-free college students. TSSP was compared between the two groups with the low (< 50) and high (>50 and <70) PAI-BOR T scores using a repeated measures ANOVA (10 ratings of average pain at each pulse in the three trials by 2 groups). The results indicated a significant interaction between group and repeated pulses after controlling for peak temperatures (F (9, 223) = 4.24, p = .01, epsilon=.25). The high PAI-BOR group reported significantly higher pain in the later pulse train. Analysis of covariance indicated that the interaction is no longer significant after controlling for depressive symptoms (p > .05). These findings suggest that the relationship between affect dysregulation and enhanced central sensitization is mediated by depressive symptoms.