(319) The role of central sensitization in pain hypersensitivity in individuals with symptoms of migraine headache

Abstract

Repeated migraine attacks are associated with maladaptive neural plasticity and lead to chronic headache. Sensitization of the pain pathways could play an important role in migraine’s pathophysiology and in the transition to the chronic forms of the disorder. In a previous study our laboratory found that subjects with a history of adverse childhood events presented a significantly increased area of capsaicin-induced secondary hyperalgesia, a measure of central sensitization, suggesting that exposure to trauma dysregulates neurogenic inflammation and pain modulatory systems. In addition, results from a recent study suggest that exposure to maltreatment can induce oxytocin dysregulation, which may also contribute to increased pain sensitivity. The goals of this study were to evaluate the differences in laboratory-induced pain and central sensitization between migraineurs and healthy controls. In addition, we explored whether childhood trauma and oxytocin levels mediate pain hypersensitivity. Thirty-three individuals with migraine headache and thirty-two healthy individuals underwent pain sensitivity testing following topical capsaicin application to the volar forearm. Childhood trauma, oxytocin levels and psychological measures were also assessed. We observed a significant increase in the area of secondary hyperalgesia (p=0.019) as well as capsaicin-induced unpleasantness (p=0.018) in migraineurs compared to healthy controls. However, no significant difference in oxytocin levels (p=0.110; Mann-Whitney U-test) and reported childhood traumatic events (p=0.055; Mann-Whitney U-test) were found between groups.