Project Summary/Abstract Primary dysmenorrhea (PD), or menstrual pain without an identified pathology, has been shown to share deficits in pain processing in the central nervous system in both behavioral and neural indices. These alterations may put some girls at risk for the development of future pain problems, although phenotyping the “at risk” group with PD has been challenging due to significant individual variation among girls with menstrual pain. Recent evidence suggests that dysregulation of the immune system may be an important biomarker for PD that could shed light on who is at risk for chronic pain. One recent study demonstrated up-regulated plasma genetic expression of inflammatory cytokines during menstruation and 5 days following menstruation in women with PD compared to women without PD. These data support the idea that prolonged inflammatory responses may be a phenotypic biomarker associated with the transition from recurrent to chronic pain. The overarching objective of this administrative supplement, “Inflammatory Processes in Adolescent Girls with Primary Dysmenorrhea,” is to evaluate the relationship between pro-inflammatory cytokines and pain responses in a sample of 212 adolescent girls (ages 14-18 years) with varying levels of menstrual pain who are not using any exogenous hormones. As originally proposed, the parent study involves all participants receiving both quantitative sensory testing (QST) of pain sensitivity and structural and functional neuroimaging upon enrollment (baseline) and again one year later. Additionally, they will be followed monthly to assess menstrual pain and symptoms, as well as non-menstrual body pain, for two years total (from enrollment). Findings from the study will help characterize the role of inflammation in this highly prevalent condition.