• Lauren E Ballina, Jacob C Ulirsch, April C Soward, Catherine Rossi, Suzanne Rotolo, Sarah D Linnstaedt, Tricia Heafner, Kelly A Foley, Jayne Batts, Renee Collette, Debra Holbrook, Stacie Zelman, and Samuel A McLean.
• TRYUMPH Research Program, University of North Carolina, Chapel Hill, North Carolina 27599-7010, USA.
• J Pain. 2013 Feb 1; 14 (2): 165171165-71.

UnlabelledPain is common after sexual assault (SA), but etiology of pain symptoms after SA is unknown. Preclinical studies suggest that the release of endogenous opioids during stress produces delayed-onset hyperalgesia. In human studies, individuals with ≥1 G allele at the μ-opioid receptor functional single nucleotide polymorphism A118G have been shown to have a reduced response to opioids. We hypothesized that if opioid-mediated hyperalgesia contributes to pain after SA, women SA survivors with 1 or more G alleles at A118G would experience reduced postassault pain. Among 52 European American women SA survivors presenting for care within 48 hours of SA, those with a G allele (12/52, 23%) experienced less severe pain (F[1,39] = 11.55, P = .002) and a reduced extent of pain (F[1,41] = 11.01, P = .002) during the 6 weeks after SA. These associations between the presence of 1 or more G alleles and reduced pain severity and reduced pain extent after SA remained significant in multivariable models controlling for age, income, education, reported pain prior to assault, and pain at the time of initial evaluation.PerspectiveThese results suggest that endogenous opioid-mediated hyperalgesia may contribute to pain symptoms after sexual assault. Further studies examining mechanisms mediating the development of pain after sexual assault, and the potential influence of opioid-mediated hyperalgesia, are needed.Copyright © 2013 American Pain Society. Published by Elsevier Inc. All rights reserved.

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