Genetic Alteration Predicts Pain Recovery After Sexual Assault

Key points
- One in five U.S. women are sexually assaulted in their lifetimes and more than half experience severe pain during the week following an attack.
- Based in Glenview, Ill., the American Pain Society (APS) is a multidisciplinary community that brings together a diverse group of scientists, clinicians and other professionals to increase the knowledge of pain and transform public policy and clinical practice to reduce pain-related suffering.
- Previous studies have reported that sexual assault victims who report having severe pain across multiple body regions are experiencing stress-induced hyperalgesia, resulting from release of endogenous opioids.
- Women 18 years and older presenting for treatment by sexual assault nurse examiners working in ten different health systems were recruited for the study.
One in five U.S. women are sexually assaulted in their lifetimes and more than half experience severe pain during the week following an attack. A study published in The Journal of Pain showed that presence of a genetic variant could significantly reduce pain severity associated with assault.
Previous studies have reported that sexual assault victims who report having severe pain across multiple body regions are experiencing stress-induced hyperalgesia, resulting from release of endogenous opioids. An initial period of analgesia is followed by delayed onset of persistent and widespread hyperalgesia. Gene variants have been associated with the u-opioid receptor and the most common variant is the single nucleotide polymorphism (SNP) A118G. Individuals with one or more copies of variant gene (allele) at the A118G have shown poor analgesic response to opioids.
A research team at the University of North Carolina hypothesized that activation of u-opioid receptors causes stress-induced hyperalgesia after a sexual assault and survivors with one or more copies of the variant gene at the A118G receptor would experience less receptor-mediated hyperalgesia and less pain in the initial weeks following the assault.
Women 18 years and older presenting for treatment by sexual assault nurse examiners working in ten different health systems were recruited for the study. The women were interviewed after one week and six weeks for evaluation of their pain symptoms. Genotyping was performed on all 52 study participants. The gene variant was found in 12 women (23%) and all were Caucasian.
The study results showed that the women with the gene variant resulting in reduced response to u-opioid receptor binding had clinically relevant reductions in pain severity. The findings suggest that women with one of more alleles at A118G may experience both a reduced analgesic response to endogenous opioids and a reduction in delayed-onset, more long-lasting opioid mediated hyperalgesia. The finding suggests that endogenous opioid-mediated hyperalgesia may contribute to pain symptoms after sexual assault.
A majority of sexual assault victims experience severe pain in the early aftermath of the crime but less than a third of these victims receive pain medications, according to research in The Journal of Pain, the peer review publication of the American Pain Society.
One in five U.S women experiences a sexual assault in their lifetimes. Like other physical trauma, severe acute pain occurs in sexual assault cases. When physical trauma is limited, factors such as stress-induced hyperalgesia may contribute to post-assault pain. Researchers from the University of North Carolina evaluated the distribution and severity of pain in sexual assault victims who presented for medical care from sexual assault nurse examiner (SANE) programs.
This was the first prospective study of pain symptoms in the early aftermath of sexual assault. Female sexual assault survivors 18 years and older who sought a SANE evaluation within 48 hours of the crime were recruited for the study. The subjects were questioned about pain intensity in eight body regions and asked to rate pain severity on a 1- to-10 scale.
Written and revised by
David Cohen, M.D.
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