ArticleThe journal of pain2019
Conditioned Pain Modulation in Sexual Assault Survivors.
Article in The journal of pain, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Development of a Momentary Digital Intervention to Prevent Sexual Revictimization Among College Women: A Qualitative Examination of Perceived Acceptability and Usefulness.Journal of child sexual abuse · 2026Article
- Article
- Childhood sexual abuse and post-cesarean pain.Pregnancy (Hoboken, N.J.) · 2025Article
- Profiles of Trauma Exposure Type and Its Associations With Pain-Related Outcomes Among Adults With Chronic Pain: A 2-Year Longitudinal Study.The journal of pain · 2024Article
- The Relationship Between Experienced Discrimination and Pronociceptive Processes in Native Americans: Results From the Oklahoma Study of Native American Pain Risk.The journal of pain · 2022Article
- Are Cardiometabolic Markers of Allostatic Load Associated With Pronociceptive Processes in Native Americans?: A Structural Equation Modeling Analysis From the Oklahoma Study of Native American Pain Risk.The journal of pain · 2021Article
- The Relationship Between Adverse Life Events and Endogenous Inhibition of Pain and Spinal Nociception: Findings From the Oklahoma Study of Native American Pain Risk (OK-SNAP).The journal of pain · 2021Article
- Characterizing Pain and Generalized Sensory Sensitivity According to Trauma History Among Patients With Knee Osteoarthritis.Annals of behavioral medicine : a publication of the Society of Behavioral Medicine · 2021Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Sexual assault (SA) is associated with an increased risk of chronic pain, but the mechanisms for this relationship are poorly understood. To explore whether disrupted descending inhibition is involved, this study used a conditioned pain modulation task to study the inhibition of pain and the nociceptive flexion reflex (NFR; a correlate of spinal nociception) in 32 pain-free SA survivors. This group was compared with 32 pain-free, trauma-exposed persons without SA and a group of 40 pain-free persons who reported no trauma exposure. Conditioned pain modulation was assessed from painful electric stimulations (test stimulus) delivered to the ankle before, during, and after participants submerged their hand in painful 10°C water (conditioning stimulus). Pain ratings and NFR were assessed in response to test stimuli. All groups demonstrated significant inhibition of pain during conditioned pain modulation. However, only the no trauma exposure group demonstrated significant inhibition of NFR. The persons without SA group showed no inhibition of NFR, whereas the SA group showed significant facilitation of the NFR. These findings suggest that trauma exposure may impair inhibitory cerebrospinal circuits, but that SA may specifically promote facilitation of spinal nociception. Perspective: This study suggests that trauma exposure disrupts the cerebrospinal inhibition of spinal nociception, but that exposure to SA further promotes chronic pain risk by facilitating spinal nociception. This finding help may help to elucidate the pain risk mechanisms in trauma survivors.
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