Sexual assault (SA) is associated with increased risk for 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 (CPM) task to study inhibition of pain and the nociceptive flexion reflex (NFR; a correlate of spinal nociception) in 32 pain-free SA survivors. This group was compared to 32 pain-free, trauma-exposed persons without SA (no-SA group) and a group of 40 pain-free persons who reported no trauma exposure (no-TE). CPM 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 CPM. However, only the no-TE group demonstrated significant inhibition of NFR. The no-SA group showed no inhibition of NFR, whereas the SA group showed significant facilitation of 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 trauma exposure disrupts cerebrospinal inhibition of spinal nociception but that exposure to sexual assault further promotes chronic pain risk by facilitating spinal nociception. This help may help elucidate the pain risk mechanisms in trauma survivors.