Menstrual cycle effects on pain modulation and autonomic arousal

Abstract

Animal research has elucidated the neurobiological substrates and environmental determinants of pain modulation. Despite these advances, relatively little is known about how psychological processes activate pain modulatory systems. One psychological process that is thought to play an important role in regulating pain sensitivity is emotion. In addition, previous research into the human menstrual cycle and the animal estrous cycle have determined that either the presence of certain gonadal hormones or the fluctuations of these hormones may lead to changes in how females perceive pain, regulate emotion, and modulate pain. The present study examines both the role of emotion and the human menstrual cycle in pain modulation. Participants were 39 female undergraduate students with a mean age of 18.7 years (SD=1.46). Results are consistent with prior studies indicating that progesterone has antiinflammatory effects. Specifically, significant effects were observed primarily in the luteal phase. Subjects in the luteal phase demonstrated less sympathetic arousal during the experiment but greater autonomic arousal during the noise stressor. Participants in the luteal phase also demonstrated an analgesic/anti-inflammatory response evidenced by an observed decrease in secondary hyperalgesia for those that did not receive the noise stressor. No such changes in pain perception were discovered in the ovulation and follicular phases. Finally, in response to the noise stressor, an inhibition of the analgesic/anti-inflammatory effects was observed in the luteal phase. No such evidence of stress-induced pain modulation was discovered in the ovulation and follicular phases. Although the specific mechanisms of this action still remain unclear, prior evidence points to the role of centrally-mediated pain modulation. It is likely that the stressor worked to inhibit the anti-inflammatory effects commonly observed in the luteal phase to persistent inflammatory pain through centrally-mediated pain modulatory mechanisms. It is hypothesized that hormone-mediated effects at the level of the amygdala influenced the impact of affective pain modulation.