The Neuroscience of Cortisol and Menstruation (Or Lack Thereof)

Painful periods, known clinically as dysmenorrhea, occur in the majority of women that menstruate. Dysmenorrhea causes more than just pain with menses. It can also cause pain with urination and sexual intercourse. With this seemingly universal experience, one would wonder how many of these women are at risk for chronic pelvic pain. With the increasing prevalence of dysmenorrhea, gynecological studies, specifically ones that take account in the neural feedback, are especially thought-provoking.

In the article “Cortical Mechanisms of Visual Hypersensitivity in Women At Risk for Chronic Pelvic Pain” by Kmecik, et al., multisensory hypersensitivity in women who reported pelvic pain, including dysmenorrhea, was studied. Multisensory hypersensitivity was studied because it is a risk factor for chronic pain. It was found that a “steeper positive relationship between unpleasantness and cortical excitation was observed in women with greater bladder pain”. From these results, it can be extrapolated that women suffering from pelvic pain are at increased risk for developing chronic pain. It can also be inferred that cortisol plays a positive role in the manifestation of pelvic pain.

But what about the neurological basis of women who can’t menstruate? Amenorrhea is characterized by the absence of a period without an organic cause, such as pregnancy or the use of hormone-altering contraceptives. Amenorrhea can cause many disruptions for a woman’s life, such as depression, dyspareunia, other forms of pelvic pain, and infertility in some cases. Pathophysiologically, the reported symptoms are similar to dysmenorrhea.

 Hypothalamic amenorrhea counts for almost a third of amenorrhea in women who have already experienced menarche. According to a study published in Therapeutic Advances and Metabolism titled “Current understanding of hypothalamic amenorrhoea”, the cause of HA is known to be a deficient secretion of GnRH (gonadotropin-releasing hormone). Increased cortisol was shown to inhibit release of GnRH.

Since both amenorrhea and dysmenorrhea present elevated levels of cortisol, more studies must be conducted to measure the impact of cortisol. Specifically, why do both have increased levels? Are they more similar than previously thought? Does the high cortisol come first, or does the amenorrhea or dysmenorrhea come first? The future of neurogynecology has much work to be done, but can yield great results. With many women experiencing painful reproductive abnormalities, neuroscience could serve as helping hand to these women.

Kmiecik, M. J., Tu, F. F., Silton, R. L., Dillane, K. E., Roth, G. E., Harte, S. E., & Hellman, K. M. (2020). Cortical Mechanisms of Visual Hypersensitivity in Women at Risk for Chronic Pelvic Pain. https://doi.org/10.1101/2020.12.03.20242032 

Roberts, R. E., Farahani, L., Webber, L., & Jayasena, C. (2020). Current understanding of hypothalamic amenorrhoea. Therapeutic Advances in Endocrinology and Metabolism. https://doi.org/10.1177/2042018820945854