Cortisol and nightmares: the role of neuroendocrine stress response

Maria R D’Orsogna

Maria R D’Orsogna

Professor, California State University, Northridge; Adjunct Professor, UCLA Biomathematics Department

Maria R D’Orsogna received her PhD in Theoretical Physics from UCLA in 2003. She is a professor of Mathematics at the California State University, Northridge and holds an adjunct professor position in the Biomathematics Department in the Medical School at UCLA. Currently, she is the Associate Director of the Institute for Pure and Applied Math at UCLA.


Her scientific interests cover a wide range of topics, primarily within biology and sociology using tools from statistical mechanics, game theory, numerical simulations, and stochastic processes. She has worked on mathematical models of virology, cell biology, neuroendocrine systems, multi-particle swarming, crime hotspot formation, sectarian violence, networks of organized crime. Collaborations with experimental or social scientists usually help inform the proper approaches to be used, to understand dynamics and mechanisms, identify optimal strategies and possibly formulate new and relevant questions.

Prof. D’Orsogna is the author of more than fifty referred publications; her work is supported by the NSF and by the Army Research Office.

Nightmares are a most prevalent feature of PTSD and other major anxiety disorders. Several studies associate frequent nightmares to an inherent deficit of stimulatory hormone levels, specifically cortisol. The latter is regulated by the hypothalamic-pituitary-adrenal (HPA) axis, a neuroendocrine system that regulates numerous physiological processes. The HPA axis is known to be disrupted in PTSD patients who generally manifest lower cortisol levels than control individuals. Nightmares/low cortisol can thus be interpreted as a hallmark of PTSD. In this talk, we present a mathematical model to describe the HPA axis which yields two steady-state configurations:  a "normal" (high basal, normal sleep, cortisol state) and a "diseased" state (low basal, frequent nightmares, cortisol state). The model includes hormonal self-upregulation, release, synthesis; interaction, delay and feedback mechanisms. External input is associated to psychological trauma, while parameter changes represent physiological damage. We show that transitions between the normal and diseased states may be induced solely by external input, with all physiological parameters unchanged, emphasizing the severe consequences of psychological trauma.