Autonomic Dysfunction

Team: Justen Geddes1, Tess Jones1, Ben Randall1, Mette Olufsen1, Brian Carlson2, Jesper Mehlsen3, Johnny Ottesen4

Affiliations:1NC State University, 2University of Michigan, 3Rigshospitalet, Denmark, 4Roskilde University

Recent Publications:

  1. Postural Orthostatic Tachycardia Syndrome explained using a baroreflex response model
    J Geddes, JT Ottesen, J Mehlsen, MS Olufsen
    Journal of Royal Society Interface, 2022
  2. Global sensitivity analysis informed model reduction and selection applied to a Valsalva maneuver model
    EB Randall, NZ Randolph, A Alexanderian, MS Olufsen
    Journal of Theoretical Biology, 2021
  3. Classification of orthostatic tolerance through data analytics
    S Gilmore, J Hart, J Geddes, CH Olsen, J Mehlsen, P Gremaud, MS Olufsen
    Medical & Biological Engineering & Computing, 2021
  4. Characterization of blood pressure and heart rate oscillations of POTS patients via uniform phase empirical mode decomposition
    J Geddes, J Mehlsen, MS Olufsen
    IEEE, 2020
  5. Persistent instability in a nonhomogeneous delay differential equation system of the Valsalva maneuver
    EB Randall, NZ Randolph, MS Olufsen
    Mathematical biosciences, 2020
  6. A model-based analysis of autonomic nervous function in response to the Valsalva maneuver
    EB Randall, A Billeschou, LS Brinth, J Mehlsen, MS Olufsen
    Journal of Applied Physiology 127, 2019

The cardiovascular system as a whole is controlled both neurally and hormonally, maintaining homeostasis. In our work, we model the reflexive neurological control systems governing blood pressure and heart rate. Primarily, we focus on the autonomic nervous system (ANS), which involuntarily controls vital bodily functions (e.g., breathing, heart rate, blood pressure, pupil dilation, etc.). When these systems do not function normally, the body suffers from ANS dysfunction can arise idiopathically or in conjunction with several diseases and disorders (e.g., Parkinson's disease, diabetes, etc.). Our goal is to understand the physiological differences between the healthy and disease states to (i) quantify these changes in cardiovascular function, (ii) detect early biomarkers for ANS dysfunction, and (iii) provide plausible hypotheses contributing to the dysfunction.


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