It is known that some individuals with chronic pain go on to develop high blood pressure. Indeed, patients with post-surgical chronic pain have nearly twice the prevalence of clinical hypertension than medical patients without pain (Bruehl, Chung, Jirjis, & Biridepalli, 2005). Accordingly, we could postulate that a person who consistently exhibited increases in muscle sympathetic nerve activity (MSNA), blood pressure and heart rate during experimental muscle pain may - if he or she developed chronic pain from an injury in the future - go on to develop hypertension (Bruehl et al., 2005). Interestingly, long-lasting experimental muscle pain induced by hypertonic saline solution in humans causes a sustained and consistent increase in muscle vasoconstrictor drive and blood pressure in some subjects, and a sustained decrease in others (Fazalbhoy, Birznieks, & Macefield, 2012, 2014). To further our understanding of the complex physiological changes that bring about these divergent responses, this thesis has explored the association of baseline physiological and psychological levels with the direction of the sympathetic response during tonic muscle pain. Furthermore, this project included combined microneurography and neuroimaging techniques to identify areas of the brain involved in generating sustained increases or decreases in sympathetic nerve activity to muscle, as well as changes in the brain associated with the generation of MSNA bursts during experimental muscle pain. The final chapter explored the effects of an audio-visual stimulus on the direction of the response. The results reported in this thesis highlight the fact that the muscle sympathetic responses to experimental muscle pain are not based on baseline physiological or psychological parameters but are associated with different signal intensity changes in important autonomic brain regions. Furthermore, distraction from the painful stimulus through audio-visual distraction does not influence the direction of the response. While this series of experiments has shed light on the neurophysiological mechanism through which the divergent sympathetic response to experimental muscle pain arises, many questions remain to be answered. For instance, it is unknown why such divergent responses would occur in humans. Furthermore, whether these responses remain sustained over a longer period of time needs to be determined.
Date of Award | 2018 |
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Original language | English |
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- myalgia
- chronic pain
- neurophysiology
- hypertension
The neurophysiological basis of the divergent sympathetic responses to long-lasting experimental muscle pain in humans
Kobuch, S. N. (Author). 2018
Western Sydney University thesis: Doctoral thesis