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Sympathetic Neural Control in Humans with Anxiety‐Related Disorders

Jeremy A. Bigalke, Jason R. Carter

10.1002/cphy.c210027

Source: Volume 12, Issue 1, January 2022

Published online: December 2021

Full Article on Wiley Online Library



Abstract

Numerous conceptual models are used to describe the dynamic responsiveness of physiological systems to environmental pressures, originating with Claude Bernard's milieu intérieur and extending to more recent models such as allostasis. The impact of stress and anxiety upon these regulatory processes has both basic science and clinical relevance, extending from the pioneering work of Hans Selye who advanced the concept that stress can significantly impact physiological health and function. Of particular interest within the current article, anxiety is independently associated with cardiovascular risk, yet mechanisms underlying these associations remain equivocal. This link between anxiety and cardiovascular risk is relevant given the high prevalence of anxiety in the general population, as well as its early age of onset. Chronically anxious populations, such as those with anxiety disorders (i.e., generalized anxiety disorder, panic disorder, specific phobias, etc.) offer a human model that interrogates the deleterious effects that chronic stress and allostatic load can have on the nervous system and cardiovascular function. Further, while many of these disorders do not appear to exhibit baseline alterations in sympathetic neural activity, reactivity to mental stress offers insights into applicable, real‐world scenarios in which heightened sympathetic reactivity may predispose those individuals to elevated cardiovascular risk. This article also assesses behavioral and lifestyle modifications that have been shown to concurrently improve anxiety symptoms, as well as sympathetic control. Lastly, future directions of research will be discussed, with a focus on better integration of psychological factors within physiological studies examining anxiety and neural cardiovascular health. © 2022 American Physiological Society. Compr Physiol 12:1‐33, 2022.

Figure 1. Figure 1. Representative baroreflex response to transient blood pressure reductions with electrocardiogram (ECG, top), blood pressure (middle), and muscle sympathetic nerve activity (MSNA, bottom) recordings at rest in a supine subject. As blood pressure falls, sympathetic nerve activity increases to normalize blood pressure back to its homeostatic set‐point (solid box). Conversely, as blood pressure begins to rise, sympathetic nerve activity is reduced (dashed box).
Figure 2. Figure 2. Neural recruitment mechanisms that contribute to increased strength of a sympathetic burst. Reused, with permission, from Macefield VG, et al., 2002 209.
Figure 3. Figure 3. Schematic representation of the relationship between occurrence of action potential clusters and integrated MSNA burst size. Larger multiunit bursts are associated with larger action potential clusters, indicating recruitment of normally silent, large axons. DBP, diastolic blood pressure. Reused, with permission, from Salmanpour A and Shoemaker JK, 2012 273.
Figure 4. Figure 4. Relationship between level of perceived stress in response to both the Stroop Color Word Task and mental arithmetic, and subsequent neurovascular responses. Asterisks (*) mark significant differences between responses to the SCWT and MA. SCWT, Stroop Color Word Task; MA, mental arithmetic; MSNA, muscle sympathetic nerve activity. Reused, with permission, from Callister R, et al., 1992 30.
Figure 5. Figure 5. Relationship between subjectively reported anxiety symptoms and sympathetic neural reactivity to mental arithmetic and cold pressor test in controls and generalized anxiety disorder patients combined. (A) Relative MSNA burst amplitude reactivity to mental arithmetic and cold pressor test compared to subjective anxiety levels, (B) MSNA burst incidence reactivity to mental arithmetic and cold pressor test compared to subjective anxiety levels. Reused, with permission, from Holwerda SW, et al., 2018 148.
Figure 6. Figure 6. Percentage of neural bursts with one, two, three, or four or more single‐unit spikes in individuals with panic disorder and healthy controls. Asterisks (* or **) indicate significant differences between individuals with PD and healthy adults. PD, panic disorder. Reused, with permission, from Lambert E, et al., 2006 193.
Figure 7. Figure 7. Reactivity of systolic blood pressure (A), diastolic blood pressure (B), mean arterial pressure (C), heart rate (D), MSNA burst frequency (E), and total MSNA (F) in response to simulated combat in individuals with posttraumatic stress disorder (PTSD) and healthy controls. SBP, systolic blood pressure; DBP, diastolic blood pressure; MAP, mean arterial pressure; HR, heart rate; MSNA, muscle sympathetic nerve activity. Reused, with permission, from Park J, et al., 2017 255.
Figure 8. Figure 8. Sympathetic neural reactivity to a cold pressor test in chronic insomniacs and healthy controls. Total MSNA reactivity to a cold pressor test (A) as well as representative microneurographic recordings from both healthy individuals (B, top) and individuals with chronic insomnia (B, bottom) are shown. Asterisks (*) indicate significantly elevated total MSNA reactivity to the cold pressor test in individuals with chronic insomnia compared to healthy controls. MSNA, muscle sympathetic nerve activity. Reused, with permission, from Carter JR, et al., 2018 39.
Figure 9. Figure 9. Chronic anxiety may result in development of disorders such as panic disorder (PD), posttraumatic stress disorder (PTSD), generalized anxiety disorder (GAD) as well as comorbid major depressive disorder (MDD). Sympathetic dysfunction has been demonstrated in these populations primarily through altered reactivity to mental stressors. However, many questions remain regarding the underlying sympathetic recruitment patterns, as well as inter‐individual differences in the dysfunctional sympathetic activity observed in highly anxious populations. BRS, baroreflex sensitivity; mMSNA, multiunit muscle sympathetic nerve activity; sMSNA, single‐unit muscle sympathetic nerve activity; AP, action potential.


Figure 1. Representative baroreflex response to transient blood pressure reductions with electrocardiogram (ECG, top), blood pressure (middle), and muscle sympathetic nerve activity (MSNA, bottom) recordings at rest in a supine subject. As blood pressure falls, sympathetic nerve activity increases to normalize blood pressure back to its homeostatic set‐point (solid box). Conversely, as blood pressure begins to rise, sympathetic nerve activity is reduced (dashed box).


Figure 2. Neural recruitment mechanisms that contribute to increased strength of a sympathetic burst. Reused, with permission, from Macefield VG, et al., 2002 209.


Figure 3. Schematic representation of the relationship between occurrence of action potential clusters and integrated MSNA burst size. Larger multiunit bursts are associated with larger action potential clusters, indicating recruitment of normally silent, large axons. DBP, diastolic blood pressure. Reused, with permission, from Salmanpour A and Shoemaker JK, 2012 273.


Figure 4. Relationship between level of perceived stress in response to both the Stroop Color Word Task and mental arithmetic, and subsequent neurovascular responses. Asterisks (*) mark significant differences between responses to the SCWT and MA. SCWT, Stroop Color Word Task; MA, mental arithmetic; MSNA, muscle sympathetic nerve activity. Reused, with permission, from Callister R, et al., 1992 30.


Figure 5. Relationship between subjectively reported anxiety symptoms and sympathetic neural reactivity to mental arithmetic and cold pressor test in controls and generalized anxiety disorder patients combined. (A) Relative MSNA burst amplitude reactivity to mental arithmetic and cold pressor test compared to subjective anxiety levels, (B) MSNA burst incidence reactivity to mental arithmetic and cold pressor test compared to subjective anxiety levels. Reused, with permission, from Holwerda SW, et al., 2018 148.


Figure 6. Percentage of neural bursts with one, two, three, or four or more single‐unit spikes in individuals with panic disorder and healthy controls. Asterisks (* or **) indicate significant differences between individuals with PD and healthy adults. PD, panic disorder. Reused, with permission, from Lambert E, et al., 2006 193.


Figure 7. Reactivity of systolic blood pressure (A), diastolic blood pressure (B), mean arterial pressure (C), heart rate (D), MSNA burst frequency (E), and total MSNA (F) in response to simulated combat in individuals with posttraumatic stress disorder (PTSD) and healthy controls. SBP, systolic blood pressure; DBP, diastolic blood pressure; MAP, mean arterial pressure; HR, heart rate; MSNA, muscle sympathetic nerve activity. Reused, with permission, from Park J, et al., 2017 255.


Figure 8. Sympathetic neural reactivity to a cold pressor test in chronic insomniacs and healthy controls. Total MSNA reactivity to a cold pressor test (A) as well as representative microneurographic recordings from both healthy individuals (B, top) and individuals with chronic insomnia (B, bottom) are shown. Asterisks (*) indicate significantly elevated total MSNA reactivity to the cold pressor test in individuals with chronic insomnia compared to healthy controls. MSNA, muscle sympathetic nerve activity. Reused, with permission, from Carter JR, et al., 2018 39.


Figure 9. Chronic anxiety may result in development of disorders such as panic disorder (PD), posttraumatic stress disorder (PTSD), generalized anxiety disorder (GAD) as well as comorbid major depressive disorder (MDD). Sympathetic dysfunction has been demonstrated in these populations primarily through altered reactivity to mental stressors. However, many questions remain regarding the underlying sympathetic recruitment patterns, as well as inter‐individual differences in the dysfunctional sympathetic activity observed in highly anxious populations. BRS, baroreflex sensitivity; mMSNA, multiunit muscle sympathetic nerve activity; sMSNA, single‐unit muscle sympathetic nerve activity; AP, action potential.
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Article Title: Sympathetic Neural Control in Humans with Anxiety‐Related Disorders
 

How to Cite

Jeremy A. Bigalke, Jason R. Carter. Sympathetic Neural Control in Humans with Anxiety‐Related Disorders. Compr Physiol 2021, 12: 3085-3117. doi: 10.1002/cphy.c210027