The Sympathetic Nervous System and Pain

Abstract

The sympathetic nervous system (SNS) and pain interact on many levels of the neuraxis. In healthy subjects, activation of the SNS in the brain usually suppresses pain mainly by descending inhibition of nociceptive transmission in the spinal cord. Furthermore, some experimental data even suggest that the SNS might control peripheral inflammation and nociceptive activation. However, even subtle changes in pathophysiology can dramatically change the effect of SNS on pain, and vice versa. In the periphery, inflammation or nociceptive activation is enhanced, spinal descending inhibition is reversed to spinal facilitation, and finally the awareness of all these changes will induce anxiety, which furthermore amplifies pain perception, affects pain behavior, and depresses mood. Unraveling the detailed molecular mechanisms of how this interaction of SNS and pain is established in health and disease will help us to treat pain more successfully in the future.

Depression, anxiety and chronic pain in patients with chronic obstructive pulmonary disease: the influence of breath

“…The splanchnic nerves cross the diaphragm through small muscular spaces [38]. The sympathetic system, when activated, can amplify the pain severity, and record information related to pain perception [39]. We can assume that, if the sympathetic nerves are compressed in the region of the diaphragm, their function and morphology can change, negatively affecting the innervated tissues.…”

Autonomic Regulation in Musculoskeletal Pain

“…At the central level there is a strong connection between autonomic activation and nociception (Jänig 2003;Schlereth and Birklein 2008). Studies based on brain imaging techniques show a close anatomical and functional overlap between cortical and sub-cortical structures involved in pain processing and those controlling autonomic regulation.…”

“…Repeated painful stimulation over time may result in habituation with reduced perceived pain intensity and increased pain threshold (Bingel et al 2007); the opposite may also occur. During acute physical or psychological stress, pain is normally suppressed via the activation of the descending antinociceptive pathways, involving opioid-dependent and noradrenalin-dependent mechanisms (Benarroch 2006;Schlereth and Birklein 2008).…”

“…With chronic musculoskeletal pain, and also with chronic stress, the interaction between the nociceptive and autonomic systems appears to become maladapted (Bruehl and Chung 2004;Schlereth and Birklein 2008). Chronic neck-shoulder pain is associated with increased local pain intensity, and reduced pain thresholds in response to sympathetic stimulation (Ge et al 2006).…”

Psychosocial Stress-Induced Analgesia: An Examination of Effects on Heat Pain Threshold and Tolerance and of Neuroendocrine Mediation

“…It is modulated by opioid [9,20] and non-opioid mechanisms involving monoamines [21,22] as well as endocrine processes [23] involved in the regulation of stress. While the involvement of the corticotropin-releasing factor as well as glucorticosteroids has been found to be important in the development of SIA in animals [23,24,25,26,27,28,29], comparable endocrine evidence in humans is scarce.…”