J Anesth Perioper Med. 2015;2(4):216-225. https://doi.org/10.24015/ebcmed.japm.2015.0029

Progress in Sympathetically Mediated Pathological Pain

Si-Si Chen, and Jun-Ming Zhang

From Pain Research Center, Department of Anesthesiology, University of Cincinnati College of Medicine, Cincinnati, USA.

Correspondence to Dr. Jun-Ming Zhang at Jun-Ming.Zhang@uc.edu.

EBCMED ID: ebcmed.japm.2015.0029 DOI: 10.24015/ebcmed.japm.2015.0029


Abstract

Aim of review
Many chronic pain conditions remain difficult to treat, presenting a high burden to society. Conditions such as complex regional pain syndrome may be maintained or exacerbated by sympathetic activity. Understanding the interactions between sympathetic nervous system and sensory system will help to improve the effective management of pathological pain including intractable neuropathic pain and persistent inflammatory pain.

Method
We first described the discovery of abnormal connections between sympathetic and sensory neurons. Subsequently, the functional roles of sympathetic sprouting in altered neuronal excitability and increased pain sensitivity were discussed. The mechanisms of the sympathetic sprouting were focusing on its relationship with neurotrophins, local inflammation, and abnormal spontaneous activity. Finally, we discussed clinical implications and conflicting findings in the laboratory and clinical research with respect to the interaction between sympathetic system and sensory system.

Recent findings
The findings that sprouting of sympathetic fibers into the sensory ganglia (dorsal root ganglion) after peripheral nerve injury, offers a possible explanation of the sympathetic involvement in pain. It is also suggested that releases of adenosine triphosphate (ATP), in addition to norepinephrine, from sympathetic nerve endings play important roles in sympathetic-mediated pain. New evidence indicates the importance of sympathetic innervation in local inflammatory responses.

Summary
Hopefully, this review will reinvigorate the study of sympathetic-sensory interactions in chronic pain conditions, and help to better understand how sympathetic system contributes to this serious clinical problem.

Article Type
Review Article

Declaration of Interests
No other potential conflict of interest relevant to this review was reported.

Acknowledgements
This review was supported in part by National Institutes of Health grants NS045594 and NS055860.

This is an open-access article, published by Evidence Based Communications (EBC). This work is licensed under the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium or format for any lawful purpose. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.