I appreciate the comments by Drs. Kakazu and Julka. Although the role of the sympathetic nervous system in certain chronic pain states, including complex regional pain syndrome (CRPS), has been well documented,1,2its role in acute pain and inflammation is still controversial.3,4A coupling between the sensory afferent and sympathetic efferent system after peripheral nerve lesions has been previously described as a causative mechanism for neuropathic pain, including CRPS.1,2However, the role of the sympathetic nervous system in acute pain still must be elucidated. The sympathetic nervous system may influence the nociceptive response to acute tissue injury in two ways.4First, there is a potentiation of the chemical mediator cascade after trauma as well as augmentation of sensitization to substance P. Second, norepinephrine and α2agonism in the dorsal horn neurons and in the locus ceruleus in the medulla play a major role in the descending medullospinal inhibition of nociception. Experimental studies in rats indicate that sympathetic postganglionic neurons may be involved in the generation of pain, hyperalgesia, and inflammation after tissue damage or trauma.5,6Sensitization of nociceptive afferent fibers in the knee joints of rats involves a cascade of events in which the mast cell and the sympathetic terminal are sequentially activated, resulting in plasma extravasation in the synovium.5,6Further, adrenal medullary-derived epinephrine can exacerbate and surgical or pharmacologic sympathectomy can decrease the severity of experimental arthritis.5Although these behavioral studies in rats point to a potential role of the sympathetic nervous system in acute inflammatory pain, neurophysiologic studies of nociceptors in rats and psychophysical studies in humans have failed to provide confirmatory evidence for the role of sympathetic efferents in inflammatory pain and hyperalgesia.3
The use of a stellate ganglion block for acute postoperative pain as described by Drs. Kakazu and Julka is intriguing. I agree with the authors that because this patient sustained his fracture 1 week before surgical correction, prolonged sensitization and alteration of nociceptive afferent pathways may have increased the risk for the development of postsurgical CRPS. However, the authors did not report whether this patient had any clinical symptoms consistent with CRPS before surgical intervention. Perhaps the surgical intervention exacerbated an underlying disease process that may have been initiated before surgery. Interestingly, since the success of our original report on the efficacy of stellate ganglion blocks for CRPS patients undergoing surgery,7many of our surgeons now request that we routinely perform this sympathetic block for non-CRPS patients who are undergoing surgical procedures and are at increased risk for development of this disease. Although stellate ganglion block may be effective for treating acute postoperative neuropathic pain, it may also be useful in the management of acute nociceptive pain. Matsuura et al. 8describe the efficacy of stellate ganglion block in 29 patients undergoing ocular surgery. These authors report a significant reduction in postoperative pain and nonsteroidal antiinflammatory drugs with the use of stellate ganglion block. These case studies highlight the importance of moving from symptom control toward a mechanism-specific pharmacologic management of postoperative pain.9We have only begun to identify the multiple neurobiologic mechanisms responsible for different pain states. We hope to be able to develop diagnostic tools that will allow us to identify these mechanisms in individual patients and target them with appropriate analgesic interventions. Future research is needed in defining the clinical significance of the interaction of the sympathetic nervous system and the somatic afferent system in the development of postoperative pain. At that time, we may have available not only the resources for eliminating acute pain but also the tools necessary for preventing the occurrence of chronic postsurgical pain.
Baystate Medical Center and the Tufts University School of Medicine, Springfield, Massachusetts. firstname.lastname@example.org