Nerve damage takes place during surgery. As a consequence, significant numbers (10%–40%) of patients experience chronic neuropathic pain termed surgically induced neuropathic pain (SNPP). The initiating surgery and nerve damage set off a cascade of events that includes both pain and an inflammatory response, resulting in “peripheral and central sensitization,” with the latter resulting from repeated barrages of neural activity from nociceptors. In affected patients, these initial events produce chemical, structural, and functional changes in the peripheral and central nervous systems (CNS). The maladaptive changes in damaged nerves lead to peripheral manifestations of the neuropathic state—allodynia, sensory loss, shooting pains, etc, that can manifest long after the effects of the surgical injury have resolved. The CNS manifestations that occur are termed “centralization of pain” and affect sensory, emotional, and other (eg, cognitive) systems as well as contributing to some of the manifestations of the chronic pain syndrome (eg, depression). Currently there are no objective measures of nociception and pain in the perioperative period. As such, intermittent or continuous pain may take place during and after surgery. New technologies including direct measures of specific brain function of nociception and new insights into preoperative evaluation of patients including genetic predisposition, appear to provide initial opportunities for decreasing the burden of SNPP, until treatments with high efficacy and low adverse effects that either prevent or treat pain are discovered.
This article evaluates the effects of traumatic induced neuropathic pain that commonly follows surgery. The complexity of the perioperative period, aside from the surgery itself, can result in chronic neuropathic pain that is not simply from a damaged peripheral nerve but changes in the central nervous system as a result of sensitization of pain.
*Department of Anesthesia and Perioperative and Pain Medicine, Boston Childrens Hospital, Harvard Medical School, Boston, MA
†Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA
‡Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA.
Reprints: David Borsook, MD, PhD, Department of Anesthesia Perioperative and Pain Medicine, Harvard Medical School, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115. E-mail: firstname.lastname@example.org.
Disclosure: This work was supported by a grant from NINDS to DB (K24 NS064050).