Peripheral tissue damage or nerve injury often leads to pathological pain processes, such as spontaneous pain, hyperalgesia and allodynia, that persist for years or decades after all possible tissue healing has occurred. Although peripheral neural mechanisms, such as nociceptor sensitization and neuroma formation, contribute to these pathological pain processes, recent evidence indicates that changes in central neural function may also play a significant role. In this review, we examine the clinical and experimental evidence which points to a contribution of central neural plasticity to the development of pathological pain. We also assess the physiological, biochemical, cellular and molecular mechanisms that underlie plasticity induced in the central nervous system (CNS) in response to noxious peripheral stimulation. Finally, we examine theories which have been proposed to explain how injury or noxious stimulation lead to alterations in CNS function which influence subsequent pain experience.

Long-term pain is a common sequela of thoracotomy, occurring in approximately 50% of patients 2 years after thoracic surgery. Despite this alarming statistic, little is known about the factors responsible for the transition of acute to chronic pain. The aim of the present study is to identify predictors of long-term post-thoracotomy pain. Follow-up was for 1.5 years for patients who had participated in a prospective, randomized, controlled trial of preemptive, multimodal analgesia. Subjects were recruited from a tertiary care center. Thirty patients who had undergone lateral thoracotomy were followed up by telephone, administered a structured interview, and classified according to long-term pain status. Present pain status was measured by a verbal rating scale (VAS). Measures obtained within the first 48 h after surgery were compared between patients with and without pain 1.5 years later. These include VAS pain scores at rest and after movement, McGill Pain Questionnaire data, patient-controlled morphine consumption (mg), and pain thresholds to pressure applied to a rib contralateral to the thoracotomy incision. Fifty-two percent of patients reported long-term pain. Early post-operative pain was the only factor that significantly predicted long-term pain. Pain intensity 24 h after surgery, at rest, and after movement was significantly greater among patients who developed long-term pain compared with pain-free patients. A significant predictive relationship was also found at 24 and 48 h using the McGill Pain Questionnaire. Cumulative morphine was comparable for the two groups. Pain thresholds to pressure applied to a rib contralateral to the incision did not differ significantly between the groups. Aggressive management of early postoperative pain may reduce the likelihood of long-term post-thoracotomy pain.

Most patients who undergo surgery recover uneventfully and resume their normal daily activities within weeks. Nevertheless, chronic postsurgical pain develops in an alarming proportion of patients. The prevailing approach of focusing on established chronic pain implicitly assumes that information generated during the acute injury phase is not important to the subsequent development of chronic pain. However, a rarely appreciated fact is that every chronic pain was once acute. Here, we argue that a focus on the transition from acute to chronic pain may reveal important cues that will help us to predict who will go on to develop chronic pain and who will not. Unlike other injuries, surgery presents a unique set of circumstances in which the precise timing of the physical insult and ensuing pain are known in advance. This provides an opportunity, before surgery, to identify the risk factors and protective factors that predict the course of recovery. In this paper, the epidemiology of chronic postsurgical pain is reviewed. The surgical, psychosocial, socio-environmental and patient-related factors that appear to confer a greater risk of developing chronic postsurgical pain are described. The genetics of chronic postsurgical pain are discussed with emphasis on known polymorphisms in human genes associated with chronic pain, genetic studies of rodent models of pain involving surgical approaches, the importance of developing accurate human chronic postsurgical pain phenotypes and the expected gains for chronic postsurgical pain medicine in the post-genomic era. Evidence is then reviewed for a preventive multimodal analgesic approach to surgery. While there is some evidence that chronic postsurgical pain can be minimized or prevented by an analgesic approach involving aggressive perioperative multimodal treatment, other studies fail to show this benefit. The transition of acute postoperative pain to chronic postsurgical pain is a complex and poorly understood developmental process, involving biological, psychological and social-environmental factors.

The purpose of this article is to describe the current state‐of‐the‐art regarding the co‐occurrence of the anxiety disorders and chronic pain. First, we describe the core characteristics of chronic pain and its co‐occurrence with the anxiety disorders. Second, we review data on the prevalence of co‐occurrence. Third, we describe the mutual maintenance and shared vulnerability models, both of which have been offered to explain the co‐occurrence of posttraumatic stress disorder (PTSD) and chronic pain and may have applicability to various other anxiety disorders. Fourth, we provide an integrative review of available research addressing the postulates of these models specific to the mechanisms of anxiety sensitivity, selective attention to threat, and reduced threshold for alarm. We conclude with general recommendations for improving assessment and treatment of patients who present with an anxiety disorder accompanied by clinically significant pain. Given that most of the available evidence has come from studies of PTSD and chronic pain, we provide a detailed agenda for future investigation of the co‐occurrence of chronic pain and other anxiety disorders. Depression and Anxiety, 2009.