Low back pain

Non-specific low back pain affects people of all ages and is a leading contributor to disease burden worldwide. Management guidelines endorse triage to identify the rare cases of low back pain that are caused by medically serious pathology, and so require diagnostic work-up or specialist referral, or both. Because non-specific low back pain does not have a known pathoanatomical cause, treatment focuses on reducing pain and its consequences. Management consists of education and reassurance, analgesic medicines, non-pharmacological therapies, and timely review. The clinical course of low back pain is often favourable, thus many patients require little if any formal medical care. Two treatment strategies are currently used, a stepped approach beginning with more simple care that is progressed if the patient does not respond, and the use of simple risk prediction methods to individualise the amount and type of care provided. The overuse of imaging, opioids, and surgery remains a widespread problem.

The tendency to "catastrophize" during painful stimulation contributes to more intense pain experience and increased emotional distress. Catastrophizing has been broadly conceived as an exaggerated negative "mental set" brought to bear during painful experiences. Although findings have been consistent in showing a relation between catastrophizing and pain, research in this area has proceeded in the relative absence of a guiding theoretical framework. This article reviews the literature on the relation between catastrophizing and pain and examines the relative strengths and limitations of different theoretical models that could be advanced to account for the pattern of available findings. The article evaluates the explanatory power of a schema activation model, an appraisal model, an attention model, and a communal coping model of pain perception. It is suggested that catastrophizing might best be viewed from the perspective of hierarchical levels of analysis, where social factors and social goals may play a role in the development and maintenance of catastrophizing, whereas appraisal-related processes may point to the mechanisms that link catastrophizing to pain experience. Directions for future research are suggested.

The role of the brain in chronic pain conditions remains speculative. We compared brain morphology of 26 chronic back pain (CBP) patients to matched control subjects, using magnetic resonance imaging brain scan data and automated analysis techniques. CBP patients were divided into neuropathic, exhibiting pain because of sciatic nerve damage, and non-neuropathic groups. Pain-related characteristics were correlated to morphometric measures. Neocortical gray matter volume was compared after skull normalization. Patients with CBP showed 5-11% less neocortical gray matter volume than control subjects. The magnitude of this decrease is equivalent to the gray matter volume lost in 10-20 years of normal aging. The decreased volume was related to pain duration, indicating a 1.3 cm3 loss of gray matter for every year of chronic pain. Regional gray matter density in 17 CBP patients was compared with matched controls using voxel-based morphometry and nonparametric statistics. Gray matter density was reduced in bilateral dorsolateral prefrontal cortex and right thalamus and was strongly related to pain characteristics in a pattern distinct for neuropathic and non-neuropathic CBP. Our results imply that CBP is accompanied by brain atrophy and suggest that the pathophysiology of chronic pain includes thalamocortical processes.