The sense of body ownership represents a fundamental aspect of our self-awareness, but is disrupted in many neurological, psychiatric, and psychological conditions that are also characterized by disruption of skin temperature regulation, sometimes in a single limb. We hypothesized that skin temperature in a specific limb could be disrupted by psychologically disrupting the sense of ownership of that limb. In six separate experiments, and by using an established protocol to induce the rubber hand illusion, we demonstrate that skin temperature of the real hand decreases when we take ownership of an artificial counterpart. The decrease in skin temperature is limb-specific: it does not occur in the unstimulated hand, nor in the ipsilateral foot. The effect is not evoked by tactile or visual input per se, nor by simultaneous tactile and visual input per se, nor by a shift in attention toward the experimental side or limb. In fact, taking ownership of an artificial hand slows tactile processing of information from the real hand, which is also observed in patients who demonstrate body disownership after stroke. These findings of psychologically induced limb-specific disruption of temperature regulation provide the first evidence that: taking ownership of an artificial body part has consequences for the real body part; that the awareness of our physical self and the physiological regulation of self are closely linked in a top-down manner; and that cognitive processes that disrupt the sense of body ownership may in turn disrupt temperature regulation in numerous states characterized by both.body image ͉ consciousness ͉ crossmodal integration ͉ homeostasis

That a minor injury can trigger a complex regional pain syndrome (CRPS) - multiple system dysfunction, severe and often chronic pain and disability - has fascinated scientists and perplexed clinicians for decades. However, substantial advances across several medical disciplines have recently increased our understanding of CRPS. Compelling evidence implicates biological pathways that underlie aberrant inflammation, vasomotor dysfunction, and maladaptive neuroplasticity in the clinical features of CRPS. Collectively, the evidence points to CRPS being a multifactorial disorder that is associated with an aberrant host response to tissue injury. Varying susceptibility to perturbed regulation of any of the underlying biological pathways probably accounts for the clinical heterogeneity of CRPS.

The pain field has been advocating for some time for the importance of teaching people how to live well with pain. Perhaps some, and maybe even for many, we might again consider the possibility that we can help people live well without pain. Explaining Pain (EP) refers to a range of educational interventions that aim to change one's understanding of the biological processes that are thought to underpin pain as a mechanism to reduce pain itself. It draws on educational psychology, in particular conceptual change strategies, to help patients understand current thought in pain biology. The core objective of the EP approach to treatment is to shift one's conceptualization of pain from that of a marker of tissue damage or disease to that of a marker of the perceived need to protect body tissue. Here, we describe the historical context and beginnings of EP, suggesting that it is a pragmatic application of the biopsychosocial model of pain, but differentiating it from cognitive behavioral therapy and educational components of early multidisciplinary pain management programs. We attempt to address common misconceptions of EP that have emerged over the last 15 years, highlighting that EP is not behavioral or cognitive advice, nor does it deny the potential contribution of peripheral nociceptive signals to pain. We contend that EP is grounded in strong theoretical frameworks, that its targeted effects are biologically plausible, and that available behavioral evidence is supportive. We update available meta-analyses with results of a systematic review of recent contributions to the field and propose future directions by which we might enhance the effects of EP as part of multimodal pain rehabilitation. Perspective: EP is a range of educational interventions. EP is grounded in conceptual change and instructional design theory. It increases knowledge of pain-related biology, decreases catastrophizing, and imparts short-term reductions in pain and disability. It presents the biological information that justifies a biopsychosocial approach to rehabilitation.

Complex regional pain syndrome type 1 (CRPS1) involves cortical abnormalities similar to those observed in phantom pain and after stroke. In those groups, treatment is aimed at activation of cortical networks that subserve the affected limb, for example mirror therapy. However, mirror therapy is not effective for chronic CRPS1, possibly because movement of the limb evokes intolerable pain. It was hypothesised that preceding mirror therapy with activation of cortical networks without limb movement would reduce pain and swelling in patients with chronic CRPS1. Thirteen chronic CRPS1 patients were randomly allocated to a motor imagery program (MIP) or to ongoing management. The MIP consisted of two weeks each of a hand laterality recognition task, imagined hand movements and mirror therapy. After 12 weeks, the control group was crossed-over to MIP. There was a main effect of treatment group (F(1, 11) = 57, P < 0.01) and an effect size of approximately 25 points on the Neuropathic pain scale. The number needed to treat for a 50% reduction in NPS score was approximately 2. The effect of treatment was replicated in the crossed-over control subjects. The results uphold the hypothesis that a MIP initially not involving limb movement is effective for CRPS1 and support the involvement of cortical abnormalities in the development of this disorder. Although the mechanisms of effect of the MIP are not clear, possible explanations are sequential activation of cortical pre-motor and motor networks, or sustained and focussed attention on the affected limb, or both.

Motor imagery reduced pain and disability in these patients with complex regional pain syndrome type I or phantom limb pain, but the mechanism, or mechanisms, of the effect are not clear.

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Disability is an important outcome from a clinical and public health perspective. However, it is unclear how disability develops in people with low back pain or neck pain. More specifically, the mechanisms by which pain leads to disability are not well understood. Mediation analysis is a way of investigating these mechanisms by examining the extent to which an intermediate variable explains the effect of an exposure on an outcome. This systematic review and meta-analysis was aimed to identify and examine the extent to which putative mediators explain the effect of pain on disability in people with low back pain or neck pain. Five electronic databases were searched. We found 12 studies (N=2,961) that examined how pain leads to disability with mediation analysis. Standardized regression coefficients (â) of the indirect and total paths were pooled. We found evidence to show that self-efficacy (â = 0.23, 95% CI = 0.10-0.34), psychological distress (â = 0.10, 95% CI = 0.01-0.18), and fear (â = 0.08, 95% CI = 0.01-0.14) mediated the relationship between pain and disability, but catastrophizing did not (â = 0.07, 95% CI = -0.06-0.19). The methodological quality of these studies was low and we highlight potential areas for development. Nonetheless, the results suggest that there are significant mediating effects of self-efficacy, psychological distress, and fear, which underpins the direct targeting of these constructs in treatment.

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