Pain normally provides our nervous system with useful information (e.g. by alerting us to potential harm). Yet sometimes pain persists long after an injury has healed, at which point it can be considered pathological. Many people with pathological pain conditions can present with neuropsychological changes that might impair sensorimotor processing, such as distorted body representations. According to the sensorimotor theory of pain (Harris, 1999), pathological pain could have a cortical origin. According to the sensorimotor theory of pain (Harris, 1999), pathological pain could have a cortical origin. He postulated that sensorimotor incongruence could be driving several pathological pain conditions. Such an incongruence was proposed to arise from a discrepancy between the predicted outcome of a movement (e.g. sensory, motor, proprioceptive), and the “true” sensory outcome (i.e. the sensory feedback). I will address this idea in my thesis, and aim to further our understanding of the role of sensorimotor incongruence in pathological pain. First, I present a comprehensive review of the existing literature to evaluate how sensorimotor processing might be altered in a broad range of pathological pain conditions, and if such changes are related to pain. I conclude that there is support for many of the hypotheses that can be derived from the theory. Next, I address some of these hypotheses experimentally in a clinical population, and a non-clinical population where pain was induced experimentally. Specifically, I look at sensorimotor processing in people with Complex Regional Pain Syndrome (CRPS), and in an experimental acute pain model. I find evidence of altered updating of bodily and spatial representations for people with CRPS, relative to controls, which is not seen in an acute pain model. Such changes could interfere with predicting the sensory outcome of a movement. In contrast, I find no evidence to suggest that sensorimotor adaptation is impaired. This finding opposes theoretical predictions, as it suggests that people with CRPS should be able to adapt to incongruent sensorimotor information. Taken together, the main contribution of my thesis is 1) to highlight areas in which sensorimotor processing might be altered in people with CRPS, which cannot be explained by the presence of acute pain, and 2) to challenge one of the assumptions underpinning the sensorimotor theory of pain. The broader findings from my thesis have implications for the sensorimotor theory of pain, and treatments that target sensorimotor processing for pain relief. For instance, they suggest that therapies focused on improving bodily and motor representations might be more appropriate for people with CRPS than those targeting sensorimotor adaptation. I conclude that the sensorimotor theory of pain does not provide a complete explanation of the changes seen in people with pathological pain conditions, and suggest ways of refining the theory. Nonetheless, the theory is a useful framework within which to generate testable hypotheses that focus on specific aspects of sensorimotor processing that appears to be altered in pathological pain conditions.
|Date of Award||16 Sep 2020|
|Sponsors||Medical Research Council|
|Supervisor||Janet Bultitude (Supervisor), Michael Proulx (Supervisor), Gavin Buckingham (Supervisor) & Mark Wilson (Supervisor)|