The sensorimotor theory of pathological pain revisited

Harris (1999) proposed that pain can arise in the absence of tissue damage because changes in the cortical representation of the painful body part lead to incongruences between motor intention and sensory feedback. This idea, subsequently termed the sensorimotor theory of pain, has formed the basis for novel treatments for pathological pain. Here we review the evidence that people with pathological pain have changes to processes contributing to sensorimotor function: motor function, sensory feedback, cognitive representations of the body and its surrounding space, multisensory processing, and sensorimotor integration. Changes to sensorimotor processing are most evident in the form of motor deficits, sensory changes, and body representations distortions, and for Complex Regional Pain Syndrome (CRPS), fibromyalgia, and low back pain. Many sensorimotor changes are related to cortical processing, pain, and other clinical characteristics. However, there is very limited evidence that changes in sensorimotor processing actually lead to pain. We therefore propose that the theory is more appropriate for understanding why pain persists rather than how it arises.

Automated summary

Harris proposed that pain can occur without tissue damage, leading to incongruences between motor intention and sensory feedback. This theory has been the basis for novel treatments for pathological pain. In this article, we review the evidence of changes in sensorimotor function in people with pathological pain and suggest that the theory is more suitable for understanding why pain persists rather than how it arises.