Sensorimotor incongruence as (one) cause of pain?

Motor actions are planned and steered from the brain. Input from eyes, muscles, joints, skin and vestibular system continuously inform the brain about actual movements. Simultaneously, this information is compared with the motion program (that what was predicted) in the brain, which is important for adjusting motor plans and ensuring smoothness of motor action. This process is normal automatic and implicit, but we can made aware of it when incongruence exists between that what the brain predicted to do (the motion program) and that what really occurred. This may lead to the experience of pain and other sensations, in the same way as a conflict between visual and vestibular input may result in motion sickness.

In a recently published paper in Rheumatology, we investigated the hypothesis that pain results from incongruence between predicted and actual sensory feedback. Interestingly, we found that inducing sensorimotor incongruence by manipulating the visual input resulted in the experience of sensations such as  loss of control, feeling of peculiarity, weight changes and discomfort, but not pain, in healthy subjects. These findings confirm the notion that sensorimotor incongruence can induce sensations, however, are in contrast with the aspect of the cortical pain model proposing that sensorimotor incongruence elicits pain.

In patients with chronic whiplash associated disorders (WAD), reducing or disturbing the visual input (via hiding a moving limb) seemed to be sufficient to exacerbate symptoms and/or elicit additional sensations. No additional effect was observed when visual input (manipulated by using a mirror) conflicts with proprioceptive feedback. These findings suggest that patients with chronic WAD rely heavily on visual input of neck and upper limbs to reassure the brain about movements. In addition, the results indicate altered perception of distorted visual feedback and support the presumption of body schema disruption in chronic WAD. Disturbing the visual input can further modify the body schema and hence, modulate pain and other sensations. Following this, therapy strategies which intend to restore the visual input and improve the sensorimotor integration at cortical level may lead to symptom relief in chronic WAD. Although further research is warranted to examine these assumptions.

In conclusion, our work shows that sensorimotor incongruence can generate sensations, but not pain, in healthy subjects and that reducing or disturbing the visual input is sufficient to exacerbate symptoms in patients with chronic WAD. Although the mechanism underpinning the abovementioned observations and its role in the development and/or maintenance of pain and other symptoms remains to be revealed and hence, requires further study. More in-depth understanding of it may help to improve treatment strategies.

 About Liesbeth Daenen

Liesbeth Daenen is a doctoral researcher at the University of Antwerp (Belgium) and the Vrije Universiteit Brussel (Belgium). She is interested in the role of central mechanism and their interaction in (chronic) unexplained pain. Her work focuses on changes in sensorimotor integration and pain processing mechanisms and, pain-motor interactions in patients with whiplash associated disorders.


Daenen L, Nijs J, Roussel N, Wouters K, Van Loo M, & Cras P (2012). Sensorimotor incongruence exacerbates symptoms in patients with chronic whiplash associated disorders: an experimental study. Rheumatology (Oxford, England), 51 (8), 1492-9 PMID: 22525161


  1. stuart miller says:

    I was wondering if there are studies that had looked at activation sequences of muscles in chronic WAD and healthy controls under conditions of sensorimotor incongruence. The concepts of local stabilizers, global stabilizers and mobilizers are obviously too simple to encompass the integrated movement patterns of humans but wondered what recent studies might have been done. I have not usually had patients with ataxia complain of pain as their primary reason for seeking my services – isn’t this a simple example of sensorimotor incongruence ? As well, the visual system anticipates movement (forward projecting) but what happens when there is decreased kinaesthetic and vestibular integration with precise visual control – vestibular rehab scratches the surface but the integration of multiple systems in therapy seem to be needed. Any help ?

  2. Interesting study.
    I wonder if you contact an auto insurance company and request statistics as to the rate of subscribers seeking care for whiplash and compare the rates of those who were at fault to those who were the victim, what that might say about the role of the mind in whiplash syndrome pain? I honestly cannot recall that in over 13 years I have treated the person at fault in an motor vehicle accident, for chronic whiplash pain!
    H. Schrader from Norway published two studies of interest to the mind-body factors possibly at work in whiplash syndrome: Lancet. 1996, 347: 1207-11 and European Journal of Neurology. 2006, 13: 1226-32.
    Also, the degree of the physical injury sustained does not correlate to the likelihood of developing chronic whiplash pain (see Malik and Lovell, Spine. 2004, 29: E315-7).
    Even more fascinating, see Castro et al, International Journal of Legal Medicine. 2001, 114:316-22… placebo induced whiplash correlated to the degree of stress present, “central autonomic and limbic priming” as I call it.
    Finally, what about demolition derby drivers?? See Simotas and Shen, Archives of Physical Medicine and Rehabilitation. 2005, 86:693-6.
    Perception of harm is a critical factor… the biology of victimization is a critical factor… pre-existing neural procedural memory, and degree of stress at time of injury, reflect central, limbic and autonomic priming, as critical factors in non-pathological “whiplash” pain. I believe the term is, in some respects (in non-pathological form), a form of collective mind-body syndrome, not unlike the prevalence of hysterical paresis prior to the advent of deep tendon reflex testing, thereafter which it largely disappeared due to lack of public acceptance and associated stigma.
    For effective treatment, see Unlearn Your Pain by Dr. Howard Schubiner.

    Karen Reply:

    Hi Matt,

    I would respectfully suggest that mechanism of injury between your two hypothetical cohorts is at play if the statistics bore fruit. The driver “at fault” usually has the foresight to brace and possibly an airbag to disperse impact forces. The driver struck, often has no luxury of warning or appreciable dispersal of impact forces. Genetic and gender predisposition to centralisation of pain are also important factors in post trauma pain experiences. Stress post trauma from reluctant insurers, medical providers and employers adds more to the cognitive burden. Imprecise neuroimmune anti-inflammatory response, especially in patients headed toward centralisation of their pain is rarely addressed. The above article provides excellent reasoning that the application of visual motor therapy as well as graded motor therapy might help resolve WAD symptoms.

    I am curious if the study results can be extrapolated to certain subgroup of failed spinal surgery patients and LBP patients who report exacerbation of symptoms walking on different incline patterns?

    Danny Reply:

    Hi Karen
    I am interested in your comment ‘imprecise neuro-immune anti-inflammatory response’. rather cheekily I am curious about your reasoning about this and the idea that you suggest it may be addressed (through gmi and visual motor therapy). Perhaps you could be more explicit?!