Pain, The Brain and Motor Control

I find this topic quite heavy going for my Brain! But I think that it is an important area of growth in knowledge that we should be aware of.

I have tried to summarise some of the key points from four of the most recent articles I have read in relation to this topic. The first article is a nice summary of the topic, the final three being quite detailed.

To finish off the post I have summarised a theory from Hodges (2011) and, Hodges and Tucker (2011), regarding Motor Control and Adaptation to Pain.

Pain, The Brain and Motor Control

Moseley and Flor (2012)

  • Pain is a conscious experience (cannot exist outside of consciousness).
  • Nociception can exist outside of consciousness.
  • Pain emerges from the brain according to the apparent danger to body tissues and the need for a concerted response from the individual, not according to activity in nociceptive fibers or the actual state of the tissues.
  • Sensitization occurs in the spinal cord and supraspinal centers. In people with chronic pain:
    • Seeing a painful limb being touched can evoke pain and swelling even when the limb is not actually touched.
    • Imagined movements of a chronically painful limb can increase pain and swelling in the absence of detectable muscle activity or limb movement.
    • These clinical observations demonstrate that sensitization is not confined to a single sensory modality and that pain can be evoked through non-nociceptive channels.
  • Cortical reorganization in people with persistent pain is not limited to sensory and motor representations. There is evidence of disruption across efferent systems. For example, perceptual and autonomic disturbances are particularly common in CRPS.
  • Patients who show high levels of pain behaviors, and are very incapacitated by their pain, appear to benefit from operant behavioral treatment.
    • The goals are to:
      • Decrease pain behaviors
      • Increase healthy behaviors related to work, leisure time, and the family
      • Reduce medication
      • Change the responses of significant others from solicitous to distracting or ignoring.
  • The cognitive-behavioral approach teaches patients various techniques to effectively deal with episodes of pain. Components include:
    • Pain coping strategies, such as diversion of attention, use of imagery or relaxation that increase self-efficacy, and cognitive reappraisal.
    • Increased activity
    • Pacing
    • Activity planning.
    • Education about pain and the factors that modulate it.
  • Conclusions:
    • A large body of evidence shows that chronic pain is associated with disruption of a range of body-related cortical representations. There is some evidence that this disruption contributes to, or maintains, chronic pain.
    • Treatments that target sensory and cognitive representations using sensory and motor strategies (to normalise cortical representations) show clear functional and symptomatic benefits.

Wand et al (2011)

  • CLBP is characterised by a range of structural, functional and neurochemical changes within the brain.
  • Neurochemical Changes:
    • Shifts in neurochemical profile in anterior cingulate cortex, thalamus and prefrontal cortex can differentiate between those with CLBP and healthy controls.
    • There is clear evidence that brain neurochemistry is awry in people with CLBP, there is no evidence to suggest that neurochemical changes cause CLBP.
  • Structural Changes:
    • Compelling evidence of reduced gray matter in the DLPFC, the right anterior thalamus, the brainstem, the somatosensory cortex and the posterior parietal cortex of people with CLBP.
  • Cortical Representation:
    • A representation can be thought of as a network of neurons that represent something else, for example a word, thought, joint, immune response, or article of knowledge.
    • Representation of the lower back in the primary somatosensory cortex (S1) is shifted medially and expanded, invading the area where the leg is normally represented and that the extent of expansion is closely associated with pain chronicity.
      • Similar findings in CLBP patients who were distressed, but not in those who were not, raises the possibility that S1 shifts may not be a feature of CLBP so much as the emotional impact of CLBP.
  • Cortical Activity and Responsiveness:
    • CLBP patients have significantly lower increases in blood flow in the periaqueductal gray (an important part of the descending antinociception system) than controls when exposed to equally painful stimuli.
    • Shifts in primary motor cortex representation have also been reported in people with CLBP.
    • Raised motor thresholds have been reported for the lumbar back muscles of CLBP patients, which suggest decreased corticospinal drive to these muscles.
  • Clinical Implications:
    • Enhanced response to noxious stimuli:
      • The neurochemical and functional changes that have been observed in people with CLBP should sensitise the neural networks that subserve nociception and pain.
      • Brain areas that demonstrate neurodegeneration are known to be involved in antinociception.
      • Changes in sensitivity away from the back (i.e. widespread) implicate cortical rather than peripheral or spinal mechanisms.
      • Hyperalgesia at remote sites has been shown to be positively correlated with self reported pain intensity, physical function and pain duration.
        • Interestingly it is negatively correlated with degenerative lumbar disc disease or radiculopathy.
    • Psychological and Cognitive Effects:
      • CLBP patients have been shown to:
        • Be impaired on a task designed to assess emotional decision making. Performance was negatively related to pain intensity.
        • Demonstrate significant impairments in memory, language skills and mental flexibility and reduced ability to shift attention away from pictures of physical activities associated with the threat of back injury.
      • Brain changes may need to be considered as an additional contributor to psychological dysfunction.
    • Altered Body Perception:
      • LBP patients:
        • Exhibit deficits in proprioception.
        • Perform poorly on a task that required subjects to make judgements on the direction of trunk rotation adopted by a model.
        • Have poorer tactile acuity.
        • Are worse at identifying letters that are traced on their back.
        • Find it difficult to delineate the outline of their back when asked to complete a drawing of ‘how it feels’.
      • It is also possible that the varied alterations in trunk muscle recruitment patterns evident in CLBP patients may be a manifestation of a disturbance in body perception.
  • Conclusions:
    • One could argue that the manifestations of cortical changes at least make rehabilitation more difficult, and indeed may prove to contribute to the problem, as well as the failure of common treatment approaches.
    • Seems reasonable to suggest that the brain may be a legitimate target for new therapies.

Apkarian (2011)

  • Brain Activity for Chronic Pain:
    • Chronic pain seems to involve brain regions far more involved in emotions and self-evaluation and less involved in the activation of regions associated with acute nociception.
  • Brain Anatomical Changes:
    • Decreased regional gray matter density was first described in chronic back pain patients………our results suggest that these changes are not specific to any fixed set of brain areas and involve widespread regions of the brain.
    • The decrease in gray matter density is at least partially reversible when underlying pain is properly treated.
      • These studies are important as they indicate that at least some of the morphological changes must be a direct consequence of the presence of the pain.
    • Recent research shows that when chronic pain is effectively treated, specific regional gray matter decreases are reversed, and this reversal is related to the extent of pain relief and also to renormalization of cognitive abilities.

Baliki et al (2011)

  • CBP has a unique brain representation different from that of acute pain.
  • Elevated spontaneous CBP pain was perpetuated by:
    • Sustained activation of the medial prefrontal cortex (a region involved in emotional/self-referential information processing) and punctuated by transient nociceptive input that perpetuate the state of continued negative affect (suffering) regarding the self in CBP patients.
    • These results, coupled with behavioral data, showing impaired performance of CBP patients on a gambling task, led us to the conclusion that chronic pain can no longer be fully characterized within the classical pain system.
    • We reasoned that CBP might indeed impact and modulate brain functions beyond the pain system itself.

Motor Control and Adaptation to Pain

If we take all of the above potential “Brain Changes” information into account then I think the following summary of Hodges (2011), and Hodges and Tucker (2011) puts forward a nice theory on Motor Control and Adaptation to Pain. The 5 key points of the theory being:

  1. Redistribution of activity within and between muscles:
    1. The new theory proposes that rather that a uniform increase or decrease of activity there is an adaptation that may vary between individuals and tasks to change the mechanical response to protect the tissues or remove threat .
  2. Altered mechanical behaviour:
    1. A central premise of the new theory is that the redistribution of activity within and between muscles changes the mechanical outcome of contraction.
    2. Redistribution of activity between trunk muscles also changes kinematics and mechanical properties of the spine.
      1. Stiffness of the trunk is increased in clinical back pain.
      2. Spinal movement is necessary to dampen forces.
      3. Some variability in performance of movement has the advantage of varying the areas of joint load, muscle activity, and ligament stress. This would be compromised if the adapted protective strategies lead to a reduction in variation.
  3. Protection from further pain or injury, or from threatened pain or injury:
    1. Many different adaptations in muscle activity may achieve protection.
    2. The unique feature proposed in the new theory is that rather than a stereotypical change that is the same in all conditions, we propose the nervous system has a range of options to achieve the goal of protection, and this may involve increased, decreased, or redistributed activity. This will involve more complex neural processes than those proposed by the existing theories that advocate stereotypical change.
  4. Changes at multiple levels of the motor system:
    1. These changes may be complementary, additive, or competitive. Examples of the changes being:
      1. The mechanisms at each site may be different. For instance:
        1. Spinal effects may be mediated by direct input of nociceptive afferents on motoneurons or functional plasticity in the spinal cord (i.e. central sensitisation)
        2. Cortical changes may be due to changes in motor planning, such as the recruitment of a more protective strategy in advance of movement or reorganisation of cortical regions.
        3. The net output of the motor system would be dependent on the relative impact of the events throughout the motor system, and this may vary between individuals and tasks, which may account for some of the variability in experimental findings.
  5. Short-term benefit, long term consequences:
    1. A final aspect of the theory is that although the adaptation achieves a short-term goal of protection from further pain/injury the adaptation may have consequences that could lead to further problems in the long term.
      1. This could be due to increased or modified load, decreased movement, decreased variability, or other changes.

An interesting topic…….discussion welcome!

References:

Apkarian AV. The brain in chronic pain: clinical implications. Pain Manag. 2011 Nov 1;1(6):577-586.

Baliki MN, Baria AT, Apkarian AV. The cortical rhythms of chronic back pain. J Neurosci. 2011 Sep 28;31(39):13981-90.

Hodges PW. Pain and motor control: From the laboratory to rehabilitation. J Electromyogr Kinesiol. 2011 Apr;21(2):220-8.

Hodges PW, Tucker K. Moving differently in pain: a new theory to explain the adaptation to pain. Pain. 2011 Mar;152(3 Suppl):S90-8.

Moseley GL, Flor H. Targeting cortical representations in the treatment of chronic pain: a review. Neurorehabil Neural Repair. 2012 Jul-Aug;26(6):646-52.

Wand BM, Parkitny L, O’Connell NE, Luomajoki H, McAuley JH, Thacker M, Moseley GL. Cortical changes in chronic low back pain: current state of the art and implications for clinical practice. Man Ther. 2011 Feb;16(1):15-20.

About the Author:

Mark is a Specialist Musculoskeletal Physiotherapist who consults at both Insight Physiotherapy and Pain Options, in Perth, Western Australia. He specialises in the assessment and management of persistent/chronic musculoskeletal pain. In addition to his clinical role he maintains regular involvement in education of the profession having held a Teaching Fellow position at the University of Western Australia for 10 years and regularly presenting at courses and seminars through the Australian Physiotherapy Association and private education sector. Mark is also a Facilitator for the Australian College of Physiotherapists Specialisation Training Program and a Branch Councillor on the Western Australian Branch of the Australian Physiotherapy Association.

Post a Comment

%d bloggers like this: