The bigger picture: Pain and Cortical Change

Neuroplasticity has been defined as “the ability of the nervous system to respond to intrinsic and extrinsic stimuli by reorganising its structure, function and connections” (Cramer 2010)

A common example of neural adaptation that all can relate to is learning. Most I am sure have heard the term ‘practice makes perfect’ and some are aware of conditioning paradigms; remember being told the story of Pavlov and his experiment with dogs?

Central sensitisation is another example of adaptation. Allodynia and Hyperalgesia are known to be a symptom of central sensitisation and occur as a consequence of repeated activation of spinal nociceptors. Both symptoms can provide a biological advantage by increasing sensitivity to peripheral inputs. Increased sensitivity can potentially optimise the possibility of tissue healing and assist in preventing further injury. However ongoing sensitisation can pose a problem of its own when its benefit is lost such as in chronic pain.
It is well evidenced that among individuals with chronic pain the mere thought of a task can evoke pain and swelling. Equally, the observing a task  can elicit a painful response and the development of swelling though no action has taken place (Acerra and Mosely, 2005 and Mosely 2004).

Phantom limb pain and neuropathic pain following spinal cord injury were among the first pain states that identified a relation between pain and primary sensory cortex reorganisation. However, a wealth of evidence has since emerged that suggests a similar correlation exists  in patients with chronic musculoskeletal pain.

Mercier and Leonard, 2011 carried out a review that looked at the relation between pain and the motor cortex in patients with phantom limb pain and complex regional pain syndrome. Due to my musculoskeletal bias and purpose of this blog I shall  cover findings around complex regional pain syndrome.The review found that indeed there was evidence of change in motor cortex reorganisation in patients with complex regional pain syndrome.  The size of cortical representation of muscles on the affected side was found to be reduced in comparison to the unaffected side. Intra-cortical inhibition was found to be reduced in the motor cortex again in the unaffected side or bilaterally. Consistent with this reduced inhibition, an fMRI study showed that during a finger tapping exercise there was greater activation within the motor cortex and other areas when the exercise was performed by the affected hand compared to the unaffected. Such findings support that these alterations in motor function may be as a consequence of changes at cortical level and not just peripheral or spinal level.The review highlighted that several other factors may contribute to the reorganisation in the motor cortex other than pain alone as patients with chronic pain often have other sensorimotor defecits that could have an impact of motor-cortex excitability.  Motor  cortex  reorganisation was also thought to be dependent on the chronicity of the pain. The review hypothesised that cortical changes may also vary  dependent on the pain population. This hypothesis was based on studies that observed changes that occur at the level of somatosensory cortices. In patients with phantom limb pain and complex regional  pain the representation of the painful area decreased but increased in patients with low back pain and patients suffering from fibromyalgia. Thus suggesting cortical responses are specific to pathologies. The review posed the question: is it pain that drives plasticity within the motor cortex or, conversely does the motor cortex plasticity contribute to the development of chronic pain? Attempting to cover this may make me diverse somewhat and so I welcome ideas from the reader.

Camille et al, 2015 investigated whether there was a difference in motor cortical organisation among those with knee osteoarthritis (OA). The study  aimed to ascertain whether there was an association between cortical organisation and accuracy of a motor task.  11 participants who had moderate to severe OA and 7 asymptomatic individuals whom served as the control group were required to perform 3 visually guided, variable force, force matching motor tasks involving isolated muscle contractions of the knee (quadriceps), ankle (tibialis anterior), and hand (finger/thumb flexors). fMRI data was used to map the location of peak activation in the motor cortex during the three tasks. The results showed that there were differences in the organisation of the motor cortex during the performance of the knee and ankle motor tasks in those participants with knee OA. The differences in organisation was also related to the quality of performance of the knee motor task in this group too.

The differences in organisation presented as an anterior shift of the knee representation and a switching of the relative anterior-posterior arrangement of the knee and ankle representations in those with OA. The range of shift in the motor cortex representation was related to poorer performance and was specific to the knee. Organisation of the ankle and hand representations did not differ.
The greater the anterior location of the site of peak motor cortex activation during the knee tasks in those with OA in comparison to the site of those without OA signified substantial remodelling of that brain region.
The difference in location was measured and a similar range of remodelling of the motor cortex was also found in a study by Tsao et al, 2011 that looked at the representation of the longissimus erector spinal muscle in the back representation. Such changes in representation of muscles in the motor cortex was also linked with reduced coordination of trunk muscles. (Tsao et al 2008)
A systematic review by Henry et al, 2011 further supports the findings by Tsao et al, 2011 in the reorganisation of the motor cortex in chronic back pain. Schabrun et al, 2015 also confirmed that cortical reorganisation is accountable for clinical features of back pain. A general consensus among the literature is that  the amount of reorganisational change in chronic back pain increases with the chronicity of pain and not the intensity of the pain.

Lastly  a study by Ngomo et al, 2015 whom looked at whether rotator cuff tendinopathy lead to changes in central motor representation of a rotator cuff muscle. 39 participants with unilateral rotator cuff tendinopathy were recruited. The motor representation of infraspinatus was assessed bilaterally. Infraspinatus was chosen as according to Reddy et al, 2000 it is a rotator cuff muscle for which its movement pattern has been shown to be altered during arm elevation among those with rotator cuff tendinopathy. Also it is the only rotator cuff muscle that electromyographic activity can be directly recorded using surface electrodes.
In contrast to findings among other papers I’ve read the results of this study did not reveal any significant differences between the two hemispheres in cortical map location. However similar to other studies the study did show a higher motor threshold indicating a decrease in corticospinal excitability on the side of a rotator cuff tendinopathy. It too proposed that cortical changes is dependent on the duration of the pain. Most  studies that analyse cortical reorganisation  use functional MRI, this study used transcranial magnetic stimulation perhaps that may have implications on the findings.

So what’s next, what do these findings mean to us as clinicians and how does it alter our practice? Part 2 to come…


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