Motor Learning in Musculoskeletal practice

As mentioned in my previous blog a common example of neural adaptation is learning.
In novel motor skill acquisition cortical neuroplastic changes are frequently associated with an advantageous change such as an increase in motor performance. Conversely, in persistent pain neuroplastic changes are often linked with unfavourable behaviour such as a decrease in motor performance.
As altered motor performance is thought to be a factor for the maintenance of pain, motor rehabilitation approaches that aim to re-establish normal motor strategies are an important factor to consider in the treatment of musculoskeletal pain disorders.


Image 1. New theory of Motor Adaptation to pain. (Hodges and Tucker 2011)

Learning from each other.  Collaboration between specialities

Much of the evidence that underpins the basis of neuroplasticity and the potential for re establishing normal motor strategies in musculoskeletal patients is based on evidence in patients with neurological disorders.

Recognising neuroplasticity as a component in patients with musculoskeletal dysfunction may lead to a greater understanding of neural mechanisms that influence musculoskeletal dysfunction. By addressing maladaptive neural organisation through the recognition of neuroplasticity the effectiveness of treatments that target motor behaviour such as movement quality and muscular strength could be improved.(Snodgrass et al 2014)
In stroke the best evidence based inventions that demonstrate a positive effect on neuroplasticity and motor learning are intensive repetitive practice and task specific training (Richards et al 2008, Van vliet 1993 and French et al 2007).
Although there is new found evidence in the role of neuroplasticity within musculoskeletal practice musculoskeletal Physiotherapists continue to be guided by exercise protocols justified through clinical trials (Bystrom et al 2013)

Shaping our practice

Prior to now I had not really considered the relation between pain and altered motor performance in the context of cortical reorganisation. I certainly never contemplated the principles of inducing plasticity when treating my patients.

Numerous studies have identified through the use of functional magnetic resonance imaging (fMRI) that during a painful experience there is an increase in activity in specific areas of the brain. These include the primary and secondary somatosensory cortex, insular, anterior cingulate cortex, prefrontal cornices and thalamus. (Peyron et al 2000, Henry 2000, Apkarian et al 2005)

Novel motor skill training in healthy individuals compared to passive assistance or repetitions of general exercise has been shown to improve task performance and provide an increase in representation of the trained muscle in the motor cortex (Karni et al 1995, Pascual-Leone et al 1995, Svensson et al 2003, Hlustik et al 2004).


Image 2. Primary motor cortex homunculous (Wikipedia)

Svensson et al 2003 showed during one week of novel tongue task training an increase in motor representation of the tongue muscle occurred and that there was an increase in cortical excitability of the tongue primary motor cortex. Increased cortical excitability was also demonstrated for the hand primary motor cortex following novel motor training in a study by Koeneke et al 2006.

Furthermore both studies suggest that neuroplastic changes in the motor cortex can occur over a short period. Improvements in motor performance and rapid changes in cortical excitability of the tongue primary motor cortex occurred immediately after just 15 minutes of novel tongue task training.

Based on the evidence that novel motor skill training is associated with rapid changes in cortical excitability and cortical reorganisation this training approach is considered relevant in the treatment of patients with musculoskeletal pain and movement dysfunction.          Image result for bOUDREAU 2010 MOTOR SKILL TRAINING

Figure 3. Cortical maps of the face primary motor cortex. Expansion of the tongue muscle representation following novel task training. (Svensson et al 2003)

Training the activation of a delayed or inhibited muscle through the use of repeated isolated voluntary contraction is an effective clinical approach commonly used in the management of musculoskeletal pain disorders.
Tsao et al, 2010 observed that maladaptive changes in the motor cortex reverted towards that of a healthy individual with task specific exercises in persons with low back pain.
Transcranial Magnetic Stimulation (TMS) revealed that deep abdominal muscle training consisting of voluntary activation of the Transverse Abdominals (TrA) independently from other trunk muscles induced an anterior and medial shift in motor cortical representation of the trained muscle towards that of healthy asymptomatic individuals in persons with low back pain compared to that of walking as a control intervention.
Subjects were positioned in crook lying and were instructed to activate their TrA. Electromyographic activity recorded the contraction once patients could activate with little use from their abdominals, contractions were held for 10 seconds whilst continuing to breath . 3 sets of 10 were performed twice a day.
Those in the control group were required to walk at their own pace for 10 minutes twice a day for 2 weeks.
Although the basis of using this approach is based on the principle of novel motor skill training, further key components in motor skill strategies have emerged that could advance  rehabilitation outcomes.

Skill or Strength

Motor skill training requires great skill and a high level of attention and precision in comparison to the mere contraction of a group of muscles such as strength training. A study by Remple et al 2001, identified that motor skill training coupled with strength training did not promote any greater cortical neuroplastic changes in the motor cortex compared to motor skill training alone. These findings are in keeping with the study by Tsao et al 2010, that showed an increase in reorganisation of the motor cortex following skilled training compared to that of just walking. The observation of improvements in the amplitude and speed of activation of the deep cervical flexor muscles through isolated training of these muscles as opposed to strengthening exercise in patients with neck pain further support the importance of motor skill training over strength training (Jull et al 2009).

Role of pain

Many studies that have examined the effects of acute experimental pain have found that pain can alter the excitability of the motor cortex.
Compared to the rapid changes that are associated with motor skill acquisition, the changes in cortical excitability that occur in association with experimental pain or persistent pain do not necessarily correspond to the muscle groups represented in the motor cortex. For example induced pain at the finger in a study by Koflet et al 1998, revealed an induced increase in excitability of the hand primary motor cortex but at the same time a decrease in excitability of the upper arm muscles. These pain related changes in excitability of the motor cortex may suggest why patients move differently when in pain. The findings would help to explain why maladaptive movements occur but not necessarily at the location of where we would expect.

Incremental gains in task performance have been shown not to occur when pain is present this is thought to be due to the effect that pain has on suppressing the rapid increase in cortical excitability (Boudreau et al 2007).
The belief that pain hinders novel skill acquisition is in keeping with other factors that are well known to hinder learning unfortunately such are commonly found in chronic pain patients. These include increased stress, reduced cognition, reduced quality of sleep and attention deficit.

What is the purpose?

A goal orientated sequential finger tapping task was associated with a significant increase in representation of the trained muscle in the motor cortex compared to a protocol that required mental rehearsal of the finger tapping task and even more so than the random performing of the finger tapping task.
Altering the complexity of the task was noted to further enhance cortical neuroplastic changes. A complex finger tapping task compared to a simple finger tapping task showed additional areas of cortical activation under fMRI (Pascual-Leone et al 1995). These findings suggest that purposful meaningful tasks that require cognitive effort contribute significantly to the extent of cortical neuroplastic changes.

How many repetitions? Quality versus Quantity

Hundreds of repetitions of movement in varying contexts are necessary for inducing cortical change (van Vliet et al 2012). However, it is important to remember that this is not always achievable without the presence of pain. As mentioned earlier pain does not support novel motor skill acquisition. There has been studies that suggest the use of imagery when pain prevents a patient from performing the task. Boudreau et al 2010, suggested that if rapid changes in cortical excitability are apparent following short training sessions (approx 60 within-session task repetitions over the course doc 10-15 minutes) such a high number of repetitions isn’t actually required and therefore the number of task repetitions should be based upon all of the principles discussed through the course of this post in order to improve the performance of a motor task.


Apkarian AV, Bushnell MC, Treede RD and Zubieta JK. Human brain mechanisms of pain perception and regulation in health and disease. Eur J Pain 2005;9:463-84 doi:10.1016/j.ejpain.2004.11.001

Boudreau S, Farina D and Falla D. The role of motor learning and neuroplasticity in designing rehabilitation approaches for musculoskeletal pain disorders. Manual Therapy 2010;15:410-414

Bystrom M, Rasmussen-Barr R and Grooten W. Motor control exercises reduces pain and disability in chronic and recurrent low back pain a matter analysis. Spin 2013; 38(6):E350-8

Figure 2. Cortical homonculous available at: last accessed 23/11/15

French B, Thomas LH, Leathley MJ, Sutton CJ, McAdam J and Forster A et al. Repetitive task training for improving functional ability after stroke. Cochrane database Syst Rev 2007 (4):CD006073

Hlustik P, Solodkin A, Noll DC and Small SL. Cortical plasticity during three-week motor skill learning. Journal of Clinical Neurophysiology 2004;21(3):180-91

Henry P, Creac’h C, Caille JM, and Allard M. Functional magnetic resonance imaging analysis of pain related brain activity after acute mechanical stimulation. American Journal of neuroradiology 2000;21:1402-1406

Hodges P and Tucker K. Moving differently in pain: A new theory to explain the adaptation to pain. Pain 2011;152:90-98

Jull GA, Falla D, Vicenzino B and Hodges PW. The effect of therapeutic exercise on activation of the deep cervical flexor muscles in people with chronic neck pain. Manual Therapy 2009;14(6):696-701

Koeneke S, Lutz K, Herwig U, Ziemann U and Jancke L. Extensive training of elementary finger tapping movements changes the pattern of motor cortex excitability. Experimental Brain Research 2006;174(2):199-209

Karni A, Meyer G, Jezzard P, Adams MM, Turner R and Ungerleider LG. Functional MRI evidence for adult motor cortex plasticity during motor skill learning. Nature 1995;377(6545):155-8

Kofler M, Glocker FX, Leis AA, Seifert C, Wissel J, Kronenberg MF and Fuhr P. Modulation of upper extremity motoneurone excitability following noxious finge tip stimulation in man: a study with transcranial magnetic stimulation. Neurosci Lett 1998;246:97-100

Pascual-Leone A, Nguyet D, Cohen LG, Brasil-Neto JP, Cammarota A, and Hallett M. Modulation of muscle responses evoked by transcranial magnetic stimulation during the acquisition of new fine motor skills. Journal of Neurophysiology 1995;74(3):1037-45

Peyron R, Laurent B and Garcia-Larrea L. Functional imaging brain responses to pain: a review and meta analysis. Neurophysiol Clin 2000;30:263-88

Remple MS, Bruneau RM, Vandenberg PM, Goertzen C and Kleim JA. Sensitivity of cortical movement representations to motor experience: evidence that skill learning but not strength training induces cortical reorganization. Behavioral Brain Research 2001;123(2):133-41

Richards LG, Stewert KC, Woodbury ML, Sensec C and Cauraugh  JH. Movement dependent stroke recovery: a systematic review and meta-analysis of TMS and fMRI evidence. Neurophy 2008;46:3-11

Snodgrass S Heneghan N, Tsao H, Stanwell P, Rivett D  and Van Vliet P. Recognising neuroplasticity in musculoskeletal rehabilitation: a basis for greater collaboration between musculoskeletal and neurological physiotherapists. Manual Therapy 2014; 19:614-617

Svenson P, Romaniello A, Arendt-Nielson L and Sessle BJ. Plasticity in corticomotor control of the human tongue musculature induced by tongue-task training. Experimental Brain Research 2003;152(1):42-51

Tsao H, Galae M and Hodges P. Driving plasticity in the motor cortex in the current low back pain European Journal of pain 2010

Van Vliet PM, Matyas T and Carey LM. Training principles to enhance learning-based rehabilitation and neuroplasticity. In: Carey LM, editor. Stroke Rehabilitation: insights from neurosciences and imaging. Oxford: University Press: 2012. pp. 115-26. ch. 9








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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