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








8 thoughts on “Motor Learning in Musculoskeletal practice

  1. Hello Kate,

    I was glad to read your post. It was very interesting and include valuable information and extensive knowledge. Yes, I agree with you that we should understand the neuroplasticity as a component in patients with musculoskeletal disorders. Also, a task oriented exercise with hundreds reps could be the best choice for some patients when we seek to a certain and specific goal, and to gain good outcomes.


    • Hello Mansour I am pleased you enjoyed the post. With regards to task repetition although to drive plastic changes high repetitions are favourable although in some cases this isn’t always practical. Do you have any thoughts on the practical application of exercise in addressing Neuroplasticity in MSK practice? Kind regards

      • Hi Kate,

        Thank for your reply. Personally, I think its difficult to apply this type of exercise with high reps in practice, especially with elderly patients, or patients who may easily get fatigue. Also, I have a question! Is there any study that compare between task oriented exercises and other functional exercises in term of functional improvement and patient satisfaction in MSK conditions?


      • Hi Kate, good post and thanks for sharing via twitter. Generally speaking you can apply strength training principles to motor learning in relation to repetitions and percentage 1RM. For neuromuscular control/learning (whatever term is vogue at the minute lol), i would generally apply <30% of 1 RM for approx 15-20 reps with rest periods of approx 2-3 minutes between sets to allow local recuperation to occur with 3-5 sets in order to achieve 45-100 reps, for 2-3 key exercises. Obviously pain free/minimal discomfort is key in order to put 'goodness into the system/individual as a whole' (along with addressing other psychosocial issues first!). I would apply these general rules for a mesocycle of approx 4-6/52 as a short term primary aim. These principles are applied widely within the MSK world but generally in younger/healthier individuals. This treatment regime has recently been applied in a patellofemoral pain webinar by simon lack ( which has really helped influence my general patient management. Again thanks for sharing via twitter.

  2. Hi Kate,
    Brilliant post, very informative and intellectual. Well done!
    Like you say in the post I don’t think I had stopped to think about what the exercise was actually doing until more recently. It’s amazing to think about how much is going on in our brains to help coordinate these movement patterns and the cortical changes that can occur. It is an interesting point that incremental gains in motor performance are reduced in the presence of pain. Often in chronic pain education, hurt is not harm is taught. So do you think the psychological belief about their pain may impact on their learning?

    • Hello Heather.Thankyou for your feedback. You have asked whether I think beliefs regarding pain can influence learning. I would say absolutely.
      It is well known psychosocial factors are linked to the development of persistent pain. In chronic pain patients the neuromatrix (the body’s network of neurones) has an increase in activity, the amygdala included which is most associated with pain memory. If patients do not have a thorough understanding of their pain in that the pain that they are feeling is an output from the brain and hold negative views regarding their pain, what it means and the consequences which most often are associated with movement and exercise skill acquisition is not likely to be successful. Many studies have shown that motor skill training is reduced when pain is present compared to when it is not. Cognition targeted exercise is an approach that is on the up in the treatment of altering pain memory. It assists in the move away from the biomedical model of practice and more towards the current biopyschosocial model that we are ever more so aware of. My 3rd post covers what we have just discussed. Feel free to take a look.

  3. Hello Kate! It is a clear demonstrated blog regarding the topic of motor learning. And it is quite practical for guiding treatment, which you discussed the topic of treatment repetition and the corporate of strength training.
    I also agree that strength training should not be perform together with motor skill training, since fatigue problem may also evolve if repetition goes to a hundred of time. While is it good to incorporate endurance training (low weight) with motor skill training, because it seems that it would be more challenging for the younger/athlete. What do you think about that?

  4. Hello kate,

    Great post about changes in motor cortex,neuroplasticity and evidences.

    I  thoroughly enjoyed reading your blog .

    I have read an article on neuroplasticity and i would like to share a part of that article here.

    I would like to have your opinion regarding this.

    Neuroplasticity is often experience dependent, time-sensitive and strongly influenced by features of environment. Motivation and attention can be critical modulators of plasticity. Skills training can improve behavioural outcomes on the backbone of neuroplasticity; in many cases, maintenance of behavioural gains depends on continued therapeutic exposure. Many covariates influence neuroplasticity. Neuroplasticity does not always have a positive impact on behavioural status and can result in negative consequences in some cases. Note too that there are many important differences between CNS disorders in neuroplasticity findings, such as the temporal course and spatial distribution of the CNS disease that incites plasticity, the extent to which ageing effects interact with plasticity, the extent to which plasticity itself directly influences disease pathogenesis, and the degree to which relevant animal models are available for the study of plasticity.

    Although a number of promising neuroplasticity-based interventions have been identified or are under study, many questions remain. Some of these have been described above, such as issues related to clinical trial methodology.

    Another principle is that not all plasticity has a positive impact on clinical status—in some cases, plasticity might have negative consequences. For example, new onset epilepsy is a common complication of cerebral trauma, often arising months to years after the insult. This delayed onset suggests that progressive changes in the brain, such as axonal sprouting and the formation of new connections, produce alterations in neuronal signalling and disinhibition that result in the induction of seizures (Prince et al). 

    Other examples suggestive of maladaptive plasticity include chronic pain and allodynia following injury to a limb (such as amputation) or to CNS (dorsal spinal cord or thalamus), dystonia after various CNS injuries and autonomic dysreflexia after spinal cord injury (Karl et al).

     Thus, recovery from trauma or disease may reflect both adaptive and maladaptive neuroplasticity, which can occur simultaneously.

    Neuropsychiatric disorders

    Brain plasticity in the setting of neuropsychiatric disorders shows some similarities with that found in the setting of CNS injury such as stroke, but also shows a number of important differences. In both settings, plasticity has been described as part of the adaptation to pathology. However, the nature of the CNS pathology in neuropsychiatric disorders results in additional forms of altered brain structure and function. Mental and addictive disorders do not result from specific localizable lesions in the nervous system, in contrast to the relatively well-defined lesions that occur in stroke and trauma. Instead, these disorders are characterized by abnormalities in the distributed limbic, prefrontal and frontostriatal neural circuits that underlie motivation, perception, cognition, behaviour, social interactions and regulation of emotion (Beauregard et al). Also in contrast to stroke and trauma, the onset of mental and addictive disorders is usually insidious; the course of illness tends to be chronic or recurring/episodic; recovery in most of these disorders is slow when present; and relapse rates are high, with each episode of illness increasing the likelihood of future episodes (Patten, 2008;Robinson and Berridge, 2008). 

    Expression of these illnesses drives change in key neural systems in the direction of ever more dysfunctional patterns underlying thoughts, emotions and complex behaviours. An important point, therefore, is that CNS plasticity, while a mechanism for achieving therapeutic gains in neuropsychiatric disorders (below) as in other settings, also has a large influence on disease pathogenesis in these disorders (Sullivan and Pfefferbaum, 2005).

    Plasticity during development can also be adaptive or maladaptive. Two cardinal examples of adaptive plasticity in relation to development are the age-dependent recovery of language and motor functions following hemispherectomy for intractable epilepsy and the ability to benefit from a cochlear implant in early childhood. After hemispherectomy, the shift of language and motor functions to the non-removed hemisphere is remarkable, but highly dependent on age, with the greatest potential for reorganization seen in children under 6 years of age (Gardner et al;Chen et alb); interpretation of such plasticity measures must bear in mind that they arise in the setting of an atypical brain at baseline. Congenitally deaf children appear to benefit most from cochlear implants within the first 3.5 years of life, a time during which the central auditory pathways show maximal plasticity. Recent research shows that the latency of the early (P1) component of the cortical auditory evoked potential falls within the normal range for age among children who receive an implant by 3.5 years of age. In contrast, those who receive implants after 7 years of age show abnormal cortical responses even years after receiving the implant (Sharma et al, 2009a).
    Another perspective on neuroplasticity with degenerative diseases is that, with increasing pathology over time, compensatory mechanisms may fail or perhaps even become pathogenic via their effects on vulnerable neuronal populations, thereby destabilizing networks (Palop et al). Neurophysiological evidence of increased association cortex responsiveness in the early stages of Alzheimer’s disease might reflect dynamic compensation for the impaired transmission of signals from primary cortex processing centres (Fernandez et al). However, over time, such compensatory activity might have detrimental consequences, possibly mediated by excitotoxic mechanisms. Similar ideas have been advanced in other neurodegenerative conditions; for example, in Huntington’s disease, the high frequency of synaptic activation required to maintain medium-sized spiny neurons in an excitable state might render these cells more susceptible to cellular stress (Milnerwood and Raymond, 2010). Clarification of whether changes in neural activity are compensatory or pathogenic may hold implications for treatment, as some network dysfunctions may be reversible. Normalization of network activity might help prevent progressive neuronal loss (Palop et al).

    so kate,

    what are your views regarding this??

    Do you think that we can use the concept of neuroplasticity in all
    the Musculoskeletal  physiotherapy patients??

    would Adult osteoarthritic patients with flare-ups and chronic pain patients would benefit from this??

    If you think yes,then are there any specific guidelines or instructions we need to consider in mind as it differs with every patient.

    Thanks a lot.

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