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








Pain. A view not so ordinary


As literature suggests there is more to pain, than what was previously thought of as merely a basic physiological reaction to a noxious stimulus. How pain is viewed, is shaped by a whole host of factors.

A function of pain is to demand attention and motivate behaviour to deal with an injury. (Eccleston & Crumbez 1999).

If pain is considered a threat, the greater the threat the more attention is given. Attention to pain may then be linked to fear and anxiety and the necessity to take action.
Vigilance, a term referring to an abnormal focus on possible signs of pain or injury (Leeuw et al 2007), provides an understanding of why a seemingly small injury can result in serious pain. This process highlights the close link between emotional and cognitive processes and attention.
Cognitive processes are used to interpret the information received. The cognitive process is closely linked with emotional processes as how we perceive a noxious stimulus is shaped by our past experiences. This would explain how it is difficult to “think about something else ” when pain is present and in contrast how when attempts to suppress pain are made the experience of pain can be heightened. Cognitive processes rationalise why sometimes an insignificant stimulus such as light touch can be experienced as severe pain or a serious injury as little or no pain.

We all posses some form of opinion on what pain is and what it would feel like to feel ‘pain’. The beliefs we hold about pain are useful as they can serve as a catalyst in the interpretation of stimuli. Accelerating the process our brain undertakes in making sense of the vast amount of stimuli that our brain needs to interpret, thus becoming a sort of automatic interpretation process. However, this natural tendency can lead to detrimental responses.
Main et al (2010) & Leeuw et al (2008) found there are a number of attitudes and beliefs related to the development of persistent pain and disability in patients with low back pain.These include the idea that “hurt is harm” that if it hurts then something serious is wrong and that “rest is the best cure” pain is a signal to rest and therefore any provoking activity should be avoided.
Buitenhuis et al (2008) supports such correlation between beliefs and pain persistence, their study found that there was a link between causal beliefs and prognostic value in patients experiencing neck pain post whiplash.

Normally when we feel pain we have some idea of its cause how it should be managed and how long we should expect before it is better. How our expectations are managed have also been proven to be good predictors of outcome by a number of studies both in patients with low back pain and neck pain.
We each make sense of incoming information differently. However, for a number of reasons some people fall into a cognitive trap where not intentionally but through error, their misinterpretation of actual or probable future events becomes reality (Linton, 2005 and Barlow 2004).
Pain catastrophising is an example of such a process. Typically catastrophic thoughts are assumptions. “The pain I have, if it continues will cause me not to walk again.”. Therefore, it is not surprising that pain catastrophising is associated with a variety of barriers that hinder recovery, thus making treatment more difficult and the chance of developing persistent pain and disability higher. In keeping with previous research into the development of chronic pain Buitenhuis et al (2008) also found that the severity of neck disability post whiplash event was related to pain catastrophising, however to what extent was unclear. Severeijns et al (2001) too concludes that pain catastrophising significantly contributes to pain related disability.

Anxiety, worry, and depression are all common emotional reactions to pain. It is well known within the literature, that emotions are powerful drivers of behaviour. Therefore, how these emotions are regulated by a person will impact on their experience of pain.
Fear, although short in duration is an emotion that prepares us for “fight or flight” a form of anxiety, that plays a huge part in our thought processes and behaviour.According to Salkovskasis and Warwick (2001) anxiety disorders are typically more prevalent in people with persistent pain than in those who aren’t.
Depression defined by Bair et al (2003) as a psychological problem characterised by negative mood, hopelessness, and despair is a common emotional state that has a powerful effect on the pain experience. There are a number of studies, that have found that patients who have depression pre treatment have poorer rehabilitation outcomes and that the incidence of developing chronic pain is a lot higher. Most research that I have found is in patients experiencing low back pain.

So… what does this all mean to us as clinicians? In my subsequent post this is something I hope to answer.

Reference List

Bair M, Robinson R, Katon W, Kroenke K Depression and pain comorbidity: A literature review Archives of Internal Medicine. 2003; 163: 10: 2433-2445

Barlow D Anxiety and it’s disorders: The Nature and Treatment of Anxiety and Panic; 2nd edition. New York, NY: Guildford Press 2004

Buitenhuis J, de Jong P, Jaspers J, Groothoff J Catastrophising and Causal beliefs in Whiplash. Spine. 2008; 33: 22: 2427-2433

Eccleston C, Crombez, G Pain demands attention: a cognitive-affective model of the interruptive function of pain. Psychological bulletin. 1999; 125: 356-366

Leeuw M, Goosens M, Linton, S The fear avoidance model of musculoskeletal pain: current state of scientific evidence. Journal of Behavioural Medicine. 2007; 30: 77-94

Leeuw M, Goosens M, Van Breukelen G Exposure in vivo versus operant graded activity in chronic low back pain patients: results of a randomised controlled trial Journal of Behavioural Medicine. 2008; 138: 192-207

Linton S, Understanding Pain for Clinical Practice. Edinborough, Scotland, elsevier, 2005

Main C, Foster N, Buchbider R How important are back pain beliefs and expectations for satisfactory recovery from back pain? Best Practice and Research Clinical Rheumatology. 2010; 24: 205-217

Severeijns R, Vlaeyen J, Van den Hout, Weber W Pain Catastrophising Predicts Pain intensity, Disability, and Psychological Distress Independent of the Level of Physical Impairment the Clinical Journal of Pain. 2001; 17: 165-172

Thompson D, Urmston M, Oldham J, Woby S The association between cognitive factors, pain and disability in patients with idiopathic chronic neck pain Disability and Rehabilitation. 2010; 32 (21): 1758-1767

Villemure C, Bushnell M Cognitive modulation of pain: how do attention and emotion influence pain processing. Journal of Pain. 2002; 95: 195-199