Live Clinically 05 Motor Cntrol

Breaking Down Motor Control

Read Time: 8-10 min

Zach Walston working on a triathlete's foot after a race.

“To believe something is to believe that it is true; therefore a reasonable person believes each of his beliefs to be true; yet experience has taught him to expect that some of this beliefs, he knows not which, will turn out to be false. A reasonable person believes, in short, that each of his beliefs is true and some of them are false”– W.V. Quine


This post is the start of a three-part series in which I am going to attempt to tackle a ‘large and complex, although sometimes we don’t treat it that way’ topic. What comes to mind when thinking of a patient with poor movement patterns? Motor control. How about weakness? Motor control. Apprehension with movement? Motor control. Aberrant movement? Motor control. An exercise that follows the recognition of any of these problems. Motor control exercise.

Get The Point

Motor control has many similarities to Pain Science. They are large, broad topics that are often blindly applied with poor understanding of its principles. This lack of understanding of the specific causes of poor motor control and the mechanisms to improve it can lead to poor outcomes. In the realm of pain science, this can be seen in the difference between acute and chronic, fear and anxiety, nocebo and placebo, nociceptive and neuropathic, etc. Misidentifying the root cause or the factors contributing to the current perception of pain can lead to improper treatments. The same is true for motor control. I will breakdown the articles from the June 2019 issue of JOSPT over the next couple posts. This issue primarily comprised of clinical commentaries reviewing motor control with respect to low back pain. I highly encourage you to explore the articles for a deeper understanding of this broad and powerful topic.

Knowledge Is Coming

What is motor control

First things first, how do we define motor control? The simplest definition is the way in which the nervous system – motor, sensory, and central processes – controls posture and movement to perform motor tasks.[1] Motor control exercises then aim to change the way a person controls their body, often with respect to the loading of the spine and adjacent structure. Clearly, motor control training occurs in many aspects of life outside the clinic.

Learning to play the guitar, kick a soccer ball, draw something more impressive than a stick figure, and drive a manual transmission all require motor learning and control. When considering our patients, we often consider motor control in the contexts of altering loads, as ongoing mechanical stimulation of tissues can potentially activate nociceptors and initiate or prolong the inflammatory responses and pain.[2] Furthermore, when determining a “diagnosis” of a patient and an approach for examination and treatment, it is important to assess across multiple biological, psychological, and social dimensions. For example, pain provocation and relief, muscle atrophy and weakness, proprioceptive impairment, pain beliefs and fear of pain and/or re-injury, depression, catastrophizing, self-efficacy, and social issues. The question is, how do all these relate to motor control? Let’s start with general categorization and building a framework for assessment. [3]

In general, motor control of the trunk comprises modulation of intrinsic stiffness through tonic muscle activity, anticipatory control, and feedback control.[2] One method of approaching motor control is determining if a patient is demonstrating ‘loose’ or ‘tight’ control. Someone displaying tight control will have increased activation of trunk muscles both at rest and during activity. This provides greater control of the spine – specifically protection against ‘excessive’ movement – but comes with the cost of higher loads on muscles and the spinal column. Conversely, loose control refers to lower muscle activation. This avoidance of high muscle forces and compressive loading leads to reduced control over movements and the potential for applying high tensile strain to tissues. When considering ‘loose’ versus ‘tight’ control as a general framework for assessing a patient’s motor control, the challenge is determining the root cause. Both excitatory and inhibitory effects on muscle activity may result from injury and nociception, as well as anticipation or fear of pain.[4] Basically, we have a ‘chicken or egg’ conundrum.

I Dont Get It

We can largely breakdown motor control tasks into three classes: [2]

  • Control of the trunk in steady state posture and movement
  • Control of trunk posture and movement when challenged by predictable perturbations (anticipatory/feedforward control)
  • Control of trunk posture and movement when challenged by unpredictable perturbations (reactive/feedback control)

Unfortunately, there are inconsistencies among patients with respect to these three classes of movements. Outside of the preference for ‘tight’ or ‘loose’ control, we see differences among patients in the order of muscle recruitment and the speed of movement. Typically, trunk movements are performed more slowly in those with LBP compared to those without LBP.[5] Additionally, patients with LBP often display poor precision with control of trunk posture, trunk movement, and force production by trunk muscles. However, while there is evidence supporting stronger coupling of pelvic and thorax movements and reduced variability of trunk movements, many studies show the exact opposite. High individual variability may reflect poor control or it may reflect purposeful movement specific to the individual’s needs, such as fear of loading. Additionally, it may be beneficial to share load between structures or to provide exposure to new options of movement to aide learning and adaptation. Are you staring to see the complexity of motor control and the need for individuality in assessment and treatment?


The different responses to pain

Speaking of complexity, let’s layer in that other broad and complex topic, pain science. There are two primary issues to consider, the current perception of pain and the fear and anxiety related to pain. Injury and nociception can directory interfere with motor control, as it can change excitability of motor pathways at different levels of the nervous system. Things are even more gray when layering on fear. When comparing patients with LBP and those without, the motor control impairments may be more pronounced in patients who are more afraid of pain.[3] Essentially, the change is a consequence of motivation of the system to adapt as a purposeful strategy to protect the body region from further pain and injury. Surprise, surprise, patients are motivated to avoid pain.

This is not a green light to start using the phrase ‘no pain, no gain.’ It simply means, seeing a motor control impairment is often more than strict weakness; avoid the temptation to immediately run for the clam band when you see medial knee collapse during squats. Let’s take it one step further. What happens when the pain is persistent? Nothing good. Structural changes – loss of segmental stiffness, muscle atrophy, and connective tissue changes – will change the relationship between motor commands and motor output and may interfere with motor control as a result.[2]


Now what happens when the pain goes away? Does the movement pattern magically improve? Unless you are only treating healthy teenagers suffering from acute grade 1 ankle sprains, often not. The complete avoidance of movement or compensatory movement patterns repeated while in pain can become learned responses and lead to further adaptations of motor control. Those same anticipatory responses can occur despite the lack of any nociception occurring.

When considering pain and the impact it has on motor control, it is helpful to develop a clinical construct consisting of three categories:[6]

  • Pain and nociception (e.g. regulation of descending nociceptive modulation)
  • Sensorimotor function (e.g. production of motor outputs, encoding sensory inputs)
  • Cognitions and emotions (e.g. encoding beliefs and thoughts)

With respect to the processing of pain and nociception, our nervous system possesses plasticity and it may be sensitized to future stimuli. Why is this a problem you ask? Well, increased sensitivity to pain, or a lowered threshold to stimulate it, can lead to avoidance of more movements as previously innocuous stimuli may now be perceived as dangerous.[6] Patients demonstrate altered activation patterns on trunk muscles in anticipation of a noxious stimulus, even if there is no threat for actual tissue damage.[7]

This does not mean our brain is dumb and needs a session of meditation to calm down. There is a reason we have altered biomechanics and increased sensitivity to pain. After an acute injury to tissue, we want to avoid loading and stressing the tissue to allow for healing. The increased sensitivity serves as a reminder. Imagine your brain plastering a giant ‘Do Not Touch’ sign on the injured area. Additionally, the changes in muscle activation serve to enhance protection. The problem is when the alterations persist beyond normal tissue healing.

Chronic suboptimal loading of spinal tissues, avoidance of certain behaviors, and withdrawal from activity can lead to a cascade of health, social, and personal issues.[6] As pain persists, there is a shift in activity toward emotional brain areas. This leads to an increased influence of neural networks that encode for unpleasantness and decreased influence of neural networks that encode for intensity and sensory features.[8] Essentially, chronic pain has a predominance of the emotional dimensions of pain – its ‘unpleasantness’ – over the sensory discriminative dimensions of pain. What’s that? You want more specific details? I am happy to oblige.

These changes lead to reduced white matter integrity, which creates a reduction in the utilization of proprioceptive signals.[9] This can impair the accuracy of the interpretation of sensory input. Beyond that, a reorganization of the sensorimotor resting-state network can occur and modify the utility of sensory signals from the back. More simply put, chronic pain results in someone being unable to reliably trust the sensations they feel. Not only that, our ability to consciously activate muscles will change even without fear of movement. There is evidence of increased responsiveness of corticomotor inputs to the bracing strategy – using superficial muscles such as the rectus abdominus – and decreased inputs to muscles involved in subtle fine-tuning of spine control – deep muscles such as the transverse abdominus – which can limit the ability to optimally load the spine.[10]

Now What

Translating to the clinic

Now that we have a decent background on the issues with motor control and the need to treat it, what is the best approach?


Wait for it….


Wait for it…..


We don’t know. While this may come as a surprise, there isn’t a single clear-cut answer and on top of that, there are several schools of thought. We’ll cover those in the next post.

To wrap up, let’s briefly look at the big picture. Training that targets motor skill learning has been shown to normalize the location of primary motor cortex networks that are involved in activating specific trunk muscles, whereas general exercises such as walking does not.[11]Additionally, extinction training can be a powerful tool, especially for chronic pain and motor control issues. It focuses on the elimination of pain-related behaviors and the increase of healthy behaviors.[12]Diving a little deeper, a disrupted body image in patients with chronic LBP in the area of usual pain suggests the need for treatment options that focus on the reinstatement of normal body image of that strength body perception. This all points to the general idea that some level of specificity is better than generic exercise. The question remains, how specific?

My challenge to each of you, is to dive a little deeper in your “motor control” assessments. Additionally, once you have a clearer picture of the why behind the impairments and behaviors of the patient’s movement patterns, develop interventions tailored to that individual. Just as ‘exercise’ and ‘manual therapy’ are broad terms that alone do not provide the necessary detail for devising a treatment strategy, ‘motor control’ is a broad term for labeling impairments and exercise interventions.


  1. Hodges, P.W., J.H. van Dieen, and J. Cholewicki, Time to Reflect on the Role of Motor Control in Low Back Pain. J Orthop Sports Phys Ther, 2019. 49(6): p. 367-369.
  2. van Dieen, J.H., et al., Motor Control Changes in Low Back Pain: Divergence in Presentations and Mechanisms. J Orthop Sports Phys Ther, 2019. 49(6): p. 370-379.
  3. van Dieen, J.H., et al., Analysis of Motor Control in Patients With Low Back Pain: A Key to Personalized Care? J Orthop Sports Phys Ther, 2019. 49(6): p. 380-388.
  4. Hodges, P.W. and K. Tucker, Moving differently in pain: a new theory to explain the adaptation to pain. Pain, 2011. 152(3 Suppl): p. S90-8.
  5. Laird, R.A., et al., Comparing lumbo-pelvic kinematics in people with and without back pain: a systematic review and meta-analysis. BMC Musculoskelet Disord, 2014. 15: p. 229.
  6. Brumagne, S., et al., Neuroplasticity of Sensorimotor Control in Low Back Pain. J Orthop Sports Phys Ther, 2019. 49(6): p. 402-414.
  7. Moseley, G.L., M.K. Nicholas, and P.W. Hodges, Does anticipation of back pain predispose to back trouble? Brain, 2004. 127(Pt 10): p. 2339-47.
  8. Baliki, M.N. and A.V. Apkarian, Nociception, Pain, Negative Moods, and Behavior Selection. Neuron, 2015. 87(3): p. 474-91.
  9. Pijnenburg, M., et al., Microstructural integrity of the superior cerebellar peduncle is associated with an impaired proprioceptive weighting capacity in individuals with non-specific low back pain. PLoS One, 2014. 9(6): p. e100666.
  10. Tsao, H., K.J. Tucker, and P.W. Hodges, Changes in excitability of corticomotor inputs to the trunk muscles during experimentally-induced acute low back pain. Neuroscience, 2011. 181: p. 127-33.
  11. Tsao, H., M.P. Galea, and P.W. Hodges, Driving plasticity in the motor cortex in recurrent low back pain. Eur J Pain, 2010. 14(8): p. 832-9.
  12. Diers, M., et al., Treatment-related changes in brain activation in patients with fibromyalgia syndrome. Exp Brain Res, 2012. 218(4): p. 619-28.



Zach Walston, PT, DPT, OCS serves as the National Director of Quality and Research at PT Solutions. Zach grew up in Northern Virginia and earned his Bachelor of Science in Human Nutrition, Foods, and Exercise at Virginia Polytechnic Institute and State University. He then received his Doctorate of Physical Therapy from Emory University before graduating from the PT Solutions’ Orthopaedic Residency Program in 2015.  Zach now serves as the Residency Program Coordinator and the director of the practice’s Clinical Mentorship Program providing training for over 100 physical therapists a year.

Zach has numerous research publications in peer-reviewed rehabilitation and medical journals. He has developed and taught weekend continuing education courses in the areas of plan of care development, exercise prescription, pain science, and nutrition. He has presented full education sessions at APTA NEXT conference and ACRM, PTAG, and FOTO annual conferences. He has also presented multiple platforms sessions and posters at CSM. He is an active member of the Orthopedic and Research sections of the American Physical Therapy Association and the Physical Therapy Association of Georgia. He currently served on the APTA Science and Practice Affairs Committee and the PTAG Barney Poole Leadership Academy.

Zach currently lives in Marietta, GA with his wife, son, and two dogs. Connect with Zach on Twitter @zachwalston and LinkedIn.