Scapula Stability Exercises, Challenging Current Practice : A guest article by Chris Littlewood

So yet again I am pleased to give you another fantastic guest article, this time from Chris Littlewood a physio and a research fellow at the University of Sheffield. He is currently undertaking a PhD in relation to rehabilitation of rotator cuff tendinopathy and has recently published a book entitled Understanding Physiotherapy Research (here). His full biography can be found here

Chris has kindly done an excellent article for us fitting in with the critical thinking theme of this site by questioning the role the scapula does or doesn't have in shoulder pains and problems, and if we are doing the right thing in giving scapula stability exercises, take it away Chris…

Scapula stabilisation exercises are commonly prescribed as a core component of rehabilitation programmes for many types of shoulder pain syndromes, particularly subacromial impingement syndrome or rotator cuff tendinopathy (Littlewood et al. 2012). There appears to have been an unquestioned proliferation of such prescription despite doubts raised in the literature about the relevance of scapula dyskinesia and the role of scapula stabilisation exercises in these painful shoulder syndromes.

This paper will consider some of the relevant evidence with the aim of stimulating the reader to question the rationale which appears to currently underpin the prescription of scapula stabilisation exercises across the spectrum of patients complaining of shoulder pain without significant movement restriction.


Normal or ideal positions and movement patterns of the scapula, in association with the glenohumeral joint, have previously been described (Kibler and McMullen 2003). Aberrations from this ideal, broadly referred to as scapula dyskinesis, are thought to contribute to the development and maintenance of various painful shoulder syndromes, including subacromial pain syndrome (Struyf et al. 2013). Broadly, scapula stabilisation exercises are prescribed to address and correct these aberrations with the intention of reducing the associated pain and disability. Such a “cause and effect” model appears plausible and logical, i.e. joint/ tissue movement deviates from normal which results in dysfunction and possible overload which subsequently results in a pain syndrome. If the movement aberration is addressed then the dysfunction and possible overload should be minimised or removed and the pain syndrome should abate. Despite the clarity and plausibility of such a pathway, messages have appeared in the literature that serve to question this reasoning process and these will now be considered in turn.

Relevance of scapula dyskinesia

It seems logical to suggest that if scapula dyskinesis contributes to painful shoulder syndromes then such movement aberrations would present more in those complaining of shoulder pain and less so in those who do not complain of shoulder pain. Previous studies have investigated whether there is such an association between dyskinesia, measured in various ways, and shoulder pain and have concluded that the evidence does not support such a theory (Catlin et al. 1995; Lucasiewicz et al. 1999). This evidence highlights that scapula dyskinesis is present in those with and without painful shoulder syndromes.

Further to this, a recent study evaluated movement of the scapula in healthy subjects (Morais and Pascoal 2013). In comparison to the scapula of the non-dominant shoulder, this study found that the scapula of the dominant shoulder showed greater retraction and upward rotation at all points during elevation of the arm. This is an interesting finding because the presence, absence or relevance of scapula dyskinesis in a painful shoulder syndrome is often identified in comparison to the asymptomatic shoulder. This study questions the validity of such an assessment process and also further highlights the presence of relative movement differences in the scapulae of asymptomatic or healthy individuals.

However, such evidence, in isolation, should not be used to discount the relevance of scapula dyskinesis entirely, at least not at this stage. It is theoretically plausible that shoulder pain presents at the end of a continuum which begins with dyskinesia and, secondary to a gradual build-up of overload, over time ends with pain. Subsequent evidence however might add weight to the argument that scapula dyskinesis is less relevant to shoulder pain than we think.

Assessment of dyskinesia

There are many different approaches to the assessment of scapula dyskinesis including static, dynamic, low-tech and high-tech approaches. If scapula dyskinesis is to be regarded as a credible basis upon which treatment is prescribed then it seems fair to suggest that practitioners should be able to agree upon its presence or absence and relevance when assessing their patients. Many researchers have investigated whether therapists can reliably detect what is considered clinically significant dyskinesis over recent years and generally they report poor levels of reliability (Ellenbecker et al. 2012). This means that whereas one practitioner might suggest that there is a deviation from normal, it is highly likely that another practitioner would disagree. Therefore even if scapula dyskinesis is related to the shoulder pain syndrome, is this a credible basis upon which to prescribe a treatment? Although such poor levels of reliability are not unique to the assessment of scapula dyskinesis, it still serves to question the credibility of such an approach.

Mechanism of action

Thus far it has been suggested that scapula dyskinesis is present in those with and without shoulder pain and that practitioners struggle to agree whether such aberrations are present, absent or relevant. Notwithstanding these concerns, scapula stabilisation rehabilitation protocols have evolved with the explicit aim of addressing such dyskinetic movement patterns (Kibler et al. 2013). Hence it seems reasonable to suggest that if these rehabilitation protocols are implemented and shoulder pain is diminished, then the dyskinetic movement patterns should also improve. A recent study evaluated this and found that despite significant improvements in shoulder pain and disability at the end of treatment and after three months, the measurements of scapula dyskinesis did not change (Struyf et al. 2013).

In contradiction to the evidence from Struyf et al (2013), Baskurt et al (2011) found that following a six-week programme of exercise which included scapula stabilisation exercises, scapula dyskinesis did improve compared to the control group who received a programme of stretching and strengthening exercises but not specifically scapula stabilisation exercises. A closer look at the study tells us that scapula dyskinesis was evaluated using the Lateral Scapula Slide Test (LSST). This test measures the distance between the thoracic spine and the inferior angle of the scapula but the reliability of this test has been questioned (Shadmehr et al. 2010). This means that any reported differences could be attributable to measurement error rather than being representative of a true difference. More importantly the LSST could have been subject to outcome assessor bias. The LSST relies on a person to take the measurements and if this person, the outcome assessor, is aware that the person they are measuring received the programme including scapula stabilisation exercises then they are more likely to assess the LSST in a favourable way, i.e. one that suggests a change has occurred. This is a common flaw in much research and is addressed by ‘blinding’ the outcome assessor. This means that the person undertaking any measurements is not aware of which treatment has been received and hence the potential for bias is minimised. However, this was not reported to have been undertaken in this study

Therefore although conclusions from Baskurt et al (2011) might be seen to question the conclusions of the Struyf et al (2013), it is possible that methodological flaws explain the reported differences.

Looking more broadly it is apparent that the finding, that stabilisation exercises do not improve stability or reduce dyskinesis, is not unique to the shoulder. A recent systematic review of studies (Laird et al. 2012) found that movement-based interventions for low back pain, e.g. stabilisation exercises, were rarely found to be effective for changing observable movement patterns, e.g. dyskinesia. These researchers were also unable to identify a relationship between changes in movement patterns and improvement in pain or disability, which fits with the studies referred to here in relation to the shoulder. These studies, and others, contribute to the increasing body of evidence which is now questioning those who approach the rehabilitation of pain syndromes from a purely biomechanical perspective.

Clinical effectiveness

In the context of what has been suggested so far, it is questionable whether the clinical effectiveness of scapula stabilisation exercises needs to be considered. However, for completeness, clinical effectiveness will be reviewed although there is a paucity of such evidence due to the emerging nature of the field. Struyf et al. (2013) investigated whether exercises focused upon the scapula were superior to a control intervention that included exercise, manual therapy, including glenohumeral mobilisation and friction massage, and electrotherapy directed at the rotator cuff. After three months there were no significant differences between the groups in terms of self-reported shoulder pain and disability as measured by the Shoulder Disability Questionnaire. There are methodological limitations associated with this study including a small sample size (n = 22) and the fact that only one therapist delivered both the control and intervention treatments which introduces the potential for therapist preference bias, i.e. the therapist has a preference for one treatment and delivers this in a different (superior) way to the non-preferred treatment. This is important in therapy-based research because if a therapist or practitioner has a strong preference for one treatment or another, which many of us do, then the process and subsequent outcomes are likely to be affected by this. Despite this potential for bias, no significant differences were reported after three months.

Buskart et al (2011) reported no significant difference when comparing one group that received stretching, strengthening and scapula stabilisation exercises and a second group that received stretching and strengthening exercises only. Both groups reported a favourable outcome at the end of the six-week treatment period. This was measured, amongst other tests, by the Western Ontario Rotator Cuff Index (WORC). The WORC is a condition-specific self-reported outcome measure that is used to evaluate the quality of life of people with problems relating to the rotator cuff (de Witte et al. 2012). As with the study by Struyf et al (2012), methodological limitations did exist. Most notable was the low number of participants recruited (n=40), which means that the study might not have adequate statistical power to detect a true difference between groups if one actually did exist.

On balance of the evidence presented so far, it is unclear whether scapula dyskinesis is relevant to shoulder pain and it is questionable whether practitioners can identify such aberrations. Furthermore, it is questionable whether scapula stabilisation exercises do “what they say on the tin” because the studies reviewed here do not convincingly show that dyskinesia changes following a scapula stabilisation rehabilitation programme. Finally, although there is a paucity of evidence and concern about the quality of the research that has been conducted to date, approaches that focus upon scapula stabilisation do not appear to confer superior clinical outcomes to other, more generalised, exercise approaches.

Implications for practice

These issues, relating to the relevance and assessment of scapula dyskinesis and the value of scapula stabilisation exercises, raise a number of implications for practice. Firstly, if the relevance of scapula dyskinesis is questionable and practitioners are unable to identify its presence reliably then it seems reasonable to suggest that time spent assessing patients in this manner is an inefficient use of resources. Secondly, if scapula stabilisation exercises do not significantly correct movement aberrations or confer superior outcomes over other existing approaches, then it also seems reasonable to suggest that prescribing treatment with the explicit aim of correcting movement aberrations is mis-guided and not evidence-based. Although there is a strong theoretical argument underpinning such an approach, this is generally not borne out by the research that has been undertaken to date.


This paper has questioned the relevance of scapula dyskinesis and the value of scapula stabilisation exercises as core components of rehabilitation strategies for shoulder pain syndromes. Currently, despite a proliferation of such assessment and prescription strategies, there is a lack of evidence to support such narrow biomechanical approaches. The time has come to pause and reflect upon the relevance of scapula dyskinesis and the rationale underpinning scapula stabilisation exercises.



Baskurt Z, Baskurt F, Gelecek N, & Ozkan M (2011). The effectiveness of scapular stabilization exercise in patients with subacromial impingement syndrome. Journal of Back and Musculoskeletal Rehabilitation, 24, 173-179.

Catlin P, Coats P, Green E, McDonald J, North C, & Greenfield B (1995). Posture in patients with shoulder overuse injuries and health individuals. Journal of Orthopaedic and Sports Physical Therapy, 21, (5) 287-295.

de Witte P, Henseler J, Nagels J, Vlieland T, & Nelissen R (2012). The Western Ontario Rotator Cuff Index in rotator cuff disease patients: A comprehensive reliability and responsiveness validation study. American Journal of Sports Medicine, 40, 1611-1619.

Ellenbecker T, Kibler W, Bailie D, Caplinger R, Davies G, & Riemann B (2012). Reliability of scapular classification in examination of professional baseball players. Clinical Orthopaedics and Related Research, 470, (6) 1540-1544.

Kibler WB, McMullen J (2003). Scapular dyskinesis and its relation to shoulder pain. Journal of the American Academy of Orthopaedic Surgeons, 11(2), 142-51.

Kibler WB, Ludewig P, McClure P, Michener L, Bak K, Sciascia (2013). Clinical implications of scapular dyskinesis in shoulder injury: the 2013 consensus statement from the ‘scapular summit.’ British Journal of Sports Medicine. Published online first: April 18, 2013 as 10.1136/bjsports-2013-092425.

Laird R, Kent P, & Keating J (2012). Modifying patterns of movement in people with low back pain – does it help? A systematic review. BMC Musculoskeletal Disorders, 13, 169.

Littlewood C, Lowe A, & Moore J (2012). Rotator cuff disorders: Survey of current UK physiotherapy practice. Shoulder & Elbow, 4, 64-71.

Lucasiewicz A, Pratt N, Sennett B, McClure P, & Michener L (1999). Comparison of 3-dimensional scapula position and orientation between subjects with and without shoulder impingement. Journal of Orthopaedic and Sports Physical Therapy, 29, (10) 574-586.

Morais N & Pascoal A (2013). Scapular positioning assessment: Is side-to-side comparison clinically acceptable? Manual Therapy, 18, (1) 46-53.

Shadmehr A, Bagheri H, Ansari N, & Sarafraz H (2010). The reliability measurements of lateral scapula slide test at three different degrees of shoulder abduction. British Journal of Sports Medicine, 44, 289-293.

Struyf F, Nijs J, Mollekens S, Jeurissen I, Truijen S, Mottram S, & Meeusen R (2013). Scapular focused treatment in patients with shoulder impingement syndrome: a randomized clinical trial. Clinical Rheumatology, 32, (1) 73-85.




  1. Chris,
    Great article here. What are your thoughts on the scapular assistance and scapular retraction tests? If the patient has a reduction in symptoms with these tests then it has been suggested that targeting scapular motor control as an intervention could be beneficial to the patient. Jeremy Lewis suggests using these types of tests with his shoulder symptom modification procedure (SSMP). However, these tests and the subsequent suggested interventions, to my knowledge, have not yet been studied to determine the effectiveness.

    • Hi Bill
      I think these tests have ‘non-specific’ effects – much like taping for patellofemoral pain. I don’t think that they indicate that scapula dyskinesis is relevant or that biomechanical aberrations are relevant. Movement simply feels easier when someone does it with you.

  2. Hi Chris
    As an individual with a scapula dyskinesis I am curious to learn your views on how the regularity of undertaking pain behaviours could affect outcome measures. e.g. Poor posture and having to raise my arm to write for 3-5 hours of lectures 5 days a week overloads my shoulder causing pain, more regularly than my summer off.
    In this case I am assuming the faulty movement pattern leads to a overload, causing inflammation and crepitius brought about by a hypertonic subscapularis grating over the rib angle. While I have undertaken rehabilitation and strengthening along side some muscular stripping and release, the pain syndrome persists.
    While this history is rather brief, would you believe functional management to be the next step in this case?
    Lastly, I lift the arm through full abduction or extension to assess the crepitis or “clunking” through the range, and while crude, is useful in indicating how painful the dyskenesis will be. Is there an outcome measure you would recommend?
    Thanks for your insights, this made great reading.
    Kind regards

  3. Hi Martyn
    My opinion is that functional, i.e. mimics the painful task, loaded exercise performed progressively, i.e. more weight, repetitions etc, over a minimum of 12 weeks is the most appropriate management strategy for most people who complain of shoulder pain diagnosed with rotator cuff tendinopathy/ subacromial impingement syndrome. For those with more severe or long-standing symptoms the programme will take longer. We advocate a programme that provokes familiar pain during exercise which goes away when the exercise is stopped.
    We use the patient specific functional scale as a way of monitoring progress in tandem with an exercise diary to monitor exercise adherence, both of which are important and we currently prefer the Shoulder Pain & Disability Index (SPADI) for measuring clinical outcomes of conservative treatment.
    I apologise for the lateness in delay but only came across your question just now. Thanks for taking the time to comment.
    Best Wishes

  4. Hi Chris
    I having been looking into best practice for managing shoulder impingement so enjoyed the article. I have worked on scapula dyskinesis with mixed results but recently saw a paper by Worsley et al 2013 that showed positive outcomes for motor control retraining – I wonder what the key is?

  5. Hi Louise
    I think we are beginning to understand some of the ‘key’ parameters but understanding is far from complete and I think it is likely that the keys will be different shapes and sizes for different individuals.
    Best Wishes

  6. Hi Chris,
    Very interesting read. I was wondering what the general strengthening and stretching exercises in the Buskart paper were? Whilst I see that scapula stabilisation exercises may not improve dyskinesis I don’t see why they shouldn’t be included to improve pain. Both the Buksart and the Struyf papers show no difference between intervention but it seems to me that the intervention in the Struyf experiment was more time efficient than the control. That considered, using scapula stability exercises PURELY for improvement in pain seems reasonable.

  7. Hi Callum, I disagree. Why bother getting ‘technical’ when you could just encourage the person to get their arm moving = similar results? Chris

  8. This is just another example of the difficulty researchers have in measuring physiotherapy interventions and the disconnect between clinical practice and academia. Chris, your argument is not the only logical conclusion that can be drawn from the research you describe. A poorly designed study (not just ones with poor internal validity, but especially those with suspect external validity—which I’d contend is most studies with impeccable internal validity) or an incomplete body of literature is not enough to invalidate a practice with which practitioners experience clinical success. Simply, your conclusions are too bold. My comments on your ‘relevance of scapular dyskinesia’ section will be longer than your section’s original text. So, I’ll stop there. But consider these arguments as a starting point for why you are limiting your opinion too much based on the paucity of evidence at hand.
    On the ‘relevance of scapula dyskinesia,’ just because Catlin et al and Lucasiewicz et al did not find an association between “scapular dyskinesia” and shoulder pain does not necessarily mean that there isn’t an association.
    1. With regard to testing scapular dyskinesia, there have been various movement faults identified in theory. For example, some discuss lateral rotation, others posterior tilt, and yet others elevation. If a study employs the Lateral Scapular Slide Test (LSST), it is only evaluating the lateral rotation; what about the other forms of dyskinesia? Could a person not have an impairment of their posterior tilt or elevation and yet be negative for scapular dyskinesia in the study, based on the LSST alone?
    2. Many people have what we call movement faults. But, not all of these people experience pain. Most nociceptive structures have a tolerance for some abuse before the problem becomes clinically relevant. Therefore, it wouldn’t be a surprise to find people with scapular dyskinesia who do not have pain.
    3. Also, there are people who have normal movement patterns and manage to overload tissues through repetitive use. So, it would not be a surprise to find people with normal movement patterns who have some pain.
    4. People employ different movement patterns for different activities. A person might employ a faulty movement pattern for some activities, but not all—perhaps not the activity tested in a given study. Arm elevation might be okay, but their tennis serve reveals the problem, as an example.
    5. The issue only gets more complicated as some activities can prompt faulty movement patterns, while others do not.
    6. Further, some activities will cause an individual pain, while other do not.
    7. It is not fair to assume that the chosen movement in a given study will expose an individual’s particular movement fault or the movement that causes the individual’s pain.
    8. Individual morphological variations such as acromion shapes and bone spurs can cause people pain despite reasonably good movement patterns.
    9. Scapulohumeral rhythm has been postulated to include not only scapulothoracic movement but also the position of the humeral head on the glenoid fossa. This is of note, because sometimes people display relatively “normal” scapular movement, but their humeral head is anterior (or moves in all directions excessively) on the glenoid fossa. Correcting the latter might be the most important concept in shoulder rehabilitation. Often centering the humeral head in the glenoid fossa alters the scapular movement pattern for better or worse. Now, one correction has changed the individual’s movement pattern completely, necessitating further coaching regarding appropriate scapular movement. Movement strategies are not fixed things. There are many variables from the type, intensity and duration of the activity to an individual’s constant experimentation with movement and change over time.
    10. All of these factors have the ability to diminish the statistical significance of a correlation between symptoms and the scapulothoracic measurements used for the specific movement chosen, in the studies described.
    In light of these considerations, if a study doesn’t find a correlation between symptoms and a specific movement pattern during a simple test, perhaps the fault remains with the study design.
    What I will conclude is that certain exercises (none of which were defined specifically in the article) may be useless in certain circumstances, as you contend, but the research that you elucidated does not prove it. Further, there is no more compelling evidence as a clinician than the observation of a movement fault coupled with predictable symptoms, whereby the symptoms resolve instantly with correction of the movement pattern fault. This is tough to study without deviating too far from the clinical reality, I’m afraid. Per usual, external validity is the greatest challenge in researching physiotherapy. Let the evidence inform practice, but we must recognize the limitations of the research in keeping up with the theory and practice.

    • Hi Justin
      First of all thank you for your well reasoned and well thought out comments, I think I will leave Chris to reply in more detail, but what I think Chris has achieved with this fantastic critical review of scapular stability is to highlight some common assumptions and misconceptions that many make when assessing and treating scapulars that just aren’t supported by the literature.
      As you say its not the only interpretation of the literature but without any robust evidence saying otherwise surely the principle of Occams Razor applies, no correlation identified therefore no correlation exists until proven otherwise, and yes I agree with you that to identify and show any correlation can be difficult if not impossible to achieve due to subtleties in assessment but herein lies the crux, if we can’t assess/test/research it how can we make claims on how best to manage / treat it?
      Thanks again for some thought provoking comments
      I look forward to Chris’s reply

  9. Thanks for your comments chaps and your clinical observations Justin. In an era of pragmatic clinical trials I think the concern about generalizability or external validity of studies is less relevant; yes, there will always be some disconnect due to the nature of evaluation but my preference is to use high quality research to inform practice rather than personal preference, anecdote and unsubstantiated theory. Herbert et al, in their book Practical Evidence-Based Physiotherapy, offer an insightful view into this.
    I’m sure we could debate all day which in part reflects current uncertainty but I would like to challenge one of the points, that the conclusions (repeated below) from the paper are too bold:
    ‘This paper has questioned the relevance of scapula dyskinesis and the value of scapula stabilisation exercises as core components of rehabilitation strategies for shoulder pain syndromes. Currently, despite a proliferation of such assessment and prescription strategies, there is a lack of evidence to support such narrow biomechanical approaches. The time has come to pause and reflect upon the relevance of scapula dyskinesis and the rationale underpinning scapula stabilisation exercises.’
    I would argue that the conclusions reflect the current body of literature and should stimulate practitioners to reflect upon their current practice.
    Best Wishes

  10. Great discussion chaps. Herein lies the crux, to me at least:
    “A recent study evaluated this and found that despite significant improvements in shoulder pain and disability at the end of treatment and after three months, the measurements of scapula dyskinesis did not change (Struyf et al. 2013).”
    Once again, in physiotherapy, we can do something which had been shown to help people, bit with a lack of “how” and “why” it works, some will argue it should not be used. As Chris said, movement of possible any sort is likely key, so is there any “harm”to using this approach, especially (for Adam’s sake) if we are up front with the patient that we think it should work but aren’t clear how and why.
    The risk is that some practitioners may file this in the “does not work ” selection of techniques they have discarded over the years, when it would appear the evidence suggests that doing nothing is the worst option.
    For the record, I can not agree with “no correlation identified therefore no correlation exists until proven otherwise” as useful here, because as we all know correlation is not causation and to me that is the more important issue. No proof of causation is also not the same as proof of no causation either.
    Very enjoyable read. Thanks

Related news