was successfully added to your cart.

by Dr. Austin Baraki, Dr. Michael Ray, and Dr. Derek Miles.

In the first article of this series we discussed the concept of “normal” or “abnormal” scapular movement (i.e., scapular dyskinesis), which is the pathomechanical foundation upon which other shoulder-related diagnoses and narratives are built. “Shoulder impingement” is one of these ideas that is commonly discussed in the coaching, rehab, and orthopedic worlds. The narrative describes soft tissue structures around the shoulder (e.g., rotator cuff tendons and bursae) becoming compressed between the bony surfaces of the joint. Two types are discussed in the scientific literature: “internal” and “external” impingement. Let’s take a critical look at these concepts, starting with “external” impingement in this article.

The Origins of “External Impingement”, a.k.a. Subacromial Impingement:

The idea of “shoulder impingement” was introduced in 1972 by orthopedic surgeon Dr. Charles Neer. We will spend a good bit of time discussing Neer’s seminal paper, Anterior Acromioplasty for the Chronic Impingement Syndrome in the Shoulder: A Preliminary Report, because it sets the stage for the next several decades of biomedical intervention.1

Dr. Neer examined the scapulae of 100 cadavers and found that 11 “revealed alterations attributable to mechanical impingement”. He hypothesized how the supraspinatus tendon might become “impinged” under the acromion process (or associated bone spurs) during certain movements, and become damaged or degenerated as a result.

He writes:

“At about 80 degrees of abduction, the critical area of the supraspinatus tendon passes beneath the acromioclavicular joint and this joint tilts with overhead elevation of the arm. With the joint in this position, it is logical to assume that excrescences on the undersurface of the anterior margin of the acromion may impinge on the cuff. Arthrograms seem to substantiate this point.”

Dr. Neer then proposes that this impingement could be fixed through surgical intervention.

“One should therefore remove the anterior edge and the undersurface of the anterior process along with the attached coraco-acromial ligament. If other pathological areas are discovered at operation, that is, a hypertrophic acromioclavicular joint, or spurs and adhesions at the long head of the biceps or greater tuberosity, they too should be removed. The attachments of the deltoid should be minimally disturbed.”

In the 1972 article, Dr. Neer claims to have been performing such procedures, known as anterior acromioplasties, since 1965. He presents a summary of 50 operations that were completed on 46 patients between 1965-1970.

The pre-operative physical exam of these patients revealed crepitus (“noise” in the joint such as clicking and popping), tenderness over the supraspinatus tendon, and the painful arc sign (pain between 70 and 120 degrees while abducting the arm), along with pain at the anterior edge of the acromion during forced elevation.1 The only common findings on imaging among the participants were cysts or sclerosis of the greater tuberosity. Dr. Neer then states, “… but on close inspection many [X-rays] showed corresponding areas of proliferation at the anterior edge of the acromion.”1 How many demonstrated this? We don’t know. Whether this is meaningful, we will discuss later.

Dr. Neer goes on to rationalize his surgical intervention:

“The value of anterior acromioplasty is thought to be that it relieves pain and inflammation from chronic impingement; that technically it improves exposure of other involved structures and allows appropriate measures to be taken with reference to them; and that it retards the wear caused by persistent impingement and may prevent rupture of the supraspinatus tendon or of the long head of the biceps, or both.”

Outcomes

Dr. Neer performs his intervention and follows up with patients anywhere from 9 months to 5 years post-operatively. If this sounds odd, that’s because it is odd to have such a broad, inconsistent range of follow-up times for subjects after intervention. This opens up the potential for natural history and regression to the mean to occur — phenomena by which patients tend to get better on their own with time — confounding the apparent effectiveness of the surgical intervention, given the lack of a control group.

Ketola et al demonstrated this in their study comparing a surgery + exercise group to an exercise-only group for shoulder impingement syndrome, and followed-up at 2 and 5 years.2 The authors report:

“The results at 2 and 5 years were similar between treatment groups and they seemed to continue to improve in a similar way in both groups after the first 2 years (to the 5-year follow up). The effects of both procedures appeared to be long-lasting and to continue to improve over time.”

The authors go on to ask the question, “Do these good results reflect the therapeutic intervention, or the natural long-term course of this syndrome?” During the study the authors allowed participants who were not satisfied with exercise alone to cross over and undergo surgery (18 participants). We might expect these patients to improve after surgery, but they actually didn’t. The authors go on to state:

“We believe that there was a similar group of patients in the combined group as well, who would not respond to surgery either. So it appears that almost one-third of all patients with this diagnosis do not respond to any sort of treatment. The remaining two-thirds will get better irrespective of the nature of the treatment. It might well be that the natural course of the shoulder impingement syndrome contributes substantially to the improvement of those patients who are “healed” after treatment, during the 5-year follow-up. It appears that patients who do not get better with nonoperative treatment do not get better with operative treatment either, although this may also partly depend on the duration of the symptoms before initiation of the treatment. This in any case challenges the previous guidelines of offering surgery to patients who “fail” with nonoperative treatment.”

The authors go on to advocate for more research with longer follow-up periods to accurately assess the natural history of subacromial impingement syndrome.

Now, back to Dr. Neer’s findings. Post-operative results are shown in table 1 below:

Post-operatively, patients were dichotomized between “satisfactory” and “unsatisfactory” outcomes:

  • Satisfactory = patient “satisfied” with surgical procedure, with no significant pain. Complete use of the shoulder, less than 20 degrees of limitation of overhead extension, and ≥ 75% of normal strength.1
  • Unsatisfactory = not meeting above standards.

Thirty-eight out of 47 (~ 80%) were considered “satisfactory” cases — pretty good for a treatment intervention. However, a major confounder was not assessed with this study: the placebo effects of surgery, which are becoming well-recognized today.3

Benedetti et al argue, Placebos are not inert substances, as thus far believed. They are made of words and rituals, symbols, and meanings, and all these elements are active in shaping the patient’s brain.”  They go on to state:

“A real placebo effect is a psychobiological phenomenon occurring in the patient’s brain after the administration of an inert substance, or of a sham physical treatment such as sham surgery, along with verbal suggestions (or any other cue) of clinical benefit. Therefore, the effect that follows the administration of a placebo cannot be attributable to the inert substance alone, for saline solutions or sugar pills will never acquire therapeutic properties. Instead, the effect is because of the psychosocial context that surrounds the inert substance and the patient.”

There was no attempt to understand or account for placebo effects in Dr. Neer’s study. There was no sham-control group, and no blinding took place despite the fact that randomized, controlled trials were standard practice in research by this time. Unfortunately, this tends to be the case for many orthopedic procedures that initially appear to make superficial sense from a biomedical perspective prior to undergoing controlled study.

The RCTs Strike Back

Now in 2017, forty-five years after Dr. Neer’s original paper, and we have a new trial published in the Lancet, Arthroscopic subacromial decompression for subacromial shoulder pain (CSAW): a multicentre, pragmatic, parallel group, placebo-controlled, three-group, randomised surgical trial.4

The CSAW (Can Shoulder Arthroscopy Work?) study aimed to compare 1) subacromial decompression versus 2) sham (“placebo” arthroscopy) versus 3) no treatment. A total of 313 patients were recruited and randomly assigned as follows: 106 to decompression surgery (removal of tissue/bone), 103 to sham arthroscopy (“placebo” surgery with no removal of tissue/bone), and 104 to no treatment. All participants were then reassessed 6 and 12 months later using the Oxford Shoulder Score as an outcome measure.4

Results showed that outcomes after surgical decompression are no better than sham surgery and both are only slightly better than no treatment at all (although the clinical significance of this difference is questionable).4 Their conclusions:

“In conclusion, we showed that, in patients with persistent subacromial shoulder pain due to impingement, improvement in Oxford Shoulder Scores with arthroscopic subacromial decompression did not differ to that achieved with arthroscopy only (placebo surgery). Although both types of surgery provide greater symptom improvement than no treatment, this difference was of uncertain clinical significance. The findings (which should be communicated to patients during the shared treatment decision-making process) question the value of this type of surgery for these indications, and might discourage some surgeons from offering decompression surgery and dissuade some patients from undergoing the surgery.”

In 2018, a similar study was conducted by Paavola et al, Subacromial decompression versus diagnostic arthroscopy for shoulder impingement: randomised, placebo surgery controlled clinical trial.5

In this study, 59 patients were randomized to subacromial decompression surgery, 61 underwent sham (placebo) arthroscopy, and 71 underwent exercise therapy. Patients were reassessed for pain severity at 3, 6, 12, and 24 months after intervention.5

Study results showed that both the subacromial decompression and sham arthroscopy groups dramatically improved, and by 24 months no differences were identified between the surgery and sham surgery groups.5

What about subacromial decompression vs. exercise therapy? Both groups demonstrated substantial improvement from baseline to 24 months. There was a statistically significant difference supporting decompression over exercise at the 24 months mark, but the mean difference between the two groups did not meet the pre-specified minimal clinically important difference (MCID).5 MCID refers to the smallest possible change in outcome that would be important to a real-world patient, or which would justify a change in a patient’s management. This means that the difference observed in the study between surgery and exercise groups was not a meaningful difference for real-world patients.

The authors conclude:

“The results of this randomised, placebo surgery controlled trial show that arthroscopic subacromial decompression provides no clinically relevant benefit over diagnostic arthroscopy in patients with shoulder impingement syndrome. The findings do not support the current practice of performing subacromial decompression in patients with shoulder impingement syndrome.”

So, It appears that pretending to relieve the mechanical subacromial impingement is just as effective at improving symptoms as actually relieving it. How can this be? This should make us question Neer’s original hypothesis attributing the syndrome to mechanical compression.

Where does this leave us? We have an outdated biomedical narrative from the 1960s that continues to be disseminated to patients, remains unsubstantiated, and results in the rationalization of an invasive treatment that offers no benefit over sham surgery.

What about less invasive treatments, such as corticosteroid injections?

A recent systematic review and meta-analysis by Steuri et al examined the research on conservative treatment options including corticosteroid injections, NSAIDs, exercise, manual therapy, ultrasound, extracorporeal shockwave therapy (ECSWT), and taping.6 It is worth noting that this review is based on very low quality evidence; with that said, the authors conclude:

“Exercise, especially shoulder-specific exercises, should be prescribed for all patients with shoulder impingement. The addition of manual therapy, tape, ECSWT and laser might add a small benefit. For other non-exercise physical therapy modalities, we cannot provide enough evidence for or against, therefore they should only be used in addition with exercise. Corticosteroid injections seems to be a valid alternative only when exercise or other modalities are not possible while NSAIDS can be helpful, if necessary, in addition to exercise.”

Take-home message: We need to get patients moving to tolerance as soon as possible, preferably with exercise geared specifically to their goals.

The Power of Narrative

An overarching theme at Barbell Medicine is the importance of the words we use with patients and clients. So, what are the issues associated with delivering this idea of tissue being “impinged” by the acromion or its bony outgrowths? Cuff et al. published a study in 2017, Subacromial impingement syndrome – What does this mean to and for the patient? A qualitative study.7 The authors examined patients’ understanding of subacromial impingement syndrome and its effect on treatment selection and rehabilitative care.

The authors argue that the diagnosis of “Subacromial Impingement Syndrome” reflects a biomedical narrative that instills fear and avoidance of movement among patients. Patients are told they have a bony outgrowth that “impinges with particular shoulder movements, thus damaging, degrading, or “fraying” underlying tissues over time.7

In response, many naturally become fearful and, potentially unbeknownst to them, begin self-selecting movements they deem “acceptable” vs. “unacceptable” for fear of precipitating further shoulder damage. As one can imagine, this can become quite detrimental to daily function and desired activity.

This mechanically-focused narrative poses an even larger problem when a patient is referred to rehab as a first step in order to “avoid” surgery. Nine patients were included in the qualitative study and all 9 reported a similar understanding of the problem:

Participant 3:

“It is the tendon being caught by this piece of bone and wearing it away.”

Participant 5:

“According to my doctor, I had a scan and I’ve got two extra bones … They did say there is inflammation and there’s something that’s rubbing and then every time it rubs that’s what causing me to have pain … He just said it was all swollen up and that there’s something that when it’s swollen up that’s what’s causing me the pain and that’s as much as I know.”

Participant 9:

“He said there was some impingement that could have been inflammation from irritation in the shoulder … things stopping my arm actually moving the way it should … I could just picture something just in the joint that got in the way at a certain point and was making it difficult for the socket to move in the way it should be moving.”

Since patients’ understanding of the problem was rooted in a mechanically-focused model, the expected treatment logically centered around this approach as well.


Participant 3:

“(How are we going to get this pain to go away?) By removing this piece of bone.”  …  “I don’t want to get to a position where it’s okay, I go back to work and it blows up again and I’m back to square one. I want it sorted you know. I said to the Physiotherapist you know, I think the only way that is going to permanently cure this is through that surgery, you know”.

Worse, this line of thinking led to patients questioning the role and efficacy of non-invasive rehabilitation treatments like exercise:

Participant 1:

If there is a physical lump or something there, all the Physiotherapy in the world isn’t going to resolve that if that doesn’t disappear. He said that it was quite likely in my case that I might well need some keyhole surgery …”

Participant 3:

“There is a possibility, I think, I think what the [Physician] was meaning was that I could have some Physio to get the inflammation down, get the swelling down, get the muscles stronger but it’s not permanent, it’s not going to be a permanent fix, this piece of bone is still there. I can’t imagine how any amount of physio is going to shift this piece of bone which is in my shoulder.”

“He said we can do keyhole surgery on it and it’ll be fine. Meanwhile, he said I want you to try a couple of months of physio first before we commit to that, which puzzles me to be honest because I thought well you know, if this piece of bone is not a big job just go in there, get rid of this bit of bone, fine. So I was a bit nonplussed when I came to physio, I thought well you know, I felt a bit sorry for the guy to be honest”.

Despite the previously discussed evidence showing equivalent outcomes from non-surgical treatments, the delivery of the standard mechanical impingement narrative appears to induce a substantial nocebo effect upon patients. That is, their expectations of benefit from non-invasive rehabilitation treatments are worsened, a phenomenon which then tends to result in worse outcomes.8

Another major issue is that these supposed “issues” are readily observed in the asymptomatic aging population. A 2014 article, A systematic review and pooled analysis of the prevalence of rotator cuff disease with increasing age, included 30 studies of 6112 shoulders.9 Overall, the prevalence of abnormalities increased from 9.7% in 20 year olds to 62% in 80 year olds and older. The prevalence increased similarly regardless of symptoms or shoulder dislocation.9 The authors conclude:

“The prevalence of rotator cuff abnormalities in asymptomatic people is high enough for degeneration of the rotator cuff to be considered a common aspect of normal human aging and to make it difficult to determine when an abnormality is new (e.g., after a dislocation) or is the cause of symptoms.”

Where do we go next?

If we’re going to dispose of the classic theory of subacromial impingement, how should we diagnose these painful shoulders instead? There is now a push to shift the terminology to things like Subacromial Pain Syndrome (SPS), Rotator Cuff Syndrome, or Rotator cuff-related shoulder pain.

Dierks et al published a 2014 review, Guideline for diagnosis and treatment of subacromial pain syndrome: a multidisciplinary review by the Dutch Orthopaedic Association. They define SPS as, “….all non-traumatic, usually unilateral, shoulder problems that cause pain, localized around the acromion, often worsening during or subsequent to lifting of the arm.”10

The authors propose that the umbrella term Subacromial Pain Syndrome encompass the following current diagnoses: bursitis, tendinosis calcarea, supraspinatus tendinopathy, partial rotator cuff tear, biceps tendinitis, or cuff tendon degeneration.10

Regardless of the selected diagnostic label, the prognosis in these scenarios likely matters more than the specific structural diagnosis. Clinicians like to supply labels for patient symptoms in order to neatly place these “problems” into biomedical boxes. We can then intervene upon these boxes with specific treatments to “fix” the patient. There are two major issues with this approach: 1) We have more evidence demonstrating what are likely not problems than what are problems, and 2) This approach leaves out a huge part of the picture as it relates to treating the person, rather than treating the bursa, the tendon, or the joint; ultimately stigmatizing the person.11

This line of thinking is one of the largest differences between the biomedical versus biopsychosocial approaches to pain treatment. With that said, how should we appropriately assess this issue clinically? According to Dierks et al:

No single test is sufficiently accurate to diagnose SPS. The inter-rater reliability of the most common tests varies greatly.”

We see this statement further supported by a Cochrane Review: Physical tests for shoulder impingements and local lesions of bursa, tendon or labrum that may accompany impingement,

There is insufficient evidence upon which to base selection of physical tests for shoulder impingements, and local lesions of bursa, tendon or labrum that may accompany impingement, in primary care. The large body of literature revealed extreme diversity in the performance and interpretation of tests, which hinders synthesis of the evidence and/or clinical applicability.12

And based on the above discussion, diagnostic imaging like X-ray or MRI is likely not beneficial in atraumatic shoulder pain situations either, given the increasing likelihood of finding a supposed “abnormality” on imaging as we age. If you are following the theme of this article, it should be apparent that the specific tissueabnormality” is less important for prognosis and outcomes.

So, what is relevant for the prognosis of SPS? According to Dierks et al:

  1. Duration of symptoms (> 3 months) is associated with poorer outcomes.
  2. Middle-aged (45-54 years) is associated with poorer outcomes.
  3. Psychosocial factors – Dierks states, “Psychosocial factors appear to have a greater association with the course and prognosis of chronic shoulder pain (> 3 months) than with that of shorter-term shoulder pain (< 6 weeks).10

Psychosocial factors are important, given our lack of evidence for strong correlations to structural issues. A recent longitudinal study on prognostic factors related to physiotherapy outcomes identified 4 relevant factors that led to better outcomes (less pain and disability):

  1. Lower baseline disability
  2. Patient expectation of “complete recovery” vs “slight improvement” due to physiotherapy treatment (which, notably, can be influenced by our words & narratives)
  3. Higher pain self-efficacy
  4. Lower pain severity at rest4

Two of these points have a substantial base of supporting evidence. A systematic review earlier this year discusses the relationship between a person’s self-efficacy and effects on prognosis for chronic musculoskeletal pain.14 The authors define self-efficacy as “the personal confidence to carry out an activity with the aim of successfully achieving a desired outcome.” The authors conclude:

“Our results suggest that higher [self-efficacy] levels are associated with greater physical functioning, physical activity participation, health status, work status, satisfaction with the performance, efficacy beliefs, and lower pain intensity, disability, disease activity, depressive symptoms, presence of tender points, fatigue and presenteeism.”

How do we instill and bolster self-efficacy in patients? Most importantly, we must ensure we are not creating unnecessary issues for us to fix, as this removes the locus of control and autonomy from the individual and creates dependency on the clinician. Instead, clinicians should guide the path to patient goals via education and demonstration of how they can take care of themselves. We should promote narratives of resilience, versus vulnerability.15

Setting expectations goes hand-in-hand with this approach. As described above, our narratives directly influence patient beliefs, which then influence treatment outcomes. We must ensure we are setting appropriate and realistic expectations for the issue being addressed as well as for treatment. For a detailed discussion of setting expectations, see Bialosky et al and Geurts et al.16,17

When it comes to treatment, education appears to be the best bet for helping patients reach their goals, followed by exercise. Now, there is certainly a chance that the benefits of exercise, much like surgery, are primarily mediated by placebo effects. Or perhaps exercise just entertains the clinician and patient while natural history and regression to the mean occur over time. However, to quote a recent JOSPT editorial by Lewis:

“… proponents of evidence-based practice would advocate that if there are 2 interventions of equal clinical effectiveness (even if the basis for that outcome is uncertain), then the choice of the economically competitive treatment should dominate that of the more expensive intervention, allowing the finite resources to be directed in a more appropriate manner. Furthermore, activity- and exercise-based interventions have significant and important health benefits.”18

Conclusions

In closing, the question remains, if not mechanical impingement of tissue(s), then what?

Although many practitioners are happy to provide confident, superficially plausible-sounding explanations for pain, we aren’t entirely sure why certain people develop shoulder pain. However, we now have a better understanding of the need to de-emphasize rigidly biomedical narratives that are overly focused on supposed structural/mechanical “abnormalities”, as we have little supportive data for a pathoanatomical or kinesiological causes.

We do have good quality research evidence on efficacious ways to mitigate the risk for development of symptoms in the athlete by focusing our attention on two primary areas, which we will discuss in further detail in the next article:

  1. Psychosocial coping skills19
  2. Load / Fatigue Management (Jones et al & Eckard et al)20,21

Additionally, attempting to answer the question of why someone became symptomatic may not be productive, as it elicits further unnecessary hypervigilance to a perceived problem rather than a solution. Focused attention to a supposed root “cause” may also perpetuate a narrative that lacks a level of acceptance for pain as a human experience while removing autonomy from the person.22 This feedback may further feed into a fear-avoidance cycle along with a continuous need to investigate for a structure-based issue.23

Speaking of fear-avoidance, we have no evidence for particular movements being “dangerous” for a shoulder joint. In the rehab or exercise world, we often hear that particular movements such as the upright row should be avoided for “shoulder health”, that one must maintain an “active shoulder”, or that shrugging at the top of an overhead movement is essential to prevent structural damage to the shoulder musculature and its associated tendons. We’ve had a rather lengthy discussion regarding the lack of substantiating evidence for this entire idea. If we instill false dichotomy-based narratives regarding shoulder movement, we continue to instill fear avoidance while perpetuating a false narrative.

For now, our best bet is to minimize unnecessary invasive, costly procedures while instilling confidence in patients and their ability to move and self-manage without unnecessary false biomedical narratives.

Next in the series: Internal impingement in the overhead athlete.


References:

  1. Neer CS. Anterior acromioplasty for the chronic impingement syndrome in the shoulder: a preliminary report. The Journal of bone and joint surgery. American volume. 1972; 54(1):41-50.
  2. Ketola S, Lehtinen J, Rousi T, Nissinen M, Huhtala H, Arnala I. Which patients do not recover from shoulder impingement syndrome, either with operative treatment or with nonoperative treatment? Acta Orthopaedica. 2015; 86(6):641-646.
  3. Benedetti F, Carlino E, Pollo A. How placebos change the patient’s brain. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. 2011; 36(1):339-54.
  4. Beard DJ, Rees JL, Cook JA, et al. Arthroscopic subacromial decompression for subacromial shoulder pain (CSAW): a multicentre, pragmatic, parallel group, placebo-controlled, three-group, randomised surgical trial The Lancet. 2018; 391(10118):329-338.
  5. Paavola M, Malmivaara A, Taimela S, et al. Subacromial decompression versus diagnostic arthroscopy for shoulder impingement: randomised, placebo surgery controlled clinical trial BMJ. 2018;
  6. Steuri R, Sattelmayer M, Elsig S, et al. Effectiveness of conservative interventions including exercise, manual therapy and medical management in adults with shoulder impingement: a systematic review and meta-analysis of RCTs. British journal of sports medicine. 2017; 51(18):1340-1347.
  7. Cuff A, Littlewood C. Subacromial impingement syndrome – What does this mean to and for the patient? A qualitative study. Musculoskeletal science & practice. 2018; 33:24-28.
  8. Rossettini G, Carlino E, Testa M. Clinical relevance of contextual factors as triggers of placebo and nocebo effects in musculoskeletal pain. BMC musculoskeletal disorders. 2018; 19(1):27.
  9. Teunis T, Lubberts B, Reilly BT, Ring D. A systematic review and pooled analysis of the prevalence of rotator cuff disease with increasing age. Journal of shoulder and elbow surgery. 2014; 23(12):1913-1921.
  10. Diercks R, Bron C, Dorrestijn O, et al. Guideline for diagnosis and treatment of subacromial pain syndrome: a multidisciplinary review by the Dutch Orthopaedic Association. Acta orthopaedica. 2014; 85(3):314-22.
  11. Cohen M, Quintner J, Buchanan D, Nielsen M, Guy L. Stigmatization of Patients with Chronic Pain: The Extinction of Empathy Pain Med. 2011; 12(11):1637-1643.
  12. Hanchard NC, Lenza M, Handoll HH, Takwoingi Y. Physical tests for shoulder impingements and local lesions of bursa, tendon or labrum that may accompany impingement . 2013.
  13. Chester R, Jerosch-Herold C, Lewis J, et al. Psychological factors are associated with the outcome of physiotherapy for people with shoulder pain: a multicentre longitudinal cohort study. Br J Sports Med 2018;52:269-275.
  14. Martinez-Calderon J, Zamora-Campos C, Navarro-Ledesma S, Luque-Suarez A. The Role of Self-Efficacy on the Prognosis of Chronic Musculoskeletal Pain: A Systematic Review. The journal of pain : official journal of the American Pain Society. 2018; 19(1):10-34.
  15. Esteve R, Bendayan R, López-Martínez AE, Ramírez-Maestre C. Resilience and Vulnerability Factors When Pain is Acute as Predictors of Disability: Findings From a Two-Year Longitudinal Study. Pain medicine (Malden, Mass.). 2017; 18(11):2116-2125.
  16. Bialosky JE, Bishop MD, Cleland JA. Individual expectation: an overlooked, but pertinent, factor in the treatment of individuals experiencing musculoskeletal pain. Physical therapy. 2010; 90(9):1345-55.
  17. Geurts JW, Willems PC, Lockwood C, van Kleef M, Kleijnen J, Dirksen C. Patient expectations for management of chronic non-cancer pain: A systematic review. Health expectations : an international journal of public participation in health care and health policy. 2017; 20(6):1201-1217.
  18. Lewis J. The End of an Era? The Journal of orthopaedic and sports physical therapy. 2018; 48(3):127-129.
  19. Ivarsson A, Johnson U, Andersen MB, Tranaeus U, Stenling A, Lindwall M. Psychosocial Factors and Sport Injuries: Meta-analyses for Prediction and Prevention. Sports medicine (Auckland, N.Z.). 2017; 47(2):353-365.
  20. Jones CM, Griffiths PC, Mellalieu SD. Training Load and Fatigue Marker Associations with Injury and Illness: A Systematic Review of Longitudinal Studies. Sports medicine (Auckland, N.Z.). 2017; 47(5):943-974.
  21. Eckard TG, Padua DA, Hearn DW, Pexa BS, Frank BS. The Relationship Between Training Load and Injury in Athletes: A Systematic Review Sports Med. 2018; 48(8):1929-1961.
  22. Karos K, Williams ACdC, Meulders A, Vlaeyen JW. Pain as a threat to the social self PAIN. 2018.
  23. Vlaeyen JW, Linton SJ. Fear-avoidance and its consequences in chronic musculoskeletal pain: a state of the art. Pain. 2000; 85(3):317-32.

Join the discussion 3 Comments

  • Scott says:

    Good article. I am an OT Cer as a Certified Hand Therapist who treats Upper Extremities. I have beenpracticing mindfulness and meditation for eight years now. For me, this has taught me to reframe my experiences without the hypervigilence that I used to go after things with. I also have changed ny language toward my patients in how I explain their “ diagnosis.”
    2. Great article . With this and your other articles I am reconsidering taking the SFMA . I was considering taking that as a way to understand but it may be completely unnecessary not just costly. Or it may be good to have as long as I jeep it in perspective. Anyway thanks and any input would be appreciated.

    Blessings
    Scott

  • Filip Klement says:

    Hi, thank you guys for great article. My name is Filip and I just started working as orthopedic surgeon. I had a conversation with my colleagues about SAD and shoulder impingement last week and only few of them are familiar with most recent studies. One of them suggested that many SAD are not correctly indicated. He only performs SAD on patients with chronic pain and significant “pathologies”. In his opinion this leads to better results. Obviously I can not speak for him but what is your opinion about acertain group of patients that could benefit from surgery (if someone like that even exist)? And what about people who dont respond to any treatment as mentioned in Ketola et al study?
    Thank you , Filip

  • Michael says:

    Hey Filip,

    Thanks for the comment and questions. Persistent pain would not be a valid indicator for surgical intervention given our current understanding of persistent pain development and appropriate management. I’d be curious how significant pathologies are being defined as indicators for surgery. At this time there doesn’t appear to be a subgroup of patients who would benefit from a surgical intervention for SIS. Which makes sense given the symptomatic presentation isn’t well correlated to the traditional biechanical narrative. Happy to discuss further.

Leave a Reply