Frozen shoulder: a syndrome on the move…

Most physiotherapists will tell you that there are a number of clinical syndromes that they particularly like or dislike, for whatever reason. What is your favourite group of patients suffering from a musculoskeletal disorder that you like treating, and do you know why?

Early on in my career I happened to stumble over a range of patients with stiff shoulders, perhaps because their disorder seemed to be so mysterious and stubborn that I got curious and developed a certain passion towards this patient group. In 1993, during my stay in Adelaide for the Master’s Course, I decided to do a literature review on frozen shoulder (FS) to find out more. As every student having to write a thesis as part of a degree course knows, this gives entrance to a very selected group of acknowledged-experts on a certain topic, and not surprisingly, in years afterwards my daily patient schedule would feature many patients with stiff shoulders, coming for treatment or an (second) opinion. However, even after reading way over 200 articles dealing with frozen shoulder/adhesive capsulitis, I wasn’t really able to come up with any more substantial explanations why this syndrome was so difficult to define, difficult to treat and difficult to explain. This view had already been expressed as early as 1934 by Codman, when he introduced the term „frozen shoulder“.

Some key features that characterize the clinical pattern of frozen shoulder:

• It seems age related, occurring mostly in the group over 40
• A classification scheme based on guidelines from the American Shoulder and Elbow Surgeons in 2011 describes a primary and a secondary sub-classification. Primary or true FS has an idiopathic onset, the secondary FS is again subdivided into one of 3 categories, depending on an assumed association with a) an intrinsic shoulder pathology, b) an extrinsic pathology remote from the shoulder or c) a systemic illness.
• Onset, course and resolution should be seen along a continuum of various stages; an inflammatory process would mark the onset of pain and the development of progressive capsular restrictions, such a „freezing“ process would lead to a „frozen joint“ that over time would enter a „thawing stage“.
• Again and again, it has been documented that this basically is a self-limiting disorder, although there is an enormous discrepancy between the reported length of the various stages, ranging from 1-3 years, and to what extend the joint recovers functionally.

Some of the questions that I was asked over the years:

• Given that it is a self-limiting process, should we bother to treat this disorder at all? Yes, we should. Even though not conclusive and robust, there are sufficient findings that indicate we have a potential role to play in management, as I will point out below.
• What components should management consist of? As always, the formulation of management should be driven by a clinical reasoning process that puts the presenting signs and symptoms in relation to the hypothesized stage of the disorder. There is ample indication that skilful applied (passive) mobilization combined with active movement strategies integrated in ADL and specific exercise regimes should be part of the overall management.
• Is there a short-cut to a quick relief of pain and recovery of function? No, there is no miracle cure, neither can a quick fix of range of movement be achieved. Patients should know this, but tell them about the self-limiting and treatable nature of the disorder. They need to understand the pathological processes and tissue pathomechanics involved, so they will recognize that your treatment of 30 mins/ 2 times per week on itself is not enough. Sufficient motivation, patience and persistence in performing self-mobilization and ADL with as much as possible normal use of the affected extremity, are necessary requirements to significantly speed up the recovery process compared to wait and see how natural history takes its course.
• How firm does such a stiff shoulder needs to be mobilized? Along the same line of reasoning: particularly in the more pain-dominant stages, vigorously applied mobilizations as EOR-procedures are likely to stir symptoms up and lead to more reflex muscle activity (motor responses, often interpreted as tissue resistance/R1-R2).
• And what about procedures that in various ways stretch the capsule, like manipulation under anaesthesia (MUA) or hydraulic joint distension, do you recommend these to patients? No, I don’t. Not only because there is hardly any evidence that such procedures significantly speed up the recovery process, but particularly as they are accompanied by a range of inherent side-effects and complications. The very first patient with FS that I treated early on in my career went for a manipulation under anaesthesia, but came to see me only a couple of hours later, with absolutely no change in range of movement. He reported that his orthopaedic surgeon had not been able to achieve a successful manipulation of the joint, being physically unable to overcome the enormous tissue resistance of the shoulder joint of the patient. This exemplifies that once the joint has entered the frozen phase, dominated by capsular and myofascial tightness, enormous forces are often required to overcome such resistance to achieve an immediate elongation (in movement diagrams terms, this would mean going beyond R2…), and as we would assume clinically, you are entering a dangerous zone. I have seen patients after MUA with CRPS, humeral fractures, nerve traction injuries of the brachial plexus and median nerve leading to longstanding severe neuropathic pain, and even know of instances where the joint luxated during an attempted shoulder manipulation. To my knowledge, there are no published data on the number needed to harm related to such procedures, but I have seen and heard of enough patient cases to know of the potential dangers involved. I have therefore in most cases discouraged patients to seek such a fast route to regaining range of movement, informing them about the risk-benefit of both conservative vs manipulation and distention methods, that the syndrome is basically self-limiting, and even though it’s course is likely to be protracted, there is a fairly good prognosis for full functional recovery within 5-9 months.
• Why does it affect the shoulder, are there other joints that „freeze“ similarly? No, frozen shoulder seems to display unique features compared to other peripheral joints. Sure, other joints can develop stiffness and show up with (capsular) patterns of contracture. However, the multi-phasic course of FS, starting insidiously, running a protracted course with a tendency to spontaneous improvement of functional movement is unparalleled, and as yet, there are no conclusive answers why this seems unique to shoulders.
• And lastly, what about the onset of the syndrome? One of the conclusions from my review back in 1993 was that the most probable way towards understanding the disorder would be through advances in understanding the pathophysiological changes that mark the onset. More recent publications have now taken FS out of its traditional research paradigms related to the fields of rheumatology and orthopaedics, and expanded their view to incorporate psychoneuroimmunology. In particular, the review by Pietzrak (2016) is worth reading to get an overview of current understanding of tissue pathophysiology in FS. Given that two of the strongest risk factors for FS are diabetes and cardiovascular disease, Pietzrak (2016) hypothesizes that metabolic syndrome and a chronic low grade inflammatory process are likely to precipitate the inflammation and capsular fibrosis seen in FS. Such a chronic low grade inflammatory process, also referred to as metaflammation,  assumed to also be involved in other obscure upper limb pain syndromes (like e.g. lateral epicondylalgia), was shown to be strongly associated with an upregulation of pro-inflammatory cytokine production, neuro-immune activation and a dysregulated autonomic nervous system that seems to be shifted to a more sympathetic mode. In summary: there is now increasing evidence that the hitherto insidious onset of the painful inflammatory stage is triggered by a combination of neuroimmune/neuroendocrine biological dysfunctions. Tissue samples demonstrated neoinnervation and neoangiogenesis in the shoulder capsule, which may underlie the pain severity and irritability of the initial stage of the disorder. Apart from these more peripheral and tissue based pathophysiological changes, FS should now also be viewed in the context of what is known about the potential effects that longstanding peripheral joint dysfunction has on the central nervous system. Considering the clinical course of the disorder, the barrage of input during the inflammatory phase combined with the loss of normal movement input due to a combination of pain and stiffness, will inevitably result in changes in afferent and efferent signalling pathways and neural networks at various levels of the central nervous system. If we only look at the findings in similar longstanding joint disorders like hip and knee OA, it can be assumed that in patients with FS too there will be considerable maladaptive neuromatrix changes reflected in abnormal muscle tone and movement patterns, alterations of proprioception and body scheme, and last but not least, secondary hyperalgesia. This makes it understandable that what we clinically feel and interpret from our movement diagrams in patients with FS is a mixture of both local tissue tightness and (protective) motor responses. These latter may clinically present as bracing, guarding and increases in muscle tone around the shoulder, and possibly even be associated with factors like fear-avoidance and anxiety. As such, FS needs to be examined and managed within a biopsychosocial framework, like any other stubborn, slow healing musculoskeletal syndrome with a tendency for chronification.

This small update of my 1993 review shows that recent literature dealing with the patho-aetiology has indeed now shed some new exciting light on this syndrome. To a large extent it is still enigmatic, but theoretical understanding has made quite some progress, giving our clinical reasoning a more solid foundation regarding diagnosis, prevention, classification and estimation of the stage and course of the disorder. We can now be more specific with movement based approaches (both active and passive), informing patients (explaining both pain and stiffness) and importantly, that when movement rehabilitation is applied on the background of a biopsychosocial reasoning framework, there is a high likelihood of a good prognosis. I must admit my interest in FS has made a bit of a revival after reading the latest reviews on pathophysiology of FS, and I guess since I will continue to keep a close eye on the upcoming publications, I might as well report back to you again with a further update of this update in another 25 years. In the meantime, it would be good if we got some more data on the specific role and contribution of active and passive movement concepts within the overall management of FS. Such research might perhaps best be conducted by way of carefully designed single case studies. So, if anybody out there hasn’t made up his/her mind about a favourite clinical syndrome yet, can I suggest to go for the group of patients with stiff shoulders.

See you later, Hugo

1. Pietrzak, M. Adhesive capsulitis: An age related symptom of metabolic syndrome and chronic low-grade inflammation? Med Hypotheses 88, 12–17 (2016).
2. Ryan, V., Brown, H., Minns Lowe, C. J. & Lewis, J. S. The pathophysiology associated with primary (idiopathic) frozen shoulder: A systematic review. BMC Musculoskelet Disord 17, 340 (2016).
3. Vermeulen, H. M., Rozing, P. M., Obermann, W. R., le Cessie, S. & Vlieland, T. P. M. V. Comparison of high-grade and low-grade mobilization techniques in the management of adhesive capsulitis of the shoulder: randomized controlled trial. Phys Ther 86, 355–368 (2006).
4. Maricar, N., Shacklady, C. & Mcloughlin, L. Effect of Maitland mobilization and exercises for the treatment of shoulder adhesive capsulitis: A single-case design. Physiother Theory Pract 25, 203–217 (2009).
5. Diercks, R. L. & Stevens, M. Gentle thawing of the frozen shoulder: a prospective study of supervised neglect versus intensive physical therapy in seventy-seven patients with frozen shoulder. Journal of Shoulder and Elbow Surgery, 499-502 (2004).
6. Stam, H. W. Frozen shoulder: a review of current concepts. Physiotherapy 80, 588–598 (1994).

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