Firstly pain is a very subjective entity and can be defined as:
“An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.”
This definition conveys just how both central peripheral systems are important in pain processing and pain development. It is vital to remember that pain is frequently a totally necessary and useful sensation. Pain after an acute injury reminds us to be careful and forces us to titrate our activity levels to a level that can be tolerated by the healing tissue. Interestingly an acute injury, such as after blunt trauma or a burn, the normal pain response involves an increase in pain sensitivity in both peripheral (peripheral sensitisation) and central (central sensitisation) pain processing (nociceptive) structures. The artificial division between peripheral and central is at the level of the spinal cord, with the sensitivity at the cord and above deemed ‘central’, while sensitivity peripheral to the cord is deemed ‘peripheral’.
Our nociception systems are not just simple afferent sensors of tissue damage, as once thought, meaning that higher systems such as emotion and mood can have powerful downward effects on the peripheral nervous system via descending modulatory circuitry. This descending circuitry consists of both direct neural routes and indirect endocrine routes such as the hypothalamic-pituitary axis. These descending systems may not only affect pain perception, but also peripheral tissue homeostasis and healing. The peripheral nervous system’s important afferent role in tissue homeostasis and healing has been relatively under researched and is consequently rather poorly understood, but it is well known the denervation is highly detrimental to the healing of both ligament and bone (http://www.ncbi.nlm.nih.gov/pubmed/12382964).
Pain may occur in the presence or absence of tissue damage, consequently there is a huge variability in the patterns of peripheral and central changes in patients presenting with shoulder pain. Some patients have significant tissue abnormality, for example a rotator cuff tear, with a very peripheral pattern of pain sensitivity, while others have no significant tissue abnormality and a very central pattern of pain sensitivity (http://www.ncbi.nlm.nih.gov/pubmed/21464489). It is also worth noting that many patients have significant tissue abnormalities without any pain or functional symptoms at all (http://www.ncbi.nlm.nih.gov/pubmed/10471998).
Pain and structure
Despite the high number of asymptomatic patients with rotator cuff tears, there is still a very strong relationship between pain symptoms and rotator cuff integrity. Rotator cuff tendinopathy (RCT) is the commonest ‘cause’ of shoulder pain and accounts for about three quarters of the patients presenting. Patients with rotator cuff tears are far more likely to have symptoms than those without (unpublished work by Oag et al), while previously asymptomatic patients are far more likely to develop symptoms as their tear size increase (http://www.ncbi.nlm.nih.gov/pubmed/16882890). It is unlikely that any one specific factor which precisely determines symptom development will ever be identified, pain is complex and many factors may contribute to its development. The glenohumeral joint kinematics change as tear size increases but this abnormality is equally prevalent in both symptomatic and asymptomatic patients (http://www.ncbi.nlm.nih.gov/pubmed/10717855,http://www.ncbi.nlm.nih.gov/pubmed/21084574).
Although the rotator cuff tendons are the most common ‘source’ of shoulder pain, damage to any structure may result in pain development, other common sources being the glenohumeral joint and capsule, the labrum, the acromioclavicular joint and the cervical spine. It can be incredibly difficult and sometimes impossible to pin point the exact ‘source’ of pain using history, examination and radiological investigations for a wide variety of complex reasons. The more a patient is highly ‘centrally sensitised’ the more difficult it can be to reach a specific diagnosis, this may be demonstrated by clinical features such as pain radiating all the way down the arm and tenderness to palpation over a wide area. It is important to realise that highly centralised patients may have a very treatable peripheral pathology in isolation, but is also vital to think of nerve entrapment in the cervical spine as part of one’s differential diagnosis.
History, examination findings including special tests and diagnostic injections (bursal injection or nerve root blocks) are all undoubtedly useful, but they can all be problematic due to a lack of specificity, for example a C6 nerve root block may abolish a patient’s ‘cuff tear related’ shoulder pain as a result of C6 innervating the shoulder joint. Both rotator cuff tears and cervical spine degeneration become increasingly common with age, meaning that many patients may well have dual pathology, and it may only sometimes be recognised that a significant contributing pathology has been missed after failed surgical intervention. Tissue abnormality can only explain so much in terms of symptomatology, and the fact that patients with massively different tissue abnormalities can have such different levels of symptoms is likely explained by individual variations in nociceptive processing, both peripherally and centrally.
Time and the placebo are great healersThe treatment of shoulder pain depends on a great number of factors including the patient’s specific diagnosis, the patient’s preferences and the treating clinician’s choice of strategy. As a natural cynic I have become increasingly convinced that many widely used treatments have little efficacy beyond the placebo effect. The placebo effect is incredibly powerful and useful in augmenting any particular treatment strategy, the patient’s belief and expectation can be huge drivers for symptomatic improvement, whether or not a treatment has a significant ‘treatment effect’.
The body has a tremendous capacity for dampening down pain over time, and amazingly this process is hardly understood at all. Huge numbers of patients with significant symptoms simply get better without any intervention, despite there being no improvement or a significant deterioration in their structural tissue abnormality. Therefore many simply never consult their primary care clinician or their secondary care specialist. Many patients do not ‘get better’ but are reasonably content to live with a certain level of pain and disability, after all this is part of what normal ageing entails; we have to be realistic about what can be achieved and setting real world patient expectations is an important part of any consultation.
It is certainly beyond this short piece to bore you with all the evidence for all the possible treatments for all the possible diagnoses of shoulder pain. What is of value is remembering that every individual is different, with a unique pattern of peripheral tissue changes, combined with certain highly variable peripheral and central nervous system changes, and that these drivers of pain symptomatology are well worth considering when embarking upon any particular treatment plan. Everything we do is imperfect; diagnosis is fraught with problems with sensitivity and specificity, we have no cures for the age-related disorders that result in so much pain and disability in those they affect. First we should try not to do any harm, and secondly we should try to appreciate that pain is a very complicated and confusing entity.
A summary of the key mechanisms involved in shoulder pain can be found here (http://www.ncbi.nlm.nih.gov/pubmed/23429268) at the British Journal of Sports Medicine.