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The following case study is focused on a patient with worsening chronic pain but no explanatory trauma, no identifiable, ‘culpable lesion’, no ‘hard signs’, no ‘pathology’, neuropathy, radiculopathy or spinal pathology.
The patient was a 40-year-old, right-handed female with an eight-month history of worsening right upper-quadrant pain of atraumatic onset. She described the pain as ‘deep, aching’ and dragging’. She could recall no precipitating trauma and denied accompanying nausea, vomiting, bulbar abnormalities, visual, periorbital, perioral or other sensory disturbances, such as dysaesthesias. Her other side was unaffected and she was otherwise healthy.
She stated her pain was almost constant (“practically 24/7”) and rated it at approximately 8/10 (at its maximum) and 4/10 on average. Intensity varied with position and activity. This means that her visual analogue scale (VAS) had a ‘true zero’, which is a relevant clinical datum. Her pain did not wake her but made it difficult for her to ‘get comfortable’ at night prior to falling asleep. Pain was worsened in static positions, especially prolonged standing and sitting, computer use and walking her dog. She could not recall specific painful movements — she had limited her habitual physical activities due to the problem, mostly to avoid “making it worse”.
She had no previous history of this complaint, though she recalled some neck dysfunction and headache “about 10” years previously (after a minor MVA while on holidays) and was unsure as to whether the two problems were related. Imaging studies taken at the time were unremarkable. She denied any significant neck or arm problems.
She related her present condition to increased “pressure” (by which she meant ‘workload’) at work and perhaps to undertaking home renovations. She recalled that onset was gradual — she awoke with discomfort in her right scapular area, which spread down her arm to the wrist and digits over a few days. She was unsure which digits were involved though she stated the thumb was spared.
She waited a few weeks before contacting her GP. The initial examination was suggestive of arm pain referred from the neck and anti-inflammatories and analgesics were prescribed. Apart from “taking the edge off the pain,” she stated that these did not help. In the interim, she consulted a chiropractor for spinal adjustments and a sports physiotherapist, who did some manual therapy, prescribed a home exercise programme and suggested Pilates. She noted no exacerbation after her medications ran out, so she elected not to renew her prescription.
I noted minor asymmetry of some shoulder girdle and neck muscles. The right shoulder girdle was slightly dropped.
Shoulder girdle and glenohumeral active and passive ROM were normal and pain-free. Cervical rotation and side-flexion were limited bilaterally, particularly to the left. Combined cervical extension, right side flexion and rotation elicited neck and upper trapezius region discomfort. She was stiff and tender to palpation anteriorly at about C3-4 on the right. Resisted testing of all upper limb muscles was clinically unremarkable, as was neurological testing.
Upper limb tension tests
These clinical tests combine neck, shoulder girdle and upper limb motions to apply mechanical stress to the neuromeningeal structures of the upper quadrant. Different combinations of movements have been shown to selectively stress different neuromeningeal structures. They are analogous to the ‘straight leg raise’ (SLR) and the ‘prone-knee bend’ (PKB) tests in the lower limb. These tests may be interpreted as indicators of neuromeningeal irritation in the upper quadrant and are clinically useful in presentations ranging from headache to referred pain, DDD, ‘whiplash’ and so on.
After establishing likely sources of the patient’s nociception, I tried to estimate the relative contribution of these tissues to the patient’s specific presentation. This patient’s assessment findings suggested that she had a problem in her cervical spine, (probably C3-4 right, of unknown aetiology, but probably degenerative in nature and possibly related to her history of MVA, some irritation of related peripheral neurogenic tissue (especially tissues related to the median nerve and its branches) and though no frank muscle injury could be identified, some muscle dysfunction in the form of active trigger points in infraspinatus and teres minor.
Trigger points are hyperactive, hyperirritable loci within skeletal muscle that, when stimulated, produce a reliable, referred pain pattern.
There is some confusion about ‘active’ and ‘passive’ trigger points. Put simply, a trigger point is ‘active’ if palpation of this trigger point reproduces the patient’s presenting symptoms and it is ‘latent’ if it reproduces a pattern that is unfamiliar to the patient. This patient had examples of both types of trigger point.
This patient had right-sided, upper-quadrant persistent pain of non-traumatic origin, resulting in significant dysfunction. It has been resistant to medical and non-medical interventions and she has no specific diagnosis or ‘mechanism of injury’. She has no overt rheumatological, neuropathic, psychiatric or orthopaedic disease to explain her symptoms.
Prior to the first encounter with the physiotherapist, the patient completes an extensive intake form. This can take them 15 minutes or more. This is followed by the face-to-face encounter with the physiotherapist.
The first visit usually takes 30 minutes but it is not unusual for components of the physiotherapy assessment process to ‘spill over’ into subsequent visits. The physiotherapist takes a history and performs a physical examination. The assessment is heavily didactic in nature: The goal is to reach a diagnosis, explain it to the patient, teach the patient how the ‘injury’ occurred (if not obvious), how the different findings are related to each other, how to avoid exacerbations and recurrences, and instruct the patient in self-management.
When my patients arrive at the clinic, I ask them to complete a VAS — I request them to rate their ‘pain’ before I meet them to give them sufficient time to think about their response, and to minimise ‘white coat syndrome’. I believe this is better than requiring that a patient provides a numerical value on a standardised measurement tool ‘unprepared’. Patients with poor literacy skills or problems with numeracy may opt to utilise the ‘faces’ component of the tool.
I prefer this approach to asking patients to provide a numerical rating during the clinical interview. It also provides me with a ‘starting point’ for the clinical interview.
By verbal or other means, establish expectations about desirable, or undesirable, responses to the patient (or vice-versa).
Pain management priorities
The priorities are to explain the pain, reduce the threat, improve patient knowledge and promote self-management — especially of chronic or intractable conditions.
Like many patient problems, this patient’s pain seemingly just ‘came out of nowhere’ — there was no explanatory trauma or even a likely change in lifestyle that would explain her symptoms. Some elements of her history pointed at a mechanism:
- Her history of previous neck problems from MVA 10 years previously;
- Her recently increased job “stresses” (increased time and workload);
- Her home decoration “around the same time”; and
- Her dog.
She had not changed occupation, had an accident or taken up a new physical activity.
Clinical thinking regarding causation
Conjectures as to diagnosis and possible source of symptoms:
- The patient’s pain could be of muscular origin; a muscle injury — one could assume that the source of symptoms was in the active trigger points in infraspinatus and teres minor and this explains why she improved with treatment directed at these muscles (needling and manual therapy).
- The patient’s pain is articular in origin — the source of symptoms was in the cervical spine, at C3-4 on the right and contributed to by her ‘old’ thoracic spine dysfunction. This would explain why treatment to these joint regions improved her symptoms.
- The patient’s pain is neuropathic in nature — the positive ULTT suggested that the source of the symptoms lay in the neuromeningeal structures of the upper quadrant, most likely the median nerve. Though she received no specific treatment to neuromeningeal structures (so called ‘nerve-stretching’ or ‘nerve-flossing’), these may have been indirectly affected by her spinal joint manual therapy.
All of these are actually wrong: The source of the patient’s pain is in her CNS.
A tendinopathy is unlikely, as all tests of upper-quadrant contractile structures were negative and no treatment was addressed at tendon.
That the patient’s pain came from a peripheral joint is unlikely. All tests of peripheral articular structures in the upper quadrant were negative and no treatment was directed at peripheral joints.
It is important to understand that the patient’s condition was successfully addressed, despite not knowing which mechanism was the ‘correct one’. It is also important to understand that this is normal — the truth is that articular, muscular and neural (and supratentorial) elements all contributed to this presentation and they can all be addressed during treatment.
In our training we are taught to ‘atomise’ the patient: To pick them apart to identify a pain-generating lesion at which we can direct our treatment. But the living human does not work like a cadaver — in clinical pain management, we have to ‘put them back together’. Think of the first process as ‘differentiation’ and the second as ‘integration’, if it helps. We are taught that the ‘pain comes from an injured or diseased ‘structure’ but this is incorrect. The pain comes from the brain — all pain comes from the brain and the body is only one of many inputs to the process of pain production (Mosely and Butler, 2013).
Advice given to patient at first visit
- Get a hip belt for walking the dog, to ‘offload’ irritated soft-tissues.
- Use a PC mouse with the other hand — temporarily or permanently.
- Self-treat trigger points with a rubber ball or tennis ball several times per day for a few minutes per session (eg, while ads are on TV) — promotes self-efficacy and is good for their ‘inactivity physiology’.
- Alignment of shoulder girdle — be mindful of ergonomics while using a computer.
- Avoid static positioning of shoulder girdle and neck — simple movements of shoulder girdle and arm every 20 minutes while at a computer or watching TV.
Treatment by physiotherapist
Deep dry needling (DDN) for active trigger points — progressing to latent trigger points, as necessary.
- MFR (myofascial release — a type of ‘sports massage’).
- Mobilisation of relevant neck joints to restore normal motion in neck and reduce neuromeningeal irritation, especially around median nerve.
- Explanation of pain mechanisms and current pain science.
- Patient is taught initial home programme and self-management strategies.
- Manual therapy administered to neck at C3-4 region, right and thoracic spine.
- Trigger point therapy for active trigger points in infraspinatus and teres minor.
Second visit – four days later
- Pain now intermittent and 5/10 maximum. Sleep undisturbed.
- Repeated manual therapy to neck and thoracic spine.
- DDN to teres minor and infraspinatus.
- Manual treatment of salient latent trigger points.
- Reinforcement of current pain science concepts.
Third visit – seven days later
- Pain intermittent and approximately 2-3/10.
- Can use computer and sleep pain-free.
- Now difficult to locate peri-scapular trigger points.
- Full range of neck motion; all tests on upper limb of neuromeningeal irritation-negative.
- Rotator cuff tests at 5/5, despite undertaking no strengthening exercises.
- Treatment — reinforcement of pain neuroscience concepts, home management and self-management strategies.
- Dry needling for active trigger points.
- Repeated manual therapy of neck and thoracic spine.
Final visit – approximately 14 days after third visit
- Patient remains pain-free for most of day.
- Re-assessment ‘NAD’.
- DDN and myofascial release for relevant muscles, repeated spinal manual therapy.
- Review and reinforcement of ergonomics (including dog lead) and neuroscience.
- As often happens in private practice, patient self-discharged.
- There was no ‘final visit’.
The following are some thoughts that are relevant to neuromusculoskeletal pain management pursuant to the case study presented here.
Nociception accompanies pain, but it is neither a required nor a sufficient precondition for it — neither is a lesion (Bayer et al, 1991).
No specific lesion was identified in this assessment and the patient’s pain symptoms were successfully treated, regardless of this fact.
No primary nociceptive source was identified — although she did have several active and latent muscle (myofascial) trigger points and these were treated with a home programme, dry needling and simple stretches. This is not uncommon.
Strictly speaking, TPs are not ‘lesions’, in that they are not an injury in a muscle.
In fact, they are a subject of lively controversy (see Simons, 2008, www.painscience.com and Quintner JL, et al. (2014).
Their algogenic properties and response to treatment are more likely to be related to neuroplastic reorganisation than changes in tissue biochemistry (see www.bodyinmind.org/trigger-point-evaluation/ for further discussion).
Often, no single explanatory lesion will be identified in assessment or during treatment.
The lesion you ‘find’ may be more related to your training, your favourite diagnostic ‘tests’ and the imaging studies (ie, more closely related to the last CPU course you did than to the patient’s pain).
Such a lesion may, or may not, be related to the patient’s presenting pain (false negatives, false positives are common. Hegedus et al, 2012).
Though your diagnosis may successfully guide thinking, intervention and recovery, it may still be wrong.
Improvements in symptoms do not require healing or ‘resolution’ of a specific lesion — whether or not you have identified it — and irrespective of the tissue in which you believe it to reside, successful rehabilitation is still possible, even in the case of a patient with persistent pain and no definitive diagnosis.
The examination may suggest more than one possible ‘pain-generating site’ at which to legitimately direct the physical treatment.
Treatment may be successful without having demonstrably altered the histological or pathological status of a lesion.
The patient must be made aware that many factors contribute to pain and recovery, and that they can personally influence some of these factors (exercise, ergonomics, home programme, attitude change, improved knowledge about pain mechanisms).
It may not be possible (or desirable) to explain to the patient which component of treatment (if any) brought about the observed ‘improvements’ in their condition — the goal is functional restoration.
Patients should do their own ‘body chart’ and pain VAS — it’s more efficient and they’re better at it.
The clinician should improve upon these during the clinical interview.
References on request