1. 1. Based on your subjective examination, please discuss your ‘diagnostic reasoning’ regarding the most likely ‘source of nociception and associated pathology’ and your hypothesis about the dominant ‘pain type’ (i.e. nociceptive, peripheral neuropathic, nociplastic), highlighting the clinical features supporting your hypotheses.

The Achilles tendon insertion is the most likely source of nociception, and tendinopathy is the most probable diagnosis/pathology (Rio et al., 2015a). Morning pain and stiffness is a hallmark of Achilles tendinopathy. It is common for this to last up to 30 minutes; anything over 60 minutes may indicate a systemic contributor or cause of the tendon pain (notably, inflammatory diseases). There are two key clinical questions that support a diagnosis of Achilles tendinopathy:

• • Where is the pain? Achilles tendon pain is localized and does not spread regardless of the length of time of the symptoms. In this case, Judy had pain at the lateral part of the insertion. Pain in the Achilles can also occur at the mid-substance, where patients commonly use two fingers to ‘pinch’ the area of pain.
  
• • What aggravates the pain? Achilles tendon pain is aggravated by activities involving high tendon loads for the Achilles, especially energy-storage loads. Lower-energy-storage-load activities include brisk walking, whereas high-energy-storage-load activities involve running or change of direction. Activities such as cycling and swimming are low tendon load, and if these are the aggravating activities, a clinician should have a high index of suspicion that the Achilles is not the source of nociception. Tendinopathy appears to be nociceptively driven, as with Judy’s presentation, and it is always intimately linked with loading. When a low-tendon-load activity is the aggravating factor, there may be another pain source, such as neural irritation or the Achilles peritendon structures. These presentations will usually have a more diffuse pain pattern than Achilles tendon pain.

In insertional Achilles tendinopathy, movement into dorsiflexion causes compressive loading, where the tendon is compressed against the calcaneus; this can aggravate both pain and pathology (Cook and Purdam, 2012a). Activities such as stretching can cause pain because of compressive load. Walking with low-heeled shoes or bare feet is typically more aggravating than with shoes with a higher heel. The Haglund prominence is an anatomical morphology, not a deformity; it reduces load on the tendon insertion into the distal calcaneus by allowing compression of the Achilles tendon against the superior calcaneus (Benjamin et al., 2004). Removing this surgically exposes the insertion to greater load, increasing load on the tendon that has not adapted to full load on the insertion. Patients who display this morphology can have successful outcomes using rehabilitation without surgery (Fahlstrom et al., 2003; Jonsson et al., 2008).

Judy does not report any symptoms associated with a nociplastic pain type; however, it is well known that the experience of pain is modulated by conceptual and contextual factors. As such, education is critical so that language does not contribute to Judy’s fear and pain experience. Therefore, increasing her understanding of tendinopathy and the rehabilitation process is likely to have a positive effect.

Posterior ankle pain has a number of differential diagnoses (Rio et al., 2015a). The key differential diagnosis is posterior ankle impingement. Patients with impingement report pain in full passive and active plantar-flexion activities, including kicking in swimming (that would not typically aggravate the Achilles tendon). The retrocalcaneal bursa is part of the Achilles enthesis and should be managed as part of an insertional Achilles tendinopathy, and is therefore not considered in any separate diagnosis. Where there is local neural entrapment or pain referral, the pain location is generally more diffuse than with Achilles tendon pathology.

1. 2. What is your interpretation of Judy’s ‘perspectives on her experience’ (e.g. her understanding of her condition, fears, stress, coping, etc.)? Do you anticipate needing to address this in your management?

1. 3. Please discuss the potential ‘contributing factors’ (intrinsic and extrinsic) to the development of Judy’s problem and to her ongoing pain and disability.

Reduction in oestrogen during menopause can contribute to tendon pathology and pain in older women. The obtained information about her menopausal status and other, sometimes associated, general health issues (see Table 15.1) was thus important to consider.

The increase in Judy’s weight has implications for both load on the Achilles and for circulating cytokines associated with visceral fat deposits that in turn are associated with tendinopathy (Gaida et al., 2008). The onset of Achilles tendon pain usually coincides with a change in load, in this case a mild change in activity and footwear that may have aggravated her tendon by direct compression on the site (rubbing) or through being too low in heel height. The presence of these other comorbidities can increase the risk of developing Achilles tendon pain, with an amplified response to changes in load.

1. 4. Can you please highlight any aspects of Judy’s presentation (e.g. pathology, clinical presentation, comorbidities, medications, previous interventions) you feel signal the need for ‘precaution in the physical examination and treatment’?

Diagnostic reasoning regarding pain type, potential sources of nociception and associated pathologies commences in the subjective examination and is continued throughout the physical examination and ongoing management, where diagnostic hypotheses are tested further. As discussed in Chapter 1, these diagnoses are formulated on the basis of established (research and experience-based) clinical patterns. The specificity of musculoskeletal diagnoses varies with different problems and diagnostic tests. When the ability to identify specific sources of nociception and associated pathology is limited (e.g. non-specific low back pain), such as where overt pathology may not exist or clinical diagnostic tests lack validity to isolate sources of nociception, impairment-based diagnoses (e.g. motion segment symptom provocation, mobility and control) become the focus. In contrast, problems such as insertional tendinopathy have clearer clinical patterns, as discussed here, that can be differentiated from other sources of nociception and pathology. Although management will be largely guided by impairment based reasoning (i.e. patient’s specific clinical presentation within the common clinical pattern), more accurate diagnostic classification enables more targeted research to identify effective management strategies that can then be tailored to the individual patient.

Judy’s clinical presentation is judged as ‘nociceptive dominant’ and typical for tendinopathy that is intimately linked with loading. However, despite this, conceptual and contextual influences on the modulation of patients’ pain experiences (e.g. Judy’s understanding of tendinopathy and associated fear) are highlighted and linked to management reasoning regarding education and care with language that may contribute to Judy’s already-expressed fears. This underscores the important reality discussed in Chapters 1, 3 and 4 that unhelpful patient perspectives, commonly associated with nociplastic pain, can present in any patient and with any dominant pain type and are therefore important to assess and manage to optimize clinical outcomes and potentially reduce the risk of progression to chronicity.

Contributing factors to the development and maintenance of patients’ problems can be intrinsic or extrinsic and modifiable or non-modifiable. As discussed in Chapter 1, identification of contributing factors is important in management, both for reducing immediate symptoms and disability and for minimizing the likelihood of recurrence. Consideration of contributing factors also informs judgements regarding the hypothesis category ‘prognosis’. This emphasizes the importance of undertaking medical/general health screening for comorbidities and their management, which may represent contributing factors that vary in the extent they are modifiable. Other factors such as patient weight, activity pattern and footwear are all modifiable and important to management reasoning, as are most physical impairments assessed in the physical examination (e.g. mobility, control/strength both locally and throughout the rest of the kinetic chain).

Similarly, the hypothesis category ‘precautions and contraindication to physical examination and treatment’ should be based on comorbidities and red flags screened, plus patients’ individual clinical features, for example, those related to constancy, severity and irritability of symptoms, as well as patient perspectives such as fear.