Fibromyalgia and Chronic Widespread Pain — Written Clinical Reasoning

SAQ 1 — Integrated Approach to Secondary Fibromyalgia (20 marks, 30 minutes)

Prompt: Outline your integrated approach to Mrs Chen's presentation, addressing: (a) the prioritised problem list and the diagnostic reasoning; (b) the 2016 ACR criteria for fibromyalgia and why the tender point examination is obsolete; (c) the pathophysiological basis for the pharmacological therapy and the explanation of why the DAS28 is elevated despite controlled inflammatory disease; (d) the management plan, including the non-pharmacological foundation, the symptom-targeted pharmacotherapy, and the approach to the opioid; (e) the communication and shared decision-making with a patient who expects a biologic escalation; and (f) the common exam trap in this patient. [1]

Model Answer

(a) Prioritised problem list and diagnostic reasoning (3 marks) [1]

The prioritised problem list is: [1]

1. Secondary fibromyalgia overlaid on well-controlled rheumatoid arthritis — the central sensitisation is driving the widespread pain, the fatigue, the unrefreshing sleep and the cognitive dysfunction, and it is inflating the DAS28. This is the primary problem.
2. Rheumatoid arthritis in remission on methotrexate and adalimumab — the inflammatory markers are normal and there is no synovitis, so the RA is not active.
3. Opioid exposure (oxycodone 20 mg per day for six months) — this is iatrogenic harm. The opioid is likely worsening the central sensitisation through opioid-induced hyperalgesia, and a deprescribing plan is needed.
4. Central sensitivity syndrome cluster — irritable bowel symptoms and tension headaches, sharing the central sensitisation mechanism.
5. Functional impairment — difficulty concentrating and the impact on her work as a teacher. [1]

The diagnostic reasoning is that the discordance between the normal inflammatory markers (CRP 2, ESR 10), the absence of synovitis, and the elevated DAS28 (4.3) is explained by the fibromyalgia component inflating the tender joint count and the patient global assessment. She meets the 2016 ACR criteria (WPI 9, SSS 7, generalised pain, more than 3 months) [1]. The inflammatory component of the RA is quiet.

(b) The 2016 ACR criteria and the obsolescence of the tender point examination (3 marks) [1]

The 2016 ACR revised criteria (Wolfe 2016) require: generalised pain in at least 4 of 5 body regions; symptoms present at a similar level for at least 3 months; and either a WPI of 7 or more with an SSS of 5 or more, or a WPI of 4 to 6 with an SSS of 9 or more [1]. Mrs Chen meets the first limb (WPI 9 with SSS 7).

The WPI counts 19 body areas; the SSS scores the severity of fatigue, waking unrefreshed and cognitive symptoms (each 0 to 3) plus the extent of somatic symptoms (0 to 3), for a maximum of 12. [1]

The tender point examination (the 1990 criteria required 11 of 18 points) is obsolete because it is not reproducible between examiners, it samples the body inadequately, and it identifies a narrower population than the condition actually affects. The 2016 criteria also explicitly state that a diagnosis of fibromyalgia does not exclude other diagnoses — so Mrs Chen can have both RA and fibromyalgia. [1]

(c) Pathophysiological basis and the elevated DAS28 (4 marks) [1]

Fibromyalgia is a disorder of central sensitisation: amplified central nervous system processing of nociceptive input produces hyperalgesia and allodynia, and the descending inhibitory system (serotonergic and noradrenergic) is deficient [2]. The neurotransmitter profile shows reduced serotonin, noradrenaline and dopamine, and elevated substance P and glutamate.

This mechanism explains the pharmacotherapy: amitriptyline (a tricyclic) and duloxetine (an SNRI) boost the deficient descending serotonergic and noradrenergic inhibition; pregabalin and gabapentin (alpha-2-delta ligands) reduce the release of the excitatory neurotransmitters (glutamate, substance P) by binding the voltage-gated calcium channel [5][6].

The elevated DAS28 (4.3) is explained by the composition of the score: the DAS28 includes a tender joint count (28 joints) and a patient global assessment, both of which are driven by the central sensitisation. The fibromyalgia makes every joint tender, inflating the tender count. The objective inflammatory components — the CRP (which is normal) and the swollen joint count (which is zero) — are quiet. The teaching point is that the DAS28 cannot distinguish inflammatory activity from central sensitisation, and this is the classic pitfall of secondary fibromyalgia. [1]

(d) The management plan (6 marks) [1]

The non-pharmacological foundation (first-line): [1]

• Patient education and validation: explain the diagnosis, the central sensitisation mechanism in plain language, and set the expectation of management rather than cure.
• Graded aerobic exercise: the only EULAR strong-for recommendation [3], with meta-analytic evidence of benefit for pain, fatigue, mood and physical function [7]. Start low (walking, swimming), progress slowly.
• Cognitive behavioural therapy: addresses catastrophising, fear-avoidance and unhelpful coping.
• Sleep hygiene: fixed sleep and wake times, a wind-down routine.
• Pacing and graded activity: to avoid the boom-and-bust cycle.

The symptom-targeted pharmacotherapy: [1]

• Given her sleep disturbance is prominent, amitriptyline 10 mg at night is the appropriate first choice, titrated to 25 mg if tolerated and if the response is partial.
• If the response is insufficient, add or switch to duloxetine 30 mg daily for one week then 60 mg daily (also addresses any comorbid low mood), or pregabalin 75 mg twice daily titrated to response (if the neuropathic component is prominent). [1]

The approach to the opioid: [1]

• Oxycodone has no role in fibromyalgia. It is likely contributing to the worsening through opioid-induced hyperalgesia [2].
• A structured deprescribing plan: explain the rationale (the opioid is worsening the central sensitisation), reduce by 10 per cent every one to two weeks, engage the GP for the longitudinal support, and substitute with the evidence-based therapy.
• This is not abrupt cessation — it is a planned taper with the non-pharmacological foundation and the symptom-targeted pharmacotherapy in place.

The explicit avoidance: no biologic escalation (the RA is in remission), no glucocorticoids (not inflammatory), no further invasive investigations for the pain. [1]

(e) Communication and shared decision-making (3 marks) [1]

Mrs Chen expects a biologic escalation because she has been told her DAS28 is high and she interprets the worsening pain as a rheumatoid flare. The communication strategy: [1]

1. Validate the pain as real — "Your pain is real. This is not in your head. We can see on your brain scans that the pain system is amplified."
2. Explain the discordance — "Your blood tests show no inflammation, your joints show no swelling, and your current biologic is working. The reason your score is high is that the fibromyalgia is making everything tender, including the joints that are not inflamed."
3. Reframe the management — "The answer is not a stronger drug for the rheumatoid arthritis. The answer is to treat the central sensitisation — with exercise, with sleep, with a tablet that calms the pain system, and by coming off the oxycodone, which is making the pain system more sensitive, not less."
4. Negotiate a shared plan and document it — the exercise programme, the amitriptyline, the opioid taper, the CBT referral, and the follow-up with the GP and the rheumatology team. [1]

(f) The common exam trap (1 mark) [1]

The common exam trap in this patient is escalating the biologic or the immunosuppression for a DAS28 that is inflated by secondary fibromyalgia. The correct response is to recognise the central sensitisation, confirm that the inflammatory component is quiet (normal CRP and ESR, no synovitis), and manage the fibromyalgia component with evidence-based therapy. [1]

SAQ 2 — Distinguishing Fibromyalgia from Inflammatory and Endocrine Mimics (10 marks, 15 minutes)

Prompt: A registrar asks you to explain how to distinguish fibromyalgia from the key mimics in the patient with chronic widespread pain. Address: (a) the clinical and investigative discriminators from inflammatory polyarthritis; (b) the discriminator from polymyalgia rheumatica in the older patient; (c) the role of the inflammatory markers and why persistent normality is the key clue; and (d) the principle of the focused investigation screen and the avoidance of over-investigation. [1]

Model Answer

(a) Discrimination from inflammatory polyarthritis (3 marks) [1]

Inflammatory polyarthritis (RA, spondyloarthritis, SLE) has: synovitis on examination (bogginess, warmth, effusion); raised CRP or ESR; prolonged morning stiffness that improves with activity (the gelling phenomenon); specific autoantibodies (RF and anti-CCP for RA, ANA and anti-dsDNA for SLE, HLA-B27 for SpA); and a structural articular pattern. Fibromyalgia has: generalised non-articular tenderness with no synovitis; normal CRP and ESR; widespread pain that does not follow an articular pattern; no specific autoantibody; and preserved range of movement despite the reported pain. [1]

(b) Discrimination from polymyalgia rheumatica (3 marks) [1]

PMR presents in patients typically above 50, with prominent shoulder and pelvic girdle stiffness, a markedly raised ESR and CRP (typically above 40 mm per hour), and a dramatic rapid response to prednisolone 15 mg daily within days. Fibromyalgia presents at any age (peak 30 to 50), has widespread pain not confined to the girdles, has normal inflammatory markers throughout, and does not respond to glucocorticoids. The single most important discriminator is the ESR and CRP: a normal result in a patient with apparent PMR symptoms should trigger fibromyalgia into the differential and should stay the hand from empiric prednisolone [2].

(c) The role of the inflammatory markers (2 marks) [1]

Persistent normality of CRP and ESR with widespread pain, over months of symptoms, is the single most important diagnostic clue supporting a central pain mechanism. A raised marker means a new or alternative diagnosis (inflammation, infection, malignancy). The exception is that SLE can have active disease with normal CRP (the acute-phase response is characteristically blunted in SLE), but SLE has other objective features (synovitis, rash, renal disease, serology) that distinguish it from fibromyalgia. [1]

(d) The focused screen and the avoidance of over-investigation (2 marks) [1]

The focused screen is: FBC, ESR, CRP, TSH, CK, creatinine, electrolytes, vitamin D, and ANA, RF and anti-CCP only if there is a clinical suggestion of inflammatory disease. The goal is to do ENOUGH to exclude the mimics, and then to make the diagnosis and resist the pressure for further negative investigations. Each normal result that is sought reinforces the illness belief that there must be a hidden peripheral cause, and each repeated scan or biopsy that is normal delays the move to evidence-based management [4].