Fibromyalgia and Chronic Widespread Pain — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mrs Susan Chen, 48 years old, primary school teacher. [1]

Presenting complaint: Eight months of worsening widespread pain, fatigue, unrefreshing sleep and difficulty concentrating at work. [1]

Background: Eight-year history of rheumatoid arthritis, currently on methotrexate 20 mg weekly and adalimumab 40 mg subcutaneously every two weeks. The RA had been well controlled until this deterioration. She also describes irritable bowel symptoms (bloating, alternating bowel habit) and tension headaches. [1]

Medications: Methotrexate 20 mg weekly, folic acid 5 mg daily, adalimumab 40 mg subcutaneously every two weeks, oxycodone 20 mg per day (started by a locum GP six months ago), paracetamol 1 g four times daily, omeprazole 20 mg daily. [1]

Examination: Looks well. No synovitis in any joint. Generalised soft-tissue tenderness across the trapezius, the paraspinal muscles, the gluteal muscles and the thighs. Full active range of movement at all major joints. No focal neurological deficit. Beighton score 4. [1]

Investigations: CRP 2 mg per litre (normal), ESR 10 mm per hour (normal), FBC normal, TSH normal, CK normal, creatinine normal, ALT normal. RF positive (known from the RA diagnosis), anti-CCP positive (known). DAS28 4.3. Widespread Pain Index 9, Symptom Severity Scale 7. [1]

Candidate's presentation (SASPOP format)

"Mrs Susan Chen is a 48-year-old primary school teacher presenting with an eight-month history of worsening widespread pain, fatigue, non-restorative sleep and cognitive dysfunction, on a background of well-controlled rheumatoid arthritis. [1]

Her symptoms are widespread pain across the neck, the upper and lower back, both arms and both legs, profound fatigue, unrefreshing sleep and difficulty concentrating. She also has irritable bowel symptoms and tension headaches. [1]

Her age is 48, she is female, she presents to the rheumatology outpatient clinic, she is a primary school teacher, and her occupation is affected by the cognitive dysfunction. [1]

Her problems are:

1. Secondary fibromyalgia overlaid on well-controlled rheumatoid arthritis.
2. Rheumatoid arthritis in remission on methotrexate and adalimumab.
3. Iatrogenic opioid exposure (oxycodone 20 mg per day).
4. A cluster of central sensitivity syndromes (irritable bowel, tension headaches).
5. Functional impairment affecting her work." [1]

Integrated management plan

Problem 1: Secondary fibromyalgia [1]

• Make the diagnosis explicitly and explain the central sensitisation mechanism in plain language. Validate the pain as real and neurobiological.
• The non-pharmacological foundation: graded aerobic exercise (start with walking or swimming, supervised by the physiotherapist, progress slowly), cognitive behavioural therapy (referral to the clinical psychologist), sleep hygiene (fixed sleep and wake times, a wind-down routine), and pacing and graded activity.
• Symptom-targeted pharmacotherapy: amitriptyline 10 mg at night as first-line (the sleep is her most distressing symptom), titrated to 25 mg if tolerated and if the response is partial. If insufficient, add or switch to duloxetine 30 mg daily for one week then 60 mg daily.
• Baseline and track the disease impact with the FIQR [8].
• Multidisciplinary referral: rheumatology (diagnosis and exclusion of mimics), GP (longitudinal continuity and pharmacotherapy titration), physiotherapy (graded exercise), clinical psychology (CBT).

Problem 2: Rheumatoid arthritis in remission [1]

• The inflammatory component is quiet (normal CRP and ESR, no synovitis). Continue methotrexate 20 mg weekly and adalimumab 40 mg subcutaneously every two weeks.
• Do NOT escalate the biologic. The elevated DAS28 is driven by the fibromyalgia component, not by inflammatory activity.
• Explain to the patient that the RA is well controlled and that the biologic is working. [1]

Problem 3: Iatrogenic opioid exposure [1]

• Oxycodone has no role in fibromyalgia. It is likely contributing to the worsening through opioid-induced hyperalgesia [2].
• Structured deprescribing plan: explain the rationale, reduce by approximately 10 per cent every one to two weeks, engage the GP for the longitudinal support, and put the evidence-based therapy in place first. Do not stop abruptly.
• Provide naloxone information given the overdose risk.

Problem 4: Central sensitivity syndromes [1]

• The irritable bowel symptoms and the tension headaches share the central sensitisation mechanism. The non-pharmacological foundation (exercise, CBT, sleep) addresses all of them. The amitriptyline may help the headaches and the irritable bowel as well as the sleep. [1]

Problem 5: Functional impairment [1]

• Address the cognitive dysfunction through the sleep and the mood management.
• Arrange a graded return-to-work plan with the occupational therapist, with workplace accommodation (flexible hours, reduced load initially). [1]

Probing questions and model answers

Q: "Why is her DAS28 elevated if her RA is in remission?" [1]

"The DAS28 is composed of a tender joint count, a swollen joint count, the CRP, and a patient global assessment. The fibromyalgia inflates the tender joint count — every joint is tender because the central pain system is amplified — and the patient global assessment. The objective inflammatory components — the CRP (normal) and the swollen count (zero) — are quiet. The DAS28 cannot distinguish inflammatory activity from central sensitisation, and this is the classic pitfall of secondary fibromyalgia [1][2]."

Q: "Would you order an MRI to look for subclinical synovitis?" [1]

"No. The normal CRP and ESR and the absence of synovitis on clinical examination make active RA very unlikely. Ordering an MRI to look for subclinical disease is over-investigation — it reinforces the illness belief that there must be a hidden peripheral cause, and a positive incidental finding could prompt an inappropriate biologic escalation. The diagnosis of secondary fibromyalgia is clear on the clinical picture and the criteria. The teaching point is to resist the pressure for further negative investigations [4]."

Q: "What would you do if she insists on a stronger painkiller?" [1]

"I would not prescribe an opioid. The evidence is that opioids worsen the central sensitisation, they carry dependence and overdose risk, and they are explicitly recommended against. My ethical response is to explain the rationale (the opioid is making the pain system more sensitive, not less), to offer the evidence-based alternatives (the exercise, the CBT, the amitriptyline, the opioid deprescribing), and to document the discussion. If the pain is severe and refractory, I involve the pain specialist for the multimodal management, not for the opioid escalation." [1]

Q: "What is her prognosis?" [1]

"Fibromyalgia is a chronic condition with a fluctuating course. With early multidisciplinary intervention — the diagnosis, the validation, the non-pharmacological foundation, the symptom-targeted pharmacotherapy, and the opioid deprescribing — she has a good chance of meaningful functional improvement and a return to work. Without the intervention, the trajectory is one of chronification, deconditioning, escalating healthcare utilisation and work disability. The role of the physician is to shift the trajectory [3]."

Communication and shared decision-making

The communication with Mrs Chen is as important as the pharmacotherapy. She expects a biologic escalation and she expects a stronger painkiller. The communication strategy: [1]

1. Validate: "Your pain is real. This is not in your head. We can see on brain scans that the pain system is amplified in fibromyalgia."
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."
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."
4. Negotiate and document: The exercise programme, the amitriptyline, the opioid taper, the CBT referral, the follow-up. Give written information. Book the follow-up. [1]

Short Case — Widespread Pain Assessment

Examination instruction

"Examine this 45-year-old woman who has widespread pain. Present your findings and offer a differential diagnosis." [1]

Systematic examination routine

1. End of bed: general inspection — the patient looks well, no distress, no deformity.
2. Hands: no synovitis, no deformity, no nodules, no skin lesions.
3. Joint examination: palpate each joint group (MCPs, PIPs, wrists, elbows, shoulders, knees, ankles, MTPs) for synovitis — bogginess, warmth, effusion — and find it absent. No joint-line tenderness.
4. Soft-tissue palpation: palpate the trapezius, the supraspinatus, the gluteal muscles, the thigh muscles, the lumbar paraspinals — find generalised soft-tissue tenderness, reproducible across regions.
5. Range of movement: full active range at all major joints, despite reported pain.
6. Neurological: no focal deficit — power, tone, reflexes, sensation and coordination all normal.
7. Hypermobility (Beighton score): screen for the five manoeuvres.
8. Screen for mimics: temporal arteries, organomegaly, proximal weakness. [1]

Key physical signs

• Generalised soft-tissue tenderness with no joint, neurological or tissue abnormality.
• Preserved range of movement despite the reported pain.
• No synovitis, no effusion, no deformity.
• The patient looks well. [1]

Presentation template

"My findings are generalised soft-tissue tenderness across the trapezius, the paraspinal muscles, the gluteal muscles and the thighs, with no synovitis, no joint-line tenderness, no effusion, no deformity, full active range of movement at all major joints, and no focal neurological deficit. The picture is of generalised tenderness with no objective joint, neurological or tissue abnormality. My synthesis is a central sensitisation syndrome. My differential is fibromyalgia (supported by the symptom cluster and the normal inflammatory markers), with polymyalgia rheumatica excluded by the normal ESR and CRP, hypothyroidism excluded by the normal TSH, and polymyositis excluded by the normal CK and the absence of proximal weakness [2]."

Discussion

Q: "How does this differ from rheumatoid arthritis?" [1]

"Rheumatoid arthritis has synovitis — bogginess, warmth, effusion in a symmetrical small-joint distribution with restricted movement and prolonged morning stiffness. Fibromyalgia has generalised soft-tissue tenderness with no synovitis, preserved movement, and a widespread non-articular pattern. The squeeze test is not discriminatory in fibromyalgia because the patient is tender everywhere." [1]

Q: "What investigations would you order?" [1]

"A focused screen to exclude the mimics: FBC, ESR, CRP, TSH, CK, creatinine, electrolytes, vitamin D. I would add ANA, RF and anti-CCP only if there is a clinical suggestion of inflammatory disease. I would not over-investigate — the persistent normality of CRP and ESR with widespread pain is the key diagnostic clue supporting a central pain mechanism [1]."