Fibromyalgia and Chronic Widespread Pain — Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mrs Susan Chen is a 48-year-old primary school teacher with an eight-year history of rheumatoid arthritis, well controlled on methotrexate 20 mg weekly and adalimumab 40 mg subcutaneously every two weeks, who presents with an eight-month history of worsening widespread pain across her neck, back, both arms and both legs, profound fatigue, unrefreshing sleep and difficulty concentrating. [1]

Her main problems are:

1. Secondary fibromyalgia overlaid on well-controlled rheumatoid arthritis — she meets the 2016 ACR criteria (WPI 9, SSS 7, generalised pain, more than 3 months), her CRP and ESR are normal, and there is no synovitis. The fibromyalgia is inflating her DAS28 to 4.3 through the tender joint count and the patient global.
2. Rheumatoid arthritis in remission on methotrexate and adalimumab — the inflammatory component is quiet.
3. Iatrogenic opioid exposure — she has been on oxycodone 20 mg per day for six months, which is likely worsening the central sensitisation through opioid-induced hyperalgesia.
4. A cluster of central sensitivity syndromes — irritable bowel symptoms and tension headaches — sharing the central sensitisation mechanism.
5. Functional impairment — the cognitive dysfunction and the fatigue are affecting her work as a teacher. [1]

My priorities are the explanation and validation of the diagnosis, the non-pharmacological foundation (graded exercise, CBT, sleep hygiene, pacing), the symptom-targeted pharmacotherapy (amitriptyline at night as first-line for the sleep), the structured opioid deprescribing, and the multidisciplinary team referral. I will explicitly not escalate the biologic, because the inflammatory component is in remission." [1]

Examiner probing questions and model answers

Q1: "How do you know the rheumatoid arthritis is in remission and not driving the pain?" [1]

"The evidence is the discordance between the composite score and the objective inflammatory measures. The CRP is 2 (normal), the ESR is 10 (normal), and there is no synovitis on examination — the swollen joint count is zero. The DAS28 of 4.3 is elevated, but the DAS28 is composed of a tender joint count, a swollen joint count, the CRP, and a patient global assessment. In Mrs Chen, the tender joint count and the patient global are inflated by the central sensitisation — the fibromyalgia makes every joint tender. The objective components — the CRP and the swollen count — are quiet. This is the classic picture of secondary fibromyalgia, and the teaching point is that the DAS28 cannot distinguish inflammatory activity from central sensitisation [1][2]."

Q2: "She meets the 2016 ACR criteria. What are they, and why are the tender points obsolete?" [1]

"The 2016 ACR revised criteria 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]. 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. 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, which is why Mrs Chen can have both RA and fibromyalgia."

Q3: "Explain the central sensitisation mechanism in a way that justifies your pharmacotherapy." [1]

"Fibromyalgia is a disorder of amplified central pain processing. The gain on the central pain system is turned up, so a normal stimulus produces a disproportionate pain experience — that is hyperalgesia — and a normally non-painful stimulus like light touch is felt as pain — that is allodynia. Functional MRI shows this objectively: equal pressure stimuli produce greater activation in the insula and the somatosensory cortex in fibromyalgia patients than in controls [2].

There are two mechanism-level problems. First, the descending inhibitory system — the serotonergic and noradrenergic pathway from the periaqueductal grey that normally suppresses incoming nociceptive signals — is deficient. Second, the excitatory neurotransmitters substance P and glutamate are elevated. The pharmacotherapy follows directly. Amitriptyline and duloxetine boost the deficient descending inhibition by increasing serotonin and noradrenaline. Pregabalin and gabapentin reduce the release of the excitatory neurotransmitters by binding the alpha-2-delta subunit of the voltage-gated calcium channel [5][6]. The treatment targets the CNS, not a peripheral tissue."

Q4: "She is on oxycodone 20 mg a day. What do you do about it?" [1]

"Oxycodone has no role in fibromyalgia. It has no evidence of sustained benefit, it worsens the central sensitisation through opioid-induced hyperalgesia — a neuroplastic phenomenon of increased pain sensitivity that paradoxically makes the pain worse as the dose escalates — and it carries dependence and overdose risk. Mrs Chen's spreading pain and her allodynia over the last six months, since the oxycodone was started, are consistent with opioid-induced hyperalgesia [2].

My approach is a structured deprescribing plan. I explain the rationale — the opioid is worsening the pain system, not helping it. I reduce by approximately 10 per cent every one to two weeks, I engage the GP for the longitudinal support, and I put the evidence-based therapy in place first — the amitriptyline, the exercise, the CBT — so that the central sensitisation is being treated as the opioid comes down. I do not stop it abruptly. I also offer the GP and the patient the naloxone information, given the overdose risk." [1]

Q5: "What is the role of exercise, and what is the evidence?" [1]

"Exercise is the cornerstone of the non-pharmacological management and it is the only therapy-based recommendation graded strong-for by the 2017 EULAR guidelines [3]. The Hauser meta-analysis of 28 randomised controlled trials showed that aerobic exercise reduces pain, fatigue and depressed mood, and improves physical fitness and health-related quality of life [7]. The mechanism is partly the central effect (exercise increases the descending inhibition and the endogenous opioid and endocannabinoid signalling) and partly the peripheral effect (deconditioning worsens the pain, and reconditioning improves it).

The key is grading — Mrs Chen should start low, with walking or swimming, and progress slowly. Starting too hard flares the pain and reinforces the fear-avoidance, which is the opposite of what I want. I involve the physiotherapist to supervise the programme." [1]

Q6: "How do you explain this to a patient who expects a stronger drug for her rheumatoid arthritis?" [1]

"I start by validating the pain — her pain is real, it is neurobiological, and it is not in her head. I then explain the discordance — the blood tests show no inflammation, the joints show no swelling, and the current biologic is working. I reframe the elevated score — the reason the DAS28 is high is that the fibromyalgia is making everything tender, including the joints that are not inflamed. I then reframe the management — the answer is not a stronger drug for the rheumatoid arthritis, it is to treat the central sensitisation, with exercise, with sleep, with a tablet that calms the pain system, and by coming off the oxycodone that is making the pain system more sensitive. [1]

I negotiate a shared plan: the exercise programme, the amitriptyline at night, the opioid taper, the CBT referral, and the follow-up. I document it, I give her written information, and I book the follow-up. The communication is as important as the pharmacotherapy — a patient who feels invalidated will not engage with a non-pharmacological plan [4]."

Short Case Discussion

The widespread pain assessment

Examiner instruction: "This 45-year-old woman has widespread pain. Examine her and present your findings." [1]

Candidate's model answer: [1]

"My routine is the end of the bed, the hands and the general inspection, the joint examination (looking for synovitis), the soft-tissue palpation (looking for the pattern of tenderness), the range of movement, the neurological examination, and the screen for hypermobility and for the mimics. [1]

End of bed. She looks well — she is in no distress, she has no obvious deformity, she is mobile. The fact that she looks well is itself a discriminating feature from active inflammatory disease, where the patient often looks systemically unwell. [1]

Hands and general inspection. No synovitis, no deformity, no nodules, no skin lesions, no muscle wasting, no rash. The hands are normal. [1]

Joint examination. I palpate each joint — the MCPs, the PIPs, the wrists, the elbows, the shoulders, the knees, the ankles, the MTPs — for synovitis. I am looking for bogginess, warmth and effusion. In this patient, I find none. There is no joint-line tenderness. I perform the squeeze test across the MCPs and the MTPs, and it may be uncomfortable, but it is non-specific because she is tender everywhere. [1]

Soft-tissue palpation. I palpate the soft tissues — the trapezius, the supraspinatus, the gluteal muscles, the thigh muscles, the lumbar paraspinals — and I find generalised tenderness. The tenderness is soft-tissue, not articular, and it is reproducible across regions. This generalised tenderness with no objective joint abnormality is the examination hallmark of fibromyalgia. [1]

Range of movement. Active range of movement is preserved at all major joints — full flexion and extension at the elbows, the wrists, the shoulders, the knees. The patient reports pain but can move through the full range. The discrepancy between full movement and reported pain is characteristic. [1]

Neurological examination. No focal deficit. Power is normal (she may report subjective weakness, but on formal testing the power is five throughout), tone is normal, reflexes are symmetrically present, sensation is intact, and coordination is normal. There is no nerve root distribution to the pain. [1]

Hypermobility screen. I perform the Beighton score — the fifth-finger dorsiflexion beyond 90, the thumb apposition to the forearm, the elbow and knee hyperextension beyond 10, and the palms to the floor. Hypermobility is over-represented in fibromyalgia and contributes a biomechanical component to the pain. [1]

Screen for mimics. I check the temporal arteries (in the older patient, for giant cell arteritis), I feel for organomegaly (for malignancy), and I look for the proximal weakness of a myopathy (she rises from a chair without difficulty). [1]

My synthesis: generalised soft-tissue tenderness with no objective joint, neurological or tissue abnormality, consistent with 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]."*

Examiner: "How do you distinguish this from rheumatoid arthritis on the examination alone?" [1]

"The distinction is the presence or absence of synovitis. In rheumatoid arthritis, I find synovial bogginess, warmth and effusion in a symmetrical small-joint distribution — the MCPs, the PIPs, the wrists, the MTPs — with restricted range of movement and morning stiffness that improves with activity. In fibromyalgia, I find generalised soft-tissue tenderness with no synovitis, preserved range of movement, and a widespread non-articular pattern. The squeeze test is not discriminatory because the fibromyalgia patient is tender everywhere. The teaching point is that the examination in suspected fibromyalgia is performed to demonstrate the generalised tenderness and the absence of the objective joint abnormality, and the inflammatory markers confirm it." [1]

Examiner: "What is the single most important lesson from this case for a registrar managing widespread pain?" [1]

"The single most important lesson is that the normal inflammatory marker is the key. A patient with widespread pain and a normal CRP and ESR, over months of symptoms, has a central pain mechanism until proven otherwise — and the response is to make the diagnosis, explain it, validate the symptoms, and start the evidence-based management, not to keep searching for a peripheral lesion that is not there. The registrar who orders the tenth ANA, the third MRI, or the empiric prednisolone trial has missed the point. The corollary is that a rising marker, a new focal deficit, or a new red flag changes everything — the diagnosis of fibromyalgia does not confer immunity to other disease, and any red flag is investigated as in any other patient [1][2]."