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, symptoms at a similar level for at least 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 patient 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 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]."