RheumatologyTier 1Disease (DEADMAN)

Fibromyalgia

Description

Chronic central pain sensitisation syndrome - widespread musculoskeletal pain with fatigue, sleep disturbance, and cognitive symptoms ("fibro fog")
A clinical diagnosis of a real physiological process, not a diagnosis of exclusion or "medically unexplained symptoms" - functional MRI and other research demonstrates objective alterations in central pain processing
Frequently overlaps with other central sensitisation/functional syndromes (IBS, chronic fatigue syndrome, chronic pelvic pain, TMJ disorder)

~2-4% of the population; F>M, though the gap narrows under newer criteria that better capture male presentations
Typical onset 30-50 years, can occur at any age including adolescence

Central sensitisation - amplified pain processing in the CNS (dorsal horn wind-up, altered descending inhibitory pathways) rather than peripheral tissue pathology - explains why standard inflammatory markers and imaging are normal
Dysregulation of neurotransmitters involved in pain modulation (serotonin, noradrenaline) - the rationale for SNRI-class treatment
Triggers/associations: physical trauma, emotional stress, infection, and a genetic predisposition to pain sensitivity - likely a final common pathway from multiple triggers in a susceptible individual
Sleep disturbance and pain appear bidirectionally reinforcing - poor sleep lowers pain threshold, pain disrupts sleep

2016 revised ACR criteria - the current standard

Widespread Pain Index (WPI) >=7 and Symptom Severity Scale (SSS) >=5, OR WPI 4-6 and SSS >=9
Generalised pain present in >=4 of 5 body regions
Symptoms present at a similar level for >=3 months
Not better explained by another diagnosis (though fibromyalgia can coexist with another rheumatological diagnosis - e.g. RA or SLE with superimposed fibromyalgia is common and each needs separate assessment)
The 2016 revision removed the requirement for physician-counted tender points used in the older 1990 criteria - diagnosis no longer depends on a formal tender point examination

Work-up - to exclude mimics/coexisting disease, not to "prove" fibromyalgia

Basic screen: FBE, CRP/ESR, TFTs, CK, vitamin D - normal in fibromyalgia itself; abnormal results should prompt investigation of an alternative/coexisting cause rather than being attributed to fibromyalgia
Avoid extensive autoimmune serology testing (ANA, RF) without a specific clinical indication - low pre-test probability drives false positives and unnecessary anxiety/referral

A. Foundational - non-pharmacological, for every patient

Patient education - explaining the central sensitisation mechanism validates the symptoms as real and improves engagement with treatment
Graded aerobic exercise - the single best-evidenced intervention, started low and progressed gradually ("boom-bust" cycling of activity worsens symptoms)
Cognitive behavioural therapy - good evidence for improving function and coping, not implying the pain is "psychological"
Sleep hygiene/management of comorbid sleep disturbance

B. Pharmacological - modest benefit, used adjunctively

Low-dose tricyclic antidepressant (amitriptyline) at night - improves sleep and pain in many patients, first-line pharmacological option
SNRIs (duloxetine, milnacipran) - address pain and mood/fatigue symptoms concurrently
Pregabalin/gabapentin - reduces pain in a subset, sedation/weight gain are limiting side effects
Opioids and NSAIDs are not recommended - poor evidence of benefit in fibromyalgia specifically, and opioids carry disproportionate harm (dependence, hyperalgesia) in this population

C. Whole-person approach

Address comorbid anxiety/depression directly
Multidisciplinary pain management program for refractory/complex cases (physiotherapy, psychology, medical management combined)
Avoid over-medicalising with repeated normal investigations once the diagnosis is established - this can reinforce illness anxiety rather than help

Irritable bowel syndrome, chronic fatigue syndrome, chronic pelvic pain, interstitial cystitis, TMJ dysfunction - overlapping central sensitisation syndromes
Depression, anxiety - common comorbidities, bidirectional relationship with pain
Can coexist with a defined inflammatory/autoimmune rheumatological disease (RA, SLE, Sjogren's) - important to assess each independently, as fibromyalgia does not respond to immunosuppression

Chronic, fluctuating course - most patients have persistent symptoms over years, though functional improvement with a sustained multidisciplinary approach is achievable
Not associated with tissue damage, joint destruction, or reduced life expectancy - an important reassurance point distinct from inflammatory arthritis
Untreated/unaddressed - significant impact on function, employment, and mental health; diagnostic delay and dismissive care experiences are a recognised source of additional distress and healthcare-seeking
Early diagnosis, validation, and a structured exercise/CBT-based approach improve long-term functional outcomes more reliably than pharmacotherapy alone

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