What is fibromyalgia?

Fibromyalgia is a chronic condition characterised by widespread musculoskeletal pain, fatigue, sleep disturbance and cognitive difficulties ("fibro fog"). It is caused by central sensitisation — abnormal amplification of pain signals in the central nervous system — rather than peripheral tissue damage or inflammation. Inflammatory blood tests (CRP, ESR) are normal; joints are normal on examination. Despite normal tests, fibromyalgia causes significant disability: it affects approximately 2-4% of the global population, predominantly women, and is one of the most common reasons for referral to rheumatology clinics.

How is fibromyalgia diagnosed?

Fibromyalgia is a clinical diagnosis — no blood test or imaging confirms it. The ACR 2010/2016 criteria: widespread pain index (WPI) ≥7 + symptom severity score (SSS) ≥5 (or WPI 4-6 + SSS ≥9); symptoms present for ≥3 months; not better explained by another diagnosis. The old approach (tender point examination) is no longer used. Before diagnosing fibromyalgia, it is important to exclude: inflammatory arthritis (rheumatoid arthritis — elevated CRP/ESR, swollen joints); lupus; hypothyroidism; vitamin D deficiency; haemochromatosis; polymyalgia rheumatica (in older adults); small fibre neuropathy.

Why are opioids harmful in fibromyalgia?

Opioids are specifically contraindicated in fibromyalgia because they cause opioid-induced hyperalgesia (OIH) — paradoxically making the pain system more sensitive rather than less. Central sensitisation is driven by overactive excitatory neurotransmitter systems; opioids upregulate these systems further and alter the descending pain inhibitory pathways, making pain more widespread and severe. Clinical practice consistently shows fibromyalgia patients on long-term opioids have worse pain, worse function and worse quality of life than those not on opioids. Evidence is strongly against opioids for fibromyalgia (ACR 2016, EULAR 2017, NICE).

What lifestyle changes help fibromyalgia?

Exercise: the single most evidence-based intervention for fibromyalgia. Aerobic exercise (swimming, walking, cycling — low-impact preferred due to joint sensitivity) reduces pain, fatigue and improves sleep and quality of life at least as effectively as drug therapy. Start extremely low and build very gradually. Aquatic exercise is particularly effective. Sleep hygiene: consistent sleep schedule; address sleep-disrupting factors (cognitive arousal before bed, noise, light); low-dose amitriptyline for sleep. Stress management: CBT addresses the catastrophising and fear-avoidance patterns that amplify pain. Social connection: isolation worsens fibromyalgia.

What are the best medications for fibromyalgia?

FDA-approved specifically for fibromyalgia: duloxetine (SNRI, 60mg/day — also treats comorbid depression), milnacipran (SNRI, 100-200mg/day), pregabalin (300-450mg/day — also improves sleep). Commonly used off-label: amitriptyline (10-50mg at night — improves sleep and pain); gabapentin (moderate evidence for sleep and pain). NOT recommended: NSAIDs (minimal benefit for central sensitisation); opioids (contraindicated — cause OIH); high-dose corticosteroids (no evidence). The approach: pharmacotherapy should complement, not replace, exercise and CBT. Most patients benefit from combining low-dose amitriptyline (sleep) + duloxetine (pain/mood) + aerobic exercise + CBT.

How does GMJ News cover fibromyalgia?

GMJ News covers WHO fibromyalgia data, central sensitisation mechanism, ACR 2010/2016 diagnostic criteria, opioid contraindication (OIH), duloxetine/milnacipran/pregabalin FDA approvals, aerobic exercise evidence, amitriptyline for sleep, CBT, comorbidities (IBS, depression, ME-CFS), and the central sensitivity syndrome concept. Fibromyalgia — affecting 2-4% of the population — is directly relevant to PHIG's NCD, chronic pain and rehabilitation programme.

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Fibromyalgia

GMJ News knowledge hub · last reviewed September 2026 · Georgian Medical Journal

Summary Statistics Glossary GMJ news FAQ Documents Organizations Research

Fibromyalgia — a chronic condition characterised by widespread musculoskeletal pain, fatigue, sleep disturbance and cognitive dysfunction (“fibro fog”), driven by central sensitisation (amplified pain processing in the CNS rather than peripheral tissue damage) — affects approximately 2-4% of the global population (predominantly women, 3-7:1 female:male ratio) and is among the most common causes of chronic pain worldwide, yet remains profoundly under-recognised, frequently dismissed, and poorly treated despite robust evidence for its neurobiological basis and multiple approved pharmacological therapies (WHO). A critical clinical rule: opioids are contraindicated in fibromyalgia — they consistently worsen outcomes through opioid-induced hyperalgesia — while approved treatments (duloxetine, milnacipran, pregabalin) and aerobic exercise have robust trial evidence.

Key messages

2-4% prevalence — most common cause of widespread pain

Fibromyalgia affects approximately 2-4% of the global population — predominantly women (3-7:1 female:male ratio). It is one of the most common causes of chronic widespread pain globally and the most common musculoskeletal condition after osteoarthritis and rheumatoid arthritis in rheumatology clinics (WHO).

Central sensitisation — not peripheral tissue damage

Fibromyalgia is driven by central sensitisation — abnormal amplification of pain signals in the central nervous system — rather than peripheral inflammation or tissue damage. Inflammatory markers (CRP, ESR) are normal; joint examination is normal. MRI and PET show altered brain pain processing networks.

Opioids are contraindicated — they worsen fibromyalgia

Opioids are specifically contraindicated in fibromyalgia — they cause opioid-induced hyperalgesia (OIH), making pain more widespread and severe. This is the opposite of the expected analgesic effect. Opioids for fibromyalgia consistently worsen outcomes in clinical practice and trials.

FDA-approved treatments: duloxetine, milnacipran, pregabalin

Three medications are FDA-approved specifically for fibromyalgia: duloxetine (SNRI — 60mg/day); milnacipran (SNRI — 100-200mg/day); pregabalin (alpha-2-delta ligand — 300-450mg/day). None achieves complete pain relief — typical benefit is approximately 30% pain reduction in approximately 50% of patients.

Aerobic exercise — the strongest single intervention

Aerobic exercise (low-to-moderate intensity swimming, walking, cycling) has the strongest evidence base in fibromyalgia — reducing pain, fatigue and improving function and quality of life. Starting low and building gradually is essential; the aim is regular, consistent activity rather than intensity. Exercise is as effective as pharmacological therapy.

Multidisciplinary treatment is most effective

The best outcomes come from combining: aerobic exercise; CBT (addressing catastrophising and fear-avoidance); sleep hygiene; patient education about central sensitisation; low-dose amitriptyline (for sleep and pain); and pharmacological therapy (duloxetine or pregabalin). Single-modality approaches are less effective than combined approaches.

Key statistics

2-4%

global population prevalence (WHO estimate)

WHO

3-7:1

female:male ratio (predominantly women)

WHO/ACR

inflammation on blood tests (normal CRP/ESR) — not inflammatory arthritis

ACR/EULAR

3 FDA-approved

specific fibromyalgia drugs: duloxetine, milnacipran, pregabalin

FDA

Contraindicated

opioids in fibromyalgia — cause opioid-induced hyperalgesia (OIH)

WHO/ACR

~50%

of fibromyalgia patients have comorbid depression or anxiety

WHO/ACR

Fibromyalgia — comorbidities and symptom domains (ACR/WHO)

Source: ACR/WHO. Fibromyalgia is rarely isolated — psychiatric and functional comorbidities are the rule, not the exception.

Glossary of key terms

Central sensitisation
WHO/NeuroscienceA state of amplified pain signalling in the central nervous system — where pain pathways become hypersensitive, responding to normally non-painful stimuli (allodynia — pain from light touch) and amplifying painful stimuli (hyperalgesia). In fibromyalgia: increased excitatory neurotransmitters (glutamate, substance P); decreased inhibitory modulation (serotonin, noradrenaline — hence the rationale for SNRIs); altered functional connectivity in pain processing brain networks (demonstrated on fMRI). Central sensitisation explains why anti-inflammatories (targeting peripheral inflammation) are ineffective, while centrally-acting drugs (duloxetine, pregabalin) have evidence.

ACR 2010/2016 diagnostic criteria
ACR/EULARNo requirement for tender point examination (replaced the 1990 ACR 11/18 tender point criterion). Current criteria (ACR 2010, modified 2016): (1) Widespread pain index (WPI) ≥7 + symptom severity scale (SSS) ≥5; OR WPI 4-6 + SSS ≥9. (2) Symptoms present at similar level for ≥3 months. (3) Not better explained by another diagnosis. WPI: count of areas with pain in past week (19 regions). SSS: fatigue severity + unrefreshing sleep severity + cognitive symptom severity (0-3 each) + presence of somatic symptoms.

Duloxetine (Cymbalta)
FDA 2008/WHOAn SNRI (serotonin-noradrenaline reuptake inhibitor) — FDA-approved for fibromyalgia (2008), also approved for depression, GAD, diabetic neuropathy, chronic musculoskeletal pain. Mechanism: enhanced descending pain inhibition via increased serotonin and noradrenaline in the spinal cord. Start 30mg, increase to 60mg/day. Evidence: approximately 30% pain reduction vs placebo in approximately 50% of patients. Side effects: nausea (usually transient), insomnia, dry mouth, increased sweating.

Pregabalin (Lyrica)
FDA 2007/WHOAn alpha-2-delta calcium channel ligand — FDA-approved for fibromyalgia (2007), also approved for neuropathic pain and partial epilepsy. Mechanism: reduces release of excitatory neurotransmitters (substance P, glutamate) from presynaptic neurons — "calming" the sensitised pain system. Standard dose: 300-450mg/day in 2-3 divided doses. Evidence: similar to duloxetine. Side effects: dizziness, sedation, peripheral oedema, weight gain; abuse potential (particularly in patients with opioid history).

Fibromyalgia and functional disorders
WHO/RheumatologyFibromyalgia frequently co-occurs with other conditions sharing the central sensitisation mechanism — collectively called central sensitivity syndromes (CSS): irritable bowel syndrome (IBS — 40% comorbidity); migraine; temporomandibular disorder (TMD — jaw pain); interstitial cystitis; chronic pelvic pain; myalgic encephalomyelitis/ME-CFS; restless legs syndrome. This syndromic overlap, combined with normal blood tests and imaging, has historically led to fibromyalgia being dismissed. Neuroscience has now established the biological basis for central sensitisation.

Low-dose amitriptyline
WHO/EULARLow-dose amitriptyline (10-50mg at night — much lower than antidepressant doses) is commonly used first-line for fibromyalgia sleep symptoms. Mechanism: sedative (antihistamine, anticholinergic effects at low doses) + weak serotonin/noradrenaline reuptake inhibition. Evidence: reduces pain and fatigue; improves sleep quality; not FDA-approved specifically for fibromyalgia but widely used (EULAR recommendation). Side effects: morning sedation, dry mouth, constipation — start at 10mg and titrate slowly.