Fibromyalgia

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Fibromyalgia is a chronic nociplastic syndrome characterised by pain in multiple body regions plus fatigue, non-restorative sleep and cognitive difficulty. Ask about distribution, fluctuation, sleep, sensory sensitivities, headaches, bowel or bladder symptoms, postural symptoms, mood, trauma, work, caring and activity effects. Clarify stiffness, swelling, fever, weight change, rashes, weakness, numbness, apnoeas and medicine use. Examination should identify synovitis, muscle weakness, neurological loss, endocrine signs and hypermobility; generalised tenderness supports the phenotype but is not a test of credibility.

Diagnosis is positive and can be made in primary care. Current criteria use widespread regions, duration, Widespread Pain Index and Symptom Severity scoring; the former 18-point tender examination is not mandatory. A focused baseline set such as FBC, CRP or ESR, renal and liver profile, calcium, TSH and CK may be reasonable when history suggests a mimic. Autoantibodies, repeated imaging and specialist panels are not screening tests and frequently generate incidental results.

A useful explanation separates pain intensity from ongoing tissue damage while acknowledging biological and social contributors. Management aims to increase function, confidence and recovery rather than promise immediate pain elimination. Choose one or two feasible changes, such as consistent wake time and brief low-intensity walking, then progress. Psychological therapies are pain skills, not a statement that symptoms are imaginary. Antidepressants can be trialled for pain, sleep or mood, but medicine burden should fall when planned functional targets are not met.

Key points

Fibromyalgia causes chronic widespread pain with fatigue, non-restorative sleep, cognitive symptoms and sensory sensitivity; examination may show diffuse tenderness but no required tender-point count.
Make a positive clinical diagnosis after history, full examination and proportionate tests show no better explanation; it can coexist with inflammatory or structural disease.
Widespread Pain Index and Symptom Severity scores can structure assessment, but complement rather than replace clinical judgement and exclusion of important mimics.
Explain nociplastic amplification: pain is real, but ongoing symptoms do not mean muscles and joints are being progressively damaged by ordinary movement.
Offer supported graded aerobic and strengthening activity, pacing that avoids boom-and-bust cycles, sleep intervention and, when appropriate, ACT or CBT for pain.
NICE allows consideration of selected antidepressants after shared discussion, even without depression; use low doses, define a target and review adverse effects and withdrawal.
Do not initiate opioids, gabapentinoids, benzodiazepines, NSAIDs or paracetamol specifically for chronic primary pain; review existing treatment safely rather than stopping abruptly.
Investigate new focal, inflammatory, neurological or systemic features independently; fibromyalgia should reduce neither vigilance nor access to ordinary care.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Multifactorial susceptibility

Genetic, neurobiological, sleep, autonomic and psychological factors alter vulnerability, but no single lesion, infection, personality type or laboratory abnormality explains all cases.

Precipitating stressors

Symptoms may follow infection, injury, surgery, childbirth or sustained emotional and occupational stress; a temporal trigger does not establish ongoing tissue damage.

Coexisting long-term disease

Fibromyalgia is more frequent with rheumatoid arthritis, lupus, axial spondyloarthritis, hypermobility, migraine, irritable bowel syndrome and mood or trauma-related disorders.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Nociplastic amplification
Central sensory networks amplify and prolong nociceptive signalling despite no adequate peripheral injury, producing widespread pain and tenderness from ordinarily tolerable input.
2
Impaired inhibitory control
Descending pain modulation becomes less effective and temporal summation increases, so repeated stimuli feel progressively more painful and symptoms persist after activity.
3
Sleep and arousal disruption
Non-restorative sleep, hypervigilance and autonomic dysregulation worsen pain threshold, concentration, fatigue and post-exertional recovery, reinforcing symptoms across systems.
4
Deconditioning feedback
Unpredictable flares promote boom-and-bust activity or avoidance; reduced fitness then makes ordinary effort more demanding, increasing pain and fatigue without structural injury.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Widespread pain

Pain affects multiple axial and limb regions for at least three months, often changing location and intensity rather than remaining anatomically focal.

Restorative failure

Patients wake unrefreshed despite sufficient time in bed and report disproportionate fatigue after ordinary physical or cognitive demands.

Cognitive symptoms

Slowed processing, word-finding difficulty and reduced concentration fluctuate with poor sleep, pain and overload and are often called fibro fog.

Sensory amplification

Diffuse pressure tenderness, headache and increased sensitivity to light, sound, temperature, odour or touch fit altered sensory processing.

Associated syndromes

Migraine, irritable bowel symptoms, temporomandibular pain, pelvic pain and postural symptoms commonly cluster but each still needs red-flag assessment.

Objective discordance

Effort may be limited by pain and fatigue, but focal weakness, atrophy, reflex change or swollen joints points to an additional diagnosis.

Red flags requiring action

Objective progressive weakness, upper-motor-neurone signs, saddle sensory change or new bladder dysfunction requires urgent neurological or spinal assessment.
Persistent fever, weight loss, focal night pain, lymphadenopathy, inflammatory joint swelling or markedly abnormal inflammatory markers suggests infection, malignancy or inflammatory disease.
Current suicidal thoughts with intent, inability to maintain safety or severe medicine withdrawal needs same-day mental-health and medical risk assessment.
New exertional chest pain, syncope, hypoxaemia or unilateral limb swelling requires acute cardiopulmonary assessment rather than attribution to sensitisation.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
First-line clinical criteriaFirst stepFirst line
Why
Document widespread symptom burden and duration while finding objective features indicating another or coexisting condition.
Interpretation and limitations
WPI and Symptom Severity scores support a positive phenotype but must not be used mechanically without examination or when an alternative explains findings better.
02
Focused baseline blood panel
Why
Exclude common reversible mimics when history or examination warrants testing.
Interpretation and limitations
FBC, CRP or ESR, renal and liver profile, calcium, TSH and sometimes CK are usually sufficient; minor isolated abnormalities require clinical interpretation.
03
Targeted nutritional tests
Why
Investigate anaemia, malabsorption, neuropathy, bone pain or endocrine features rather than screen indiscriminately.
Interpretation and limitations
Select ferritin, B12, folate, vitamin D, phosphate or other tests from a specific clue and never assume one deficiency explains every symptom.
04
Targeted inflammatory evaluation
Why
Assess persistent swelling, inflammatory back pain, rash, Raynaud features, uveitis or true proximal weakness.
Interpretation and limitations
Use examination, markers and disease-specific serology or imaging only when pre-test probability exists; positive ANA alone is common and non-diagnostic.
05
Sleep assessment
Why
Identify sleep apnoea, restless legs, circadian disruption or medicine-related sedation contributing to fatigue and pain.
Interpretation and limitations
Snoring, witnessed apnoea, obesity, hypertension or daytime sleepiness justifies formal assessment; routine polysomnography is unnecessary for everyone.
06
Imaging for a local question
Why
Investigate trauma, focal bone pain, neurological compression or objective joint pathology not explained by the widespread syndrome.
Interpretation and limitations
Degenerative changes are frequent incidental findings; link abnormalities anatomically and functionally before presenting them as the cause of generalised pain.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Inflammatory rheumatic disease

Rheumatoid arthritis, polymyalgia, myositis and spondyloarthritis produce objective synovitis, prolonged stiffness, weakness, uveitis or raised markers, although fibromyalgia may amplify symptoms.

Endocrine and nutritional disease

Hypothyroidism, osteomalacia, iron deficiency, B12 deficiency and electrolyte disorders can cause fatigue, pain or weakness and are identified through focused assessment.

Neurological and sleep disorders

Neuropathy, multiple sclerosis, myopathy, restless legs and sleep apnoea have localising findings or characteristic physiology not explained by widespread tenderness alone.

Medicine and mood effects

Statins, sedatives, opioid-induced hyperalgesia, depression, anxiety and post-traumatic symptoms contribute; mood disorders are treated without reducing physical symptoms to psychology.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First-line diagnosisName the syndrome and retain vigilanceFirst stepFirst lineWidespread pain, sleep disturbance, fatigue and cognitive symptoms have persisted for at least three months.

1Take a whole-person history and perform musculoskeletal, neurological and general examination, documenting both typical clustering and discordant objective features.
2Use symptom criteria to support a positive diagnosis and request only focused tests needed for common mimics or history-led alternatives.
3Explain that altered processing produces genuine pain without requiring continuing tissue damage while preserving a route to assess new focal or systemic change.
4Agree the most important functional problem and a small initial treatment target rather than an unmanageable dense package.

02Preferred non-drug treatmentRebuild activity, sleep and controlPreferredAlternativeThe diagnosis is sufficiently accepted to begin rehabilitation and no unstable alternative limits participation.

1Start low-intensity aerobic or strengthening activity below the level provoking prolonged flare, then increase one variable gradually with support when needed.
2Replace overactivity-and-collapse cycles with planned pacing, consistent waking and recovery while maintaining valued work, family and social roles.
3Offer ACT or CBT for pain when accessible, focusing on coping, sleep, fear, mood and valued action rather than proving a psychological cause.
4Address sleep apnoea, restless legs, depression, anxiety, trauma, obesity or hypermobility as parallel treatable contributors.

03Medicine trialUse an explicit target and stop ruleNon-pharmacological care is under way but sleep, mood or pain remains limiting enough for a cautious antidepressant trial.

1Discuss that amitriptyline or duloxetine use for fibromyalgia pain is off-label in the UK, identify the primary target and review interactions.
2Begin low, titrate only if tolerated and review within four to eight weeks for functional benefit, adverse effects, blood pressure, sedation and mood.
3Continue only when benefit outweighs harm; taper gradually if ineffective because withdrawal can intensify the symptom complex.
4Do not initiate opioids, gabapentinoids, benzodiazepines, NSAIDs or paracetamol specifically for chronic primary pain.

04Existing dependence-prone treatmentReview safely without abandonmentThe patient already receives an opioid, gabapentinoid, benzodiazepine or another medicine offering little value or excess harm.

1Assess benefit, dose, duration, dependence, sedation, falls, driving and concurrent substances, and explain why change may improve long-term function.
2Agree a slow individual reduction with pauses when needed, never using abrupt cessation as a test of commitment or withdrawing care during symptoms.
3Strengthen non-drug, sleep and mental-health support and seek specialist pain or dependence input when dose, comorbidity or withdrawal risk is complex.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

A low-dose antidepressant trial may improve sleep and pain interference even without depression, alongside active rehabilitation.

Amitriptyline off-label

Start 10 mg orally at night, increasing after one to two weeks to 20–25 mg at night if needed and tolerated; review after four to eight weeks and taper if ineffective.

Sedation, dry mouth, constipation, urinary retention, blurred vision, falls and QT effects limit use, especially in older adults; avoid MAO inhibitors and seek advice in pregnancy, bipolar disorder or suicide risk.

May be considered when pain interference coexists with depression or anxiety after discussing off-label UK use and modest average benefit.

Duloxetine off-label

Start 30 mg orally once daily for one to two weeks, then increase to 60 mg once daily if tolerated; review by four to eight weeks and taper gradually when stopping.

Check blood pressure, liver and renal disease, bleeding medicines, hyponatraemia and serotonergic combinations; nausea, insomnia, sexual dysfunction and withdrawal occur, and reproductive advice is needed.

Reduces dependence-prone treatment lacking durable chronic-primary-pain benefit while maintaining therapeutic support and function-focused care.

Existing opioid or gabapentinoid taper

There is no universal schedule; agree small proportional reductions, commonly 5–10% every two to four weeks, slowing or pausing for withdrawal, dose, duration and mental-health risk.

Abrupt withdrawal can cause severe autonomic, gastrointestinal, mood, pain and sleep symptoms; benzodiazepine or high-dose opioid withdrawal may be dangerous, requiring overdose assessment and specialist input.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Functional restriction

Pain, cognitive difficulty and fatigue can impair employment, caring, exercise and self-care, especially when activity repeatedly alternates between overexertion and prolonged recovery.

Sleep and mental health

Chronic insomnia, demoralisation, anxiety, depression and suicide risk may develop, requiring direct assessment and treatment alongside pain rehabilitation.

Iatrogenic dependence

Repeated investigation, long-term opioids, benzodiazepines or gabapentinoids can add incidental findings, sedation, tolerance, withdrawal, falls and dependence without restoring function.

Diagnostic overshadowing

A fibromyalgia label can delay recognition of infection, inflammatory disease, malignancy or neurological injury when a new symptom is assumed to be another flare.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Use the same patient-selected outcomes, such as work attendance, walking, sleep regularity or recovery time, rather than chasing a zero pain score.
Increase activity in small increments only after the current level is repeatable; review post-activity duration, fear, technique and competing illness when progress stalls.
For antidepressants, review mood, suicidality, sleep, function, blood pressure where relevant, adverse effects and withdrawal risk within four to eight weeks.
Reassess red flags when symptoms become focal, objective weakness appears, a joint swells, inflammatory stiffness emerges or systemic health changes.
Monitor opioids, sedatives and gabapentinoids for escalation, dependence, falls, cognition, driving and breathing risk, with collaborative taper when harm exceeds benefit.
Schedule follow-up proactively after diagnosis so explanation is linked to implementation, review and access to rehabilitation.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Diagnosis is positive

A recognisable symptom cluster and normal objective examination support diagnosis; exhaustive exclusionary testing is neither necessary nor harmless.

Coexistence is common

Fibromyalgia can amplify pain in controlled rheumatoid or lupus disease, but cannot prove inflammation absent when objective signs recur.

Tender points are historical

The fixed 18-site tender-point count is no longer required; distribution and severity of pain, fatigue, sleep and cognition provide broader assessment.

Exercise dose is individual

Starting below current tolerance and progressing consistently is more useful than repeatedly testing maximum capacity with a generic vigorous programme.

Withdrawal resembles flare

Pain, insomnia, anxiety and autonomic symptoms during rapid reduction can be misread as proof that an ineffective medicine was beneficial.

11Common pitfallsFrequent interpretation and management errors.

01
Do not tell a patient that normal tests mean nothing is wrong; explain the positive nociplastic mechanism and provide active care.
02
Do not order broad autoimmune panels without compatible signs because incidental antibodies create anxiety and inappropriate pathways.
03
Do not equate symptom severity with inflammation activity in coexisting rheumatic disease; assess both processes objectively.
04
Do not prescribe exercise as a vague instruction; define a tolerable starting dose, progression rule and response to flare.
05
Do not initiate opioid or gabapentinoid treatment for chronic primary fibromyalgia pain, and never abruptly abandon someone already dependent.
06
Do not attribute a new emergency to fibromyalgia; chest pain, neurological loss, fever, swollen joints and suicidal risk retain ordinary urgency.