Fibromyalgia — Symptoms, Causes & Treatment | MyMedicPlus

Fibromyalgia is a chronic, centralised pain condition characterised by widespread musculoskeletal pain, profound fatigue, non-restorative sleep, and cognitive difficulties — collectively termed 'fibro-fog'. It represents a paradigm of central sensitisation: amplified pain signal processing within the central nervous system rather than peripheral tissue damage or inflammation. Functional MRI studies consistently demonstrate altered neural activity in pain-processing regions including the anterior cingulate cortex and insula, with heightened connectivity between pain-amplifying circuits. Fibromyalgia affects approximately 2–4% of the global population — an estimated 200–400 million people worldwide — with a 3:1 female predominance, though this ratio may reflect diagnostic bias as male fibromyalgia is likely underdiagnosed. Onset typically occurs between ages 25 and 55, but the condition affects all ages including children (juvenile fibromyalgia). Fibromyalgia is the second most common rheumatological diagnosis after osteoarthritis and accounts for approximately 15% of new rheumatology outpatient referrals. Critically, it is not a diagnosis of exclusion — it has positive diagnostic criteria (the 2016 ACR diagnostic criteria) and coexists with other conditions rather than being a label applied only when all other diagnoses have been ruled out. The condition carries substantial disability — approximately 30–40% of fibromyalgia patients cannot maintain full-time employment — and significant health resource utilisation, with mean annual healthcare costs 2–3 times higher than matched controls.

Fibromyalgia is caused by central sensitisation — a state of pathological amplification of nociceptive (pain) signal processing in the brain and spinal cord. Neuroimaging demonstrates that fibromyalgia patients perceive as painful stimuli that controls rate as non-painful; they have up to 11 times greater neural activity in pain-processing brain regions in response to equivalent pressure. Precipitating factors include physical trauma (motor vehicle accidents, whiplash, surgery), infectious illness (Epstein-Barr virus, Lyme disease, COVID-19 — 'long COVID fibromyalgia' is now formally recognised), or a major psychological stressor — though fibromyalgia also develops without any identifiable trigger. Genetic susceptibility: twin studies suggest 50% heritability; polymorphisms in genes encoding catecholamine pathways (COMT — catechol-O-methyltransferase; SLC6A4 — serotonin transporter) affect pain modulation thresholds and are enriched in fibromyalgia populations. Psychological factors: adverse childhood experiences (ACE) — physical, emotional, and sexual abuse during childhood — are found in 40–65% of fibromyalgia patients and are associated with hypothalamic-pituitary-adrenal (HPA) axis dysregulation and altered stress response. Depression (found in 30–40% of patients) and anxiety disorders have bidirectional relationships with fibromyalgia — mood disorders lower pain thresholds, and chronic pain worsens mood. Autonomic nervous system dysfunction (increased sympathetic and reduced parasympathetic tone) explains sleep disruption, irritable bowel features, and widespread allodynia in fibromyalgia.

Widespread body pain affecting multiple body regions for at least three months is the hallmark symptom of fibromyalgia. Pain is typically described as deep aching, burning, or stabbing, migrating throughout the body, and fluctuating in intensity depending on activity, sleep, weather changes, and stress. Allodynia (pain from normally non-painful stimuli — light touch, mild pressure, temperature changes) and hyperalgesia (amplified pain response to normally painful stimuli) are neurophysiological hallmarks. Profound fatigue, described as 'bone-deep exhaustion', occurs in over 90% of patients — it is disproportionate to exertion and not fully relieved by rest. Non-restorative sleep: despite spending an adequate number of hours in bed, patients wake unrefreshed — formal polysomnography reveals alpha-wave intrusion into slow-wave (delta) sleep, fragmenting restorative sleep stages and correlating with pain severity the following day. Cognitive dysfunction ('fibro-fog'): difficulties with working memory, sustained attention, word-finding, and information processing speed — documented on neuropsychological testing in 70–80% of patients. Headaches (tension-type or migraine) affect 50% of fibromyalgia patients. Irritable bowel syndrome (IBS) coexists in 30–70%. Overactive bladder and interstitial cystitis are common. Restless legs syndrome affects 30–40%. Temporomandibular joint disorder (TMJ) is present in 40%. These overlapping conditions share central sensitisation pathophysiology and are now collectively termed 'central sensitivity syndromes'.

Fibromyalgia is a clinical diagnosis based on positive diagnostic criteria — no laboratory test or imaging modality confirms the diagnosis. The 2016 revised ACR criteria require: widespread pain index (WPI) score of 7 or more and a symptom severity score (SSS) of 5 or more, or WPI of 4–6 with SSS of 9 or more, with symptoms present at a similar level for at least 3 months, and not better explained by another diagnosis. The WPI counts the number of areas (out of 19 body sites) where the patient has experienced pain in the past week; the SSS rates the severity of fatigue, waking unrefreshed, and cognitive symptoms (each 0–3 scale, maximum score 9) plus a sum of somatic symptoms. Unlike the older 1990 criteria, the 2016 criteria do not require the '18 tender points' examination — which was unreliable, examiner-dependent, and excluded male patients who had fewer tender points than females despite equivalent symptoms. Blood tests are ordered not to confirm fibromyalgia but to exclude other diagnoses — FBC (anaemia, inflammatory arthritis), ESR/CRP (significantly elevated ESR above 50 suggests systemic inflammatory disease), thyroid function (TSH — hypothyroidism mimics fibromyalgia), calcium (hypercalcaemia), vitamin D (deficiency contributes to musculoskeletal pain), CPK (myositis), ANA (if suspicion of lupus or Sjögren's syndrome — typically negative in fibromyalgia), RF and anti-CCP (rheumatoid arthritis). MRI is indicated only when neurological symptoms suggest a structural cause. Assessment of psychiatric comorbidities using validated scales — PHQ-9 (depression), GAD-7 (anxiety) — is essential as they significantly influence treatment and prognosis.

Fibromyalgia management requires a multimodal, biopsychosocial approach. Exercise is the single most effective intervention — supervised aerobic exercise (aquatherapy, walking, cycling — 30 minutes, 3–4 times weekly) reduces pain intensity (NRS) by 1–2 points and significantly improves fatigue and function; resistance training also improves outcomes; complete rest worsens fibromyalgia by deconditioning and reinforcing pain behaviours. Cognitive behavioural therapy (CBT): evidence-based psychological treatment targeting catastrophising, pain-related fear, and maladaptive behaviours — reduces pain catastrophising, improves self-efficacy, and decreases disability; mindfulness-based stress reduction (MBSR) and acceptance and commitment therapy (ACT) are effective alternatives. FDA-approved pharmacotherapy: Duloxetine (Cymbalta — SNRI, 60–120 mg/day): reduces pain in approximately 50% of patients by 30% or more; also treats comorbid depression. Milnacipran (Savella — SNRI, 100–200 mg/day): approved specifically for fibromyalgia; similar efficacy to duloxetine. Pregabalin (Lyrica — alpha-2-delta calcium channel ligand, 300–450 mg/day): improves pain and sleep; first licensed fibromyalgia drug (2007). Gabapentin (1,200–2,400 mg/day): less robust evidence than pregabalin but used widely due to lower cost. Low-dose amitriptyline (10–50 mg nocte): improves sleep architecture and morning pain at doses well below antidepressant range — used as add-on therapy. Cyclobenzaprine (muscle relaxant, 5–40 mg at bedtime): improves sleep and reduces pain. NSAIDs and opioids: NSAIDs have limited efficacy in fibromyalgia (which is not inflammatory) and should not be primary treatment; opioids are not recommended and worsen central sensitisation through opioid-induced hyperalgesia. Tramadol (weak mu-opioid and SNRI properties) may benefit some patients short-term. Low-dose naltrexone (4.5 mg/day — off-label): emerging evidence shows anti-neuro-inflammatory effects and pain reduction in fibromyalgia.

Fibromyalgia causes profound, long-term functional impairment across multiple life domains: approximately 30–40% of patients are unable to maintain full-time employment, with substantial socioeconomic consequences. Disability and work loss represent the greatest measurable burden — physical component scores on the SF-36 quality-of-life questionnaire in fibromyalgia patients are lower than in populations with diabetes, chronic obstructive pulmonary disease, and end-stage renal disease on dialysis. Depression and anxiety disorders are present in 30–40% of fibromyalgia patients, existing in a bidirectional reinforcing cycle with chronic pain — inadequately managed fibromyalgia carries a substantially elevated risk of suicidal ideation (approximately 2-fold increased rate compared to the general population), and psychiatric comorbidity must be systematically assessed. Opioid dependence is a significant iatrogenic complication — fibromyalgia patients are frequently prescribed opioids despite evidence that they worsen central sensitisation, cause opioid-induced hyperalgesia (paradoxical increase in pain sensitivity with increasing dose), and carry addiction risk; up to 40% of fibromyalgia patients seen in specialist centres have been prescribed long-term opioids inappropriately. Social isolation, reduced participation in leisure activities, relationship strain (sexual dysfunction is common), and impaired parenting are psychosocial complications. Physical deconditioning from pain-avoidance behaviours creates a reinforcing cycle — reduced activity increases pain sensitivity, fatigue, and sleep disturbance, worsening all core symptoms.

Fibromyalgia cannot be fully prevented, as the precise aetiology involves genetic, neurobiological, and environmental factors that are not fully controllable. However, certain interventions reduce the risk of onset and flare severity: maintaining regular aerobic exercise (at least 150 minutes of moderate-intensity activity weekly) sustains conditioned pain modulation (CPM — the brain's descending pain inhibitory system) and reduces central sensitisation risk; aerobic fitness is inversely associated with pain sensitivity in population studies. Prompt psychological support after significant traumatic events, surgery, or serious illness — particularly structured trauma-focused CBT or EMDR (eye movement desensitisation and reprocessing) after post-traumatic stress events — may reduce the risk of fibromyalgia developing in susceptible individuals by preventing maladaptive central sensitisation. Sleep quality optimisation: treating obstructive sleep apnoea, practising consistent sleep hygiene, and addressing insomnia with CBT-I (cognitive behavioural therapy for insomnia) before it becomes chronic reduces the inflammatory and neurobiological consequences of sleep deprivation that drive central sensitisation. Stress management: chronic stress dysregulates the HPA axis and sympathetic nervous system — practices including mindfulness, yoga, and structured relaxation reduce allostatic load. Early recognition and treatment of prior central sensitivity syndromes (IBS, migraines, chronic pelvic pain) may prevent the spread of central sensitisation to produce the full fibromyalgia syndrome.

See your GP if you have widespread pain lasting more than 3 months affecting multiple body regions, associated with fatigue, sleep problems, cognitive difficulties, or other symptoms of fibromyalgia — early assessment prevents unnecessary investigations and allows targeted management to begin. Ask for referral to a rheumatologist or pain specialist if: your GP is unable to confirm the diagnosis, your symptoms are severe enough to significantly impair daily function, or initial treatments (exercise, sleep hygiene, amitriptyline) have not produced improvement after 3–6 months. Seek urgent review for: sudden new neurological symptoms (weakness, numbness, bladder or bowel dysfunction) — these are not typical fibromyalgia and require urgent investigation to exclude spinal cord or nerve compression. Seek emergency care for: chest pain, breathlessness, or cardiovascular symptoms occurring in a fibromyalgia patient — fibromyalgia does not cause these, and a cardiac cause must always be excluded.