Fibromyalgia

Fibromyalgia is a chronic centralised pain syndrome characterised by widespread musculoskeletal pain, fatigue, sleep disturbance and cognitive difficulty. It is understood to result from disordered central pain processing (central sensitisation) rather than peripheral inflammatory or structural pathology.

It frequently coexists with, and is triggered or perpetuated by, other painful or inflammatory conditions.

Pathophysiology

Central sensitisation, characterised by amplified pain signal processing within the central nervous system, altered descending pain inhibitory pathways, and dysregulation of neurotransmitters involved in pain modulation (including serotonin, noradrenaline and glutamate), underlies the widespread pain and sensory amplification characteristic of this condition.

Sleep disturbance, psychological stress and, in a proportion of patients, a preceding physical or emotional trauma or infection, appear to contribute to onset and perpetuation, though the precise causal pathway remains incompletely understood.

Widespread, chronic (present for at least three months) musculoskeletal pain affecting both sides of the body and above and below the waist is the core feature, often described as aching, burning or throbbing, and fluctuating in intensity and location.

Profound fatigue, frequently as disabling as the pain itself, and non restorative sleep with frequent waking are near universal.

Cognitive difficulty ("fibro fog") with impaired concentration, memory difficulty and word finding problems is a recognised and often distressing component.

Additional somatic symptoms are common, including headache, irritable bowel syndrome, bladder symptoms, paraesthesia, temporomandibular joint pain and heightened sensitivity to sensory stimuli including light, sound and temperature.

Mood disturbance, particularly anxiety and depression, coexists in a substantial proportion and interacts bidirectionally with the pain and fatigue burden.

Examination classically reveals tenderness at multiple soft tissue sites without objective signs of inflammation (no synovitis, no rash, normal muscle strength once pain is accounted for), and the absence of these findings is itself diagnostically important.

Diagnosis is clinical, based on validated criteria. These assess the widespread pain index (number of painful body regions) and symptom severity scale (fatigue, waking unrefreshed, cognitive symptoms and somatic symptom burden) over a period of at least three months.

The historical tender point examination is not relied on and has been superseded in current diagnostic frameworks.

Investigation is directed at excluding alternative or coexisting conditions that might explain or contribute to the symptoms, rather than confirming fibromyalgia itself, which has no specific diagnostic test.

Full blood count, inflammatory markers, thyroid function, creatine kinase, vitamin D and calcium are reasonable baseline tests.

Inflammatory markers and autoantibody testing are typically normal or negative in isolated fibromyalgia, and their elevation should prompt evaluation for a coexisting inflammatory or autoimmune condition rather than being attributed to fibromyalgia itself.

Screening for and identification of coexisting conditions (inflammatory arthritis, connective tissue disease, hypothyroidism, obstructive sleep apnoea, depression and anxiety) is important given their frequent coexistence and the need to address them alongside the fibromyalgia diagnosis.

Avoid excessive repeated investigation once a reasonable initial workup is negative and the clinical picture is characteristic, since this can reinforce illness anxiety and delay engagement with effective management.

Patient education explaining the mechanism of central sensitisation in accessible terms, validating the reality of symptoms while explaining the absence of tissue damage, is a foundational and often therapeutic first step that improves engagement with subsequent management.

Graded aerobic exercise is among the most effective interventions with the strongest evidence base, started at a very low, tolerable level and progressed gradually given the tendency for symptom flare with overexertion, ideally with physiotherapy guidance.

Cognitive behavioural therapy and other psychologically informed approaches (including acceptance and commitment therapy) have good evidence for improving pain coping, function and quality of life.

Sleep hygiene measures and treatment of any coexisting sleep disorder (including screening for obstructive sleep apnoea, which is underrecognised in this population) are important given the central role of non restorative sleep in symptom perpetuation.

Pharmacological options include low dose tricyclic antidepressants (amitriptyline) or serotonin noradrenaline reuptake inhibitors (duloxetine) for pain and sleep, and gabapentinoids (pregabalin, gabapentin) for pain, with all agents offering modest benefit at best and requiring careful discussion of realistic expectations, dose titration and side effect monitoring.

Opioids are not recommended and should generally be avoided, given a lack of efficacy evidence in this specific pain mechanism and the substantial risks of dependence, tolerance and opioid induced hyperalgesia with long term use.

Multidisciplinary pain management programmes, combining education, graded exercise, psychological therapy and pharmacological optimisation, offer the most full and evidence supported approach for patients with significant functional impairment.

Address and treat coexisting depression and anxiety actively, recognising the bidirectional relationship with pain severity and the potential for shared pharmacological treatment (certain antidepressants addressing both).

Set realistic, function focused goals with the patient, given that complete symptom resolution is uncommon, while meaningful improvement in function and quality of life is achievable with sustained, consistent, multimodal management.