Fibromyalgia is a non-inflammatory, non-autoimmune diffuse pain syndrome characterised by combinations of hyperalgesia, disordered non-restorative sleep and low mood. It can occur on its own (primary) or in association with chronically painful conditions such as rheumatoid arthritis (secondary). Primary fibromyalgia is considered under the umbrella term of ‘soft-tissue rheumatism’ and the objective absence of (peri-)articular disease is crucial both in terms of diagnosis and management.

There are no good epidemiological studies but primary fibromyalgia may affect up to 4% of the population overall. The overwhelming majority of patients are women, and the average age at diagnosis is early middle-age (40–50 years). Indeed, the development of disabling fatigue and pain in older age groups should prompt a considered search for alternative sinister diagnoses such as chronic infection or occult malignancy.

The characteristic clinical features of fibromyalgia are chronic diffuse pain in association with combinations of morning stiffness, fatigue and non-restorative sleep, depression, anxiety and headache. More rarely the presence of parasthesiae or Raynaud’s phenomenon can add to diagnostic difficulty. Examination is normal, except for the presence of classic ‘trigger points’ – evidence of hyperalgesia at specific soft-tissue sites (see below). However, if fibromyalgia occurs as a secondary phenomenon due to another condition such as RA, then the clinical findings are those one would expect from the underlying disease (e.g. synovitis, effusions and joint destruction).

• Pain: is characteristically diffuse, with non-inflammatory spinal pain being a common feature. The pain is hard to localise and patients frequently massage their whole arm/leg, describing it as ‘deep inside’. It may not follow the diurnal pattern or relation to exercise of inflammatory or degenerative disease, and patients frequently experience good days and bad days.
  
• Sleep: is non-restorative leading to daytime fatigue, which may be extreme. The sleep disturbance is characterised by alpha-delta sleep, in which delta (restorative, restful and deep) sleep is interrupted by alpha-waves (found early in the approach to sleep). As a result, late and restorative non-REM stage IV sleep is dramatically reduced. This sleep pattern also occurs during times of emotional stress and is found in other causes of chronic pain such as RA; the fatigue in inflammatory disease is compounded by circulating cytokines, which are not a feature of primary fibromyalgia.

• Depression: the relationship between pain and mood is reciprocal. Low mood is understandably a common component of chronically painful syndromes and mood impacts profoundly on pain perception. Low mood may also engender a sense of helplessness in the patient, reducing their ability or desire to adhere to treatment strategies. Successful rehabilitation is a frequently a significant challenge.
  
• Parathesiae and neurological features: these are classically non-dermatomal/anatomical in distribution and are not accompanied by abnormal investigations such as EMG findings.
  
• Raynaud’s phenomenon: occurs in up to 10% of patients with fibromyalgia, but there are no associated systemic features of either SLE or scleroderma.

The clinical examination in primary fibromyalgia is essentially normal, with no objective evidence of articular or systemic disease. However, the presence of multiple tender trigger points (see figure opposite) is highly suggestive of fibromyalgia. These are specific areas on the body that are sensitive to applied pressure, even in normal people. In the context of a pain amplification syndrome, such as fibromyalgia, these areas are exquisitely tender when only moderate pressure is applied (i.e. enough to blanch the examiner’s thumbnail). There are 18 specific points, of which 11, represented in all 4 quadrants of the body, should be tender to consider the diagnosis.

The aetiology of fibromyalgia is unknown. Unlike the closely-related chronic fatigue syndrome, in which a precipitating episode (usually viral illness) is frequently clearly identifiable, patients may not identify a particular trigger for fibromyalgia. Where present, common precipitating events include viral illness, emotional stress or minor injury such as whiplash. Withdrawal from medications, particularly glucocorticoids, may also be implicated.

The pathogenesis of fibromyalgia is likely to be an abnormality of central processing, manifesting as a problem of pain perception or amplification; abnormalities in the descending analgesia and endogenous endorphin systems, alpha-delta sleep disturbance, affective spectrum disorder and somatoform disorder may all play a role in initiation and perpetuation of the condition. MRIs of patients’ brains are normal but functional imaging studies have suggested reduced blood flow to thalamus and caudate nucleus, which has been reported in other causes of chronic pain.

Treatment for fibromyalgia is a combination of:

• Patient education.
  
• Physical therapy and aerobic exercise.
  
• Analgesia.
  
• Correction of sleep disturbance.
  
• Treatment of any associated disorders.

Patient education is particularly crucial and must be sensitively handled: there should be agreement that the symptoms are both real and disabling, but strong reassurance that the patient has substantial control over the impact, treatment and outcome of the condition. A steadily graded aerobic exercise system is also vital.

Medical therapy is based on low dose tricyclic antidepressants (TCAs) to improve sleep quality and alter pain perception: a standard approach would be amitriptyline 10 mg several hours before going to bed (to try to avoid hang-over effect). This can be increased gradually to a maintenance dose of 30–40mg daily. If TCA side-effects such as dry mouth or constipation prove troublesome, there is some evidence of the efficacy of SSRIs such as venlafaxine.

The prognosis is variable and depends profoundly on patient-physician interaction and the patient’s ability to engage with rehabilitation programmes.