How can we treat fibromyalgia?
Howard A. Bird, Professor of Pharmacological Rheumatology University of Leeds, United Kingdom
ABSTRACT:
Since there is no diagnostic test for fibromyalgia, the diagnosis is essentially one of exclusion. The pitfall in primary care is to miss a more serious treatable diagnosis that has mimicked fibromyalgia. A careful history and examination, checking this against existing diagnostic criteria for fibromyalgia, is therefore important. However, the behaviour of pressure points can be fluctuant so in cases of doubt careful investigation may also be necessary.
Studies in primary care in the United Kingdom have noted higher rates of illness and health care resource use for as much as ten years prior to the formal diagnosis of fibromyalgia being made, suggesting that illness behaviour may play a role. Overlap with chronic fatigue syndrome and hypermobility syndrome has been suggested. Sometimes there is a family history. Sleep disturbance is often striking though the establishment of a formal neuro-endocrine link, perhaps associated with loss of diurnal rhythm, has proved elusive.
Management is likely to be with a multidisciplinary team and the majority of these patients are treated in primary care. Patient education remains important. Psychological counselling, certainly with relief of any previousdepression, is important since physiotherapy often aggravates though an ergonomic occupational therapy assessment may be of value. Patients should be taught to pace themselves in the knowledge that a proportion will improve over the years.
Drug treatment is often successful though analgesics have a limited role and NSAIDs are normally ineffective. The most successful group of drugs have been the tricyclic anti-depressants though there has also been recent interest in serotonin uptake inhibitors or in the use of these drugs in various combinations. Normally the dose required is substantially less than that needed for the treatment of frank depression.
Novel therapeutic options have included manipulation of the sympathetic nervous system, pregabalin, sodium channel blockers and melatonin, any of which might be tried in general practice. There is also a suggestion that interleukins, particularly IL-6 or IL-8, may be relevant in pathogenesis, prompting the need for formal trials in this
area.
MANUSCRIPT:
The term ‘fibromyalgia’ may well cover a variety of diagnoses for which we have no formal diagnostic tests though diagnostic criteria have been suggested both from Smythe and the American College of Rheumatology. Before commencing treatment it is therefore prudent to confirm the diagnosis, essentially one of exclusion, beyond any doubt with a careful history and examination in addition to any investigations deemed appropriate.
In particular, there may be some overlap in classification between fibromyalgia, particularly on a day when tenderness of pressure points is minimal, and other conditions. Both over-use syndromes (repetitive strain injury and hypermobility syndrome) probably associate with fibromyalgia and some variants of the condition mimic Sudek’s algodystrophy. Even Gulf War syndrome has been discussed as a fibromyalgia variant. There is some evidence that trauma precipitates fibromyalgia particularly at certain sites, e.g. the neck. Autonomic dysfunction may be present as well as pronounced sleep disturbance. Fibromyalgia is sometimes considered to be a mild psychiatric illness7 and studies in primary care in the U.K.have noted higher rates of illness and health care resource use for as much as ten years prior to the formal diagnosis of fibromyalgia being made, suggesting that illness behaviour may play a role. Others have suggested a neuroendocrine aetiology.
Management is likely to be with a multidisciplinary team, the majority of these patients treated in primary care. Patient education remains very important, not least because patients will need to pace themselves against their symptoms. Often these patients are vocal and informed about their disease. Psychological counselling is therefore likely to be of benefit though physiotherapy, particularly if extreme, often seems to aggravate this condition. An ergonomic occupational therapy assessment may be of value however. There have been controlled trials of aerobic exercise and cognitive behavioural therapy as well as of
hypnotherapy, transcutaneous nerve stimulation and homeopathy.
Analgesics may be of some use, initially paracetamol, and a specific action has been claimed in fibromyalgia for the more potent weak opioid antagonist tramadol. Stronger opiates should be avoided. Non-steroidal antiinflammatory drugs only play a limited role since the condition is not characterised by inflammation. Tricyclic anti-depressants, particularly amitriptyline, remain the mainstay of treatment. These drugs are of proven efficacy and given as a small nocturnal dose. Improvement, if it is to occur, is normally noted within two weeks so the drug should be prescribed in escalating dosage for a trial of up to eight weeks, the patient warned that improvement might not be immediate. Dosulepin (Dothiepin) is an alternative.
Initial enthusiasm for the use of serotonin uptake inhibitors has been tempered by disappointment in controlled trials though it may be more rational to use these drugs in combination with amitriptyline. In this regard Venlafaxine, which inhibits both serotonin and noradrenaline re-uptake, suggests the simultaneous blocking of two transmitters may the most appropriate.
Novel therapeutic options have included manipulation of the sympathetic nervous system, pregabalin, sodium channel blockers, melatonin, monoamine oxidase inhibitors and counter-irritants such as capsaicin applied topically. Recent research has focussed on a possible aetiological role for cytokines. IL-6 appears the most incriminating, increasing heart rate in fibromyalgia and also induces hyperalgesia, fatigue and depression, though this may in part also be through the action of IL-8.
