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SP0125 Management of Fibromyalgia
  1. F. Mckenna
  1. Dept of Rheumatology, Trafford General Hospital, Manchester, United Kingdom

Abstract

There is little consensus in the management of fibromyalgia (FM) leading to significant disparity of treatment protocols in different rheumatology and pain clinics. The problem in developing effective management guidelines has been the paucity of appropriate clinical trial data. Some management programmes focus on physical and cognitive therapy but may neglect drug therapy. In order to develop a logical approach it is necessary to consider both the symptoms and pathophysiology of the disease.

Most patients with FM have a recognisable phenotype and may be described as psychologically vulnerable. A number of studies have documented that a history of physical or sexual abuse is more common in FM compared to control populations. Depression, ill health and catastrophising behaviour are often present prior to the onset of FM and persistent symptoms often lead to treatment focussed on behavioural therapy. However, this is only one facet of the illness.

Evidence for augmented processing of pain and impaired endogenous pain inhibition in FM may help to explain the mechanism of altered pain perception. Controlled functional magnetic resonance imaging (fMRI) studies have demonstrated that patients with FM exhibit higher sensitivity to pain provocation – a reduced stimulus in FM causes the same activity in the brain compared with a stronger painful stimulus in controls. This may be explained by a lack of response to painful stimuli in the rostral anterior cingulate cortex (rACC) – part of the descending pain regulating system. More recent studies have suggested that this may result from reduced connectivity of the rACC with the amygdala, hippocampus, and brainstem in FM patients compared with healthy controls.

Although the cause of these abnormalities is unclear, we can hypothesise that disordered sleep architecture may explain the development of abnormal pain mechanisms in vulnerable patients. We know from volunteer studies that pain threshold is significantly reduced following deprivation of slow wave sleep (SWS), and fMRI studies of sleep have found reduced activity in a number of structures relating to pain pathways including the ACC, especially during SWS. Longitudinal population studies have found sleep disturbance to be a major risk factor for developing FM, and polysomnographic studies support the hypothesis that fibromyalgia may be a primary disorder of sleep. Altered sleep architecture is found in most studies.

There is evidence that fatigue in fibromyalgia is causally related to sleep disturbance. Following restoration of deep sleep with sodium oxybate treatment in FM, fatigue improves in addition to significant improvement in pain and other symptoms. Current data therefore supports the hypothesis that both fatigue and chronic widespread pain in FM result from abnormalities in sleep architecture in patients with psychological vulnerability, leading to dysfunction in the descending pain regulating system.

These data suggest that management of FM should be multifaceted. In addition to physical, behavioural and other psychological therapies, treatment programmes must include active management of sleep pathology.

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.6286

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