Fibromyalgia pathogenesis provides drug target clues

Fibromyalgia (FM) has been described as a condition of heightened generalised sensitisation to sensory input presenting as a complex of symptoms dominated by chronic widespread pain characterised by hyperalgesia and allodynia. A range of co-morbidities of variable intensity, such as fatigue, sleep disturbance, cognitive impairment, anxiety and depression, are often present (Figure 1; page 46). The prevalence of this condition, which is more common in females than males, is reported to be 2-8% of the population and presents a major financial and social burden to patients and healthcare systems. Neuronal excitability associated with amplified responses of the central nervous system (CNS) to peripheral input leading to central sensitisation is believed to underlie the pathophysiology1,2. Peripheral nociceptive generators, such as nerve pathologies, neuro-inflammation, skeletal muscle abnormalities and ischaemia, play a role in the enhancement of the central components and the pain experienced by FM patients3,4.