Abstract
Fibromyalgia is a common, high-impact condition of chronic widespread pain and sensory dysfunction associated with altered central and peripheral sensory processing. A growing body of evidence supports the role of neuroinflammation and immune changes in fibromyalgia, and a narrative review of this literature was undertaken. Published data suggest that the interactions between the neural pain networks and the immune system in fibromyalgia appear to be bidirectional and operate both centrally and peripherally. There is a growing focus on processes occurring in the dorsal root ganglia and the role of maladaptive microglial cell activation. Ongoing insight into neuroinflammatory mechanisms in fibromyalgia opens potential avenues for the development of mechanism-based therapies in what is, at present, a challenging-to-manage condition.