Fibromyalgia (FM) is a chronic pain disorder characterized by widespread musculoskeletal pain, persistent fatigue, and cognitive difficulties. This condition affects millions globally, impacting daily life. The disorder involves an altered perception of pain within the nervous system. The complex relationship between FM and inflammation has long been debated, but modern research is providing a nuanced answer regarding its inflammatory component.
Understanding Fibromyalgia
Fibromyalgia is classified as a central pain syndrome, meaning it is a disorder of pain processing in the brain and spinal cord. The hallmark symptom is chronic, widespread pain affecting multiple body areas, often described as deep, burning, or aching. People with FM also commonly experience unrefreshing sleep, which contributes to fatigue not relieved by rest.
The cognitive difficulties, often termed “fibro fog,” involve problems with memory, concentration, and thought speed. Diagnosis is primarily clinical, based on these characteristic symptoms persisting for at least three months. The underlying issue is an amplification of pain signals within the central nervous system (CNS), distinct from traditional tissue damage.
The Traditional Absence of Systemic Inflammation
FM was traditionally not considered an inflammatory condition because patients typically do not show signs of systemic inflammation. Standard blood tests used to detect inflammation, such as C-Reactive Protein (CRP) and Erythrocyte Sedimentation Rate (ESR), are normal in people with FM. This absence of elevated systemic markers is a primary factor that distinguishes FM from classic inflammatory conditions like Rheumatoid Arthritis or Lupus.
The traditional view held that since no generalized inflammation was detectable, the pain was solely related to central nervous system dysfunction. However, some recent studies using high-sensitivity CRP (hsCRP) have detected low-grade systemic inflammation in certain patient subgroups, often correlated with factors like obesity. This suggests that while FM is not primarily an inflammatory disease, a mild systemic inflammatory state may coexist in some individuals.
Evidence for Localized Neuroinflammation
While systemic inflammation is generally absent, research points to localized inflammation within the central nervous system, referred to as neuroinflammation. This discovery shifts the understanding of FM’s biological basis. Studies using advanced imaging techniques show activation of non-neuronal cells in the brain and spinal cord.
These activated cells are glial cells (microglia and astrocytes), which act as the resident immune cells of the CNS. When activated, glial cells release pro-inflammatory substances, including cytokines, into the surrounding neural tissue. Elevated levels of pro-inflammatory cytokines, such as Interleukin-8 (IL-8) and Interleukin-6 (IL-6), have been demonstrated in the cerebrospinal fluid (CSF) of people with FM. The presence of these markers in the CSF, rather than peripheral blood, provides direct evidence of a localized inflammatory process affecting the CNS.
Connecting Neuroinflammation to Heightened Pain Sensitivity
The localized neuroinflammation driven by activated glial cells directly contributes to FM’s pain symptoms. The substances released by these cells act on nearby neurons, promoting Central Sensitization. Central Sensitization is a persistent, heightened responsiveness of neurons in the central nervous system to normal or sub-threshold sensory input.
This process causes the brain to over-interpret normal sensations as painful. The consequence is allodynia—pain caused by a stimulus that does not normally provoke pain, such as light touch. It also leads to hyperalgesia, an exaggerated response to painful stimuli. Neuroinflammation acts as a continuous irritant that maintains this sensitized state, transforming the central nervous system into a chronic pain generator.