Pathophysiology of Fibromyalgia

Core Pathophysiological Mechanisms

The primary mechanism of fibromyalgia is central sensitization, where the central nervous system amplifies pain signals, leading to widespread pain despite no evidence of actual tissue damage or nerve injury, according to the American Academy of Neurology 1
Fibromyalgia is classified as a "nociplastic" pain condition, distinct from neuropathic or inflammatory pain, because pain arises from altered nociception despite no clear evidence of actual or threatened tissue damage, as defined by the International Association for the Study of Pain 1

Fibromyalgia is characterized by chronic widespread pain, fatigue, non-restorative sleep, mood disturbance, and cognitive impairment, with significant impact on quality of life, as reported by the European League Against Rheumatism 2

The American College of Rheumatology recommends avoiding the mistake of diagnosing fibromyalgia as a diagnosis of exclusion, but rather as a positive clinical diagnosis based on characteristic features of central sensitization, with normal laboratory results and imaging supporting the diagnosis 2
The National Institute of Neurological Disorders and Stroke suggests that fibromyalgia is fundamentally a central nervous system disorder, not a peripheral neuropathy, and symptoms should not be attributed to peripheral nerve damage 1