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Neurophysiopathogenesis of fibromyalgia syndrome: A unified hypothesis
Rheumatic Disease Clinics of North America, 08/11/09

Russell IJ et al. – This review briefly summarizes the peripheral component of FMS neurophysiopathogenesis and proposes a unifying model that embodies many testable subhypotheses. Theoretical integrated neurobiophysiopathogenesis model of the FMS:

The model begins with one or more of the genetic associations that might predispose the individual to undergo brain degeneration or atrophy in response to an undefined stimulus
Time and a variety of cofactors: age, physical trauma, febrile illness, inflammation, dysfunctional sleep, and antipolymer antibody (APA) may contribute to this process
Degeneration of cortical tissue, medications, and chronic sleep deprivation cause the patient to feel insecure
Injury to cortical tissue prompts increased production of nerve growth factor (NGF)
HIgh levels of NGF establish a new, higher steady state concn for substance P (SP) in the brain and spinal fluid
Elevated levels of SP cause sleep dysfunction, depression, low CSF levels of biogenic amines, and inhibition of the stress response system
These changes result in allodynia/spontaneous pain, chronic insomnia, depression, and impotent stress responses
The combination of the cognitive insecurity with the allodynia, insomnia, depression, and poor stress response embodies the features of FMS

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