What Actually Causes Fibromyalgia? The Mitochondrial, Mast Cell, and Small Fiber Neuropathy Mechanisms Standard Treatment Misses — Why the current fibromyalgia model produces variable results

The dominant current model of fibromyalgia is the "central sensitization" model. Pain processing in the central nervous system is amplified. The amplification produces hypersensitivity to normal stimuli (allodynia) and exaggerated response to painful stimuli (hyperalgesia). Treatment targets the pain processing itself: pregabalin and gabapentin act on alpha-2-delta calcium channels reducing neurotransmitter release, duloxetine and milnacipran act on serotonin and norepinephrine reuptake increasing descending inhibition, cyclobenzaprine acts at the brainstem to reduce muscle tone and improve sleep architecture. This model has produced effective acute treatments. It has not produced curative treatments. Long-term outcomes are modest. The model is correct in describing what is happening in central pain processing. It is incomplete in describing why the central sensitization developed in the first place and why it persists despite treatment. The questions the current model does not adequately address: what triggers the central sensitization in a specific patient? Why do some patients develop central sensitization after a specific event (infection, trauma, surgery) while others develop it gradually without an identifiable trigger? What sustains the sensitization despite treatment that targets the relevant neurotransmitter systems? Why do specific subsets of fibromyalgia patients hav