Fibromyalgia originates in the central nervous system, where pain-processing pathways become hyperactive. In healthy individuals, the brain filters and modulates incoming pain signals through descending inhibitory pathways. In fibromyalgia, these regulatory mechanisms malfunction, amplifying normal sensory input by up to 300% compared to healthy controls, according to functional MRI studies.
This central sensitization creates a state where the spinal cord and brain respond to non-painful stimuli as though they were painful, a phenomenon called allodynia. Neurotransmitter imbalances, including elevated levels of substance P and glutamate alongside reduced serotonin and norepinephrine, further amplify the pain signal cascade.
The neuroinflammatory component compounds these changes. Elevated levels of pro-inflammatory cytokines and activated glial cells in the central nervous system sustain the sensitized state, creating a self-perpetuating cycle where the nervous system remains locked in a heightened pain response even without ongoing tissue damage.
