The cause of fibromyalgia is unknown.but there are probably a number of factors involved. Many people associate the development of fibromyalgia with a physically or emotionally stressful or traumatic event, such as an automobile accident. Some connect it to repetitive injuries. Others link it to an illness. For others, fibromyalgia seems to occur spontaneously.
However, several hypotheses have been developed including “central sensitization”. This theory proposes that people with fibromyalgia have a lower threshold for pain because of increased reactivity of pain-sensitive nerve cells in the spinal cord or brain. Neuropathic pain and major depressive disorder often co-occur with fibromyalgia – the reason for this comorbidity appears to be due to shared genetic abnormalities, which leads to impairments in monoaminergic, glutamatergic, neurotrophic, opioid and proinflammatory cytokine signaling.
In these vulnerable individuals psychological stress or illness can cause abnormalities in inflammatory and stress pathways which regulate mood and pain. Eventually a sensitisation and kindling effect occurs in certain neurons leading to the establishment of fibromyalgia and sometimes a mood disorder. The evidence suggests that the pain in fibromyalgia results primarily from pain processing pathways functioning abnormally.
In simple terms it can be described as the volume of the neurons being set too high and this hyper-excitability of pain processing pathways and under-activity of inhibitory pain pathways in the brain results in the affected individual experiencing pain.
Some scientists speculate that a person’s genes may regulate the way his or her body processes painful stimuli. According to this theory, people with fibromyalgia may have a gene or genes that cause them to react strongly to stimuli that most people would not perceive as painful. There have already been several genes identified that occur more commonly in fibromyalgia patients, and NIAMS-supported researchers are currently looking at other possibilities.