Fibromyalgia has no known cause. This can be very frustrating because without a cause it difficult to come up with a cure or to try to prevent the disease. It is much easier for patients and physicians to manage diseases that they understand fully.
The research over the last 20 years has increasingly shown that that it is a neurological problem and not a muscle problem as thought of before. In the recent past, it was thought to be a primarily soft tissue problem, such as issues with the muscles, and their coverings, and their attachments to bones. This better understanding has helped to change how we treat the disease.
Fibromyalgia is a condition of altered pain processing in the brain and spinal cord (central nervous system or CNS), with the CNS in a persistent “hyper-reactive” mode. Central sensitization means the patient is “hyper-reactive” or “hypersensitive” to any stimuli, including pain and pressure, sounds, smells or sights, stress and temperature. Another name for central sensitization is amplified pain processing.
There are several factors that can lead to central sensitization. One is what state the nervous system is in before developing fibromyalgia or the injury that leads to it. Central sensitization is associated with cognitive problems, such as poor memory and difficulties with concentration. Central sensitization can also be caused by increased levels of emotional distress, especially anxiety. Remember, the nervous system is responsible for not only sensations, like pain, but also emotions. When the nervous system is stuck in a constant state of hyper-reactivity, patients tend to experience the emotion of anxiety as their default way of being.
Studies in patients with fibromyalgia have shown altered levels of many different brain chemicals (called neurotransmitters) that communicate from one brain cell to another. Two specific neurotransmitters related to fibromyalgia are serotonin and norepinephrine. These neurotransmitters are involved in mood, sleep, and pain regulation. Higher levels of the chemical glutamate can also be associated with lower pain thresholds.
Other research has shown evidence of central inflammation in fibromyalgia to include increased cerebrospinal fluid interleukin-8 levels. Yet other research has shown higher levels of substance P in the fluid, a pain mediator. Brain activities have been noted to be different on functional MRIs in fibromyalgia patients compared to patients without fibromyalgia.
The onset of fibromyalgia may be associated with stressors in many patients. This can be any prolonged stress, both emotional and physical. Some examples may be a car accident or bomb blast, psychological trauma such as an abusive childhood or marriage, or a rape. Medical illnesses like a systemic infection or other illnesses can also trigger it. Other things associated might be peri-menopause (just before menopause in women) and certain rheumatologic diseases like lupus.
Though these stressors may be the trigger, physicians also note the state of the nervous system before the condition arises. For example, if someone is already anxious or depressed, they have a higher chance of developing chronic pain including fibromyalgia later in life.
The stress-response is thought to play a role in the development of central sensitization. Studies have shown that stress and anxiety can actually lower a patient’s pain thresholds and make him/her more sensitive to pain.
There is also a strong genetic component. Family members with fibromyalgia often have other family members with it as well. First degree relatives of patients who have the condition are eight and a half times more likely to have it. There are genes that have been identified that affect pain thresholds, in general. These genes are involved in modulating neurotransmitters involved in pain.