Nobody gets fibromyalgia from a single cause. It develops through a combination of genetic vulnerability, changes in how the brain processes pain signals, and one or more triggering events, whether physical, infectious, or psychological. The condition affects roughly 1 to 5 percent of the population, most commonly appearing between ages 25 and 55, and is diagnosed far more often in women (about 87 percent of cases).
Understanding what drives fibromyalgia means looking at several layers: what’s happening in the nervous system, what makes certain people susceptible, and what sets the whole process in motion.
What Changes in the Nervous System
Fibromyalgia is fundamentally a disorder of pain processing. In a healthy nervous system, pain signals travel from the body through the spinal cord to the brain, where they’re interpreted and, when appropriate, dialed down. In fibromyalgia, that system becomes stuck in an amplified state, a process researchers call central sensitization. The brain and spinal cord begin magnifying incoming pain signals and, in some cases, generating the sensation of pain when there’s no painful stimulus at all.
This isn’t imagined pain. It reflects measurable changes in the central nervous system. Brain imaging studies show altered patterns of connectivity and chemical activity in people with fibromyalgia, which contribute to both the widespread nature of the pain and the mood disturbances that often accompany it. One key finding: levels of substance P, a chemical messenger involved in transmitting pain signals, are consistently elevated in the spinal fluid of fibromyalgia patients.
There are two leading explanations for how this sensitization begins. The “bottom up” theory holds that repeated or intense pain signals from the body eventually overwhelm the central nervous system, rewiring it to stay in a heightened state even after the original source of pain is gone. The “top down” theory suggests that changes already present in the brain drive the perception of pain regardless of what’s happening in the body. Most researchers now think both pathways play a role, and the balance likely varies from person to person.
Genetics and Family Risk
Fibromyalgia runs in families. If you have a first-degree relative with the condition (a parent, sibling, or child), your risk of developing it is about eight times higher than the general population’s. That said, there’s no single “fibromyalgia gene.” The genetic component appears to involve small contributions from many different genes, each nudging risk upward slightly.
The genes studied so far are telling. They tend to be involved in producing, transporting, or breaking down neurotransmitters, the chemical messengers the brain uses to process pain, regulate mood, and manage stress. One well-studied candidate, the COMT gene, helps control how quickly the brain clears certain neurotransmitters. Variations in this gene can alter pain sensitivity. Other candidate genes affect serotonin transport and the function of stress-related receptors. In short, what you inherit isn’t fibromyalgia itself but a nervous system that may be more prone to the kind of sensitization described above.
Physical Trauma as a Trigger
A significant physical injury, particularly one involving the neck and spine, can set off fibromyalgia in susceptible people. Whiplash injuries have received the most research attention. One early study found that the probability of developing fibromyalgia within a year was 13 times greater in patients with cervical (neck) injuries than in those with leg fractures. In a larger cohort of people with persistent neck pain three months after a whiplash injury, about 14 percent met the diagnostic criteria for fibromyalgia.
The relationship isn’t straightforward, though. Not all studies have confirmed an increased risk, and in the cohort study above, 63 percent of patients who initially met fibromyalgia criteria no longer did after about six months of treatment. This suggests that for some people, the post-injury pain state is temporary, while for others it becomes entrenched. Major surgeries, repetitive strain, and other forms of sustained physical stress can also serve as triggers.
Infections That Precede Onset
Certain infections are linked to fibromyalgia developing in their aftermath. The NHS identifies Epstein-Barr virus (the virus behind mononucleosis) and Lyme disease as notable examples. The mechanism likely involves the intense, prolonged immune and pain signaling that accompanies these infections. In a nervous system already genetically primed for sensitization, weeks or months of inflammatory signaling may be enough to flip the switch to a chronic pain state.
Psychological Trauma and Chronic Stress
The link between psychological trauma and fibromyalgia is one of the strongest and most consistent findings in the field. In one study comparing fibromyalgia patients to healthy controls, 75 percent of those with fibromyalgia reported a history of trauma (primarily emotional and physical), compared to 53 percent in the control group. Fibromyalgia patients also reported a higher average number of traumatic experiences (2.47 versus 1.16).
Among those whose trauma preceded their pain, the types of trauma and the age at which they occurred varied widely, from childhood experiences to events in middle age. The fibromyalgia diagnosis typically followed 2 to 14 years after the most significant traumatic event. About 64 percent of fibromyalgia patients with a trauma history said their most troublesome trauma came before their pain began. Another 13 percent reported having some pain since childhood that worsened after trauma.
The connecting thread appears to be chronic anxiety and hyperarousal. Trauma, especially when unresolved, can keep the body’s stress response system activated long term. This sustained state of physiological alertness disrupts sleep, alters pain processing, and erodes coping resources, creating conditions in which central sensitization can take hold. Researchers at the International Society for Traumatic Stress Studies have highlighted that this state of chronic hyperactivation may be key to how fibromyalgia develops after trauma, with poor sleep and compounding life stress feeding the cycle.
Existing Pain Conditions Raise Risk
People who already live with a chronic inflammatory or autoimmune disease are significantly more likely to develop fibromyalgia. Women with lupus are nearly six times more likely to have fibromyalgia than women without it. Women with rheumatoid arthritis face about four and a half times the risk. For men, the pattern holds: those with rheumatoid arthritis are six times more likely to also have fibromyalgia.
This makes biological sense. Autoimmune conditions generate persistent pain and inflammation, exactly the kind of ongoing nociceptive input that can drive central sensitization over time. The fibromyalgia that develops alongside these conditions isn’t simply a symptom of the underlying disease. It becomes its own self-sustaining pain process, which is why treating the autoimmune condition alone often doesn’t resolve fibromyalgia symptoms.
How Fibromyalgia Gets Diagnosed
There’s no blood test or scan that confirms fibromyalgia. Diagnosis relies on a clinical assessment using criteria developed by the American College of Rheumatology. The current (2016) criteria require two things: pain in at least four of five body regions, and symptoms lasting at least three months.
Doctors use two scoring tools together. The first is a widespread pain index, where you indicate which of 19 body locations (including both sides of the jaw, shoulders, arms, hips, legs, plus the neck, chest, abdomen, and upper and lower back) have been painful in the past week. The second is a symptom severity score that rates three core symptoms, fatigue, unrefreshing sleep, and cognitive difficulties (often called “fibro fog”), on a scale from none to severe. It also adds points for headaches, abdominal pain or cramping, and depression present over the previous six months.
A fibromyalgia diagnosis is made when the widespread pain index is 7 or higher with a symptom severity score of 5 or more, or when the pain index is at least 4 with a severity score of 9 or higher. These thresholds capture the reality that fibromyalgia isn’t just about pain. For some people, the fatigue, cognitive symptoms, and sleep disruption are equally debilitating.
Why It All Adds Up Differently for Each Person
What makes fibromyalgia frustrating to pin down is that no two people arrive at it the same way. One person develops it after a car accident. Another traces it to a period of extreme emotional stress. A third notices it creeping in alongside rheumatoid arthritis, with no single triggering event they can identify. The common thread is a nervous system that, through some combination of genetic predisposition and accumulated stressors, crosses a threshold into a state where pain signals are persistently amplified. Once that central sensitization is established, it tends to maintain itself, which is why fibromyalgia is a chronic condition even when the original trigger has long since resolved.