Cause

The cause of fibromyalgia is unknown. However, several hypotheses have been developed including "central sensitization".This theory proposes that fibromyalgia patients 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 of the neurochemical abnormalities that occur in fibromyalgia also regulate mood, sleep and energy, thus explaining why mood, sleep and fatigue problems are commonly co-morbid with fibromyalgia.

Psychological factors

There is strong evidence that major depression is associated with fibromyalgia (1999), although the nature of the association is debated. A comprehensive review into the relationship between fibromyalgia and major depressive disorder (MDD) found substantial similarities in neuroendocrine abnormalities, psychological characteristics, physical symptoms and treatments between fibromyalgia and MDD, but currently available findings do not support the assumption that MDD and fibromyalgia refer to the same underlying construct or can be seen as subsidiaries of one disease concept.

Pathophysiology
Dopamine dysfunction

The "dopamine hypothesis of fibromyalgia" proposes that the central abnormality responsible for symptoms associated with fibromyalgia is a disruption of normal dopamine-related neurotransmission.Insufficient dopamine in a part of the body is termed hypodopaminergia. Dopamine is a catecholamine neurotransmitter with roles in pain perception and natural analgesia. There is also strong evidence for a role of dopamine in restless leg syndrome.

Serotonin metabolism

In 1975, researchers hypothesized that serotonin, a neurotransmitter that regulates sleep patterns, mood, concentration and pain, could be involved in the pathophysiology of fibromyalgia-associated symptoms.

Brain imaging studies

Evidence of abnormal brain involvement in fibromyalgia has been provided via functional neuroimaging. The first findings reported were decreased blood flow within the thalamus and elements of the basal ganglia and mid-brain (i.e., pontine nucleus)

Prognosis

Although in itself neither degenerative nor fatal, the chronic pain of fibromyalgia is pervasive and persistent. Most fibromyalgia patients report that their symptoms do not improve over time. An evaluation of 332 consecutive new fibromyalgia patients found that disease-related factors such as pain and psychological factors such as work status, helplessness, education, and coping ability had an independent and significant relationship to FM symptom severity and function.

Epidemiology

Fibromyalgia is estimated to affect 2–8% of the population, with a female to male incidence ratio that is somewhere between 7:1 and 9:1.It is most commonly diagnosed in individuals between the ages of 20 and 50, though onset can occur in childhood.