A number of investigators have proposed that chronic emotional stress plays a causal role in FM.7 This hypothesis is consistent with evidence that people with FM have high rates of disorders characterized by chronic stress, including depression, posttraumatic stress disorder, and other anxiety disorders.8,9 The importance of stress is supported by research that indicates that high proportions (more than 75%) of people with FM report that stress aggravates the symptoms.10 Moreover, a significant percentage of people with FM report that the symptoms began following physical or emotional stress.10
Longitudinal data also support the hypothesis that psychological dysfunction and distress increase the risk for FM.11 On the other hand, there is little doubt that living with FM and its associated symptoms serves as an ongoing stressor. Thus, high levels of emotional distress among people with FM might be construed as a consequence of the difficulties they face in adapting to the condition.
Investigators of the HPA axis function have generally found that people with FM are in a state of physiological exhaustion or “burnout.” Studies of autonomic nervous system function report blunting of phasic responses to acute stressors but argue that these responses are by-products of chronic hyperarousal.12 Therefore, stress may be both a causal and maintaining factor.
Research investigating sensory processing in FM has consistently demonstrated that patients have a lower pain threshold than do age- and sex-matched healthy persons.13 Based on these results, a hypervigilance model of FM in which increased attention to somatosensory stimuli is a predisposing factor for developing the syndrome has been proposed.14 Vigilance to sensory information in FM may not be limited to pain. Some data indicate that patients with FM are more sensitive to cold, noise, and environmental irritants.15
Dysfunction of sensory modulation
There is growing agreement that FM is characterized by an augmentation of central processing of sensory stimuli, to the extent that there is disordered pain regulation and a lowered threshold for noxious stimulation of unknown cause.5 This might account for the widespread pain and myriad symptoms.
There is increasing evidence for a genetic predisposition for FM, including the possible role of polymorphisms in the serotonergic, dopaminergic, and catecholaminergic systems.16 The abnormal sensitivity to pain may be the result of heightened generalized sensitivity from pathological nociceptive processing within the CNS—central sensitization.17 The genetic predisposition may be expressed following instigation by a physical or emotional trauma—a diathesis-stress model.18
There has been ongoing debate in the FM literature about whether psychological factors are causal or a reaction to the presence of a large number of symptoms with unknown cause and no cure. Some have suggested that FM is one of a set of depression-spectrum disorders.19 Others note that the lifetime prevalence of psychiatric disorders is high in FM, yet not all patients have a significant psychiatric history.20-22 Anxiety, depression, and anger have each been shown to be important in the etiology, maintenance, and exacerbation of symptoms, adaptation, and response to treatments by patients with FM.