In patients with FMS, a reduced hypothalamic-pituitary-adrenal (HPA) axis response to stress has been demonstrated.41,42,43 The neuroendocrine response acts normally under baseline conditions, but not when subjected to stress or even normal activities of daily living. However, this deficit might have more impact on depression, a common associated feature of FMS as well as chronic pain. Patients with FMS often report experiencing previous stressful or traumatic events. A reduced HPA axis response to stress can contribute to FMS development or worsening of FMS. The HPA axis is also linked to the autonomic nervous system, which is involved in modulating sleep, mood, pain, and cardiovascular activities (including microcirculation of muscles). This could explain many clinical features and the association of FMS with sympathetic nerve system over activity, although more detailed mechanistic studies will be needed to confirm a causative relationship. Abnormal HPA axis activity has also been observed to a lesser extent in chronic low back pain sufferers, therefore it does appear to be linked to chronic pain.
Hormones such as cortisol, growth hormone (GH), and thyroid hormone can be affected particularly in patients with an altered HPA axis. Studies have reported increased levels of adrenocortical trophic hormone (ACTH) and decreased levels of insulin-like growth factor (IGF-1), triiodothyronine (T3), GH, estrogen, and urinary cortisol.44
A reduction in IGF-1 levels has also been proposed as a contributing factor for FMS development/symptomatology. Bennett et al.45 observed that FMS patients had declining levels over the following one to two years. These patients with a low level of IGF-1 also failed to secrete GH after stimulation with clonidine and L-dopa suggesting that low IGF-I levels in patients with FMS are a secondary phenomenon due to hypothalamic-pituitary-GH axis dysfunction.
Some have suggested that the HPA deficit may be a secondary phenomenon rather than having a causative role as it has been observed in people with sleep disturbances. FMS patients have been reported to have a reduction of stage 4 non-REM, or deep sleep, which also leads to reduced pressure pain thresholds, increased aching and fatigue.46 FMS patients are frequently more painful and tender in the morning and experience significant morning stiffness, this is lessened after nights where they have had more restful sleep. Although a cause and effect relationship has not been established, this does appear to be an important factor in FMS.
Another hypothesis involves the role of proin-flammatory cytokines which could induce hyperalgesia in the central nervous system (CNS). Release of these cytokines can be triggered by chronic stress. They are known to directly contribute to peripheral and central neuropathic pain as well as depression and can lead to exaggerated pain states similar to those seen in FMS.47 A recent study in 40 patients with chronic widespread pain, including 26 with FMS and 40 age- and sex-matched healthy controls, found lower relative gene expression for the anti-inflammatory cytokines interleukin-4 and interleukin-10.48
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