Neuroendocrine abnormalities in fibromyalgia

Abstract

Fibromyalgia is a disorder of unknown etiology characterized by chronic, widespread musculoskeletal pain and symptoms such as fatigue, poor sleep, gastrointestinal complaints, and psychologic problems that are similar to those experienced by patients with hormone deficiencies. This review summarizes the available data on the neuroendocrine function in fibromyalgia, including data on hormone secretion, circadian phase, and autonomic nervous system function. Studies suggest that there may be lower activity of a number of hypothalamic-pituitary-peripheral gland axes and altered autonomic nervous system function in patients with fibromyalgia. These reductions in activity are mild to moderate and do not result from alterations in circadian rhythms. The reduced hormonal and autonomic responses appear to reflect an impairment in the hypothalamic or central nervous system response to stimuli rather than a primary defect at the level of the pituitary gland or the peripheral glands. A combination of multiple, mild impaired responses may lead to more profound physiologic and clinical consequences as compared with a defect in only one system, and could contribute to the symptoms of fibromyalgia.

Sleep Disorders and Fibromyalgia

“…Among environmental factors, chronic stress has been considered the underlying factor for the neuroendocrine dysfunctions described in fibromyalgia, such as hyperactive and hyporeactive hypothalamic-pituitary-adrenal axis, which can directly or indirectly affect the adjustment of cortisol response and lead to variable manifestation of the characteristic symptoms of fibromyalgia, including fatigue, pain, depressed mood, and nonrestorative sleep [19][20][21]. Alterations in HPA axis function also may provide an explanation for the observation of subnormal growth hormone (GH) secretion in some patients with fibromyalgia, which may contribute to the development of impaired cognition, fatigue, muscle weakness, and decreased exercise tolerance [19].…”

“…Alterations in HPA axis function also may provide an explanation for the observation of subnormal growth hormone (GH) secretion in some patients with fibromyalgia, which may contribute to the development of impaired cognition, fatigue, muscle weakness, and decreased exercise tolerance [19]. Given that GH and somatomedin C are necessary for the repair of muscle microtrauma, sleep disturbances may impair the healing of muscle tissue damage, thereby prolonging the transmission of sensory stimuli from damaged muscle tissue to the CNS and enhancing the perception of muscle pain [47].…”

“…Conversely, the development of chronic pain may influence sleep through physical and functional modifications of the CNS. The increased sympathetic activity [18], underactivated hypothalamic-pituitary-adrenal axis [19][20][21], and the release of proinflammatory cytokines from glial cells [22,23] have been proposed as the underlying mechanisms of disordered sleep in fibromyalgia. Notwithstanding, the reciprocal relationship between sleep disturbance and pain in fibromyalgia [9,[24][25][26][27][28] still remains controversial in terms of the impact of such an interaction in fibromyalgia manifestations [29].…”

Salivary cortisol and suicidal behavior—A follow-up study

“…Hypocortisolism has been reported in patients with stress related disorders, such as Chronic Fatigue Syndrome (CFS) (Wyller, 2007), fibromyalgia (Adler et al, 2002), Post Traumatic Stress Disorder (PTSD) (Ehlert et al, 2001), and depression with atypical features (Antonijevic, 2006). Since these disorders also share some symptoms (including enhanced stress sensitivity, pain, and fatigue), common underlying physiological abnormalities have been suggested (Heim, Ehlert et al 2000).…”

Fibromyalgia syndrome—current concepts

“…9,37 Numerous studies have been performed to evaluate the hypothalamic-pituitary-adrenal axis in FM patients and many abnormalities have been documented, including relative adrenal insufficiency, low levels of growth hormone and a relative inability for stress events (such as infection or physical and emotional stress) to activate the HPA-axis. 2 FM seldom presents spontaneously. Most patients relate an acute injury, infection or emotional stressor as a precipitating event.…”