Abstract
Fibromyalgia, characterised by persistent pain, fatigue, sleep disturbance and cognitive dysfunction, is a central sensitivity syndrome that also involves abnormality in peripheral generators and in the hypothalamic pituitary adrenal axis. Heterogeneity of clinical expression of fibromyalgia with a multifactorial aetiology has made the development of effective therapeutic strategies challenging. Physiological properties of the neurohormone melatonin appear related to the symptom profile exhibited by patients with fibromyalgia and thus disturbance of it’s production would be compatible with the pathophysiology. Altered levels of melatonin have been observed in patients with fibromyalgia which are associated with lower secretion during dark hours and higher secretion during daytime. However, inconsistencies of available clinical evidence limit conclusion of a relationship between levels of melatonin and symptom profiles in patients with fibromyalgia. Administration of melatonin to patients with fibromyalgia has demonstrated suppression of many symptoms and an improved quality of life consistent with benefit as a therapy for the management of this condition. Further studies with larger samples, however, are required to explore the potential role of melatonin in the pathophysiology of fibromyalgia and determine the optimal dosing regimen of melatonin for the management of fibromyalgia.
Highlights
Fibromyalgia, characterised by persistent pain, fatigue, sleep disturbance and cognitive dysfunction, is a central sensitivity syndrome [1,2]
Altered levels of melatonin have been observed in patients with fibromyalgia which are associated with lower secretion during dark hours and higher secretion during daytime
The physiological processes maintained by the availability of melatonin are relevant to the clinical features of fibromyalgia where persistent pain, fatigue, sleep disorder and cognitive impairment are characteristic
Summary
Fibromyalgia, characterised by persistent pain, fatigue, sleep disturbance and cognitive dysfunction (i.e. attentional capacity and memory), is a central sensitivity syndrome [1,2]. Central sensitization (CS) with neuronal excitability linked to amplified responses of the central nervous system (CNS) to peripheral input has been proposed to underlie the pathophysiology of fibromyalgia [2]. Peripheral sensory generators, such as nerve pathologies, neuroinflammation, skeletal muscle abnormalities and ischaemia, have been reported to contribute to this heightened activity of the CNS [3,4]. MEDLINE database, Web of Science and Google Scholar were used to identify relevant studies and publications up to August 2019 using the terms ‘melatonin’ and ‘fibromyalgia’
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