Neuroendocrine immunology of fibromyalgia.
The pathophysiology of fibromyalgia (FM) is not completely understood. The disease is characterized by a central sensitization with an amplification of pain perception. A combination of interactions among external stressors, behavioral constructs, neurotransmitters, hormones, immune, and sympathetic nervous systems appears to be involved. It is known that the neuroimmunoendocrine system has a role in the pathogenesis of the disease and multiple abnormalities have been demonstrated in the peripheral and central nervous systems. Bidirectional mechanisms involving peripheral nociceptive input as well as abnormal central pain processing are involved. Hypothalamic-pituitary-adrenal axis alterations have also been shown with abnormal response to stress. Recent data highlight the putative role of cytokines in the pathogenesis of FM. The autonomic nervous system is implicated in the maintenance of the physiological homeostasis and sympathetic activity appears increased in FM. Neuropeptide Y and its receptors Y1 and Y2 seem to have a complex role in pain modulation.
Di Franco
Manuela
M
Department of Clinical and Medical Therapy, Rheumatology Unit, Sapienza University of Rome, Rome, Italy. manuela.difranco@uniroma1.it
Iannuccelli
Cristina
C
Valesini
Guido
G
D001341:Autonomic Nervous System / Q000503:physiopathology; D016207:Cytokines / Q000502:physiology; D005356:Fibromyalgia / Q000503:physiopathology*; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology; D015213:Neuroimmunomodulation; D009490:Neurosecretory Systems / Q000503:physiopathology*; D018384:Oxidative Stress; D010146:Pain / Q000503:physiopathology; D010913:Pituitary-Adrenal System / Q000502:physiology; D013564:Sympathetic Nervous System / Q000503:physiopathology
D016207:Cytokines