1813 01 REUMA3 Editoriale - ME/CFS Australia

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32 S. Stisi et al.stress, obtained, for instance, through relaxationtraining or exercise training, produces a decrease inthe sympathetic activity (as evaluated via spectralanalysis, resting heart rate, circulating levels of catecholamines).Pain may also explain the reduced neuroendocrineand ANS responsiveness since there is a high levelof substance P in the CSF in FMS, and substance Pis a potent inhibitor of CRH.CONCLUSIONSUnderstanding of pathogenetic pathways in FMShas advanced from observing patient responses toneurophysiologically targeted therapies and basicresearch. The model of central sensitization representsthe most common and most accepted hypothesesabout the underlying mechanisms in thepathogenesis of FMS.SUMMARYFibromyalgia syndrome (FMS) is a common chronic condition of widespread pain with causal mechanisms that are largelyunknown. It is characterized by moderate to severe musculoskeletal pain and allodynia, but its pathogenesis appearsconfined to the nociceptive structures of the central nervous system. FMS is often triggered by negative environmentalinfluences, especially if they occur in childhood. In a fetus, these environmental triggers may influence the developmentof the autonomic nervous system (ANS) and the hypothalamic-pituitary-adrenal axis (HPA). Increasing evidence supportsthe comorbidity of psychological conditions including depression, panic disorders, anxiety, and post-traumaticstress disorder (PTSD). Recent evidence suggests that genetic factors may play a role in the pathogenesis of FMS. Centralsensitization has long been associated with FMS pain. It describes enhanced excitability of dorsal horn neurons, whichleads to transmission of altered nociceptive information to the brain. Understanding of pathogenetic pathways in FMShas advanced beyond observing patient responses to neurophysiologically targeted therapies and basic research.Key words - Central sensitization, neuroendocrine abnormalities, genetic factors, autonomic nervous system.Parole chiave - Sensibilizzazione centrale, alterazioni neuroendocrine, fattori genetici, alterazioni del sistema nervoso.REFERENCES1. Sarnoch H, Adler F, Scholz OB. Relevance of muscularsensitivity, muscular activity, and cognitive variablesfor pain reduction associated with EMG feedbackin fibromyalgia. Percept Mot Skills 1997; 84:1043-50.2. Jacobsen S, Petersen IS, Danneskiold-Samsoe B.Clinical features in patients with chronic muscle painwith special reference to fibromyalgia. Scand JRheumatol 1993; 22: 69-76.3. Kajantie E. Fetal origins of stress-related adult disease.Ann NY Acad Sci 2006; 1083: 11-27.4. Phillips DI and Jones A. Fetal programming of autonomicand HPA function: do people who were smallbabies have enhanced stress response? J Phisiol 2006;572: 45-50.5. McBeth J, Morris S, Benjamin S, Silman AJ, MacfarlaneGJ. Associations between adverse events inchildhood and chronic widespread pain in adulthood:are they explained by differential recall? J Rheumatol2001; 28: 2305-9.6. Imbierowicz K, Egle UT. Childhood adversities inpatients with fibromyalgia and somatoform pain disorder.Eur J Pain 2003; 7: 113-9.7. Crofford LJ. Violence, stress, and somatic syndromes.Trauma Violence Abuse 2007; 8: 299-313.8. Ablin JN, Shoenfeld Y, Buskila D. Fibromyalgia, infectionand vaccination: two more parts in the etiologicalpuzzle. J Autoimmun 2006; 27: 145-52.9. Goldenberg DL: Do infections trigger fibromyalgia?(editorial). Arthritis Rheum 1993; 36: 1489-92.10. Cruz BA, Catalan-Soares B, Proietti F. Higher prevalenceof fibromyalgia in patients infected with humanT cell lymphotropic virus type I. J Rheumatol 2006;33: 2300-3.11. Moldofsky H, Scarisbrick P, England R, Smythe H.Musculoskeletal symptoms and non-REM sleep disturbancein patients with “fibrositis syndrome” andhealthy subjects. Psychosom Med 1975; 47: 341-51.12. Lavigne G, Brousseau M, Kato T Mayer P, ManziniC, Guitard F, et al. Experimental pain perception remainsequally active over all sleep stages. Pain 2004;110: 646-55.13. Burckhardt CS, Clark SR, Campbell SM, O’ReillyCA and Bennett RM. Events and comorbidities associatedwith the onset of fibromyalgia. J MusculoskelPain 1995; 3: 71.14. Kosek E and Ordeberg G. Abnormalities of somatosensoryperception in patients with painful osteoarthritisnormalize following successful treatment.Eur J Pain 2000; 4: 229-38.15. McBeth J and Silman AJ. The role of psychiatric disordersin fibromyalgia. Curr Rheumatol Reports 2001;3: 157-64.16. Bell IR, Baldwin CM, Schwartz GE. Illness from low
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