PubMed · 14805481
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J CYRIAX. 1951-02-03. [Fibrositis].. https://pubmed.ncbi.nlm.nih.gov/14805481/
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Fibromyalgia (FM) pain is frequent in the general population but its pathogenesis is only poorly understood. Many recent studies have emphasized the role of central nervous system pain processing abnormalities in FM, including central sensitization and inadequate pain inhibition. However, increasing evidence points towards peripheral tissues as relevant contributors of painful impulse input that might either initiate or maintain central sensitization, or both. It is well known that persistent or intense nociception can lead to neuroplastic changes in the spinal cord and brain, resulting in central sensitization and pain. This mechanism represents a hallmark of FM and many other chronic pain syndromes, including irritable bowel syndrome, temporomandibular disorder, migraine, and low back pain. Importantly, after central sensitization has been established only minimal nociceptive input is required for the maintenance of the chronic pain state. Additional factors, including pain related negative affect and poor sleep have been shown to significantly contribute to clinical FM pain. Better understanding of these mechanisms and their relationship to central sensitization and clinical pain will provide new approaches for the prevention and treatment of FM and other chronic pain syndromes.
The hypothesis that fibromyalgia (FM) should be classified as a somatoform disorder was assessed by reviewing current clinical studies. According to the ICD-10, somatic illness beliefs of the patient, high health care utilization, and frustrating patient-doctor relationships are diagnostic criteria of somatoform disorders. For the diagnosis of a somatoform pain disorder, a temporal association between the manifestation of pain and emotional or psychosocial conflicts and the exclusion of a depressive disorder are additionally required. Empirical studies demonstrate a higher lifetime and current prevalence of psychiatric disorders, childhood adversities, life events, and daily hassles and a higher health care utilization of FM patients. Studies also reveal that most patients believe that both somatic and psychosocial factors have caused their disorder. The patient-doctor relationship is characterized to be disappointing for both. Yet in all studies there were patients who did not fulfill the ICD-10 criteria of a somatoform (pain) disorder. A biopsychosocial model of FM differentiating between biological as well as psychosocial predisposing, triggering, and perpetuating factors in the pathogenesis of FM is presented as an alternative model. Hopefully the biopsychosocial model and the distinction of subgroups will enable more differentiated and tailored psychotherapeutic and pharmacological treatment strategies.
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