It is considered a useful measure of disease impact. Other questionnaires
Other measures include the Hospital Anxiety and Depression Scale, Multiple Ability Self-Report Questionnaire, Multidimensional Fatigue Inventory, and Medical Outcomes Study Sleep Scale. Differential diagnosis
As of 2009, as many as two out of every three people who are told that they have fibromyalgia by a rheumatologist may have some other medical condition instead. Fibromyalgia could be misdiagnosed in cases of early undiagnosed rheumatic diseases such as preclinical rheumatoid arthritis, early stages of inflammatory spondyloarthritis, polymyalgia rheumatica, myofascial pain syndromes and hypermobility syndrome. Neurological diseases with an important pain component include multiple sclerosis, Parkinsons disease and peripheral neuropathy. Other medical illnesses that should be ruled out are endocrine disease or metabolic disorder (hypothyroidism, hyperparathyroidism, acromegaly, vitamin D deficiency), gastro-intestinal disease (celiac and non-celiac gluten sensitivity), infectious diseases (Lyme disease, hepatitis C and immunodeficiency disease) and the early stages of a malignancy such as multiple myeloma, metastatic cancer and leukemia/lymphoma. Other systemic, inflammatory, endocrine, rheumatic, infectious, and neurologic disorders may cause fibromyalgia-like symptoms, such as systemic lupus erythematosus, Sjögren syndrome, ankylosing spondylitis, Ehlers-Danlos syndromes, psoriatic-related polyenthesitis, a nerve compression syndrome (such as carpal tunnel syndrome), and myasthenia gravis. In addition, several medications can also evoke pain (statins, aromatose inhibitors, biophosphonates, and opioids).The differential diagnosis is made during the evaluation on the basis of the persons medical history, physical examination, and laboratory investigations. The patients history can provide some hints to a fibromyalgia diagnosis.
Increased baseline ACTH and increase in response to stress have been observed, hypothesized to be a result of decreased negative feedback. Immune system
Inflammation has been suggested to have a role in the pathogenesis of fibromyalgia. People with fibromyalgia tend to have higher levels of inflammatory cytokines IL-6, and IL-8. There are also increased levels of the pro-inflammatory cytokines IL-1 receptor antagonist. Increased levels of pro-inflammatory cytokines may increase sensitivity to pain, and contribute to mood problems. Anti-inflammatory interleukins such as IL-10 have also been associated with fibromyalgia.A repeated observation shows that autoimmunity triggers such as traumas and infections are among the most frequent events preceding the onset of fibromyalgia. Neurogenic inflammation has been proposed as a contributing factor to fibromyalgia. Digestive system
Gut microbiome
Gut bacteria may play a role in fibromyalgia. People with fibromyalgia are more likely to show dysbiosis, a decrease in microbiota diversity. There is a bidirectional interplay between the gut and the nervous system. Therefore, the gut can affect the nervous system, but the nervous system can also affect the gut. Neurological effects mediated via the autonomic nervous system as well as the hypothalamic pituitary adrenal axis are directed to intestinal functional effector cells, which in turn are under the influence of the gut microbiota. Gut-brain axis
The gut-brain axis, which connects the gut microbiome to the brain via the enteric nervous system, is another area of research. Fibromyalgia patients have less varied gut flora and altered serum metabolome levels of glutamate and serine, implying abnormalities in neurotransmitter metabolism.