Diagnosis
There is no single pathological feature, laboratory finding, or biomarker that can diagnose fibromyalgia and there is debate over what should be considered diagnostic criteria and whether an objective diagnosis is possible. In most cases, people with fibromyalgia symptoms may have laboratory test results that appear normal and many of their symptoms may mimic those of other rheumatic conditions such as arthritis or osteoporosis. The specific diagnostic criteria for fibromyalgia have evolved over time. American College of Rheumatology 1990
The first widely accepted set of classification criteria for research purposes was elaborated in 1990 by the Multicenter Criteria Committee of the American College of Rheumatology. These criteria, which are known informally as "the ACR 1990", defined fibromyalgia according to the presence of the following criteria:

A history of widespread pain lasting more than three months – affecting all four quadrants of the body, i.e., both sides, and above and below the waist. Tender points – there are 18 designated possible tender points (although a person with the disorder may feel pain in other areas as well).The ACR criteria for the classification of patients were originally established as inclusion criteria for research purposes and were not intended for clinical diagnosis but have later become the de facto diagnostic criteria in the clinical setting. A controversial study was done by a legal team looking to prove their clients disability based primarily on tender points and their widespread presence in non-litigious communities prompted the lead author of the ACR criteria to question now the useful validity of tender points in diagnosis.
By using Southern blot analysis of leukocytes, it was revealed that the patients (on average) had expanded repeats ranging from 280 to 380 bp which was the equivalent of more than 90 repeats of CGG, when the LRP12 gene of 1,000 control subjects was tested with the same method, it was revealed that they (on average) had between 13 and 45 repeat units of the same nucleotides, with the exception of two out of the 1,000 controls, who had expanded repeats without any symptoms of the condition.In 2020, Deng et al. discovered beterozygous trinucleotide repeat expansions in the 5-prime untranslayed region of the GIPC1 gene of multiple affected members from 3 Chinese families, this trinucleotide sequence consisted of two Gs (guanine) and one C (cytosine). This mutation was later identified by the same team of researchers in 16 patients, of which 9 were Chinese and 7 were Japanese.In 2020, Ogasawara et al. discovered heterozygous trinucleotide repeat expansions in the non-coding region of the NOTCH2NLC gene of 7 un-related Japanese patients with the condition, the trinucleotide sequence consisted of one C (cytosine) and two Gs (guanine), all 5 patients had more than 100 repeats of the trinucleotide sequence, one of which had two expansions consisting of 217 and 674 repeats. See also
Myopathy
Familial episodic pain syndrome


== References ==