Key points

Pain syndromes seen by upper extremity surgeons have a variety of presentations. Compression neuropathies, neuromas, enthesopathies, tendinopathies, synovitis, arthritis, ischemia, trauma, and degenerative disorders may all play a role in the pain that afflicts our patients. Most conditions require either therapy exercises, immobilization, or anti-inflammatories. The history and physical examination become extremely important in helping the surgeon to differentiate surgical versus nonsurgical management in painful conditions and the upper extremity. Challenges arise, however, when the patient has multiple symptoms that do not seem to condense to a specific site or surgically manageable pathology. In fact, upper extremities surgeons often see patients with some distinct pathology, such as carpal metacarpal joint arthritis of the thumb or carpal tunnel syndrome, but the patient has complaints of chronic pain and tenderness in various areas in the upper extremity or the entire body. The patient may also complain of many conditions, such as a history of migraine headaches, irritable bowel syndrome, interstitial cystitis, myofascial pain syndrome, or restless leg syndrome. For the busy surgeon, this can be easily dismissed as they try to focus on one specific area that can be treated quickly and efficiently to render the patient pain free. The multiple symptoms outside of those to a specific area in the upper extremity should alert the hand surgeon to other conditions such as fibromyalgia.

Fibromyalgia is a complex systemic disorder characterized by generalized pain, specific sites of musculoskeletal tenderness, fatigue, sleep disturbance, headaches, and a myriad of other visceral and cognitive maladies. ^, Fibromyalgia may be confused with other pain syndromes ( Box 1 ). Previous fibromyalgia criteria used the term chronic wide spread pain defined as pain on the right or left side of the body, pain above or below the waist, or axial skeletal pain. Currently, regions of generalized pain are considered a more useful criteria. Once termed fibrositis, fibromyalgia is now believed to be a part of the central sensitivity syndrome and not an inflammatory process. With that being said, the triggers for the central sensitization are unclear. It is possible that inflammatory states or autoimmune conditions or physical trauma can be the initial trigger to fibromyalgia. Ultimately, the condition is manifest by abnormal intense perception of pain with minimal stimuli. Abnormalities along the entire pain pathway, from the peripheral activation of nociceptors, to neurotransmitter changes, to the somatosensory cortical interpretation of the central nervous system, have been identified in patients with fibromyalgia. Abnormalities in functional MRI provide objective evidence that fibromyalgia has its foundation in an organic pathology. ^{, , ,} Similarly, sustained higher levels of substance P and other pain-modulating neurotransmitters have been identified in the cerebral spinal fluid of patients with fibromyalgia. ^, Even more compelling is the recent finding by Albrecht and colleagues, demonstrating an increase in radioligands and uptake in specific brain regions through activated brain glia and neuroinflammation in patients with fibromyalgia.

The prevalence of fibromyalgia is said to be in the range of 0.5% to 12.0% of the population with a female to male ratio 3 to 1. Patients with fibromyalgia should be thought of as patients with a pain-prone phenotype, often experiencing episodes of chronic pain not only focused on the musculoskeletal system, but on all areas of the body. Therefore, obtaining an extensive history defining the chronicity and regionality of the pain will direct management appropriately. Surgery and opioid use to relieve the pain is more often than not unresponsive in the pain-prone patient. Furthermore, the pain sensitivity is thought to be polygenic. Patients with fibromyalgia seem to have a familial preponderance of the condition with variable expression1. ^,

The diagnosis of fibromyalgia can be difficult, but is based predominantly on the patient’s history. It often takes more than 2 years to confirm the diagnosis, with patients seeing an average of 3.7 physicians and or surgeons during this time. Many conditions may have similar clinical scenarios that mimic fibromyalgia; therefore, care should be taken into consideration during the workup of afflicted patients to try to identify ailments that will be treated differently. The differential diagnosis of fiber myalgia can be categorized into musculoskeletal, neurologic, psychiatric psychological, and drug-related disorders ( Box 2 ).

Diagnostic dilemmas in the evaluation of a patient with chronic pain prompted the formation of the Analgesic, Anesthetic, and Addiction Clinical Trial Translations Innovation Opportunities and Networks public–private partnership with the US Food and Drug Administration and the American Pain Society initiation of the Analgesic, Anesthetic, and Addiction Clinical Trial Translations Innovation Opportunities and Networks–American Pain Society Pain Taxonomy group to develop a consistent diagnosis system for the various pain disorders. As a result, the Analgesic, Anesthetic, and Addiction Clinical Trial Translations Innovation Opportunities and Networks–American Pain Society Pain Taxonomy identified 5 dimensions to differentiate diagnosis ( Box 3 ). ^{, ,} Further clarifications were made through structured, focused fibromyalgia working groups to reach our current understanding of appropriate criteria for diagnosing fibromyalgia ( Box 4 ). Biomarkers do not exist for fibromyalgia, although increases in serum haptoglobin and fibrinogen levels offer some promise. Systemic inflammation is not characteristic of this condition. Recent evidence, however, suggests that profiles of microRNAs in saliva and cerebral spinal fluid may help to diagnose patients with fibromyalgia. Proteomic analysis have shown increases in seotransferin, alpha-enolase, phosphoglycerate-mutase-I, and trans-aldolase in patients with fibromyalgia relative to healthy, migraine, or rheumatoid arthritis patients. Similarly, Ramirez-Tejero and colleagues identified 33 different proteins expressed in the plasma of patients with fibromyalgia and suggested that inflammation may have a role in the pathology. Metabolomic screening has recently differentiated patients with fibromyalgia from those patients with lupus and rheumatoid arthritis, identified through the analysis of vibrational spectra tyrosine residues in proteins, which highlighted possible roles of aromatic and carboxylic acid molecules, including tryptophan as potential biomarkers.

Box 4

The 2019 Analgesic, Anesthetic, and Addiction Clinical Trial Translations Innovation Opportunities and Networks–American Pain Society Pain Taxonomy diagnostic criteria established for patients with fibromyalgia

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