One of the tautological matters that bothers us when we participate with algologists in meetings concerning chronic pain is the idea that it is a syndrome per se and does not require any aetiopathogenetic or clinical differentiation. As physicians, we have been taught to look at the cause(s) of a disease or syndrome because this usually helps to define a specific treatment strategy. Although specific symptoms may become a syndrome per se , and pain may represent a model for this assumption, we feel this needs to be more critically examined, as developed in the following thoughts. Chronic pain can be categorised as localised, regional or widespread on the basis of its distribution. In many cases, it seems to originate from the musculoskeletal system and is commonly associated with pain hypersensitivity, specifically mechanical hyperalgesia.

Epidemiological studies have found that chronic widespread pain (CWP) is very prevalent in the general population (5–10%) and is characterised by pain in all four body quadrants and the neck and back. However, the majority of these studies are telephone surveys, which may be imprecise. Population studies indicate that women report chronic musculoskeletal pain more frequently than men (the ratio is 3:1), and the difference is even more marked in the case of fibromyalgia (FM, 9:1). This may reflect a gender bias inherent to the current criteria, which do not take into account the fact that women generally have lower pressure pain thresholds.

CWP not only has a different distribution from that of localised pain, but also affects lives differently. Multiple pain sites are associated with greater pain intensity, longer pain duration and more severe disability. Anxiety and depression are more common in patients with CWP than in those with localised pain or pain-free controls.

Chronicity takes time. When recording a patient’s clinical history, it soon becomes clear that it may take years for full-blown chronic pain to develop, and the speed or acute appearance of diffuse pain is often related to stressful events or psycho-affective problems.

CWP is not a discrete disorder and its diagnosis requires the assessment of other symptoms (sleep disturbances, fatigue, mood disorders, cognitive dysfunction and chemical sensitivity) as well as other common concomitant and overlapping rheumatic and psychiatric disorders, infections and pain states.

The treatment of CWP requires an individualised approach and often involves multimodal and multidisciplinary management. Clinical trial data show that a number of pharmacotherapies are effective in treating pain and other symptom domains, and these should be combined with non-pharmacological modalities, such as cognitive behavioural therapy and exercise. The World Health Organization (WHO) scale of pain severity indicates that patients with CWP or FM should be treated with opioids, but there is little evidence to support the use of opioids to treat FM symptoms.

We believe that there is a difference between the diagnoses of CWP and FM, and prefer to use the terms ‘localised’ or ‘widespread’ pain in accordance with the new 2010 preliminary American College of Rheumatology (ACR) classification criteria. However, the cluster of FM symptoms not only includes pain, but also fatigue, sleep alterations and cognitive dysfunction, and these additional domains demonstrate the possible consequences when pain becomes chronic. The ideas that abnormal pain behaviour may arise from an aberrant nociceptive system, on the one hand, or be entirely explained by a biopsychosocial model, on the other, must be filtered by the fact that FM may not develop in the absence of a genetic predisposition.

Can the problems of terminology be solved? Should chronic pain be considered a syndrome rather than a symptom? It may be easier, but we feel that this would not be correct. Most of our patients present with mixed pain: for example, the pain of osteoarthritis may keep relapsing and, as the flares of this peripheral pain pattern of pain cause central pain amplification, patients need to be treated with both central and peripheral pain-relieving drugs.

In conclusion, chronic musculoskeletal pain can be considered localised, regional or diffuse. Pain responses tend not to be amplified in patients with chronic localised pain (e.g., shoulder periarthritis, neck or low back pain and local myofascial pain), which often continues to wax and wane without greatly interfering with the psycho-affective dimension. In some other patients, chronic pain is associated with a type of central sensitivity syndrome (such as irritable bowel syndrome, headache or chronic fatigue), but does not substantially affect the muscle nociception system. However, there are patients who develop full-blown FM involving the interaction of multiple biological, psychological and behavioural elements. Although not completely understood, it is thought that increased central sensory input, neuroendocrine and neuropeptide abnormalities, family and genetic factors and psychosocial stressors may all play a role, and these aetiological complexities are reflected in the array of symptom domains associated with FM.

What should these different types of pain syndrome be called? On the basis of our experience, we believe that the topographical definition can be used if the pain is localised, CWP if the pain is regional or diffuse but there are few ancillary symptoms and the term FM can be used if there are many ancillary symptoms. This is the type of terminology we have for now, until there are better and perhaps more objective measures, such as neuroimaging techniques, to characterise chronic pain patients.