Abstract
Pain is associated with the different types of rheumatic syndromes because it is often the most troubling symptom of patients affected by any of these diseases. Some risk factors clearly play a major role in the clinical expression of pain and related syndromes, including genetics, age, gender, co-morbidities, traumas and psychological patterns, but there are no specific clinical, laboratory or neuroimaging markers that can indicate why and when a patient’s localised pain will become chronic and widespread. Any type of pain must be treated not only appropriately, but also rapidly because the likelihood of developing some form of chronic pain is related to the duration of the peripheral pain stimulus. Chronic pain inevitably has a major impact on patients’ quality of life because the loss of function undermines their ability to do everyday activities. Pain can be most effectively treated by carefully selecting various pharmacological and non-pharmacological interventions based on the characteristics of the pain itself, disease factors, psychological coping abilities, and lifestyle.
Rheumatology is a branch of medicine in which pain (particularly chronic pain) is the cornerstone of most clinical presentations and diagnoses . Over the last 20 years, we have learned to distinguish various underlying mechanisms that can cause chronic pain, and this information has led to significant changes in the way patients are treated. During the 1990s, rheumatologists mainly used non-steroidal anti-inflammatory drugs (NSAIDs) or steroids to treat all types of pain, which were only distinguished in terms of their severity, whereas we now easily use opioids, anticonvulsants and antidepressants together with non-pharmacological approaches. We have also learned that most individuals with chronic pain have more than one underlying mechanism for their pain, and thus different patients with the same disease causing their pain may need to be treated with different treatments with differing underlying mechanisms . Thus, it is increasingly important to understand the mechanisms of pain present in each individual and personalise their treatment(s) based on this information. This is no less than a Copernican revolution in causing rheumatologists to use all of the weapons available in the armamentarium more actively.
Setting, adjusting and achieving realistic therapeutic goals requires not only a combination of pharmacological, non-pharmacological and rehabilitative approaches but also a strong therapeutic alliance between patients and physicians . Therefore, planning the treatment of persistent pain involves clearly understanding patients’ goals and expectations, co-morbidities and cognitive and functional status .
Pain in systemic rheumatic diseases
This issue concentrates on the different types of pain associated with the different types of rheumatic syndromes because pain is often the most troubling symptom of patients affected by any of these diseases.
Rheumatic pain affects bones, muscles and joints, and it is most frequently associated with diseases such as osteoarthritis (OA), rheumatoid arthritis (RA) and other types of inflammatory arthritis and osteoporosis . However, pain may invariably be among the constellation of symptoms peculiar to practically any type of rheumatic disease.
The distinction between ‘acute’ and ‘chronic’ pain in musculoskeletal pain disorders is not very clear. Patients with arthritis may experience recurrent acute pain mainly related to exercise related or almost continuous pain that is present even at rest, whereas unremitting pain is more a feature of chronic widespread pain (CWP); furthermore, some patients with RA and OA feel pain mainly at rest and they find that it improves with exercise . Consequently, an all-encompassing description such as ‘chronic’ pain does not usually reflect individual experience accurately.
Chronicity is a feature of most rheumatic diseases that is often highlighted by the persistence of symptoms whose physiopathological characteristics may change over time. For example, the pain associated with RA is probably nociceptive in origin, when the joints are inflamed, but it may gradually become centralised as it spreads through the body. This means that it may be simultaneously nociceptive and centralised for long periods of time and, consequently, it may be necessary to treat (or prevent) the centralised aspects of pain while providing anti-nociceptive relief.
The extent of pain varies widely in patients with rheumatic diseases. Some may experience pain and tenderness over much of the body surface as in the case of CWP or fibromyalgia (FM), whereas in others the pain will be much more regional and only affect tissues with ongoing damage or inflammation. However, although CWP and FM are sometimes seen as being distinct from other rheumatic diseases (differentiated by the extent of tenderness), there is still no physiological justification for this distinction ; therefore, in the current study, they will be considered as falling within the spectrum of musculoskeletal pain disorders.
Pathophysiology of pain
Learning to distinguish nociceptive, neuropathic, centralised and mixed pain has been a significant achievement. As rheumatic diseases may be characterised by any of these, physicians must develop an understanding of the type of pain affecting an individual patient and tailor the treatment accordingly . However, in any disease, the presence of mixed pain may make diagnosis and treatment extremely difficult: for example, a patient with RA may subsequently develop a ‘centralised pain’ syndrome such as FM, headache, irritable bowel syndrome (IBS), temporomandibular joint disorder (TMJD) and interstitial cystitis (IC), all of which have been shown to be familial/genetic and to strongly co-aggregate in individuals and families . The symptoms experienced by patients with central pain syndromes have been well characterised: multifocal pain (a current and lifetime history of pain in many body regions) and a cluster of co-occurring somatic symptoms (i.e., fatigue, sleep disorders and memory difficulties) .
Current evidence suggests that genetic and immunological factors may contribute to increasing sensitivity to pain, thus making it more likely that chronic pain will develop during the course of a lifetime . It has been shown that various sets of genes are involved in these two processes, including catechol-O-methyltransferase (COMT) (an oestrogen-sensitive enzyme that may play a more prominent role in females), a number of sodium channel mutations, guanosine triphosphate (GTP) cyclohydroxylase, type 2 and 3 adrenergic receptors and the KCNS potassium channel gene .
The most widely accepted pathogenic theory to explain the association of central pain states with the clustering of co-occurring somatic symptoms and higher than expected rates of mood disorders is that the centrally acting neurotransmitters known to be involved in causing the pain (low norepinephrine, gamma-aminobutyric acid (GABA), serotonin, high glutamate levels and substance P) also play prominent roles in controlling sleep, mood, alertness, etc. . Clinicians might better understand pain and sensory processing by considering it to be controlled in a manner similar to the control of immune function.
Pathophysiology of pain
Learning to distinguish nociceptive, neuropathic, centralised and mixed pain has been a significant achievement. As rheumatic diseases may be characterised by any of these, physicians must develop an understanding of the type of pain affecting an individual patient and tailor the treatment accordingly . However, in any disease, the presence of mixed pain may make diagnosis and treatment extremely difficult: for example, a patient with RA may subsequently develop a ‘centralised pain’ syndrome such as FM, headache, irritable bowel syndrome (IBS), temporomandibular joint disorder (TMJD) and interstitial cystitis (IC), all of which have been shown to be familial/genetic and to strongly co-aggregate in individuals and families . The symptoms experienced by patients with central pain syndromes have been well characterised: multifocal pain (a current and lifetime history of pain in many body regions) and a cluster of co-occurring somatic symptoms (i.e., fatigue, sleep disorders and memory difficulties) .
Current evidence suggests that genetic and immunological factors may contribute to increasing sensitivity to pain, thus making it more likely that chronic pain will develop during the course of a lifetime . It has been shown that various sets of genes are involved in these two processes, including catechol-O-methyltransferase (COMT) (an oestrogen-sensitive enzyme that may play a more prominent role in females), a number of sodium channel mutations, guanosine triphosphate (GTP) cyclohydroxylase, type 2 and 3 adrenergic receptors and the KCNS potassium channel gene .
The most widely accepted pathogenic theory to explain the association of central pain states with the clustering of co-occurring somatic symptoms and higher than expected rates of mood disorders is that the centrally acting neurotransmitters known to be involved in causing the pain (low norepinephrine, gamma-aminobutyric acid (GABA), serotonin, high glutamate levels and substance P) also play prominent roles in controlling sleep, mood, alertness, etc. . Clinicians might better understand pain and sensory processing by considering it to be controlled in a manner similar to the control of immune function.
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