Why don't we use a body map in every chronic pain patient yet?

Abstract

The excellent article by Johnson and colleagues used genetic data from a very large sample from the UK Biobank and performed a longitudinal study examining factors contributing to the development of symptomatic knee osteoarthritis (OA).7 The previously published Genome Wide Association Study findings for widespreadedness of pain (termed multisite chronic pain [MCP] in this study) were used as the surrogate for central factors and of body mass index (BMI) as the surrogate for peripheral factors. The authors showed what appear to be strong causal independent and synergistic contributions for both central and peripheral factors. In this analysis, the authors found the peripheral factors to be stronger than central but that may have been partly driven by the use of BMI for the surrogate of peripheral factors (because BMI is strongly related to MCP in population-based studies). Other studies suggest that peripheral and central factors may be playing differentially important roles in different phases of osteoarthritis. Because no one disagrees that peripheral nociceptive pain is important in OA, rather than quibbling about the relative contributions, these data should further reinforce the importance of central factors in OA. Most clinicians are unaware of the plethora of data that shows that central factors are important in OA (and in any other chronic pain condition) and that this information can already be used in clinical practice to guide treatment decisions. Any type of body map should be given to any chronic pain patient to assess for widespreadedness of pain—because this single measure is being repeatedly shown to be a good surrogate for what is now referred to as nociplastic pain.5 Although some of us work to develop formal criteria for nociplastic pain, there is unanimity that the widespreadedness or spatial extent of pain is a very important component because when the central nervous system is driving the pain, it should be more widespread than if peripheral factors are the driver.4 Many studies in OA and other pain conditions have shown that a body map alone can be very powerful in determining which patients with pain are most likely to respond to peripherally or centrally directed therapies. Treatments that work primarily in the periphery are more likely to be effective in individuals with localized pain, whereas individuals with multisite pain are more likely to respond to centrally directed therapies. Patients with knee OA getting arthroplasty are much more likely to respond if they have localized than widespread pain,3 but these OA patients with widespread pain are more likely to respond to duloxetine—a centrally acting analgesic.6 Similar findings showing that pain widespreadedness predicts poorer pain relief following surgery have been noted in other surgeries done to relieve pain, such as hysterectomy,2 and better outcomes with centrally acting analgesics such as duloxetine in other chronic pain conditions such as low back pain.1 For those unfamiliar with the use of a body map for this purpose, it does not matter what body map you use because what is most important is how many regions of pain an individual has. Although body maps with many sites can be helpful for precise anatomic location of pain, one cannot simply count the number of pain sites on a body map to assess widespreadedness because contiguous regional pain is miscounted as multisite. For example, an individual with sciatica could have as many as 5 to 6 contiguous sites of pain from the buttock to foot—from a single peripheral problem. Thus, one should distill any body map to 7 or 8 regions (head and neck, 2 arms/shoulders, 2 legs, front of trunk and back of trunk, ± pelvis as a separate site) and look at how many regions of pain an individual is experiencing. Most individuals with pain have some contributions from both sets of factors, but those with prominent nociplastic components will generally have pain in 3 or more regions. There are other phenotypic features of central sensitization/nociplastic pain that may end up being part of the formal criteria for nociplastic pain because these features are known to be much more common in central nervous system-driven pain. For example, individuals with nociplastic pain have higher levels of sleep and memory problems and fatigue, and these symptoms are even risk factors for the development of multisite or widespread pain.8 These items are included in the 2011 Fibromyalgia Survey Questionnaire that our group and others have used as a surrogate measure of central sensitization/nociplastic pain.12 Individuals with nociplastic pain are also not just more sensitive to pain, they are more sensitive to a number of other nonpainful stimuli, such as the brightness of lights, loudness of noises, and measures of global sensory sensitivity, which may be helpful in identifying these individuals.11 Another way to phenotype of individuals for this trait is to look at the number of chronic overlapping pain conditions, such as fibromyalgia, headache, irritable bowel, and the like the individual has experienced, using International Classification of Diseases codes to compute such a phenotype.9,10 Although we wait for the IASP and other organizations to develop formal criteria for nociplastic pain, we can and should rapidly translate some of these findings into clinical practice. Every one of us who teaches providers how to diagnose and manage pain should require a body map as part of the history and physical of any chronic pain patient. The information gleaned is extremely easy to attain and too important to ignore. Conflict of interest statement The author has no conflict of interest to declare.

Topics & Concepts