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Does Neuropathic Pain Augment Risk of Developing Chronic Widespread Pain?

January 8, 2020
A prospective study follows participants a year after an initial pain survey.

with Don Goldenberg, MD

A condition that is known to increase mortality,1 chronic widespread pain (CWP) is defined by the American College of Rheumatology (ACR) as pain affecting the axial skeleton (skull, spine, or rib cage) and “at least two contralateral quadrants of the body” for at least three months.2

According to Don Goldenberg, MD, professor emeritus of medicine at Tufts University School of Medicine and member of PPM’s Editorial Advisory Board, while CWP is the central feature of fibromyalgia, cases of the latter constitute only a subset of the former. “CWP occurs in approximately 11% of the population throughout the world,” said Dr. Goldenberg, while fibromyalgia has around a 3% prevalence.

Treatment for CWP is lacking, but past research has identified risk factors for developing the condition, including female sex, greater age, depression, and a family history of pain.3 However, Dr. Goldenberg emphasized that “the biggest risk factor for somebody getting CWP is whether they have regional pain to begin with.”

Regional pain, like CWP, is defined more or less by its location or distribution. What remains unclear is whether specific types of pain—and not just the areas affected—could serve as predictors of CWP.

One such candidate is neuropathic pain, defined in part by a patient’s description as burning, tingling, freezing, shock-like, numbness, pins and needles, or itching. Neuropathic pain is often reported by patients with fibromyalgia, and past research has shown that heritability of neuropathic pain and CWP overlap.4

John McBeth, PhD, a professor of chronic disease epidemiology at the University of Manchester, UK, set out to evaluate neuropathic pain as a risk factor for developing CWP in a prospective study.5

(Source: 123RF)

Neuropathic Pain: Too Rare to Serve as a Risk Factor?

McBeth and his colleagues surveyed 1,162 English people (662 women and 500 men, ages 53 to 67) without CWP, grouping participants into three classes based on the pain they reported:

  • no pain (523)
  • regional pain without neuropathic pain (562)
  • and regional pain with neuropathic pain (77).

The participants completed the same survey 12 months later, at which point 153 of them had developed CWP. This group of 153 included:

  • 3.6% of those who reported no baseline pain
  • 19.2% of those who reported baseline pain without neuropathic pain
  • and 33.8% of those who reported baseline pain with neuropathic pain.

Comparing the three groups, the proportion of participants who ended up with CWP was greatest among the group reporting neuropathic pain at baseline. However, because neuropathic pain was relatively rare, regional pain without neuropathic pain served as a more meaningful predictor in hindsight. Among the participants with CWP, those who had initially reported pain without neuropathic pain outnumbered those who had reported pain with neuropathic pain (108 to 26, over 4:1).

The survey included the Douleur Neuropathique 4 (DN4), a common tool used to assess neuropathic pain.6 McBeth and his team used the ACR definition of CWP to identify those with the condition at both survey time points. Also included in the survey were key demographics, occupation, current pain medications, and measures of anxiety, depression, and sleep quality.

The researchers found that those who had regional pain without neuropathic pain at baseline were three times as likely as those without pain to have CWP at follow-up—a finding that held even after controlling for all the other variables in the survey. In comparison, those who had regional pain with neuropathic pain at baseline were twice as likely as those without pain to have CWP at follow-up after adjusting for covariates.

McBeth and colleagues also calculated partial population attributable risks. They reported that the medical community could potentially prevent 6.0% of CWP cases by eliminating regional pain with neuropathic pain, while 41.3% of CWP cases could be prevented by eliminating regional pain without neuropathic pain.

Unexpected Results

These findings surprised Dr. Goldenberg, who has studied fibromyalgia extensively and expected that neuropathic pain at baseline would be a greater predictor of CWP development. He applauded the research, noting the inherent challenges in carrying out a prospective study with over 1,000 participants. However, a common critique of research on chronic conditions such as this study is that even a 1-year study period only offers a snapshot of a chronic condition. Dr. Goldenberg speculated whether neuropathic pain would remain a relatively poor predictor of future CWP if the study followed patients for 5 to 10 years.

Another limitation was the lack of data collected between the baseline and 12-month follow-up surveys. McBeth noted the possibility that his team may have missed cases of CWP that developed and resolved during these intervening months, but it is also unclear whether regional pain for participants persisted throughout the one-year period. The study also failed to report on the prevalence of neuropathic pain at follow-up among the participants who developed CWP.

Still, these findings help delineate the relationships between neuropathic pain, CWP, and fibromyalgia, suggesting that neuropathic pain could be a key difference between CWP when it occurs as part of fibromyalgia, and CWP on its own.

While more research is needed, the results challenge the notion that neuropathic pain augments the risk of developing CWP among patients with regional pain. The study may give pause to clinicians who have gauged the risk of CWP by asking patients if they would describe their pain as burning, tingling, itching, etc. “Maybe that is not an important question,” suggested Dr. Goldenberg.

Last updated on: January 9, 2020
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