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12 Articles in Volume 12, Issue #4
Causes of Postoperative Pain Following Inguinal Hernia Repair: What the Literature Shows
Persistent Postsurgical Pain
Managing Adverse Drug Effects in Pain: Focus on Triptans and NSAIDs
Nonsurgical Treatments for Ankle Arthritis
Opioid Disposal: Dos and Don’ts
Survey Shows More Education About Fibromyalgia Needed Among Healthcare Providers
Anxiety in a Headache Patient: Case Challenge
“Centralized Pain”: A New Consensus Phrase
Tooth Loss in the Chronic Pain Population
When Prescribed Opioids Go Unused
May 2012 Pain Research Updates
May 2012 Letters to the Editor

“Centralized Pain”: A New Consensus Phrase

Editor's Memo from May 2012

The framework or mechanism of how peripheral pain may “become centralized” is now known and understood due to a number of outstanding and dedicated basic scientists. I use the word “dedicated” since I am well aware that Linda R. Watkins, PhD, among others, have diligently and steadfastly pursued the understanding of this framework for more than 20 years.1,2 Put another way, these scientists originally had some great hypotheses. Through their extensive research, they were able to prove they “got it right” for the benefit of millions of suffering pain patients. A problem for practitioners, though, has been what to call this pathologic phenomenon.

To review, some inflammatory mediators generated in the peripheral injury site (activation of glial and opioid receptors) enter the spinal cord and central nervous system (CNS) creating an inflammatory/pain response. If the inflammatory response is excessive (and not treated quickly), tissue destruction occurs in the CNS. In this process, the memory of the pain becomes encoded or “trapped.” If the neuroinflammation generated by glial cell activation is not contained, a number of pathologic changes take place. They include cellular and receptor overstimulation (“sensitization”), tissue loss, hypothalamic-pituitary activation, and excess autonomic efferent and sympathetic discharge.3,4 In essence, the pain develops an inflammatory site within the CNS that encodes and produces hyperarousal of the autonomic nervous system. A good way to grasp this phenomenon is to know that phantom pain is the quintessential example of “centralized” pain.

A problem for practitioners has been what to call this pathologic phenomenon. Researchers originally began to call this occurrence “central sensitization” because the CNS was hyperaroused and over-reactive to painful stimuli, which resulted in such symptoms as hyperalgesia and allodynia. The term “central sensitization” has no real meaning to clinicians or patients, so it hasn’t been used much outside research circles. A few clinical groups wanted to call the centralization phenomenon “maldynia” to indicate that the pain was “malignant” and serious. This suggestion, however, has been a nonstarter.

A lot of practitioners have started to use the term “central pain syndrome.” Unfortunately, this term has caused confusion with the classic definition of “central” pain.5 For several decades, “central pain” or “central pain syndrome” has been used to describe the pain that may occur after a classic CNS disease such as Parkinson’s disease, multiple sclerosis, stroke, or amyotrophic lateral sclerosis.6 Another confusion in the picture is a group of painful conditions, which may, apparently, originate in the CNS. These include fibromyalgia, interstitial cystitis, irritable colon, and temporal mandibular joint dysfunction.7 It is most appropriate to state that these conditions are “centralized.”

To make it clear to all parties, the term “centralized pain” has emerged among many academic and clinical groups to indicate that pain may have started in the periphery but is now in the CNS. We recommend continued use of the phrase “centralized pain.” “Central pain” or “central pain syndrome” should be reserved for pain that occurs following a known CNS disease.

Given the seriousness of centralized pain, it is now far more important to the patient to have a diagnosis of centralized or peripheral pain than it is to classify the pain as nociceptive, visceral, or neuropathic. Why? Once pain is centralized, the originating peripheral injury site may or may not be an active painful, inflammatory lesion. Peripheral treatments may not only be useless, but even harmful. It’s time we educate ourselves and all concerned parties regarding this profound discovery and its related clinical condition. Now that we have the picture, we can move on to developing better—and targeted—treatments.

Last updated on: August 11, 2015
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