Chronic Pain may be More than Central Sensitization

Identifying Central Sensitization May Not Tell the Whole Story by Charles E Argoff, MD – Sept 2018

Though this article addresses only chronic pelvic pain (CPP), I believe it can be generalized across many other painful disorders of unknown cause.

Levesque et al. describe in this edition of the Journal their development of a consensus-based tool using the Delphi process to assist in establishing clinical criteria of central sensitization in chronic pelvic pain and perineal pain (CPP).

However, the very premise that the authors make—“The concept of central sensitization may allow better understanding and management of patients with chronic pelvic pain (CPP), which is why we decided to elaborate a clinical evaluation tool designed to simply identify central sensitization in pelvic pain”—as the only important neural mechanism in CPP is itself unproven.

My purpose in writing this Editorial is to raise several points that advance the possibility that central sensitization may not be the only primary mechanism of CPP; if this possibility in fact has merit, then identifying central sensitization in CPP may be important but may not be sufficient in assessing and treating patients.  

First, while the authors note how complicated CPP is to diagnose and effectively treat, stating, “The gap between clinical symptoms and pathological signs is a constant feature of these pain syndromes,” and while the general concept of sensitization can be applied to CPP, the authors do not provide clear evidence that central sensitization is the primary initiating mechanism or the perpetuating mechanism of CPP; therefore, how does their proposed tool lead to better assessment and treatment?

Second, recently published findings have noted that the prevalence of skin biopsy–confirmed small fiber polyneuropathy in patients with complex chronic pelvic pain was much higher than the prevalence reported in the general population (64% vs 0.053%).

the observation that small fiber polyneuropathy is prevalent in CPP should be incorporated into any current and future approach to our evaluation and treatment of CPP

Given this, how does one conclude that central sensitization alone is key to the evaluation and treatment of CPP?

Third, the authors note fibromyalgia not once but twice among the 12 items that achieved a strong consensus for establishing their criteria “history of fibromyalgia” and “history of dysfunctional pain, temporomandibular joint dysfunction, migraine, fibromyalgia syndrome.”

Although fibromyalgia has been described as a central pain disorder associated with central sensitization, multiple recent publications have demonstrated that a notable proportion of patients fulfilling the most recent American College of Rheumatology diagnostic criteria for fibromyalgia have skin biopsy findings consistent with small fiber polyneuropathy.

We do not take care of general populations; rather, we take care of individual patients, closer therefore to a subgroup than to a large heterogeneous cohort. This point cannot be overlooked when developing new tools for the assessment and treatment of our patients.

I previously posted about the problem of population risk misapplied to individual risk: Population Risk Does Not Equal Individual Risk.

Finally, although we generally acknowledge that both peripheral sensitization and central sensitization are important mechanisms in the initiation and maintenance of chronic pain, little attention has been focused on the role of peripheral nervous system mechanisms in ongoing chronic pain.

Perhaps future tools can be developed to examine a more integrated approach to pain mechanisms. Such an approach may further assist in our ability to assess and treat CPP than this tool.

Other thoughts?

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