Neurology -- Correspondence for Treede et al., 70 (18) 1630-1635

Correspondence published:

Neuropathic pain: Redefinition and a grading system for clinical and research purposes: Jose L. Ochoa, MD, PhD, DSc (29 August 2008)

Neuropathic pain: Redefinition and a grading system for clinical and research purposes 29 August 2008

Jose L. Ochoa, MD, PhD, DSc,
Oregon Nerve Center LLC
1040 NW 22nd Avenue, Suite 600, Portland, Oregon 97210
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Re: Neuropathic pain: Redefinition and a grading system for clinical and research purposes

jochoa{at}nervesense.net Jose L. Ochoa, MD, PhD, DSc

I read the article by Treede et al. with interest. [1] The IASP definition of neuropathic pain: “pain from a lesion or dysfunction of the nervous system,” is inadequate as patients displaying pain behavior and sensorimotor phenomena without demonstrable neuropathophysiology lack evidence of disease.
However, the clinical resemblance between patients with and without such evidence has been taken to indicate that both profiles are neuropathic, but the second profile is due to a “dysfunctional set of neurons.” [2] For neurologists, such resemblance is superficial and the “dysfunctional set of (central) neurons” has not been proven. [3]
The present redefinition by neurologists shifts pain medicine from folk towards the scientific paradigm. “Pain arising as a direct consequence of a lesion or disease affecting the somatosensory system”...and this “cannot be determined without a physical (neurological) examination of the patient.” Therefore, “neuropathic” cannot be diagnosed in patients who communicate pain associated with sensorimotor clinical displays in the absence of clinical or neurophysiological equivalents of neuropathology.
Self-reported escalation following uncomplicated acute focal injury, perpetual allodynia or unexplainable symptom spread is not enough; neither is the collapse of voluntary muscle power nor impaired sensory acuity during psychophysical examination. In pain clinics, where most of these patients are managed, mandatory neurological evaluation is substandard leaping from initial observation to concluding thesis while bypassing intermediate hypothesis and test.
One tacit contribution from this revision concerns the CRPS I controversy. By virtue of the intriguing criterion #4 (International Association for the Study of Pain, 1994), CRPS I has remained a descriptive label by default, rather than the diagnosis of a validated disease process. The label CRPS I pertained only when the treating doctor could not explain the patient’s medical nature. This fallacy is addressed in the Introduction to the latest CRPS book. [4] Treede et al [1] must now go back to the virtual concept of secondary "central sensitization," a pathophysiologically-loaded attribution that largely addresses pseudoneurological phenomena. Its hypothesized mechanism, again "a dysfunctional set" of hyperexcitable central neurons, cannot be directly tested in behaving patients, and it's ad hoc animal models follow nerve injury, not CRPS I. [4]
References
1. Treede RD, Jensen T., Campbell JN, et al. Neuropathic pain: Redefinition and a grading system for clinical and research purposes. Neurology 2008;70: 630-1635.
2. Merskey H. Clarifying definition of neuropathic pain. Pain 2002;96 408-409.
3. Ochoa J. The irritable human nociceptor under microneurography: from skin to brain In Advances in Clinical Neurophysiology. Vol 57. Eds. Hallett M., Phillips II L H, Schomer D L, Massey, J M; Elsevier Sciences 2004;57:15-23.
4. Loeser, J.D. CRPS: Current Diagnosis and Therapy, Progress in Pain Research and Management. Introduction by J.D. Loeser, Seattle, IASP Press. Eds. Peter R. Wilson, Michael Stanton-Hicks, R. Norman Harden. 2005;32:3-7.
Disclosure: The authors report no disclosures.
Editor’s Note: The authors of the article were offered the opportunity to respond but declined.