Central sensitization, a wording derived from the animal neurophysiological literature, is undoubtedly in fashion in the field of pain medicine and is frequently articulated by clinical researchers when referring to any spread of pain-related sensitivity and is used by clinicians to explain strange clinical phenomenologies. In more strict neurophysiological terms central sensitization is a form of activity-dependent neuronal plasticity and has recently been described regarding its highly complex cellular and molecular mechanisms [1] and potential implications for the diagnosis and treatment of pain [2].
Acquainting data from animal experiments on altered neuronal excitability as a result of challenging input in nocieptive afferents with the clinical literature on local/regional and remote hypersensitivity to normally non-painful and painful stimuli in patients with localized pain conditions, non-critical interpretations of data are commonly found in the latter [3,4]. The pre-clinical literature on the subject offers insights into use-dependent synaptic plasticity in dorsal horn neurons in or near the segment receiving nociceptive input from the periphery. The clinical literature demonstrates local and remote widespread hypersensitivity in conditions with a fairly well understood pathophysiology (and in less well understood conditions) which frequently and indiscriminately is interpreted in terms of central sensitization. The presentation will:
draw attention to the mismatch between pre-clinical and clinical data on central sensitization,
discuss suggested features of the clinical phenotype that may rely on homo- and heterotopic central sensitization,
suggest exercising caution when interpreting clinical data in terms of central sensitization,
point to alternative explanations and nomenclature for widespread increased sensitivity.
Currently, central sensitization lacks diagnostic criteria in the clinical scenario and should hence be employed warily, if at all, in such a setting. In the interest of pursuing a mechanism-based classification and treatment of pain translational aspects of pain medicine would benefit from more cautious interpretations of findings in human studies. Repeated use of an unproven concept has caught on in the pain community and may leave translational aspects of pain trivialized and us ridiculed by those who know better.
References
[1] Woolf CJ. Central sensitization: Implications for the diagnosis and treatment of pain. Pain 2011;152:S2–15.Search in Google Scholar
[2] Latremoliere A, Woolf CJ. Central sensitization: a generator of pain hypersensitivity by central neural plasticity. Journal of Pain 2009;9:895–926.Search in Google Scholar
[3] Fernandez-Carnero J, et al. Widespread mechanical pain hypersensitivity as sign of central sensitization in unilateral epicondylalgia. Clinical Journal of Pain 2009;25:555–61.Search in Google Scholar
[4] Cesar Fernandez-de-las-Penas C, et al. Bilateral widespread mechanical pain sensitivity in carpal tunnel syndrome: evidence of central processing in unilateral neuropathy. Brain 2009;132:1472–9.Search in Google Scholar
© 2012 Scandinavian Association for the Study of Pain