• Andrea Westermann, Anne-Kathrin Rönnau, Elena Krumova, Sabrina Regeniter, Peter Schwenkreis, Roman Rolke, Rolf-Detlef Treede, Helmut Richter, and Christoph Maier.
• Department of Pain Management, Berufsgenossenschaftliches Universitätsklinikum Bergmannsheil GmbH, Bochum, Germany. andrea.westermann@ruhr-uni-bochum.de
• Clin J Pain. 2011 Nov 1;27(9):782-9.

ObjectivesA mixture of sensory loss and gain is a hallmark of neuropathic pain. But hypesthesia and hyperalgesia also occur with experimentally induced acute pain. Here, we assessed sensory profiles in chronic non-neuropathic pain (osteoarthritis, OA) using the quantitative sensory testing (QST) protocol of the German Research Network on Neuropathic Pain (DFNS).MethodsTwenty individuals with OA [mean pain intensity on the numerical rating scale (NRS, 0-10): 5.6±1.5] were tested on the painful and contralateral hand and compared with 20 healthy volunteers matched for age, sex, and handedness.ResultsIn the OA group, analysis of variance revealed increased detection thresholds to tactile stimuli bilaterally and to thermal stimuli restricted to the more painful hand (all P<0.05). Pin-prick hypoalgesia was present restricted to the patients' more affected hand. Neither hyperalgesia nor allodynia was found. QST parameters were correlated with average pain intensity (r between 0.48 and 0.51).ConclusionsThese results suggest that chronic non-neuropathic pain may induce slight sensory impairment for large fiber function (bilateral) and small fiber function (ipsilateral). However, all changes are within the normal range, in contrast to patients with neuropathy. Inhibition of central pathways by nociceptive input and altered sensory processing due to disuse of the hand are possible mechanisms. These functional sensory alterations do not interfere with the diagnosis of neuropathy.

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