• Tanja Stammler, Roberto De Col, Frank Seifert, and Christian Maihöfner.
• Department of Neurology, Schwabachanlage 6, 91054 Erlangen, University Hospital Erlangen, Germany.
• Neuroimage. 2008 Sep 1;42(3):1151-63.

AbstractIt is increasingly recognized that pain-induced plasticity may provoke secondary sensory decline, i.e. centrally-mediated hypoesthesia and hypoalgesia. We investigated perceptual changes induced by conditioning electrical stimulation of C-nociceptors differing in stimulation frequencies and duty cycles provoking either sensory gain (i.e. mechanical hyperalgesia; Stim1) or sensory decline (i.e. hypoesthesia and hypoalgesia; Stim2). Underlying brain processing was investigated using functional magnetic resonance imaging. Before conditioning stimuli, tactile stimulation and pin-prick stimuli led to differential activations of primary and secondary somatosensory cortices (S1, S2), insula and prefrontal cortices (PFC). After induction of mechanical hyperalgesia (Stim1), increased activations were detected in somatosensory/pain-related areas (S1, S2, insula, cingulate cortex) and networks involved in attentional and cognitive processing (parieto-frontal, parieto-cingulate and frontal circuits). In contrast, after induction of hypoesthesia and hypoalgesia (Stim2) the degree of sensory decline for touch and mechanical pain was directly correlated with deactivations within S1, whereas networks associated with attentional and cognitive processing showed increased activation. Therefore, our results demonstrate that brain processing underlying pain-induced sensory gain substantially differs from pain-induced sensory decline. A potential neurobiological mechanism of secondary CNS-mediated hypoesthesia and hypoalgesia may involve modification of local inhibitory networks within somatosensory cortices.

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