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RIII reflex changes in neuropathic pain induced by spinal cord lesions Patients with spinal cord lesions have provided the basis for a unique clinical model for evaluating the anatomo-functional substrate of descending inhibitory pathways modulating the spinal transmission of nociceptive information. In tetraplegic patients suffering from a clinically complete spinal cord transection at the cervical level, Roby-Brami et al. [121] found that the RIII was normally elicited. In these patients, HNCS application below the level of transection did not produce any effect on the RIII.

Should this data be confirmed, it would suggest that a parallel processing in SI and SII has remained functional in humans for noxious inputs, whereas hierarchical processing from SI toward SII has emerged for non-noxious somatosensory modalities [2, 97]. The main problems in interpreting pain-evoked potentials are the fact that attentional activation is an unavoidable concomitant of noxious activation. Pain-evoked potentials are therefore a mixture of sensory and cognitiveattentional responses, and should be interpreted as such.

RIII reflex changes in neuropathic pain induced by supraspinal lesions RIII change studies in supraspinal lesions have yielded valuable information for the understanding of pain induced by thalamic lesions and of diffuse noxious inhibitory controls (DNIC). Willer et al. [170] studied changes of the RIII threshold in thalamic syndromes. They found that the threshold was increased on the pain side compared to the unaffected side, where it was normal. Treatment with a selective serotonin reuptake inhibitor (indalpine) caused an increase similar to that observed in normal subjects on the non-painful side, whereas on the pain side a further increase in the reflex threshold, but not in the subjective pain threshold, was observed.

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