Comparison of the pain suppressive effects of clinical and experimental painful conditioning stimuli.

Studies in healthy volunteers suggested that the classical counterirritation phenomenon (i.e. pain inhibits pain effect) might depend on diffuse noxious inhibitory controls (DNIC), which modulate the spinal transmission of nociceptive signals. In the present study, we sought to determine whether similar mechanisms were at play in patients with different subtypes of neuropathic pain. Ten patients presenting with a traumatic peripheral nerve injury associated with dynamic mechano-allodynia (i.e. pain triggered by brushing) or static mechano-allodynia (i.e. pain triggered by light pressure stimuli) were included in this study. To investigate counterirritation mechanisms in these patients, we analysed the RIII nociceptive flexion reflex and concomitant painful sensation elicited by electrical stimulation of the sural nerve. We compared the effects of heterotopic 'clinical' conditioning stimuli (i.e. pain evoked by brushing or pressure within the allodynic area located in the upper limb or chest) to those of experimental heterotopic noxious stimuli (HNCS) consisting of a cold pressor test or tourniquet test applied to the normal upper limb. Static mechano-allodynia induced inhibitions of both the RIII reflex and the concomitant painful sensation. These effects were similar to those induced by HNCS and were probably due to an increased activation of DNIC. In contrast, in patients with dynamic allodynia, brushing within the allodynic area reduced the pain sensation at the foot, but did not inhibit the electrophysiological responses, suggesting that in this case the counterirritation effect may take place at the supraspinal level. Thus, the mechanisms of counterirritation are not univocal, but depend on the pathophysiological mechanisms of clinical pain.