Modulation de la douleur par la contrestimulation nociceptive hétérotopique et l'attention sélective chez des patients atteints de lombalgie chronique non spécifique

Pain is a subjective experience that can be modulated by regulatory neurophysiological mechanisms and psychological factors. It has alarming and protective functions, but it sometimes persist beyond the time required for tissue healing and becomes chronic. Among chronic pain syndromes, chronic non-specific low back pain is a very prevalent and incapacitating condition. In order to better understand the pathophysiology of chronic non-specific low back pain, it is crucial to evaluate the integrity of endogenous pain modulation mechanisms. The latter can be evaluated experimentally by a nociceptive counterstimulation paradigm (pain-inhibit-pain phenomenon).  First, we developed an experimental protocol to assess the contribution of attention to hypoalgesia induced by nociceptive counter-stimulation. Healthy volunteer participants received a series of painful transcutaneous electrical stimulations applied over the sural nerve at an individually-adjusted intensity to evoke the nociceptive flexion reflex (RIII) and moderate pain. Pain was modulated by a cold non-painful stimulation applied on the arm (non-nociceptive counterstimulation) and by a frozen gel pack causing pain on the forearm (nociceptive counterstimulation). The direction of attention was manipulated across two sessions. As expected, pain induced by electrical stimulations was inhibited by nociceptive counterstimulation relative to baseline (p < 0.01). In addition, the hypoalgesic effect of nociceptive counterstimulation was greater than that of non-nociceptive counterstimulation (p < 0.01). Moreover, this inhibition was greater when attention was directed towards counterstimulation than towards electrical stimulation (p = 0.02). As for inhibition of spinal nociceptive transmission, the RIII was significantly inhibited by counterstimulation relative to baseline (p < 0.01) and the effect was significantly greater for nociceptive than for non-nociceptive counterstimulation (p = 0.03). However, this effect was not modulated by the direction of attention (p = 0.35). The results of this study indicate that selective attention and nociceptive counterstimulation produce additive inhibition of pain. This additive effect was not observed for the RIII, which suggests the implication of a cerebral mechanism independent of spinal nociceptive transmission.   Secondly, we investigated pain modulation mechanisms in patients with chronic non-specific low back pain, which pathophysiology is not well defined. In this study, we used the experimental paradigm described above to which we added a control session. During this session, participants received electrical stimulation only, without counterstimulation. This allowed measuring and controlling for non-specific temporal effects. In addition to measuring pain and RIII, evoked potentials were recorded in order to measure the modulation of pain-related brain activity. The inhibition of pain by counterstimulation or by selective attention was not significantly different between patients and controls (p = 0.99). However, for both groups combined, nociceptive counterstimulation produced a marginal inhibition of pain (p = 0.06) as well as significant inhibition of the N100 and N150 components of the evoked potentials (p < 0.001). Also, selective attention induced significant hypoalgesia (p < 0.01) and significantly inhibited the N100 component (p < 0.001). The results of this study suggest that nonspecific chronic low back pain does not rely on a deficit of the pain inhibition mechanisms assessed in this study.

Keyphrases: Attention, Pain, Heterotopic noxious counterstimulation, Descending modulation, RIII-reflex, Somatosensory evoked-potentials