Deficient conditioned pain modulation after spinal cord injury correlates with clinical spontaneous pain measures

The contribution of endogenous pain modulation dysfunction to clinical and sensory measures of neuropathic pain (NP) has not been fully explored. Habituation, temporal summation, and heterotopic noxious conditioning stimulus-induced modulation of tonic heat pain intensity were examined in healthy noninjured subjects (n = 10), and above the level of spinal cord injury(SCI) in individuals without (SCI-noNP, n = 10) and with NP (SD-NP, n = 10). Thermoalgesic thresholds, Cz/AFz contact heat evoked potentials (CHEPs), and phasic or tonic (30 seconds) heat pain intensity were assessed within the C6 dermatome. Although habituation to tonic heat pain intensity (0-10) was reported by the noninjured (10 s: 3.5 +/- 0.3 vs 30s: 2.2 +/- 0.5 numerical rating scale; P = 0:003), loss of habituation was identified in both the SCI-noNP (3.8 +/- 0.3 vs 3.6 +/- 0.5) and SCI-NP group (4.2 +/- 0.4 vs 4.9 +/- 0.8). Significant temporal summation of tonic heat pain intensity was not observed in the 3-groups. Inhibition of tonic heal pain intensity induced by heterotopic noxious conditioning stimulus was identified in the noninjured (-29.7%+/- 9.7%) and SCI-noNP groups (-19.6%+/- 7.0%), but not in subjects with SCI-NP (+1.1%+/- 8:0%; P<0.05). Additionally, the mean conditioned pain modulation response correlated positively with Cz/AFz CHEP amplitude (rho = 0.8; P = 0.015) and evoked heat pain intensity (p = 0.8; P = 0.007) in the SCI-NP group. Stepwise regression analysis revealed that the mean conditioned pain modulation (R-2 = 0.72) correlated with pain severity and pressing spontaneous pain in the SCI-NP group. Comprehensive assessment of sensory dysfunction above the level of injury with tonic thermal test and conditioning stimuli revealed less-efficient endogenous pain modulation in subjects with. SCI-NP.