Evidence for central hypersensitivity in patients with acute low back pain assessed with somatosensory evoked potentials

P.H. VUILLEUMIER; A.Y. NEZIRI; J.A. BIURRUN MANRESA; S. MLEKUSCH; F.G. ARGUISSAIN; A. ENACHE; O.K. ANDERSEN; L. ARENDT-NIELSEN; M. CURATOLO

Buenos Aires

Congreso; 15th World Congress on Pain; 2014

Aim of Investigation: Altered endogenous pain modulation is one of the possible mechanisms underlying chronic pain conditions. Conditioned pain modulation (CPM) is a method to assess endogenous pain modulation in humans, based on the attenuation of painful test stimulus by a concurrent painful conditioning stimulus. Most of the existing studies have used subjective pain response to assess the CPM efficiency. Furthermore, little is known on the efficiency of CPM in acute low back pain. In the present study CPM was tested using electroencephalography in an acute low back pain population. Methods: Eleven patients with acute low back pain (LBP group) of less than 4 weeks duration, without history of chronic low back pain, and having a pain intensity of at least 3 (numerical rating scale 0-10) were compared to eleven healthy age- and sex-matched volunteers (CTRL group). As test stimuli, bursts of five 1-ms electrical pulses of an intensity 1.5 times the pain threshold (200 ms inter-stimulus interval) were applied percutaneously every 5 seconds to the median nerve of the left hand for 10 minutes (baseline condition). Then subjects immersed their right hand in ice-water (conditioning stimulus), while the same electrical stimulation was applied for the next 10 minutes to investigate CPM. Somatosensory evoked potentials (SEP) in response to electrical stimulation were measured before and during ice-water stimulation using 128-chanel electroencephalography sampled at 2 kHz. EEG data was segmented in epochs of 1850 ms. The first long latency negative component of the SEP responses from the vertex were analyzed after the 1st (N1) and the 5th (N1r) pulse in each burst. Data are presented as means ±SD. Mixed-model ANOVA was used for analysis. Results: For the baseline condition, N1 was detected at 93.7 ± 22.8 ms for the CTRL group and at 62.3 ± 21.5 ms in the LBP group. During ice water (CPM condition), the N1 was identified at 91.9 ± 23.6 ms and 64.5 ± 16.9 ms for CTRL and LBP group, respectively.For the baseline condition, the N1r was located at 88.2 ± 15.5 ms in the CTRL group and at 77.6 ± 15.1 ms in the LBP group. During ice water, the N1r was located at 103.3 ± 19.7 ms and 74.6 ± 13.7 ms for CTRL and LBP group, respectively.For the N1, the ANOVA revealed significant differences between groups in SEP responses (F(1,20)=13.032, p=0.002). There was no significant effect of condition (baseline vs. icewater) (F(1,20)=0.03, p=0.954), and no interaction between condition and group (F(1,20)=2.22, p=0.642).For the N1r, ANOVA revealed significant differences between groups (F(1,20)= 7.29, p= 0.013) and conditions (F(1,20)=8.15,p=0.009), as well as interaction between condition and group (F(1,20)=14.46, p=0.001). Post hoc analysis revealed significantly longer latencies in the control group compared to the LBP group during ice-water stimulation (p=0.003).Conclusions: To our knowledge, this is the first study showing altered CPM in patients with acute low back pain using EEG. This effect was found for the 5th stimulus in a train of 5 stimuli, but not for the 1st one. Further studies are needed to investigate if CPM deficiencies in acute low back pain patients translate into a risk factor to develop chronic low back pain.