Psychophysical and electrophysiological evidence for enhanced pain facilitation and unaltered pain inhibition in acute low back pain patients.

Vuilleumier, Pascal Henri; Arguissain, Federico Gabriel; Biurrun Manresa, José Alberto; Neziri, Alban Ymer; Nirkko, Arto Christian; Andersen, Ole Kæseler; Arendt-Nielsen, Lars; Curatolo, Michele (2017). Psychophysical and electrophysiological evidence for enhanced pain facilitation and unaltered pain inhibition in acute low back pain patients. The journal of pain, 18(11), pp. 1313-1323. Elsevier 10.1016/j.jpain.2017.05.008

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The aim of this case-control study was to examine differences in neural correlates of pain facilitatory and inhibitory mechanisms between acute low back pain patients and healthy individuals. Pressure pain tolerance (PPT), electrical pain detection thresholds (EDT), pain ratings to repetitive suprathreshold electrical stimulation (SES) and conditioned pain modulation (CPM) were assessed in 18 patients with acute low back pain (LBP) and 18 healthy controls (CTRL). Furthermore, event-related potentials (ERPs) in response to repetitive SES were obtained from high-density electroencephalography. Results showed that the LBP group presented lower PPT and higher pain ratings to SES compared to the CTRL group. Both groups displayed effective CPM, with no differences in CPM magnitude between groups. Both groups presented similar reductions in ERP amplitudes during CPM, but ERP responses to repetitive SES were significantly larger in the LBP group. In conclusion, acute low back pain patients presented enhanced pain facilitatory mechanisms, whereas no significant changes in pain inhibitory mechanisms were observed. These results provide new insight into the central mechanisms underlying acute low back pain. This study was registered in the Clinical Trials Protocol Registration System (NCT00892411, available at https://clinicaltrials.gov/ct2/show/NCT00892411).

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This article present evidence that acute low back pain patients show enhanced pain facilitation and unaltered pain inhibition compared to pain-free volunteers. These results provide new insight into the central mechanisms underlying acute low back pain.

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