Neuroscience. 2016 Dec 17;339:511-524. doi: 10.1016/j.neuroscience.2016.10.032. Epub 2016 Oct 19.

Neural mechanisms and functional correlates of altered postural responses to perturbed standing balance with chronic low back pain.

Jacobs JV¹, Roy CL², Hitt JR³, Popov RE⁴, Henry SM⁵.

Author information

1: Department of Rehabilitation and Movement Science, University of Vermont, 305 Rowell Building, 106 Carrigan Dr., Burlington, VT 05405, USA; Center for Physical Ergonomics, Liberty Mutual Research Institute for Safety, 71 Frankland Road, Hopkinton, MA 01748, USA. Electronic address: jesse.jacobs@libertymutual.com.
2: Department of Rehabilitation and Movement Science, University of Vermont, 305 Rowell Building, 106 Carrigan Dr., Burlington, VT 05405, USA. Electronic address: carrieinvt@gmail.com.
3: Department of Rehabilitation and Movement Science, University of Vermont, 305 Rowell Building, 106 Carrigan Dr., Burlington, VT 05405, USA. Electronic address: Juvena.Hitt@med.uvm.edu.
4: Department of Rehabilitation and Movement Science, University of Vermont, 305 Rowell Building, 106 Carrigan Dr., Burlington, VT 05405, USA. Electronic address: roman.popov@uvm.edu.
5: Department of Rehabilitation and Movement Science, University of Vermont, 305 Rowell Building, 106 Carrigan Dr., Burlington, VT 05405, USA; Department of Rehabilitation Therapy, University of Vermont Medical Center, 111 Colchester Avenue, Burlington, VT 05401, USA. Electronic address: Sharon.Henry@uvmhealth.org.

Abstract

This study sought to determine the effects of chronic low back pain (LBP) on the cortical evoked potentials, muscle activation, and kinematics of postural responses to perturbations of standing balance. Thirteen subjects with chronic, recurrent, non-specific LBP and 13 subjects without LBP participated. The subjects responded to unpredictably timed postural perturbations while standing on a platform that randomly rotated either "toes up" or "toes down". Electroencephalography (EEG) was used to calculate the negative peak (N1) and subsequent positive peak (P2) amplitudes of the perturbation-evoked cortical potentials. Passive-marker motion capture was used to calculate joint and center-of-mass (CoM) displacements. Surface electromyography was used to record muscle onset latencies. Questionnaires assessed pain, interference with activity, fear of activity, and pain catastrophizing. Results demonstrated that subjects with LBP exhibited significantly larger P2 potentials, delayed erector spinae, rectus abdominae, and external oblique onset latencies, as well as smaller trunk extension yet larger trunk flexion, knee flexion, and ankle dorsiflexion displacements compared to subjects without LBP. For the subjects with LBP, CoM displacements significantly and positively correlated with knee displacements as well as activity interference and fear scores. The P2 potentials significantly and negatively correlated with CoM displacements as well as activity interference, catastrophizing, and fear scores. These results demonstrate that people with LBP exhibit altered late-phase cortical processing of postural perturbations concomitant with altered kinematic and muscle responses, and these cortical and postural response characteristics correlate with each other as well as with clinical reports of pain-related fears and activity interference.