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Background: People with low back pain exhibit altered postural coordination that has been suggested as a target for treatment, but heterogeneous presentation has rendered it difficult to identify appropriate candidates and protocols for such treatments. This study evaluated the associations of task-related and person-related factors with the effect of low back pain on anticipatory postural adjustments.Methods: Thirteen subjects with and 13 without low back pain performed seated, rapid arm flexion in self-initiated and cued conditions. Mixed-model ANOVA were used to evaluate group and condition effects on APA onset latencies of trunk muscles, arm-raise velocity, and pre-movement cortical potentials. These measures were evaluated for correlation with pain ratings, Fear Avoidance Beliefs Questionnaire scores, and Modified Oswestry Questionnaire scores.Findings: Delayed postural adjustments of subjects with low back pain were greater in the cued condition than in the self-initiated condition. The group with low back pain exhibited larger-amplitude cortical potentials than the group without pain, but also significantly slower arm-raise velocities. With arm-raise velocity as a covariate, the effect of low back pain remained significant for the latencies of postural adjustments but not for cortical potentials. Latencies of the postural adjustments significantly correlated with Oswestry and Fear Avoidance Beliefs scores.Interpretation: Delayed postural adjustments with low back pain appear to be influenced by cueing of movement, pain-related disability and fear of activity. These results highlight the importance of subject characteristics, task condition, and task performance when comparing across studies or when developing treatment of people with low back pain. [ABSTRACT FROM AUTHOR]

Background Motor retraining for non-specific chronic low back pain (LBP) often focuses on voluntary postural tasks. This training, however, may not transfer to other known postural impairments, such as automatic postural responses to external perturbations. Objectives To evaluate the extent current treatments of motor retraining ameliorate impaired postural coordination when responding to a perturbation of standing balance. Design Planned secondary analysis of a prospectively registered ( NCT01362049 ), randomized controlled trial with a blinded assessor. Method Sixty-eight subjects with chronic, recurrent, non-specific LBP were allocated to perform a postural response task as a secondary assessment one week before and one week after receiving either stabilization or Movement System Impairment (MSI)-directed treatment over 6 weekly 1-h sessions plus home exercises. For assessment, subjects completed the Oswestry disability and numeric pain rating questionnaires and then performed a postural response task of maintaining standing balance in response to 3 trials in each of 4 randomly presented directions of linear surface translations of the platform under the subjects' feet. Integrated amplitudes of surface electromyography (EMG) were recorded bilaterally from the rectus abdominis (RA), internal oblique (IO), and external oblique (EO) muscles during the postural response task. Results No significant effects of treatment on EMG responses were evident. Oswestry and numeric pain ratings decreased similarly following both treatments. Conclusions Stabilization and MSI-directed treatments do not affect trunk EMG responses to perturbations of standing balance in people with LBP, suggesting current methods of motor retraining do not sufficiently transfer to tasks of reactive postural control. [ABSTRACT FROM AUTHOR]

Interventions that target trunk muscle impairments in people with LBP have been promoted; however, the treatment effects on muscle activation impairments during postural tasks remain unclear. Thus, our objective was to evaluate the effects trunk stabilization vs. general strength and conditioning exercises on the automatic postural response in persons with chronic low back pain (LBP). Fifty-eight subjects with chronic, recurrent LBP ( n = 58) (i.e., longer than six months) were recruited and randomly assigned to one of two, 10-week physical therapy programs: stabilization ( n = 29) or strength and conditioning ( n = 29). Pain and function were measured at 11 weeks and 6 months post-treatment initiation. To quantify postural following support surface perturbations, surface electrodes recorded electromyography (EMG) of trunk and leg muscles and force plates recorded forces under the feet, to calculate the center of pressure. Both groups demonstrated significant improvements in pain and function out to 6 months. There were also changes in muscle activation patterns immediately post-treatment, but not at 6 months. However, changes in center of pressure (COP) responses were treatment specific. Following treatment, the stabilization group demonstrated later onset of COP displacement, while the onset of COP displacement in the strengthening group was significantly earlier following treatment. Despite two different treatments, clinical improvements and muscle activation patterns were similar for both groups, indicating that the stabilization treatment protocol does not preferentially improve treatment outcomes or inter-muscle postural coordination patterns for persons with LBP. Clinical Trial Registration Number NCT01611792. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Abstract: There is increasing evidence that individuals with non-specific low back pain (LBP) have altered movement coordination. However, the relationship of this neuromotor impairment to recurrent pain episodes is unknown. To assess coordination while minimizing the confounding influences of pain we characterized automatic postural responses to multi-directional support surface translations in individuals with a history of LBP who were not in an active episode of their pain. Twenty subjects with and 21 subjects without non-specific LBP stood on a platform that was translated unexpectedly in 12 directions. Net joint torques of the ankles, knees, hips, and trunk in the frontal and sagittal planes as well as surface electromyographs of 12 lower leg and trunk muscles were compared across perturbation directions to determine if individuals with LBP responded using a trunk stiffening strategy. Individuals with LBP demonstrated reduced peak trunk torques, and enhanced activation of the trunk and ankle muscle responses following perturbations. These results suggest that individuals with LBP use a strategy of trunk stiffening achieved through co-activation of trunk musculature, aided by enhanced distal responses, to respond to unexpected support surface perturbations. Notably, these neuromotor alterations persisted between active pain periods and could represent either movement patterns that have developed in response to pain or could reflect underlying impairments that may contribute to recurrent episodes of LBP. [Copyright &y& Elsevier]