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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]

Individuals with a history of non-specific low back pain (LBP) while in a quiescent pain period demonstrate altered automatic postural responses (APRs) characterized by reduced trunk torque contributions and increased co-activation of trunk musculature. However, it is unknown whether these changes preceded or resulted from pain. To further delineate the relationship between cyclic pain recurrence and APRs, we quantified postural responses following multi-directional support surface translations, in individuals with non-specific LBP, following an active pain episode. Sixteen subjects with and 16 without LBP stood on two force plates that were translated unexpectedly in 12 directions. Net joint torques of the ankles, knees (sagittal only), hips, and trunk, in the frontal and sagittal planes, were quantified and the activation of 12 muscles of the lower limb unilaterally and the dorsal and ventral trunk, bilaterally, were recorded using surface electromyography (EMG). Peaks and latencies to peak joint torques, rates of torque development (slopes), and integrated EMGs characterizing baseline and active muscle contributions were analyzed for group by perturbation direction (torques) and group by perturbation by epoch interaction (EMG) effects. In general, the LBP cohort demonstrated APRs that were of similar torque magnitude and rate but peaked earlier compared to individuals without LBP. Individuals with LBP also demonstrated increased muscle activity following perturbation directions in which the muscle was acting as a prime mover and reduced muscle activity in opposing directions, proximally and distally, with some proximal asymmetries. These altered postural responses may reflect increased muscle spindle sensitivity. Given that these motor alterations are demonstrated proximally and distally, they likely reflect the influence of central nervous system processing in this cohort. [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]

People with a history of low back pain (LBP) exhibit altered responses to postural perturbations, and the central neural control underlying these changes in postural responses remains unclear. To characterize more thoroughly the change in muscle activation patterns of people with LBP in response to a perturbation of standing balance, and to gain insight into the influence of early- vs. late-phase postural responses (differentiated by estimates of voluntary reaction times), this study evaluated the intermuscular patterns of electromyographic (EMG) activations from 24 people with and 21 people without a history of chronic, recurrent LBP in response to 12 directions of support surface translations. Twofactor general linear models examined differences between the 2 subject groups and 12 recorded muscles of the trunk and lower leg in the percentage of trials with bursts of EMG activation as well as the amplitudes of integrated EMG activation for each perturbation direction. The subjects with LBP exhibited 1) higher baseline EMG amplitudes of the erector spinae muscles before perturbation onset, 2) fewer early-phase activations at the internal oblique and gastrocnemius muscles, 3) fewer late-phase activations at the erector spinae, internal and external oblique, rectus abdominae, and tibialis anterior muscles, and 4) higher EMG amplitudes of the gastrocnemius muscle following the perturbation. The results indicate that a history of LBP associates with higher baseline muscle activation and that EMG responses are modulated from this activated state, rather than exhibiting acute burst activity from a quiescent state, perhaps to circumvent trunk displacements. [ABSTRACT FROM AUTHOR]

Evaluation of postural control in multiple planes is necessary to determine the movement strategies used to respond to unexpected perturbations. The present study quantified net joint torques of the lower limbs and trunk in the sagittal and frontal planes following multi-directional surface translations. Twenty-one healthy subjects stood with feet on separate force plates mounted on a moveable platform, translated unexpectedly in one of 12 directions. Peak net torque magnitudes and latencies following perturbation onset were determined as were the relative contributions of each joint to total torque production. Magnitude of net torque generated by each leg varied by perturbation direction, with the largest individual joint magnitude elicited in directions of limb loading. Relative contributions of individual joint torques to the total response were dependent upon perturbation direction. Results suggest that a redistribution of the relative contributions of hip/trunk versus ankle strategies occurs dependent on perturbation direction, with a significant contribution by the knee joint in response to forward perturbations. Direction-specific redistribution of proximal versus distal strategies appears to depend upon the biomechanical constraints imposed by a given perturbation direction. Thus, it appears that sagittal and frontal plane posture-righting responses may not be uniquely controlled, and may instead be governed similarly, with modulation of relative torque contributions among joints when necessary, given direction-specific anatomical constraints. [ABSTRACT FROM AUTHOR]