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Study Design: Randomized trial., Objective: To implement an algorithm enabling the automated segmentation of spinal muscles from open magnetic resonance images in healthy volunteers and patients with adult spinal deformity (ASD)., Summary of Background Data: Understanding spinal muscle anatomy is critical to diagnosing and treating spinal deformity.Muscle boundaries can be extrapolated from medical images using segmentation, which is usually done manually by clinical experts and remains complicated and time-consuming., Methods: Three groups were examined: two healthy volunteer groups (N = 6 for each group) and one ASD group (N = 8 patients) were imaged at the lumbar and thoracic regions of the spine in an upright open magnetic resonance imaging scanner while maintaining different postures (various seated, standing, and supine). For each group and region, a selection of regions of interest (ROIs) was manually segmented. A multiscale pyramid two-dimensional convolutional neural network was implemented to automatically segment all defined ROIs. A five-fold crossvalidation method was applied and distinct models were trained for each resulting set and group and evaluated using Dice coefficients calculated between the model output and the manually segmented target., Results: Good to excellent results were found across all ROIs for the ASD (Dice coefficient >0.76) and healthy (dice coefficient > 0.86) groups., Conclusion: This study represents a fundamental step toward the development of an automated spinal muscle properties extraction pipeline, which will ultimately allow clinicians to have easier access to patient-specific simulations, diagnosis, and treatment., (Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)

Study Design: Basic science study of the relationship between spine pathology and the contractile ability of the surrounding muscles., Objective: The aim of this study was to investigate single muscle fiber contractile function in a model of progressive spine mineralization (ENT1-/- mice)., Summary of Background Data: Altered muscle structure and function have been associated with various spine pathologies; however, studies to date have provided limited insight into the fundamental ability of spine muscles to actively contract and generate force, and how this may change in response to spine pathology., Methods: Experiments were performed on two groups (ENT1-/- [KO] and ENT1+/+ [WT]) of mice at 8 months of age (n = 12 mice/group). Single muscle fibers were isolated from lumbar multifidus and erector spinae, as well as tibialis anterior (a non-spine-related control) and tested to determine their active contractile characteristics., Results: The multifidus demonstrated decreases in specific force (type IIax fibers: 36% decrease; type IIb fibers: 29% decrease), active modulus (type IIax: 35% decrease; type IIb: 30% decrease), and unloaded shortening velocity (Vo) (type IIax: 31% decrease) in the ENT1-/- group when compared to WT controls. The erector spinae specific force was reduced in the ENT1-/- mice when compared to WT (type IIax: 29% decrease), but active modulus and Vo were unchanged. There were no differences in any of the active contractile properties of the lower limb TA muscle, validating that impairments observed in the spine muscles were specific to the underlying spine pathology and not the global loss of ENT1., Conclusion: These results provide the first direct evidence of cellular level impairments in the active contractile force generating properties of spine muscles in response to chronic spine pathology.Level of Evidence: N/A., (Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)

Study Design: Basic science study of the relationship between the structural properties of the spine and its surrounding musculature., Objective: To determine whether an increase in spine stiffness causes an inverse compensatory change in the passive stiffness of the adjacent paraspinal muscles., Summary of Background Data: Intervertebral disc degeneration causes an increase in multifidus passive stiffness; this was hypothesized to compensate for a decrease in spine stiffness associated with disc degeneration. Mice lacking equilibrative nucleoside transporter 1 (ENT1) develop progressive ectopic calcification of the fibrous connective tissues of the spine, which affects the lumbar spine by 6 months of age and likely creates a mechanically stiffer spine., Methods: Experiments were conducted on four groups of mice (n = 8 mice/group): wild-type (WT) and ENT1 knockout (KO) at 2 or 8 months of age. Lumbar spines were removed and tested in cyclic axial compression to determine neutral zone length and stiffness. Single muscle fibers and bundles of fibers were isolated from lumbar multifidus and erector spinae, as well as tibialis anterior (a non-spine-related control) and tested to determine elastic modulus (passive stiffness)., Results: At 2 months of age, neither spine nor muscle stiffness was different between KO and WT. At 8 months of age, compared with WT the lumbar spines of ENT1 KO mice had a stiffer and shorter neutral zone, and the paraspinal muscle fibers were less stiff; however, fiber bundles were not different. In addition, tibialis anterior was not different between KO and WT., Conclusion: This work has confirmed that calcification of spinal connective tissues in the ENT1 KO mouse results in a stiffened spine, whereas the concurrent decrease in muscle fiber elastic modulus in the adjacent paraspinal muscles suggests a direct compensatory relationship between the stiffness of the spine and the muscles that are attached to it., Level of Evidence: N/A.

Study Design: Basic science study of the rabbit multifidus muscle response to intervertebral disc degeneration., Objective: To assess changes in passive mechanical properties, associated protein structure, and histology of multifidus in response to disc degeneration produced by experimental needle puncture., Summary of Background Data: Relationships have been reported between muscle dysfunction and low back injury; however, little is known about the cause and effect of such relationships., Methods: Twelve rabbits were studied; 4 in each of 3 groups: control, 4-weeks postintervertebral disc injury (4-week disc degeneration), and 12-weeks postintervertebral disc injury (12-week disc degeneration). Single multifidus fibers and bundles of fibers were isolated and tested for slack sarcomere length and elastic modulus. Titin isoform mass, myosin heavy chain distribution, and muscle histology were also examined., Results: Compared to control, individual muscle fibers were 34% stiffer and fiber bundles 107% stiffer in the 12-week disc degeneration group. No changes were detected at 4-week disc degeneration. No statistically significant change was found for MHC distribution in the 12-week disc degeneration group when compared to control, whereas titin isoforms were larger (P < 0.05) in the 12-week disc degeneration group. Histology revealed select regions of multifidus, at 12-week disc degeneration, with increased space between bundles of fibers, which in some instances was partly occupied by adipose tissue., Conclusion: Multifidus becomes stiffer, both in individual fibers and fiber bundles, in response to experimentally induced intervertebral disc degeneration. This cannot be explained by change in fiber-type due to reduced muscle use, nor by the increased size of the protein titin (which would reduce stiffness). We hypothesize that fiber bundles become stiffer by proliferation and/or reorganization of collagen content within the muscle but the basis for fiber stiffening is not known.

Study Design: A repeated measures biomechanical analysis of the effects of abdominal bracing in preparation for a quick release of the loaded trunk., Objectives: To quantify the ability of individuals to abdominally brace the externally loaded trunk, and assess their success in achieving and enhancing appropriate spine stability., Summary of Background Data: Spine stability requires trunk muscle coactivation, which demands motor control skill that differs across people and situations. The quick release protocol may offer insight into the motor control scheme and subsequent effect on spine stability., Methods: There were 10 individuals who sat, torso upright, in an apparatus designed to foster a neutral spine position. They were instructed to support a posteriorly directed load to the trunk in either their naturally chosen manner, or by activating the abdominal muscles to 10%, 20%, or 30% of maximum ability. The externally applied load was then quickly released, thereby unloading the participant. Muscle pre-activation patterns, spine stability, and kinematic measures of trunk stiffness were quantified., Results: Participants were able to stabilize their spine effectively by supporting the load in a naturally selected manner. Conscious, voluntary overdriving of this natural pattern often resulted in unbalanced muscular activation schemes and corresponding decreases in stability levels., Conclusions: Individuals in an externally loaded state appear to select a natural muscular activation pattern appropriate to maintain spine stability sufficiently. Conscious adjustments in individual muscles around this natural level may actually decrease the stability margin of safety.