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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: Preclinical study in rodents., Objective: To investigate changes in biomechanical properties of paraspinal muscles following a posterior spinal surgery in an animal model., Summary of Background Data: Posterior spine surgery damages paraspinal musculature per histological and imaging studies. The biomechanical effects of these changes are unknown., Methods: 12 Sprague-Dawley rats were divided equally into sham and surgical injury (SI) groups. For sham, the skin and lumbodorsal fascia were incised at midline. For SI, the paraspinal muscles were detached from the vertebrae, per normal procedure. Thirteen weeks postsurgery, multifidus and longissimus biopsies at L1, L3, and L5 levels were harvested on the right. From each biopsy, three fibers and three to six bundles of fibers (∼10-20 fibers ensheathed in their extracellular matrix) were tested mechanically to measure their passive elastic modulus. The collagen content and fatty infiltration of each biopsy were also examined histologically by immunofluorescence staining. Nonparametric statistical methods were used with a 1.25% level of significance., Results: A total of 220 fibers and 279 bundles of fibers were tested. The elastic moduli of the multifidus and longissimus fibers and longissimus fiber bundles were not significantly different between the SI and sham groups. However, the elastic modulus of multifidus fiber bundles was significantly greater in the SI group compared to sham (SI median 82 kPa, range 23-284; sham median 38 kPa, range 23-50, P = 0.0004). The elastic modulus of multifidus fiber bundles in the SI group was not statistically different between spinal levels (P = 0.023). For histology, only collagen I deposition in multifidus was significantly greater in the SI group (median 20.8% vs. 5.8% for sham, P < 0.0001)., Conclusion: The surgical injury increased the passive stiffness of the multifidus fiber bundles. Increased collagen content in the extracellular matrix is the likely reason and these changes may be important in the postoperative compensation of the spine.Level of Evidence: N/A., (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.