The goal of this review is to discuss the mechanisms of postural degeneration, particularly the loss of lumbar lordosis commonly observed in the elderly in the context of evolution, mechanical, and biological studies of the human spine and to synthesize recent research findings to clinical management of postural malalignment. Lumbar lordosis is unique to the human spine and is necessary to facilitate our upright posture. However, decreased lumbar lordosis and increased thoracic kyphosis are hallmarks of an aging human spinal column. The unique upright posture and lordotic lumbar curvature of the human spine suggest that an understanding of the evolution of the human spinal column, and the unique anatomical features that support lumbar lordosis may provide insight into spine health and degeneration. Considering evolution of the skeleton in isolation from other scientific studies provides a limited picture for clinicians. The evolution and development of human lumbar lordosis highlight the interdependence of pelvic structure and lumbar lordosis. Studies of fossils of human lineage demonstrate a convergence on the degree of lumbar lordosis and the number of lumbar vertebrae in modern Homo sapiens . Evolution and spine mechanics research show that lumbar lordosis is dictated by pelvic incidence, spinal musculature, vertebral wedging, and disc health. The evolution, mechanics, and biology research all point to the importance of spinal posture and flexibility in supporting optimal health. However, surgical management of postural deformity has focused on restoring posture at the expense of flexibility. It is possible that the need for complex and costly spinal fixation can be eliminated by developing tools for early identification of patients at risk for postural deformities through patient history (genetics, mechanics, and environmental exposure) and tracking postural changes over time.

Recent demographics demonstrate an increase in the number of elderly spinal cord injury patients, motivating the desire for a better understanding of age effects on injury susceptibility. Knowing that age and disease affect neurological tissue, there is a need to better understand the sensitivity of spinal cord injury mechanics to variations in tissue behavior. To address this issue, a plane-strain, geometrically nonlinear, finite element model of a section of a generic human thoracic spinal cord was constructed to model the response to dorsal compression. The material models and stiffness responses for the grey and white matter and pia mater were varied across a range of reported values to observe the sensitivity of model outcomes to the assigned properties. Outcome measures were evaluated for percent change in magnitude and alterations in spatial distribution. In general, principal stresses (114–244% change) and pressure (75–119% change) were the outcomes most sensitive to material variation. Strain outcome measures were less sensitive (7–27% change) than stresses (74–244% change) to variations in material tangent modulus. The pia mater characteristics had limited (<4% change) effects on outcomes. Using linear elastic models to represent non-linear behavior had variable effects on outcome measures, and resulted in highly concentrated areas of elevated stresses and strains. Pressure measurements in both the grey and white matter were particularly sensitive to white matter properties, suggesting that degenerative changes in white matter may influence perfusion in a compressed spinal cord. Our results suggest that the mechanics of spinal cord compression are likely to be affected by changes in tissue resulting from aging and disease, indicating a need to study the biomechanical aspects of spinal cord injury in these specific populations.

A cross-sectional study. The aim of this study was to assess fatty infiltration and asymmetry of the multifidus (MF), semispinalis cervicis (SCer), semispinalis capitis (SCap), and splenius capitis (SPL) muscles in patients with degenerative cervical myelopathy (DCM), and evaluate their correlations with clinical symptoms and functional scores. Cervical muscle alterations have been reported in patients with chronic neck pain, but the assessment of cervical muscle morphology has been overlooked in patients with DCM. Thirty-eight patients diagnosed with DCM and spinal cord compression at C4-C5 or C5-C6 (first level of compression) were included. Cervical muscle measurements of cross-sectional area (CSA) and ratio of functional CSA (fat-free area, FCSA) to total CSA were obtained from T2-weighted axial images at the level above, same, and level below the most cranial level of spinal cord compression. Muscle fatty infiltration and asymmetry was assessed at every level and their associations with respect to clinical signs and symptoms and functional scores were investigated. There was a significant increase in fatty infiltration (decrease in FCSA/CSA ratio) of the MF (P = 0.001) and SPL (P < 0.001) muscles at the level below the spinal cord compression. A significant increase in MF CSA asymmetry was also observed at the level below the compression. Lower MF FCSA/CSA ratio was associated with longer 30-m walking test time. Lower SCer FCSA/CSA was associated with corticospinal distribution motor deficits and atrophy of the hands. Greater asymmetry in SCap CSA was associated with higher Neck Disability Index (NDI) scores, whereas lower asymmetry in MF CSA was associated with a positive Hoffman sign and weakness. A significant increase in muscle fatty infiltration and CSA asymmetry at the level below the compression was observed in patients with DCM. Our results also suggest an association between cervical muscle morphology and DCM clinical symptoms and functional status. Level of Evidence: 2

A rat model of thoracic spinal cord contusion was used to examine the effect of velocity on the primary injury. The overall objective of this study was to determine the effect of the contusion velocity (slow vs. fast) on damage to the spinal cord immediately following mechanical injury. Secondary objectives were to demarcate between damage in the gray and white matters and to observe damage to the mechanical elements of the neurons (i.e., neurofilaments). Although studies have explored the effect of impact velocity on spinal cord damage and functional deficits, no study has addressed regional tissue damage of the primary injury (e.g., between the gray and white matter) as a function of velocity. A modified Spinal Cord Injury Research System generated 1 mm contusions in 24 male, Sprague-Dawley rats (210-320 g) at T10, using slow (3 mm/s) and fast (300 mm/s) velocities. The primary lesion (<2 minutes postinjury) was assessed using hematoxylin and eosin staining for hemorrhage volume and immunostaining for nonphosphorylated heavy neurofilament damage. The volume of hemorrhage in the white matter was significantly increased following fast impact (fast = 0.61 mm3, slow = 0.24 mm3, P = 0.013) whereas the total hemorrhage volume (fast = 1.51 mm, slow = 1.21 mm, P = 0.22) showed no effect. Complete axonal disruption was evident in the fast injury group around the injury epicenter. A significant increase in nonphosphorylated neurofilament staining (P = 0.013) was observed for fast impacts. Hemorrhage in the gray matter was similar between the slow and fast groups, but an increase in neurofilament dephosphorylation was observed in the gray matter following fast contusion (P = 0.03). We conclude that contusion velocity has an effect on the magnitude of injury within the white matter during spinal cord injury and the amount of neuronal damage in the gray matter. The results of this study demonstrate the importance of including high impact velocity as a variable in models of spinal cord injury.

The development of a non-human primate (NHP) model of spinal cord injury (SCI) based on mechanical and computational modeling is described. We scaled up from a rodent model to a larger primate model using a highly controllable, friction-free, electronically-driven actuator to generate unilateral C6-C7 spinal cord injuries. Graded contusion lesions with varying degrees of functional recovery, depending upon pre-set impact parameters, were produced in nine NHPs. Protocols and pre-operative magnetic resonance imaging (MRI) were used to optimize the predictability of outcomes by matching impact protocols to the size of each animal's spinal canal, cord, and cerebrospinal fluid space. Post-operative MRI confirmed lesion placement and provided information on lesion volume and spread for comparison with histological measures. We evaluated the relationships between impact parameters, lesion measures, and behavioral outcomes, and confirmed that these relationships were consistent with our previous studies in the rat. In addition to providing multiple univariate outcome measures, we also developed an integrated outcome metric describing the multivariate cervical SCI syndrome. Impacts at the higher ranges of peak force produced highly lateralized and enduring deficits in multiple measures of forelimb and hand function, while lower energy impacts produced early weakness followed by substantial recovery but enduring deficits in fine digital control (e.g., pincer grasp). This model provides a clinically relevant system in which to evaluate the safety and, potentially, the efficacy of candidate translational therapies.