Dysfunctional paraspinal muscles in adult spinal deformity patients lead to increased spinal loading

Abstract

Purpose Decreased spinal extensor muscle strength in adult spinal deformity (ASD) patients is well-known but poorly understood; thus, this study aimed to investigate the biomechanical and histopathological properties of paraspinal muscles from ASD patients and predict the effect of altered biomechanical properties on spine loading. Methods 68 muscle biopsies were collected from nine ASD patients at L4–L5 (bilateral multifidus and longissimus sampled). The biopsies were tested for muscle fiber and fiber bundle biomechanical properties and histopathology. The small sample size (due to COVID-19) precluded formal statistical analysis, but the properties were compared to literature data. Changes in spinal loading due to the measured properties were predicted by a lumbar spine musculoskeletal model. Results Single fiber passive elastic moduli were similar to literature values, but in contrast, the fiber bundle moduli exhibited a wide range beyond literature values, with 22% of 171 fiber bundles exhibiting very high elastic moduli, up to 20 times greater. Active contractile specific force was consistently less than literature, with notably 24% of samples exhibiting no contractile ability. Histological analysis of 28 biopsies revealed frequent fibro-fatty replacement with a range of muscle fiber abnormalities. Biomechanical modelling predicted that high muscle stiffness could increase the compressive loads in the spine by over 500%, particularly in flexed postures. Discussion The histopathological observations suggest diverse mechanisms of potential functional impairment. The large variations observed in muscle biomechanical properties can have a dramatic influence on spinal forces. These early findings highlight the potential key role of the paraspinal muscle in ASD.

The effect of fatty infiltration, revision surgery, and sex on lumbar multifidus passive mechanical properties

“…In an animal model of intervertebral disc degeneration, both multifidus muscle fibers and fiber bundles were stiffer 12 weeks after injury, 30 although in a model of spinal stiffness induced by ectopic calcification in ENT1‐deficient mice, reduced single fiber stiffness was observed, with no change in fiber bundle mechanics 31 . Interestingly, a recent study investigating passive mechanical properties of the multifidus muscle in individuals with adult spinal deformity demonstrated extremely high fiber bundle elastic modulus in some patients, resulting in increased simulated spinal compressive loads of over 500% 32 . Similar to our own data, this study reported histopathological findings of fibro‐fatty replacement and muscle degeneration in these patients.…”

“…31 Interestingly, a recent study investigating passive mechanical properties of the multifidus muscle in individuals with adult spinal deformity demonstrated extremely high fiber bundle elastic modulus in some patients, resulting in increased simulated spinal compressive loads of over 500%. 32 T A B L E 1 Patient demographics of stratified by fatty atrophy and surgery status. The lower elastic modulus in individuals with severe fatty infiltration is, perhaps, not surprising given that adipocytes often accumulate in the interstitium, although our biopsy samples were carefully cleaned of extramuscular fatty tissue prior to passive mechanical testing.…”

Glycerol induced paraspinal muscle degeneration leads to hyper-kyphotic spinal deformity in wild-type mice

“…Recent work demonstrated large variability in the active (specific force) and passive (elastic modulus) functional properties of paraspinal muscle biopsies from degenerative adult spinal deformity patients, reporting values that appear to be impaired compared to age-matched literature skeletal muscle norms 24 . Nonetheless, whether muscle alterations are consequences of spine degeneration and deformity or whether they precede, drive, or accompany the disorder progression is unknown; causative data are needed to address such hypotheses.…”

Understanding the Interplay Between Paraspinal Muscle Atrophy and Lumbar Endplate Degeneration

“…10 Atrophy of the PM can increase segmental instability, resulting in unbalanced load distribution during flexion and increase force transmission through the intervertebral disk, as demonstrated by finite element analysis. 11 This is assumed to accelerate degenerative processes once the regenerative capabilities are overtaxed, although limited clinical literature exists. 12 Inflammation and arthrogenic reflex inhibition due to degenerative processes have been associated with increased atrophy, 13,14 which complicates the causative analysis.…”

“…Atrophy of the psoas muscle is typically described by a reduction in muscle area as the tendency for FI of the psoas muscle is less pronounced 10 . Atrophy of the PM can increase segmental instability, resulting in unbalanced load distribution during flexion and increase force transmission through the intervertebral disk, as demonstrated by finite element analysis 11 . This is assumed to accelerate degenerative processes once the regenerative capabilities are overtaxed, although limited clinical literature exists 12 .…”