Introduction: Decreased spinal extensor muscle strength in adult spinal deformity (ASD) patients is well-known but poorly understood. Whether this decreased strength results from altered muscle properties due to fibrosis, fatty infiltration, or other causes, is unknown. 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 (66±8 years old; five males and four females) at L4-L5 (bilateral multifidus and longissimus sampled). The ASD patients comprised group I (four patients) with no sagittal imbalance (SI) and no usage of compensatory mechanisms (CMs); group II (three patients) with no SI through usage of CMs; and group III (two patients) with SI despite usage of CMs. The biopsies were tested for muscle fiber and fiber bundle biomechanical properties (i.e. passive elastic modulus, active specific force, in situ and slack sarcomere lengths) 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 stiffness, up to 20 times greater than has been reported previously (Figure 1). Active contractile specific force was consistently less than literature values (Figure 2), with notably 24% of samples exhibiting no contractile ability. Both in situ and slack sarcomere lengths presented a large variation, with in situ sarcomere length exceeding literature data in most cases (Figure 3). Histological analysis of 28 biopsies revealed frequent fibro-fatty replacement with a range of muscle fiber abnormalities (Figures 4 and 5). In general, the degree of abnormality was more severe in patients with greater deformity. Biomechanical modelling predicted that high muscle stiffness could increase the compressive loads in the spine by over 500%, particularly in flexed postures (Figure 6).

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.