Study Design Retrospective chart analysis of 199 individuals aged 18-80 years scheduled for lumbar spine surgery. Objective The purpose of this study was to quantify changes in muscle cross sectional area (CSA) and fat signal fraction (FSF) with age in men and women with lumbar spine pathology and compare them to published normative data. Summary of Background Data Pathological changes in lumbar paraspinal muscle are often confounded by age-related decline in muscle size (CSA) and quality (fatty infiltration). Individuals with pathology have been shown to have decreased CSA and fatty infiltration of both the multifidus and erector spinae muscles, but the magnitude of these changes in the context of normal aging is unknown. Methods Individuals aged 18-80 years who were scheduled for lumbar surgery for diagnoses associated with lumbar spine pain or pathology were included. Muscle CSA and FSF of the multifidus and erector spinae were measured from preoperative T2-weighted magnetic resonance images at the L4 level. Univariate and multiple linear regression analyses were performed for each outcome using age and gender as predictor variables. Statistical comparisons of univariate regression parameters (slope and intercept) to published normative data were also performed. Results There was no change in CSA with age in either gender (p>0.05), but women had lower CSA's than men in both muscles (p<0.0001). There was an increase in FSF with age in erector spinae and multifidus muscles in both genders (p<0.0001). Multifidus FSF values were higher in women with lumbar spine pathology than published values for healthy controls (p=0.03), and slopes tended to be steeper with pathology for both muscles in women (p<0.08) but not in men (p>0.31). Conclusions Lumbar muscle fat content, but not CSA changes with age in individuals with pathology. In women, this increase is more profound than age-related increases in healthy individuals.

Histological and cell-level changes in the lumbar musculature in individuals with chronic lumbar spine degenerative conditions are not well characterized. Although prior literature supports evidence of changes in fiber type and size, little information exists describing the tissue quality and biology of pathological features of muscle in this population. The purpose of this study was to quantify multifidus tissue composition and structure, inflammation, vascularity, and degeneration in individuals with chronic degenerative lumbar spine pathology. Human multifidus biopsies were acquired from 22 consecutive patients undergoing surgery for chronic degenerative lumbar spine pathology. Relative fractions of muscle, adipose, and extracellular matrix were quantified along with muscle fiber type and cross-sectional area (CSA) and markers of inflammation, vascularity, satellite cell density, and muscle degeneration. On average, multifidus biopsies contained 48.5% muscle, 11.7% adipose tissue, and 26.1% collagen tissue. Elevated inflammatory cell counts (48.5 ± 30.0 macrophages/mm2) and decreased vascularity (275.6 ± 69.4 vessels/mm2) were also observed compared to normative values. Satellite cell densities were on average 13 ± 9 cells per every 100 muscle fibers. Large fiber CSA (3,996.0 ± 1,909.2 um2) and a predominance of type I fibers (61.8 ± 18.0%) were observed in addition to evidence of pathological degeneration-regeneration cycling (18.8 ± 9.4% centrally nucleated fibers, and 55.2 ± 24.2% of muscle regions containing degeneration). High levels of muscle degeneration, inflammation, and decreased vascularity were commonly seen in human multifidus biopsies of individuals with lumbar spine pathology in comparison to normative data. Evidence of active muscle degeneration suggests that changes in muscle tissue are more complex than simple atrophy.

Many chronic musculoskeletal conditions are associated with loss of muscle volume and quality, resulting in functional decline. While atrophy has long been implicated as the mechanism of muscle loss in these conditions, recent evidence has emerged demonstrating a degenerative phenotype of muscle loss consisting of disrupted muscle fiber membranes, infiltration of cells into muscle fibers, and as previously describer, possible replacement of muscle fibers by adipose tissue. Here, we use human lumbar spine pathology as a model system to provide a more comprehensive analysis of the morphological features of this mode of muscle loss between early and late stages of disease, including an analysis of the cell populations found in paraspinal muscle biopsies from humans with acute vs chronic lumbar spine pathology. Using longitudinal sections, we show that degeneration of muscle fibers is localized within a fiber (ie, focal), and is characterized by discontinuous or ragged membrane disruption, cellular infiltration, and apparently vacant space containing limited numbers of nuclei and hyper‐contractile cell debris. Samples from patients with acute and chronic pathology demonstrate similar magnitudes of muscle degeneration, however, larger proportions of PDGFRβ‐positive progenitor cells and leukocytes were observed in the acute group, with no differences in myogenic cells, macrophages, or T‐cells. By better understanding the cell population behaviors over the course of disease, therapies can be optimized to address the appropriate targets and timing of administration to minimize the functional consequences of muscle degeneration in lumbar spine pathology.

Both open and percutaneous posterior techniques following LLIF significantly improved clinical outcomes. Open procedures resulted in significantly better radiographic improvements but also higher complication rates. LLIF with percutaneous posterior fixation, without decompression, should be considered part of the algorithm in select ADS patients with remaining compensatory mechanisms and understanding that greater degrees of correction may require an open, more extensive approach.