• Alex M Noonan, Masoud Malakoutian, Iraj Dehghan-Hamani, Stephen Lewis, John Street, Thomas R Oxland, and BrownStephen H MSHMDepartment of Human Health and Nutritional Sciences, University of Guelph, 50 Stone Road East, Guelph, ON, N1G 2W1, Canada. shmbrown@uoguelph.ca..
• Department of Human Health and Nutritional Sciences, University of Guelph, 50 Stone Road East, Guelph, ON, N1G 2W1, Canada.
• Eur Spine J. 2024 Oct 14.

BackgroundParaspinal and spinopelvic muscular dysfunction are hypothesized to be a causative factor for spinal degeneration and deformity; however, our fundamental understanding of paraspinal muscle (dys)function remains limited.MethodsTwelve surgical patients with spinal degeneration were recruited and categorized into group DEG (four patients) with no sagittal imbalance and no usage of compensatory mechanisms; group DEG-COMP (four patients) with no sagittal imbalance through use of compensatory mechanisms; and group DEG-COMP-UNBAL (four patients) with sagittal imbalance despite use of compensatory mechanisms. From each patient, four biopsies were collected from right and left multifidus (MULT) and longissimus (LONG) for single fibre contractile and structural measurements.ResultsEight of 48 (17%) biopsies did not exhibit any contractile properties. Specific force was not different between groups for the MULT (p = 0.47) but was greater in group DEG compared to group DEG-COMP-UNBAL for the LONG (p = 0.02). Force sarcomere-length properties were unusually variable both within and amongst patients in all groups. Thin filament (actin) lengths were in general shorter and more variable than published norms for human muscle.ConclusionThis study is the first to show a heightened intrinsic contractile muscle disorder (i.e. impaired specific force generation) in patients with spinal degeneration who are sagittally imbalanced (compared to patients without deformity). Additionally, there are clear indications that patients with spinal degeneration (all groups) have intrinsic force sarcomere-length properties that are dysregulated. This provides important insight into the pathophysiology of muscle weakness in this patient group.© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.

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