Department of Human Health and Nutritional Sciences, University of Guelph, 50 Stone Road East, Guelph, ON, N1G 2W1, Canada.
Department of Mechanical Engineering, University of British Columbia, Vancouver, Canada.
Eur Spine J. 2024 Dec;33(12):4605-4618. doi: 10.1007/s00586-024-08509-x. Epub 2024 Oct 14.
Paraspinal 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.
Twelve 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.
Eight 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.
This 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.
脊柱旁和脊柱骨盆肌肉功能障碍被认为是脊柱退化和畸形的一个致病因素;然而,我们对脊柱旁肌肉(功能障碍)的基本理解仍然有限。
招募了 12 名患有脊柱退化的手术患者,并将其分为无矢状面失衡且不使用代偿机制的 DEG 组(4 名患者);无矢状面失衡但使用代偿机制的 DEG-COMP 组(4 名患者);以及尽管使用代偿机制仍存在矢状面失衡的 DEG-COMP-UNBAL 组(4 名患者)。从每位患者身上采集右侧和左侧多裂肌(MULT)和最长肌(LONG)的 4 个活检样本,用于单纤维收缩和结构测量。
48 个活检样本中有 8 个(17%)没有表现出任何收缩特性。MULT 的组间特定力无差异(p=0.47),但与 DEG-COMP-UNBAL 组相比,DEG 组的 LONG 特定力更大(p=0.02)。各组患者的力-肌小节长度特性在个体内和个体间均异常多变。细丝(肌动蛋白)长度通常比公布的人类肌肉正常值更短且更易变。
这项研究首次表明,矢状面失衡的脊柱退化患者(与无畸形患者相比)存在固有收缩性肌肉疾病(即特定力生成受损)。此外,有明确迹象表明,脊柱退化患者(所有组)均存在固有肌小节力长度特性失调。这为该患者群体肌肉无力的病理生理学提供了重要的见解。