Zhang Jiaqi, Liu Yinhao, Zeng Yan, Li Weishi
Department of Orthopedics, Peking University Third Hospital, Beijing, China.
Beijing Key Laboratory of Spinal Disease Research, Peking University Third Hospital, Beijing, China.
Orthop Surg. 2025 Jul;17(7):2048-2056. doi: 10.1111/os.70075. Epub 2025 May 23.
Late-onset neurological deficit is a severe complication usually attributed to the medullary compression at the apex as the kyphotic deformity develops gradually. However, little is known about another rare cause of proximal adjacent segment degeneration (ASD) above the kyphosis. This study aimed to report the surgical outcome of rigid posttraumatic thoracolumbar kyphosis combined with neurological deficits and to illustrate the different causes of late-onset spinal cord dysfunction and their relationship to spinopelvic alignment.
In this retrospective cohort study, 39 patients with rigid posttraumatic thoracolumbar kyphosis who underwent surgical correction were enrolled. All patients had late-onset spinal cord dysfunction, and the causes were classified according to the location of the lesion. Patients were divided into Group A (patients without proximal ASD) and Group B (patients with proximal ASD). Neurologic status was graded using the American Spinal Injury Association (ASIA) Impairment Scale. The visual analog scale (VAS) and Japanese Orthopedic Association scores-29 (JOA-29) were utilized for clinical assessment. Radiographic parameters of X-ray and MRI were compared between the two groups.
Twenty-three patients (59.0%) had neurological deficits only resulting from the kyphosis itself, and 10 patients (25.6%) had developed neurological dysfunction related to thoracic stenosis above the kyphosis. The remaining six patients (15.4%) had coexisting compression both at and above the kyphotic apex. All the ASD occurred in the lower thoracic spine, and the level of T10/11 was the most involved site. Patients who developed proximal ASD had significantly smaller adjacent thoracic kyphosis (ATK) (1.2 ± 9.6 vs. 14.4 ± 11.6, p < 0.001). These patients had significantly worse preoperative ASIA grades and lower JOA-29 at final follow-up.
Proximal ASD above kyphosis could cause late-onset neurological deterioration. Compensatory lordosis in the lower thoracic spine might be associated with degenerative spinal stenosis. The dominant compensatory mechanism might be a decisive factor in developing proximal ASD.
迟发性神经功能缺损是一种严重并发症，通常归因于随着后凸畸形逐渐发展，顶点处的髓质受压。然而，对于后凸上方近端相邻节段退变（ASD）的另一种罕见原因知之甚少。本研究旨在报告创伤后僵硬性胸腰椎后凸畸形合并神经功能缺损的手术结果，并阐明迟发性脊髓功能障碍的不同原因及其与脊柱骨盆对线的关系。
在这项回顾性队列研究中，纳入了39例行手术矫正的创伤后僵硬性胸腰椎后凸畸形患者。所有患者均有迟发性脊髓功能障碍，病因根据病变部位分类。患者分为A组（无近端ASD的患者）和B组（有近端ASD的患者）。使用美国脊髓损伤协会（ASIA）损伤量表对神经功能状态进行分级。采用视觉模拟量表（VAS）和日本矫形外科学会评分-29（JOA-29）进行临床评估。比较两组的X线和MRI影像学参数。
23例患者（59.0%）的神经功能缺损仅由后凸畸形本身引起，10例患者（25.6%）出现了与后凸上方胸椎狭窄相关的神经功能障碍。其余6例患者（15.4%）在驼背顶点处及上方同时存在压迫。所有ASD均发生在下胸椎，T10/11水平是最常受累部位。发生近端ASD的患者相邻胸椎后凸（ATK）明显更小（1.2±9.6 vs. 14.4±11.6，p<0.001）。这些患者术前ASIA分级明显更差，末次随访时JOA-29更低。
后凸上方的近端ASD可导致迟发性神经功能恶化。下胸椎的代偿性前凸可能与退行性脊柱狭窄有关。主要的代偿机制可能是发生近端ASD的决定性因素。
