Abstract
OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.