Response to the letter to the editor: Predicting residual neurologic deficits using the Spinal Infection Treatment Evaluation score after surgery for thoracic and lumbar spinal epidural abscess: a retrospective study in Taiwan

Dear Editors,

We thank you for the opportunity to respond to the letter to the editor concerning our article entitled “Predicting residual neurologic deficits using the Spinal Infection Treatment Evaluation score after surgery for thoracic and lumbar spinal epidural abscess: a retrospective study in Taiwan” [1]. We sincerely appreciate the authors’ careful review of our work and their constructive comments.

First, previous studies have proposed a pathogenetic classification of spinal epidural abscess (SEA) into primary SEA (PSEA) and secondary SEA (SSEA) [2]. PSEAs arise directly in the epidural space, most commonly in the dorsal region, without vertebral involvement, typically via hematogenous or lymphatic spread. In contrast, SSEAs develop per continuitatem from adjacent infections, such as spondylodiscitis or paravertebral abscesses. In our cohort, both primary and secondary SEAs were included in the analysis. Six of the 45 patients (13.3%) were classified as PSEA due to hematogenous spread, while 39 patients (86.7%) had SSEA secondary to spondylodiscitis. Owing to the limited number of cases, a subgroup analysis comparing outcomes between PSEA and SSEA was not feasible.

Second, we would like to clarify the exclusion criteria of this study. Only de novo thoracic and lumbar SEAs were included. Patients with a history of prior spinal surgery were excluded to avoid confounding from deep surgical site infections. In addition, patients with previously treated spinal infections or recurrent spinal infections were excluded to ensure cohort homogeneity.

Third, all included patients underwent posterior-only surgical intervention. Surgical indications included the presence of neurological deficits or mechanical instability. Surgical procedures consisted of posterior decompression with or without instrumented fusion. For patients with PSEAs without spinal instability, posterior decompression alone was performed. For patients with SSEAs accompanied by vertebral destruction, we uniformly applied long-segment posterior instrumentation (two levels above and two levels below the infected segment) combined with short-segment posterolateral fusion (one level above and one level below), following our previously published surgical protocol [3]. We believe that this strategy provides effective infection control, correction of kyphotic deformity, and maintenance of spinal alignment. Notably, no patient in our cohort underwent short-segment instrumentation alone.

We hope that these clarifications adequately address the concerns raised and further strengthen the interpretation of our findings.