STUDY DESIGN: A retrospective study. SUMMARY OF BACKGROUND DATA: Posterior lumbar interbody fusion (PLIF) increases mechanical stress and can cause degenerative changes at the adjacent segment. However, the precise causes of adjacent segment disease (ASD) after PLIF are not known, and it is unclear whether simultaneous decompression surgery for symptomatic ASD is effective. OBJECTIVE: To study, radiographically and symptomatically, the risk factors for adjacent segment disease (ASD) in the lumbar spine after L4/5 PLIF and to examine whether decompression surgery for the adjacent segment (L3/4) reduces the occurrence of symptomatic ASD. METHODS: Fifty-four patients who underwent L4/5 PLIF for L4 degenerative spondylolisthesis and could be followed up for at least 2 years were included. Of these, 37 were treated simultaneously with decompression surgery at L3/4. We measured radiographic changes and assessed symptoms from the cranial adjacent segment. RESULTS: Thirty-one patients (57.4%) met radiologic criteria for ASD. The length of follow-up (P=0.004) and simultaneous decompression surgery at L3/4 (P=0.009) were statistically significant factors for radiologic diagnosis of ASD. Seven patients (13.0%) had symptomatic ASD: 6 in the decompression group (16.2%) and 1 in the PLIF-only group (5.9%). Simultaneous decompression surgery did not reduce the incidence of symptomatic ASD (P=0.256). Local lordosis at the fused segment (P=0.005) and the sagittal angle of the facet joint at L3/4 (P=0.024) were statistically significant predictors of symptomatic ASD, which was accompanied by postoperative anterior listhesis above the fused segment (S group, 8.4%±8.0%; nonsymptomatic group: -0.7%±5.0%, P=0.024). CONCLUSIONS: Patients whose facet joint at the adjacent segment had a more sagittal orientation had postoperative anterior listhesis, which caused symptomatic ASD. Simultaneous decompression surgery without fusion at the adjacent level was not effective for these patients, but rather, there was a possibility that it induced symptomatic ASD.
STUDY DESIGN: A retrospective study. SUMMARY OF BACKGROUND DATA: Posterior lumbar interbody fusion (PLIF) increases mechanical stress and can cause degenerative changes at the adjacent segment. However, the precise causes of adjacent segment disease (ASD) after PLIF are not known, and it is unclear whether simultaneous decompression surgery for symptomatic ASD is effective. OBJECTIVE: To study, radiographically and symptomatically, the risk factors for adjacent segment disease (ASD) in the lumbar spine after L4/5 PLIF and to examine whether decompression surgery for the adjacent segment (L3/4) reduces the occurrence of symptomatic ASD. METHODS: Fifty-four patients who underwent L4/5 PLIF for L4 degenerative spondylolisthesis and could be followed up for at least 2 years were included. Of these, 37 were treated simultaneously with decompression surgery at L3/4. We measured radiographic changes and assessed symptoms from the cranial adjacent segment. RESULTS: Thirty-one patients (57.4%) met radiologic criteria for ASD. The length of follow-up (P=0.004) and simultaneous decompression surgery at L3/4 (P=0.009) were statistically significant factors for radiologic diagnosis of ASD. Seven patients (13.0%) had symptomatic ASD: 6 in the decompression group (16.2%) and 1 in the PLIF-only group (5.9%). Simultaneous decompression surgery did not reduce the incidence of symptomatic ASD (P=0.256). Local lordosis at the fused segment (P=0.005) and the sagittal angle of the facet joint at L3/4 (P=0.024) were statistically significant predictors of symptomatic ASD, which was accompanied by postoperative anterior listhesis above the fused segment (S group, 8.4%±8.0%; nonsymptomatic group: -0.7%±5.0%, P=0.024). CONCLUSIONS:Patients whose facet joint at the adjacent segment had a more sagittal orientation had postoperative anterior listhesis, which caused symptomatic ASD. Simultaneous decompression surgery without fusion at the adjacent level was not effective for these patients, but rather, there was a possibility that it induced symptomatic ASD.