The current study shows that the radiographic decompression effect of LLIF for Schizas grade D segments was comparable with the effect on other grades. However, patients with extreme lumbar spinal stenosis are not good candidates for LLIF alone. Stand-alone LLIF is not suggested for such patients, but with concomitant posterior decompression, LLIF can achieve a satisfactory clinical outcome for extreme lumbar spinal stenosis.
Although the indirect neural decompression effect of LLIF for lumbar stenosis has been addressed in previous studies(3, 4, 9–13), the current study was the first to evaluate the indirect neural decompression effect in patients with extreme lumbar spinal stenosis. The average changes in CD and CCA of grade D were 2.50 ± 1.25 mm and 16.11 ± 10.70 mm2, which was comparable with the effects in other grades, which indicated that the indirect decompression effect is not compromised in patients with extreme spinal stenosis. However, the average rates of change CD and CCA of grade D were 79.69 ± 86.23% and 52.91 ± 34.41% respectively, both of which increased from grade A to D (Figure.3B), and in accordance with Fujibayashi’s finding(14) that the greater the stenosis preoperatively, the greater the improvement rate in neural decompression with LLIF compared with milder stenosis. Oliviera et al(11) described increases of 2.4 mm (33.1%) and 12.4 mm2 (8.4%), respectively, in central canal diameter and canal area after XLIF. Elowitz et al(15) found a 3.8 mm improvement in anterior-posterior diameter of the dural sac and the area of the dural sac increased an average of 83 mm2 (143%) after XLIF. Castellvi et al(12) found that the central canal area was improved by 10 mm (27%) and 23 mm2 (17%) at 3 months and 1 year, respectively, after XLIF. At the 3-month follow-up, Isaacs et al(3) found an increase in the central canal area of 20.8 mm2 and in the central canal diameter of 1.2 mm after XLIF. Except for the results reported by Elowitz et al., the improvement of central canal stenosis in patients with Schizas grade D is comparable with those studies(3, 11, 12).
With regard to the indirect decompression effect on foraminal stenosis, Oliviera et al(11) described an increase of 2.48 mm (13.1%) of foraminal height after XLIF. In another retrospective study with 90 patients undergoing LLIF, Alimi et al(16) found foraminal height increased by 3.1 mm (20%). At 3-month follow-up, Isaacs et al(3) found an increase in the approach-side foraminal height of 2.16 mm and in the contralateral-side foraminal height of 1.39 mm after XLIF. For segments with Schizas grade D, we found an increase of foraminal height of 2.11 ± 1.75 mm (12.20 ± 10.28%) on the left -side and 2.05 ± 1.83 mm (11.83 ± 10.82%) on right-side, which is comparable with those studies and not significantly different from the improvement seen with other grades. Likewise, as to the change of anterior and posterior disk height and segment angle, grade D showed no significant difference from other grade. Thus, we consider that preoperative central canal stenosis does not significantly influence the degree of change of indirect decompression after LLIF.
In our group, the mean ODI and VAS scores were both significantly improved at the last follow-up. Post-operatively, the average axial CCA of grade D was 49.87 ± 18.81 mm2, which was significantly smaller than the average preoperative axial CCA of grade C (82.06 ± 26.97 mm2). Sixteen of 18 (88.89%) segments with stenosis of grade D received posterior direct decompression. We believed that additional posterior decompression after LLIF was important to ensure sufficient decompression in patients with extreme lumbar spinal stenosis. In addition, it is extremely dangerous to perform posterior instrumentation without direct decompression in patients with severe stenosis exhibiting preoperative paralysis(17). The clinical indications for posterior decompression after LLIF were inconsistent. There have been studies which claimed that factors likely to cause failure of indirect decompression include cage subsidence, low bone mineral density, severe central canal stenosis, ligamentum flavum hypertrophy, and osteophytes in the lateral recess and foraminal canal (11, 14, 18–22). Among them, severe central canal stenosis might be the major risk factor. Nakashima et al(17) claimed that patients with preoperative lower limb paralysis and severe stenosis were at a higher risk of perioperative neurological deterioration and that this was particularly true for patients exhibiting ligament ossification around the spinal canal. Moreover, factors that are less likely to influence indirect decompression in LLIF are cage position, cage type, side of approach, preoperative sagittal/coronal alignment, presence of facet arthropathy, spinal level (upper or lower lumbar spine), and number of operated spinal levels (9, 21, 23–26).
In the current group, seven out of eight patients with extreme lumbar stenosis who underwent single-level LLIF received second-stage posterior decompression. One patient who was treated with single-level stand-alone LLIF reported worse of back pain and neurological deterioration at the last follow-up. Lack of posterior supplemental fixation may lead to a loss of acquired indirect decompression after the operation. Thus, we do not suggest stand-alone surgery for patients with extreme spinal stenosis. Posterior lumbar interbody fusion may be a better surgical option for patients with single-level extreme lumbar spinal stenosis.
There are some limitations to this study including the retrospective nature of the study, the limited follow-up, and the small sample size of grade D. Since CT and MRI were not performed during follow-up in most cases, we could not show the radiographic changes during follow-up. The clinical outcomes of patients with extreme lumbar stenosis were not compared with those with mild lumbar stenosis.