کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5629578 | 1580275 | 2017 | 5 صفحه PDF | دانلود رایگان |
- The best evidence points out to a reduction in Modic type I frequency on fused segments.
- There was a predominance of new type II changes in postoperative images.
- No study described the Modic changes in adjacent levels.
- Clinical and functional outcomes were significantly improved at follow-up.
According to the original description by Modic et al., the natural course of bone marrow signal abnormalities is an inexorable, progressive one, however recent evidence has demonstrated in healthy individuals and those suffering from lumbar disc herniation that the course of endplate degenerative changes is rather dynamic and sometimes regressive. The evolution of such changes in lumbar fused segments and adjacent levels is largely unknown. The literature relevant to the course of Modic changes on fused and adjacent levels, as well as its clinical correspondence in patients undergoing posterolateral lumbar fusion was collected. Two studies met the criteria. Of 38 patients with Modic type I signals preoperatively, 6 regressed to type 0, 22 progressed to type 2, and 10 remained the same postoperatively. Of 12 patients with Modic type 2 signals preoperatively, 2 regressed to type 0 and 10 remained the same postoperatively. None of the articles described the Modic changes in adjacent levels. Clinical and functional outcomes were significantly improved at follow-up regardless of the endplate signal changes. The best available evidence points out to a reduction in Modic type I frequency on fused segments, either regressive or progressive. There was a predominance of new type II changes in postoperative images, which might represent improvement of instability. This study calls into attention the controversial role of Modic changes as an indicator of clinical significance, since clinical and functional outcomes significantly improved regardless of the endplate signal changes.
Journal: Journal of Clinical Neuroscience - Volume 41, July 2017, Pages 6-10