Remodeling Pattern of Spinal Canal after Full Endoscopic Uniportal Lumbar Endoscopic Unilateral Laminotomy for Bilateral Decompression: One Year Repetitive MRI and Clinical Follow-Up Evaluation

Objective: There is limited literature on repetitive postoperative MRI and clinical evaluation after Uniportal Lumbar Endoscopic Unilateral Laminotomy for Bilateral Decompression. Methods: Clinical visual analog scale, Oswestry Disability Index, McNab's criteria evaluation and MRI evaluation of the axial cut spinal canal area of the upper end plate, mid disc and lower end plate were performed for patients who underwent single-level Uniportal Lumbar Endoscopic Unilateral Laminotomy for Bilateral Decompression. From the evaluation of the axial cut MRI, four types of patterns of remodeling were identified: type A: continuous expanded spinal canal, type B: restenosis with delayed expansion, type C: progressive expansion and type D: restenosis. Result: A total of 126 patients with single-level Uniportal Lumbar Endoscopic Unilateral Laminotomy for Bilateral Decompression were recruited with a minimum follow-up of 26 months. Thirty-six type A, fifty type B, thirty type C and ten type D patterns of spinal canal remodeling were observed. All four types of patterns of remodeling had statistically significant improvement in VAS at final follow-up compared to the preoperative state with type A (5.59 +/- 1.58), B (5.58 +/- 1.71), C (5.58 +/- 1.71) and D (5.27 +/- 1.68), p < 0.05. ODI was significantly improved at final follow-up with type A (49.19 +/- 10.51), B (50.00 +/- 11.29), C (45.60 +/- 10.58) and D (45.60 +/- 10.58), p < 0.05. A significant MRI axial cut increment of the spinal canal area was found at the upper endplate at postoperative day one and one year with type A (39.16 +/- 22.73; 28.00 +/- 42.57) mm(2), B (47.42 +/- 18.77; 42.38 +/- 19.29) mm(2), C (51.45 +/- 18.16; 49.49 +/- 18.41) mm(2) and D (49.10 +/- 23.05; 38.18 +/- 18.94) mm(2), respectively, p < 0.05. Similar significant increment was found at the mid-disc at postoperative day one, 6 months and one year with type A (55.16 +/- 27.51; 37.23 +/- 25.88; 44.86 +/- 25.73) mm(2), B (72.83 +/- 23.87; 49.79 +/- 21.93; 62.94 +/- 24.43) mm(2), C (66.85 +/- 34.48; 54.92 +/- 30.70; 64.33 +/- 31.82) mm(2) and D (71.65 +/- 16.87; 41.55 +/- 12.92; 49.83 +/- 13.31) mm(2) and the lower endplate at postoperative day one and one year with type A (49.89 +/- 34.50; 41.04 +/- 28.56) mm(2), B (63.63 +/- 23.70; 54.72 +/- 24.29) mm(2), C (58.50 +/- 24.27; 55.32 +/- 22.49) mm(2) and D (81.43 +/- 16.81; 58.40 +/- 18.05) mm(2) at postoperative day one and one year, respectively, p < 0.05. Conclusions: After full endoscopic lumbar decompression, despite achieving sufficient decompression immediately postoperatively, varying severity of asymptomatic restenosis was found in postoperative six months MRI without clinical significance. Further remodeling with a varying degree of increment of the spinal canal area occurs at postoperative one year with overall good clinical outcomes

Remodeling Pattern of Spinal Canal after Full Endoscopic Uniportal Lumbar Endoscopic Unilateral Laminotomy for Bilateral Decompression: One Year Repetitive MRI and Clinical Follow-Up Evaluation

Objective: There is limited literature on repetitive postoperative MRI and clinical evaluation after Uniportal Lumbar Endoscopic Unilateral Laminotomy for Bilateral Decompression. Methods: Clinical visual analog scale, Oswestry Disability Index, McNab’s criteria evaluation and MRI evaluation of the axial cut spinal canal area of the upper end plate, mid disc and lower end plate were performed for patients who underwent single-level Uniportal Lumbar Endoscopic Unilateral Laminotomy for Bilateral Decompression. From the evaluation of the axial cut MRI, four types of patterns of remodeling were identified: type A: continuous expanded spinal canal, type B: restenosis with delayed expansion, type C: progressive expansion and type D: restenosis. Result: A total of 126 patients with single-level Uniportal Lumbar Endoscopic Unilateral Laminotomy for Bilateral Decompression were recruited with a minimum follow-up of 26 months. Thirty-six type A, fifty type B, thirty type C and ten type D patterns of spinal canal remodeling were observed. All four types of patterns of remodeling had statistically significant improvement in VAS at final follow-up compared to the preoperative state with type A (5.59 ± 1.58), B (5.58 ± 1.71), C (5.58 ± 1.71) and D (5.27 ± 1.68), p < 0.05. ODI was significantly improved at final follow-up with type A (49.19 ± 10.51), B (50.00 ± 11.29), C (45.60 ± 10.58) and D (45.60 ± 10.58), p < 0.05. A significant MRI axial cut increment of the spinal canal area was found at the upper endplate at postoperative day one and one year with type A (39.16 ± 22.73; 28.00 ± 42.57) mm2, B (47.42 ± 18.77; 42.38 ± 19.29) mm2, C (51.45 ± 18.16; 49.49 ± 18.41) mm2 and D (49.10 ± 23.05; 38.18 ± 18.94) mm2, respectively, p < 0.05. Similar significant increment was found at the mid-disc at postoperative day one, 6 months and one year with type A (55.16 ± 27.51; 37.23 ± 25.88; 44.86 ± 25.73) mm2, B (72.83 ± 23.87; 49.79 ± 21.93; 62.94 ± 24.43) mm2, C (66.85 ± 34.48; 54.92 ± 30.70; 64.33 ± 31.82) mm2 and D (71.65 ± 16.87; 41.55 ± 12.92; 49.83 ± 13.31) mm2 and the lower endplate at postoperative day one and one year with type A (49.89 ± 34.50; 41.04 ± 28.56) mm2, B (63.63 ± 23.70; 54.72 ± 24.29) mm2, C (58.50 ± 24.27; 55.32 ± 22.49) mm2 and D (81.43 ± 16.81; 58.40 ± 18.05) mm2 at postoperative day one and one year, respectively, p < 0.05. Conclusions: After full endoscopic lumbar decompression, despite achieving sufficient decompression immediately postoperatively, varying severity of asymptomatic restenosis was found in postoperative six months MRI without clinical significance. Further remodeling with a varying degree of increment of the spinal canal area occurs at postoperative one year with overall good clinical outcomes

Comparison of 5 Different Rat Models to Establish a Standard Animal Model for Research Into Interstitial Cystitis

Purpose We evaluated 5 different rat models using different agents in order to establish a standard animal model for interstitial cystitis (IC) in terms of the functional and pathologic characteristics of the bladder. Methods Five IC models were generated in 8-week-old female Sprague-Dawley rats via transurethral instillation of 0.1M hydrogen chloride (HCl) or 3% acetic acid (AA), intraperitoneal injection of cyclophosphamide (CYP) or lipopolysaccharide (LPS), or subcutaneous injection of uroplakin II (UPK2). After generating the IC models, conscious cystometry was performed on days 3, 7, and 14. All rats were euthanized on day 14 and their bladders were obtained for histological and pro-inflammatory-related gene expression analysis. Results In the cystometric analysis, all experimental groups showed significantly decreased intercontraction intervals compared with the control group on day 3, but only the LPS and UPK groups maintained significantly shorter intercontraction intervals than the control group on day 14. The histological analysis revealed that areas with severe urothelial erosion (HCl, AA, and UPK) and hyperplasia (CYP and LPS), particularly in the UPK-treated bladders, showed a markedly increased infiltration of toluidine blue-stained mast cells and increased tissue fibrosis. In addition, significantly elevated expression of interleukin-1b, interleukin-6, myeloperoxidase, monocyte chemotactic protein 1, and Toll-like receptors 2 and 4 was observed in the UPK group compared to the other groups. Conclusions Among the 5 different agents, the injection of UPK generated the most effective IC animal model, showing consequent urothelial barrier loss, inflammatory reaction, tissue fibrosis stimulation, and persistent hyperactive bladder