• K Miaki, H Matsui, M Nakano, and H Tsuji.
• Department of Orthopaedic Surgery, Toyama Medical and Pharmaceutical University, Japan.
• Eur Spine J. 1999 Jan 1; 8 (4): 310-6.

AbstractLaminectomy-induced cauda equina adhesion has been proved by rat experiments and postoperative serial MRI in humans. A degenerative change of the cauda equina has been proved when cauda equina adhesion has been prolonged. Since it has not been reported how the nutritional supply is changed in such a condition, we evaluated the glucose supply to the adhered cauda equina in rats. Wistar rats were divided into the following three groups: the control group which received no operation, the laminectomy group which underwent L5-L6 laminectomy only, and the koalin group which received 5 mg of kaolin on the dorsal extradural space following L5-L6 laminectomy. Based on 3H-methyl-glucose uptake study, we analyzed (1) glucose transport from the intraneural vessels to the nerve tissue, and (2) glucose transport from the cerebrospinal fluid to the nerve tissue. We evaluated the relation between the severity of cauda equina adhesion and 3H uptake into the cauda equina. Cauda equina adhesion was observed in 2 of 12 rats in the control group, in 3 of 12 rats in the laminectomy group, and in 18 of 20 rats in the kaolin group. In the 3H-methyl-glucose uptake study, at 12 weeks the glucose transport to the cauda equina from the vessels increased by 44%, and that from the cerebrospinal fluid decreased by 64% in the kaolin group compared with the control group. In the condition of complete cauda equina adhesion, the glucose transport to the cauda equina from the vessels increased by 53% and that from the cerebrospinal fluid remarkably decreased by 72% compared with the normal cauda equina. Considering the greater nutritional importance of the cerebrospinal fluid in the cauda equina, it is most likely that the impairment of nutritional supply to adhered cauda equina may lead to eventual neural degeneration.

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