IntroductionAdhesive spinal arachnoiditis in the lumbar spine is considered to be a sequence of inflammatory changes in the cauda equina and the pia-arachnoid membrane. The possible etiologic factors have been reported as infections [6], prolapsed intervertebral disc [7,8,23], spinal surgery [1,22,26,28], myelographic dyes [2,7,11,12], and spinal anesthesia [1,22]. Recently, clumping of the cauda equina in the central and peripheral region in the thecal sac has been described in MRI studies [5,15,24]. To date, among the possible etiologic factors in lumbar adhesive arachnoiditis, posterior surgical intervention to the lumbar spine seems to be the most possible and frequently associated cause. In the previous study, it was reported that tranAbstract Laminectomy-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 3 H-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 3 H 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 3 H-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 thecontrol 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.
