The neuroendoscopic third ventriculostomy is becoming the standard treatment for aquired aqueduct stenosis because of its exellent results and very low morbidity. Usually the floor of third ventricle is perforated by closed forcep. Fogarty catheter, laser, saline torch, monopolar coagulator and endoscope itself. Whatever the method of ventriculostomy, the obstruction may occur. Recently the author experienced a case of obstruction at the previous site of third ventriculostomy. A 54 yr old man who had long standing ataxia developed headache, vomiting and urinary incontinence suddenly. It was revealed that he had cerebellar tumor, which had compressed the aqueduct of Sylvius anteriorly. I performed the endoscopic third ventriculostomy by monopolar coagulator and Fogarty ballon catheter. During this procedure, there was some bleeding from opening margin but all these bleedings were stopped by rinsing and electric coagulation. He was improved immediately in the postoperative period. 1 month later, the reattack of hydrocephalus developed and it was operated. On intraoperative view, the newly grown gliotic plug originated from the right mammillary body. On 5th day after reoperation., the patency of the artficial aqueduct was confirmed by 2-D cine PC MR CSF(2 dimensional cine phase contrast magnetic resonance cerebrospinal fluid) flow study.

I may suggest that in order to minimize the occlusion the opening should be made at the center of midline, thinnest area in front of both mammillary bodies, with less bleeding and without electric coagulation.

For the purpose of ascertaining the role and magnitude of ischemia of the spin-al cord following trauma the authors determine the lactate concentrations in cere-brospinal fluid(CSF). Laminectomies were performed at L2 under general anes-thesia with aseptic techniques. Paraplegia was produced by 400 gm-cm impact injury with impounder. Significant increases in CSF lactate levels occurring at Day 5. The prolonged elevation of CSF lactate indicates that tissue hypoxia plays a role in spinal cord damage and that there is a continuing hypoxia of metabolically active spinal cord tissue for several days post injury.