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  • Author or Editor: Takamitsu Yamamoto x
  • Journal of Neurosurgery: Spine x
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Chikashi Fukaya, Yoichi Katayama, Masahiko Kasai, Jun Kurihara, Sadahiro Maejima and Takamitsu Yamamoto

Object. Histopathological studies on spinal cord injury (SCI) have demonstrated time-dependent spread of tissue damage during the initial several hours postinjury. When the long tract within the spinal cord is stimulated, a large monophasic positivity occurs at the injury site. This type of potential, termed the killed-end evoked potential (KEEP), indicates that a nerve impulse approaches but does not pass beyond the injury site. The authors tested the hypothesis that the damage spread can be evaluated as a progressive shift of the KEEP on a real-time basis. The effect of high-dose methylprednisolone sodium succinate (MPSS) on the spread of tissue damage was also examined by this methodology.

Methods. The KEEP was recorded using an electrode array placed on the spinal cord at the T-10 level in cats. This electrode array consisted of multiple 0.2-mm-diameter electrodes, each separated by 0.5 mm. Spinal cord injury was induced using a vascular clip (65 g pinching pressure for 30 seconds). The midline posterior surface of the spinal cord was stimulated bipolarly at the C-7 level by applying a single pulse at supramaximal intensity. During the initial period of 6 hours postinjury, the localization of the largest KEEP shifted progressively up to 2.5 mm rostral from the injury site. The amplitude of the KEEP recorded at the injury site decreased to 55 to 70% and became slightly shortened in latency as the localization of the largest KEEP shifted rostrally. These findings imply that the injury site KEEP represents the volume-conducted potential of the largest KEEP at the site of the conduction block. It moved away from the injury site in association with the damage spread, and this was confirmed histopathologically. A decrease in amplitude of KEEP at the injury site appeared to be the most sensitive measure of the damage spread, because the amplitude of the volume-conducted KEEP is inversely proportional to the square of the distance between the recording site and site of conduction block. Administered immediately after SCI, MPSS clearly inhibited these events, especially within 30 minutes postinjury.

Conclusions. The KEEP enables sequential evaluation to be made of the time-dependent spread of tissue damage in SCI in the same animal. It is, therefore, useful for detecting the effect of therapeutic interventions and for determining the therapeutic time window. The efficiency of MPSS to inhibit the spread of damaged tissue appeared to be maximized when it was administered within the initial 30-minute period postinjury.

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Shinya Okuda, Akira Miyauchi, Takenori Oda, Takamitsu Haku, Tomio Yamamoto and Motoki Iwasaki

Object

Previous studies of surgical complications associated with posterior lumbar interbody fusion (PLIF) are of limited value due to intrastudy variation in instrumentation and fusion techniques. The purpose of the present study was to examine rates of intraoperative and postoperative complications of PLIF using a large number of cases with uniform instrumentation and a uniform fusion technique.

Methods

The authors reviewed the hospital records of 251 patients who underwent PLIF for degenerative lumbar disorders between 1996 and 2002 and who could be followed for at least 2 years. Intraoperative, early postoperative, and late postoperative complications were investigated.

Intraoperative complications occurred in 26 patients: dural tearing in 19 patients and pedicle screw malposition in seven patients. Intraoperative complications did not affect the postoperative clinical results. Early postoperative complications occurred in 19 patients: brain infarction occurred in one, infection in one, and neurological complications in 17. Of the 17 patients with neurological complications, nine showed severe motor loss such as foot drop; the remaining eight patients showed slight motor loss or radicular pain alone, and their symptoms improved within 6 weeks. Late postoperative complications occurred in 17 patients: hardware failure in three, nonunion in three, and adjacent-segment degeneration in 11. Postoperative progression of symptomatic adjacentsegment degeneration was defined as a condition that required additional surgery to treat neurological deterioration.

Conclusions

The most serious complications of PLIF were postoperative severe neurological deficits and adjacent-segment degeneration. Prevention and management of such complications are necessary to attain good long-term clinical results.