A NEW MODEL FOR TETHERED CORD SYNDROME - A BIOCHEMICAL, ELECTROPHYSIOLOGICAL, AND ELECTRON-MICROSCOPIC STUDY

Citation
A. Kocak et al., A NEW MODEL FOR TETHERED CORD SYNDROME - A BIOCHEMICAL, ELECTROPHYSIOLOGICAL, AND ELECTRON-MICROSCOPIC STUDY, Pediatric neurosurgery, 26(3), 1997, pp. 120-126
Citations number
20
Journal title
ISSN journal
10162291
Volume
26
Issue
3
Year of publication
1997
Pages
120 - 126
Database
ISI
SICI code
1016-2291(1997)26:3<120:ANMFTC>2.0.ZU;2-E
Abstract
In order to investigate the pathophysiology of the tethered cord syndr ome, a few experimental models have been developed and used previously . In this study, the authors present a new experimental model to inves tigate the biochemical, electrophysiological, and histopathological ch anges in the tethered spinal cord syndrome. A model was produced in gu inea pigs using an application of cyanoacrylate to fixate the filum te rminale and the surrounding tissue to the dorsal aspect of the sacrum following 5-gram stretching of the spinal cord. The experiments were p erformed on 40 animals divided into two groups. The responses to tethe ring were evaluated with hypoxanthine and lipid peroxidation, somatose nsory and motor evoked potentials, and transmission electron microscop e examination. The hypoxanthine and lipid peroxidation levels signific antly increased, indicating an ischemic injury (p < 0.01). The average hypoxanthine level in the control group was 478.8 +/- 68.8 nmol/g wet tissue, while ii, was 651.2 +/- 71.5 nmol/g in the tethered cord grou p, The lipid peroxidation level in group I Nas 64.0 +/- 5.7 nmol/g wet tissue, whereas it Nas 84.0 +/- 4.7 nmol/g in group II. In the tether ed cord group, the latencies of the somatosensory and motor evoked pot entials significantly increased, and the amplitudes decreased. These c hanges indicated a defective conduction in the motor and sensorial ner ve fibers. In the transmission electron microscopic examinations, besi des the reversible changes like edema and destruction in the gray-whit e matter junction, irreversible changes like scarcity of neurofilament s and destruction in axons and damage in myelin sheaths were observed. We consider that this work can be used as an experimental model for t ethered cord syndrome.