A new model for tethered cord syndrome: A biochemical, electrophysiological, and electron microscopic study

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dc.authoridcirak, bayram/0000-0002-3946-0456
dc.authorwosidKilic, Abdullah/AAI-2792-2021
dc.contributor.authorKocak, A
dc.contributor.authorKilic, A
dc.contributor.authorNurlu, G
dc.contributor.authorKonan, A
dc.contributor.authorKilinc, K
dc.contributor.authorCirak, B
dc.contributor.authorColak, A
dc.date.accessioned2024-08-04T20:11:52Z
dc.date.available2024-08-04T20:11:52Z
dc.date.issued1997
dc.departmentİnönü Üniversitesien_US
dc.description.abstractIn order to investigate the pathophysiology of the tethered cord syndrome, a few experimental models have been developed and used previously. In this study, the authors present a new experimental model to investigate the biochemical, electrophysiological, and histopathological changes in the tethered spinal cord syndrome. A model was produced in guinea pigs using an application of cyanoacrylate to fixate the filum terminale and the surrounding tissue to the dorsal aspect of the sacrum following 5-gram stretching of the spinal cord. The experiments were performed on 40 animals divided into two groups. The responses to tethering were evaluated with hypoxanthine and lipid peroxidation, somatosensory and motor evoked potentials, and transmission electron microscope examination. The hypoxanthine and lipid peroxidation levels significantly 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 group, 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 tethered cord group, the latencies of the somatosensory and motor evoked potentials significantly increased, and the amplitudes decreased. These changes indicated a defective conduction in the motor and sensorial nerve fibers. In the transmission electron microscopic examinations, besides the reversible changes like edema and destruction in the gray-white matter junction, irreversible changes like scarcity of neurofilaments and destruction in axons and damage in myelin sheaths were observed. We consider that this work can be used as an experimental model for tethered cord syndrome.en_US
dc.identifier.doi10.1159/000121176
dc.identifier.endpage126en_US
dc.identifier.issn1016-2291
dc.identifier.issn1423-0305
dc.identifier.issue3en_US
dc.identifier.pmid9419028en_US
dc.identifier.scopus2-s2.0-0030710227en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage120en_US
dc.identifier.urihttps://doi.org/10.1159/000121176
dc.identifier.urihttps://hdl.handle.net/11616/93055
dc.identifier.volume26en_US
dc.identifier.wosWOS:A1997YJ66500003en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherKargeren_US
dc.relation.ispartofPediatric Neurosurgeryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectcyanoacrylateen_US
dc.subjectevoked potentialsen_US
dc.subjectfree radicalsen_US
dc.subjectmotor evoked potentialsen_US
dc.subjectsomatosensory evoked potentialsen_US
dc.subjecttethered cord syndromeen_US
dc.titleA new model for tethered cord syndrome: A biochemical, electrophysiological, and electron microscopic studyen_US
dc.typeArticleen_US

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