4.2 Article

Pathophysiology of tethered cord syndrome and other complex factors

Journal

NEUROLOGICAL RESEARCH
Volume 26, Issue 7, Pages 722-726

Publisher

MANEY PUBLISHING
DOI: 10.1179/016164104225018027

Keywords

tethered cord syndrome; oxidative metabolism; redox of cytochrome oxidase; cord elongation; hypoxia; axonal degeneration

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There are different interpretations of tethered cord syndrome (TCS) partly due to difficulty in understanding the concept of this syndrome as a functional disorder not merely based on gross anatomy of congenital anomalies. The essential mechanical factor of cord tethering is that any of the inelastic structures fastening the caudal end of the spinal cord produces traction effects on the lumbosacral cord. The production of such traction is the key to understanding this disorder. In a significant number of patients who present with the typical clinical signs and symptoms of le TCS, the diameter of the filum terminale is found within normal limits and the caudal end of the spinal cord is located in the normal position. Therefore, the definition of TCS requires the demonstration that there is a posterior displacement of the conus and filum by MRI, lack of viscoelasticity by the stretch test of the filum during surgery, and fibrous displacement of glial tissue within the filum by histological studies. This is because there is inconsistency from such studies as ultrasonography, MRI and CT myelography, which attempt to establish the presence of a tight filum terminale. A goal of this article is to provide basic understanding of TCS so that clinicians can use the concept of stretch-induced spinal cord dysfunction for proper diagnosis and treatment of this disorder.

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