Abstract
BackgroundSyringomyelia is a serious complication of spinal cord trauma, occurring in approximately 28% of spinal cord injuries. Treatment options are limited and often produce unsatisfactory results. Post-traumatic syringomyelia (PTS) is presumably related to abnormalities of cerebrospinal fluid (CSF) and interstitial fluid hydrodynamics, but the exact mechanisms are unknown.MethodsTransmission electron microscopy (TEM) was used to investigate in detail the interfaces between fluid and tissue in the spinal cords of healthy Sprague–Dawley rats (n = 3) and in a rat model of PTS (n = 3). PTS was induced by computer-controlled impact (75 kDyn) to the spinal cord between C6 and C8, followed by a subarachnoid injection of kaolin to produce focal arachnoiditis. Control animals received a laminectomy only to C6 and C7 vertebrae. Animals were sacrificed 12 weeks post-surgery, and spinal cords were prepared for TEM. Ultra-thin spinal cord sections at the level of the injury were counterstained for structural anatomy.ResultsSpinal cords from animals with PTS displayed several abnormalities including enlarged perivascular spaces, extracellular edema, cell death and loss of tissue integrity. Additionally, alterations to endothelial tight junctions and an abundance of pinocytotic vesicles, in tissue adjacent to syrinx, suggested perturbations to blood-spinal cord barrier (BSCB) function.ConclusionsThese findings support the hypothesis that perivascular spaces are important pathways for CSF flow into and out of the spinal cord, but also suggest that fluid may enter the cord through vesicular transport and an altered BSCB.
Highlights
Syringomyelia is a serious complication of spinal cord trauma, occurring in approximately 28% of spinal cord injuries
From months to decades after a spinal cord trauma, Post-traumatic syringomyelia (PTS) may develop within spinal cord tissue [1,2,3]
The extracellular space was described as the space between parenchymal cells separated from the cerebrospinal fluid (CSF)-filled areas of the subarachnoid and perivascular space by the foot processes of astrocytes
Summary
Syringomyelia is a serious complication of spinal cord trauma, occurring in approximately 28% of spinal cord injuries. Treatment options are limited and often produce unsatisfactory results. From months to decades after a spinal cord trauma, PTS may develop within spinal cord tissue [1,2,3]. The fluidfilled cavities (syrinxes) that develop in PTS can enlarge over time and alter surrounding nervous tissue integrity. Damage to cord tissue can result in pain and neurological deficits. Treatment options for syringomyelia are limited to surgical decompression or correction of deformity, arachnolysis or shunting procedures to facilitate drainage [4,5,6]. Carry high risks of complication, and result in unsatisfactory long-term success rates in approximately 50% of cases [2]. An improved understanding of the neuropathology of PTS is necessary to mitigate poor treatment outcomes
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