• Johnny Wong, Sarah Hemley, Nigel Jones, Shaokoon Cheng, Lynne Bilston, and Marcus Stoodley.
• Australian School of Advanced Medicine, Macquarie University, Sydney, New South Wales, Australia.
• Neurosurgery. 2012 Aug 1;71(2):474-80; discussion 480.

BackgroundPosttraumatic syringomyelia affects approximately 28% of spinal cord injury patients, and current treatments are often ineffective. The pathogenesis of this condition remains poorly understood. Previous reports have focused on pathways and mechanisms of fluid inflow; however, disturbances of fluid outflow mechanisms and pathways may be important in syrinx formation and enlargement.ObjectiveTo determine the route of fluid outflow from a syrinx in an animal model of posttraumatic syringomyelia.MethodsA model of posttraumatic syringomyelia using excitotoxic amino acid and kaolin-induced arachnoiditis was created in 12 Merino wethers. Six weeks after syrinx induction, the cavities were localized and a cerebrospinal fluid tracer, horseradish peroxidase (HRP), was injected into the syrinx under ultrasonic guidance. After 10 minutes, the animals were killed and the spinal cords harvested for microscopy.ResultsAn extracanalicular syrinx developed in 6 of the 12 sheep. HRP was successfully injected into 5 of the 6 syrinx cavities. HRP reaction product was observed in gray and white matter adjacent to the syrinx in a diffuse pattern. There were moderate amounts of HRP around the central canal and perivascular spaces and minimal amounts in the dorsal subarachnoid space.ConclusionIn this model of posttraumatic syringomyelia, fluid outflow occurred in a diffuse manner into the surrounding extracellular space and toward the central canal and perivascular spaces. Fluid outflow may be an important consideration in the pathogenesis of syringomyelia and the development of new therapies.

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