Fluid outflow in a large-animal model of posttraumatic syringomyelia

Johnny Wong, Sarah Hemley, Nigel Jones, Shaokoon Cheng, Lynne Bilston, Marcus Stoodley

    Research output: Contribution to journalArticleResearchpeer-review

    Abstract

    BACKGROUND: Posttraumatic 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. OBJECTIVE: To determine the route of fluid outflow from a syrinx in an animal model of posttraumatic syringomyelia. METHODS: A 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. RESULTS: An 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. CONCLUSION: In 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.

    LanguageEnglish
    Pages474-480
    Number of pages7
    JournalNeurosurgery
    Volume71
    Issue number2
    DOIs
    Publication statusPublished - Aug 2012

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    Syringomyelia
    Syringes
    Animal Models
    Horseradish Peroxidase
    Arachnoiditis
    Kaolin
    Subarachnoid Space
    Extracellular Space
    Spinal Cord Injuries
    Ultrasonics
    Cerebrospinal Fluid
    Microscopy
    Spinal Cord
    Sheep
    Amino Acids
    Therapeutics

    Cite this

    Wong, Johnny ; Hemley, Sarah ; Jones, Nigel ; Cheng, Shaokoon ; Bilston, Lynne ; Stoodley, Marcus. / Fluid outflow in a large-animal model of posttraumatic syringomyelia. In: Neurosurgery. 2012 ; Vol. 71, No. 2. pp. 474-480.
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    abstract = "BACKGROUND: Posttraumatic 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. OBJECTIVE: To determine the route of fluid outflow from a syrinx in an animal model of posttraumatic syringomyelia. METHODS: A 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. RESULTS: An 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. CONCLUSION: In 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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    Fluid outflow in a large-animal model of posttraumatic syringomyelia. / Wong, Johnny; Hemley, Sarah; Jones, Nigel; Cheng, Shaokoon; Bilston, Lynne; Stoodley, Marcus.

    In: Neurosurgery, Vol. 71, No. 2, 08.2012, p. 474-480.

    Research output: Contribution to journalArticleResearchpeer-review

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    AU - Hemley, Sarah

    AU - Jones, Nigel

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    AU - Stoodley, Marcus

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    N2 - BACKGROUND: Posttraumatic 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. OBJECTIVE: To determine the route of fluid outflow from a syrinx in an animal model of posttraumatic syringomyelia. METHODS: A 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. RESULTS: An 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. CONCLUSION: In 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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