Role of the blood-spinal cord barrier in posttraumatic syringomyelia: Laboratory investigation

Research output: Contribution to journalArticleResearchpeer-review

Abstract

Object. Posttraumatic syringomyelia produces a significant burden of pain and neurological deficits in patients with spinal cord injury. The mechanism of syrinx formation is unknown and treatment is often ineffective. A possible explanation for syrinx formation is fluid leakage from the microcirculation in the presence of a compromised blood-spinal cord barrier (BSCB). The aim of this study was to investigate the structural and functional integrity of the BSCB in a model of posttraumatic syringomyelia. Methods. The excitotoxic amino acid and arachnoiditis model of syringomyelia was used in 27 Sprague-Dawley rats. Structural integrity of the BSCB was assessed using immunoreactivity to endothelial barrier antigen (EBA), and loss of functional integrity was assessed by extravasation of intravascular horseradish peroxidase. Animals were studied after 3 days, or at 1, 3, 6, or 12 weeks after surgery. There were laminectomy-only and saline injection control animals for comparison at each time point. Results. Syrinxes formed in 16 of the 17 animals injected with excitotoxic amino acid. Loss of structural and functional integrity of the BSCB in syrinx animals was noted at all time points. Disruption of the BSCB was most dramatic in tissue adjacent to the syrinx, and in the central and dorsal gray matter. Changes in EBA expression generally corresponded with altered vascular permeability, although in the acute stages, widespread vascular permeability occurred without a corresponding decrease in EBA expression. At the later time points (3-12 weeks) EBA expression was often absent, although no vascular leakage was observed. Conclusions. This study demonstrated a prolonged structural and functional disruption of the BSCB in this model of posttraumatic syringomyelia. Loss of functional integrity of the BSCB, with fluid entering the interstitial space of the spinal cord, may contribute to initial cyst formation after spinal cord injury and subsequent enlargement of the cyst, to produce posttraumatic syringomyelia.

LanguageEnglish
Pages696-704
Number of pages9
JournalJournal of Neurosurgery: Spine
Volume11
Issue number6
DOIs
Publication statusPublished - Dec 2009

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Syringomyelia
Spinal Cord
Syringes
Capillary Permeability
Spinal Cord Injuries
Cysts
Arachnoiditis
Amino Acids
Laminectomy
Extracellular Fluid
Horseradish Peroxidase
Microcirculation
Blood Vessels
Sprague Dawley Rats
Pain
Injections
rat endothelial barrier antigen

Cite this

@article{3a1de338a0bd4763837e35332a4b3bdd,
title = "Role of the blood-spinal cord barrier in posttraumatic syringomyelia: Laboratory investigation",
abstract = "Object. Posttraumatic syringomyelia produces a significant burden of pain and neurological deficits in patients with spinal cord injury. The mechanism of syrinx formation is unknown and treatment is often ineffective. A possible explanation for syrinx formation is fluid leakage from the microcirculation in the presence of a compromised blood-spinal cord barrier (BSCB). The aim of this study was to investigate the structural and functional integrity of the BSCB in a model of posttraumatic syringomyelia. Methods. The excitotoxic amino acid and arachnoiditis model of syringomyelia was used in 27 Sprague-Dawley rats. Structural integrity of the BSCB was assessed using immunoreactivity to endothelial barrier antigen (EBA), and loss of functional integrity was assessed by extravasation of intravascular horseradish peroxidase. Animals were studied after 3 days, or at 1, 3, 6, or 12 weeks after surgery. There were laminectomy-only and saline injection control animals for comparison at each time point. Results. Syrinxes formed in 16 of the 17 animals injected with excitotoxic amino acid. Loss of structural and functional integrity of the BSCB in syrinx animals was noted at all time points. Disruption of the BSCB was most dramatic in tissue adjacent to the syrinx, and in the central and dorsal gray matter. Changes in EBA expression generally corresponded with altered vascular permeability, although in the acute stages, widespread vascular permeability occurred without a corresponding decrease in EBA expression. At the later time points (3-12 weeks) EBA expression was often absent, although no vascular leakage was observed. Conclusions. This study demonstrated a prolonged structural and functional disruption of the BSCB in this model of posttraumatic syringomyelia. Loss of functional integrity of the BSCB, with fluid entering the interstitial space of the spinal cord, may contribute to initial cyst formation after spinal cord injury and subsequent enlargement of the cyst, to produce posttraumatic syringomyelia.",
author = "Hemley, {Sarah J.} and Jian Tu and Stoodley, {Marcus A.}",
year = "2009",
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language = "English",
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pages = "696--704",
journal = "Journal of Neurosurgery: Spine",
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Role of the blood-spinal cord barrier in posttraumatic syringomyelia : Laboratory investigation. / Hemley, Sarah J.; Tu, Jian; Stoodley, Marcus A.

In: Journal of Neurosurgery: Spine, Vol. 11, No. 6, 12.2009, p. 696-704.

Research output: Contribution to journalArticleResearchpeer-review

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T1 - Role of the blood-spinal cord barrier in posttraumatic syringomyelia

T2 - Journal of Neurosurgery: Spine

AU - Hemley, Sarah J.

AU - Tu, Jian

AU - Stoodley, Marcus A.

PY - 2009/12

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N2 - Object. Posttraumatic syringomyelia produces a significant burden of pain and neurological deficits in patients with spinal cord injury. The mechanism of syrinx formation is unknown and treatment is often ineffective. A possible explanation for syrinx formation is fluid leakage from the microcirculation in the presence of a compromised blood-spinal cord barrier (BSCB). The aim of this study was to investigate the structural and functional integrity of the BSCB in a model of posttraumatic syringomyelia. Methods. The excitotoxic amino acid and arachnoiditis model of syringomyelia was used in 27 Sprague-Dawley rats. Structural integrity of the BSCB was assessed using immunoreactivity to endothelial barrier antigen (EBA), and loss of functional integrity was assessed by extravasation of intravascular horseradish peroxidase. Animals were studied after 3 days, or at 1, 3, 6, or 12 weeks after surgery. There were laminectomy-only and saline injection control animals for comparison at each time point. Results. Syrinxes formed in 16 of the 17 animals injected with excitotoxic amino acid. Loss of structural and functional integrity of the BSCB in syrinx animals was noted at all time points. Disruption of the BSCB was most dramatic in tissue adjacent to the syrinx, and in the central and dorsal gray matter. Changes in EBA expression generally corresponded with altered vascular permeability, although in the acute stages, widespread vascular permeability occurred without a corresponding decrease in EBA expression. At the later time points (3-12 weeks) EBA expression was often absent, although no vascular leakage was observed. Conclusions. This study demonstrated a prolonged structural and functional disruption of the BSCB in this model of posttraumatic syringomyelia. Loss of functional integrity of the BSCB, with fluid entering the interstitial space of the spinal cord, may contribute to initial cyst formation after spinal cord injury and subsequent enlargement of the cyst, to produce posttraumatic syringomyelia.

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U2 - 10.3171/2009.6.SPINE08564

DO - 10.3171/2009.6.SPINE08564

M3 - Article

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