Abstract
Introduction: Post-traumatic syringomyelia produces a significant burden of pain and neurological deficits for patients with spinal cord injury. The mechanism of syrinx formation is unknown and treatment is often ineffective. Previous studies have demonstrated that fluid flow enters syrinxes from the subarachnoid space via perivascular spaces, however other pathways may be involved. It has been proposed that a damaged blood-spinal cord barrier (BSCB) provides another pathway for fluid to enter syrinxes. The purpose of this study was to investigate whether or not the integrity of the BSCB is compromised in an animal model of post-traumatic syringomyelia, and if so, whether this deficiency plays a role in the induction or subsequent enlargement of a syrinx.
Methods: The excitotoxic amino acid and arachnoiditis model of syringomyelia was used to study the structural and functional integrity of the BSCB in 27 Sprague-Dawley rats. In this model, quisqualic acid is injected into the cord to create an initial cyst. The addition of subarachnoid kaolin to create arachnoiditis results in a reliable model of syringomyelia [1]. Structural integrity of the blood-spinal cord barrier was assessed using immunoreactivity to endothelial barrier antigen (EBA) and loss of functional integrity was assessed by extravasation of intravascular horseradish peroxidise (HRP). Animals were studied at 3 days, or 1, 3, 6, or 12 weeks after surgery. There were laminectomy-only and saline injection controls at each time point.
Results: Syrinxes formed in 15 of 17 animals injected with excitotoxic amino acid. There was loss of structural and functional integrity of the BSCB in the syrinx animals at all time points. There was wide-spread disruption of the barrier at early time points, followed by recovery of the barrier except for vessels immediately adjacent to the syrinx.
Discussion: This study has demonstrated a prolonged structural and functional disruption of the BSCB. Loss of functional integrity of the barrier, 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 form post-traumatic syringomyelia.
Correspondence should be addressed to Dr Owen Williamson, Editorial Secretary, Spine Society of Australia, 25 Erin Street, Richmond, Victoria 3121, Australia.
