Object. More than a quarter of spinal cord injured patients will develop an enlarging cystic cavity, or syrinx, within the spinal cord up to 30 years following the initial trauma. Enlarging syrinxes can cause progressive loss of function in patients who often already have a disability. Less than half the affected patients can be expected to improve following treatment. A lack of understanding of the pathophysiology of the disease is hampering attempts to improve on this poor prognosis. Investigation into the mechanisms of fluid flow and the role of ischaemia in this type of syringomyelia may help understand the causative mechanisms and lead to improved treatment outcomes. Materials and methods. Temporal and dose profiling of an animal model of post-traumatic syringomyelia was performed in Sprague Dawley rats. The cerebrospinal fluid tracer, horseradish peroxidase, was used for detailed analysis of the routes of fluid flow into the syrinx. The effects of variations in subarachnoid space compliance on syrinx formation and fluid flow were examined using shunt insertion, pseudomeningocele formation, and animals without subarachnoid adhesions. Local spinal cord blood flow was investigated with Doppler flowmetry, and the intracellular levels of ATP and adenosine phosphates were measured with a bioluminescence technique. Results. A reliable animal model that mimicked human syrinx pathology was refined. Excitotoxic injury selectively damaged neurones, and induced syrinx formation in a dose and time dependent fashion. Cerebrospinal fluid flows from the subarachnoid space along perivascular spaces into the cord and syrinx. Flow occurred along the perivascular spaces of the central branches of the anterior spinal artery, and was maximal at the level of the syrinx. Improving compliance by shunt insertion reduced syrinx size but preferential fluid movement into the syrinx was maintained. If arachnoid adhesions were absent, this preferential flow ceased and syrinxes were smaller. Pseudomeningocele formation proved technically difficult and was unhelpful in changing cord compliance. Spinal cord blood flow was decreased following syrinx formation. Early reductions occurred in ATP and ADP levels, and the intracellular ATP/ADP ratio remained below 0.2 at all time points following syrinx induction. Conclusions. CSF moves into the syrinx and spinal cord along perivascular spaces. Arachnoid adhesions may act to decrease localized subarachnoid space compliance and encourage fluid flow from the subarachnoid space along perivascular spaces and into the syrinx. Increasing distal subarachnoid space compliance does not prevent this preferential flow but may reduce the amount of flow. Fluid accumulation within the syrinx causes ischaemia through pressure effects on the surrounding spinal cord tissue, and may further syrinx enlargement by apoptosis. The results support and are consistent with a local arterial pulsation dependent pumping mechanism of cerebrospinal fluid flow.
| Identifer | oai:union.ndltd.org:ADTP/187864 |
| Date | January 2003 |
| Creators | Brodbelt, Andrew Robert, Prince of Wales Medical Research Institute, Faculty of Medicine, UNSW |
| Publisher | Awarded by:University of New South Wales. Prince of Wales Medical Research Institute |
| Source Sets | Australiasian Digital Theses Program |
| Language | English |
| Detected Language | English |
| Rights | Copyright Andrew Robert Brodbelt, http://unsworks.unsw.edu.au/copyright |
Page generated in 0.002 seconds