Abstract
Introduction: Modern imaging techniques have demonstrated that up to 28% of patients with spinal cord injury develop syringomyelia. Cyst formation and enlargement are thought to be related to abnormalities of cerebrospinal fluid hydrodynamics, however the exact mechanism and route of entry into the spinal cord remain incompletely understood. Previous work in rats has demonstrated that experimental post-traumatic syrinxes occur more reliably and are larger when the excitotoxic injury is combined with arachnoiditis produced by subarachnoid kaolin injection. A sheep model of post-traumatic syringomyelia (P.T.S.) has been characterised and studies of cerebrospinal fluid dynamics are currently being undertaken. The aim of this study was to assess the effect of focal subarachnoid space blockage on spinal fluid pressures and flow.
Methods: Arachnoiditis was induced in 5 sheep by injection of 1.5 mls of kaolin in the subarachnoid space (SAS) of upper thoracic spinal cord. The animals were left for 6–8 weeks before C.S.F. studies were undertaken. In another 5 sheep, a ligature was passed around the spinal cord to simulate an acute blockage of the subarachnoid space. Fluid-coupled monitors were used to measure blood pressure, central venous pressure and subarachnoid pressure (1cm rostral and 1 cm caudal to the arachnoiditis or ligature). Fiberoptic monitors were used to measure intracranial pressure. In the ligature group, subarachnoid pressures were also measured prior to tying the ligature to obliterate the SAS and served as baseline control pressures. The effects of Valsalva and Queckenstedt manoeuvres on SAS pressures were examined in both groups.
CSF flow was studied at 0 and 10 minutes after injection of the CSF tracer horseradish peroxidase (HRP). Vibratome sections of the spinal cord were processed using tetramethylbenzidine and sections examined under light microscopy.
Results: The mean SAS pressure rostral to the arachnoiditis was found to be greater than the mean caudal SAS pressure by 1.7 mmHg. In the ligature group, the difference was 0.9 mmHg, being higher in the caudal SAS. Queckenstedt manoeuvre exaggerated this difference to 3 mmHg in the Kaolin group and 4 mmHg in the ligature group. The effect of Valsalva was much less marked in both groups.
Perivascular spaces were enlarged in most cases of arachnoiditis and HRP was seen to stain these spaces and the central canal within 10 minutes.
Discussion: Post-traumatic syrinxes are usually juxtaposed to the injury site with 80% occurring rostral, 4% caudal and 15%in both directions. The finding of a higher subarachnoid pressure rostral to the injury site may help explain this phenomenon. We hypothesize that a reduction of compliance in subarachnoid space increases the pulse pressure and hence increases perivascular flow of C.S.F. contributing to the formation and enlargement of PTS. We are currently investigating this hypothesis by measuring subarachnoid space compliance directly in the sheep model of arachnoiditis described above.
The abstracts were prepared by Dr Robert Moore. Correspondence should be addressed to him at Spine Society of Australia, c/o the Adelaide Centre for Spinal Research, Institute of Medical and Veterinary Science, PO Box 14, Rundle Mall, Adelaide SA 500, Australia.
