title: Fluid flow in an animal model of post-traumatic syringomyelia.
abstract: More than a quarter of patients with spinal cord injury develop syringomyelia, often with progressive neurological deficit. Treatment options remain limited and long-term failure rates are high. The current poor understanding is impeding development of improved therapies. The source and route of fluid flow into syringes has been investigated using cerebrospinal fluid (CSF) tracers. Previous work using a model of canalicular syringomyelia has shown that fluid enters the dilated central canal from perivascular spaces. The aim of this study was to determine the source and route of fluid flow in an animal model of extracanalicular (post-traumatic) syringomyelia. A model of post-traumatic syringomyelia was established in 25 Sprague-Dawley rats with intraparenchymal injections of quisqualic acid and kaolin-induced arachnoiditis. Rats survived for 6 weeks before injection of the CSF tracer horseradish peroxidase into the cisterna magna. Examination of the spatial distribution of horseradish peroxidase at 0, 3, 5, 10, or 20 min after injection was used to determine the route of fluid flow. Horseradish peroxidase rapidly spread to the ventromedian fissure, perivascular spaces, central canal, and extracanalicular syrinx. Flow occurred into the syrinx prior to significant perivascular flow in the rostral spinal cord. Preferential flow into the syrinx occurred from the perivascular spaces of the central penetrating branches of the anterior spinal artery in the grey matter. Transparenchymal flow into the syrinx was less prominent than perivascular flow. This is the first report of fluid flow within the spinal cord in a model of post-traumatic syringomyelia. Fluid from perivascular spaces moves preferentially into extracanalicular syringes and the surrounding parenchyma. Obstruction to CSF flow and loss of compliance from traumatic arachnoiditis might potentiate fluid flow in the perivascular space.
authors.affiliation: Prince of Wales Medical Research Institute, University of New South Wales, Barker Street, Randwick, NSW 2031, Australia. abrodbelt@doctors.org.uk
authors.forename: Andrew R
authors.initials: AR
authors.lastname: Brodbelt
authors.forename: Marcus A
authors.initials: MA
authors.lastname: Stoodley
authors.forename: Amy M
authors.initials: AM
authors.lastname: Watling
authors.forename: Jian
authors.initials: J
authors.lastname: Tu
authors.forename: Nigel R
authors.initials: NR
authors.lastname: Jones
mesh_terms: D000818:Animals; D001100:Arachnoiditis / Q000503:physiopathology; D002555:Cerebrospinal Fluid / Q000502:physiology*; D015170:Cerebrospinal Fluid Pressure / Q000502:physiology*; D004195:Disease Models, Animal; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D005110:Extracellular Space / Q000502:physiology; D006735:Horseradish Peroxidase; D019581:Neuropil / Q000502:physiology; D016318:Quisqualic Acid / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow / Q000502:physiology; D013116:Spinal Cord / Q000473:pathology / Q000503:physiopathology*; D013119:Spinal Cord Injuries / Q000150:complications* / Q000473:pathology / Q000503:physiopathology*; D013595:Syringomyelia / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology*
chemical_list: D018690:Excitatory Amino Acid Agonists; D016318:Quisqualic Acid; D006735:Horseradish Peroxidase