title: Altered subarachnoid space compliance and fluid flow in an animal model of posttraumatic syringomyelia.
abstract: METHODS
  A histologic study of cerebrospinal fluid tracers in Sprague-Dawley rats undergoing lumboperitoneal shunt insertion in the excitotoxic animal model of posttraumatic syringomyelia (PTS).
  
  
  OBJECTIVE
  To determine the effects of cerebrospinal fluid (CSF) diversion from the subarachnoid space on perivascular flow (PVS) and syrinx formation in posttraumatic syringomyelia.
  
  
  BACKGROUND
  In an animal model of PTS, fluid enters syringes from the subarachnoid space via perivascular spaces. Preferential PVS flow occurs at the level of the syrinx. It has been suggested that arachnoiditis predisposes to posttraumatic syringomyelia formation by obstructing subarachnoid cerebrospinal fluid flow and enhancing perivascular flow.
  
  
  METHODS
  Thirty-two male Sprague-Dawley rats were investigated using the CSF tracer horseradish peroxidase (HRP), the excitotoxic model of PTS, and lumboperitoneal shunt insertion. Five experimental groups consisted of normal controls, syrinx only and shunt only controls, and shunt insertion before or after syrinx formation. In all groups except normal controls, CSF flow studies were performed 6 weeks after the final intervention. Grading scales were used to quantify HRP staining.
  
  
  RESULTS
  All excitotoxic model animals formed syringes. Perivascular flow was greatest at the level of the syrinx. Cerebral cortex perivascular flow was significantly reduced after shunt insertion in animals with a syrinx (P < 0.05). Shunt insertion did not alter syrinx length or size. There were no significant differences between shunt and syrinx first groups.
  
  
  CONCLUSIONS
  Increasing caudal subarachnoid space compliance with a shunt does not affect local CSF flow into the spinal cord and syrinx. These results suggest that localized alterations in compliance, as opposed to obstruction from traumatic arachnoiditis, may act as an important factor in syrinx pathogenesis.
authors.affiliation: Prince of Wales Medical Research Institute, Barker Street, Randwick, New South Wales 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: Seán
authors.initials: S
authors.lastname: Burke
authors.forename: Nigel R
authors.initials: NR
authors.lastname: Jones
mesh_terms: D000818:Animals; D001100:Arachnoiditis / Q000473:pathology / Q000503:physiopathology; D002555:Cerebrospinal Fluid / Q000502:physiology*; D015170:Cerebrospinal Fluid Pressure; D004195:Disease Models, Animal; D006735:Horseradish Peroxidase / Q000008:administration & dosage / Q000378:metabolism; D007267:Injections; D008279:Magnetic Resonance Imaging; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013119:Spinal Cord Injuries / Q000150:complications; D013346:Subarachnoid Space / Q000503:physiopathology; D013595:Syringomyelia / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*
chemical_list: D006735:Horseradish Peroxidase