title: The pressure distribution of cerebrospinal fluid responds to residual compression and decompression in an animal model of acute spinal cord injury.
abstract: METHODS
  In vivo large animal (pig) model study of cerebrospinal fluid (CSF) pressures after acute experimental spinal cord injury (SCI).
  
  
  OBJECTIVE
  To determine how the CSF pressure (CSFP) and CSF pulse pressure amplitude (CSFPPA) cranial and caudal to the injury site change after an acute SCI with subsequent thecal occlusion and decompression.
  
  
  BACKGROUND
  Lowering intrathecal pressure via CSF drainage is currently instituted to prevent ischemia-induced SCI during thoracoabdominal aortic aneurysm surgery and was recently investigated as a potential intervention for acute traumatic SCI. However, in SCI patients, persistent extradural compression commonly occludes the subarachnoid space. This may generate a CSFP differential across the injury site, which cannot be appreciated with lumbar catheter pressure measurements.
  
  
  METHODS
  Anesthetized pigs were subjected to an acute contusive SCI at T11 and 8 hours of sustained compression (n = 12), or sham surgery (n = 2). CSFP was measured cranial and caudal to the injury site, using miniature pressure transducers, during compression and for 6 hours after decompression.
  
  
  RESULTS
  The cranial-caudal CSFP differential increased (mean, 0.39 mm Hg/h), predominantly due to increased cranial pressure. On decompression, cranial CSFP decreased (mean, -1.16 mm Hg) and caudal CSFP increased (mean, 0.65 mm Hg). The CSFP differential did not change significantly after decompression. Cranial CSFPPA was greater than caudal CSFPPA, but this differential did not change during compression. On decompression, the caudal CSFPPA increased in some but not all animals.
  
  
  CONCLUSIONS
  Although extradural compression exists at the site of injury, lumbar CSFP may not accurately indicate CSFP cranial to the injury. Decompression may provide immediate, though perhaps partial, resolution of the pressure differential. CSFPPA was not a consistent indicator of decompression in this animal model. These findings may have implications for the design of future clinical protocols in which CSFP is monitored after acute SCI.
authors.affiliation: Orthopaedic and Injury Biomechanics Laboratory, Departments of Mechanical Engineering and Orthopaedics, University of British Columbia, Vancouver, British Columbia, Canada. claire.jones@alumni.ubc.ca
authors.forename: Claire F
authors.initials: CF
authors.lastname: Jones
authors.forename: Robyn S
authors.initials: RS
authors.lastname: Newell
authors.forename: Jae H T
authors.initials: JH
authors.lastname: Lee
authors.forename: Peter A
authors.initials: PA
authors.lastname: Cripton
authors.forename: Brian K
authors.initials: BK
authors.lastname: Kwon
mesh_terms: D000208:Acute Disease; D000818:Animals; D062186:Arterial Pressure; D015170:Cerebrospinal Fluid Pressure; D019299:Decompression, Surgical / Q000379:methods*; D004195:Disease Models, Animal; D004322:Drainage; D005260:Female; D007427:Intracranial Pressure; D008991:Monitoring, Physiologic / Q000295:instrumentation; D013117:Spinal Cord Compression / Q000134:cerebrospinal fluid / Q000503:physiopathology / Q000601:surgery*; D013119:Spinal Cord Injuries / Q000134:cerebrospinal fluid / Q000503:physiopathology / Q000601:surgery*; D013552:Swine; D013556:Swine, Miniature; D013997:Time Factors; D014160:Transducers, Pressure; D014690:Venous Pressure