Intracanal pressure in compressive @entity1566 : reduction with XXXX .

@entity1 @entity432 @entity1566 @entity35 @entity2332
Most cases of @entity1 @entity1566 ( @entity1566 ) are accompanied by continuing cord compression. Experimentally, compression results in rapid neurological decline over hours, suggesting a rise in intracanal pressure local to the site of injury. The aim of this study was to measure the rise in local intracanal pressure accompanying progressive @entity432 and to determine the relationship between raised intracanal pressure and neurological outcome. We also aimed to establish whether @entity2332 was able to reduce raised intracanal pressure. We demonstrate that, following @entity1566 in F344 @entity35 , local intracanal pressure remains near normal until @entity432 exceeds 30% of diameter, whereupon a rapid increase in pressure occurs. Intracanal pressure appears to be an important determinant of neurological recovery, with poor long-term behavioural and histological outcomes in animals subject to 8   h of 45% @entity432 , in which intracanal pressure is significantly elevated. In contrast, good neurological recovery occurs in animals with near normal intracanal pressure (animals undergoing 8   h of 30% @entity432 or those undergoing immediate decompression). We further demonstrate that @entity2332 is an effective therapy to control raised intracanal pressure, rapidly reducing elevated intracanal pressure accompanying critical (45%) @entity432 to near normal. Overall these data indicate that following @entity1566 only limited canal narrowing is tolerated before local intracanal pressure rapidly rises, inducing a sharp decline in neurological outcome. Raised intracanal pressure can be controlled with @entity2332 , which may be a useful therapy to emergently decompress the spinal cord prior to surgical decompression.
