Intracanal pressure in compressive spinal cord injury: reduction with hypothermia.

Most cases of human spinal cord injury (SCI) 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 canal occlusion and to determine the relationship between raised intracanal pressure and neurological outcome. We also aimed to establish whether hypothermia was able to reduce raised intracanal pressure. We demonstrate that, following SCI in F344 rats, local intracanal pressure remains near normal until canal occlusion 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% canal occlusion, 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% canal occlusion or those undergoing immediate decompression). We further demonstrate that hypothermia is an effective therapy to control raised intracanal pressure, rapidly reducing elevated intracanal pressure accompanying critical (45%) canal occlusion to near normal. Overall these data indicate that following SCI 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 hypothermia, which may be a useful therapy to emergently decompress the spinal cord prior to surgical decompression.

Hypothermia prior to decompression: buying time for treatment of acute spinal cord injury.

Human spinal cord injury (SCI) is usually accompanied by persistent cord compression. Experimental data demonstrate that compression of the traumatized cord results in rapid neurological decline over hours. Undertaking decompression in humans within this time frame has proved impractical, with the time to surgery in studies of urgent decompression averaging between 10 and 24 h. There is, therefore, an important need for a therapy to prevent the neurological deterioration of patients prior to decompressive surgery. The aim of this study was to determine if hypothermia prevents compressive SCI, thereby limiting neurological decline. Rats were subjected to a moderate mid-thoracic SCI and spacers were inserted to compress the spinal cord by 45%. Decompression, by removal of the spacer, was performed immediately, and at 2 or 8 h post-injury. Hypothermia (33 degrees C) was commenced in half the animals at 30 mins post-injury and maintained for 7.5 h, with the other half remaining normothermic (37.3 degrees C). Motor recovery was assessed weekly, and the volume and area of tissue damage determined at the end of the 8-week study period. The results demonstrate that hypothermia significantly improves the behavioral and histological outcome of animals undergoing 8 h of compressive injury (the primary outcome measure). The hypothermia-treated group regained weight-supported locomotion (Basso-Beattie-Bresnahan [BBB] locomotor assessment score 9.5 +/- 0.9), while the normothermic group remained severely paraparetic (BBB score 5.3 +/- 0.6; p