OBJECTIVE: To evaluate the effect of expansion speed on chronic compressive spinal cord injury in the rat. METHODS: Thirty-six Sprague-Dawley rats were divided into four groups: a control group, a group receiving compressor in the C5-C6 epidural space with instant compression (group 1), and two other groups receiving water-absorbing polyurethane polymer sheets with two expansion speeds, which reached maximum volume in 2 h (group 2: fast expansion) or 24 h (group 3: slow expansion). A C6 laminectomy was performed in the control group. Neurological function, MRI, large motoneuron number in the ventral horn, and myelin staining intensity in the posterior funiculus were evaluated. RESULTS: In the instant compression group, compression was confirmed on T2-weighted images by a hypointense signal change in the intramedulla. In the gradual compressive injury groups, large motoneuron number (p<0.001), but not myelin staining intensity, was significantly decreased in both the fast and slow expansion groups compared with the instant compression group. However, there was no difference in Basso Beattie Bresnahan score, cord distortion in T2-weighted image, large motoneuron numbers, or myelin staining between the fast and slow expansion groups. CONCLUSION: Instant spinal cord compression caused acute injury. Gradual expansion compression induced reliable pathology and MRI characteristics consistent with chronic compressive spinal cord injury. The speed of expansion is not a significant problem for establishing a reliable model if the chronic compression is induced by gradual expansion.
OBJECTIVE: To evaluate the effect of expansion speed on chronic compressive spinal cord injury in the rat. METHODS: Thirty-six Sprague-Dawley rats were divided into four groups: a control group, a group receiving compressor in the C5-C6 epidural space with instant compression (group 1), and two other groups receiving water-absorbing polyurethane polymer sheets with two expansion speeds, which reached maximum volume in 2 h (group 2: fast expansion) or 24 h (group 3: slow expansion). A C6 laminectomy was performed in the control group. Neurological function, MRI, large motoneuron number in the ventral horn, and myelin staining intensity in the posterior funiculus were evaluated. RESULTS: In the instant compression group, compression was confirmed on T2-weighted images by a hypointense signal change in the intramedulla. In the gradual compressive injury groups, large motoneuron number (p<0.001), but not myelin staining intensity, was significantly decreased in both the fast and slow expansion groups compared with the instant compression group. However, there was no difference in Basso Beattie Bresnahan score, cord distortion in T2-weighted image, large motoneuron numbers, or myelin staining between the fast and slow expansion groups. CONCLUSION: Instant spinal cord compression caused acute injury. Gradual expansion compression induced reliable pathology and MRI characteristics consistent with chronic compressive spinal cord injury. The speed of expansion is not a significant problem for establishing a reliable model if the chronic compression is induced by gradual expansion.