Objective To investigate the effect of methylprednisolone sodium succinate (MP) and mouse nerve growth factor (mNGF) for injection in treating acute spinal cord injury (ASCI) and cauda equina injury. Methods Between December 2004 and December 2007, 43 patients with ASCI and cauda equina injury were treated, including 33 males and 10 females with an average age of 43 years (range, 32-66 years). Injured vertebral columns were C2 in 1 case, C4 in 5 cases, C5 in 7cases, C6 in 3 cases, T8 in 1 case, T10 in 1 case, T11 in 2 cases, T12 in 3 cases, L1 in 9 cases, L2 in 5 cases, L3 in 3 cases, L4 in 1 case, and L5 in 2 cases. All the patients had sensory disturbance and motor dysfunction at admission. The Frankel scale was used for assessment of nerve function, 5 cases were rated as Grade A, 12 as Grade B, 22 as Grade C, and 4 as Grade D before operation. In 43 patients, 23 cases were treated with MP and mNGF (group A), 20 cases with MP only (group B). There was no significant difference in general data between 2 groups (P gt; 0.05). All the patients were admitted, received drug treatment within 8 hours of injury, and were given spinal canal decompression, bone transplantation, and internal fixation within 48 hours. The neurological function score systems of American Spinal Injury Association (ASIA) were used for neurological scores before treament, at 1 week and 2 years after treatment. The scores of the activity of daily l iving (ADL) were evaluated and compared. Results All the patients achieved heal ing of incision by first intention. Forty-three cases were followed up 24-61 months with an average of 30 months. Bone graft fusion was achieved after 6-17 months, 11 months on average with stable fixation. No death and compl ications of osteonecrosis and central obesity occurred. There was no significant difference in neurological function scores and ADL scores between 2 groups before treatment (P gt; 0.05); however, the neurological function scores and ADL scores at 1 week and 2 years after treatment were higher than those before treatment (P lt; 0.01) in 2 groups. Group A had higher neurological function scores and ADL scores than group B (P lt; 0.01). At 1 week and 2 years after treatment, the improvement rates of neurological function of group A (47.8%, 11/23 and 91.3%, 21/23) were significantly higher (P lt; 0.01) than those of group B (30.0%, 6/20 and 70.0%, 14/20). Conclusion MP and mNGF play an important role in improving the neurological function in patients with ASCI and cauda equina injury.
Objective To study the changes of blood flow of the already-compressed cauda equina under dynamic burden, high frequency stimulation (HFS) and increased additional compression, and to clarify the mechanism of neurogenic intermittent claudication. Methods Thirty SD rats were divided into 5 groups, 6 in each. All groups were operated with laminectomy of the fifth lumbar verfebra. One hour after the measurement of blood flow,in 4experimental groups, the silicon sheets were inserted into the spinal canal of L4 and L6 to cause double level compression of cauda equina by 30%. Two hours after onset of compression, no dynamic burden was introduced to the subjects of the experimental group 1. Only HFS was introduced to the subjects of the experimental group 2 for 6 minutes. Both HFS and increased additional compression were introduced to the subjects of the experimental group 3 for 6 minutes. While only increased additional compression was introduced to the subjects of the experimental group 4 for 6 minutes. The subjects of control group only underwent laminectomy of the fifth lumbar vertebra and HFS 6 minutes. The blood flow of cauda equina was measured with laser Doppler flowmeter. Results In the first 2 hours, there was no significant change of cauda equina blood flow in the control group. During the time of HFS, the blood flow increased significantly to 186.4%±31.5% of initial value (Plt;0.05). In the experimental group 1, there was no blood flow change during the period of dynamic burden（110.4％±7.5％，Pgt;0.05）. After introduction of dynamic burden, there was no blood flow changes in the experimental group 2 (111.6％±17.6％，Pgt;0.05). The blood flow in the experimental group 3 decreased to 65.3%±10.7% of initial value (Plt;0.05); and the blood flow in the experimental group 4 decreased to 60.1%±9.2% of initial value (Plt;0.01). There was no significant difference between the experimental groups 3 and 4 (Pgt;0.05). Conclusion The results above show that during the period of increased impulse transmission, double level compression of cauda equina may limit the increase of blood flow, which maycause relative ischemia. If there is increased additional compression along with increased impulse transmission, the blood flow will decrease significantly, which will cause absolute ischemia.
OBJECTIVE: To study the changes of neural electrophysiology properties of cauda equina under double level compression and dynamic burdens, and to clarify the mechanisms of intermittent neurogenic claudication. METHODS: Thirty SD rats were divided into 5 groups (6 in each group). The laminectomy of L5 was performed in control group. In the experimental groups, the silicon sheets were inserted into the spinal canal of L4 and L6 to cause double level compression of cauda equina by 30%. Two hours after onset of compression, no dynamic burden was introduced in experimental group 1. Only high frequency stimulation(HFS) was introduced for 6 minutes in experimental group 2. Both HFS and additional increased compression were introduced for 6 minutes in experimental group 3. While only additional increased compression was introduced for 6 minutes in experimental group 4. After 6 minutes of dynamic burdens, all were returned to the status of static compression for another 30 minutes and then electrical examination was made. RESULTS: After 2 hours of compression, motor and sensory nerve conduction velocity (NCV) of all the four experimental groups decreased significantly (P lt; 0.05), but there was no significant difference between them. There was no significant change in the control group. There was no significant change of NCV in experimental group 1 during the last 30 minutes of experiment. NCV in the other three experimental groups decreased after introduction of dynamic burdens, especially in the experimental group 3. CONCLUSION: The above results showed that NCV of cauda equina decreased significantly under dynamic burdens during static compression. Two kinds of dynamic burdens introduced at the same time can cause more profound change than a single one.