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.
ObjectiveTo study the effect of combined treatment using pancreatic kinionogenase enteric-coated tab and mecobalamin injection on diabetic peripheral neuropathy (DPN) patients. MethodsWe collected 84 subjects with DPN who received treatment from January 2012 to December 2012 in our hospital, and we randomly divided them into treatment group (42 subjects, using pancreatic kinionogenase enteric-coated tab and methylcobalamin injection) and control group (42 subjects, using mecobalamine only). Subjects in the treatment group were given oral pancreatic kininogenase at 120 unit/times and 3 times/day, and methylcobalamin intravenous injection at 1 mg/day for 14 days. Subjects in the control group were only given methylcobalamin intravenous injection at 1 mg/day for 14 days. ResultsIn the treatment group, 22 subjects showed excellent, 19 subjects effective and 1 subject ineffective outcome. In the control group, 8 subjects showed excellent, 22 effective and 12 ineffective outcome. The difference between the two groups is statistically significant (P<0.01). Compared with no treatment, the nerve conduction velocity in both the two groups has been improved. The improvement in the treatment group is significantly better than that of the control group (P<0.01), and all of them had no obvious adverse reaction during the treatment. ConclusionThe combined treatment using pancreatic kinionogenase enteric-coated tab and methylcobalamin injection on DPN is better than using methylcobalamin only.