| Cauda equina injury is comprehensive in clinical disease or injury of lumbar spine. The causes for cauda equine injury can be diverse, but most of them are related to direct compression leading to not only the damage of the cauda equine, but also the injury of sacral nerve. The cauda equina consists of peripheral nerves, both motor and sensory, below the level of the conus medullaris and within the spinal canal. The conus medullaris contains the myelomeres of the five sacral nerve roots. damage to any part of this structure may result in the cauda equina syndrome (CES). The clinical symptoms of CES are manifest by low back pain, sciatica, saddle and perineal hypoesthesia or anesthesia, a decrease in anal tone, absent ankle, knee, or bulbocavernous reflexes, and bowel and bladder dysfunction. Judicious physical examination and prompt diagnosis remain the cornerstones of effective management of this syndrome, but when it does occur it can lead to poor outcomes with significant legal implications. Expeditious surgery is a significant factor that can affect outcome in this syndrome. Timing of surgical intervention, attack mechanism, early diagnosis can all affect outcome of CES. Part of patients with cauda equina injury, however, contract other severe complications, which result in infeasibility of timely surgical intervention.Therefore, we should find some remedial measures to improve it.Neurotrophin-3/neurotrophic factor 3 is the important member of neurotrophin family, which can prevent embryonic and postnatal motoneuron death, maintain neuron survival, promote reparation and regeneration after nervous injury, and regulate synapse activity of neuron. Experiment in vitro indicate NT-3 has satisfactory effect on neuronal survive and axonal growth, however, the effect research in vivo is less comparatively.In this study, we establish an animal model of acute compressed cauda equina injury of a close similarity with the clinical situation, and detect the level of NT-3 in sacral cord at different times after operation, so that a way of rejection of apoptosis of sacral neurons after cauda equina injury was confirmed and data would be helpful for clinical application.1. Establishment of acute compressed cauda equina injury model in the ratObjective: To establish an animal model of acute compressed cauda equina injury in the rat. Methods:Thirty-six rats were randomly divided into control group (Group A), 1 d experimental group (Group B), 7 d experimental group (Group C) and 21 d experimental group (Group D), 9 rats in each group. Metal screws without tip were used to drill into vertebral canal through the lamina of L6 sticking the spinous processes tightly in experimental groups. At different time (1, 7, 21 d) after operation, animal's comprehensive evaluation was carried out in combined behavioral score(CBS), latency changes of spinal cord evoked potential(SCEP) and observation of the morphological changes in the sacral cords using H-E staining under light microscopes. Results:H-E staining showed the form of anterior horn cells changed significantly after the screw was drilled into the vertebral canal. At the different time points (1, 7, 21 d ) after operation, combined behavioral score (17.89±1.27, 9.78±1.30, 9.33±1.41) and SCEP latency (ms, 4.29±0.51, 4.35±0.54, 4.91±0.50) were significantly different from those in the control group (P<0.05). Conclusion: Techniques for creating this acute compressed cauda equina injury model are simple and can be highly replicable. It provides an available basis for the further study on acute compressed cauda equina injury.2. The change on the expression of NT-3 of the conus medullaris following cauda equina compressed injury in ratsObjective: To observe of expression of NT-3 of the conus medullaris neuron with cauda equina compressed injury. Methods: Replicating acute compressed cauda equina injury model in the rat, at the followtimes (1d, 7d, 21d), animals were given a lethal overdose of pentobarbital and perfused Cardiac with NS and 40 g/L paraformaldehyde. The conus medullaris was removing. Samples were put in fixative overnight, and serial 5μm coronal sections were immunohistochemistry: ABC method and microscope were used to observe the expression. Result: NT-3 positive products were mainly distributed in cytoplasm. The 7d and 21d groups were significantly higher than the normal and 24 h groups on the NT-3 positive neurons counting in the ventral horn following cauda equine injury(P<0.01), only 21 d group was significantly higher than the normal group in the dorsal horn (P>0.01). Conclusion: The number of NT-3 positive neurons is increased in the conus medullaris ventral and dorsal horns following cauda equina and the increased endogenous NT-3may play a role in early repairment of nerve injury. |
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