Research Of Relationship Between The Time Of Spinal Cord Compression And Long-Term Pathophysiology

Object:spinal cord injury is very common in clinic, which cause a heavy burden to patients and society. Recently many scholars researched pathophysiology, prevention and rehabilitation of spinal cord. The treatment of spinal cord injury was one of the difficult problems that puzzled medical science. The extent of the intial damage to the spinal cord produced by a spinal cord injury depends on factors such as force of impact, cord displacement, kinetic energy of compression and acceleration. Spinal cord compression and displacement from bone fragments, ligaments or hematoma within the spinal cord may contribute to the initial damage by stimulating this secondary injury cascde. The primary injury is followed by secondary injury mechanisms that are associated with physiological, biochemical, immunological, and cellular changes in the injury cord. Mitigation of this secondary injury process by spinal cord decompression may be an important factor in the preservation of neurological function, but the time of decompression was not confirmed, the pathology, physiology and the blood flow of secondary injury was not clear. The relationship between pathology and blood flow and SEP was notclear too. We make use of the model of dogs spinal cord injury to explore the mechanism of secondary injury, analyse the pathophysiology and regional blood flow after spinal cord injury. The object of this study is to determine whether there is a relationship between the duration of sustained spinal cord compression and the extent of spinal cord injury and neurological recovery after decompression .Methods:With the somatosensory evked potentials were continuously monitored, twenty-four beagle dogs weighing 11-15kg were anesthetized with sodium thiopental (15-20mg/kg) intravenous induction. The dogs were intubated. All animals received normal 0.9% saline solution infused at lOml/kg/hr. With use of sterile technique, a laminectomy at the thirteenth thoracic segment (T13) was performed. We incise the dorsimesal skin about 5cm, separate the muscles blantedly along the spinous process. T12-L1 apeared. Cut off the spinous process of T13, get rid of vertebral lamina by bone rongeur. Pay attention to protect the dura. A hydraulic piston was suspended over the dura and attached to the transvere processes of T13. The diameter of piston was 7mm. We calculated the ratio of the cortical evoked response to stimulation of the median nerve in the upper extremity to the cortical evorked response to stimulation of the posterior tibial nerve in the lower extremity. It is necessary to use this ratio to eliminate the influence of cumulative anesthetic effects. When the amplitudes of SEP in the lower extremity were reduced by approximately 50% of thebaseline value, the position of the piston was maintained for either thiry minutes or 180 minutes. SEP were monitored during a sixty-minute recovery periods as well as twenty eight days after the injury. Funtional motor recovery was judged throughout a twenty-six day period after the injury with use of a battery of motor tasks. The volume of the lesion and damage to the tissue were assesses with histological analysis. The lacoal blood flow were measured by the radiolabelling microsphere technique.ResultsrThere was continuous decline in the ampitude of the somatosensory, which did not return until the cord was decompressed within one hour after the decompression. The dogs in thirty-minute-compression group had recovery of somatosensory evoked potentials with recovery to 63% of the baseline value at ninety minutes after decompression. Twenty-eight days after the injury, the mean amplitude of the SEP was 42% of the baseline in the thiry-minute -compression group. In contrast in 180-minute-compression group, decompression did not result in recovery of SEP either early or late.Motor test demonstrated rapid recovery of hindlimb motor funtion in the thiry-minute-compression group, but there were considerable impairment in the 180 minute-compression group. By twenty one day all ten animals remaining in the thiry minute-compression group were walking normally. Incontrast four of ten dogs remaining in the 180 minute group werecapabale of weight -bearing, although none were ever capable of walking normally. With two weeks after the injury, balance, cadence, stair-climbing were significantly better in the thiry-minute-compression group. All the animals in thirty-minute group recovered normal balance and normal cadence within twenty six day test period. Whereas none of the animals in 180-minute-compression group recovered normal balance and normal cadence. Nine of ten animals in thirty minute group recovered a normal ability to climb stair within the twenty-six-day test period, whereas none of the animal in the 180-minute group recovered normal stair-climbing ability. All dogs in the thiry-minute-compression group could walk up the inclined plane by fourteen days after injury. It took nearly twice as long (twenty-six days) for half of the dog in the 180-minute-group to be able to walk up the inclined plane.The longer duration of compression produced lesions of significantly greater volume which corresponded to the long -term functional outcome. Thiry-minute-compression group: Isolate areas of central cord necrosis were seen, the lesion volune is 13.22%. The residual neurons and white matter mainly perfect. The residul white matter was 67.70%. Myelin sheat and axon mainly perfect. Only a small part axon was disorder. 180-minute-group: a small part of gray matter was seen but anterior horn and posterior horn was incompleted. Neurons were elema rare and the residual neurons were elema and deformed. Central cord necrosis was more severe and the lesion volume...