Experimental Study Of Chronic Thoracolumbar Cord Injury By Method Of The Progressive Screw Compression In Rats

[Backgrounds] Chronic mechanical compression of spinal cord is a commoncause of neruological disablity among the elderly, resluting in myelopathy, whichis commonly caused by disc herniation, calcification of posterior longitudinalligaments, ossification of yellow ligaments, tumor and spinal deformities. Chronicmechanical compression myelopathy impairs motors and sensory functionsinsidiously and progressively. The condition of many patients remainsasymptomatic for many years, and once the disease becomes symptomatic, motorsand sensory disturbances progress with changes in the impairments. Althoughsymptoms in many patients has improved after surgical procedures, includingafter decompression and stabilization, some of them have remained unchanged orhave even deteriorated. The exact pathophysiological mechanisim of chronicspinal cord compression remains to be elucidated. That pose a big controversy tomake an early clinical treatment and time of surgical decompression.[Aims] To apply and improve the animal model of chronic spinal cordcompression caused by method of progressive screw, It was evaluated through thechange of the neurobehavior assesement, histopathology, electrophysiology, andradiology. Furthermore, the stability and possibility of the animal model wasstudied to provide experimental data for determining the surgical time ofdecompression.[Methods] forty-five adult SD rats were operated at the posterior thoracolumbar.The flat plastic screw (pitch0.05mm, diameter3mm, height9mm) was implantedon the exposed spinal cord between the T12-L1vertebrae after drilling. Corticalsomatosensory evoked potential (CSEP) was detected during the surgery. Thescrew was tightened1complete turn every week for4weeks to create differentlevel of chronic spinal cord compression. Forty-five SD rats were randomlydivided into surgery group (40), which was subdivided into1week group,2weekgroup,3week group and4week group, and control group (5). In the control group, the laminae was drilled while no screw was implanted. After surgery, BBBscore was performed weekly. At8week, all the animals were harvested andexamined histologically(H-E and Luxol fast blue staining). In addition, theMicro-CT was scanned and three parameters were measure including the CTheigh on axial images, total canal cross-sectional area and CT compression ratioon mid-sagittla images.[Results] Progressive motor dysfunction of the lower limbs was seen at theoperative group. BBB score was reducing. The score in the3week and4weekgroups at the same time point was significantly lower than the other two groups.Decreased amplitude in the1week and2week surgery groups changedsignificantly at30minutes after surgery(P<0.05). Delayed latency period in the3week and4week groups was longer than was before surgery (P<0.05). Severity ofspinal cord compression was progressive in Mirco-CT scan. The CT compressionrate at mid-sagittal images, the CT height and total canal cross-sectional area weresignificantly different among the groups(P<0.05). The number of motor neuronsdecreased progressive in gray matter, demyelination and cavitation changes werenoted in white matter in the surgery group.[Conclusion] An ideal animal model of chronic spinal cord compression wascreated by method of the progressive screw compression. The changes ofamplitude were more sensitive instead of latency. However, at the later stage ofthe chronic compression, delayed latency was a reliable parameter. The spinalcord compression was more three-dimensionally and spatially observed throughMicro-CT. There were great combinations and interactions among the dysfuctionsof spinal cord, the degree of canal compression, the changes of CSEP,neurobehavior assesement and histopathology, which will provide experimentaldata for determine the time of surgical decompression.