Abstract
PurposeThis study aimed to establish an animal model in which we can precisely displace the spinal cord and therefore mimic the chronic spinal compression of cervical spondylotic myelopathy.MethodsIn vivo intervertebral compression devices (IVCDs) connected with subcutaneous control modules (SCCMs) were implanted into the C2-3 intervertebral disk spaces of sheep and connected by Bluetooth to an in vitro control system. Sixteen sheep were divided into four groups: (Group A) control; (Group B) 10-week progressive compression, then held; (Group C) 20-week progressive compression, then held; and (Group D) 20-week progressive compression, then decompression. Electrophysiological analysis (latency and amplitude of the N1-P1-N2 wave in somatosensory evoked potentials, SEP), behavioral changes (Tarlov score), imaging test (encroachment ratio (ER) of intraspinal invasion determined by X-ray and CT scan), and histological examinations (hematoxylin and eosin, Nissl, and TUNEL staining) were performed to assess the efficacy of our model.ResultsTarlov scores gradually decreased as compression increased with time and partially recovered after decompression. The Pearson correlation coefficient between ER and time was r = 0.993 (p < 0.001) in Group B at 10 weeks and Groups C and D at 20 weeks. And ER was negatively correlated with the Tarlov score (r = -0.878, p < 0.001). As compression progressed, the SEP latency was significantly extended (p < 0.001), and the amplitude significantly decreased (p < 0.001), while they were both partially restored after decompression. The number of abnormal motor neurons and TUNEL-positive cells increased significantly (p < 0.001) with compression.ConclusionOur implantable and wireless intervertebral compression model demonstrated outstanding controllability and reproducibility in simulating chronic cervical spinal cord compression in animals.
Highlights
Cervical spondylotic myelopathy (CSM) is one of the most common diseases causing spinal cord dysfunction
The most widely accepted mechanism underlying the pathogenesis of CSM is chronic spinal cord compression, which is related to intervertebral disk herniation, bone hyperplasia, ligament hypertrophy, ossification, and others [1, 2]
One sheep in Group B had the subcutaneous control modules (SCCMs) break down 24 days after the operation, which was corrected by replacing the SCCM in a second operation on Day 26
Summary
Cervical spondylotic myelopathy (CSM) is one of the most common diseases causing spinal cord dysfunction. The most widely accepted mechanism underlying the pathogenesis of CSM is chronic spinal cord compression, which is related to intervertebral disk herniation, bone hyperplasia, ligament hypertrophy, ossification, and others [1, 2]. European Spine Journal compression models [12] All these models have common drawbacks, such as poor controllability, high risk of surgical trauma and infection, and poor reproducibility. Karadimas et al [10] simulated the pathogenesis of cervical spinal cord compression, caused by the ossification of the ligamentum flavum, by promoting local calcium and phosphorus deposition and new bone formation. The compression caused by the ossification-inducing material was not controllable, and the process of inducing ossification between different experimental animals lacked consistency and repeatability. The appearance of miniaturized, fully implantable platforms with wireless capabilities and battery-free operation makes biocompatibility and controllability possible
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
