STUDY DESIGN: Cervical spondylotic myelopathy (CSM) represents the most commonly acquired cause of spinal cord dysfunction among individuals over 55 years old. The pathophysiology of the disease involves static and dynamic mechanical factors, which are the result of chronic degeneration. The clinical course of the disease remains unpredictable. In the past, many experimental animal models have been developed to study the cellular and molecular mechanisms underlining the pathophysiology of the disease. OBJECTIVES: To create a new animal model of CSM, which will reproduce the temporal course of the disease and the local microenvironment at the site of spinal cord compression. METHODS: We performed posterior laminectomy to New Zealand rabbits at the level of C7, and a thin sheet (5-7 μm) of aromatic polyether was implanted with microsurgical technique at the epidural space underneath C5-C6 laminae. Motor function evaluation was performed after the operation and once a week thereafter. RESULTS: After 20 weeks, the animals were killed, and the histological evaluation of spinal cord at the site of compression above and below it, using eosin hematoxylin, immonohistochemistry and Kluver-Barrera techniques reveals axonal swelling and demyelination, interstitial edema and myelin sheet fragmentation. Moreover, histological evaluation of C5 and C6 laminae reveals osteophyte formation. CONCLUSION: We believe that this CSM model reproduces the temporal evolution of the disease and creates a local microenvironment at the site of spinal cord compression, which shares the same characteristics with that of human disease.
STUDY DESIGN: Cervical spondylotic myelopathy (CSM) represents the most commonly acquired cause of spinal cord dysfunction among individuals over 55 years old. The pathophysiology of the disease involves static and dynamic mechanical factors, which are the result of chronic degeneration. The clinical course of the disease remains unpredictable. In the past, many experimental animal models have been developed to study the cellular and molecular mechanisms underlining the pathophysiology of the disease. OBJECTIVES: To create a new animal model of CSM, which will reproduce the temporal course of the disease and the local microenvironment at the site of spinal cord compression. METHODS: We performed posterior laminectomy to New Zealand rabbits at the level of C7, and a thin sheet (5-7 μm) of aromatic polyether was implanted with microsurgical technique at the epidural space underneath C5-C6 laminae. Motor function evaluation was performed after the operation and once a week thereafter. RESULTS: After 20 weeks, the animals were killed, and the histological evaluation of spinal cord at the site of compression above and below it, using eosin hematoxylin, immonohistochemistry and Kluver-Barrera techniques reveals axonal swelling and demyelination, interstitial edema and myelin sheet fragmentation. Moreover, histological evaluation of C5 and C6 laminae reveals osteophyte formation. CONCLUSION: We believe that this CSM model reproduces the temporal evolution of the disease and creates a local microenvironment at the site of spinal cord compression, which shares the same characteristics with that of human disease.
Authors: Paula Martin-Vaquero; Ronaldo C da Costa; Matthew J Allen; Sarah A Moore; Jeremy K Keirsey; Kari B Green Journal: Spine (Phila Pa 1976) Date: 2015-05-01 Impact factor: 3.468