The Pathophysiology of Chronic Compressive Cervical Myelopathy
Discussions about the pathophysiology of chronic compressive myelopathy are shrouded by controversy, and a number of questions about our understanding of myelopathy remain unanswered. No previous animal model has adequately reproduced the condition of humans with myelopathy, and the two primary hypotheses concerning the cause (vascular and mechanical) do not fully explain the clinical aspects of cervical spondylotic myelopathy.
To simulate the course of cervical spondylotic myelopathy in humans, we developed a canine model of cervical cord compression that produced a delayed onset of neurologic abnormalities. The cervical spines of 14 dogs were compressed both anteriorly and posteriorly. Four additional dogs underwent sham operations and served as controls. Twelve of the dogs undergoing compression eventually developed clinical signs of myelopathy; the mean latent period to the onset was seven months. These 12 animals were divided into two groups matched according to the degree of neurologic deficit. The spinal cords of six of these animals were then decompressed through removal of the anteriorly-placed device, and these dogs showed subsequent neurologic-improvement. No spontaneous improvement in neurologic function was seen in the dogs whose spinal cords remained compressed. After the animals were sacrificed, histopathologic abnormalities were seen almost exclusively within the gray matter, and included necrosis, cavitation, changes in vascular morphology, and the loss of large motor neurons. The severity of the morphologic changes correlated with the neurologic deficits. Magnetic resonance images, somatosensory evoked potentials, local blood flow measurements and microangiographic data were collected throughout the study.
In comparison to previous models, this animal model of chronic compressive cervical myelopathy more accurately reflects the disease process seen in humans, and provides a basis for a more precise theory of the pathophysiology of CSM.
