EXPERIMENTAL CHRONIC COMPRESSIVE CERVICAL MYELOPATHY

A canine model simulating both cervical spondylosis and its results in delayed progressive myelopathy is presented. This model allowed contr ol of compression, an ongoing assessment of neurological deficits, and evaluation using diagnostic images, frequent electrophysiological tes ts, local blood flow measurements, and postmortem histological examina tions. Subclinical cervical cord compression was achieved in 14 dogs b y placing a Teflon washer posteriorly and a Teflon screw anteriorly, p roducing an average of 29% stenosis of the spinal canal. Four dogs und ergoing sham operations were designated as controls. Twelve of the ani mals undergoing compression developed delayed and progressive clinical signs of myelopathy, with a mean latent period to onset of myelopathy of 7 months. Spinal cord blood flow studies using the hydrogen cleara nce method showed a significant transient increase in blood flow immed iately after compression and a decrease before sacrifice. Somatosensor y evoked potential studies indicated progressive deterioration during. the period of compression. Magnetic resonance images revealed intramed ullary changes. Histological studies showed abnormalities overwhelming ly within the gray matter, including changes in vascular morphology, l oss of large motor neurons, necrosis, and cavitation. Axonal degenerat ion and obvious demyelination were rarely seen. The most profound morp hological changes occurred at the site of greatest compression. It is proposed that a momentary arrest of microcirculation occurs during ext ension of the neck because of loss of the reserve space in the comprom ised spinal canal. This microcirculatory disturbance is predominant in the watershed area of the cord and mainly affects the highly vulnerab le anterior horn cells, leading to neuronal death, necrosis, and event ual cavitation at the junction of the dorsal and anterior horns. Addit ional supportive evidence of this hypothesis was derived from the lite rature.