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  • By Author: Al-Mefty, Ossama x
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H. Louis Harkey, Ossama Al-Mefty, Isam Marawi, Dudley F. Peeler, Duane E. Haines and Lon F. Alexander

✓ Twelve dogs developed a delayed onset of neurological abnormalities from chronic cervical cord compression that was characteristic of myelopathy. The animals were divided into two groups and matched according to degree of neurological deficit. Six animals underwent decompression through removal of the anteriorly placed compressive device. Throughout the experiment, serial neurological examinations and somatosensory evoked potential studies were performed on each animal. Spinal cord blood flow measurements were obtained during each surgical procedure and at sacrifice. Magnetic resonance images were obtained after compression and before sacrifice.

All animals in the decompressed group showed significant neurological improvement after decompression; no spontaneous improvement in neurological function was seen in the compressed group. On pathological examination, irreversible changes including large motor neuron loss, necrosis, and cavitation were seen in four of the animals in the decompressed group and five in the compressed group.

Cervical spondylotic myelopathy in humans is known to respond to decompression; this study provides further evidence that this animal model for chronic compressive cervical myelopathy accurately reflects the disease process seen in humans.

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Ossama Al-Mefty, H. Louis Harkey, Isam Marawi, Duane E. Haines, Dudley F. Peeler, Harvey I. Wilner, Robert R. Smith, Howard R. Holaday, Joseph L. Haining, William F. Russell, Brent Harrison and Troy H. Middleton

✓ A canine model simulating both cervical spondylosis and its results in delayed progressive myelopathy is presented. This model allowed control of compression, an ongoing assessment of neurological deficits, and evaluation using diagnostic images, frequent electrophysiological tests, local blood flow measurements, and postmortem histological examinations. Subclinical cervical cord compression was achieved in 14 dogs by placing a Teflon washer posteriorly and a Teflon screw anteriorly, producing an average of 29% stenosis of the spinal canal. Four dogs undergoing sham operations were designated as controls. Twelve of the animals 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 clearance method showed a significant transient increase in blood flow immediately after compression and a decrease before sacrifice. Somatosensory evoked potential studies indicated progressive deterioration during the period of compression. Magnetic resonance images revealed intramedullary changes. Histological studies showed abnormalities overwhelmingly within the gray matter, including changes in vascular morphology, loss of large motor neurons, necrosis, and cavitation. Axonal degeneration and obvious demyelination were rarely seen. The most profound morphological changes occurred at the site of greatest compression. It is proposed that a momentary arrest of microcirculation occurs during extension of the neck because of loss of the reserve space in the compromised spinal canal. This microcirculatory disturbance is predominant in the watershed area of the cord and mainly affects the highly vulnerable anterior horn cells, leading to neuronal death, necrosis, and eventual cavitation at the junction of the dorsal and anterior horns. Additional supportive evidence of this hypothesis was derived from the literature.