Acute dorsal compression of the spinal cord was applied to adult cats, and magnetic resonance signal intensity, spinal cord evoked potentials, and morphologic changes of the spinal cord were examined after 5 hours.
The present study investigated the correlation of magnetic resonance signal intensity with spinal cord evoked potentials and spinal cord morphology after 5 hours of spinal cord compression in cats.
Neurologic prognosis of the injury might be predicted by an analysis of magnetic resonance signal intensity pattern. Little information is available on relationships between magnetic resonance images and functional or morphologic damage of spinal cord in acute animal experiments.
Acute dorsal compression of the spinal cord was performed in 24 anesthetized cats. After laminectomy, the L2 segment was compressed for 5 hours. Spinal cord evoked potentials were recorded by electrodes placed in the epidural space at L4, and the spinal cord was stimulated at T12. The animals were divided into four groups based on changes in the amplitude of spinal cord evoked potentials. Immediately after compression for 5 hours, magnetic resonance images were obtained. Signal intensity of the spinal cord was measured on sagittal midline images. Morphologic changes were assessed.
Spinal compression significantly increased the signal intensity of the L1, L2, and L3 segments on T2-weighted and proton density-weighted images. The increase in signal intensity was remarkable in the animals whose spinal cord evoked potentials were reduced greatly (< 40% of the control group). Histologically, edema was present in the high intensity area on T2-weighted and proton density-weighted images.
In summary, the present study documents that spinal compression causes tissue edema, which produces high signal intensity on magnetic resonance imaging. The magnetic resonance signal intensity is correlated closely with decreased amplitude of spinal cord evoked potentials.
From the *Departments of Orthopaedic Surgery and †Radiology, and the ‡Division of Neuropathology, Institute of Neurological Sciences, Faculty of Medicine, Tottori University, Yonago, Japan.
Acknowledgment date: September 12, 1994.
First revision date: January 5, 1995.
Acceptance date: March 2, 1995.
Device status category: 1.
Address reprint requests to: Toshiaki Takahashi, MD; Department of Orthopaedic Surgery; Faculty of Medicine; Tottori University; 36-1 Nishi-machi, Yonago 683; Japan