Somatosensory- and motor-evoked potentials in a rabbit model of spinal cord ischemia and reperfusion injury

• Published in: Spine (Philadelphia, Pa. 1976) Pa. 1976), 1997-05, Vol.22 (9), p.1013-1017
• Main Authors: ZHAO, M, ZHANG, Y, LIU, L, LIU, Y, LIAO, W
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Cerebrospinal fluid. Meninges. Spinal cord; Disease Models, Animal; Evoked Potentials, Motor - physiology; Evoked Potentials, Somatosensory - physiology; Ischemia - physiopathology; Male; Medical sciences; Nervous system (semeiology, syndromes); Neurology; Rabbits; Reperfusion Injury - physiopathology; Spinal Cord - blood supply
• ISSN: 0362-2436; 1528-1159
• DOI: 10.1097/00007632-199705010-00014

Occlusion of the infrarenal abdominal aorta was applied to adult rabbits, which induced spinal cord ischemia, followed by disocclusion and reperfusion. Cortical somatosensory- and motor-evoked potentials were monitored continuously up to 24 hours and correlated to hind limb motor and sensory status. To investigate cortical somatosensory-, and motor-evoked potentials in the rabbit model of spinal cord ischemia and reperfusion injury, especially their changes during reperfusion and their relationship to hind limb motor and sensory function. Various evoked potentials have been widely studied in neurologic prognosis of spinal cord ischemia. Little information is available from previous studies to correlate cortical somatosensory- and motor-evoked potentials with secondary paraplegia occurring during the reperfusion phase. Acute spinal cord ischemia was induced in eight anesthetized rabbits by occlusion of the infrarenal abdominal aorta just beneath left renal artery for 40 minutes. Cortical somatosensory-evoked potentials, elicited by stimulating the posterior tibial nerve and recorded at the skull surface corresponding to sensory projection area, and motor-evoked potentials, elicited by stimulating the skull surface corresponding to the motor projection area and recorded at L4 lamina of the vertebral arch, were monitored immediately before and at different time points during ischemia and reperfusion up to 24 hours after disocclusion. Hind limb motor and sensory functions were evaluated and correlated with cortical somatosensory- and evoked-potentials. Cortical somatosensory-evoked potentials disappeared gradually after the start of occlusion and reappeared during reperfusion. Motor-evoked potentials did not change significantly during occlusion, but deteriorated after disocclusion; they correlated well with hind limb motor and sensory status. Reperfusion injuries to the spinal cord might occur in the rabbit model after disocclusion. Cortical somatosensory-evoked potentials seemed to be a very sensitive index for spinal cord ischemia, whereas motor-evoked potentials correlated well with the course of reperfusion injuries after disocclusion and reflected long-term follow-up hind limb motor function better than cortical somatosensory-evoked potentials.