To the Editor:—
The animal study on postischemic spinal cord cooling by Kakinohana et al. 1touches on important therapeutic implications concerning ischemic injury to the spinal cord. Their study indicated that a very narrow window of 0–10 min exists after aortic balloon occlusion for hypothermia to be efficacious. A clinical study by Davison et al. 2on epidural cooling during thoracoabdominal aneurysm repair indicated the feasibility of using this method during the surgical procedure.
It is important to point out that the therapeutic window for experimental traumatic spinal cord injury, on the other hand, is considerably longer. In 1968, Albin et al. 3demonstrated functional recovery after spinal cord injury (weight-drop technique) in the subhuman primate when localized cooling (to 10.0°C in spinal cord) was instituted 4 h after trauma and conducted for 3 h. All of the controls without hypothermia developed permanent hind leg paraplegia. Kakinohana et al. noted the positive correlation between the paravertebral muscle temperature and that of the lumbar intrathecal space at the L3 level. Because the anatomic target of both ischemia and hypothermia is the spinal cord itself, do the authors have any data indicating the order of magnitude of the decrease in spinal cord temperature per se ? The decrease in spinal cord temperature seems to be inferred because the authors measured temperature in the lumbar intrathecal space, reflecting cerebrospinal fluid temperature and not that of intrinsic spinal cord. Might it be possible that the therapeutic window could be enlarged if intrinsic spinal cord temperature were reduced to lower levels? Our studies in various species 4,5indicate that localized spinal cord perfusion cooling has no deleterious effect functionally or histologically even when cord temperature was decreased to < 10°C for at least 3 h.