Review of experimental spinal cord injury with emphasis on the local and systemic circulatory effects.

Studies of experimental spinal cord injury began approximately 100 years ago, and since then many useful models of acute experimental spinal cord injury have been developed which stimulate many of the common types injuries in man. This review will describe some of these models and the information they have provided about the acute pathophysiological mechanisms in the injured spinal cord. There is good experimental evidence that the spinal cord suffers both a primary or mechanical injury and then a secondary injury which may worsen the prognosis for recovery. This review will emphasize the concept of the secondary injury, especially with respect to the vascular mechanisms. There is evidence from our laboratory and others to support the concept of the secondary injury and that the chief mechanism of the secondary injury is posttraumatic ischemia and infarction of the spinal cord. We have found evidence for the role of vascular mechanisms in three different injury models of acute spinal cord injury (A.S.C.I.) in three species of experimental animals. This review will describe the microangiographic and blood flow methods for assessing the microcirculation of the spinal cord after trauma. In addition, to these local vascular effects, this review will also describe the systemic vascular effects of A.S.C.I. which cause the neurogenic shock in this condition. It is our hypothesis that these local and systemic vascular effects are principal causes of the secondary injury leading to posttraumatic ischemia and infarction of the spinal cord after A.S.C.I. Furthermore, it is our hypothesis that early treatment of these microcirculatory changes and neurogenic shock can lead to improved recovery after A.S.C.I.