Abstract
There are two mechanisms of damage to the spinal cord after acute spinal cord injury(SCI): the primary mechanical injury and a secondary injury due to one or more additional damaging processes initiated by the primary injury (Collins, 1983; Sandier and Tator, 1976a,b). Many pathophysiological processes are involved in the secondary injury mechanisms including vascular, electrolyte and biochemical changes, edema and loss of energy metabolism (Tator and Fehlings, 1991). Of the several postulated mechanisms, the vascular theory has considerable supporting evidence based on biochemical, pathological, angiographic, blood blow and therapeutic studies. Acute spinal cord trauma causes numerous vascular changes which may be divided into systemic and local effects. Several studies have shown that acute SCI produces immediate damage to the microvasculature of the cord followed by a secondary injury to these vessels, and this combination induces spinal cord ischemia which may be progressive (Tator, 1991 and 1994; Dohrmann et al., 1971; Hall et al., 1989). One of the most direct methods of observing the spinal cord ischemia caused by SCI is to measure spinal cord blood flow (SCBF).
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Li, S., Tator, C.H. (1998). Spinal cord blood flow and evoked potentials as outcome measures for experimental spinal cord injury. In: Stålberg, E., Sharma, H.S., Olsson, Y. (eds) Spinal Cord Monitoring. Springer, Vienna. https://doi.org/10.1007/978-3-7091-6464-8_14
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