• Anna V Leonard, Emma Thornton, and Robert Vink.
• 1 Adelaide Centre for Neuroscience Research, School of Medical Sciences The University of Adelaide , South Australia, Australia .
• J. Neurotrauma. 2015 Mar 15;32(6):397-402.

AbstractRaised intrathecal pressure (ITP) after traumatic spinal cord injury (SCI) is a critically important aspect of injury development that may result in significantly greater tissue damage and worsened functional outcome. Raised ITP is caused by the accumulation of blood and/or water (edema), and while their occurrence after traumatic SCI has been well established, the relative contribution of both processes to the development of ITP after SCI has not yet been determined. Accordingly, the current study investigates the temporal profile of raised ITP after traumatic SCI in relation to both hemorrhage and edema development. A closed balloon compression injury was induced at T10 in New Zealand White rabbits. Animals were thereafter assessed for spinal water content (edema), ITP, lesion and hemorrhage volume, and albumin immunoreactivity from 5 h to 1 week post-SCI. Early increases in ITP at 5 h post-injury were associated with significant increases in blood volume. ITP, however, was maximal at 3 days post-SCI, at which time there was an associated significant increase in edema that persisted for 1 week. We conclude that raised ITP after traumatic SCI is initially driven by volumetric increases in hemorrhage, while edema becomes the primary driver of ITP at 3 days post-injury.

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