MECH 598/698 Seminar
Friday November 19th, 2010
8-9am, Blusson Spinal Cord Centre
Presenter: Claire Jones
Supervisor: Peter Cripton
Title: Cerebrospinal fluid pressure distribution and spinal cord morphological changes after acute spinal cord injury and subsequent surgical decompression in a large animal model: implications for the clinical and surgical management of traumatic SCI.
Abstract: My thesis has focused on the role of cerebrospinal fluid (CSF) at the instant of spinal cord injury (SCI) and in the immediate post-injury phase. We have developed a pig model of acute SCI which has human-like anatomy and physiology and is therefore suitable for studying many aspects of the biomechanical and physiological response to injury. This talk will focus on how we have used this model to study the changes in CSF pressure distribution along the spine and in the spinal cord morphology during the immediate post-injury phase. These parameters cannot currently be studied in a patient population for ethical and practical reasons. Our findings have implications for the design of clinical protocols that aim to reduce CSF pressure via lumbar CSF drainage in the acute SCI population and give some insight into the response of the spinal cord to surgical decompression. They suggest that it may be important to reduce cord swelling and increase tissue perfusion after acute SCI in order to optimize the clinical outcome.
Study 1. Lowering intrathecal pressure via CSF drainage improves neural tissue perfusion and is currently instituted for traumatic brain injury and to prevent SCI in thoracoabdominal aortic aneurysm surgery. It has recently been investigated in both animals and humans as an intervention for traumatic SCI. However, this treatment may be of limited value if the pressure thresholds measured in the lumbar region are not an accurate measure of peak CSF pressure along the spine. It is unclear how the CSF pressure and pulse pressure amplitude cranial and caudal to the injury site change after an acute SCI with subsequent subarachnoid occlusion. Using miniature pressure transducers implanted in the intrathecal space, we profiled the change in CSF pressure distribution and pulse pressure amplitude after a moderate and severe acute experimental SCI. To simulate a typical SCI patient presentation, this included eight hours of simulated compression and six hours in the decompressed state.
Study 2. The role of surgical decompression for treatment of traumatic SCI is currently a topic of debate. Following a direct surgical decompression, surgeons are often able to intra-operatively confirm that bony impingement upon the thecal sac and underlying spinal cord has been relieved. However, subsequent postoperative imaging often reveals that the cord has swollen to fill the subarachnoid space and is compressed against the dura. Little is known about the magnitude and timing of spinal cord swelling immediately after surgical decompression. Ongoing dural “compression” may attenuate the benefits of surgical decompression, and obstruction of CSF flow may have implications on spinal cord perfusion pressure. Our objective was to use ultrasound to study the morphologic response of the spinal cord and dura during the six hours immediately following surgical decompression in a large animal model of traumatic SCI.