"The cause is attributed to rapid cord expansion with acutely increased blood supply to the affected area following surgical decompression of a chronically compressed part of the spinal cord (e.g. due to tumour). These sudden changes are believed to result in a disruption in the blood-brain barrier (BBB) and the blood–spinal cord barrier (BSB). Such breakdown of the BBB and BSB may lead to increased permeability of inflammatory factors, resulting in neuronal apoptosis 1-5. The other well-established consequence of reperfusion is that significant amounts of free radical oxygen species (oxidants) are generated during the reperfusion, and thus, oxidative stress plays a crucial role in neural elements damage."
"The cause is attributed to rapid cord expansion with acutely increased blood supply to the affected area following surgical decompression of a chronically compressed part of the spinal cord (e.g. due to tumour). These sudden changes are believed to result in a disruption in the blood-brain barrier (BBB) and the blood–spinal cord barrier (BSB). Such breakdown of the BBB and BSB may lead to increased permeability of inflammatory factors, resulting in neuronal apoptosis 1-5. The other well-established consequence of reperfusion is that significant amounts of free radical oxygen species (oxidants) are generated during the reperfusion, and thus, oxidative stress plays a crucial role in neural elements damage."
"The cause is attributed to rapid cord expansion with acutely increased blood supply to the affected area following surgical decompression of a chronically compressed part of the spinal cord (e.g. due to tumour). These sudden changes are believed to result in a disruption in the blood-brain barrier (BBB) and the blood–spinal cord barrier (BSB). Such breakdown of the BBB and BSB may lead to increased permeability of inflammatory factors, resulting in neuronal apoptosis 1-5. The other well-established consequence of reperfusion is that significant amounts of free radical oxygen species (oxidants) are generated during the reperfusion, and thus, oxidative stress plays a crucial role in neural elements damage."
"The cause is attributed to rapid cord expansion with acutely increased blood supply to the affected area following surgical decompression of a chronically compressed part of the spinal cord (e.g. due to tumour). These sudden changes are believed to result in a disruption in the blood-brain barrier (BBB) and the blood–spinal cord barrier (BSB). Such breakdown of the BBB and BSB may lead to increased permeability of inflammatory factors, resulting in neuronal apoptosis 1-5. The other well-established consequence of reperfusion is that significant amounts of free radical oxygen species (oxidants) are generated during the reperfusion, and thus, oxidative stress plays a crucial role in neural elements damage."