Degeneration of the corticospinal tract following portosystemic shunt associated with spinal cord infarction.

The clinicopathological aspects of a case of myelopathy that followed the creation of a surgical porto-caval shunt for hepatic cirrhosis and oesophageal varices are presented. Degeneration of the lateral corticospinal tracts associated with diffuse bilateral ischaemic changes of the spinal gray matter and proliferation of Alzheimer type 2 glia in the brain and brain stem were the most prominent findings. The association of corticospinal tract degeneration and ischaemic lesions of spinal gray matter in absence of any anatomical cause of spinal cord infarction suggests that a modification of the spinal blood flow caused by creation of portosystemic shunts might be the basic pathogenetic mechanism of this complication of severe liver disease.