Hypoglycorrhachia

The maintenance of CSF glucose levels is controlled by several mechanisms, including glucose transport into and out of the CSF as well as glucose utilization by cells. Glucose enters the CSF through the blood-brain barrier at the choroid plexus with the help of glucose transport proteins (such as GLUT1) and can either be used by cells or exit through the arachnoid villi into the venous system 1, 19. The pathophysiology behind hypoglycorrhachia is not fully understood but is likely multifactorial. Possible contributors include decreased glucose delivery to the choroid plexus because of reduced blood flow, decreased transport across the blood-brain barrier, increased metabolism in the brain, and increased glucose transport out of the CSF into the venous system 1. While it was once thought that an increased rate of glycolysis by bacterial or immune cells was the primary cause of hypoglycorrhachia, this is no longer conventional thought1, 20, 21. 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4065645/#__ffn_sectitle