Two years after the first description of lumbar puncture by Quincke,1 Lichtheim noted the sugar content of the cerebrospinal fluid (CSF) to be decreased in bacterial meningitis.2 This observation was confirmed by other early investigators3 and, along with the demonstration of micro-organisms by smear or culture, has been recognized as the sine qua non of purulent meningitis for over 50 years. Diminution in CSF sugar to a slighter degree has been described in meningeal infections due to tubercle bacilli, yeasts, and spirochetes,4 sarcoidosis of the nervous system,5 diffuse leptomeningeal carcinomatosis6,7 and subarachnoid hemorrhage.8
Despite the unquestioned validity of these empiric observations, and the recognized importance of hypoglycorrhachia in differential diagnosis, the mechanism governing the disappearance of sugar from the CSF in any or all of these disease entities remains obscure. Cells, micro-organisms, alterations in meningeal permeability, and accelerated utilization of glucose by