It has been known for over 100 years that the cerebrospinal fluid contains a reducing substance, for nearly 75 years that this material consists predominantly of glucose, and for almost 50 years that glucose disappears from the spinal fluid in purulent meningitis. Subsequently it has been demonstrated repeatedly that the C.S.F. sugar may also be diminished in tuberculosis, syphilis, brain abscess, cryptococcosis, sarcoidosis, carcinomatosis of the leptomeninges, and subarachnoid hemorrhage. Despite this plethora of clinical data, the reason for hypoglycorrhachia in one or all of these states has been the subject of long debate and extensive study.* This analysis will deal primarily with bacterial meningitis since it seems to be the prototype of diseases in which a fall in C.S.F. sugar occurs.This does not imply, however, that the mechanisms governing the decrease in glucose in one disease are the same as in another.Normally the level of glucose in the C.S.F. closely parallels that in the blood. This has been corroborated in artificially induced hyper-and hypoglycemia in ani¬ mals and man. In bacterial, including tuberculous, and fungal meningitis this rela¬ tionship is disrupted and the C.S.F. sugar reaches abnormally low levels. In most viral meningitides, however, it remains within the normal range. This suggested to many early investigators that the bacteria were instrumental in producing glycolysis in the spinal fluid and that in their absence this phenomenon did not take place. Some doubt was shed upon this interpretation, however, by the inconsistent results obtained when a variety of bacterial species were incubated in sterile spinal fluid in vitro.24 Under these conditions either no glycolysis occurred or the number of bac¬ teria necessary to produce a fall in sugar far exceeded that usually seen in clinical infections. Employing pneumococci, we have observed that these organisms con-The reader is referred to a recent review for a summary of the older literature and pertinent references.