The CSF glucose concentration is normally in the range of 45 to 80 mg/dL, that is, about two-thirds of that in the blood (0.6 to 0.7 of serum concentrations). Higher levels parallel the blood glucose in this proportion; but with marked hyperglycemia, the ratio of CSF to blood glucose is reduced (0.5 to 0.6). With extremely low serum glucose, the ratio becomes higher, approximating 0.85. In general, CSF glucose values below 35 mg/dL are abnormal. After the intravenous injection of glucose, 2 to 4 h is required to reach equilibrium with the CSF; a similar delay follows the lowering of blood glucose. For these reasons, samples of CSF and blood for glucose determinations should ideally be drawn simultaneously in the fasting state or the serum should be obtained a few hours before the puncture but (this is often not practical). Low values of CSF glucose (hypoglycorrhachia) in the presence of pleocytosis usually indicate bacterial, tuberculous, or fungal meningitis, although similar reductions are observed in some patients with widespread neoplastic infiltration of the meninges and occasionally with sarcoidosis, subarachnoid hemorrhage (usually in the first week) and in chemically induced inflammation.
For a long time it was assumed that in meningitis the bacteria lowered the CSF glucose by their active metabolism, but the fact that the glucose remains at a subnormal level for 1 to 2 wk after effective treatment of the meningitis suggests that another mechanism is operative. Theoretically at least, an inhibition of the entry of glucose into the CSF, because of an impairment of the membrane transfer system, can be implicated. As a rule, viral infections of the meninges and brain do not lower the CSF glucose, although low glucose values have been reported in a small number of patients with mumps meningoencephalitis, and rarely in patients with herpes simplex and zoster infections. The almost invariable rise of CSF lactate in purulent meningitis probably suggests that some of the glucose is undergoing anaerobic glycolysis by polymorphonuclear leukocytes and by cells of the meninges and adjacent brain tissue.
CSF testing for cryptococcal surface antigen has become widely available as a rapid method if this infection is suspected. On occasion, a false-positive reaction is obtained in the presence of high titers of rheumatoid factor or antitreponemal antibodies, but otherwise the test is diagnostically more dependable than the formerly used India ink preparation. The nontreponemal antibody tests of the blood—Venereal Disease Research Laboratories (VDRL) slide flocculation test and rapid plasma reagin (RPR) agglutination test—can also be performed on the CSF. When positive, these tests are usually diagnostic of neurosyphilis, but false-positive reactions may occur with collagen diseases, malaria, and yaws, or with contamination of the CSF by seropositive blood. Tests that depend on the use of treponemal antigens, including the Treponema pallidum immobilization test and the fluorescent treponemal antibody test, are more specific and assist in the determination of false-positive RPR and VDRL reactions. The value of CSF examinations in the diagnosis and treatment of neurosyphilis is discussed in Chap. 31, but testing of CSF for treponemal antibodies is no longer routine. Serologic tests for the Lyme spirochete are useful in circumstances of suspected infection of the CNS with this agent.