In a group of such patients studied at the Mayo Clinic, 33 of 39 underwent a natural resolution and 2 died; 14 were still symptomatic at the time of the report (Smith and Aksamit). In another series from New Zealand of 83 patients, Anderson and Willoughby ultimately found tuberculosis to be the most common identifiable cause, a smaller number being accounted for by neoplastic and cryptococcal meningitis; in fully one-third of the patients, no cause could be established. Charleston and colleagues reported a subgroup of these patients who were responsive to steroids; in only 7 of 17 patients could medication eventually be withdrawn without recurrence; 4 required treatment indefinitely and the remaining 6 died after many months or years. The outcome and response to steroids in our patients have been much the same. These series excluded chemical or irritative meningitis, which should be considered if there had been spinal surgery or infusion of even apparently innocuous substances into the spinal space.
The special problem of chronic neutrophilic meningitis has been mentioned in the preceding chapter in relation to Nocardia, Aspergillus, Actinomyces, or certain Mycobacterium species; other causes include coccidioidomycosis, histoplasmosis, and blastomycosis, (see Peacock, cited in Chap. 31). Also of interest is an unusual group of meningitides with disproportionate numbers (to peripheral blood) of eosinophils. This includes parasitic disorders, Hodgkin lymphoma infiltrating the meninges, widespread cholesterol emboli, and sometimes, with allergic meningitis associated with nonsteroidal anti-inflammatory drugs such as ibuprofen.
A reasonable approach in patients with chronic meningitis is to repeat the lumbar puncture several times to obtain all cultures including for fungi and cytology of CSF, using markers to detect uniform populations of B and T lymphocytes and tumor cells, biochemical tests that are sensitive to neoplastic meningitis (such as b2-microglobulin, lactate dehydrogenase [LDH]), and PCR amplification of herpesviruses, serologic tests mainly for HIV, syphilis, coccidioidomycosis, Brucella, and Lyme disease. MRI of the brain and spinal cord with gadolinium should also be performed to detect parameningeal collections. If hydrocephalus develops, it should be managed along the lines described in Chap. 29.
A trial of broad-spectrum antibiotics may be justified until cultures are negative, although we have had limited success in our last several patients. We sometimes resort to a biopsy of the meninges over the frontal convexity or at a site that demonstrates infiltration or marked enhancement if the diagnosis has not been clarified in 6 to 12 months or if febrile meningitis persists for more than several weeks, but examination of this tissue has proved to be of limited value. In Anderson et al’s (1995) series, mentioned earlier, biopsy yielded a diagnosis in 5 of 25 patients. Finally, if bacterial and fungal infection, including tuberculosis, has been reasonably excluded, corticosteroids may be administered for several weeks and then tapered while observing the patient and resampling the CSF.