In the neoplastic group, leukemias and lymphomas are the most common sources of meningeal infiltrations. In children, leukemic “meningitis” with cells (lymphoblasts or myeloblasts) in the CSF numbering in the thousands may occur. In leptomeningeal metastases (carcinomatous meningitis), neoplastic cells extend throughout the leptomeninges and involve cranial and spinal nerve roots, producing a picture of meningoradiculitis with normal or low CSF glucose values. There is also a primary CNS lymphomatous meningitis. Lymphocytic meningitis that is accompanied by cranial-nerve palsies may prove to be tuberculous if the patient is febrile and the CSF glucose is low (or even without these signs in an endemic area); it is likely to be neoplastic if the patient is afebrile and the CSF glucose is normal or mildly decreased. Concentrated cytologic preparations and tumor cell markers may permit identification of the tumor cells. Chapter 30 discusses neoplastic meningitis in detail.
Occlusion of many small cerebral blood vessels by cholesterol emboli may also excite a reaction in meningeal vessels and a pleocytosis that includes eosinophils.
In summary, the temporal history of the illness, associated clinical findings, and laboratory tests usually provide clues to the diagnosis of nonviral and chronic forms of aseptic meningitis. It is useful to keep in mind the possibility of neoplasia, HIV, tuberculosis, cryptococcosis, sarcoidosis, syphilis, borreliosis, allergic reactions, parameningeal collection, and inadequately treated bacterial meningitis—each of which presents an urgent diagnostic problem.
From the foregoing discussion, it is evident that the separation of the clinical syndromes of aseptic meningitis and encephalitis is not always clear. In some patients with aseptic meningitis, mild drowsiness or confusion may be present, suggesting cerebral involvement. The common practice is to assume that viral meningitis causes only fever, headache, stiff neck, and photophobia; if any other CNS symptoms are added, the condition is generally called meningoencephalitis. As has been emphasized, the same spectrum of viruses gives rise to both meningitis and encephalitis. It is our impression that many cases of enteroviral and practically all cases of mumps and LCM encephalopathy are little more than examples of intense meningitis in which the subpial surface of the brain is inflamed. Rarely have they caused demonstrable postmortem cerebral lesions, and surviving patients have no residual neurologic signs. Conversely, several agents, notably the arboviruses, may cause encephalitic lesions with only mild meningeal symptoms.
The core of the encephalitis syndrome consists of an acute febrile illness with evidence of various combinations of seizures, delirium, confusion, stupor or coma; aphasia, hemiparesis with asymmetry of tendon reflexes and
Babinski signs, involuntary movements, ataxia, and myoclonic jerks; and nystagmus, ocular palsies, and facial weakness. The meningitic component may be prominent, have mild manifestations such as headache, or be entirely inapparent. The spinal fluid invariably, or eventually, shows a cellular reaction and the protein is slightly elevated. Imaging studies of the brain are most often normal but may show diffuse edema or enhancement of the cortex and, in certain infections, subcortical and deep nuclear involvement as well as, in the special case of HSV encephalitis, selective damage of the inferomedial temporal and frontal lobes.