The initial elevation of intracranial pressure and threatening temporal lobe or cerebellar herniation can be managed by the use of intravenous mannitol (or hypertonic saline) and dexamethasone, 6 to 12 mg q6h. If improvement does not begin promptly, it becomes necessary to aspirate the abscess stereotactically or remove it by an open procedure that also allows precise etiologic diagnosis by Gram stain and culture. The decision regarding aspiration or open removal of the abscess is governed by its location and the course of clinical signs and by the degree of mass effect and surrounding edema as visualized by repeated scans.
Only if the abscess is solitary, superficial, and well encapsulated or associated with a foreign body should total excision be attempted; if the abscess is deep, aspiration performed stereotactically and repeated if necessary is currently the method of choice. If the location of the abscess is such that it causes obstructive hydrocephalus, for example, in the thalamus adjacent to the third ventricle or in the cerebellum, it is advisable to remove or aspirate the mass and to drain the ventricles externally for a limited time. While it has been our practice to recommend either complete excision for posterior fossa and fungal abscesses or aspiration if they are deep, there is still a lack of unanimity as to the optimal surgical approach. Some neurosurgeons instill antibiotics into the abscess cavity following aspiration, but the efficacy of this treatment is difficult to judge.
The least satisfactory results are obtained if the patient is comatose before treatment is started; more than 50 percent of such patients in the past have died. If treatment is begun while the patient is alert, the mortality is in the range of 5 to 10 percent, and even multiple metastatic abscesses may respond. Approximately 30 percent of surviving patients are left with neurologic residua. Of these, focal epilepsy is the most troublesome. Following successful treatment of a cerebral abscess in a patient with congenital heart disease, correction of the cardiac anomaly is indicated to prevent recurrence. One may even consider closing a patent foramen ovale using interventional or open surgical methods if no other explanation for the abscess is apparent.
There are many infectious processes that induce an inflammation of the leptomeninges of lesser intensity and more chronicity than the acute forms described earlier. Included are some bacterial and most fungal infections, tuberculosis, syphilis, Lyme disease, HIV infection, and presumed noninfectious causes, such as lymphoma, sarcoidosis, Wegener granulomatosis, and others. As pointed out by Ellner and Bennett many decades ago, the clinical syndrome of chronic meningitis comprises confusion or cognitive decline, seizures, an absence of lateralizing and focal cerebral signs, with or without headache, and mild stiffness of the neck. In most cases, there is little or no fever or other manifestation of infection. The CSF will often not divulge the causative agent, as the organisms are usually by nature more difficult to detect and culture. The main identifiable forms of subacute and chronic meningitis are described below. Chapter 32 addresses the approach to the complicated problem of chronic nonbacterial meningitis (aseptic meningitis) in which no cause can be found, and should be referred to along with this section.