Headache is probably the most frequent initial symptom of intracranial abscess but this varies and a considerable number of cases are revealed incidentally. Other early symptoms, roughly in order of their frequency are drowsiness and confusion; focal or generalized seizures; and focal motor, sensory, or speech disorders. Fever and leukocytosis are not consistently present, depending on the phase of the development of the abscess at the time of presentation (see in the following text). In patients who harbor chronic ear, sinus, or pulmonary infections, a recent activation of the infection frequently precedes the onset of cerebral symptoms. In patients without an obvious focus of infection, headache or other cerebral symptoms may appear abruptly on a background of mild general ill health or congenital heart disease. In some patients, bacterial invasion of the brain may be asymptomatic or may be attended only by a transitory focal neurologic disorder, as might happen when a septic embolus briefly lodges in a brain artery. Sometimes stiff neck accompanies generalized headache, suggesting the diagnosis of meningitis (especially a partially treated one).
Localizing neurologic signs become evident sooner or later, but, like papilledema, they occur relatively late in the course of the illness. The nature of the focal neurologic defect will, of course, depend on the location of the abscess as fully explicated in Chap. 21. In cerebellar abscess, the headache is generally postauricular or occipital; the signs are those expected for disease of this part of the brain.
The treacherous aspect of brain abscess is that the signs of systemic infection may be entirely absent. The invasive stage of cerebral infection may be so inconspicuous, and the course so indolent, that the entire clinical picture may not differ from that of malignant brain tumor. Although slight fever is characteristic of the early invasive phase of cerebral abscess, the temperature may return to normal as the abscess becomes encapsulated; the same is true of leukocytosis. The sedimentation rate is usually elevated. Although lumbar puncture is not recommended, in the early stages of abscess formation the CSF pressure is moderately increased; and there is a mild to moderate pleocytosis with 10 to 80 percent neutrophils; and the protein content is modestly elevated, rarely more than 100 mg/dL. Glucose values are not lowered, and the CSF is sterile unless there is concomitant bacterial meningitis. As already mentioned, the combination of brain abscess and acute bacterial meningitis occurs only infrequently. In some patients, abscess is combined with subdural empyema; in these instances the clinical picture can be very complicated, although headache, fever, and focal signs again predominate. In a small number of cases, especially partially treated ones, there are no spinal fluid abnormalities and the sedimentation rate may be normal.
It is apparent from this overview that the clinical picture of brain abscess is far from stereotyped. Whereas headache is the most prominent feature in most patients, seizures or certain focal signs may predominate in others, and a considerable number of patients will present with only signs of increased intracranial pressure. In some instances the symptoms evolve swiftly over a week, new ones being added day by day. In such cases the abscess may become apparent only when cerebral imaging performed for the evaluation of headache or other symptoms discloses a ring-enhancing mass. Even then, the imaging identification is not always straightforward, depending often on the presence of a uniform, enhancing capsule that is typical of a mature abscess (see in the following text). An impressive feature of cerebral abscess is the unpredictability with which the symptoms may evolve, particularly in children. Thus, a patient whose clinical condition seems to have stabilized may, in a matter of hours or a day or two, advance to an irreversible state of coma. Often this is caused by rupture of the abscess into the subarachnoid or ventricular CSF.