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tions; and anaerobic streptococci are commonly metastatic from the lung and paranasal sinuses The organisms associated with acute bacterial endocarditis have been mentioned above Predisposing to nocardial brain abscess is pulmonary nocardial infection, often in immunosuppressed patients; this diagnosis is doubtful without a pneumonic in ltrate Thus knowledge of the site of the abscess and the antecedent history enables one to institute appropriate therapy while awaiting the results of bacterial and fungal cultures Pathology Localized in ammatory exudate, septic thrombosis of vessels, and aggregates of degenerating leukocytes represent the early reaction to bacterial invasion of the brain Surrounding the necrotic tissue are macrophages, astroglia, microglia, and many small veins some of which show endothelial hyperplasia, contain brin, and are cuffed with polymorphonuclear leukocytes There is interstitial edema in the surrounding white matter At this stage, which is rarely observed postmortem, the lesion is poorly circumscribed and tends to enlarge by a coalescence of in ammatory foci The term cerebritis is loosely applied to this local suppurative encephalitis or immature abscess Within several days, the intensity of the reaction begins to subside and the infection tends to become delimited The center of the abscess takes on the character of pus; at the periphery, broblasts proliferate from the adventitia of newly formed blood vessels and form granulation tissue, which is readily identi ed within 2 weeks of the onset of the infection As the abscess becomes more chronic, the granulation tissue is replaced by collagenous connective tissue It has also been noted, both in experimental animals and in humans, that the capsule of the abscess is not of uniform thickness, frequently being thinner on its medial (paraventricular) aspect These factors account for the propensity of cerebral abscesses to spread deeply into the white matter and to produce daughter abscesses or a chain of abscesses and extensive surrounding cerebral edema In some instances the process culminates in a catastrophic rupture into the ventricles.

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Clinical Manifestations Headache is the most frequent initial symptom of intracranial abscess 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 below) 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 lodges in a brain artery Sometimes stiff neck accompanies generalized headache, suggesting the diagnosis of meningitis (especially a partially treated one) These early symptoms may improve in response to antimicrobial agents, but within a few days or weeks, recurrent headache, slowness in mentation, focal or generalized convulsions, and obvious signs of increased intracranial pressure provide evidence of an in ammatory mass in the brain Localizing neurologic signs become evident sooner or later, but, like papilledema, they occur relatively late in the course of the illness However, as stated above, some patients present only with focal neurologic signs The nature of the focal neurologic defect will, of course, depend on the location of the abscess In temporal lobe abscess, headache in the early stages is usually on the same side as the abscess and is localized to the frontotemporal region If the abscess lies in the dominant temporal lobe, there is characteristically an anomic aphasia An upper homonymous quadrantanopia may be demonstrable owing to interruption of the inferior portion of the optic radiation This may be the only sign of abscess of the right temporal lobe; contralateral motor or sensory defects in the limbs tend to be minimal, though weakness of the lower face is often observed In frontal lobe abscess, headache, drowsiness, inattention, and general impairment of mental function are prominent Contralateral hemiparesis with motor seizures and a motor disorder of speech (with dominant hemisphere lesions) are the most frequent neurologic signs An abscess of the parietal lobe will give rise to a series of characteristic but sometimes subtle focal disturbances (page 400) The main manifestation of an occipital lobe lesion is a homonymous hemianopia All of the aforementioned focal signs may be obscured by inattentiveness, drowsiness, and stupor, and one must be persistent in searching for them When abscesses are multiple and widely distributed in the cerebral and cerebellar hemispheres, the ultimate syndrome is unpredictable; but most often, in our experience, it has taken the form of a global encephalopathy, like that of a metabolic confusional state, with a subtle hemiparesis or seizure In cerebellar abscess, headache in the postauricular or suboccipital region is usually the initial symptom and may at rst be ascribed to infection in the mastoid cells Coarse nystagmus, weakness of conjugate gaze to the side of the lesion, cerebellar ataxia of the ipsilateral arm and leg, and ataxia of gait are the usual signs The ataxia may be dif cult to demonstrate if the patient is very ill and cannot sit up or walk As a general rule, the signs of increased intracranial pressure are more prominent with cerebellar abscesses than with cerebral ones Mild contralateral or bilateral corticospinal tract signs are often misleading, being evidence of brainstem compression or hydrocephalus rather than a frontal lobe lesion In the.

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