Precontrast and postcontrast computed tomographic (CT) scans of patients with brain abscesses were quantitatively studied to determine if the degree of encapsulation could be predicted. The findings in these cases correlated closely to the CT criteria for encapsulation previously established in an experimental model. Time-density curves of serial delayed postcontrast CT scans and the precontrast CT appearance yielded accurate criteria for determining the degree of encapsulation. The effect of corticosteroid treatment on contrast enhancement of brain abscess was also studied in one patient.

The neuropathological progression of brain abscess formation induced by a mixed anaerobic culture of Bacteroides fragilis and Staphylococcus epidermidis was studied experimentally in dogs. Histological findings were correlated with computerized tomographic (CT) brain scans. The evolution of brain abscess formation could be divided into three stages based on histological criteria: early cerebritis (Days 1 to 3); late cerebritis (Days 4 to 9); and capsule formation (Day 10 and later). Capsule formation could not be divided into early and late stages because encapsulation was delayed compared with a previously reported model of alpha-Streptococcus brain abscess. Histologically, there was evidence for a very virulent infection. Leptomeningitis was significant even in the late stages. Early ventricular rupture occurred in 25% of the animals. A pattern of extensive purulent encephalitis was seen in 25% of the animals. In the early cerebritis stage, blood vessels near the necrotic center were engorged and were surrounded by hemorrhage and/or protein-rich fluid. Cerebral edema was extensive. Although fibroblasts appeared in late cerebritis, there was marked delay of capsule formation. Three-week-old lesions still had areas of incomplete capsule formation and foci of uncontrolled infection. In the cerebritis stages, CT scans showed an area of ring enhancement which was incomplete on early scans (at 5 minutes after injection of contrast material) but partially filled in and thickened on delayed scans (at 20 to 45 minutes). On even later delayed scans there was no decrease in intensity of ring enhancement. Lesions in which capsule formation occurred also showed ring enhancement, but delayed scans showed a decrease in the intensity of enhancement. The lesions that ruptured into the ventricular system showed atypical CT findings, with either lack of contrast enhancement (histologically there was minimal cerebritis adjacent to the abscess cavity) or a marked delay in contrast enhancement (cerebritis was more extensive and corresponded to the width of ring of enhancement). This study suggests that Bacteroides fragilis is a virulent organism in the brain. The developing abscesses enlarged quickly, were prone to early ventricular rupture, and showed incomplete and delayed encapsulation.

A short term, high dose corticosteroid treatment protocol was investigated to determine its clinical utility in staging an experimental brain abscess. Corticosteroids were shown to decrease the degree of contrast enhancement of brain abscess 12 h after administration but the magnitude of the effect was not consistent enough to be clinically useful in staging. The corticosteroid effect progressively diminished as the inflammatory lesion encapsulated over time. This effect emphasized that a decreasing ring diameter and not diminished contrast enhancement should be the CT criterion for brain abscess resolution.

The neuropathological progression of brain abscess formation was studied experimentally in paired immunosuppressed and control dogs. The immunosuppressed animals received azathioprine and prednisone beginning 7 days prior to intracerebral inoculation with alpha streptococcus. Histological findings were correlated with computerized tomography (CT) brain scans. The evolution of brain abscess in the immunosuppressed animals could be divided into three stages based on histological evaluation: cerebritis stage (1 to 11 days), early-capsule stage (12 to 17 days), and late-capsule stage (18 days and later). There was a significant delay in the evolution of alpha streptococcus brain abscess compared to the authors' previous studies. Histologically, abscesses in immunosuppressed dogs were characterized by a decrease and delay in collagen formation, a reduction in polymorphonuclear leukocytes and macrophages, longer persistence of bacterial organisms, and an increase in gliosis. During the cerebritis stage, abscesses in control animals were consistently larger and more edematous than those in immunosuppressed animals and reached their maximum size by Day 8, whereas abscesses in immunocompromised animals reached their maximum size around Day 12. In the late-capsule stage, abscesses in immunosuppressed animals remained larger than those of control animals and continued to show signs of delayed development. This was evidenced by diffusion of contrast medium into the lucent center of ring-enhancing lesions on delayed CT scans. The results suggest that the decreased inflammatory response and edema formation in the immunosuppressed host resulted in less initial mass effect from brain abscess, but that the eventual size and area of the abscess may have become larger due to the less effective host response.

The effect of short-term corticosteroid treatment on contrast enhancement was investigated in an experimental brain abscess model. The degree of enhancement was reduced in the cerebritis stage, unaffected in the capsule stage, and intermediate in the transitional stage. The area and pattern of enhancement were also altered in the cerebritis stage. Although the magnitude of the entire cerebritis time-density curve (extended for 60 minutes) was decreased by the steroids, its configuration was unchanged. Prior to steroid administration, the 10- and 60-minute components of the curve discriminated between cerebritis and capsule stages, with the latter exhibiting a far lower 60-minute value. Implications for treatment of brain abscesses are discussed.