Role of vascular proliferation on angiographic appearance and encapsulation of experimental traumatic and metastatic brain abscesses

Abstract

Experimental traumatic abscesses were produced in rhesus monkeys by intracerebral injection of nutrient agar contaminated with Staphylococcus epidermidis, and metastatic abscesses were induced by intracarotid embolization of silicone cylinders contaminated with Staphylococcus epidermidis. All monkeys underwent preoperative and serial postoperative carotid angiography. Traumatic abscesses produced early capsular blushes and progressive anterior cerebral artery displacements. Metastatic abscesses induced transient midline shifts but no capsular stains. Postmortem studies on the monkeys showed that mean capsular thickness and segmental wall vascularity of the traumatic and metastatic abscesses were significantly different (p less than 0.001), despite equal abscess ages and similar abscess volumes. In comparison to traumatic abscesses, metastatic abscesses demonstrated reduced inflammatory cell infiltration and retarded collagen formation around proliferating capsular vessels. Brain surrounding the metastatic abscesses demonstrated ischemic changes. The results suggest that 1) capsular blushes during cerebral angiography are secondary to vascular proliferation within the capsule and not to compression of surrounding brain, 2) vascular staining reflects capsular thickness, 3) capsular vascularity contributes to collagen formation, 4) encapsulation is dependent upon the integrity of surrounding brain, and 5) adjacent cerebral ischemia may impede inflammatory responses involved in capsule formation.