Ki-67 Immunoreactivity in Type II Malformations of Cortical Development

Abstract

Malformations of cortical development (MCD) are a well-recognized cause of chronic epilepsy. Most MCD are defined by the neuronal component of the lesion and are considered to be relatively "static" lesions. Twenty-one cases of MCD type II (Taylor type cortical dysplasia) were retrospectively evaluated with Ki-67 antibody looking for evidence of cell proliferation and evaluating populations of cells that may be proliferating. Resections were from 13 males and 8 females who ranged in age at the time of surgery from 6 weeks to 57 years (mean 8.6 y) and who had a duration of seizures before surgery of 1.5 months to 34.4 years (mean 6.5 y). Dysmorphic neurons were observed in all cases and balloon cells in 18/21 (86%) cases. Ki-67 labeling indices ranged from 0.2% to 4.9% (mean 2.0%). Coimmunolabeling with Ki-67 and antibodies to glial fibrillary acidic protein, CD68, and CD45RB showed that the majority of the Ki-67-positive cells were astrocytic (glial fibrillary acidic protein positive). In 9/21 cases (43%), endothelial cell staining with Ki-67 was also observed. These results suggest that low rates of cell proliferation are observable in type II MCD. The proliferating cells appear to be primarily astrocytic and endothelial in nature and suggest that these lesions are not static. Dysmorphic neurons and balloon cells in MCD were not observed to stain with Ki-67.