[Ultrastructural study of experimental cerebrocortical necrosis in calves (author's transl)]

Cerebrocortical necrosis (CCN) was experimentally induced in three calves with the thiamine antagonist Amprolium. The calves were followed clinically. At the time of development of typical clinical signs of CCN the calves were killed and necropsied and a complete histopathologic examination was performed. The light microscopic lesions of the cerebral cortex were those of middle laminar necrosis and deep laminar edema. The necrotic zone consisted of fine vesicles and differed only slightly from the edema zone. In the former some neurons were morphologically normal, others showed signs of injury, while in the latter all neurons were injured. The lesions are consistent with those found in natural cases of CCN. Biopsies from the cerebral cortex were taken at the time of early clinical signs. Ultrastructural studies of these biopsies showed no clear difference between the zones of necrosis and edema observed light microscopically. The ultrastructural changes were characterized by dilatations in the neuropil. The cytoplasm and foot plates of the astrocytes had a "watery" appearance and contained dilated mitochondria and large vesicles. The vesicles were continuous with the granular endoplasmic reticulum. It was concluded that the initial morphologic changes in CCN in calves were indicative of a cytotoxic edema of the astrocytes. This may be due to a cytotoxic edema with subsequent loss of cell volume control. The primary astrocytic changes could then lead to neuronal injury.