Ultrastructural pathology of Golgi apparatus of nerve cells in human brainedema associated to brain congenital malformations, tumours and trauma

The alterations induced by ischemia and anoxia upon smooth endoplasmic memb ranes are studied in 38 patients with congenital malformations, brain rumou rs and brain trauma. The effects of vasogenic and cytotoxic brain edema are examined in the Golgi apparatus of nerve and endothelial cells. Samples of cortical biopsies were conventionally processed for transmission electron microscopy. Cortical biopsies were performed according to the basic princip les of Helsinki declaration. Slices of 2 to 5 mm were immediately fixed in the surgical room in 4% glutaraldehyde-0.1 M sodium phosphate buffer, pH 7. 4 at 4 degrees C, and postfixed in 1% osmium tetroxide in similar buffer. T he pathological alterations of the Golgi complex were studied in samples wi th moderate and severe brain edema. Moderate edema was mainly found in cong enital malformations and severe edema in brain trauma and rumours. In some severely edematous neurons, observed in hydrocephalus associated to Arnold- Chiari malformation, small vesicular type Golgi complexes and atrophic ones were observed, characterized mainly by partial or total disappearance of s tacked Golgi cisternae and presence of congregated vesicular profiles. In b rain trauma and rumours the Golgi complex showed enlargement and fragmentat ion of the stacked cis- medial- and trans-Golgi cisternae and vacuolization of trans-Golgi network. In addition, an increased formation of Golgi and c oated vesicles was observed in the cis-and trans-Golgi regions. Most Golgi and clathrin coated vesicles were observed throughout the cytoplasm suggest ing an increased vesicular transport. In severe edema the nerve cell plasma membranes appeared fragmented, presumably due to an interference of the pr otein insertion process into the plasma membrane. In brain trauma, a hypert rophic Golgi complex was observed in some nerve cells and endothelial cells of cortical capillaries, with increased formation of Golgi and coated vesi cles. The ischemia and anoxia associated to the vasogenic and cytotoxic bra in edema induced enlargement, fragmentation and disappearance of stacked Go lgi cisternae.