Abstract

The goal of this paper is to correlate the traumatic injury-induced edematous changes and the derangement of nerve cell Golgi apparatus and interrupted axonal flow with the synaptic degeneration. We postulate the following hypothesis: The damage of the nerve cell Golgi apparatus, normally involved in the storage of most synaptic proteins and the source of synaptic vesicles, and the interrupted axonal flow are related to synaptic degeneration in the traumatic brain edema? Cortical biopsies of the cerebral cortex of 10 patients with severe traumatic head injuries complicated with subdural and extradural hematoma or hygroma were examined. They were immediately fixed in buffered glutaraldehyde fixative in the surgical room and conventionally processed for transmission electron microscopy. A notably edematous Golgi apparatus featured by marked enlargement of Golgi stack cisternae in pyramidal nerve cells, and with minor edematous changes in the perineuronal oligodendroglial cells were observed. Extremely swollen and fragmented Golgi complexes were found in nonpyramidal neurons and endothelial cells. Beaded shaped degenerated myelinated axons did not exhibit axonal flow of mitochondria and Golgi apparatus derived vesicles. Coexisting degenerated axodendritic contacts were observed in the neighboring edematous neuropil. Conclusions: The electron microscopic images suggest that the derangement of Golgi complex and the interruption of axoplasmic flow in the traumatic brain injury primarily participate in the synaptic degeneration, and secondarily the ischemic process, calcium overload, glutamate and hemoglobin cytotoxicity, and lipid peroxidation.