Nerve cell death types in the edematous human cerebral cortex.
Cortical biopsies of 18 patients with clinical diagnosis of congenital hydrocephalus, brain trauma, and vascular anomaly were examined with the transmission electron microscope to study the distinct and overlapped morphological cell types of nerve cell death in the human edematous cerebral cortex. The nerve cells showed lobulated and shrunken nucleus, irregular enlargement and fragmentation of perinuclear cistern, with areas of apparently intact nuclear pore complexes alternating with regions of nuclear pore complex disassembly. The nucleolus appears unaltered in moderate edema and with distorted nucleolar subcompartments in severe edema. Most nonpyramidal nerve cells, astrocytes and oligodendrocytes underwent an oncotic-apoptotic-necrotic continuum featured by swollen nucleoplasm, cytoplasm, and cell organelles, chromatin condensation and marginalization, and formation of apoptotic bodies. In a lesser proportion other nonpyramidal nerve cells, astrocytes and oligodendrocytes only showed apoptosis or oncosis. Autophagic cell death characterized by presence of autophagic vacuoles of lysosomal origin was rarely seen. The above findings suggest that different mechanisms of nerve cell death occur in the human edematous cerebral cortex related with brain trauma, congenital hydrocephalus, vascular anomaly, and their anoxic-ischemic conditions. An oncotic-apoptotic continuum process leading to necrosis predominates in human cerebral cortex nerve cell populations. The nerve cell death is discussed in relation with the severity of brain edema, anoxic-ischemic conditions of brain parenchyma, oxidative stress, glutamate excitotoxicity, calcium overload, and caspase dependent and independent mechanisms.
Castejón
O J
OJ
Institute of Biological Investigations, Faculty of Medicine, University of Zulia, Maracaibo, Venezuela. ocastejo@cantv.net
Arismendi
G J
GJ
D000293:Adolescent; D000328:Adult; D000369:Aged, 80 and over; D017209:Apoptosis; D001139:Arnold-Chiari Malformation / Q000473:pathology; D001253:Astrocytes / Q000648:ultrastructure*; D001929:Brain Edema / Q000473:pathology*; D001930:Brain Injuries / Q000473:pathology; D015687:Cell Hypoxia; D002467:Cell Nucleus / Q000648:ultrastructure; D002540:Cerebral Cortex / Q000473:pathology*; D003593:Cytoplasm / Q000648:ultrastructure; D005260:Female; D006801:Humans; D006849:Hydrocephalus / Q000473:pathology; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D046529:Microscopy, Electron, Transmission; D008875:Middle Aged; D009336:Necrosis; D009836:Oligodendroglia / Q000648:ultrastructure*