ELECTRON-MICROSCOPIC ANALYSIS OF CORTICAL BIOPSIES IN PATIENTS WITH TRAUMATIC BRAIN INJURIES AND DYSFUNCTION OF NEUROBEHAVIORAL SYSTEM

Authors
Citation
Oj. Castejon, ELECTRON-MICROSCOPIC ANALYSIS OF CORTICAL BIOPSIES IN PATIENTS WITH TRAUMATIC BRAIN INJURIES AND DYSFUNCTION OF NEUROBEHAVIORAL SYSTEM, Journal of submicroscopic cytology and pathology, 30(1), 1998, pp. 145-156
Citations number
59
Categorie Soggetti
Cell Biology",Pathology
ISSN journal
11229497
Volume
30
Issue
1
Year of publication
1998
Pages
145 - 156
Database
ISI
SICI code
1122-9497(1998)30:1<145:EAOCBI>2.0.ZU;2-Q
Abstract
Cortical biopsies of eight patients with craniocerebral trauma complic ated with subdural or epidural hematoma were examined with the transmi ssion electron microscope. The patients showed posttraumatic neurobeha vioural disorders and moderate or severe vasogenic brain edema. The ca pillary wall displayed increased vacuolar and vesicular endothelial tr ansport, basement membrane thickening and vacuolization and swollen as trocytic end-feet. Pericapillary and parenchymatous hemorrhages were a lso observed. The extracellular space appeared considerably enlarged w ith presence of proteinaceous hematogenous edema fluid and fibrinous o rganization. Pyramidal and non-pyramidal neurons showed intracellular edema featured by irregular enlargement of rough endoplasmic reticulum , nuclear envelope and Golgi apparatus. The myelinated axons exhibited clear or black type axoplasmic degeneration, varicose fiber swelling, myelin sheath distortion, formation of myelin ovoids and increased am ount of oligodendroglial ad-axonal layer. The dendrites also showed cl ear or dark and beaded shape degeneration. Synaptic degeneration was c haracterized by swollen and shrunken pre-and postsynaptic endings, clu mping, enlargement and depletion of synaptic vesicles, synaptic membra ne complex disassembly and detachment of glial ensheathment. Perivascu lar and perineuronal astrocytes appeared remarkably swollen. Phagocyti c astrocytes were also found. Oligodendrocytes displayed hydropic and reactive changes. Reactive oligodendrocytes induced myelinolysis. The brain barrier dysfunction, the vasogenic and cytotoxic edema and the s ubsequent neuronal and neuroglial cell reactive and degeneration proce sses might represent the morphological substrate responsible for the p ost-traumatic neurobehavioural disorders.