Castejón O J
Institute of Biological Investigations, Faculty of Medicine, University of Zulia, Maracaibo, Venezuela.
J Submicrosc Cytol Pathol. 1998 Jan;30(1):145-56.
Cortical biopsies of eight patients with craniocerebral trauma complicated with subdural or epidural hematoma were examined with the transmission electron microscope. The patients showed post-traumatic neurobehavioural disorders and moderate or severe vasogenic brain edema. The capillary wall displayed increased vacuolar and vesicular endothelial transport, basement membrane thickening and vacuolization and swollen astrocytic end-feet. Pericapillary and parenchymatous hemorrhages were also observed. The extracellular space appeared considerably enlarged with presence of proteinaceous hematogenous edema fluid and fibrinous organization. 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 amount of oligodendroglial ad-axonal layer. The dendrites also showed clear or dark and beaded shape degeneration. Synaptic degeneration was characterized by swollen and shrunken pre- and postsynaptic endings, clumping, enlargement and depletion of synaptic vesicles, synaptic membrane complex disassembly and detachment of glial ensheathment. Perivascular and perineuronal astrocytes appeared remarkably swollen. Phagocytic 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 subsequent neuronal and neuroglial cell reactive and degeneration processes might represent the morphological substrate responsible for the post-traumatic neurobehavioural disorders.
对8例颅脑外伤合并硬膜下或硬膜外血肿患者的皮质活检组织进行了透射电镜检查。这些患者表现出创伤后神经行为障碍以及中度或重度血管源性脑水肿。毛细血管壁显示空泡和囊泡状内皮运输增加、基底膜增厚和空泡化以及星形胶质细胞终足肿胀。还观察到毛细血管周围和实质内出血。细胞外间隙明显扩大,存在含蛋白质的血性水肿液和纤维组织。锥体细胞和非锥体细胞显示细胞内水肿,其特征为粗面内质网、核膜和高尔基体不规则增大。有髓轴突表现为清亮型或黑色型轴浆变性、曲张纤维肿胀、髓鞘扭曲、髓鞘卵圆体形成以及少突胶质细胞轴突周围层增多。树突也表现为清亮型或深色型串珠状变性。突触变性的特征是突触前和突触后末梢肿胀和萎缩、突触小泡聚集、增大和耗竭、突触膜复合体解体以及神经胶质包裹分离。血管周围和神经周围的星形胶质细胞明显肿胀。还发现了吞噬性星形胶质细胞。少突胶质细胞表现出水肿性和反应性改变。反应性少突胶质细胞引起髓鞘溶解。脑屏障功能障碍、血管源性和细胞毒性水肿以及随后的神经元和神经胶质细胞反应性及变性过程可能是创伤后神经行为障碍的形态学基础。