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. 2017 May 10;51(3):292–305. doi: 10.4132/jptm.2017.02.17

Fig. 4.

Fig. 4.

Ultrastructural findings during the early stage of stroke involving the poster limb of internal capsule (PLIC). In the control group, a myelinated axon unit in PLIC had a compact lamellar sheath closely encompassing an axon (A, ×6,000). Each axon was filled with intermediate filament structures, called neurofilaments, and mitochondria. The lesion group presents early pathologic changes; nodular swelling and loosening of the myelin sheath, empty cystic change of submyelin space, polygonal wrinkling of axons, and accentuated cleft along the nuclear membrane of an oligodendrocyte (B, ×3,000) at 3 hours post-ischemia. Progressive loosening of the myelin sheath covers crinkled axons developing characteristic laminating whorled appearance (C, ×10,000) at 6 hours post-ischemia. Axonal swelling with a reactive change of the glial cells presented at 12 hours to 1 day post-ischemia (D-G). Swollen axons full of mitochondria, vesicles, and granules surrounded by acompact myelin sheath appeared. Fibrin thrombosis in capillary lumen (asterisk), a ruptured myelin sheath with extrusion of axonal organelles (arrows), and cystic vacuoles in the vicinity of swollen axons presented (D, ×12,000). Club-shaped processes of reactive astrocytes (arrows) intimately contacted swollen axons and organelles drifted from injured myelinated axons (E, ×6,000). Degenerative changes in an oligodendrocyte appear as an isolated cell with nuclear cytoplasmic dissociation by an irregular cleft, vesicles, and swollen mitochondria in the cytoplasm, and nuclear chromatin condensation along the nuclear membrane (F, ×6,000). Note the different stages of myelinated axon injury; from swollen axons filled with electrondense organelles surrounded by a loosely arranged, laminating myelin sheath to demyelinated ghost axons formed by cystic vacuoles containing sparsely granular or myeloid debris (G, ×6,000). A series of myelinated axonal injury, from loosening myelin sheath to macrophages infiltration phagocytized myelin and other cellular debris, was present at 4 days post-ischemia (H, ×6,000).