Fig. 3.

Light microscopy findings of stroke involving the poster limb of the internal capsule (PLIC). Coronal sectioning reveals a poorly defined focal lesion characterized by loss of hematoxylin and eosin (H&E) staining (A) and increased glial fibrillary acidic protein (GFAP) staining (B) at 3 hours post-ischemia. A well-demarcated, pale, whitish lesion is identified by low magnification microscopy via H&E and luxol fast blue–periodic acid-Schiff (LBPAS) staining (C, D), and GFAP and neurofilament protein immunostaining (E, F) at 12 hours to 1 day post-ischemia. The focal lesion shows central necrosis surrounded by macrophages (G) phagocytized with myelinated axon debris (H) by LBPAS staining, and GFAP-positive hypertrophic astrocytes along the lesion periphery (I) at 4 days post-ischemia. The necrotic center is gradually reduced in volume, and infiltrating macrophages decrease in number at 7 days post-ischemia. However, macrophages persist, and phagocytize periodic acid-Schiff–positive myelin debris as shown through LBPAS staining (J). At 14 to 21 days post-ischemia, the infarct lesion presents as a pseudocystic cavity consisting of reactive astrocytes, macrophages, and newly formed capillaries. The motor recovery at 14 to 21 days post-ischemia is related to the completeness of axonal injury in the PLIC. In the moderate recovery group, LBPAS staining in the PLIC revealed a pseudocystic lesion surrounded by GFAP-positive reactive astrocytes (K), and partially preserved myelinated axons passing in the PLIC periphery (L). In the poor recovery group, myelinated axons in the PLIC were completely disrupted as shown by LBPAS staining (M) and were replaced by a cystic cavity surrounded by GFAP-positive reactive astrocytes (N).