Neuropathological Features

Knowledge of the pathological anatomical changes induced by stroke is essential to understand the basic radiological features that reflect the evolution of cellular and tissue changes. On standard MR, only macroscopic neuropathological alterations give rise to signal changes, whereas the technique is scarcely sensitive to early cellular and subcellular injury. Therefore, hyper-acute-phase ischaemia is not depicted on standard, even high-field, images.

The biochemical bases of the ischaemic event are not yet completely clear. It has been demonstrated that the ischaemic area shrinks within a few minutes of the event. The hypoxia-induced disruption of anaerobic glycolysis triggers a histopathological cascade, with alteration of the Na+/K+ pump and consequent intracel-lular accumulation of water (cytotoxic oedema). This can be seen microscopically 2 h from the vessel occlusion, during which time the water molecules remain „trapped" in the intracellular space, with a consequent reduction in their diffusion. The cellular injury caused by water accumulation and progressive microvacuoli-zation is reversible over the first 6 h. After this time, the necrotic process becomes established due to accumulation of lactic acid, pH reduction, damage to the microcirculation, and an increased concentration of excitatory neurotransmitters. Subsequently, damage to the blood-brain barrier (BBB) causes an accumulation of extracellular water, or vasogenic oedema. At 12-24 h, the cytotoxic oedema and related cell degeneration manifest macroscopically as a „pale" area, while the vasogenic oedema can be visualized radiologically. Unlike other organs, in which necrotic tissue is replaced by scar fibrosis, in the brain it is completely removed by macrophages and replaced by a fluid-filled cavity (porencephaly), whose walls are made up of nerve parenchyma exhibiting an intense proliferation of mesodermal elements (fibroblasts, fibrocytes) with formation of new capillaries. In this phase, defined as gliosis, which can last several weeks, the proliferative phenomena result in increasingly sharp borders of the affected area. Finally, months from the stroke, the ischaemic focus develops as a cavity with more or less regular borders that, due to scar retraction, may undergo deformation together with the adjacent parenchyma [2].

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