PMC4357158_01
Fluid-attenuated inversion recovery (FLAIR) images in the affected regions. A: bilateral hyperintensity in the white matter involving the parietal and occipital lobules and the internal capsule. B: Increment in the extension and intensity of the parietal lesion, one month after diagnosis. C: Complete resolution of the lesion, one year after diagnosis.
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Fig1
Magnetic resonance imaging (MRI) of the brain showed a bilateral hyperintensity (Figure 1A) in the white matter involving the parietal and occipital lobules and the internal capsule; there was no mass effect, edema, hemorrhagic or ischemic lesions. In the subsequent weeks, the neurological condition of the patient continued to deteriorate, with continuous epileptic fits, motor impairment with left hemiparesia, along with an increment in the extension and intensity of the parietal lesion, as revealed by a further MRI one month after diagnosis (Figure 1B). Thereafter, neurological condition and the MRI findings progressively improved and a year after diagnosis the patient achieved an almost complete resolution of the lesion as indicated by MRI, despite persisting residual motor impairment and epilepsy (Figure 1C).
Histological examination. A: Infiltration of the brain tissue by foamy macrophages and mature lymphocytes with perivascular clustering. B: Immunohistochemical staining for neurofilaments revealed a loss of myelin. Compare affected tissue at the bottom with normal brain tissue at the upper corner of the picture. C: Reactive astrocytes with polymorphic nuclei and prominent nucleoli.
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Fig2
Histological examination of the sample revealed infiltration of the brain tissue by foamy macrophages and mature lymphocytes with perivascular clustering (Figure 2A). Immunohistochemical staining for neurofilaments revealed a loss of myelin (Figure 2B). Within the lesion, astrocytes were reactive and exhibited polymorphic nuclei and prominent nucleoli (Figure 2C).