PMC3562210_01
Serial magnetic resonance imaging (3 Tesla) and computed tomography scans showing progressive bilateral reversible posterior leukoencephalopathy syndrome. (A-E) Magnetic resonance imaging immediately after the patient was admitted showed (A) marked hyperintensity in T2 and fluid-attenuated inversion recovery (FLAIR) sequences of the posterior lesions. Diffusion-weighted imaging exhibited restricted diffusion (B) with a decreased signal on apparent diffusion coefficient mapping (C) consistent with cytotoxic edema. Lesions showed slight contrast enhancement (D). Susceptibility-weighted imaging (SWI) showed signal loss indicating the beginning of hemorrhagic lesion transformation (E). (F-J) Magnetic resonance imaging two days after the patient was admitted showed progressive confluent lesions in T2 and FLAIR sequences (F). Increasing areas of restricted diffusion (G) and volume expansion (H) indicated progressive cytotoxic edema. Lesions were still slightly contrast enhancing (I). SWI showed progressive signal loss indicating advancing hemorrhagic lesion transformation (J). (K) A computed tomography scan immediately after admission demonstrates well-demarcated bilateral hypodensities in posterior brain regions. (L) The computed tomography scan on day 3 after admission reveals global cerebral swelling, subsequent upper and lower brainstem herniation and brainstem compression as well as generalized thrombosis of the cerebral sinus and veins.
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F1
However, an initial cerebral computed tomography (CT) scan showed bilateral posterior hypodense lesions (Figure 1K). An MRI of the brain on the same day demonstrated cortical and subcortical lesions in the occipital lobes with combined vasogenic and cytotoxic edema atypical for both venous congestion and arterial infarction (Figure 1A-D). Follow-up MRI two days after admission demonstrated more widespread and confluent cytotoxic edematous lesions in different arterial territories clearly exceeding the vertebrobasilar territory (Figure 1F-H), hemorrhagic transformation (Figure 1J) and mild contrast enhancement (Figure 1I). By contrast, three days after admission follow-up CT revealed global cerebral swelling, subsequent upper and lower brainstem herniation and brainstem compression as well as generalized thrombosis of the cerebral sinus and veins (Figure 1L).
Neuropathological analysis revealing laminar necrosis and hypoxic neuronal cell death in the absence of overt arterial pathology. (A,B) Gross appearance revealed cortical discoloration due to laminar necrosis ( ) and small white matter hemorrhage ( ) in occipitotemporal regions. (C) Histopathological analysis showed hypoxic neuronal damage (arrows) (that is, nerve cells with eosinophilic and shrunken cytoplasm and hyperchromatic condensed nucleus (hematoxylin and eosin stain x100)) (D,E) but no evidence of any arterial vascular pathology except for minor arteriosclerosis of intracerebral (D) and basal vessels (E) (elastica-van Gieson stain x100).
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F2
Histological evaluation showed isolated hypoxic neuronal damage preferentially in the basal ganglia, hippocampus, pons, medulla oblongata and substantia nigra and laminar necrosis with edema in several cortical areas (Figure 2A-C).