PMC3806676_01
MRI features. FLAIR images (a-c), contrast-enhanced T1-weighted image (g), diffusion-weighted image (h), and apparent diffusion coefficient map (i) performed 3 days after SE onset. d-f FLAIR images 1 month later. Evidence of bilateral involvement of the entire temporal lobe (cortex and white matter), from the temporal pole up to the hippocampus, with signs of laminar necrosis (a, d, white arrowheads), is easily recognizable after gadolinium (g). The edema is significantly more prominent 3 days after SE onset (a, b), compared with 1 month later (e). The high signal in the apparent diffusion coefficient map demonstrates it is vasogenic (h, i). b, e, f Cortical involvement outside the temporal lobe (f, white arrows), in particular of the left precuneus (black arrows), is far more evident in the second MRI. c, f The left pulvinar shows hyperintensity, which increased 1 month later, with involvement of the contralateral nucleus (black arrowheads).
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F1
SE onset, showed signal hyperintensity of the temporal lobe bilaterally and symmetrically in T2 and FLAIR sequences, with involvement of both the cortex and white matter, deep into the hippocampus and pulvinar (fig. 1). Signs of laminar necrosis were detected in the superior and medium temporal giri bilaterally (fig. 1a, d, e). Magnetic resonance diffusion-weighted images, including apparent diffusion coefficient mapping, permitted us to identify the presence of vasogenic edema (fig. 1h, i). Follow-up brain MRI studies, performed within 4 weeks, demonstrated an unvaried neuroradiological picture, but with a reduction of vasogenic edema in the temporal lobes (fig. 1f) and more evident involvement of the pulvinar bilaterally (fig. 1g).