PMC3975751_01
Flash-evoked visual potentials show prolonged N2 and P2 latencies in both sides at 9 months after disease onset (a, b); marked improvement 9 months later (c, d). 3T MRI coronal T2-weighted images show increased signals in both optic nerves, more prominent on the right (e).
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F1
Upper and lower limb somatosensory and motor evoked potentials elicited slightly reduced amplitudes on the left side; conversely, flash-evoked visual potentials showed prolonged N2 and P2 latencies (fig. 1).
Brain MRI at neurological presentation shows multifocal hyperintense lesions within the basal ganglia (a) and midbrain (b); significantly reduced lesion load after 9 months (c, d).
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F2
In July 2012, a brain scan using a 3T MR scanner detected multiple and partially confluent punctate foci of T2/FLAIR hyperintensity, unenhanced after gadolinium, bilaterally in the basal telencephalon, diencephalon, external capsulae, subcortical insula, periventricular white matter, temporal horns, corpus callosum, and optic nerves as well as the ventral cerebral peduncles, pontine-mesencephalic junction and dorsal pons (fig. 2). In March 2013, brain MRI showed that most alterations had disappeared and residual lesions were no longer contrast enhanced (fig. 2).
Axial (a, b) and coronal (c) brain 18F-FDG PET slices showing reduced glucose uptake in the left caudate nucleus, putamen, thalamus and bilateral mesial temporal lobes.
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F3
A PET brain scan showed a reduced glucose metabolism in the temporal lobes and the left striatum, relative to other cortical areas (fig. 3).