Article Figures & Data
Figures
- Fig 1.
MR imaging findings of subject 1, presenting with delirium and severe generalized seizures. Transient bilateral laminar signal alterations of the insula (short black arrows), amygdala, and ventral hippocampus (open white arrows) mimicking limbic encephalitis are most prominent 9 days after the onset of neurologic symptoms. Marked DWI signal increase in the bilateral thalamus (open black arrows) corresponds with unaltered ADC values (not shown), indicative of vasogenic edema. Signal alterations shift from the bilateral mediolateral thalamus to the left posterolateral thalamus (pulvinar) with time. Note transient patchy diffusion restriction with low ADC values (not shown) in the left amygdala and hippocampal complex, suggestive of cytotoxic edema (either as a result from status epilepticus or as a neurotoxic and/or inflammatory effect). Additionally, bilateral round signal hyperintensities (filled white arrows) can be visualized in the central pons, normalizing with clinical improvement.
- Fig 2.
MR imaging findings of subject 2 presenting with aphasia, apraxia, and memory deficits. At the level of the fourth ventricle, symmetric round signal hyperintensities (filled white arrows) can be visualized in the central pons, normalizing with clinical improvement at day 17. (The DWI image on day 4 has been modified from Reference 22.)
- Fig 3.
MR imaging findings of subject 3, presenting with delirium and memory deficits. Note the patchy hyperintensities on T2WI and FLAIR images in the frontal periventricular white matter (white arrows) 3 weeks after the onset of neurologic symptoms (supposedly as a result of HUS encephalopathy because they could not be detected on day 5). DWI shows no restriction, indicating that no ischemia is present. At this stage, the patient did not show any neurologic symptoms. After 10 weeks, these lesions are still visible despite complete clinical recovery.
Tables
Main MR imaging findings in patients with HUS with neurologic complicationsa
Peracute (Day 0) Acute (Days 1–5) Subacute (Days 10–28) Late Follow-Up (Days 41–102) Vasogenic edema of central pons 0/2 5/9 1/5 0/11 Symmetric patchy subcortical/cortical hyperintensities 0/2 3/9 3/5 4/11 Symmetric patchy or laminar hyperintensities of basal ganglia 0/2 4/9 2/5 2/11 Mesiotemporal signal changes 0/2 1/9 1/5 1/11 ↵a MRI presentation of HUS encephalopathy at different stages of the disease (days of MR imaging performance after the onset of neurologic symptoms) presented in relation to all patients imaged at this phase of disease. Note that not all patients underwent imaging at 4 different time points.
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