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| ADEM (Krupp 2013) [4] | MERS type 1 | MERS type 2 (Notebaert 2013) [20] |
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Clinical manifestations | (i) A first polyfocal, clinical CNS event with presumed inflammatory demyelinating cause | (i) Clinical onset associated with neuropsychiatric symptoms within 1 sweek after fever onset. |
(ii) Encephalopathy that cannot be explained by fever | (ii) Encephalitis or encephalopathy: speech difficulties, drowsiness, decreased consciousness, delirium, seizures, irritability, agitation, and disorientation |
(iii) No new clinical and MRI findings emerge three months or more after the onset | (iii) Complete recovery without sequelae, mostly within 10 days after the onset of neuropsychiatric symptoms |
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Brain MRI | (i) Diffuse, poorly demarcated, large (>1–2 cm) lesions involving predominantly the cerebral white matter | (i) High-signal-intensity lesions on T2-weighted images, isointense to hypointense lesions on T1-weighted imaged and a homogenously reduced diffusion | (i) High-signal-intensity lesions on T2-weighted images, isointense to hypointense lesions on T1-weighted imaged and a homogenously reduced diffusion |
(ii) T1 hypointense lesions in the white matter are rare | (ii) Lesions are seen in the midline of the splenium of the corpus callosum without contrast-enhancement | (ii) Lesions affect in a variable degree the corpus callosum (from its anterior aspect to its totality) and in a bilateral and symmetrical fashion the center semiovale without contrast-enhancement |
(iii) Deep grey matter lesions (e.g. thalamus or basal ganglia) can be present | (iii) Complete resolution of the splenial lesion on repeat imaging within 1 week, with no residual signal changes or atrophy |
(iv) Gadolinium enhancement of one or more lesions occurs in 14–30% of cases | (iii) Complete resolution of the splenial lesion on repeat imaging within 1 week, with no residual signal changes or atrophy |
(v) In addition to findings on brain MRI, patients with ADEM can have extensive lesions on spinal MRI |
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