case_images: PMC6218758_01
case_images: PMC6218758_02
case_images: MRI scans: (a, e) T2-weighted; (b,f) Fluid Attenuated Inversion Recovery (FLAIR); (c,g) diffusion-weighted imaging; (d,h) apparent diffusion coefficient (ADC) map. The first MRI imaging (a,b,c,d) showed bilateral and symmetrical hyperintensity () inT2, FLAIR and diffusion of the occipital and frontal lobes, cerebellar hemispheres, periventricular white matter, and basal ganglia with low ADC related to cytotoxic edema. After 9 days, control MRI (e, f, g, h) highlighted progressive volume loss of cerebrum with decreased hypersignal and increased ADC in cerebellar hemispheres, fontal and occipital lobes. Hypersignal persists in T2, FLAIR, and diffusion in periventricular white matter with ADC restriction and in basal ganglia without ADC restriction.
case_images: CRICC2018-8304375.001.jpg
case_images: PMC6218758_02_CRICC2018-8304375.001.jpg
case_images: fig1
case_images: A brain MRI scan with sagittal T1 spin echo (SE), Axial T1SE/T2 SE/FLAIR and diffusion, and apparent diffusion coefficient (ADC) map was performed (within 24 hours after ICU admission), showing a cytotoxic cerebral edema (Figure 1) with bilateral and symmetrical hyperintensity inT2, FLAIR, and diffusion of the occipital lobes, cerebellar hemispheres, and periventricular white matter with low ADC related to cytotoxic edema. Hypersignal persists in T2, FLAIR, and diffusion in periventricular white matter with ADC restriction and in basal ganglia without ADC restriction (Figure 1).