case_images: PMC10512083_01
case_images: (A) Timeline of major clinical events, Imaging findings and immunosuppressive treatments. A1: CT scon at time of mental status change-bilateral thalamic hypodensities. A2-5: T2 Flair MRI at level of thalamus at indicated time points-time course of resolution of bilateral thalamic lesions. (B) Additional relevant MRI imaging findings. B1: T2 Flair MRI at time of initial MRI-bilateral pontine hyperintensity, subtle right temporal lobe edema. B2: T2 Flair MRI on day 2 - midbrain edema. B3: T1 with contrast MRI demonstrating ring enhancing thalamic lesions. B4: Diffusion weighted imaging (DWI) MRI-core of thalamic lesions restrict diffusion. B5: Susceptibility weighted imaging (SWI) MRI hemorrhage in thalamic lesions.
case_images: fneur-14-1239746-g002.jpg
case_images: PMC10512083_01_fneur-14-1239746-g002.jpg
case_images: fig2
case_images: On the night of admission, she acutely developed diplopia, hallucinations, and progressive lethargy over several hours with head computed tomography (CT) demonstrating symmetric hypodensities in the bilateral thalami (Figure 2). MRI brain, with and without contrast, showed symmetric, bi-thalamic T2 hyperintensity with central oval shaped cystic areas with rim-enhancement, faint hemorrhage, circumferential diffusion restriction, and multifocal T2 hyperintense lesions, consistent with vasogenic edema, in the bilateral cortex, juxtacortical white matter, bilateral hippocampi, midbrain, pons and cerebellum (Figure 2). She was given a loading dose of IV MP 500 mg 22.5 h after acute mental status decline (Figure 2) and continued IV MP 375 mg every 6 h (total daily dose 30 mg/kg) for four more days. Repeat brain MRI 14 days after her initial study demonstrated marked improvement of previously noted edema with minimal residual abnormal T2 signal in the bilateral thalami, inferior and high frontal cortex (Figure 2).