Fig. 3

Multi-parametric MRI dynamic changes of the brain of a 7-year-old patient who recovered completely. He presented with fever, tonic colonic convulsions, then DCL, behavior changes, abnormal movement, and agitation, was diagnosed with ANEC. At the onset of the disease, axial images (a), T1 WI (b), T2 WI (c and d) FLAIR show lesions on bilateral swollen thalamus, posterior limb of internal capsule, tegmen of pons, and right WM cerebellar parenchyma being low signal in T1WI with small focus of high signal in the center of the thalamic lesions (hemorrhage), heterogeneous high signal in T2WI, and FLAIR. e and f DWI and ADC show peripheral restriction on DWI and typical tricolor pattern of thalamic lesions on ADC. g Contrast-enhanced T1WI shows bilateral thalamic homogenous enhancement. h and i SWI shows signal drop of hemosiderin deposition in the bilateral thalami and posterior brain stem. j Single-voxel MRS (TE, 115) of left thalamic lesion shows reduced NNA peak, increased glutamate/glutamine complex peak intensities at 2.3 ppm (arrow), and lipid/lactate complex peak intensities at 1.5 ppm. Broadening of the line-width may be caused by the occurrence of petechial hemorrhage within the lesion. Follow-up after 6 weeks, axial images (k and l) T2 WI reveal disappearance of WM cerebellar lesion, impressive regression of the thalamic size, and brain stem lesion with subtle bright signal. m SWI shows no signal drop. n MRS shows absence of the lactate and glutamate/glutamine peak and the NAA peak returns within the normal range