case_images: PMC10539899_01
case_images: Cerebral MRI (2022.11): (A) T1WI; (B) T2WI; (C) SWI; (D) DWI. No signals in the right thalamus on the images acquired with these imaging sequences. MRI (A-D) conducted before the onset of the patient, and no abnormal signals were found. As a group of normal controls, we found subsequent changes in thalamic lesions. Cerebral MRI (2023.1.6): E: T1WI; (F) T2WI; (G) SWI hypointense punctate foci. (H) No DWI hyperintensity. Cerebral MRI (2023.1.19): (I) T1WI hypointensity in the right thalamus. (J) T2WI hyperintensity in the right thalamus; (K) SWI hypointense punctate foci in the right thalamus; (L) No DWI hyperintensity,represented the signal contrast of the rest of the MR Sequence; (N) T2WI hyperintensity in the right thalamus disappeared; (O) SWI hypointense punctate foci in the right thalamus; (P) No DWI hyperintensity.
case_images: fneur-14-1227505-g002.jpg
case_images: PMC10539899_01_fneur-14-1227505-g002.jpg
case_images: fig2
case_images: A brain MR was performed prior to the patient's onset (2022.11), and no abnormal signals were detected (Figures 2A-D). Following admission, the patient underwent a subsequent cerebral MRI re-examination, which revealed slightly elevated signals (T2) and low signals in the right thalamus (SWI) (Figures 2F,G). T1 or DWI (Figures 2E,H). The patient was treated with intravenous immunoglobulin (IVIG 0.4 g/kg d) for 5 days. MRI revealed that the right thalamus had T1 hypointensity and a more pronounced T2 hyperintensity than before. Moreover, hypointensity was detected on the susceptibility-weighted imaging (SWI), while no hyperintensity was noted on the diffusion-weighted imaging (DWI) (Figures 2I-L). Only the hypointense lesion on SWI was visible (Figures 2M-P).