Figure 2. Brain images obtained on admission. Magnetic resonance imaging (MRI) at initial presentation revealed multiple abnormal lesions in the right frontoparietal lobe (white arrows), characterized by low signal intensity on T1-weighted sequences (A) and high signal intensity on T2-weighted sequences (B) and fluid-attenuated inversion recovery (FLAIR) sequences (C). The exact nature of these lesions remained uncertain. No notable abnormalities were observed in the N-acetyl-aspartate (NAA) and choline (Cho) peaks, while an inverted lactate peak was detected at 1.33 ppm (D). A follow-up brain MRI performed 20 days later revealed a decrease in T1 signal (E), an increase in T2 signal (F), and a decrease in FLAIR signal (G) in the right frontal lobe lesion compared with the initial examination (A–C), indicating liquefaction and necrosis. Magnetic resonance spectroscopy (MRS) revealed reduced NAA peak and abnormal lactate peak (H). During a second attack over a month later, new abnormal signal shadows (white arrows) in the right parietal lobe and left frontotemporal and parieto-occipital lobes in comparison with the initial hospitalization were obvious (I–K). The adjacent brain tissue was compressed, causing a shift of midline structures to the right (black arrow). The observed lesions exhibited characteristics consistent with vascular distribution. Subsequent analysis of computed tomography angiography and computed tomography venography did not reveal any significant abnormalities in the major blood vessels (L, P). After 15 days of treatment, a follow-up MRI showed the smaller focus with signs of necrolysis and liquefaction (M–O), prompting consideration of thrombosis or inflammation in small blood vessels leading to tissue necrosis.