A 52-year-old woman was admitted with intermittent headache lasting for 5 months. The patient's headache gradually worsened 1 week before admission, and vomiting occurred 2 days before hospitalization. Physical examination revealed normal findings. The patient had a history of hypertension and hyperlipidemia. No abnormality was found in the laboratory test results, which included blood routine examination, C-reactive protein, and erythrocyte sedimentation rate measurement. The serum tuberculosis antibody, toxoplasma antibody, and tumor markers were all negative. Serologic tests revealed positive results of the T. pallidum particle agglutination (TPPA) and toluidine red unheated serum test (TRUST), with a TRUST titer of 1:64. The human immunodeficiency virus (HIV) test was negative. Cerebrospinal fluid (CSF) examination was not performed. The patient denied any history related to venereal diseases, and the skin mucous membrane was free of rash and erythema. Conventional MR, proton MR spectroscopy, and perfusion MRI were carried out in the patient. All MR images were obtained using a 3.0 T clinical MR scanner (Discovery MR750, General Electric Healthcare, Milwaukee, WI, United States) with an eight-channel head coil. The conventional MRI sequences and parameters were as follows: axial T2-weighted imaging [repetition time (TR)/echo time (TE) = 5,200/90 ms, matrix = 512 x 512, field of view (FOV) = 24 cm, thickness = 5 mm, gap = 1.5 mm], axial T1-weighted imaging (TR/TE 1,750/25 ms, matrix = 320 x 256, FOV = 24 cm, thickness = 5 mm, gap = 1.5 mm), and diffusion-weighted imaging (TR/TE = 3,000/10 ms, matrix = 160 x 160, FOV = 24 cm, thickness = 5 mm, gap = 1.5 mm, b-value = 0, 1,000). Axial, sagittal, and coronal T1-weighted images after injection of gadolinium contrast agent (0.1 mmol/kg) were acquired. Perfusion imaging was performed by using a three-dimensional pseudo-continuous arterial spin labeling (ASL) technique with the specific imaging parameters: TR/TE = 4,600/10 ms, PLD = 1,525 ms, matrix = 128 x 128, FOV = 24 cm, thickness = 4 mm. ASL images were transferred to the workstation (ADW4.6, General Electric Healthcare) for post-processing and analyzed using FuncTool software (General Electric Healthcare) with the quantitative perfusion cerebral blood flow (CBF) map. Proton MR spectroscopy was obtained using a single-voxel point-resolved spectroscopy sequence (TR = 1,500 ms, TE = 35 ms). A volume of interest of 2 x 2 x 2 cm3 was selected from the lesion identified on the T2-weighted imaging sequence, and saturation bands were placed around the voxel. The process of shimming and water suppression was completed by the automatic pre-scanning program, making the bandwidth <7 and water suppression >97%. The MR machine's individual configuration software was applied to complete the correction of the baseline, identification of each compound, and analysis of peak value and ratio of each compound. MRI (Figures 1A-C) revealed multiple nodules with evident perilesional edema in the right temporal lobe, which was characterized by hypointensity on T1-weighted images, mostly hyperintensity on T2-weighted images, and slight hyperintensity on diffusion-weighted imaging. Contrast-enhanced T1-weighted images (Figures 1D-F) showed significant enhancement of the nodules and adjacent meninges ("dural tail"). In addition, the right ventricle was compressed and the middle line structure was skewed to the left. Single-voxel MR spectroscopy with an echo time of 35 ms (Figures 2A,B) revealed a slightly increased choline (Cho) peak and a slight decrease in the peaks of creatine (Cr) and N-acetylaspartate (NAA). The Cho/Cr and Cho/NAA ratio over the lesion was 1.24 and 0.932, respectively. A peak rising between 0.9 and 1.3 ppm represented the lipid/lactate. Perfusion MRI (Figure 2C) suggested that regional CBF in the nodule area was lower than that of the contralateral normal regions, with the highest relative CBF value of 0.84 in the lesion area, while the edema area around the lesion presented less perfusion. Merely based on the clinical manifestations, laboratory results, and conventional MR images, the diagnosis of inflammatory granuloma should be first suspected, while a differential diagnosis including neoplastic lesions such as meningiomas and brain metastasis should also be considered. However, the findings of advanced techniques such as MR spectroscopy and MR perfusion provide more clues in diagnosing inflammatory granuloma and have effectively ruled out meningioma and brain metastasis. Considering the evident mass effect of the lesion, the patient underwent surgical resection of the nodules. During the surgery, multiple solid nodules were seen protruding from the dura of the temporal lobe into the adjacent cerebral cortex and had an unclear boundary, hard and brittle texture, and general blood supply. Severe edema in the brain tissue of the right temporal lobe was also observed. Post-operative pathology (Figure 3) revealed granulation tissue with ischemic necrosis surrounded by multinucleated giant cells, plasmacytes, and lymphocytes. Based on the above findings, the clinical diagnosis of cerebral syphilitic gumma was made. Penicillin treatment (18 million U/day) was given for 2 weeks after the operation, and the patient's symptoms were relieved gradually. On the seventh day post-op, the patient was examined with non-contrast computed tomography (CT). The post-op CT (Figure 1G) showed no nodules, and a certain amount of hypodense edematous zone could be found on the right temporal lobe. After 6 months, the patient's headache disappeared completely.