On November 2017, a 66-year-old woman with left-sided hemiparesis and left motor seizures was admitted to the emergency room (ER). On November 21, 2017, an initial multi-slice computed tomography (MSCT) brain scan revealed a right temporal hypodensity and chronic small vessel ischemic changes in the deep white matter that were suggestive of cerebrovascular stroke (Fig. 1).
On November 22, the patient underwent magnetic resonance imaging (MRI) brain scans, which showed a poorly circumscribed T1-hypointense and T2-fluid-attenuated inversion recovery (FLAIR)-hyperintense lesion at the medial aspect of the right temporal lobe with partially restricted MRI apparent diffusion coefficient (ADC) values and surrounding edema. Diffusion-weighted imaging (DWI) determined that diffusion was also partially restricted (Fig. 1, 2).
In clinical correlation with the patient’s seizures, this temporal lobe lesion was thought to be a radiological feature of herpetic encephalitis. CSF analysis revealed lymphocytic pleocytosis, normal glucose levels, and increased protein levels. Furthermore, the CSF polymerase chain reaction (PCR) test was positive for herpes simplex virus 1 (HSV-1). Therefore, a herpetic encephalitis diagnosis was recommended and anti-encephalitic measures were initiated. Despite treatment, the patient’s clinical condition deteriorated. On November 30, another MSCT brain scan was performed and revealed ill-defined bilateral temporal lobe hypodensities with surrounding edema. On December 2, another MRI brain scan was subsequently recommended and conducted; it confirmed that bilateral T1-hypointense and T2-FLAIR-hyperintense lesions were present in both temporal lobes with surrounding edema and that the lesions were exerting mass effect on the nearby anterior horns of the lateral ventricles (Fig. 1, 2, 3).
Upon follow-up on December 14, an MRI brain scan performed showed a slight progression of the size of the temporal lesions with evident restriction on the ADC map (Fig. 1, 2, 3, 4).
On March 12, 2018, the temporal lobe masses became evident. After the previous MRI brain scan, they had significantly increased in size and developed the classical radiological features of glioblastoma with heterogeneous signals, peripheral vasogenic edema, infiltration into surrounding brain tissue, and high signal intensity on the ADC map (Fig. 1, 2, 3, 4, 5).
On March 22, MRI perfusion was done and revealed high relative cerebral blood volume (r-CBV) and infiltration into surrounding normal-looking brain tissue (Fig. 2). The patient then underwent surgical resection of the right temporal lobe mass due to extensive mass effect and uncal and subfalcine herniation. Histopathology confirmed the glioblastoma multiform diagnosis. Histopathology of the specimen revealed a cellular neoplasm with vascular proliferation and areas of necrosis. The tumor was composed of areas of hypercellularity and areas of hypocellularity, and the individual cells exhibited moderate pleomorphism and abundant eosinophilic cytoplasm. The cells were also actively undergoing mitosis.
Fully informed consent was prospectively obtained from the study participant and can be requested at any time. The study protocol conformed to the ethical guidelines of the 1975 Helsinki Declaration.