Neurocysticercosis (NCC) and glioblastoma present overlapping radiological features, particularly multiple ring-enhancing lesions with surrounding vasogenic edema, posing a significant diagnostic challenge. NCC typically progresses through four distinct pathological stages: vesicular, colloidal vesicular, granular nodular, and calcified nodular. The colloidal vesicular stage is most frequently associated with ring enhancement and pronounced perilesional edema, owing to the host’s robust inflammatory response to the degenerating parasite. This specific appearance closely mimics neoplastic processes.
Although glioblastoma conventionally presents as a solitary, irregular, and infiltrative mass with central necrosis, atypical presentations featuring multiple relatively well-defined cystic or ring-enhancing lesions complicate its differentiation from infectious etiologies. We report a rare case in which glioblastoma closely mimicked the colloidal NCC vesicular stage, clinically and radiologically, leading to an initial misdiagnosis.
CASE
A 73-year-old Korean woman presented to the emergency department with a one-month history of progressive left-sided weakness. Her medical history included hypertension, chronic kidney disease, osteoporosis, and seropositive rheumatoid arthritis. The latter was maintained on methotrexate (10 mg/week) and oral corticosteroids, which had been tapered and discontinued approximately one month prior to symptom onset. She had no history of seizures, recent travel to highly endemic areas, or raw meat consumption.
Neurological examination revealed mild left-sided hemiparesis (Medical Research Council [MRC] grade IV+ in the upper extremity and IV- in the lower extremity) without other focal neurological deficits or signs of increased intracranial pressure.
Initial brain magnetic resonance imaging (MRI) revealed multiple ring-enhancing nodular lesions in the right primary motor cortex, premotor cortex, and centrum semiovale. The lesions, surrounded by significant vasogenic edema, demonstrated central signal intensities similar to those of cerebrospinal fluid on T1- and T2-weighted images (Fig. 1A–1C). A distinct hypointense rim was noted on T2-weighted imaging, and diffusion-weighted imaging (DWI) showed no definite central diffusion restriction. An eccentric, scolex-like enhancing nodule protruding into one of the lesions was observed (Fig. 1D).
Given the patient’s history of immunosuppression and imaging findings, neurocysticercosis in the colloidal vesicular stage was initially considered the most likely diagnosis. The routine laboratory test results and inflammatory marker levels were unremarkable. Cerebrospinal fluid (CSF) analysis revealed a normal opening pressure (18 cm H2O), no pleocytosis (0 RBC/μL, 0 WBC/μL), and normal protein (42 mg/dL) and glucose levels. Serum and CSF cysticercosis antibodies tested negative. Further infectious workups, including toxoplasmosis serology, interferon-gamma release assay (IGRA) for tuberculosis, and Echinococcus antibodies, were negative.
The patient was empirically treated with intravenous dexamethasone, leading to left-sided motor strength improvement to MRC grade IV+ and a reduction in perilesional edema on follow-up MRI (Fig. 2A). However, subsequent imaging revealed a mixed response: while some lesions slightly decreased in size, others became more prominent (Fig. 2B), and a new focal-enhancing lesion appeared (Fig. 2C). Antiparasitic therapy with albendazole and praziquantel was initiated but had to be temporarily discontinued due to pancytopenia development.
Due to equivocal progression, a navigation-guided open brain biopsy was performed one month after admission. The formal pathology report of the cystic wall revealed “extensive hemorrhage and some vasculature,” with a few lymphocytes but no malignant cells. Assuming a treated, dying parasite, the patient was discharged.
One month later, the patient was readmitted due to worsening left hemiplegia. Follow-up MRI revealed significant interval progression of all enhancing nodules (Fig. 3), with increased cerebral blood volume (CBV) and diffuse T2 hyperintensity, suggestive of tumor infiltration. Subsequently, a craniotomy with subtotal tumor removal was performed.
Histopathological examination of the resected tissue revealed an adult-type diffuse glioma. Immunohistochemistry was positive for glial fibrillary acidic protein and showed positive ATRX, negative p53, and a Ki-67 labeling index of approximately 8%, although the overall radiological and clinical features were consistent with high-grade glioma. Molecular profiling was consistent with an Isocitrate dehydrogenase (IDH)-wild-type status. The final integrated diagnosis was IDH wild-type glioblastoma (grade 4).1 The patient subsequently received postoperative palliative radiotherapy (45 Gy/15 Fx) but eventually experienced disease progression.
After the patient’s death, a written informed consent for the publication of this case report and accompanying images was obtained from the patient’s son.
DISCUSSION
This case highlights the profound diagnostic difficulty in distinguishing atypical, multifocal glioblastoma from neurocysticercosis when imaging features heavily overlap.
The initial radiologic presentation of multiple ring-enhancing lesions with significant edema and a T2-hypointense rim strongly suggested a colloidal vesicular stage of NCC. At this stage, the host immune system attacks the dying parasite. Critically, however, the scolex undergoes degeneration during this phase and does not appear as a distinct, enhancing nodule2-4; a discrete intracystic scolex (the “dot-in-a-hole” appearance) is a hallmark of the earlier vesicular stage. Consequently, the persistent, distinct scolex-like nodule observed within the patient’s lesions was discordant with the colloidal vesicular stage, which should have been recognized as a key diagnostic clue and prompted early suspicion of a neoplastic process (an eccentric tumor necrosis or an enhancing tumor nodule closely mimicking a scolex). When a distinct enhancing nodule is identified alongside features of the colloidal vesicular stage, clinicians should maintain a high suspicion index for tumor mimicry. The stage-specific imaging features of NCC underpinning this reasoning are summarized in Table 1.
Meticulous differential diagnosis is critical for multiple ring-enhancing lesions, particularly for those with a T2-hypointense rim.5 Central diffusion restriction on DWI was notably absent in this patient. The patient’s negative IGRA and normal CSF profile excluded tuberculomas. Fungal infections were considered but deeper central nervous system involvement or concomitant pulmonary findings were absent. Metastases were largely excluded based on negative systemic computed tomography imaging. While negative serology does not absolutely exclude NCC, particularly in solitary or heavily calcified lesions, the lack of epidemiological risk factors and the absence of serum and CSF cysticercosis antibodies in active, multiple, and highly edematous lesions are atypical and should prompt consideration of neoplastic processes.6
This case illustrates the limitations of initial brain biopsies in highly heterogeneous tumors. The first open biopsy revealed extensive hemorrhage and vascular tissue. Glioblastomas are characterized by chaotic angiogenesis and microvascular proliferation, which are highly prone to hemorrhage. Sampling errors in areas of tumor hemorrhage or necrosis easily produce false-negative histopathological results, delaying oncological treatment.
Ultimately, the mixed radiological response to steroids, failure of antiparasitic therapy, and CBV progression on perfusion MRI were critical glioblastoma indicators.7 Therefore, while negative serology does not absolutely exclude NCC, the presence of progressive lesions despite empirical therapy should strongly prompt reconsideration of alternative diagnoses, such as high-grade gliomas.
Glioblastoma can convincingly mimic neurocysticercosis on imaging, particularly when presenting as multiple ring-enhancing lesions resembling the colloidal vesicular stage. Negative serologic and CSF findings, the absence of epidemiological risk factors, and equivocal responses to empirical therapy must prompt a rapid clinical pivot. When clinical suspicion diverges from initial benign biopsy results, physicians must account for tumor heterogeneity and sampling error, pursuing serial imaging and repeat tissue diagnosis to avoid critical delays in glioblastoma management.
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