1. Introduction

Astroblastoma is an uncommon primary CNS tumor, traditionally recognized by a circumscribed growth pattern, astroblastic perivascular pseudorosettes and variable vascular hyalinization. The 2021 WHO CNS classification incorporated astroblastoma, MN1-altered as a molecularly defined entity within circumscribed astrocytic gliomas. Histology remains important, but recent literature demonstrates that morphology alone may overlap with ependymoma and other neuroepithelial tumors. Molecular profiling has consequently become central to contemporary classification.

Recent molecular work has shown that the group previously classified as astroblastoma, MN1-altered is heterogeneous. A 2026 cohort of 200 tumors identified three fusion-defined groups, including MN1::BEND2, EWSR1::BEND2 and MN1::CXXC5, with clinically different outcomes. This makes precise molecular characterization particularly important when interpreting older histopathological diagnoses.

The present case is clinically unusual because it occurred in a 59-year-old man with a giant left frontoparietal cystic lesion. The patient recovered completely after gross total macroscopic resection but died suddenly on postoperative day 3 from autopsy-confirmed pulmonary thromboembolism.

2. Case Presentation

A 59-year-old man with known arterial hypertension presented with a three-month history of progressive headache, dysarthria and progressive reduction in strength of the right hemibody. He subsequently developed depressed consciousness. On admission, the Glasgow Coma Scale was 14/15, with right hemiplegia. Karnofsky Performance Status was greater than 70. There was no documented previous intracranial neoplasm.

2.1. Neuroimaging

Non-contrast CT demonstrated a large left frontoparietal hypodense lesion with a central cystic component and discrete enhancement of the solid component after contrast administration. MRI demonstrated a predominantly cystic and nodular left frontoparietal lesion, hypointense on T1 and hyperintense on T2, measuring approximately 7.5 × 5.0 × 5.4 cm, with approximately 10 mm of midline shift and compression of the lateral ventricles.

Figure 1. Preoperative CT (1 and 2) and MRI (3 and 4) demonstrating the large left frontoparietal cystic-nodular lesion with mass effect and midline shift.

Figure 1. Preoperative CT (1 and 2) and MRI (3 and 4) demonstrating the large left frontoparietal cystic-nodular lesion with mass effect and midline shift.

2.2. Surgical Procedure

A left frontoparietal osteoplastic craniotomy was performed using five burr holes, followed by an inferiorly based curvilinear durotomy. The cystic component was punctured and aspirated, yielding brown-colored fluid. Corticotomy was performed at the parietal level while avoiding the primary motor cortex. The solid mural component was dissected and resected circumferentially in all directions, aiming for gross total macroscopic removal. After confirmation of no visible residual tumor, the operative cavity showed apparently healthy surrounding brain. Hemostasis was achieved with bipolar coagulation and Spongostan. The cavity was irrigated with 0.9% saline, the dura was closed hermetically, the bone flap was replaced and an epidural drain was positioned. No intraoperative complication was reported.

Figure 2. Intraoperative photograph showing the left frontoparietal exposure during tumor surgery.

2.3. Histopathology

Histological examination demonstrated blood elements and a neoplastic proliferation composed of rounded and oval cells. Areas of small cells arranged radially around blood vessels formed perivascular pseudorosette-like structures. Mitotic figures were very uncommon. The morphology was interpreted as compatible with astroblastoma with low proliferative activity. No molecular testing for MN1/BEND2/CXXC5 or DNA methylation profiling was available.

Figure 3. Histopathological examination (hematoxylin and eosin) showing a cellular neoplastic proliferation with numerous vascular structures and perivascular architectural patterns compatible with astroblastic pseudorosettes.

2.4. Postoperative Course and Autopsy

The immediate postoperative course was excellent, with complete improvement of the preoperative neurological deficits. The patient's Karnofsky Performance Status reached 100. As thromboprophylaxis, enoxaparin (0.3 mL subcutaneously once daily) was administered. However, on postoperative day 3, the patient developed acute respiratory failure followed by cardiac arrest. Cardiopulmonary resuscitation, including the administration of vasoactive drugs, was unsuccessful. Autopsy demonstrated findings consistent with pulmonary thromboembolism, which was considered the cause of death despite the administration of pharmacological thromboprophylaxis.

Figure 4. Autopsy findings demonstrating pulmonary thromboembolism.

3. Discussion

The present case expands the clinical spectrum of astroblastoma because of the patient's age and sex. Contemporary literature indicates that astroblastoma predominantly affects children, adolescents and young adults, with a female predominance. A 2024 series of eight molecularly tested cases had a median age of 35.1 years and a female-to-male ratio of 1.6:1, while a systematic review of adults with MN1-altered CNS tumors also emphasized marked demographic and clinical heterogeneity. The present 59-year-old male is therefore unusual, although elderly molecularly confirmed cases have been reported.

The imaging phenotype is nevertheless compatible with the recognized spectrum. Astroblastomas are often circumscribed supratentorial tumors with solid, cystic or mixed morphology. Radiology-pathology correlation studies describe well-defined cystic-solid masses, sometimes with a bubbly or mural-nodular appearance. Our lesion was very large, measured 7.5 cm in its greatest dimension and produced 10 mm of midline shift and ventricular compression, explaining the progressive motor deficit and impaired consciousness.

Histologically, the presence of perivascular pseudorosette-like architecture and low mitotic activity supported the original diagnosis. However, contemporary studies show that the diagnosis cannot always be reliably established by morphology alone. MN1::BEND2-positive tumors may lack classic astroblastoma morphology, while EWSR1::BEND2, YAP1::BEND2, MAMLD1::BEND2 and TCF3::BEND2 rearrangements have been reported in astroblastoma-like CNS tumors. Therefore, the most defensible wording for this case is 'astroblastoma based on characteristic histopathological findings, with low proliferative activity; molecular characterization was not available.'

The 2026 study of 200 tumors is particularly relevant. DNA methylation and sequencing identified three groups: MN1::BEND2-enriched supratentorial Group A, EWSR1::BEND2-enriched Group B, and MN1::CXXC5 Group C. Five-year progression-free survival was 47%, 14% and 75%, respectively, while 10-year overall survival was 89%, 54% and 89%. These data show that astroblastoma is not biologically uniform and that molecular subgrouping may become central to risk-adapted treatment.

Surgery remains the principal treatment for accessible symptomatic tumors. Individual-patient meta-analysis and recent series support gross total resection as the main modality associated with disease control, although the evidence is observational. In our patient, complete macroscopic resection was followed by complete neurological recovery and KPS 100, consistent with the favorable immediate neurological outcomes reported after extensive resection. Recent pediatric cases with MN1::BEND2 fusion have likewise shown stability after gross total resection.

The fatal event in our patient was not evidence of tumor progression. The patient developed acute respiratory failure on postoperative day 3, and autopsy established pulmonary thromboembolism. A 2024 meta-analysis of patients undergoing craniotomy for brain tumors reported a clinically relevant prevalence of postoperative venous thromboembolism. Current perioperative neurosurgical guidance emphasizes individualized prophylaxis because clinicians must balance thrombotic risk against intracranial bleeding risk. The available case data do not document the exact prophylaxis strategy; therefore, no conclusion should be drawn about adequacy or causality.

The case also demonstrates the value of autopsy in sudden postoperative deterioration. In a neurosurgical patient, acute respiratory collapse may have several possible causes, and autopsy can establish the diagnosis when clinical circumstances are uncertain. Here, it separated the systemic postoperative complication from the neurological and oncological outcome.

A further implication is the importance of molecular testing. If archival paraffin-embedded material remains available, MN1/BEND2/CXXC5 fusion testing, RNA sequencing or DNA methylation profiling could be considered. Such testing could potentially refine the diagnosis and permit comparison with current molecular subgroups. The lack of molecular testing is the main limitation of this report.

Overall, the case demonstrates a striking divergence between immediate neurosurgical outcome and short-term systemic outcome: complete neurological recovery followed by fatal pulmonary thromboembolism. This combination, together with the patient's advanced age and giant cystic frontoparietal lesion, constitutes the principal contribution of the report.

4. Comparative Outcome