Zhijie Yang, Ling Ai, Jun Shen, Aibin Zhou, Shaolin Zhang
This case highlights an exceptionally rare presentation of primary IDH-wildtype glioblastoma with spontaneous transdural extension and contiguous calvarial/mastoid osteolysis before any cranial intervention. In addition to expanding the clinicoradiological spectrum of GBM, this case underscores the diagnostic value of integrating MRI, MRS, histopathology, and molecular profiling in skull-invasive lesions. Our literature review suggests that superficially located tumors with prolonged dural contact may facilitate transdural spread, whereas molecular alterations associated with aggressive mesenchymal-like behavior and extracellular matrix remodeling may contribute to osseous invasion. This report adds a contemporary molecularly characterized example to the limited literature on skull-invasive GBM.
BACKGROUND: Glioblastoma (GBM) is the most common and most aggressive primary malignant tumor of the central nervous system in adults. Although GBM is characterized by highly infiltrative growth within the brain parenchyma, spontaneous transdural extension with direct invasion of the calvarium and skull base at initial presentation is exceptionally rare. Such cases may radiologically mimic metastatic skull tumors or other extra-axial lesions, creating diagnostic and therapeutic challenges.
CASE PRESENTATION: We report the case of a 63-year-old man who presented with dizziness, slowed responses, and progressive gait impairment. Magnetic resonance imaging revealed a heterogeneously enhancing right temporal lobe mass with marked peritumoral edema, while computed tomography demonstrated contiguous osteolytic destruction of the right temporal calvarium and mastoid region. Magnetic resonance spectroscopy showed a markedly elevated choline peak, reduced N-acetylaspartate, and increased lipid/lactate peak, supporting a high-grade infiltrative glioma. The patient underwent gross total resection of the intracranial tumor together with resection of the involved skull lesion and cranioplasty. Histopathology confirmed glioblastoma, CNS WHO grade 4. Molecular testing demonstrated an IDH-wildtype profile with TERT promoter mutation, CDKN2A/CDKN2B homozygous deletion, PTEN loss, chromosome 10 loss, MGMT promoter unmethylation, and absence of 1p/19q codeletion. Postoperatively, the patient received radiotherapy to the tumor bed (60 Gy/30 fractions) and surrounding low-risk field (54 Gy/30 fractions) with concurrent temozolomide, followed by adjuvant temozolomide. Early postoperative MRI indicated gross total resection. At 3-month follow-up, the patient remained alive without radiographic progression, with relief of headache and no new neurological deficits.
CONCLUSION: This case highlights an exceptionally rare presentation of primary IDH-wildtype glioblastoma with spontaneous transdural extension and contiguous calvarial/mastoid osteolysis before any cranial intervention. In addition to expanding the clinicoradiological spectrum of GBM, this case underscores the diagnostic value of integrating MRI, MRS, histopathology, and molecular profiling in skull-invasive lesions. Our literature review suggests that superficially located tumors with prolonged dural contact may facilitate transdural spread, whereas molecular alterations associated with aggressive mesenchymal-like behavior and extracellular matrix remodeling may contribute to osseous invasion. This report adds a contemporary molecularly characterized example to the limited literature on skull-invasive GBM.