Transdural Skull Base Infiltration by Glioblastoma: Case Report and Review of the Literature

We report the rare occurrence of a temporal glioblastoma multiforme (GBM) showing transdural tumor extension into adjacent mastoid cells. As the dura mater provides a barrier to intraaxial tumors, GBM seldom penetrates into the skull base, even though it is a high-grade astrocytoma with a tendency to spread. Yet, some mechanisms of GBM-induced skull invasion have been identified, making this entity a very rare but nonetheless relevant differential diagnosis in otherwise ambiguous cases of an intracerebral tumor extending into the skull base. In addition, imaging markers that may assist in distinguishing extra- from intraaxial tumor infiltration of the temporal bone are described.


Introduction
GBM is the most common primary malignant tumor of the central nervous system (CNS). It accounts for approximately 45% of tumors in this category, with an annual incidence of up to 5 per 100,000 persons [1]. As GBM is typically confned to the CNS, no TNM classifcation for the assessment of cancer spreading has been established.
Te incidence of extraneural metastasis of GBM has been defned as being as low as 0.2% [3]. Primary transdural skull base infltration by glioblastoma represents an even rarer fnding [4].

Case
A 61-year-old male patient presented to the emergency department because of left-sided brachiofacial hemiparesis. Te patient's history was otherwise unremarkable. Te cranial computed tomography (CCT) on admission disclosed a right temporal mass lesion with perifocal edema and lytic changes of the adjacent petrous bone (Figure 1(a)), indicative of tumorous infltration. Corresponding to the lytic bone changes seen on CCT, there was an extension of contrast-enhancing tumor components into the mastoid cells on contrast-enhanced magnetic resonance imaging (MRI; Figure 1(b)). MRI otherwise revealed an enhancing, cystic necrotic tumor, showing marked perifocal edema within the right temporal lobe (Figures 2(a) and 2(b)). Audiometric testing disclosed a hearing impairment.
Intraoperatively, glioblastoma-like tissue with necrotic areas, thrombosed vessels, and an infltration zone at the tumor margins was encountered. Following macroscopically complete resection, re-resection was performed under 5-ALA fuorescence, resulting in a 5-ALA-negative tumor resection cavity.
Early postoperative MRI confrmed complete intracranial resection, while questionable residual tumor was disclosed in the deep right mastoid cells.
Adjuvant treatment according to the CeTeG protocol was started including standard radiotherapy with 60 Gy (30 × 2 Gy) and six 42-day cycles with oral administration of Lomustine (CCNU) on days 1 and temozolomide (TMZ) on

Discussion
Our case showed typical features of a glioblastoma: an irregularly circumscribed, contrast-enhancing tumor with central necrosis, extensive vasogenic edema, and evidence of peritumoral neovascularization. In 2009, Kwak and Shatzkes [6] cited altogether twelve case reports of transdural tumor infltration from 1962 to 1996. Since then, only a few additional cases have been documented [4,[7][8][9].
Extracranial GBM dissemination is explicable in the case of prior skull base injuries, such as craniotomies, biopsies, or shunt placement [6]. Possible routes of transdural infltration, not facilitated by prior dural defects, include spreading through a dural slit, transdural herniation due to increased intracranial pressure, direct dural infltration by tumor cells and tumor migration through the dura mater via the cranial nerve foramina.
In our case, no previous skull base surgery was present, making iatrogenic dural defects as the route of infltration less probable. Yet, the mastoid tegmen is known as a thin bony plate, which may develop defects for various reasons, one of which being tumorous lesions and increased intracranial pressure [10].
In our case, we hypothesize that the combination of a rapidly growing tumor within the medial cranial fossa in combination with the low-resistance mastoid tegmen may have facilitated herniation and subsequent infltration of tumorous tissue into the upper mastoid cells.
Regarding imaging-based tumor assessment, the absence of a peritumoral cerebrospinal fuid (CSF) boundary (the CSF cleft sign) and a relatively narrow dural attachment (absence of the dural tail sign) helped to diferentiate the GBM from a common extraaxial mass such as a meningioma.

. Conclusion
Our case illustrates that in the setting of an ambiguous intracerebral tumor with transdural skull base invasion, glioblastoma represents a rare but nonetheless relevant diferential diagnosis.

Data Availability
Te image data used to support the fndings of this study are included within the article.

Conflicts of Interest
Te authors declare that there are no conficts of interest.