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LETTER TO THE EDITOR
Year : 2015  |  Volume : 11  |  Issue : 4  |  Page : 1044

Intracranial high grade glioma masquerading as a skull base lesion: Report of two unusual cases


1 Department of Neurosurgery, Sri Sathya Sai Institute of Higher Medical Sciences, Bengaluru, Karnataka, India
2 Department of Pathology, Sri Sathya Sai Institute of Higher Medical Sciences, Bengaluru, Karnataka, India

Date of Web Publication15-Feb-2016

Correspondence Address:
Sumit Thakar
Department of Neurosurgery, Sri Sathya Sai Institute of Higher Medical Sciences, EPIP Area, Whitefield, Bengaluru - 560 066, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-1482.158199

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How to cite this article:
Thakar S, Mohan D, Srinivasa R, Ghosal N, Hegde AS. Intracranial high grade glioma masquerading as a skull base lesion: Report of two unusual cases . J Can Res Ther 2015;11:1044

How to cite this URL:
Thakar S, Mohan D, Srinivasa R, Ghosal N, Hegde AS. Intracranial high grade glioma masquerading as a skull base lesion: Report of two unusual cases . J Can Res Ther [serial online] 2015 [cited 2019 Sep 21];11:1044. Available from: http://www.cancerjournal.net/text.asp?2015/11/4/1044/158199

Sir,

Though gliomas primarily affect the white or gray matter of the brain, they are rarely known to invade and destroy the skull base. We report two unusual cases in which high grade gliomas presented with features of skull base lesions without having caused any significant intracranial symptoms.

A 53-year-old man presented with right sided proptosis and a right temporal swelling. Computed tomography and magnetic resonance imaging (MRI) [Figure 1] showed an enhancing lesion in the right middle cranial fossa eroding the right sphenoid, maxillary sinus, squamous temporal bone, and orbit. Aspiration cytology of the temporal swelling was reported as malignant astrocytoma [Figure 2]. He underwent a right temporal craniotomy and tumor debulking. The involved dura with an adjacent bony rim were excised as well. Histopathology was suggestive of a glioblastoma mutiforme (GBM) (WHO Grade IV) with marked desmoplasia [Figure 3].
Figure 1: Computed tomography brain showing a lesion in the right middle cranial fossa floor (a). Erosion of the right maxillary sinus and orbit (b), and of the right sphenoid and squamous temporal bones (c). T2 magnetic resonance imaging (MRI) showing a lesion in the right temporal and subtemporal regions (d). T1 gadolinium MRI (e). Inferior extent of the lesion into the infratemporal fossa (f)

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Figure 2: Smear preparation showing oval to spindle tumor cells with cytoplasmic projections

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Figure 3: Paraffin section demonstrating tumor cells (curved arrow) with marked desmoplasia (straight arrow) (a); nuclear pleomorphism (b); mitotic activity (straight arrow) (c) and immunopositivity for glial fibrillary acidic protein (d). (H and E, [a] ×100, [b and c] ×400) (avidin biotin complex immunoperoxidase [d] ×100)

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The second patient was a 42-year-old man who presented with proptosis of the left eye. He had previously undergone excision, radiation, and chemotherapy for a left frontal anaplastic oligodendroglioma (AO). MRI brain at his first admission [Figure 4]a] had shown a heterogeneously enhancing mass in the left frontal lobe. Follow-up MRI 4 years later had shown no recurrence [Figure 4]b]. MRI at this admission [Figure 4]c-f] showed a recurrent lesion in the left frontal region extending into the orbit. He underwent a left frontal recraniotomy and decompression of the lesion. The osteo-dural defect in the orbital roof was repaired with a pericranial patch. Histopathology was suggestive of an AO [Figure 5]. The previous slides were reviewed [Figure 6], and the histological features of both the specimens were found to be similar.
Figure 4: T1 magnetic resonance imaging (MRI) brain during the first admission showing a large, enhancing mass in the left frontal lobe (a). Follow-up MRI showing no recurrence (b). T2 MRI at the second admission showing a recurrent lesion in relation to the left orbit (c). Axial section showing heterogeneous enhancement of the lesion (d). Cranial-caudal extent of the lesion (e). Extension of the lesion into the orbit (f)

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Figure 5: Paraffin section showing perinuclear halo (straight arrow) (a) with tumor cell infiltration in dura and (inset) immunopositivity for GFAP (b). (H and E, [a] ×400; [b] ×100) (avidin biotin complex immunoperoxidase, [inset] ×100)

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Figure 6: Paraffin section at the time of the first surgery showing round tumor cells with a perinuclear halo (a). High power view of the same (b). (H and E, [a] ×100; [b] ×400)

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Bony invasion in malignant gliomas have been classified into two categories. In the first type of invasion, tumors on the convexity invade the adjoining calvarium. The second type of invasion is seen in temporal lobe tumors that involve the middle fossa floor. [1] There have, however, been reports of gliomas invading other skull base regions. [2] Macroscopically, extradural extension of gliomas has been described to occur through perivascular or dural slits; along the cranial nerves; or via., direct dural destruction. [3] The latter route is the implicated mechanism following radiation therapy or a previous surgery.

The phenomenon of a "skull base glioma" (SBG), with the tumor masquerading clinico-radiologically as a skull base lesion, is rare in glioma literature. Gliomas typically present with seizures, nonlocalizing symptoms or focal neurological deficits. This is in contrast to skull base lesions that present with symptoms related to the structures on the cranial base or with localized headache related to dural stretch or to periosteal or bony expansion.

The histopathology in most of the previously reported SBGs was GBM. [4] Our second case is the first report of an AO presenting as a SBG. This pathology has been reported earlier to have extraneural metastasis, with molecular markers such as 1p and 19q deletions, PTEN exon mutations, and hypermethylation of the MGMT promoter predisposing to this occurrence. [5] Further studies are required to validate whether any such genetic errors predispose AOs and other gliomas for skull base invasion.

 
 > References Top

1.
Russell DS, Rubinstein LJ, editors. Pathology of Tumours of the Nervous System. 5 th ed. London: Edward Arnold; 1989.  Back to cited text no. 1
    
2.
Tomac D, Chudy D, Lambaša S, Topic I, Grahovac G, Zoric A. Extracranial propagation of glioblastoma with extension to pterygomaxillar fossa. World J Surg Oncol 2011;9:53.  Back to cited text no. 2
    
3.
Kawano N, Yada K, Ogawa Y, Sasaki K. Spontaneous transdural extension of malignant astrocytoma. Case report. J Neurosurg 1977;47:766-70.  Back to cited text no. 3
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4.
Rainov NG, Holzhausen HJ, Meyer H, Burkert W. Local invasivity of glioblastoma multiforme with destruction of skull bone. Case report and review of the literature. Neurosurg Rev 1996;19:183-8.  Back to cited text no. 4
    
5.
Li G, Zhang Z, Zhang J, Jin T, Liang H, Gong L, et al. Occipital anaplastic oligodendroglioma with multiple organ metastases after a short clinical course: A case report and literature review. Diagn Pathol 2014;9:17.  Back to cited text no. 5
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