Journal of Cancer Research and Therapeutics

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


Sumit Thakar1, Dilip Mohan1, Rakshith Srinivasa1, Nandita Ghosal2, Alangar S Hegde1,  
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

Correspondence Address:
Sumit Thakar
Department of Neurosurgery, Sri Sathya Sai Institute of Higher Medical Sciences, EPIP Area, Whitefield, Bengaluru - 560 066, Karnataka
India




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;11:1044-1044


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 2020 Sep 18 ];11:1044-1044
Available from: http://www.cancerjournal.net/text.asp?2015/11/4/1044/158199


Full Text

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}{Figure 2}{Figure 3}

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}{Figure 5}{Figure 6}

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

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3Kawano N, Yada K, Ogawa Y, Sasaki K. Spontaneous transdural extension of malignant astrocytoma. Case report. J Neurosurg 1977;47:766-70.
4Rainov 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.
5Li 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.