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| LETTER TO EDITOR |
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| Year : 2013 | Volume
: 61
| Issue : 4 | Page : 433-434 |
Intracranial germ cell tumor mimicking granulomatous inflammation
Sumit Thakar, Sunil V Furtado, Nandita Ghosal, Alangar S Hegde
Department of Neurosurgery, Sri Sathya Sai Institute of Higher Medical Sciences, Whitefield, Bangalore - 560 066, Karnataka, India
| Date of Submission | 14-Apr-2013 |
| Date of Decision | 08-Jun-2013 |
| Date of Acceptance | 22-Jul-2013 |
| Date of Web Publication | 4-Sep-2013 |
Correspondence Address:
Sumit Thakar
Department of Neurosurgery, Sri Sathya Sai Institute of Higher Medical Sciences, Whitefield, Bangalore - 560 066, Karnataka
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0028-3886.117597
How to cite this article:
Thakar S, Furtado SV, Ghosal N, Hegde AS. Intracranial germ cell tumor mimicking granulomatous inflammation. Neurol India 2013;61:433-4 |
Sir,
A combination of optico-chiasmatic and periventricular involvement in a patient with a pituitary-hypothalamic lesion ordinarily invokes the possibility of granulomatous inflammatory disorders like sarcoidosis, histiocytosis, and tuberculosis. This report, with such a radiological picture being secondary to a germ cell tumour (GCT) at its initial presentation, is the first-of- its-kind in indexed literature.
An 8-year-old girl presented with progressive and painless visual deterioration in both eyes since 6 months and altered behavior since 1 week. Based on her imaging findings, she had been empirically started on antitubercular therapy and steroids by a local physician. Neurological examination revealed bilateral primary optic atrophy and absent perception of light. There were no signs of meningeal irritation. Magnetic resonance imaging (MRI) brain [Figure 1]a-d showed a diffuse, contrast enhancing lesion with contiguous components in the sellar-suprasellar, optico-chiasmatic, and periventricular regions. There was no hydrocephalus. Hormone evaluation was normal. In view of the diffuse nature of the disease, she was planned for a biopsy of the lesion. At surgery via a transnasal transphenoidal route, a reddish, soft, and vascular tumor was encountered in the sella. Histopathological examination of the tissue [Figure 2] revealed a malignant tumor with large round to oval cells showing nuclear pleomorphism and brisk mitotic activity. Few large cells with smudged nuclei were seen with sprinkling of lymphocytes. Tumor cells were diffusely positive for cytokeratin, variably positive for alpha fetoprotein and negative for glial fibrillary acidic protein. Focal positivity for S-100 and placental alkaline phosphatase was also seen. These findings were suggestive of a malignant mixed GCT. Spinal imaging and a systemic workup including serum and cerebrospinal analysis for tumor markers (alpha fetoprotein and beta-human chorionic gonadotropin) were negative. She succumbed to her illness a month after commencing local and whole-ventricular radiation therapy. | Figure 1: MRI brain (a) T2‑weighted axial section showing a heterogeneous periventricular lesion along the frontal horns of the lateral ventricles. Postcontrast T1 axial sections demonstrating (b) enhancement in bilaterally thickened optic nerves and in the chiasm and (c) intense ependymal enhancement along the bodies of the lateral ventricles. (d) Sagittal section showing the contiguous enhancing components in the optico‑chiasmatic, sellar‑suprasellar, and periventricular regions
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 | Figure 2: Microphotographs of the lesion: (a) Large tumor cells with large nuclei, prominent nucleoli and abundant, clear cytoplasm are noted among reactive inflammatory cells. (b) Tumor cells demonstrating reactivity to placental alkaline phosphatase (PLAP) (microphotographs are original magnification ×400)
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While a nonexophytic involvement of the optic apparatus occurs commonly in gliomas and sarcoidosis, periventricular enhancement occurs in pathologies like bacterial or tuberculous ventriculitis in the clinical context of infection, and in tumors like lymphoma, ependymoma, and metastases. The type of enhancement may also give a hint to the pathology: Nodular enhancement favors a tumoral process; a thin linear pattern suggests a viral etiology, while a band pattern may occur in viral, lymphomatous, or tuberculous inflammation. [1]
Visual symptoms caused by GCTs are usually due to compression of the optic apparatus by an expanding suprasellar mass. Infiltration of the optic nerves or chiasm by disseminated subarachnoid disease occurs late in the clinical course, though their primary involvement by the tumor has also been rarely reported. [2] Periventricular spread is another late phenomenon in the disease, and is usually synonymous with recurrence. [3] Radiological demonstration of these features at presentation in our patient was indicative of the aggressiveness of the GCT, a fact that was underscored by the rapidly fatal outcome.
| » References | |  |
| 1. | Guerini H, Helie O, Leveque C, Adem C, Hauret L, Cordoliani YS. Diagnosis of periventricular ependymal enhancement in MRI in adults. J Neuroradiol 2003;30:46-56. 
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| 2. | DiLuna ML, Two AM, Levy GH, Patel T, Huttner AJ, Duncan CC, et al. Primary, non-exophytic, optic nerve germ cell tumors. J Neurooncol 2009;95:437-43.
[PUBMED] |
| 3. | Alapetite C, Brisse H, Patte C, Raquin MA, Gaboriaud G, Carrie C, et al. Pattern of relapse and outcome of non-metastatic germinoma patients treated with chemotherapy and limited field radiation: The SFOP experience. Neuro Oncol 2010;12:1318-25.
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[Figure 1], [Figure 2]
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