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LETTER TO EDITOR |
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Year : 2014 | Volume
: 62
| Issue : 4 | Page : 444-446 |
Bilateral thalamic gliomas: Report of two cases with review of literature
Bi-Wu Wu1, Yi Zhang2, Wen-Gang Li1, Zhi-Qi Li2, Bi-Wu Wu1, Yi Zhang2, Wen-Gang Li1, Zhi-Qi Li2
1 Department of Neurosurgery, 5th People's Hospital of Shanghai, Shanghai, China 2 Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China
Date of Web Publication | 19-Sep-2014 |
Correspondence Address: Yi Zhang Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai China Yi Zhang Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai China
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0028-3886.141247
How to cite this article: Wu BW, Zhang Y, Li WG, Li ZQ, Wu BW, Zhang Y, Li WG, Li ZQ. Bilateral thalamic gliomas: Report of two cases with review of literature. Neurol India 2014;62:444-6 |
Sir,
Bilateral thalamic gliomas (BTGs), extremely rare central nervous system tumors, hence this report.
Case 1: A 9-year-old girl who presented with headaches with progressive intensity and vomiting of 4 months duration and decline in the physical and mental activity of 2 months duration and recent memory disturbances. Neurological examination showed recent memory disturbances, diplopia, and unsteady gait. Magnetic resonance imaging (MRI) revealed a non-contrast enhancing mass (5.5 Χ 4.0 Χ 4.0 cm) lesion occupying both the thalami, hypointense on T1-weighted [Figure 1]a, and hyperintense on T2-weighted and fluid attenuation inversion recovery (FLAIR) images [Figure 1]b-d. MR spectroscopy (MRS) further revealed increase in the levels of choline and creatinine, with the latter being higher than the former and lower levels of N-acetylaspartate (NAA) [Figure 1]e. Partial (50%) resection of the tumor was performed through interhemispheric transcallosal approach [Figure 2]a-d. Post-operative period was uneventful. Histopathology showed anaplastic astrocytoma (WHO grade III) [Figure 3]a-c. After discharge, she received radiotherapy (60 Gy) and chemotherapy (Temozolomide). The follow-up MRI at 3 months showed a reduction in lesion size [Figure 1]f. A year after operation, she died because of tumor recurrence. | Figure 1: On preoperative axial MR images, a homogeneous BTG is hypointense on T1-weighted image (a) and hyperintense on T2-weighted (b) and FLAIR (c) images. After Gd injection, no contrast enhancement is observed (d). Mild enlargement of the lateral ventricles is also observed. MRS shows higher levels of choline and creatinine, and lower level of NAA (e). Postoperative Gd-enhanced MRI shows a reduction in lesion size (f)
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 | Figure 2: Intraoperative photographs show exposure of the tumor following separation of the corpus callosum (a). The right lateral tumor was partially excised (b), and then the contralateral tumor was readily observed (c). Partial resection of both lateral tumors resulted in a large cavity (d). cc - Corpus callosum, T – Tumor
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 | Figure 3: Photomicrographs show atypical nuclear staining observed with H&E staining (a) and positive expression of glial fi brillary acidic protein (GFAP) by tumor cells detected by immunohistochemistry (b). Immunohistochemistry staining was also used to calcluate a molecular immunology borstel (MIB) index value of 6% (c). Original magnifi cation, ×400
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Case 2: A 37-year-old female presented with dizziness and drowsiness of 2 months duration. Neurological examination revealed altered mentation. Magnetic resonance imaging revealed a large (6.0 Χ 5.0 Χ 4.0 cm) heterogeneous contrast enhancing mass lesion involving both thalami and third ventricle. It was hypointense on T1-weighted and hyperintense on T2-weighted and FLAIR images. MR spectroscopy showed similar findings as in Case 1. The tumor was partially (50%) resected because of midbrain infiltration. Postoperatively he developed mutism. Histopathological diagnosis was WHO grade III astrocytoma. Family refused for any adjuvant therapy. She died 3 months later due to tumor recurrence.
The incidence of thalamic tumors among intracranial tumors has been reported to range from 0.84% to 5.2%, [1],[2] yet the frequency of BTG is less defined. Only 66 cases have been reported to date, and of them, only three had tumor resection [Table 1]. [3],[4],[5] The clinical presentations of BTG can be variable due to the complex and various anatomical and functional connections of the thalamic structures. Increased intracranial pressure usually represents a mass effect of these tumors, while hydrocephalus is usually absent or mild. [5] Magnetic resonance imaging is the choice of detecting these lesions. Lesions appear hyperintense on T2-weighted and FLAIR, and hypo- to iso-intense on T1-weighted images. On MRS, there is increase in the levels of creatinine and choline (with the former greater than the latter) and a decrease in the levels of NAA. These features are proposed to be a unique metabolic pattern of BTG. [6]
Most bithalamic lesions are histologically low-grade astrocytomas. [7] Of the reported cases (with six cases excluded due to absence of a histopathological diagnosis), 71.7% (43/60) have been low-grade astrocytomas, and only 28.3% (17/60) have been of high grade. In addition, unlike other gliomas that widely diffuse through white matter fiber, the thalamic nuclei of BTG have been found to respect the gray white matter border for an extended period of time. [8]
The prognosis for BTG is poor due to the diffuse and bilateral involvement of thalamic nuclei, which prevents complete resection. Therefore, surgical modalities are limited to biopsy and cerebrospinal fluid diversion procedures for cases of associated hydrocephalus. What is worse, the role of adjuvant therapies including radiotherapy and/or chemotherapy is not sure. [9] Although we tried to remove the tumor as much as possible, and to combine with adjuvant therapy to prolong patients' survival period, the outcome was not encouraging as previously reported. [3],[4],[5] In conclusion, the clinical, radiological, and metabolic features of BTG are different from those of unilateral thalamic tumours, and the treatment for BTG is still a great challenge to neurosurgeons.
» References | |  |
1. | Habek M, Brinar VV, Mubrin Z, Barun B, Zarkoviæ K. Bilateral thalamic astrocytoma. J Neurooncol 2007;84:175-7.  |
2. | Douis H, Jafri M, Sherlala K. Bilateral thalamic glioma. Arch Neurol 2008;65:1666-7.  |
3. | Di Rocco C, Iannelli A. Bilateral thalamic tumors in children. Childs Nerv Syst 2002;18:440-4.  |
4. | Puget S, Crimmins DW, Garnett MR, Grill J, Oliveira R, Boddaert N, et al. Thalamic tumors in children: A reappraisal. J Neurosurg 2007;106 (5 Suppl):354-62.  |
5. | Rajput DK, Mehrotra A, Srivastav AK, Kumar R, Mahapatra AK. Bilateral thalamic glioma in a 6-year-old child. J Pediatr Neurosci 2010;5:45-8.  [PUBMED] |
6. | Esteve F, Grand S, Rubin C, Hoffmann D, Pasquier B, Graveron-Demilly D, et al. MR spectroscopy of bilateral thalamic gliomas. AJNR Am J Neuroradiol 1999;20:876-81.  |
7. | Jain P, Mohamed A, Sigamani E, Suri V, Mahapatra AK, Kumar A, et al. Bilateral thalamic lesions in a child. Eur Neurol 2013;70:33-4.  |
8. | Menon G, Nair S, Sudhir J, Rao BR, Krishnakumar K. Bilateral thalamic lesions. Br J Neurosurg 2010;24:566-71.  |
9. | Gelabert-González M, Seramito-García R, Bandín-Diéguez J, Allut AG. Bilateral thalamic tumours. Three case reports and a review of the literature. Rev Neurol 2007;45:599-603.  |
[Figure 1], [Figure 2], [Figure 3]
[Table 1]
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