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|LETTER TO EDITOR
|Year : 2015 | Volume
| Issue : 3 | Page : 449-452
Multiple glioblastoma: A diagnostic challenge and controversies in management
Ankur Kapoor1, Sandeep Mohindra1, Navneet Singla1, Harsimrat Bir Singh Sodhi1, Debjyoti Chatterjee2, Sunil K Gupta1
1 Department of Neurosurgery, PGIMER, Chandigarh, India
2 Department of Histopathology, PGIMER, Chandigarh, India
|Date of Web Publication||5-Jun-2015|
Department of Neurosurgery, PGIMER, Chandigarh
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Kapoor A, Mohindra S, Singla N, Sodhi HB, Chatterjee D, Gupta SK. Multiple glioblastoma: A diagnostic challenge and controversies in management. Neurol India 2015;63:449-52
|How to cite this URL:|
Kapoor A, Mohindra S, Singla N, Sodhi HB, Chatterjee D, Gupta SK. Multiple glioblastoma: A diagnostic challenge and controversies in management. Neurol India [serial online] 2015 [cited 2020 Feb 21];63:449-52. Available from: http://www.neurologyindia.com/text.asp?2015/63/3/449/158267
We present three patients who were harboring multiple intracranial lesions. Their histopathology revealed a glioblastoma [Table 1]. The first case was a 50-year-old female patient who presented with headache lasting for the last 2 months. Her neurological examination revealed a right-sided hemiparesis and sensory aphasia. The magnetic resonance imaging (MRI) demonstrated a heterogeneously enhancing lesion in the left temporal lobe, along with two more lesions (located in the left posterior frontal lobe and the left thalamus). The patient underwent a left temporal craniotomy and excision of the lesion. Postoperatively, she did not regain consciousness. Her computed tomography scan showed an increasing mass effect by the posterior thalamic lesion. She was placed on elective ventilation to control the intracranial pressure but succumbed to her illness on the sixth postoperative day. The histopathology revealed a glioblastoma with high cellularity. The tumor cells were oval to elongated with frequent mitosis (2-3/HPF) and with a high Ki-67 proliferative index (15-20%). Some areas (10%) were composed of undifferentiated small cells with a high nuclear-cytoplasmic ratio. Necrosis, microvascular proliferation and thrombosed vessels were evident. The tumor was infiltrating into the adjacent brain with evidence of peri-neuronal satellitosis [Figure 1].
|Figure 1: (a) FLAIR image showing a left posterior thalamus hyperintensity; (b,c and d) T2W coronal,T1W contrast coronal, and T1W contrast axial images showing separate non-contiguous lesions in the left frontal, temporal and posterior thalamus; (e) Low power photomicrograph showing a highly cellular tumor with palisading necrosis, endovascular proliferation (H and E, ×100); and, (f) Higher magnification showing pleomorphic tumor cells with a high mitotic activity (H and E, ×400)|
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|Table 1: Characteristics of all three patients in terms of clinical features, radiological presentation, and management|
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The second case was a male patient aged 30 years, who was brought in an unconscious state with a history of low-grade fever and reduced verbal output for 5 days. His MRI [Figure 2] revealed a heterogenous solid-cystic lesion in the left frontal lobe with sub-falcine herniation and a midline shift, and another ill-defined lesion, minimally contrast-enhancing in the right temporal lobe. The patient underwent surgery for the left frontal lesion. The lesion was vascular, friable, with evidence of necrosis and thrombosed vessels. Postoperatively, the patient regained consciousness and was discharged on the fifth postoperative day. The histopathological examination showed findings suggestive of a glioblastoma. The central portion of the tumor contained necrotic material surrounded by neutrophils and nuclear debris while its periphery showed histiocytic collection, as highlighted by the CD68 stain. The tumor cells showed a high mitosis and Ki-67 proliferation index (10-12%). Stereotactic biopsy for the other lesion also revealed a glioblastoma.
|Figure 2: (a and b) T2W images showing a hyperintensity in the left frontal and right temporal region with vasogenic edema; (c and d) T1W contrast images showing an irregular, heterogeneous ring-enhancing lesion with necrosis in the left frontal lobe, and a heterogeneous lesion with a diffuse and faint enhancement in the right temporal lobe; (e) Photomicrograph of the left frontal lesion showing a high-grade glial tumor with neutrophilic infiltration; (f) Photomicrograph of the right temporal lesion showing a highly cellular astrocytic tumor with focal necrosis (H and E, ×20)|
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The third case was a 50-year-old female patient who presented with progressively increasing headache of 3-month duration. Her MRI [Figure 3] revealed an intensely enhancing mass in the right frontal lobe, which was excised via a frontal craniotomy. The histopathology revealed a cellular glial tumor composed of many tumor giant cells with abundant eosinophilic cytoplasm and single-to-multiple nuclei with vesicular chromatin. These cells showed increased mitotic activity, focal necrosis, and microvascular proliferation. The Ki-67 index was high (7-8%). With a diagnosis of giant cell glioblastoma, the patient was administered adjuvant radiotherapy. The follow-up MRI scan after 2 years revealed a new lesion in the contralateral frontal lobe. The patient was operated again and the contralateral frontal lobe lesion also excised. This also turned out to be a glioblastoma.
|Figure 3: T2W and T1W contrast images showing a right frontal heterogeneous lesion with evidence of necrosis; (a and b) T1W image showing no residual or recurrent lesion at 1-year follow-up; (c): T2W and T1W contrast images after 2 years showing a left frontal heterogeneously enhancing lesion; (d and e) Note the clear right frontal area at the time of recurrence; and, (f) Photomicrograph showing a cellular glial tumor with many tumor giant cells (H and E, ×400)|
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Multiple glioblastomas, first reported by Gower in 1896, represent approximately 2-16% of all glioblastomas.  These may arise by dissemination through the established anatomical pathways of spread such as the commissural pathways, cerebrospinal fluid and blood. Local metastatic spread through satellite lesion formation may also occur. The most common histology prevalent in multiple gliomas is the glioblastoma, while other less frequently seen lesions include the anaplastic gliomas, low-grade gliomas, oligodendrogliomas, and ependymomas.  The exact cause of occurrence of multiplicity is unknown. These lesions may be the result of neoplastic transformation of a field, rendering a wide area of the brain susceptible to neoplastic growth. Multiple embryonic residues scattered at different sites, and the role of cells with blastomere potential, have also been implicated.  A solitary glioblastoma has an overall survival of 11-18 months while the overall survival is just 4-7 months in the case of multiple glioblastomas. The disease process may remain quiescent for some time, manifesting later with a rapid growth, as seen in the third case. It is believed that migration of glial tumor cells to new sites and changing from traveling mode to growing mode is the basis for multiplicity.  In clinical presentation, these tumors have no localizing signs and are usually more aggressive due to the multiplicity.  Our second case presented with an ultra-short clinical history of 5 days, raising the suspicion of an inflammatory pathology. Radiologically, these lesions pose a diagnostic dilemma especially in the absence of typical clinical findings.  These lesions may masquerade a metastasis or a brain abscess. Management of these lesions remains controversial. One school of thought proposes aggressive surgery for all lesions citing the possibility of a better outcome related to the administration of adjuvant radiotherapy after tumor debulking; the other school, however, advocates surgery only for larger lesion and proposes establishement of a histological diagnosis by stereotactic biopsy for the remaining lesions. Surgery for a single lesion in multiple glioblastomas may cause further clinical deterioration due to an ipsilateral brain shift, which may prove fatal. This management decision is in contrast to the management of multiple low-grade gliomas where surgery for multiple lesions may be justified and may give optimum results. 
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[Figure 1], [Figure 2], [Figure 3]
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