Letters to the Editor
Cerebellar glioblastoma multiforme in an adult Access this article online Website: www.cancerjournal.net
Quick Response Code:
DOI: 10.4103/0973-1482.139132 PMID: ***
Dear Sir, Although glioblastomas constitute approximately 15-20% of the entire intracranial tumors,[1] occurrence of primary cerebellar glioblastoma multiforme (GBM) in adults is extremely rare (about 1% of all intracranial glioblastomas) with only few cases reported in the literature.[2‑4] A 47‑year‑old gentleman presented with the complaints of decreased hearing in right ear of 6 month’s duration and giddiness of similar duration. He also noticed decreased eyelid movements on right side and decrease movement of face on right side with drooling of saliva while eating food. He was able to walk with support. He took some treatment at a local hospital without any relief. He was a chronic alcoholic and was treated for tuberculosis in 1994 and took antitubercular treatment for 6 months. Physical examination and laboratory tests were within normal limits. Neurological examination revealed nystagmus, right‑sided 7th nerve lower motor neuron type of palsy, decreased hearing in the right ear, and impaired gag reflex on right side. There was presence of right‑sided cerebellar signs including cerebellar ataxia, tandem gait, dysmetria, and dysdiadochokinesia. An investigation with brain computed tomography (CT) and magnetic resonance imaging (MRI) scan showed a heterogenic contrast‑enhancing expanding process in the right cerebellar hemisphere [Figure 1]. The MRI further showed an intraaxial, infiltrative, heterogenic mass localized in the right cerebellar hemisphere with extension into the right middle and superior cerebellar peduncle and brainstem. The lesion was hypointense on T1‑weighted (T1W) images and hyperintense on T2W and fluid‑attenuated inversion recovery (FLAIR) images with poorly‑defined borders and mild peritumoral edema, and after the gadolinium administration there was ill‑defined, heterogeneous enhancement. There was evidence of mass effect on the fourth ventricle, but no hydrocephalus was present. To rule out the metastatic lesion, the patient underwent chest X‑ray and abdominal sonography; but these studies were normal. The patient underwent right retromastoid suboccipital craniectomy. During surgery a yellowish tumor with necrotic change and abnormal vessels that had indistinct margins from
adjacent normal white matter in the deep part of cerebellum was identified. A partial decompression of the tumor was performed. The postoperative course was uneventful and his symptoms and neurologic signs gradually improved. Histological examination showed a cellular tumor, consistent with glioblastoma, composed of elongated, spindle‑shaped cells with irregular, moderately pleomorphic nuclei, as well as proliferative blood vessels and necrosis [Figure 2]. Upon recovery from surgery, the patient underwent received radiotherapy and chemotherapy (temozolomide). However, he survived only for 8 months. Cerebellar glioblastoma is a very malignant tumor, with rapid onset of symptoms and has a poor prognosis with median overall survival of approximately 10 months, with a very less 1‑year overall survival.[3] The majority of the cerebellar glioblastomas occur in adult age range with male preponderance.[3] It has been estimated that by tissue volume, if the average human cerebrum is taken as 1,034 mL and cerebellum as 114 mL, then relative cerebellar volume is 11% of cerebral volume,[5] if all other factors were equal then it is expected that 11% of all glioblastomas would occur in the cerebellum; however, the incidence of primary cerebellar glioblastomas is less than 0.5% of all cases (20 times lower than expected).[3,4] In most of the studies, the authors failed to show the explanation for the rarity of cerebellar GBM,[6] but it has been proposed that there is a lesser tendency of cerebellar astrocytes to
a
b
c
d
Figure 1: Magnetic resonance imaging (MRI) axial images revealed the presence of hypo‑ and hyperintense lesions in the right cerebellum in T1‑weighted (a), T2‑weighted (b), and fluid‑attenuated inversion recovery (FLAIR) images (c). Note the enhancement of the lesion after contrast administration (d)
Journal of Cancer Research and Therapeutics - July-September 2014 - Volume 10 - Issue 3
777
Letters to the Editor
Amit Agarwal, Arvind Bhake1, Anand Kakani, Kishore M. Hiwale1, Sk. Khairul Enam2 Departments of Neurosurgery, 1Pathology, 2Surgery, Datta Meghe Institute of Medical Sciences, Sawangi, Wardha, Maharashtra, India
Figure 2: Histological examination of the removed tumor specimen suggestive of glioblastoma multiforme
suffer malignant transformation description.[3,4] Primary glioblastomas usually develop in older patients, while secondary glioblastomas develop in younger patients and contain TP53 mutations as the earliest detectable change.[3] Recently, there is evidence pointing to signaling pathwayas an initiating and growth‑enhancing path in glioblastomas.[4] The major clinical manifestations relates to cerebellar dysfunction and the existence of a mass lesion in the posterior fossa (i.e. unsteady gait, imbalance, headache, dizziness, slurred speech nausea, and vomiting); none of these are specific for glioblastoma.[3,6] CT scan can be used for the initially evaluation for these mass lesions;[7] however, because of good tissue resolution, lack of major bone artifacts, and multiplanar capabilities; MRI is far superior to CT for evaluation of these patients.[8] On MRI cerebellar glioblastomas usually appear hypointense in T1 and hyperintense in T2 and reveal heterogeneous and irregular enhancement after contrast, mild‑to‑moderate perilesional edema and deformity of the fourth ventricle.[8] MR diffusion/ perfusion imaging and MR spectroscopy examinations would further facilitate the characterization of the lesions and the differential diagnosis.[8] Subtotal excision of the lesion and pathological analysis provides the definite diagnosis of GBM.[8,9] This can be followed by radiotherapy and the temozolomide chemotherapy.[10]
For correspondence: Dr. Amit Agrawal, Department of Neurosurgery, Datta Meghe Institute of Medical Sciences, Sawangi, Meghe, Wardha ‑ 442 004, Maharashtra, India. E‑mail: [email protected]
REFERENCES 1. Bigner DD, McLendon RE, Bruner JM. Russell and Rubinstein’s Pathology of Tumors of the Nervous System. 7th ed. London: Hodder Arnold; 2006. 2. Hur H, Jung S, Jung TY, Kim IY. Cerebellar glioblastoma multiforme in an adult. J Korean Neurosurg Soc 2008;43:194‑7. 3. Grahovac G, Tomac D, Lambasa S, Zoric A, Habek M. Cerebellar glioblastomas: Pathophysiology, clinical presentation and management. Acta Neurochir (Wien) 2009;151:653‑7. 4. Kast RE. Why cerebellar glioblastoma is rare and how that indicates adjunctive use of the FDA‑approved anti‑emetic aprepitant might retard cerebral glioblastoma growth: A new hypothesis to an old question. Clin Transl Oncol 2009;11:408‑10. 5. Ekinci N, Acer N, Akkaya A, Sankur S, Kabadayi T, Sahin B. Volumetric evaluation of the relations among the cerebrum, cerebellum and brain stem in young subjects: A combination of stereology and magnetic resonance imaging. Surg Radiol Anat 2008;30:489‑94. 6. Chamberlain MC, Silver P, Levin VA. Poorly differentiated gliomas of the cerebellum. A study of 18 patients. Cancer 1990;65:337‑40. 7. Bhimani S, Virapongse C, Spencer D, Kim J. CT appearance of cerebellar glioblastoma multiforme. J Comput Assist Tomogr 1983;7:889‑91. 8. Demir MK, Hakan T, Akinci O, Berkman Z. Primary cerebellar glioblastoma multiforme. Diagn Interv Radiol 2005;11:83‑6. 9. Gupta V, Goyal A, Sinha S, Singh AK, Tatke M, Kumar S, et al. Glioblastoma of the cerebellum. A report of 3 cases. J Neurosurg Sci 2003;47:157‑64. 10. Saito T, Hama S, Kajiwara Y, Sugiyama K, Yamasaki F, Arifin MT, et al. Prognosis of cerebellar glioblastomas: Correlation between prognosis and immunoreactivity for epidermal growth factor receptor compared with supratentorial glioblastomas. Anticancer Res 2006;26:1351‑7.
Human papilloma virus: A diagnostic dilemma for dentist variety of possible etiologic factors. Hence, we encountered a rare case of oral squamous papilloma (OSP) caused by human papilloma virus (HPV) in a 14 year ‑ old young male patient, which clinically mimicked granulomatous lesion of the palate.
Access this article online Website: www.cancerjournal.net
Quick Response Code:
DOI: 10.4103/0973-1482.139158 PMID: ***
Sir, Granulomatous lesions of the oral and orophrayngeal tissue present a diagnostic dilemma to the dentist due to the wide 778
OSP is a benign proliferation of the stratified squamous epithelium, which results in a papillary or verrucous exophytic mass induced by HPV. This tumor is of low virulence i.e. it is not contagious. HPV is a deoxyribonucleic acid virus of the papilloma viridae family that cannot be cultivated.[1,2] The viruses considered to be of high oncogenic potential include HPVs 16, 18, 31, 33, 35, 39, 45, 51, 55, 56,
Journal of Cancer Research and Therapeutics - July-September 2014 - Volume 10 - Issue 3
Copyright of Journal of Cancer Research & Therapeutics is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
Cerebellar glioblastoma multiforme in an adult Access this article online Website: www.cancerjournal.net
Quick Response Code:
DOI: 10.4103/0973-1482.139132 PMID: ***
Dear Sir, Although glioblastomas constitute approximately 15-20% of the entire intracranial tumors,[1] occurrence of primary cerebellar glioblastoma multiforme (GBM) in adults is extremely rare (about 1% of all intracranial glioblastomas) with only few cases reported in the literature.[2‑4] A 47‑year‑old gentleman presented with the complaints of decreased hearing in right ear of 6 month’s duration and giddiness of similar duration. He also noticed decreased eyelid movements on right side and decrease movement of face on right side with drooling of saliva while eating food. He was able to walk with support. He took some treatment at a local hospital without any relief. He was a chronic alcoholic and was treated for tuberculosis in 1994 and took antitubercular treatment for 6 months. Physical examination and laboratory tests were within normal limits. Neurological examination revealed nystagmus, right‑sided 7th nerve lower motor neuron type of palsy, decreased hearing in the right ear, and impaired gag reflex on right side. There was presence of right‑sided cerebellar signs including cerebellar ataxia, tandem gait, dysmetria, and dysdiadochokinesia. An investigation with brain computed tomography (CT) and magnetic resonance imaging (MRI) scan showed a heterogenic contrast‑enhancing expanding process in the right cerebellar hemisphere [Figure 1]. The MRI further showed an intraaxial, infiltrative, heterogenic mass localized in the right cerebellar hemisphere with extension into the right middle and superior cerebellar peduncle and brainstem. The lesion was hypointense on T1‑weighted (T1W) images and hyperintense on T2W and fluid‑attenuated inversion recovery (FLAIR) images with poorly‑defined borders and mild peritumoral edema, and after the gadolinium administration there was ill‑defined, heterogeneous enhancement. There was evidence of mass effect on the fourth ventricle, but no hydrocephalus was present. To rule out the metastatic lesion, the patient underwent chest X‑ray and abdominal sonography; but these studies were normal. The patient underwent right retromastoid suboccipital craniectomy. During surgery a yellowish tumor with necrotic change and abnormal vessels that had indistinct margins from
adjacent normal white matter in the deep part of cerebellum was identified. A partial decompression of the tumor was performed. The postoperative course was uneventful and his symptoms and neurologic signs gradually improved. Histological examination showed a cellular tumor, consistent with glioblastoma, composed of elongated, spindle‑shaped cells with irregular, moderately pleomorphic nuclei, as well as proliferative blood vessels and necrosis [Figure 2]. Upon recovery from surgery, the patient underwent received radiotherapy and chemotherapy (temozolomide). However, he survived only for 8 months. Cerebellar glioblastoma is a very malignant tumor, with rapid onset of symptoms and has a poor prognosis with median overall survival of approximately 10 months, with a very less 1‑year overall survival.[3] The majority of the cerebellar glioblastomas occur in adult age range with male preponderance.[3] It has been estimated that by tissue volume, if the average human cerebrum is taken as 1,034 mL and cerebellum as 114 mL, then relative cerebellar volume is 11% of cerebral volume,[5] if all other factors were equal then it is expected that 11% of all glioblastomas would occur in the cerebellum; however, the incidence of primary cerebellar glioblastomas is less than 0.5% of all cases (20 times lower than expected).[3,4] In most of the studies, the authors failed to show the explanation for the rarity of cerebellar GBM,[6] but it has been proposed that there is a lesser tendency of cerebellar astrocytes to
a
b
c
d
Figure 1: Magnetic resonance imaging (MRI) axial images revealed the presence of hypo‑ and hyperintense lesions in the right cerebellum in T1‑weighted (a), T2‑weighted (b), and fluid‑attenuated inversion recovery (FLAIR) images (c). Note the enhancement of the lesion after contrast administration (d)
Journal of Cancer Research and Therapeutics - July-September 2014 - Volume 10 - Issue 3
777
Letters to the Editor
Amit Agarwal, Arvind Bhake1, Anand Kakani, Kishore M. Hiwale1, Sk. Khairul Enam2 Departments of Neurosurgery, 1Pathology, 2Surgery, Datta Meghe Institute of Medical Sciences, Sawangi, Wardha, Maharashtra, India
Figure 2: Histological examination of the removed tumor specimen suggestive of glioblastoma multiforme
suffer malignant transformation description.[3,4] Primary glioblastomas usually develop in older patients, while secondary glioblastomas develop in younger patients and contain TP53 mutations as the earliest detectable change.[3] Recently, there is evidence pointing to signaling pathwayas an initiating and growth‑enhancing path in glioblastomas.[4] The major clinical manifestations relates to cerebellar dysfunction and the existence of a mass lesion in the posterior fossa (i.e. unsteady gait, imbalance, headache, dizziness, slurred speech nausea, and vomiting); none of these are specific for glioblastoma.[3,6] CT scan can be used for the initially evaluation for these mass lesions;[7] however, because of good tissue resolution, lack of major bone artifacts, and multiplanar capabilities; MRI is far superior to CT for evaluation of these patients.[8] On MRI cerebellar glioblastomas usually appear hypointense in T1 and hyperintense in T2 and reveal heterogeneous and irregular enhancement after contrast, mild‑to‑moderate perilesional edema and deformity of the fourth ventricle.[8] MR diffusion/ perfusion imaging and MR spectroscopy examinations would further facilitate the characterization of the lesions and the differential diagnosis.[8] Subtotal excision of the lesion and pathological analysis provides the definite diagnosis of GBM.[8,9] This can be followed by radiotherapy and the temozolomide chemotherapy.[10]
For correspondence: Dr. Amit Agrawal, Department of Neurosurgery, Datta Meghe Institute of Medical Sciences, Sawangi, Meghe, Wardha ‑ 442 004, Maharashtra, India. E‑mail: [email protected]
REFERENCES 1. Bigner DD, McLendon RE, Bruner JM. Russell and Rubinstein’s Pathology of Tumors of the Nervous System. 7th ed. London: Hodder Arnold; 2006. 2. Hur H, Jung S, Jung TY, Kim IY. Cerebellar glioblastoma multiforme in an adult. J Korean Neurosurg Soc 2008;43:194‑7. 3. Grahovac G, Tomac D, Lambasa S, Zoric A, Habek M. Cerebellar glioblastomas: Pathophysiology, clinical presentation and management. Acta Neurochir (Wien) 2009;151:653‑7. 4. Kast RE. Why cerebellar glioblastoma is rare and how that indicates adjunctive use of the FDA‑approved anti‑emetic aprepitant might retard cerebral glioblastoma growth: A new hypothesis to an old question. Clin Transl Oncol 2009;11:408‑10. 5. Ekinci N, Acer N, Akkaya A, Sankur S, Kabadayi T, Sahin B. Volumetric evaluation of the relations among the cerebrum, cerebellum and brain stem in young subjects: A combination of stereology and magnetic resonance imaging. Surg Radiol Anat 2008;30:489‑94. 6. Chamberlain MC, Silver P, Levin VA. Poorly differentiated gliomas of the cerebellum. A study of 18 patients. Cancer 1990;65:337‑40. 7. Bhimani S, Virapongse C, Spencer D, Kim J. CT appearance of cerebellar glioblastoma multiforme. J Comput Assist Tomogr 1983;7:889‑91. 8. Demir MK, Hakan T, Akinci O, Berkman Z. Primary cerebellar glioblastoma multiforme. Diagn Interv Radiol 2005;11:83‑6. 9. Gupta V, Goyal A, Sinha S, Singh AK, Tatke M, Kumar S, et al. Glioblastoma of the cerebellum. A report of 3 cases. J Neurosurg Sci 2003;47:157‑64. 10. Saito T, Hama S, Kajiwara Y, Sugiyama K, Yamasaki F, Arifin MT, et al. Prognosis of cerebellar glioblastomas: Correlation between prognosis and immunoreactivity for epidermal growth factor receptor compared with supratentorial glioblastomas. Anticancer Res 2006;26:1351‑7.
Human papilloma virus: A diagnostic dilemma for dentist variety of possible etiologic factors. Hence, we encountered a rare case of oral squamous papilloma (OSP) caused by human papilloma virus (HPV) in a 14 year ‑ old young male patient, which clinically mimicked granulomatous lesion of the palate.
Access this article online Website: www.cancerjournal.net
Quick Response Code:
DOI: 10.4103/0973-1482.139158 PMID: ***
Sir, Granulomatous lesions of the oral and orophrayngeal tissue present a diagnostic dilemma to the dentist due to the wide 778
OSP is a benign proliferation of the stratified squamous epithelium, which results in a papillary or verrucous exophytic mass induced by HPV. This tumor is of low virulence i.e. it is not contagious. HPV is a deoxyribonucleic acid virus of the papilloma viridae family that cannot be cultivated.[1,2] The viruses considered to be of high oncogenic potential include HPVs 16, 18, 31, 33, 35, 39, 45, 51, 55, 56,
Journal of Cancer Research and Therapeutics - July-September 2014 - Volume 10 - Issue 3
Copyright of Journal of Cancer Research & Therapeutics is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
