[Downloaded free from http://www.neurologyindia.com on Thursday, May 15, 2014, IP: 202.177.173.189] || Click here to download free Android application for th journal Letters to Editor
doxorubicin, vincristine, and prednisolone regimen. In November 1997, first relapse was treated with six cycles of chlorambucil. In May 2000, second relapse was treated with six cycles of fludarabine. In April 2003, she presented with confusion and memory disturbance, left hemiparesis and bi-temporal hemianopsia. IgM peak was at 4.9 g/L. Brain MRI showed a right frontal lesion. 1 month later, biopsy of the lesion showed DLBC. CSF analysis showed 2.35 g/L of protein with abnormal lymphoma cells. Systemic CT scan was unremarkable. The patient received high-dose MTX, lomustine, procarbazine and prednisone. 1 month later, a brain CT scan showed a progressive disease in context of neurological deterioration. The patient died 3 months after DLBCL diagnosis due to brain lymphoma. Waldenström macroglobulinemia is characterized by lymphoplasmacytic bone marrow infiltration with IgM monoclonal gammapathy. Neurological manifestations of WM are peripheral neuropathy, myelopathy, ischemic, or hemorrhagic cerebral stroke and cerebral tumoral infiltration, called BNS.[2] It is interesting to note that both our patients presented BNS independently of WM status. Two historical forms of BNS were described:[3] the most common characterized by diffuse cerebral infiltrations of WM cells;[4] the second “tumoral form” involves the occurrence of tumor mass as analyzed on neuro-imaging. Here we propose a new histological classification of BNS: A first infiltrative form by lymphoplasmocytoid cells and a second tumoral-DLBCL form. WM is a low-grade lymphoma, which is known to be at risk for developing high-grade lymphoma in rare cases (Richter syndrome).[5] Moreover, two reported BNS histologies[3,6] revealed the association of both tumoral populations’ cells, suggesting a cerebral transformation of WM. Therefore, BNS in its “tumoral form” could be assimilated to a Richter syndrome, a new BNS entity. Therapy of BNS appeared to be extremely variable, more related to WM treatment.[7,8] However, these therapies are not recommended for primary cerebral lymphoma for which current treatment is high-dose MTX.[5,9] Our two patients received high-dose MTX and one of them achieved a prolonged CR. Bing-Neel syndrome remains a rare complication of WM. It can be classified into two categories: infiltration by lymphoplasmacytic cells and cerebral DLBCL transformation. The latter form can be considered as a Richter transformation. There is no consensual treatment for BNS, but high-dose MTX-based regimen could represent an interesting option.
Emeline Tabouret1,2, Diane Coso2, Mona Matta1, Maryline Barrié1, Reda Bouabdallah2, Olivier Chinot1 230
1
Departement of Neuro-Oncology, APHM, Timone Hospital, 13005, Marseille, 2Departement of Hematology, Paoli Calmettes Institute, 13273, cedex9, Marseille, France E-mail: [email protected]
References 1. 2. 3.
4. 5.
6. 7.
8.
9.
Bing J, Neel AV. Two cases of hyperglobulinemia with affection of the central nervous system on a toxi-infection basis. Acta Med Scan 1936;88:492-506. Monteiro PL, Wildi E. Waldenstrom’s macroglobulinemia with lymphorproliferative changes in the central nervous system. 4 cases. Schweiz Arch Neurol Neurochir Psychiatr 1975;116:59-82. Imai F, Fujisawa K, Kiya N, Ninomiya T, Ogura Y, Mizoguchi Y, et al. Intracerebral infiltration by monoclonal plasmacytoid cells in Waldenstrom’s macroglobulinemia: Case report. Neurol Med Chir (Tokyo) 1995;35:575-9. Fintelmann F, Forghani R, Schaefer PW, Hochberg EP, Hochberg FH. Bing-Neel Syndrome revisited. Clin Lymphoma Myeloma 2009;9:104-6. Lin P, Mansoor A, Bueso-Ramos C, Hao S, Lai R, Medeiros LJ. Diffuse large B-cell lymphoma occurring in patients with lymphoplasmacytic lymphoma/Waldenström macroglobulinemia. Clinicopathologic features of 12 cases. Am J Clin Pathol 2003;120:246-53. Garderet L, Baudel JL, Cervera P, Azizi L, Maury E, Guidet B, et al. ‘Indolent’ Waldenstrom’s macroglobulinemia and a cerebrospinal fluid protein level of 16 g/L. Eur J Haematol 2006;77:80-2. Grewal JS, Brar PK, Sahijdak WM, Tworek JA, Chottiner EG. Bing-Neel syndrome: A case report and systematic review of clinical manifestations, diagnosis, and treatment options. Clin Lymphoma Myeloma 2009;9:462-6. Dimopoulos MA, Gertz MA, Kastritis E, Garcia-Sanz R, Kimby EK, Leblond V, et al. Update on treatment recommendations from the Fourth International Workshop on Waldenstrom’s Macroglobulinemia. J Clin Oncol 2009;27:120-6. Ferreri AJ, Reni M, Foppoli M, Martelli M, Pangalis GA, Frezzato M, et al. High-dose cytarabine plus high-dose methotrexate versus high-dose methotrexate alone in patients with primary CNS lymphoma: a randomised phase 2 trial. Lancet 2009;374:1512-20. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.132451
Received: 24-11-2013 Review completed: 01-01-2014 Accepted: 13-04-2014
Primary ventral foramen magnum meningeal melanocytoma Sir, Primary meningeal melanocytomas are intriguing because of their rarity and unusual radiological appearance. [1] They are usually located around Neurology India | Mar-Apr 2014 | Vol 62 | Issue 2
[Downloaded free from http://www.neurologyindia.com on Thursday, May 15, 2014, IP: 202.177.173.189] || Click here to download free Android application for this journal Letters to Editor
the cervicomedullary junction and upper cervical spine. [2] Of interest, melanocytoma at the ventral foramen magnum has never been reported. We report one such case. A 22-year-old male presented with headache, intermittent diplopia on left lateral gaze, and correctable neck tilt to the right of 3 months duration. Examination revealed mild papilledema. Magnetic resonance imaging (MRI) revealed dural based lesion at ventral foramen magnum, isointense on T1 and T2 with brilliant enhancement suggesting a meningioma. Both vertebral arteries (VA) (right more than left) appeared to be encased within the lesion. Interestingly, a T1 hyper and T2 hypointense intralesional nodule (suspicious of blood or melanin) was seen abutting one of the VA [Figure 1]. He was operated through right far lateral approach , by the senior author PS. The arachnoid was opened, and a moderately vascular, reddish-black friable lesion was encountered that was apparently infiltrating the cranial nerves and encasing VAs. However, patient dissection revealed an arachnoid layer making peeling of the tumor from each cranial nerve and VA (engulfment and not encasement) possible. The lesion was attached to the dura ventrally up to C2 level [Figure 2]. The area corresponding to the nodule was fleshy and firm. Total excision could be achieved. Histopathology and immunohistochemistry confirmed melanocytoma [Figure 3]. Following surgery, the diplopia and neck tilt improved. The positron emission tomography-computed tomography (CT) ruled out lesions at other sites. He received 45 Grays of radiation and is doing well at 6 months follow-up. Radiology at 6 months follow-up ruled out recurrence or residual lesion [Figure 4].
Figure 1: The top row shows ventrally located lesion at the foramen magnum. The lesion is iso-hyper-dense on computed tomography, isointense on T1 and T2. The vertebral arteries (VA) appear to be encases. There is nodule close to the left vertebral artery, hyper on T1 and hypointense on T2. The middle row shows no attenuation on FLAIR, sagittal T2 showing the extent and the MR angio showing the VA. The bottom row shows the extent and Brilliant enhancement of lesion on contrast
Neurology India | Mar-Apr 2014 | Vol 62 | Issue 2
Melanocytes are neural crest derivatives and their abnormal differentiation in the central nervous system can give rise to diffuse leptomeningeal melanocytosis, meningeal melanocytoma or primary melanoma.[1] Melanocytes occur in the highest concentration ventrolateral to the medulla oblongata and making this a common site for intracranial meningeal melanocytomas. Extensive review by Fan et al. showed various locations of melanocytoma.[2] However, a ventrally located foramen magnum melanocytoma has not been described yet. These lesions have a propensity to arise in proximity to nerves as they exit the brainstem and spinal cord.[1] Meningeal melanocytoma may present with raised intracranial pressure, neuropsychiatric symptoms, seizures, or rarely spinal cord compression. Commonly, the tumor appears hyper- or iso-dense on CT scan with contrast enhancement. It is usually hyperintense on T1-weighted and Fluid Attenuated Inversion Recovery (FLAIR), and hypointense on T2-weighted MRI with contrast enhancement.[1] However, these radiological features are not definitive and may mimic a meningioma. Grossly, the lesion appears black, mimicking bleed. It is firmly attached to the underlying meninges at some point and is vascular. These lesions have a propensity to invade along the cranial and spinal nerves, which makes their gross total excision difficult.[1,3] Contrary to this, we found a well-maintained arachnoid plane and with patience, the tumor could be dissected from each nerve and the vessel. Microscopy shows melanin granules. Immunohistochemically, the lesion shows S-100 protein, antimelanoma antibodies (HMB-45) and vimentin positivity, and stains negative for keratin, epithelial membrane antigen and glial fibrillary acidic protein.[1,3]
Figure 2: Intraoperative images showing sequential excision of the tumor from lower cranial nerves and both vertebral arteries. The arachnoid plane is well-maintained. A - arachnoid, T - tumor, VA - Vertebral artery, PICA - Posterior inferior cerebellar artery, 12th N - hypoglossal nerve, 11th N - spinal accessory nerve, 9 to 10th N - Glossopharyngeal and vagus nerve, BS - Brain stem
231
[Downloaded free from http://www.neurologyindia.com on Thursday, May 15, 2014, IP: 202.177.173.189] || Click here to download free Android application for this journal Letters to Editor
a
c
b
Figure 3: (a) It shows loose nests of oval to spindle cells containing variable melanin pigment H and E, ×20. There are no mitoses. The tumor is well-circumscribed and shows extensive pigment and spindle cells in other areas (b) immunohistochemistry showing negative staining for epithelial membrane antigen and (c) strong melan A positivity (×40)
Figure 4: Contrast-enhanced magnetic resonance imaging, at 6 months follow-up showing no recurrence or residual lesion
Gross total resection (GTR) is the most important predictor of good long-term outcome.[4] The 5-year survival rates are 100% after GTR with or without radiotherapy (RT). Adjuvant RT improves the survival in cases of incomplete resection (IR) to 100% as compared with 46% without RT.[4] Though appearing benign, melanocytoma may follow an aggressive course. Local recurrences are common even after GTR and may occur earlier with malignant transformation. Therefore, surveillance MRI should be obtained at regular 6 monthly intervals. In addition, metastasizing meningeal melanocytomas do occur. The 5-year local control rate was 80% after GTR alone, 100% after GTR-RT, and 72% after IR-RT versus 18% after IR alone. RT doses of 45–55 Gray have shown to achieve better control than 35-40 Gray.[4] Gamma knife radiosurgery has shown to reduce the tumor size and improve clinical outcome. Intrathecal methotrexate or interleukins too have been tried in few cases. Currently, GTR with adjuvant RT provides the best local control and survival.[1] Apart from the unusual location, this report highlights the importance of patient dissection following a good surgical planning to achieve total excision, which is desirable in such lesions as it bears a good long-term outcome.
Harsimrat Bir Singh Sodhi, Pravin Salunke,
232
Sushanta K. Sahoo, B. D. Radotra1, Narendra Kumar2 Departments of Neurosurgery, 1Histopathology, and 2 Radiotherapy, PGIMER, Chandigarh, India E-mail: [email protected]
References 1. 2. 3.
4.
Liubinas SV, Maartens N, Drummond KJ. Primary melanocytic neoplasms of the central nervous system. J Clin Neurosci 2010;17:1227-32. Fan MC, Wang JF, Fu WW, Liu K, Li LD, Sun P. Primary meningeal melanocytoma located in foramen magnum: A case report and review of the literatures. Chin Med Sci J 2012;27:115-20. Jaiswal S, Vij M, Tungria A, Jaiswal AK, Srivastava AK, Behari S. Primary melanocytic tumors of the central nervous system: A neuroradiological and clinicopathological study of five cases and brief review of literature. Neurol India 2011;59:413-9. Rades D, Schild SE, Tatagiba M, Molina HA, Alberti W. Therapy of meningeal melanocytomas. Cancer 2004;100:2442-7.
Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.132452
Received: 10-01-2014 Review completed: 02-02-2014 Accepted: 19-04-2014
Neurology India | Mar-Apr 2014 | Vol 62 | Issue 2
Copyright of Neurology India 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.
doxorubicin, vincristine, and prednisolone regimen. In November 1997, first relapse was treated with six cycles of chlorambucil. In May 2000, second relapse was treated with six cycles of fludarabine. In April 2003, she presented with confusion and memory disturbance, left hemiparesis and bi-temporal hemianopsia. IgM peak was at 4.9 g/L. Brain MRI showed a right frontal lesion. 1 month later, biopsy of the lesion showed DLBC. CSF analysis showed 2.35 g/L of protein with abnormal lymphoma cells. Systemic CT scan was unremarkable. The patient received high-dose MTX, lomustine, procarbazine and prednisone. 1 month later, a brain CT scan showed a progressive disease in context of neurological deterioration. The patient died 3 months after DLBCL diagnosis due to brain lymphoma. Waldenström macroglobulinemia is characterized by lymphoplasmacytic bone marrow infiltration with IgM monoclonal gammapathy. Neurological manifestations of WM are peripheral neuropathy, myelopathy, ischemic, or hemorrhagic cerebral stroke and cerebral tumoral infiltration, called BNS.[2] It is interesting to note that both our patients presented BNS independently of WM status. Two historical forms of BNS were described:[3] the most common characterized by diffuse cerebral infiltrations of WM cells;[4] the second “tumoral form” involves the occurrence of tumor mass as analyzed on neuro-imaging. Here we propose a new histological classification of BNS: A first infiltrative form by lymphoplasmocytoid cells and a second tumoral-DLBCL form. WM is a low-grade lymphoma, which is known to be at risk for developing high-grade lymphoma in rare cases (Richter syndrome).[5] Moreover, two reported BNS histologies[3,6] revealed the association of both tumoral populations’ cells, suggesting a cerebral transformation of WM. Therefore, BNS in its “tumoral form” could be assimilated to a Richter syndrome, a new BNS entity. Therapy of BNS appeared to be extremely variable, more related to WM treatment.[7,8] However, these therapies are not recommended for primary cerebral lymphoma for which current treatment is high-dose MTX.[5,9] Our two patients received high-dose MTX and one of them achieved a prolonged CR. Bing-Neel syndrome remains a rare complication of WM. It can be classified into two categories: infiltration by lymphoplasmacytic cells and cerebral DLBCL transformation. The latter form can be considered as a Richter transformation. There is no consensual treatment for BNS, but high-dose MTX-based regimen could represent an interesting option.
Emeline Tabouret1,2, Diane Coso2, Mona Matta1, Maryline Barrié1, Reda Bouabdallah2, Olivier Chinot1 230
1
Departement of Neuro-Oncology, APHM, Timone Hospital, 13005, Marseille, 2Departement of Hematology, Paoli Calmettes Institute, 13273, cedex9, Marseille, France E-mail: [email protected]
References 1. 2. 3.
4. 5.
6. 7.
8.
9.
Bing J, Neel AV. Two cases of hyperglobulinemia with affection of the central nervous system on a toxi-infection basis. Acta Med Scan 1936;88:492-506. Monteiro PL, Wildi E. Waldenstrom’s macroglobulinemia with lymphorproliferative changes in the central nervous system. 4 cases. Schweiz Arch Neurol Neurochir Psychiatr 1975;116:59-82. Imai F, Fujisawa K, Kiya N, Ninomiya T, Ogura Y, Mizoguchi Y, et al. Intracerebral infiltration by monoclonal plasmacytoid cells in Waldenstrom’s macroglobulinemia: Case report. Neurol Med Chir (Tokyo) 1995;35:575-9. Fintelmann F, Forghani R, Schaefer PW, Hochberg EP, Hochberg FH. Bing-Neel Syndrome revisited. Clin Lymphoma Myeloma 2009;9:104-6. Lin P, Mansoor A, Bueso-Ramos C, Hao S, Lai R, Medeiros LJ. Diffuse large B-cell lymphoma occurring in patients with lymphoplasmacytic lymphoma/Waldenström macroglobulinemia. Clinicopathologic features of 12 cases. Am J Clin Pathol 2003;120:246-53. Garderet L, Baudel JL, Cervera P, Azizi L, Maury E, Guidet B, et al. ‘Indolent’ Waldenstrom’s macroglobulinemia and a cerebrospinal fluid protein level of 16 g/L. Eur J Haematol 2006;77:80-2. Grewal JS, Brar PK, Sahijdak WM, Tworek JA, Chottiner EG. Bing-Neel syndrome: A case report and systematic review of clinical manifestations, diagnosis, and treatment options. Clin Lymphoma Myeloma 2009;9:462-6. Dimopoulos MA, Gertz MA, Kastritis E, Garcia-Sanz R, Kimby EK, Leblond V, et al. Update on treatment recommendations from the Fourth International Workshop on Waldenstrom’s Macroglobulinemia. J Clin Oncol 2009;27:120-6. Ferreri AJ, Reni M, Foppoli M, Martelli M, Pangalis GA, Frezzato M, et al. High-dose cytarabine plus high-dose methotrexate versus high-dose methotrexate alone in patients with primary CNS lymphoma: a randomised phase 2 trial. Lancet 2009;374:1512-20. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.132451
Received: 24-11-2013 Review completed: 01-01-2014 Accepted: 13-04-2014
Primary ventral foramen magnum meningeal melanocytoma Sir, Primary meningeal melanocytomas are intriguing because of their rarity and unusual radiological appearance. [1] They are usually located around Neurology India | Mar-Apr 2014 | Vol 62 | Issue 2
[Downloaded free from http://www.neurologyindia.com on Thursday, May 15, 2014, IP: 202.177.173.189] || Click here to download free Android application for this journal Letters to Editor
the cervicomedullary junction and upper cervical spine. [2] Of interest, melanocytoma at the ventral foramen magnum has never been reported. We report one such case. A 22-year-old male presented with headache, intermittent diplopia on left lateral gaze, and correctable neck tilt to the right of 3 months duration. Examination revealed mild papilledema. Magnetic resonance imaging (MRI) revealed dural based lesion at ventral foramen magnum, isointense on T1 and T2 with brilliant enhancement suggesting a meningioma. Both vertebral arteries (VA) (right more than left) appeared to be encased within the lesion. Interestingly, a T1 hyper and T2 hypointense intralesional nodule (suspicious of blood or melanin) was seen abutting one of the VA [Figure 1]. He was operated through right far lateral approach , by the senior author PS. The arachnoid was opened, and a moderately vascular, reddish-black friable lesion was encountered that was apparently infiltrating the cranial nerves and encasing VAs. However, patient dissection revealed an arachnoid layer making peeling of the tumor from each cranial nerve and VA (engulfment and not encasement) possible. The lesion was attached to the dura ventrally up to C2 level [Figure 2]. The area corresponding to the nodule was fleshy and firm. Total excision could be achieved. Histopathology and immunohistochemistry confirmed melanocytoma [Figure 3]. Following surgery, the diplopia and neck tilt improved. The positron emission tomography-computed tomography (CT) ruled out lesions at other sites. He received 45 Grays of radiation and is doing well at 6 months follow-up. Radiology at 6 months follow-up ruled out recurrence or residual lesion [Figure 4].
Figure 1: The top row shows ventrally located lesion at the foramen magnum. The lesion is iso-hyper-dense on computed tomography, isointense on T1 and T2. The vertebral arteries (VA) appear to be encases. There is nodule close to the left vertebral artery, hyper on T1 and hypointense on T2. The middle row shows no attenuation on FLAIR, sagittal T2 showing the extent and the MR angio showing the VA. The bottom row shows the extent and Brilliant enhancement of lesion on contrast
Neurology India | Mar-Apr 2014 | Vol 62 | Issue 2
Melanocytes are neural crest derivatives and their abnormal differentiation in the central nervous system can give rise to diffuse leptomeningeal melanocytosis, meningeal melanocytoma or primary melanoma.[1] Melanocytes occur in the highest concentration ventrolateral to the medulla oblongata and making this a common site for intracranial meningeal melanocytomas. Extensive review by Fan et al. showed various locations of melanocytoma.[2] However, a ventrally located foramen magnum melanocytoma has not been described yet. These lesions have a propensity to arise in proximity to nerves as they exit the brainstem and spinal cord.[1] Meningeal melanocytoma may present with raised intracranial pressure, neuropsychiatric symptoms, seizures, or rarely spinal cord compression. Commonly, the tumor appears hyper- or iso-dense on CT scan with contrast enhancement. It is usually hyperintense on T1-weighted and Fluid Attenuated Inversion Recovery (FLAIR), and hypointense on T2-weighted MRI with contrast enhancement.[1] However, these radiological features are not definitive and may mimic a meningioma. Grossly, the lesion appears black, mimicking bleed. It is firmly attached to the underlying meninges at some point and is vascular. These lesions have a propensity to invade along the cranial and spinal nerves, which makes their gross total excision difficult.[1,3] Contrary to this, we found a well-maintained arachnoid plane and with patience, the tumor could be dissected from each nerve and the vessel. Microscopy shows melanin granules. Immunohistochemically, the lesion shows S-100 protein, antimelanoma antibodies (HMB-45) and vimentin positivity, and stains negative for keratin, epithelial membrane antigen and glial fibrillary acidic protein.[1,3]
Figure 2: Intraoperative images showing sequential excision of the tumor from lower cranial nerves and both vertebral arteries. The arachnoid plane is well-maintained. A - arachnoid, T - tumor, VA - Vertebral artery, PICA - Posterior inferior cerebellar artery, 12th N - hypoglossal nerve, 11th N - spinal accessory nerve, 9 to 10th N - Glossopharyngeal and vagus nerve, BS - Brain stem
231
[Downloaded free from http://www.neurologyindia.com on Thursday, May 15, 2014, IP: 202.177.173.189] || Click here to download free Android application for this journal Letters to Editor
a
c
b
Figure 3: (a) It shows loose nests of oval to spindle cells containing variable melanin pigment H and E, ×20. There are no mitoses. The tumor is well-circumscribed and shows extensive pigment and spindle cells in other areas (b) immunohistochemistry showing negative staining for epithelial membrane antigen and (c) strong melan A positivity (×40)
Figure 4: Contrast-enhanced magnetic resonance imaging, at 6 months follow-up showing no recurrence or residual lesion
Gross total resection (GTR) is the most important predictor of good long-term outcome.[4] The 5-year survival rates are 100% after GTR with or without radiotherapy (RT). Adjuvant RT improves the survival in cases of incomplete resection (IR) to 100% as compared with 46% without RT.[4] Though appearing benign, melanocytoma may follow an aggressive course. Local recurrences are common even after GTR and may occur earlier with malignant transformation. Therefore, surveillance MRI should be obtained at regular 6 monthly intervals. In addition, metastasizing meningeal melanocytomas do occur. The 5-year local control rate was 80% after GTR alone, 100% after GTR-RT, and 72% after IR-RT versus 18% after IR alone. RT doses of 45–55 Gray have shown to achieve better control than 35-40 Gray.[4] Gamma knife radiosurgery has shown to reduce the tumor size and improve clinical outcome. Intrathecal methotrexate or interleukins too have been tried in few cases. Currently, GTR with adjuvant RT provides the best local control and survival.[1] Apart from the unusual location, this report highlights the importance of patient dissection following a good surgical planning to achieve total excision, which is desirable in such lesions as it bears a good long-term outcome.
Harsimrat Bir Singh Sodhi, Pravin Salunke,
232
Sushanta K. Sahoo, B. D. Radotra1, Narendra Kumar2 Departments of Neurosurgery, 1Histopathology, and 2 Radiotherapy, PGIMER, Chandigarh, India E-mail: [email protected]
References 1. 2. 3.
4.
Liubinas SV, Maartens N, Drummond KJ. Primary melanocytic neoplasms of the central nervous system. J Clin Neurosci 2010;17:1227-32. Fan MC, Wang JF, Fu WW, Liu K, Li LD, Sun P. Primary meningeal melanocytoma located in foramen magnum: A case report and review of the literatures. Chin Med Sci J 2012;27:115-20. Jaiswal S, Vij M, Tungria A, Jaiswal AK, Srivastava AK, Behari S. Primary melanocytic tumors of the central nervous system: A neuroradiological and clinicopathological study of five cases and brief review of literature. Neurol India 2011;59:413-9. Rades D, Schild SE, Tatagiba M, Molina HA, Alberti W. Therapy of meningeal melanocytomas. Cancer 2004;100:2442-7.
Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.132452
Received: 10-01-2014 Review completed: 02-02-2014 Accepted: 19-04-2014
Neurology India | Mar-Apr 2014 | Vol 62 | Issue 2
Copyright of Neurology India 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.
