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Calcifying pseudoneoplasm of the cerebellomedullary cistern: A case report and review of the literature Sir, Calcifying pseudoneoplasms (CPNs) are rare, calcified, non‑neoplastic lesions and can occur in any part of the central nervous system (CNS). They were first described by Rhodes and Davis.[1] In the pathophysiology, although there is not a complete consensus among authors, they are thought to occur after a reactive or metaplastic process in the neuraxis. Our patient is the first reported case in this anatomic location and second time reported case of CPN with its imaging features in the literature. Medical history of 59‑year‑old female patient with a long‑lasting headache was unremarkable. Neurological examination was intact. Brain computed tomography (CT) revealed that a hyperdense [Figure 1], brain magnetic resonance imaging (MRI) demonstrated an extra‑axial mass lesion located in cerebellomedullary cistern. Mass lesion was showing linear band‑style extension with intense enhancement toward choroid plexus of the fourth ventricle [Figure 2]. As meningiomas and ependymomas were the differentials and patient was symptomatic, surgical treatment was considered. The mass was totally excised with a midline suboccipital craniectomy. The tumor was extremely tough, solid, white, and with a good cleavage from the normal tissue. On histopathological examination of tumor tissue, tissues showed calcified chondroid and osseous metaplasia. In focal areas, epithelial structures in papilla‑like patterns were observed without surrounding atypia. Epithelial cells were widespread positively stained with GFAP, keratin, and S‑100, and negative staining were detected with epithelial membrane antigen (EMA) mucin and PAS‑A blue [Figure 3]. Staining pattern‑observed cells were evaluated as choroid plexus cells, and the histopathologic diagnosis of tumor was reported to be compatible with CPN. Including our patient, 39 cases of intracranial CPN have been published in the literature [Table 1]. Although clinical findings vary according to location and size of the lesion, they mostly present with headache and seizures. Of 33 cases described in the literature that underwent operation, 22 had gross total resection and 11 had subtotal resection. In the 22 patients, average follow‑up was of 57.9 months, no recurrence was reported in patients who underwent gross total resection, and a recurrence had been reported after 3 years from the first operation in one patient who underwent subtotal Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4
resection.[2] In two patients, growth of the lesions were observed 5 and 8 years after initial diagnosis of the lesion, and these patients had been operated.[3,4] Other calcified intracranial lesions should be considered in differential diagnosis. Calcifying pseudoneoplasms
a
b Figure 1: At the cerebellomedullary cistern, computed tomography showed hyperdens lesion bouth on brain (a) and bone (b) windows
a
c
b
d
Figure 2: Brain MRI showed a lesion hypointense on T1-weighted images (a) and heterogeneous in appearance T2-weighted images (b). The lesion was densyl enhanced after Gd. injection (c,d)
Figure 3: Focal chondroid metaplasia with amorphous calcified material and chondromyxoid matrix (H and E, original magnification ×200)
443
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Table 1: Summary of 39 reported cases of intracranial CPN
Authors, years
Location
Presentation
Treatment
Outcame/follow‑up (month)
Right frontal Brain, dura Left cerebellum Brain, dura Choroid Pineal Brain, dura Corpus callosum
HA Autopsy Autopsy Autopsy Autopsy Autopsy Autopsy HA, n/v
STR
Jun, 1984
27/F 55/F 60/M 74/F 46/M 62/M 83/M 55/M
NED/84 m NR NR NR NR NR NR NED/12–24 m
Garen, 1989 Bertoni, 1990
44/M 31/M
Atypical facial pain HA, hoarseness
Mohapatra, 2010 Hodges, 2011
32/F 59/M 6/M 67/F 67/F 16/M 35/M 49/F 59/M 48/M 34/M
Dura, Meckel’s cave Left cerebellopontine angle, jugular foramen Foramen magnum Skullbase/cerebellum Left frontal Skull base Right parietal Left temporal Parasagittal frontal region Right side of upper cervical/ clivus region Temporal Foramen magnum L temporal Right cerebellar hemisphere Right inferior colliculus Temporal horn Temporal Hippocampus Parietal Right temporobasal Left cerebellopontine angle
Ghosal, 2011
50/M
Third ventricle
Fletcher, 2012
19/M
Anterior skull base
Nonaka, 2012
56/M
Anterior infratemporal fossa
35/M
Left cerebellum, left occipital condyle Right frontal periventricular region
Rhodes, 1978
Tsugu, 1999 Qian, 1999
Shrier, 1999 Tatke, 2001 Rodriguez, 2008 Montibeller, 2009 Aiken, 2009
Age (years)/ sex
50/M 48/M 32/M 58/M 22/F 33/F 47/F 49/M
Neck/occipital pain Right CN XI paralysis Epilepsy Hoarseness Seizures Developmental delay Seizures Progressive stiffness of the low extremities Incidental Neck pain Seizures Incidental Dizziness Incidental Seizures Seizures Left arm numbness Complex partial seizures HA, tinnitus, dizziness, blurry vision, fatigue HA and emesis, generalized tonic-clonic seizure HA, clear nasal discharge, retro-orbital pain, left eye blurry vision Right-sided facial numbness and occasional orbital pain HA, generalized fatigue, tinnitus, and dizziness Worsening headache, ataxic gait, blurred vision, and poor memory Simple partial seizures, hallucinosis
Salim, 2012
47/F
Stienen, 2013
46/M
Right parietal lobe
Kerr, 2013
56/F 56/M
Left frontoparietal lobe Right lateral medullar space
HA
Grabowski , 2013 Present case
47/F 59/F
Corpus callosum Cerebellomedullary cistern
HA HA
Progression after 8 years follow‑up, GTR GTR STR
NED/122 m Recurrens/36 m
STR GTR GTR STR GTR GTR GTR GTR
NED/42 m NED/228 m NED/360 m Lost to follow‑up NED/96 m NED/31 m NED/36 m NED/90 m
GTR GTR STR STR GTR GTR GTR GTR GTR GTR STR
NED/12 m NED/12m NED/6 m NR NED/18 m NR NR NR NR NR NED/7 m
GTR
NED/6 m
GTR
NR
GTR
NR
STR
NR
GTR
NR
STR
NED/10 m
STR Progression after 3 years follow-up, STR GTR GTR
NED/22 m NED/6 m NR/21 m NR/6 m
CPN - Calcifying pseudoneoplasms, F - Female, M - Male, STR - Subtotal resection, GTR - Gross total resection, NED - No evidence of disease, NR - Not reported
are observed radiographically as a hyperdense lesion on CT. On MRI, they are usually hypointense on T1‑ and T2‑weighted sequences in appearance. They show different contrast enhancement after the injection of Gd. In most cases, interlinear or rim‑type contrast enhancement is observed, whereas besides our case, 444
intense contrast enhancement has been reported only in one case in the literature.[5] In addition, in two of the reported cases, there has been no contrast enhancement.[6] Typical histopathological findings of CPN are typical chondromyxoid matrix in nodular pattern, palisading Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4
[Downloaded free from http://www.neurologyindia.com on Thursday, September 25, 2014, IP: 202.177.173.189] || Click here to download free Android application for this journal Letters to Editor
spindle to epithelioid cells, varying amounts of fibrous stroma, calcification, osseous metaplasia, scattered psammoma body and foreign body reaction with giant cells.[6] These findings may not be all together. Mitosis and necrosis have not been reported. Although a wide variety of immunohistochemical stains have been used to characterize CPN, they show highly positive staining with EMA and vimentin and highly negative staining with GFAP and S‑100.[4] Most authors, on the basis of findings of granulomatous inflammation surrounding these, believe that these calcified lesions occur after a reactive process in neuraxis. [2,6,7] Rodriguez et al.[8] presented a CPN case coexisting with ependymomas. They reported that CPN might have developed due to reactive process around ependymomas. Salim et al. [9] reported a CPN in touch with an intra‑axial lipoma and reported that CPN might most likely occur as a result of reactive process. It has been suggested, but not proven, that CPN may develop as a healing response to an array of inciting factors, which can account for the variations in histopathologic features. The causal factors are not yet understood, but response to possible trauma, infection, or inflammation has been proposed. [10] It is impossible to give some diagnostic and treatment algorithms because of rarity of the condition. Imaging methods are insufficient for a definitive diagnosis in growing number of these reported lesions, and they should be considered in the differential diagnosis of calcified lesions. Moreover, these lesions may grow and have recurrence risk. Thus, surgical resection seems to be the rationalistic treatment for now. Surgical removal of lesions is important both in elimination of the patient’s symptoms and obtaining histopathological diagnosis, and besides prevention of aggressive adjuvant treatments. To have enough opinion for the course of the disease, we think that there is a need for a greater number of patients and longer follow‑up period.
Aydemir Fatih, Cekinmez Melih, Kardes Ozgur, Sarica B. Feyzi, Tufan Kadir, Kayaselcuk Fazilet1 Departments of Neurosurgery, and Pathology, Faculty of Medicine, Adana Practice and Research Center, Baskent University, Adana, Turkey E‑mail: [email protected] 1
References 1. Rhodes RH, Davis RL. An unusual fibro‑osseous componentn intracranial lesions. Hum Pathol 1978;9:309‑19. 2. Bertoni F, Unni KK, Dahlin DC, Beabout JW, Onofrio BM. Calcifying pseudoneoplasms of the neural axis. J Neurosurg 1990;72:42‑8. 3. Jun C, Burdick B. An unusual fibro‑osseous lesion of the brain. Case Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4
report. J Neurosurg 1984;60:1308‑11. 4. Kerr EE, Borys E, Bobinski M, Shahlaie K. Posterior fossa calcifyingpseudoneoplasm of the central nervous system. J Neurosurg 2013;118:896‑902. 5. Montibeller GR, Stan AC, Krauss JK, Nakamura M. Calcifying pseudoneoplasm of the inferior colliculus: An unusual location for a rare tumor: Case report. Neurosurgery 2009;65:E1005‑6. 6. Qian J, Rubio A, Powers JM, Rosenblum MK, Pilcher WH, Shrier DA, et al. Fibro‑osseous lesions of the central nervous system: Report of four cases and literature review. Am J Surg Pathol 1999;23:1270‑5. 7. Tatke M, Singh AK, Gupta V. Calcifying pseudoneoplasm of the CNS. Br J Neurosurg 2001;15:521‑3. 8. Rodriguez FJ, Scheithauer BW, Fourney DR, Robinson CA. Ependymoma and intraparenchymal calcifying pseudoneoplasm of the neural axis: İncidental collision or unique reactive phenomenon? Acta Neuropathol 2008;115:363‑6. 9. Salim AA, Wilson PJ, Cherukuri RK, McKenzie S, Buckland ME. An unusual association of calcifying pseudoneoplasm of the neuraxis with interhemispheric lipoma and agenesis of corpus callosum. Pathology 2012;44:657‑9. 10. Aiken AH, Akgun H, Tihan T, Barbaro N, Glastonbury C. Calcifying pseudoneoplasms of the neuraxis: CT, MR imaging, and histologic features. AJNR Am J Neuroradiol 2009;30:1256‑60. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.141255
Received: 11-06-2014 Review completed: 13-06-2014 Accepted: 10-08-2014
Brain metastasis from cardiac angiosarcoma Sir, Angiosarcomas are rare malignant tumors, accounting for less than 1% of all sarcomas,[1] and are the second most common histological type of cardiac sarcoma. These tumors are more frequent in men and usually occur in the third to fifth decades of life.[2] Involvement of brain, either primary or metastatic, is extremely rare.[3] A 28‑year‑old male presented with headache and vomiting of 15 days duration. Neurologic examination was essentially normal. Magnetic resonance imaging (MRI) revealed a left frontal mass with heterogeneous contrast enhancement and peri‑lesional edema [Figure 1]. Thirteen months before this admission, he was evaluated for progressive chest pain and was found to have a right atrial mass. On that occasion, the cardiac mass could not be completely resected because of invasion of the vena cava. Histopathology revealed cardiac angiosarcoma with positive staining for CD31 and CD34. The Ki‑67 labeling index was about 80% [Figure 2]. Patient received 445
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.
Calcifying pseudoneoplasm of the cerebellomedullary cistern: A case report and review of the literature Sir, Calcifying pseudoneoplasms (CPNs) are rare, calcified, non‑neoplastic lesions and can occur in any part of the central nervous system (CNS). They were first described by Rhodes and Davis.[1] In the pathophysiology, although there is not a complete consensus among authors, they are thought to occur after a reactive or metaplastic process in the neuraxis. Our patient is the first reported case in this anatomic location and second time reported case of CPN with its imaging features in the literature. Medical history of 59‑year‑old female patient with a long‑lasting headache was unremarkable. Neurological examination was intact. Brain computed tomography (CT) revealed that a hyperdense [Figure 1], brain magnetic resonance imaging (MRI) demonstrated an extra‑axial mass lesion located in cerebellomedullary cistern. Mass lesion was showing linear band‑style extension with intense enhancement toward choroid plexus of the fourth ventricle [Figure 2]. As meningiomas and ependymomas were the differentials and patient was symptomatic, surgical treatment was considered. The mass was totally excised with a midline suboccipital craniectomy. The tumor was extremely tough, solid, white, and with a good cleavage from the normal tissue. On histopathological examination of tumor tissue, tissues showed calcified chondroid and osseous metaplasia. In focal areas, epithelial structures in papilla‑like patterns were observed without surrounding atypia. Epithelial cells were widespread positively stained with GFAP, keratin, and S‑100, and negative staining were detected with epithelial membrane antigen (EMA) mucin and PAS‑A blue [Figure 3]. Staining pattern‑observed cells were evaluated as choroid plexus cells, and the histopathologic diagnosis of tumor was reported to be compatible with CPN. Including our patient, 39 cases of intracranial CPN have been published in the literature [Table 1]. Although clinical findings vary according to location and size of the lesion, they mostly present with headache and seizures. Of 33 cases described in the literature that underwent operation, 22 had gross total resection and 11 had subtotal resection. In the 22 patients, average follow‑up was of 57.9 months, no recurrence was reported in patients who underwent gross total resection, and a recurrence had been reported after 3 years from the first operation in one patient who underwent subtotal Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4
resection.[2] In two patients, growth of the lesions were observed 5 and 8 years after initial diagnosis of the lesion, and these patients had been operated.[3,4] Other calcified intracranial lesions should be considered in differential diagnosis. Calcifying pseudoneoplasms
a
b Figure 1: At the cerebellomedullary cistern, computed tomography showed hyperdens lesion bouth on brain (a) and bone (b) windows
a
c
b
d
Figure 2: Brain MRI showed a lesion hypointense on T1-weighted images (a) and heterogeneous in appearance T2-weighted images (b). The lesion was densyl enhanced after Gd. injection (c,d)
Figure 3: Focal chondroid metaplasia with amorphous calcified material and chondromyxoid matrix (H and E, original magnification ×200)
443
[Downloaded free from http://www.neurologyindia.com on Thursday, September 25, 2014, IP: 202.177.173.189] || Click here to download free Android application fo this journal Letters to Editor
Table 1: Summary of 39 reported cases of intracranial CPN
Authors, years
Location
Presentation
Treatment
Outcame/follow‑up (month)
Right frontal Brain, dura Left cerebellum Brain, dura Choroid Pineal Brain, dura Corpus callosum
HA Autopsy Autopsy Autopsy Autopsy Autopsy Autopsy HA, n/v
STR
Jun, 1984
27/F 55/F 60/M 74/F 46/M 62/M 83/M 55/M
NED/84 m NR NR NR NR NR NR NED/12–24 m
Garen, 1989 Bertoni, 1990
44/M 31/M
Atypical facial pain HA, hoarseness
Mohapatra, 2010 Hodges, 2011
32/F 59/M 6/M 67/F 67/F 16/M 35/M 49/F 59/M 48/M 34/M
Dura, Meckel’s cave Left cerebellopontine angle, jugular foramen Foramen magnum Skullbase/cerebellum Left frontal Skull base Right parietal Left temporal Parasagittal frontal region Right side of upper cervical/ clivus region Temporal Foramen magnum L temporal Right cerebellar hemisphere Right inferior colliculus Temporal horn Temporal Hippocampus Parietal Right temporobasal Left cerebellopontine angle
Ghosal, 2011
50/M
Third ventricle
Fletcher, 2012
19/M
Anterior skull base
Nonaka, 2012
56/M
Anterior infratemporal fossa
35/M
Left cerebellum, left occipital condyle Right frontal periventricular region
Rhodes, 1978
Tsugu, 1999 Qian, 1999
Shrier, 1999 Tatke, 2001 Rodriguez, 2008 Montibeller, 2009 Aiken, 2009
Age (years)/ sex
50/M 48/M 32/M 58/M 22/F 33/F 47/F 49/M
Neck/occipital pain Right CN XI paralysis Epilepsy Hoarseness Seizures Developmental delay Seizures Progressive stiffness of the low extremities Incidental Neck pain Seizures Incidental Dizziness Incidental Seizures Seizures Left arm numbness Complex partial seizures HA, tinnitus, dizziness, blurry vision, fatigue HA and emesis, generalized tonic-clonic seizure HA, clear nasal discharge, retro-orbital pain, left eye blurry vision Right-sided facial numbness and occasional orbital pain HA, generalized fatigue, tinnitus, and dizziness Worsening headache, ataxic gait, blurred vision, and poor memory Simple partial seizures, hallucinosis
Salim, 2012
47/F
Stienen, 2013
46/M
Right parietal lobe
Kerr, 2013
56/F 56/M
Left frontoparietal lobe Right lateral medullar space
HA
Grabowski , 2013 Present case
47/F 59/F
Corpus callosum Cerebellomedullary cistern
HA HA
Progression after 8 years follow‑up, GTR GTR STR
NED/122 m Recurrens/36 m
STR GTR GTR STR GTR GTR GTR GTR
NED/42 m NED/228 m NED/360 m Lost to follow‑up NED/96 m NED/31 m NED/36 m NED/90 m
GTR GTR STR STR GTR GTR GTR GTR GTR GTR STR
NED/12 m NED/12m NED/6 m NR NED/18 m NR NR NR NR NR NED/7 m
GTR
NED/6 m
GTR
NR
GTR
NR
STR
NR
GTR
NR
STR
NED/10 m
STR Progression after 3 years follow-up, STR GTR GTR
NED/22 m NED/6 m NR/21 m NR/6 m
CPN - Calcifying pseudoneoplasms, F - Female, M - Male, STR - Subtotal resection, GTR - Gross total resection, NED - No evidence of disease, NR - Not reported
are observed radiographically as a hyperdense lesion on CT. On MRI, they are usually hypointense on T1‑ and T2‑weighted sequences in appearance. They show different contrast enhancement after the injection of Gd. In most cases, interlinear or rim‑type contrast enhancement is observed, whereas besides our case, 444
intense contrast enhancement has been reported only in one case in the literature.[5] In addition, in two of the reported cases, there has been no contrast enhancement.[6] Typical histopathological findings of CPN are typical chondromyxoid matrix in nodular pattern, palisading Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4
[Downloaded free from http://www.neurologyindia.com on Thursday, September 25, 2014, IP: 202.177.173.189] || Click here to download free Android application for this journal Letters to Editor
spindle to epithelioid cells, varying amounts of fibrous stroma, calcification, osseous metaplasia, scattered psammoma body and foreign body reaction with giant cells.[6] These findings may not be all together. Mitosis and necrosis have not been reported. Although a wide variety of immunohistochemical stains have been used to characterize CPN, they show highly positive staining with EMA and vimentin and highly negative staining with GFAP and S‑100.[4] Most authors, on the basis of findings of granulomatous inflammation surrounding these, believe that these calcified lesions occur after a reactive process in neuraxis. [2,6,7] Rodriguez et al.[8] presented a CPN case coexisting with ependymomas. They reported that CPN might have developed due to reactive process around ependymomas. Salim et al. [9] reported a CPN in touch with an intra‑axial lipoma and reported that CPN might most likely occur as a result of reactive process. It has been suggested, but not proven, that CPN may develop as a healing response to an array of inciting factors, which can account for the variations in histopathologic features. The causal factors are not yet understood, but response to possible trauma, infection, or inflammation has been proposed. [10] It is impossible to give some diagnostic and treatment algorithms because of rarity of the condition. Imaging methods are insufficient for a definitive diagnosis in growing number of these reported lesions, and they should be considered in the differential diagnosis of calcified lesions. Moreover, these lesions may grow and have recurrence risk. Thus, surgical resection seems to be the rationalistic treatment for now. Surgical removal of lesions is important both in elimination of the patient’s symptoms and obtaining histopathological diagnosis, and besides prevention of aggressive adjuvant treatments. To have enough opinion for the course of the disease, we think that there is a need for a greater number of patients and longer follow‑up period.
Aydemir Fatih, Cekinmez Melih, Kardes Ozgur, Sarica B. Feyzi, Tufan Kadir, Kayaselcuk Fazilet1 Departments of Neurosurgery, and Pathology, Faculty of Medicine, Adana Practice and Research Center, Baskent University, Adana, Turkey E‑mail: [email protected] 1
References 1. Rhodes RH, Davis RL. An unusual fibro‑osseous componentn intracranial lesions. Hum Pathol 1978;9:309‑19. 2. Bertoni F, Unni KK, Dahlin DC, Beabout JW, Onofrio BM. Calcifying pseudoneoplasms of the neural axis. J Neurosurg 1990;72:42‑8. 3. Jun C, Burdick B. An unusual fibro‑osseous lesion of the brain. Case Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4
report. J Neurosurg 1984;60:1308‑11. 4. Kerr EE, Borys E, Bobinski M, Shahlaie K. Posterior fossa calcifyingpseudoneoplasm of the central nervous system. J Neurosurg 2013;118:896‑902. 5. Montibeller GR, Stan AC, Krauss JK, Nakamura M. Calcifying pseudoneoplasm of the inferior colliculus: An unusual location for a rare tumor: Case report. Neurosurgery 2009;65:E1005‑6. 6. Qian J, Rubio A, Powers JM, Rosenblum MK, Pilcher WH, Shrier DA, et al. Fibro‑osseous lesions of the central nervous system: Report of four cases and literature review. Am J Surg Pathol 1999;23:1270‑5. 7. Tatke M, Singh AK, Gupta V. Calcifying pseudoneoplasm of the CNS. Br J Neurosurg 2001;15:521‑3. 8. Rodriguez FJ, Scheithauer BW, Fourney DR, Robinson CA. Ependymoma and intraparenchymal calcifying pseudoneoplasm of the neural axis: İncidental collision or unique reactive phenomenon? Acta Neuropathol 2008;115:363‑6. 9. Salim AA, Wilson PJ, Cherukuri RK, McKenzie S, Buckland ME. An unusual association of calcifying pseudoneoplasm of the neuraxis with interhemispheric lipoma and agenesis of corpus callosum. Pathology 2012;44:657‑9. 10. Aiken AH, Akgun H, Tihan T, Barbaro N, Glastonbury C. Calcifying pseudoneoplasms of the neuraxis: CT, MR imaging, and histologic features. AJNR Am J Neuroradiol 2009;30:1256‑60. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.141255
Received: 11-06-2014 Review completed: 13-06-2014 Accepted: 10-08-2014
Brain metastasis from cardiac angiosarcoma Sir, Angiosarcomas are rare malignant tumors, accounting for less than 1% of all sarcomas,[1] and are the second most common histological type of cardiac sarcoma. These tumors are more frequent in men and usually occur in the third to fifth decades of life.[2] Involvement of brain, either primary or metastatic, is extremely rare.[3] A 28‑year‑old male presented with headache and vomiting of 15 days duration. Neurologic examination was essentially normal. Magnetic resonance imaging (MRI) revealed a left frontal mass with heterogeneous contrast enhancement and peri‑lesional edema [Figure 1]. Thirteen months before this admission, he was evaluated for progressive chest pain and was found to have a right atrial mass. On that occasion, the cardiac mass could not be completely resected because of invasion of the vena cava. Histopathology revealed cardiac angiosarcoma with positive staining for CD31 and CD34. The Ki‑67 labeling index was about 80% [Figure 2]. Patient received 445
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.
