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Neuropathology 2015; ••, ••–••
doi:10.1111/neup.12198
C a se Repor t
Multiple calcifying pseudoneoplasms of the neuraxis Molly Hubbard,1 Rabia Qaiser,1 H Brent Clark2 and Ramachandra Tummala1 Departments of 1Neurosurgery and 2Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, Minnesota, USA
Calcified pseudoneoplasms of the neuraxis (CAPNON) are a rare diagnostic entity. They have been reported intra-cranially as well as in the spine, and are most commonly found at the skull base. This is a case report of a 38-year-old woman who presented with bilateral CAPNON, diagnosed 8 years apart. While there are approximately 46 reported in the current literature of cerebral and spinal fibro-osseous lesions, this is the first report of separate lesions. Keywords: CAPNON, calcification, pseudotumor, multiple, seizures.
INTRODUCTION Calcifying pseudoneoplasms of the neuraxis (CAPNON), are a rare diagnostic entity. There are 46 reports in the literature, 12 in the spinal canal and 34 intracranially. Typically, intracranial lesions are found at the skull base. Regardless of their location, they seem to have a benign course, and symptoms are caused primarily by secondary mass effect or irritation of local tissue. The precise etiology is not defined, and there seems to be a 1.5:1 male to female predominance. To our knowledge, this is the first case report of a patient presenting with two separate lesions in remote locations from each other. Additionally, it supports the current literature findings that these lesions demonstrate slow growth over time.1–3
Correspondence: Molly Hubbard, MD, Department of Neurosurgery, University of Minnesota, MMC 96, Room D429, Mayo Building, 420 Delaware St SE, Minneapolis, MN 55455, USA. Email: hubba166@ umn.edu Received 3 October 2014; revised 9 January 2015 and accepted 10 January 2015. This case report was presented as an e-poster at the AANS meeting in April, 2013.
© 2015 Japanese Society of Neuropathology
CASE REPORT A 46-year-old woman with congenital deafness secondary to prenatal measles presented with diffuse headaches that were worse on the left side. Recent MRI of the brain showed progressive growth in a known left posterior frontal lobe mass. She was referred to us for further management. Eight years earlier, she presented to an outside hospital with episodic left facial numbness, and her medical records describe bilateral calcified intra-axial frontoparietal lesions on MRI. The right-sided mass measured 13 mm × 12 mm and the left one measured 4 mm × 4 mm. She underwent a stereotactic needle biopsy of the right-sided lesion, but the results were nondiagnostic. The patient subsequently underwent a craniotomy and a transcortical resection of the right parietal mass. The operative records from the outside hospital describe a lesion that was so firm that en bloc resection was necessary. It was described as densely calcified and surrounded by glial parenchyma, not suggestive of neoplasm. The cells within the calcification were fibroblastic. The pathologist from the outside hospital believed that this was suggestive of a CAPNON. When she came to our attention 8 years later, we found her to have decreased sensation in the left cheek, left pronator drift, and mildly slow left finger movements, all sequelae of the original operation. At current presentation, the lesion on the left side had increased in size, and now measured 12 mm × 11 mm. On MRI, it appeared as a heterogeneously enhancing mass in the posterior left frontal lobe with surrounding edema (Fig. 1). Computed tomography revealed central calcification measuring 10.7 mm × 11.9 mm with surrounding hypodensity (Fig. 2). Postoperative changes were seen in the right parietal lobe with no obvious residual lesion. She underwent frameless stereotactic guided craniotomy and a trans-sulcal approach to resect the left-sided mass. Intraoperative cortical stimulation revealed that the lesion was at the base of the precentral gyrus. Intraoperative biopsies of the edematous brain anterior
2
M Hubbard et al.
A
B Fig. 2 Non-contrast CT scan, lesion measuring 10.7 mm × 11.9 mm with surrounding hypodensity consistent with edema. There is evidence of prior craniotomy on right.
C
Fig. 1 (A) Axial T1-weighted MRI with contrast, from 2009. A lesion with heterogeneous enhancement measuring 9 mm. (B) Axial T1-weighted MRI with contrast, from 2012, with increase in size of the lesion to 12 mm. (C) Axial T2-weighted MRI with edema surrounding the mass lesion, measuring 3 cm.
to the lesion revealed reactive gliosis. The calcific mass was removed en bloc and sent for permanent pathology. She awoke from surgery with no new neurological deficits. Pathological examination demonstrated a calcified mass with foci of mature adipose tissue, and occasional nests of chronic inflammatory cells. The calcified material was densely basophilic and rather amorphous except for a non-lamellar linear fibrillary appearance. This was diagnosed as a CAPNON. Surrounding the lesion was dense reactive gliosis (Fig. 3a, b). Eighteen months later, her headaches were improved but not resolved, she was at her neurological baseline, and there was no evidence of recurrence on MRI. The histopathological appearance was a calcified mass that when decalcified contained a chondromyxoid matrix with fibrillary radiating striations at the periphery. The outer margins were often rimmed by cells with eccentric eosinophilic cytoplasm. Intercalated within the mass were areas of delicate stroma often accompanied by metaplastic adipose tissue. There were no areas suggestive of meningeal or glial neoplasia. Immunohistochemical staining for epithelial membrane antigen (EMA), S100protein, GFAP and CD68 did not label the plump cells at the margin. Occasional macrophages in this region were CD68-positive. Some of the surrounding brain tissue that had been resected separately had reactive gliosis but was not involved by the calcified process. The diagnosis was calcified pseudoneoplasm of the neuraxis (CAPNON). © 2015 Japanese Society of Neuropathology
Multiple CAPNON: a case report
A
B
Fig. 3 Photomicrographs of the pathologic specimen, HE staining. (A) Low-power view of one fragment of the lesion showing an admixture of chondromyxoid matrix and stroma. Scale bar = 500 μm. (B) There are radiating fibrillary striations within the matrix. There are cells with eccentric eosinophilic cytoplasm lining the edge of the lesion. Scale bar = 50 μm.
DISCUSSION Rhodes and Davis first described CAPNON in 1978;4 six of their first seven cases were diagnosed post mortem. The surviving patient was a woman who suffered from bilateral headaches and a calcified mass was seen near the right orbital roof on skull X-ray. Since then, several authors1,5–9 have reported additional patients with calcified intracranial and spinal masses. The resected lesion has the classical appearance of CAPNON described in the literature with the chondromyxoid matrix, delicate stroma, radiating fibrillary striations and rimming by eccentric “epithelioid” cells.8 There is low cellularity without convincing evidence of neoplastic component. Adipose differentiation, presumably metaplastic, within these lesions also has been reported.10 Inflammatory changes, including foreign-body reaction also are frequently seen. The cell of origin of this © 2015 Japanese Society of Neuropathology
3 process is uncertain but arachnoidal cells or fibroblasts have been proposed.6 Most pathologists believe it is a reactive rather than neoplastic condition.3,8 The fact that the rimming “epithelioid” cells often are immunoreactive for EMA suggests an association with, if not origin from, the leptomeninges. However, in the present case there was no immunoreactivity for EMA or markers for glia or macrophages in those cells. There is one case report where a CAPNON was associated with a neoplastic lesion, namely a contiguous ependymoma.11 These authors noted only that this was supportive of a reactive etiology of CAPNON, and not indicative of transformation of the CAPNON to a neoplasm. It has been hypothesized that these lesions develop from fibroblasts or arachnoid cells;7 however, this remains controversial. Others report that these develop as a reactive process5,9 from an unclear etiology. There is one case report where a CAPNON was associated with a malignant lesion, namely a contiguous ependymoma.11 These authors noted only that this was supportive of a reactive etiology of CAPNON, and not indicative of transformation of the CAPNON to a malignant tumor. This case is unusual in the fact that both of her lesions were described to be subcortical in location. The exact etiology can only be hypothesized; however, it is possibly due to invaginations of pia, then subsequent reactive changes occurring. Others have proposed that these represent calcifications of lowgrade neoplasms2 While there have been increasing numbers of spinal and cranial CAPNON reported in the literature, there are no reports of multifocal lesions in an individual patient. Also, the increasing size of the lesion over time is consistent with what was reported by Kerr et al3 as well as others,1,2 and it is possible that her increased seizure frequency was associated with the slow growth of the lesion and increased irritation of the surrounding cortex. There was increased edema around the mass, over time, which was consistent with what has been reported with other cases.11,12Most cases of intraparenchymal CAPNON are associated with seizures,13 and while our patient’s symptoms were initially diagnosed as transient ischemic attacks, they more likely represented simple partial seizures. As there are few reports of these masses, it is not known whether resection results in decreased seizure frequency. As there are no reports of multiple lesions in a single patient, the pathology results from the patient’s first operation did not alter the management in this patient. The differential diagnosis for intracranial calcified lesions is broad. The most common calcified lesion at the skull base in the differential diagnosis is meningioma,13 but also includes chordoma, chondroma, and vestibular schwannoma.13,14 Intra-axial calcified lesions include oligodendroglioma, cavernous malformations and arteriovenous
4
M Hubbard et al.
malformations. Cavernous malformations often are seen to be hyperintense with central hypointensity on T2 MRI, which often distinguishes these lesions from fibro-osseous lesions. Choroid plexus tumors, ependymomas, and meningiomas are intraventricular tumors with potential calcifications. The differential diagnosis for calcified lesions within the spinal cord is similar, in addition to calcified disc herniation and calcified synovial cyst. Radiographically, CAPNON have been described as well circumscribed, solidly calcified masses on CT scan. They are typically hypointense on T1 and T2, and rarely show surrounding edema;13 however, edema has been noted on larger lesions.3,12 They occasionally will demonstrate peripheral enhancement with gadolinium, thought to be secondary to the stromal elements within the lesions.12 Spine lesions are less well classified, but have been described as well-circumscribed extradural lesions with isointense signal on T1 but increased signal on T2 sequences8 while others describe lesions with isointense signal on T1 and T2. All spine lesions reported have been extradural.15 Regarding recurrence, it appears that complete resection of the lesions is curative;3 however, there are no long-term studies specifically addressing this question. This is the first report of a patient with multiple calcified pseudoneoplasms of the neuraxis. In conclusion, while CAPNON are not common lesions, they should be in the differential diagnosis of a solidly calcifying intracranial or spinal canal lesion. Interestingly, in this patient, the lesion was seen to grow in size over the 8 years between surgical interventions, yet remained histologically the same as the first lesion. This supports that these are less likely a neoplastic entity, or if it is, that it remains histologically benign despite growth. Treatment currently is limited to surgical resection and should be considered based on the patient’s clinical presentation, location of the lesion and surgical risk.
REFERENCES 1. Jun C, Burdick B. An unusual fibro-osseus calcifying pesudotumor of the axis. Case report. J Neurosurg 1984; 60: 1308–1311. 2. Smith DM, III, Berry A. Unusual fibro-osseus lesion of the spinal cord with positive staining for glial fibrillary acidic protein and radiological progression: a case report. Hum Pathol 1994; 25: 835–838.
3. Kerr E, Borys E, Bobinski M, Shahlaie K. Posterior fossa calcifying pseudoneoplasm of the central nervous system. J Neurosurg 2013; 118: 896–902. 4. Rhodes RH, Davis RL. An unusual fibro-osseus component in intracranial lesions. Hum Pathol 1978; 9: 309– 319. 5. Bertoni F, Unni KK, Dahlin DC. Calcifying pseudoneoplasms of the neural axis. J Neurosurg 1990; 72: 42–48. 6. Fletcher AM, Greenlee JJD, Chang KE, Smoker WR, Kirby PA, O’Brien EK. Endoscopic resection of calcifying pseudoneoplasm of the neuraxis (CAPNON) of the anterior skull base with sinonasal extension. J Clin Neurosci 2012; 19: 1048–1049. 7. Tatke M, Singh AK, Gupta V. Calcifying pseudoneoplasm of the CNS. Br J Neurosurg 2001; 15: 521–528. 8. Park P, Schmidt LA, Shah GV, Tran NK, Gandhi D, LaMarca F. Calcifying pseudoneoplasm of the spine. Clin Neurol Neurosurg 2008; 110: 392–395. 9. Qian J, Rubio A, Powers JM et al. Fibro-Osseus Lesions of the Central Nervous System: report of four cases and literature review. Am J Surg Pathol 1999; 23: 1270–1275. 10. Jentoft ME, Scheithauer BW, Bertoni F, Abood C, Chang HT. Calcifying pseudoneoplasm of the neuraxis with single nerve rootlet involvement. Can J Neurol Sci 2012; 39: 840–842. 11. Rodriguez FJ, Scheithauer BW, Fourney DR, Robinson CA. Ependymoma and intraparenchymal calcifying pseudoneoplasm of the neural axis: incidental collison or unique reactive phenomenon. Acta Neuropathol 2007; 115: 363–366. 12. Shrier DA, Melville D, Qian J et al. Fibro-osseus lesions involving the brain: MRI. Diagn Neuroradiol 1999; 41: 18–21. 13. Aiken AH, Akgun H, Tihan T, Barbaro N, Glastonbury C. Calcifying pseudoneoplasms of the neuraxis: CT, MR imaging and histologic features. Am J Neuroradiol 2009; 30: 1256–1260. 14. Hodges TR, Karikari IO, Nimjee SM et al. Calcifying pseudoneoplasm of the cerebellopontine angle: case report. Neurosurgery 2011; 69 (1 Suppl Opoerative): 117–120. 15. Bartanusz V, Ziu M, Jimenez DF, Henry JM. Calcifying pseudoneoplasm of the atlantoaxial joint in a child. J Neurosurg Spine 2013; 18: 367–371.
© 2015 Japanese Society of Neuropathology
Neuropathology 2015; ••, ••–••
doi:10.1111/neup.12198
C a se Repor t
Multiple calcifying pseudoneoplasms of the neuraxis Molly Hubbard,1 Rabia Qaiser,1 H Brent Clark2 and Ramachandra Tummala1 Departments of 1Neurosurgery and 2Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, Minnesota, USA
Calcified pseudoneoplasms of the neuraxis (CAPNON) are a rare diagnostic entity. They have been reported intra-cranially as well as in the spine, and are most commonly found at the skull base. This is a case report of a 38-year-old woman who presented with bilateral CAPNON, diagnosed 8 years apart. While there are approximately 46 reported in the current literature of cerebral and spinal fibro-osseous lesions, this is the first report of separate lesions. Keywords: CAPNON, calcification, pseudotumor, multiple, seizures.
INTRODUCTION Calcifying pseudoneoplasms of the neuraxis (CAPNON), are a rare diagnostic entity. There are 46 reports in the literature, 12 in the spinal canal and 34 intracranially. Typically, intracranial lesions are found at the skull base. Regardless of their location, they seem to have a benign course, and symptoms are caused primarily by secondary mass effect or irritation of local tissue. The precise etiology is not defined, and there seems to be a 1.5:1 male to female predominance. To our knowledge, this is the first case report of a patient presenting with two separate lesions in remote locations from each other. Additionally, it supports the current literature findings that these lesions demonstrate slow growth over time.1–3
Correspondence: Molly Hubbard, MD, Department of Neurosurgery, University of Minnesota, MMC 96, Room D429, Mayo Building, 420 Delaware St SE, Minneapolis, MN 55455, USA. Email: hubba166@ umn.edu Received 3 October 2014; revised 9 January 2015 and accepted 10 January 2015. This case report was presented as an e-poster at the AANS meeting in April, 2013.
© 2015 Japanese Society of Neuropathology
CASE REPORT A 46-year-old woman with congenital deafness secondary to prenatal measles presented with diffuse headaches that were worse on the left side. Recent MRI of the brain showed progressive growth in a known left posterior frontal lobe mass. She was referred to us for further management. Eight years earlier, she presented to an outside hospital with episodic left facial numbness, and her medical records describe bilateral calcified intra-axial frontoparietal lesions on MRI. The right-sided mass measured 13 mm × 12 mm and the left one measured 4 mm × 4 mm. She underwent a stereotactic needle biopsy of the right-sided lesion, but the results were nondiagnostic. The patient subsequently underwent a craniotomy and a transcortical resection of the right parietal mass. The operative records from the outside hospital describe a lesion that was so firm that en bloc resection was necessary. It was described as densely calcified and surrounded by glial parenchyma, not suggestive of neoplasm. The cells within the calcification were fibroblastic. The pathologist from the outside hospital believed that this was suggestive of a CAPNON. When she came to our attention 8 years later, we found her to have decreased sensation in the left cheek, left pronator drift, and mildly slow left finger movements, all sequelae of the original operation. At current presentation, the lesion on the left side had increased in size, and now measured 12 mm × 11 mm. On MRI, it appeared as a heterogeneously enhancing mass in the posterior left frontal lobe with surrounding edema (Fig. 1). Computed tomography revealed central calcification measuring 10.7 mm × 11.9 mm with surrounding hypodensity (Fig. 2). Postoperative changes were seen in the right parietal lobe with no obvious residual lesion. She underwent frameless stereotactic guided craniotomy and a trans-sulcal approach to resect the left-sided mass. Intraoperative cortical stimulation revealed that the lesion was at the base of the precentral gyrus. Intraoperative biopsies of the edematous brain anterior
2
M Hubbard et al.
A
B Fig. 2 Non-contrast CT scan, lesion measuring 10.7 mm × 11.9 mm with surrounding hypodensity consistent with edema. There is evidence of prior craniotomy on right.
C
Fig. 1 (A) Axial T1-weighted MRI with contrast, from 2009. A lesion with heterogeneous enhancement measuring 9 mm. (B) Axial T1-weighted MRI with contrast, from 2012, with increase in size of the lesion to 12 mm. (C) Axial T2-weighted MRI with edema surrounding the mass lesion, measuring 3 cm.
to the lesion revealed reactive gliosis. The calcific mass was removed en bloc and sent for permanent pathology. She awoke from surgery with no new neurological deficits. Pathological examination demonstrated a calcified mass with foci of mature adipose tissue, and occasional nests of chronic inflammatory cells. The calcified material was densely basophilic and rather amorphous except for a non-lamellar linear fibrillary appearance. This was diagnosed as a CAPNON. Surrounding the lesion was dense reactive gliosis (Fig. 3a, b). Eighteen months later, her headaches were improved but not resolved, she was at her neurological baseline, and there was no evidence of recurrence on MRI. The histopathological appearance was a calcified mass that when decalcified contained a chondromyxoid matrix with fibrillary radiating striations at the periphery. The outer margins were often rimmed by cells with eccentric eosinophilic cytoplasm. Intercalated within the mass were areas of delicate stroma often accompanied by metaplastic adipose tissue. There were no areas suggestive of meningeal or glial neoplasia. Immunohistochemical staining for epithelial membrane antigen (EMA), S100protein, GFAP and CD68 did not label the plump cells at the margin. Occasional macrophages in this region were CD68-positive. Some of the surrounding brain tissue that had been resected separately had reactive gliosis but was not involved by the calcified process. The diagnosis was calcified pseudoneoplasm of the neuraxis (CAPNON). © 2015 Japanese Society of Neuropathology
Multiple CAPNON: a case report
A
B
Fig. 3 Photomicrographs of the pathologic specimen, HE staining. (A) Low-power view of one fragment of the lesion showing an admixture of chondromyxoid matrix and stroma. Scale bar = 500 μm. (B) There are radiating fibrillary striations within the matrix. There are cells with eccentric eosinophilic cytoplasm lining the edge of the lesion. Scale bar = 50 μm.
DISCUSSION Rhodes and Davis first described CAPNON in 1978;4 six of their first seven cases were diagnosed post mortem. The surviving patient was a woman who suffered from bilateral headaches and a calcified mass was seen near the right orbital roof on skull X-ray. Since then, several authors1,5–9 have reported additional patients with calcified intracranial and spinal masses. The resected lesion has the classical appearance of CAPNON described in the literature with the chondromyxoid matrix, delicate stroma, radiating fibrillary striations and rimming by eccentric “epithelioid” cells.8 There is low cellularity without convincing evidence of neoplastic component. Adipose differentiation, presumably metaplastic, within these lesions also has been reported.10 Inflammatory changes, including foreign-body reaction also are frequently seen. The cell of origin of this © 2015 Japanese Society of Neuropathology
3 process is uncertain but arachnoidal cells or fibroblasts have been proposed.6 Most pathologists believe it is a reactive rather than neoplastic condition.3,8 The fact that the rimming “epithelioid” cells often are immunoreactive for EMA suggests an association with, if not origin from, the leptomeninges. However, in the present case there was no immunoreactivity for EMA or markers for glia or macrophages in those cells. There is one case report where a CAPNON was associated with a neoplastic lesion, namely a contiguous ependymoma.11 These authors noted only that this was supportive of a reactive etiology of CAPNON, and not indicative of transformation of the CAPNON to a neoplasm. It has been hypothesized that these lesions develop from fibroblasts or arachnoid cells;7 however, this remains controversial. Others report that these develop as a reactive process5,9 from an unclear etiology. There is one case report where a CAPNON was associated with a malignant lesion, namely a contiguous ependymoma.11 These authors noted only that this was supportive of a reactive etiology of CAPNON, and not indicative of transformation of the CAPNON to a malignant tumor. This case is unusual in the fact that both of her lesions were described to be subcortical in location. The exact etiology can only be hypothesized; however, it is possibly due to invaginations of pia, then subsequent reactive changes occurring. Others have proposed that these represent calcifications of lowgrade neoplasms2 While there have been increasing numbers of spinal and cranial CAPNON reported in the literature, there are no reports of multifocal lesions in an individual patient. Also, the increasing size of the lesion over time is consistent with what was reported by Kerr et al3 as well as others,1,2 and it is possible that her increased seizure frequency was associated with the slow growth of the lesion and increased irritation of the surrounding cortex. There was increased edema around the mass, over time, which was consistent with what has been reported with other cases.11,12Most cases of intraparenchymal CAPNON are associated with seizures,13 and while our patient’s symptoms were initially diagnosed as transient ischemic attacks, they more likely represented simple partial seizures. As there are few reports of these masses, it is not known whether resection results in decreased seizure frequency. As there are no reports of multiple lesions in a single patient, the pathology results from the patient’s first operation did not alter the management in this patient. The differential diagnosis for intracranial calcified lesions is broad. The most common calcified lesion at the skull base in the differential diagnosis is meningioma,13 but also includes chordoma, chondroma, and vestibular schwannoma.13,14 Intra-axial calcified lesions include oligodendroglioma, cavernous malformations and arteriovenous
4
M Hubbard et al.
malformations. Cavernous malformations often are seen to be hyperintense with central hypointensity on T2 MRI, which often distinguishes these lesions from fibro-osseous lesions. Choroid plexus tumors, ependymomas, and meningiomas are intraventricular tumors with potential calcifications. The differential diagnosis for calcified lesions within the spinal cord is similar, in addition to calcified disc herniation and calcified synovial cyst. Radiographically, CAPNON have been described as well circumscribed, solidly calcified masses on CT scan. They are typically hypointense on T1 and T2, and rarely show surrounding edema;13 however, edema has been noted on larger lesions.3,12 They occasionally will demonstrate peripheral enhancement with gadolinium, thought to be secondary to the stromal elements within the lesions.12 Spine lesions are less well classified, but have been described as well-circumscribed extradural lesions with isointense signal on T1 but increased signal on T2 sequences8 while others describe lesions with isointense signal on T1 and T2. All spine lesions reported have been extradural.15 Regarding recurrence, it appears that complete resection of the lesions is curative;3 however, there are no long-term studies specifically addressing this question. This is the first report of a patient with multiple calcified pseudoneoplasms of the neuraxis. In conclusion, while CAPNON are not common lesions, they should be in the differential diagnosis of a solidly calcifying intracranial or spinal canal lesion. Interestingly, in this patient, the lesion was seen to grow in size over the 8 years between surgical interventions, yet remained histologically the same as the first lesion. This supports that these are less likely a neoplastic entity, or if it is, that it remains histologically benign despite growth. Treatment currently is limited to surgical resection and should be considered based on the patient’s clinical presentation, location of the lesion and surgical risk.
REFERENCES 1. Jun C, Burdick B. An unusual fibro-osseus calcifying pesudotumor of the axis. Case report. J Neurosurg 1984; 60: 1308–1311. 2. Smith DM, III, Berry A. Unusual fibro-osseus lesion of the spinal cord with positive staining for glial fibrillary acidic protein and radiological progression: a case report. Hum Pathol 1994; 25: 835–838.
3. Kerr E, Borys E, Bobinski M, Shahlaie K. Posterior fossa calcifying pseudoneoplasm of the central nervous system. J Neurosurg 2013; 118: 896–902. 4. Rhodes RH, Davis RL. An unusual fibro-osseus component in intracranial lesions. Hum Pathol 1978; 9: 309– 319. 5. Bertoni F, Unni KK, Dahlin DC. Calcifying pseudoneoplasms of the neural axis. J Neurosurg 1990; 72: 42–48. 6. Fletcher AM, Greenlee JJD, Chang KE, Smoker WR, Kirby PA, O’Brien EK. Endoscopic resection of calcifying pseudoneoplasm of the neuraxis (CAPNON) of the anterior skull base with sinonasal extension. J Clin Neurosci 2012; 19: 1048–1049. 7. Tatke M, Singh AK, Gupta V. Calcifying pseudoneoplasm of the CNS. Br J Neurosurg 2001; 15: 521–528. 8. Park P, Schmidt LA, Shah GV, Tran NK, Gandhi D, LaMarca F. Calcifying pseudoneoplasm of the spine. Clin Neurol Neurosurg 2008; 110: 392–395. 9. Qian J, Rubio A, Powers JM et al. Fibro-Osseus Lesions of the Central Nervous System: report of four cases and literature review. Am J Surg Pathol 1999; 23: 1270–1275. 10. Jentoft ME, Scheithauer BW, Bertoni F, Abood C, Chang HT. Calcifying pseudoneoplasm of the neuraxis with single nerve rootlet involvement. Can J Neurol Sci 2012; 39: 840–842. 11. Rodriguez FJ, Scheithauer BW, Fourney DR, Robinson CA. Ependymoma and intraparenchymal calcifying pseudoneoplasm of the neural axis: incidental collison or unique reactive phenomenon. Acta Neuropathol 2007; 115: 363–366. 12. Shrier DA, Melville D, Qian J et al. Fibro-osseus lesions involving the brain: MRI. Diagn Neuroradiol 1999; 41: 18–21. 13. Aiken AH, Akgun H, Tihan T, Barbaro N, Glastonbury C. Calcifying pseudoneoplasms of the neuraxis: CT, MR imaging and histologic features. Am J Neuroradiol 2009; 30: 1256–1260. 14. Hodges TR, Karikari IO, Nimjee SM et al. Calcifying pseudoneoplasm of the cerebellopontine angle: case report. Neurosurgery 2011; 69 (1 Suppl Opoerative): 117–120. 15. Bartanusz V, Ziu M, Jimenez DF, Henry JM. Calcifying pseudoneoplasm of the atlantoaxial joint in a child. J Neurosurg Spine 2013; 18: 367–371.
© 2015 Japanese Society of Neuropathology
