Department of Neurological Sciences-Neurosurgery, University of Rome "La Sapienza" (PC, MD, MS), Rome, and Department of Neurosurgery, University of Siena (LP), Siena, Italy Neurosurgery 31; 1113-1116, 1992 ABSTRACT: THIS REPORT PRESENTS a very rare case of metastatic meningioma of the parotid gland from a recurring intracranial lesion. The primary tumor, intracranial residues, and parotid metastasis were histologically benign. Meningiomas rarely metastasize; even rarer are cases in which both the primary and the secondary tumors have benign histological characteristics. The 11 cases reported in the literature have been critically reviewed. The case we present is noteworthy also for the exceptional localization of the metastasis in the parotid gland. KEY WORDS: Intracranial tumors; Meningiomas; Metastases; Parotid gland tumors It has been calculated that approximately 0.1% of meningiomas metastasize (27). The regions most frequently affected are the lungs and pleura, the musculoskeletal system, and the liver (7,27,29), but single metastases have also been found in anomalous regions such as the thymus (24). In 70% of cases, the metastases are observed in patients who undergo one or more craniotomies (24). The venous system, and particularly the sagittal sinus, is considered the route of diffusion of neoplastic cells (24); however, occasional cells swept away in the blood stream from biologically benign meningiomas, as a rule, do not have the ability to form distant metastases (12). Even if all the histological subtypes have been involved in spreading metastases, in the majority of cases, both the primary and the secondary tumors belong to borderline histological patterns, such as the angioblastic or the hemangiopericytic types, or are frankly malignant (7,12,19,20,23-27). Residues, recurrences, and eventual metastasis from a benign lesion can show malignant histological features (1,15, 20,28) . We present a unique case of a histologically benign meningioma metastasizing to the parotid gland and a review of the literature about this peculiar occurrence. CASE REPORT An 11-year-old boy first came to our notice in January 1973 with a 3-month history of cephalalgia and vomiting. At the age of 6 months, he had undergone radiotherapy of the scalp (35 Gy) and of
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AUTHOR(S): Celli, Paolo, M.D.; Palma, Lucio, M.D.; Domenicucci, Maurizio, M.D.; Scarpinati, Marco, M.D.
the thorax (15 Gy) for two cutaneous localizations of angioma planus. At admission, the only sign was bilateral papilledema. No evidence of neurofibromatosis was seen. After a cerebral angiogram, he underwent his first operation (January 1973) for the total removal of a right, precoronal, parasagittal tumor, the size of an orange, emerging from the cortical surface. There was no infiltration of the falx or the longitudinal sinus. A histological examination showed an endotheliomatous meningioma with no atypical features (Fig. 1A). 1 year and 10 months later, after an angiogram documented tumor recurrence, a second operation (November 1974) was performed. This entailed the total removal of the lesion together with the infiltrated falx, approximately 8 cm of the anterior longitudinal sinus, as well as the infiltrated part of the bone. The histological examination showed an endotheliomatous meningioma without aspects of malignancy. In 1980, after a control computed tomographic (CT) scan, the patient was admitted a third time for a third operation (January 1981), which included the total removal of a meningiomatous lesion growing from the left orbital roof involving the dural base of the implant. The histological examination showed an endotheliomatous meningioma (Fig. 1B). In 1984, a control CT scan was positive for a neoformation the size of an egg at the level of the medium aspect of the left sphenoid wing (Fig. 2A). The patient underwent his fourth operation (December 1984) involving the total removal of the lesion and the infiltrated dura. The histological examination showed an endotheliomatous meningioma with no atypical features (Fig. 1C). In 1985, the patient became aware of a painful growth the size of a nut in the region of the right parotid. An echotomographic scan revealed a solid intraparenchymatous neoformation, measuring 2 × 1.2 cm. A CT scan without contrast medium (Fig. 2B) showed an overall increase in the volume of the parotid gland. The patient underwent surgery for a suspected parotid tumor. On the surface of the gland, a hard and fibrous tumor was exposed. This lesion appeared easily cleavable from the glandular tissue and was in no way connected with the facial nerve. A histological examination showed a benign endotheliomatous meningioma with features comparable with the previous intracranial meningiomas (Fig. 3A and B). No facial nerve deficit was seen at discharge. Two years later, the patient underwent the fifth operation (December 1987) to remove a left orbital tumor through exeresis of the eyeball. The histological examination showed an endotheliomatous meningioma with no histological signs of malignancy (Fig. 1D). In 1988, two operations were performed to remove a right paramedian basal frontal region (March, sixth operation) and a left paramedian frontal lesion (September, seventh operation). The histological examination of the specimen obtained from these operations confirmed the presence of a totally benign endotheliomatous meningioma. To date (January 1992), successive, regular CT scans performed at 6-
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Neurosurgery 1992-98 December 1992, Volume 31, Number 6 1113 Histologically Benign Recurrent Meningioma Metastasizing to the Parotid Gland: Case Report and Review of the Literature Case Report
ACKNOWLEDGMENT The authors wish to thank Lucio Paniccia'-Bonifazi for preparing the histological slides and the photomicrographs pertinent to this case. Received, October 22, 1991. Accepted, June 5, 1992. Reprint requests: Dr. Marco Scarpinati, Dipartimento di Neuroscienze Sezione di Neurochirurgia, Via dell'Università 30a, 00185 Roma, Italy. REFERENCES: (1-33) 1. 2. 3. 4. 5. 6. 7.
8.
9.
10. 11. 12.
Arnould G, Lepoire J, Pierson, Barrucand D: Les meningiomes malins (A propos d'une observation) Rev Neurol 105:469-479, 1961. Aumann JLTM, van den Bosch JMM, Elbers JRJ, Wagenaar SJSC: Metastatic meningioma of the lung. Thorax 41:487-488, 1986. Balsys R, Norton GA: Intracranial meningioma presenting as a mass in the neck. Neuroradiology 19:89-91, 1980. Binns PM: Jugular foramen syndrome caused by meningioma. Trans Pa Acad Ophthalmol Otolaryngol 76:1368-1370, 1972. Binns PM, Fairman HD: Lesions in the temporal bone causing multiple nerve damage. J Laryngol Otol 80:125-137, 1966. Farr HW, Gray GF Jr, Vrana M, Panio M: Extracranial meningioma. J Surg Oncol 5:411420, 1973. Glasauer FE, Yuan RHP: Intracranial tumors with extracranial metastases. Case report and review of the literature. J Neurosurg 20:474492, 1963. Haratake J, Ishii N, Horie A, Yoshida A, Lin M: Meningioma of the parapharyngeal space: A unique extension of intracranial tumor. Laryngoscope 94:1372-1375, 1984. Hoshino T, Nagashima T, Murovic JA, Wilson CB, Davis RL: Proliferative potential of human meningiomas of the brain: A cell kinetic study with bromodeoxyuridine. Cancer 58:1466- 1472, 1986. Hoye SJ, Hoar CS, Murray JE: Extracranial meningioma presenting as a tumor of the neck. Am J Surg 100:486-489, 1960. Karasick JL, Mullan SF: A survey of metastatic meningiomas. J Neurosurg 39:206212, 1974. Kepes JJ (ed): Meningiomas: Biology,
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DISCUSSION The discovery of extraneuroaxial meningiomas poses the question of their origin. Hoye et al.(10) proposed subdividing the meningiomas occurring in atypical sites into four main groups: 1) primary intracranial meningiomas with extracranial direct extension; 2) meningiomas originating from arachnoid cell rests of cranial nerve sheaths with extracranial growth; 3) ectopic meningiomas without connection to nervous structures or cranial nerves; and 4) metastases from intracranial meningiomas. The direct extension from an intracranial meningioma through the cranial base foramina causes the extracranial portion to be found in regions contiguous to the skull, such as the neck or parotid region (3-5,8). Normally, this induces deficits of the cranial nerves. However, rare cases without cranial deficit are reported (18). In our case, the possibility that the parotid tumor could have originated from the direct extension of an intracranial meningioma is hardly acceptable, given the lengthy follow-up and the numerous control CT scans regularly performed. Wolff et al. (33) and Farr et al. (6) reported, respectively, one and three cases of ectopic meningiomas of the parotid gland region in the absence of intracranial lesions. Considering the clinical history of our patient, the parotid meningioma should be, in all probability, an extraneuroaxial metastasis of a primary intracranial tumor. In 1982, Kepes (12) in his critical review of reports of benign metastasizing meningiomas considered only four cases. Apart from our own, we have found only 11 reported cases of cerebral metastasizing meningiomas with well-documented histological benignity of both primary and secondary lesions (2,13, 16,17,21,24,31,32) . In this restricted group (Table 1), there is a preponderance of male patients (mean age, 42.5). The lesions in all cases were parasagittal and, in 6 of 12 (50%), aggressive and locally invasive. All but one of the patients had undergone neurosurgical procedures. Apart from the histological benignity, the characteristics of these benign metastasizing meningiomas, such as male prevalence, parasagittal localization, tendency to local residues, and pulmonary localization of the metastasis, are analogous to those observed in malignant metastasizing meningiomas (7,11,12,30). The average survival time of those patients, who have since died, was 6 years after the first craniotomy. In our case, the patient is still alive and well 19 years after the first neurosurgical operation. Of the five cases for which the cause of death is known, three were not directly due to the tumor of the metastasis (13,17,32), and in the other two, the cause was attributed to pulmonary diffusion of the secondary localizations (21,31). In the two cases with atypical localizations, the thymus in Russell's case (24) and the parotid in our own, the metastasis seems well defined and cleavable from the glandular parenchyma. This could suggest an
important role for the site of the metastasis in the patients' prognosis, even in the case of well-defined histological benignity. The recurrences and the metastases of our case could be due to a high proliferative activity of the neoplastic cells. The proliferative potential of benign intracranial meningiomas, determined with the monoclonal antibodies against bromodeoxyuridine (9,14) or Ki-67 (22), can be different. This could help to explain the aggressive biological behavior of the tumor, despite a well-defined histological benignity.
Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.
month intervals have shown no further intracranial residues or recurrences.
15.
16. 17. 18. 19. 20. 21. 22.
23.
24. 25. 26. 27. 28. 29.
30.
31.
33.
Wende S, Bohl J, Schubert R, Schulz V: Lung metastasis of a meningioma. Neuroradiol 24:287-291, 1983. Wolff M, Rankow RM: Meningioma of the parotid gland: An insight into the pathogenesis of extracranial meningiomas. Hum Pathol 2:453- 459, 1971.
COMMENTS This interesting and unusual case highlights some of the puzzling issues of the biological behavior of benign meningiomas. Radiation in the infancy of this young patient, 10 years before the diagnosis of a meningioma, is undoubtedly related to the induction of the tumor. The multiple recurrences associated with shorter recurrence-free intervals is typical. The case of this patient emphasizes the inadequacy of predicting the behavior of meningiomas from their pathological features. As the authors point out, a study that addresses the proliferative tendencies of these tumors, such as bromodeoxyridine, Ki-68, or proliferating cell nuclear antigen, should be applied in the current evaluation of resected meningiomas. With the repeated craniotomies, metastasis to facial structures is not surprising. The role of implantation or lymphatic spread might come into play. Of note, however, is the total encapsulation of this metastasis in the parotid gland. Ossama Al-Mefty Maywood, Illinois This report describes the rare occurrence of a metastasis from a histologically benign-appearing intracranial meningioma. A helpful review of reported cases of "benign" metastasizing meningiomas is also provided. It is increasingly understood that the biological behavior of any neoplasm is not only dependent on its histological nature, but also on a set of biological markers (i.e., proliferation index) that are likely to provide practical information concerning the expected behavior of a given neoplasm. This type of information has been reliably applied to predict the time to recurrence of meningiomas (1). No information is yet available concerning the potential for metastasis. Fortunately, this remains an exceedingly rare event. Raymond Sawaya Houston, Texas REFERENCES: (1) 1.
Shibuya M, Hoshino T, Ito S, Wacker M, Prados M, Davis R, Wilson C: Meningiomas: Clinical implications of a high proliferative potential determined by bromodeoxyuridine labeling. Neurosurgery 30:494-498, 1992.
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14.
32.
Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.
13.
Pathology and Differential Diagnosis. New York, Masson, 1982, pp 190-199. Kruse MF Jr: Meningeal tumors with extracranial metastasis. Neurology 10:197201, 1960. Lee KS, Hoshino T, Rodriguez LA, Bederson J, Davis RL, Wilson CB: Bromodeoxyuridine labeling study of intracranial meningiomas: Proliferative potential and recurrence. Acta Neuropathol 80:311-317, 1990. LeMay DR, Bucci MN, Farhat SM: Malignant transformation of recurrent meningioma with pulmonary metastases. Surg Neurol 31:365368, 1989. Miller DC, Ojemann R, Proppe KH, Mc Ginnis BD, Grillo HC: Benign metastasizing meningioma. J Neurosurg 62:763-766, 1985. Ng THK, Wong MP, Chan KW: Benign metastasizing meningioma. Clin Neurol Neurosurg 92:152-154, 1990. Nichols RD, Knighton RS, Chason JL, Strong DD: Meningioma in the parotid region. Laryngoscope 97:693-696, 1987. Palacios E, Azar-Kia B: Malignant metastasizing angioblastic meningiomas. J Neurosurg 42:185- 188, 1975. Repola D, Weatherbee L: Meningioma with sarcomatous changes and hepatic metastasis. Arch Pathol Lab Med 100:667-669, 1976. Ringsted J: Meningeal tumours with extracranial metastases. Acta Pathol Microbiol Scand 43:9- 20, 1958. Roggendorf W, Schuster T, Pfeiffer J: Proliferative potential of meningiomas determined with the monoclonal antibody Ki67. Acta Neuropathol 73:361-364. Rubinstein LJ: Tumors of the central nervous system, in Atlas of Tumor Pathology. Armed Force Institute of Pathology Washington, DC, 1972, second series, fascicle 6, pp 169-190. Russell DS, Rubinstein LJ: Pathology of Tumours of the Nervous System. Baltimore, Williams & Wilkins, 1989, pp 504-529. Russel T, Moss T: Metastasizing meningioma. Neurosurgery 19:1028-1030, 1986. Salvati CA: Metastatic meningioma. Clin Neurol Neurosurg 83:170-172, 1981. Shuangshoti S, Hongsaprabhas C, Netsky MG: Metastasizing meningioma. Cancer 26:832-841, 1970. Simpson D: The recurrence of intracranial meningiomas after surgical treatment. J Neurol Neurosurg Psychiatry 20:27-39, 1957. Stoller JK, Kavuru M, Mehta AC, Weinstein CE, Estes ML, Gephardt GM: Intracranial meningioma metastatic to the lung. Cleve Clin J Med 54:521-527, 1987. Strang RR, Tovi D, Nordenstam H: Meningioma with intracerebral, cerebellar and visceral metastases. J Neurosurg 21:10981102, 1964. Tognetti F, Donati R, Bollini C: Metastatic spread of benign intracranial meningioma. J Neurosurg Sci 31:23-27, 1987.
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Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.
Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.
Figure 2. Radiological pictures. A, axial CT scan, after intravenous contrast medium, showing a left sphenoidal wing meningioma. B, axial CT scan of the parotid region, without contrast medium, showing a specific and overall increase in volume of the gland.
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Figure 1. Pathological pictures of intracranial tumors indicating endotheliomatous meningioma (hematoxylin and eosin stain, various magnifications). A, first operation: right frontal parasagittal tumor. B, third operation: left anterior cranial fossa tumor. C, fourth operation: third medium of the left sphenoid wing tumor. D, fifth operation: left orbital tumor.
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Figure 3. Pathology pictures of the parotid gland meningioma (hematoxylin and eosin stain). A, metastases of endotheliomatous meningioma to the parotid gland. Tumor is seen on the left of the field; on right, normal parotid tissue can be seen clearly (×120). B, detail of the preceding field (×250).
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Table 1. Intracranial Metastasizing Meningiomas
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AUTHOR(S): Celli, Paolo, M.D.; Palma, Lucio, M.D.; Domenicucci, Maurizio, M.D.; Scarpinati, Marco, M.D.
the thorax (15 Gy) for two cutaneous localizations of angioma planus. At admission, the only sign was bilateral papilledema. No evidence of neurofibromatosis was seen. After a cerebral angiogram, he underwent his first operation (January 1973) for the total removal of a right, precoronal, parasagittal tumor, the size of an orange, emerging from the cortical surface. There was no infiltration of the falx or the longitudinal sinus. A histological examination showed an endotheliomatous meningioma with no atypical features (Fig. 1A). 1 year and 10 months later, after an angiogram documented tumor recurrence, a second operation (November 1974) was performed. This entailed the total removal of the lesion together with the infiltrated falx, approximately 8 cm of the anterior longitudinal sinus, as well as the infiltrated part of the bone. The histological examination showed an endotheliomatous meningioma without aspects of malignancy. In 1980, after a control computed tomographic (CT) scan, the patient was admitted a third time for a third operation (January 1981), which included the total removal of a meningiomatous lesion growing from the left orbital roof involving the dural base of the implant. The histological examination showed an endotheliomatous meningioma (Fig. 1B). In 1984, a control CT scan was positive for a neoformation the size of an egg at the level of the medium aspect of the left sphenoid wing (Fig. 2A). The patient underwent his fourth operation (December 1984) involving the total removal of the lesion and the infiltrated dura. The histological examination showed an endotheliomatous meningioma with no atypical features (Fig. 1C). In 1985, the patient became aware of a painful growth the size of a nut in the region of the right parotid. An echotomographic scan revealed a solid intraparenchymatous neoformation, measuring 2 × 1.2 cm. A CT scan without contrast medium (Fig. 2B) showed an overall increase in the volume of the parotid gland. The patient underwent surgery for a suspected parotid tumor. On the surface of the gland, a hard and fibrous tumor was exposed. This lesion appeared easily cleavable from the glandular tissue and was in no way connected with the facial nerve. A histological examination showed a benign endotheliomatous meningioma with features comparable with the previous intracranial meningiomas (Fig. 3A and B). No facial nerve deficit was seen at discharge. Two years later, the patient underwent the fifth operation (December 1987) to remove a left orbital tumor through exeresis of the eyeball. The histological examination showed an endotheliomatous meningioma with no histological signs of malignancy (Fig. 1D). In 1988, two operations were performed to remove a right paramedian basal frontal region (March, sixth operation) and a left paramedian frontal lesion (September, seventh operation). The histological examination of the specimen obtained from these operations confirmed the presence of a totally benign endotheliomatous meningioma. To date (January 1992), successive, regular CT scans performed at 6-
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Neurosurgery 1992-98 December 1992, Volume 31, Number 6 1113 Histologically Benign Recurrent Meningioma Metastasizing to the Parotid Gland: Case Report and Review of the Literature Case Report
ACKNOWLEDGMENT The authors wish to thank Lucio Paniccia'-Bonifazi for preparing the histological slides and the photomicrographs pertinent to this case. Received, October 22, 1991. Accepted, June 5, 1992. Reprint requests: Dr. Marco Scarpinati, Dipartimento di Neuroscienze Sezione di Neurochirurgia, Via dell'Università 30a, 00185 Roma, Italy. REFERENCES: (1-33) 1. 2. 3. 4. 5. 6. 7.
8.
9.
10. 11. 12.
Arnould G, Lepoire J, Pierson, Barrucand D: Les meningiomes malins (A propos d'une observation) Rev Neurol 105:469-479, 1961. Aumann JLTM, van den Bosch JMM, Elbers JRJ, Wagenaar SJSC: Metastatic meningioma of the lung. Thorax 41:487-488, 1986. Balsys R, Norton GA: Intracranial meningioma presenting as a mass in the neck. Neuroradiology 19:89-91, 1980. Binns PM: Jugular foramen syndrome caused by meningioma. Trans Pa Acad Ophthalmol Otolaryngol 76:1368-1370, 1972. Binns PM, Fairman HD: Lesions in the temporal bone causing multiple nerve damage. J Laryngol Otol 80:125-137, 1966. Farr HW, Gray GF Jr, Vrana M, Panio M: Extracranial meningioma. J Surg Oncol 5:411420, 1973. Glasauer FE, Yuan RHP: Intracranial tumors with extracranial metastases. Case report and review of the literature. J Neurosurg 20:474492, 1963. Haratake J, Ishii N, Horie A, Yoshida A, Lin M: Meningioma of the parapharyngeal space: A unique extension of intracranial tumor. Laryngoscope 94:1372-1375, 1984. Hoshino T, Nagashima T, Murovic JA, Wilson CB, Davis RL: Proliferative potential of human meningiomas of the brain: A cell kinetic study with bromodeoxyuridine. Cancer 58:1466- 1472, 1986. Hoye SJ, Hoar CS, Murray JE: Extracranial meningioma presenting as a tumor of the neck. Am J Surg 100:486-489, 1960. Karasick JL, Mullan SF: A survey of metastatic meningiomas. J Neurosurg 39:206212, 1974. Kepes JJ (ed): Meningiomas: Biology,
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DISCUSSION The discovery of extraneuroaxial meningiomas poses the question of their origin. Hoye et al.(10) proposed subdividing the meningiomas occurring in atypical sites into four main groups: 1) primary intracranial meningiomas with extracranial direct extension; 2) meningiomas originating from arachnoid cell rests of cranial nerve sheaths with extracranial growth; 3) ectopic meningiomas without connection to nervous structures or cranial nerves; and 4) metastases from intracranial meningiomas. The direct extension from an intracranial meningioma through the cranial base foramina causes the extracranial portion to be found in regions contiguous to the skull, such as the neck or parotid region (3-5,8). Normally, this induces deficits of the cranial nerves. However, rare cases without cranial deficit are reported (18). In our case, the possibility that the parotid tumor could have originated from the direct extension of an intracranial meningioma is hardly acceptable, given the lengthy follow-up and the numerous control CT scans regularly performed. Wolff et al. (33) and Farr et al. (6) reported, respectively, one and three cases of ectopic meningiomas of the parotid gland region in the absence of intracranial lesions. Considering the clinical history of our patient, the parotid meningioma should be, in all probability, an extraneuroaxial metastasis of a primary intracranial tumor. In 1982, Kepes (12) in his critical review of reports of benign metastasizing meningiomas considered only four cases. Apart from our own, we have found only 11 reported cases of cerebral metastasizing meningiomas with well-documented histological benignity of both primary and secondary lesions (2,13, 16,17,21,24,31,32) . In this restricted group (Table 1), there is a preponderance of male patients (mean age, 42.5). The lesions in all cases were parasagittal and, in 6 of 12 (50%), aggressive and locally invasive. All but one of the patients had undergone neurosurgical procedures. Apart from the histological benignity, the characteristics of these benign metastasizing meningiomas, such as male prevalence, parasagittal localization, tendency to local residues, and pulmonary localization of the metastasis, are analogous to those observed in malignant metastasizing meningiomas (7,11,12,30). The average survival time of those patients, who have since died, was 6 years after the first craniotomy. In our case, the patient is still alive and well 19 years after the first neurosurgical operation. Of the five cases for which the cause of death is known, three were not directly due to the tumor of the metastasis (13,17,32), and in the other two, the cause was attributed to pulmonary diffusion of the secondary localizations (21,31). In the two cases with atypical localizations, the thymus in Russell's case (24) and the parotid in our own, the metastasis seems well defined and cleavable from the glandular parenchyma. This could suggest an
important role for the site of the metastasis in the patients' prognosis, even in the case of well-defined histological benignity. The recurrences and the metastases of our case could be due to a high proliferative activity of the neoplastic cells. The proliferative potential of benign intracranial meningiomas, determined with the monoclonal antibodies against bromodeoxyuridine (9,14) or Ki-67 (22), can be different. This could help to explain the aggressive biological behavior of the tumor, despite a well-defined histological benignity.
Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.
month intervals have shown no further intracranial residues or recurrences.
15.
16. 17. 18. 19. 20. 21. 22.
23.
24. 25. 26. 27. 28. 29.
30.
31.
33.
Wende S, Bohl J, Schubert R, Schulz V: Lung metastasis of a meningioma. Neuroradiol 24:287-291, 1983. Wolff M, Rankow RM: Meningioma of the parotid gland: An insight into the pathogenesis of extracranial meningiomas. Hum Pathol 2:453- 459, 1971.
COMMENTS This interesting and unusual case highlights some of the puzzling issues of the biological behavior of benign meningiomas. Radiation in the infancy of this young patient, 10 years before the diagnosis of a meningioma, is undoubtedly related to the induction of the tumor. The multiple recurrences associated with shorter recurrence-free intervals is typical. The case of this patient emphasizes the inadequacy of predicting the behavior of meningiomas from their pathological features. As the authors point out, a study that addresses the proliferative tendencies of these tumors, such as bromodeoxyridine, Ki-68, or proliferating cell nuclear antigen, should be applied in the current evaluation of resected meningiomas. With the repeated craniotomies, metastasis to facial structures is not surprising. The role of implantation or lymphatic spread might come into play. Of note, however, is the total encapsulation of this metastasis in the parotid gland. Ossama Al-Mefty Maywood, Illinois This report describes the rare occurrence of a metastasis from a histologically benign-appearing intracranial meningioma. A helpful review of reported cases of "benign" metastasizing meningiomas is also provided. It is increasingly understood that the biological behavior of any neoplasm is not only dependent on its histological nature, but also on a set of biological markers (i.e., proliferation index) that are likely to provide practical information concerning the expected behavior of a given neoplasm. This type of information has been reliably applied to predict the time to recurrence of meningiomas (1). No information is yet available concerning the potential for metastasis. Fortunately, this remains an exceedingly rare event. Raymond Sawaya Houston, Texas REFERENCES: (1) 1.
Shibuya M, Hoshino T, Ito S, Wacker M, Prados M, Davis R, Wilson C: Meningiomas: Clinical implications of a high proliferative potential determined by bromodeoxyuridine labeling. Neurosurgery 30:494-498, 1992.
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14.
32.
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13.
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Figure 2. Radiological pictures. A, axial CT scan, after intravenous contrast medium, showing a left sphenoidal wing meningioma. B, axial CT scan of the parotid region, without contrast medium, showing a specific and overall increase in volume of the gland.
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Figure 1. Pathological pictures of intracranial tumors indicating endotheliomatous meningioma (hematoxylin and eosin stain, various magnifications). A, first operation: right frontal parasagittal tumor. B, third operation: left anterior cranial fossa tumor. C, fourth operation: third medium of the left sphenoid wing tumor. D, fifth operation: left orbital tumor.
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Figure 3. Pathology pictures of the parotid gland meningioma (hematoxylin and eosin stain). A, metastases of endotheliomatous meningioma to the parotid gland. Tumor is seen on the left of the field; on right, normal parotid tissue can be seen clearly (×120). B, detail of the preceding field (×250).
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Table 1. Intracranial Metastasizing Meningiomas
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