J Neurosurg 77:788-791, 1992
Leptomeningeal dissemination of cerebellar pilocytic astrocytoma Case report KAZUHIKO MISHIMA, M.D., MASANAO NAKAMURA, M.D., HIROHIKO NAKAMURA, M.D., OSAMU NAKAMURA~ M.D., NOBUAKI FUNATA, M.D., AND NOBUYUKI SHITARA~ M.D. Department of Neurosurgeo, and Pathology, Tokyo Metropolitan Komagome General Hospital, Tokyo, Japan u- A case of surgically treated pilocytic astrocytoma in the cerebellar vermis is reported in a patient who subsequently demonstrated multiple subarachnoid nodular masses in the cerebrum and spinal cord 6 years after the initial surgery. The nodular tumors did not indicate a growth tendency on computerized tomography or magnetic resonance imaging over a 2-year observation period. The histology of the nodular masses in the cerebrum and spinal cord was similar to that of the original tumor. The bromodeoxyuridine labeling index indicated low proliferative activity (0.5%). The peculiar pattern of dissemination of the pilocytic astrocytoma is described. KEY WORDS 9 pilocytie astrocytoma bromodeoxyuridine labeling index
EREBELLAR pilocytic astrocytomas occurring in children have one of the most favorable prognoses of all intracranial tumors. Juvenile pilocytic astrocytomas are usually extremely benign, and it is well established that, even with incomplete resection, patients have survived for years without progression of the tumor. However, several cases of late malignant recurrence of pilocytic astrocytoma have been reported, l"~'SA2"lT"2twith some authors suggesting that the malignant transformation after a prolonged interval was induced by radiation therapy. 4~~2~2~ It has also been considered that the benign astrocytoma underwent malignant transformation because the recurrent tumor contained areas that showed histological features identical to those of the original tumor. 2~ Other case reports with early recurrence suggest that areas of focal anaplasia within a benign cerebellar astrocytoma were missed when the initial tumor specimen was examined34-'~ The case reported here is unusual in that, 6 years after surgery, a histologically benign astrocytoma disseminated to the supratentorial and spinal regions without pathologically malignant transformation or apparent regrowth of the primary tumor. The growth rate of the disseminated tumor was very low and the biological behavior was quite different from that of malignant glial tumors.
C
788
9 dissemination
Case Report
This 6-year-old boy was initially evaluated at another neurosurgical center for symptoms of increased intracranial pressure. Computerized tomography (CT) performed at that time demonstrated a multicystic tumor in the cerebellar vermis and obstructive hydrocephalus with no dissemination (Fig. 1). A ventriculoperitoneal shunt was placed, and 30 Gy of radiation therapy was administered. Subsequently, the tumor was totally resected. Histologically, a juvenile pilocytic astrocytoma was diagnosed (Fig. 2). Postoperatively, a total dose of 40 Gy was administered to the posterior fossa. During the 6 years after the operation, the patient did well and showed no signs of recurrence. Examination and Operation. Six years after the initial operation, at the age of 11 years, the patient was referred to our hospital with the diagnosis of leptomeningeal dissemination. Neurologically, the child remained asymptomatic. A cranial CT scan revealed a small enhanced mass lesion in the fourth ventricle; however, there was no evidence of recurrence of the primary vermian tumor. Gadolinium-diethylenetriamine penta-acetic acid (Gd-DTPA)-enhanced cranial magnetic resonance (MR) imaging demonstrated multiple leptomeningeal nodular, round masses with no J. Neurosurg. / Volume 77/Novernber, 1992
Disseminated pilocytic astrocytoma
FIG. 1. Initial contrast-enhanced computerized tomography scan showing a multicystic mass in the cerebellar vermis.
evidence of cerebellar tumor recurrence (Fig. 3B). On Gd-DTPA-enhanced spinal MR imaging, subarachnoid metastases were demonstrated at T-3 and T-4 (Fig. 3C). However, the nonenhanced T~- and T~-weighted images (Fig. 3A) did not clearly visualize the metastatic deposits. Cytological examination of the eerebrospinal fluid (CSF) was negative. To clarify the histology of the tumor, a right frontotemporal craniotomy was performed. A soft, reddish-gray tumor was located mainly in the subarachnoid space of the sylvian fissure and was partially adherent to the brain parenchyma. The tumor was totally resected. Pathological Examination. Histologically, the disseminated tumor was essentially the same as the original neoplasm. No nuclear atypism, mitotic figure, necrosis, or vascular endothelial proliferation was observed. Rosenthal fibers were abundantly present. Immunohistological stains revealed the presence of glial fibrillary acidic protein in the tumor cells. A diagnosis of pilocytic astrocytoma was made for this tumor (Fig. 4). Postoperative Course. Radiation therapy with a total dose of 40 Gy was delivered to the cervical and upper-thoracic spinal regions. Three months after completion of radiation therapy, the tumors at T-3 and T4 showed no change in size on MR imaging and the spinal cord was still compressed. Therefore, a decompressive laminectomy from T-2 to T-4 was performed. These tumor masses were primarily extramedullary in location. Histologically, they were similar to the previously resected tumor from the sylvian fissure. To estimate the proliferation potential of the original, we also analyzed the bromodeoxyuridine (BUdR) labeling index (LI) of these tumors. Two hours before spinal tumor resection, the patient received a 150-mg intravenous infusion of BUdR over a period of 30 minutes; the BUdR LI of these tumors was 0.5%. Two years after the diagnosis of dissemination, the radiological findings J. Neurosurg. / Volume 77/November. 1992
FIG. 2. Photomicrograph of the original tumor of the cerebellar vermis. The typical histology of juvenile pilocytic astrocytoma showing interwoven elongated piloid cells with microcystic degeneration is seen. H & E, • 32.
of the residual nodular masses had not changed and the patient remained well. Discussion
This case is unique in that the cerebellar tumor showed no local recurrence and the disseminated tumor demonstrated no anaplastic features. Moreover, the size and number of the disseminated tumor nodules did not change over a 2-year follow-up period. A long interval between the first radiological signs and the beginning of clinical symptoms is one of the characteristic features in this type of CSF dissemination. Generally, seeding of an anaplastic astrocytoma or glioblastoma herald the end stage of disease. ~'~ Therefore, the growth character, biological behavior, and clinical course of the disseminated pilocytic astrocytoma were clearly different from that of the malignant gliomas. It has been reported that the BUdR LI reflects the growth activity of gliomas and is closely correlated to patient prognosis and survival duration. I-Ioshino, et al., ~ reported that low-grade gliomas with a BUdR LI of 1% or more showed a tendency to recur rapidly, whereas patients in whom the glioma BUdR LI is less than 1% survived longer. The BUdR LI and clinical course in this case were consistent with these findings. The possibility exists that the multiplicity of pilocytic astrocytomas might be due to the multiple genesis of the tumors. However, the tumor in this case was located mainly in the CSF space and was loosely attached to the brain parenchyma. Therefore, CSF dissemination of the original tumor is most likely in this case. One mechanism for dissemination is that the viable tumor cells gain access to the subarachnoid or ventricular fluid spaces. In patients with cerebellar pilocytic astrocytomas, extension into the subarachnoid space is common but is not necessarily associated with aggressive behavior or leptomeningeal seedingY '~'--~~ MeLaughlin ~3 reported five cases of extracerebellar pilo789
K. Mishima, et al.
FI6. 3. Follow-up magnetic resonance images obtained 6 years after the initial operation. Multiple nodular masses in the subarachnoid spaces thal cannot be detected on the axial T j-weighted image of the head (A) are seen on the Gd-DTPA-enhanced Tt-weighted image (B, arrowheads). A sagiltal Gd-DTPA-cnhanced T~weighted image (C) of the spine demonstrates several enhancing nodular lesions/arrm~'~') adjacent 1o the spinal cord.
tumor appears to be aggressive surgery, where possible. Recently, the efficacy of MR imaging has been evaluated in patients with meningeal tumor spread. 7'~5 Although noncontrast-enhanced MR imaging is rather insensitive, Gd-DTPA-enhanced MR imaging is useful when searching for leptomeningeal tumor deposits to prevent patient deterioration. In conclusion, although seeding from a cerebellar pilocytic astrocytoma rarely occurs, it is difficult to predict the occurrence of dissemination even by histological examination. Therefore, careful follow-up review with contrast-enhanced MR imaging is important even in cases of histologically benign pilocytic astrocytoma. FiG. 4. Photomicrograph of the disseminated tumors (brain and spinal) showing pilocytic astrocytoma without malignant features. Rosenthal fibers are also seen. H & E, • 32.
cytic astrocytoma demonstrating subarachnoid spread and invasion of surrounding structures. They concluded that a tumor showing nuclear pleomorphism or oligodendrocytomatous areas had a poor prognosis. Shapiro and Shulman ~s reported three of 72 patients with histologically benign cerebellar astrocytomas in whom the tumor seeded the spinal subarachneid space without malignant transformation. They mentioned that the seeding did not indicate the patient's imminent demise and believed that this was part of the natural history of this tumor. The treatment of the disseminated tumor remains controversial. In our patient, radiotherapy to the disseminated lesions was ineffective. Kepes, et al.? ~ and Auer, el al., 2 demonstrated the ineffectiveness of radiotherapy in controlling dissemination. With this background, the most reliable treatment of the disseminated 790
Reference
l. Alpers CE, Davis RL, Wilson CB: Persistence and late malignant transformation of the childhood cerebellar astrocytoma. Case report. J Neurosurg 57:548-551, 1982 2. Auer RN, Rice GPA, Hinton GG, et air Cerebellar astrocytoma with benign histology and malignant clinical course. Case report. J Neurosurg 54:128-132, 1981 3. Awad I, Bay JW, Rogers L: Leptomeningeal metastasis from supratentorial malignant gliomas. Neurosurgery 19: 247-251, 1986 4. Bernell WR, Kepes J J, Seitz EP: Late malignant recurrence of childhood cerebellar astrocytoma. Report of two cases. J Neurosurg 37:470-474, 1972 5. Budka H: Partially resected and irradiated cerebellar astrocytoma of childhood: malignant evolution after 28 years. Acta Neurochir 32:139-146, 1975 6. Burger PC, Scheithauer BW, Vogel FS: Surgical Pathology of the Nervous System and Its Coverings, ed 3. New York: Churchill Livingstone, 1991, pp 251-261 7. Davis PC, Friedman NC, Fry SM, et al: Leptomeningeal metastasis: MR imaging. Radiology 163:449-454, 1987 8. Hoshino T, Rodriguez LA, Cho KG, et al: Prognostic implications of the proliferative potential of low-grade astrocytomas. J Neurosnrg 69:839-842, 1988 J. Neurosurg. / r#)/ume 77/November. 1992
Disseminated pilocytic astrocytoma 9. llgren EB, Stiller CA: Cerebellar astrocytomas. Part I. Macroscopic and microscopic features. Clin Neuropathol 6:185-200, 1987 10. Kandt RS, Shinnar S, D'Souza BJ, et al: Cerebrospinal metastases in malignant childhood astrocytomas. J Neurooncol 2:123-128, t984 1l. Kepes JJ, Lewis RC, Vergara GG: Cerebellar astrocytoma invading the musculature and soft tissues of the neck. Case report. J Neurnsurg 52:414-418, 1980 12. Kleinman GM, Schoene WC, Walshe TM I11, et al: Malignant transformation in benign cerebellar astrocytoma. Case report. J Neurosurg 49:111-118, 1978 13. McLaughlin JE: Juvenile astrocytomas with subarachnoid spread. J Pathol 118:101-107, 1976 14. Ringertz N, Nordenstam H: Cerebellar astrocytoma. J Neuropathol Exp Neuroi 10:343-367, 1951 15. Rippe DJ, Boyko OB, Friedman HS, et ah Gd-DTPAenhanced MR imaging of leptomeningeal spread of primary intracranial CNS tumor in children. AJNR 11: 329-332, 1990 16. Russell DS, Rubinstein LJ: Pathology of Tumours of the Nervous System, ed 5. Baltimore: Williams & Wilkins, 1989, pp 152-159
J. Ne~lrosurg. / Vohtme 77/No'~,ember, 1992
17. Scott RM, Ballantine HT Jr: Cerebellar astrocytoma: malignant recurrence after prolonged postoperative survival. Case report. J Neurosurg 39:777-779, 1973 18. Shapiro K, Shulman K: Spinal cord seeding from cerebellar astrocytomas. Childs Brain 2:177-186, 1976 19. Steinberg GK, Shuer LM, Conley FK, et al: Evolution and outcome in malignant astroglial neoplasms of the cerebellum. J Neurosurg 62:9-17, 1985 20. Szrnfisy J, Slowik F: Prognosis of benign cerebellar astrocytomas in children. Childs Brain 10:39-47, 1983 21. Ushio Y, Arila N, Yoshimine T, et al: Malignant recurrence of childhood cerebellar astrocytoma: case report. Neurosnrgery 21:251-255, 1987
Manuscript received December 13, 1991. Accepted in final form May 13, 1992. Address reprint requests to: Kazuhiko Mishima, M.D., Department of Neurosurgery, Tokyo Metropolitan Komagome General Hospital, 3-18-22, Honkomagome, Bunkyoku, Tokyo 113, Japan.
791
Leptomeningeal dissemination of cerebellar pilocytic astrocytoma Case report KAZUHIKO MISHIMA, M.D., MASANAO NAKAMURA, M.D., HIROHIKO NAKAMURA, M.D., OSAMU NAKAMURA~ M.D., NOBUAKI FUNATA, M.D., AND NOBUYUKI SHITARA~ M.D. Department of Neurosurgeo, and Pathology, Tokyo Metropolitan Komagome General Hospital, Tokyo, Japan u- A case of surgically treated pilocytic astrocytoma in the cerebellar vermis is reported in a patient who subsequently demonstrated multiple subarachnoid nodular masses in the cerebrum and spinal cord 6 years after the initial surgery. The nodular tumors did not indicate a growth tendency on computerized tomography or magnetic resonance imaging over a 2-year observation period. The histology of the nodular masses in the cerebrum and spinal cord was similar to that of the original tumor. The bromodeoxyuridine labeling index indicated low proliferative activity (0.5%). The peculiar pattern of dissemination of the pilocytic astrocytoma is described. KEY WORDS 9 pilocytie astrocytoma bromodeoxyuridine labeling index
EREBELLAR pilocytic astrocytomas occurring in children have one of the most favorable prognoses of all intracranial tumors. Juvenile pilocytic astrocytomas are usually extremely benign, and it is well established that, even with incomplete resection, patients have survived for years without progression of the tumor. However, several cases of late malignant recurrence of pilocytic astrocytoma have been reported, l"~'SA2"lT"2twith some authors suggesting that the malignant transformation after a prolonged interval was induced by radiation therapy. 4~~2~2~ It has also been considered that the benign astrocytoma underwent malignant transformation because the recurrent tumor contained areas that showed histological features identical to those of the original tumor. 2~ Other case reports with early recurrence suggest that areas of focal anaplasia within a benign cerebellar astrocytoma were missed when the initial tumor specimen was examined34-'~ The case reported here is unusual in that, 6 years after surgery, a histologically benign astrocytoma disseminated to the supratentorial and spinal regions without pathologically malignant transformation or apparent regrowth of the primary tumor. The growth rate of the disseminated tumor was very low and the biological behavior was quite different from that of malignant glial tumors.
C
788
9 dissemination
Case Report
This 6-year-old boy was initially evaluated at another neurosurgical center for symptoms of increased intracranial pressure. Computerized tomography (CT) performed at that time demonstrated a multicystic tumor in the cerebellar vermis and obstructive hydrocephalus with no dissemination (Fig. 1). A ventriculoperitoneal shunt was placed, and 30 Gy of radiation therapy was administered. Subsequently, the tumor was totally resected. Histologically, a juvenile pilocytic astrocytoma was diagnosed (Fig. 2). Postoperatively, a total dose of 40 Gy was administered to the posterior fossa. During the 6 years after the operation, the patient did well and showed no signs of recurrence. Examination and Operation. Six years after the initial operation, at the age of 11 years, the patient was referred to our hospital with the diagnosis of leptomeningeal dissemination. Neurologically, the child remained asymptomatic. A cranial CT scan revealed a small enhanced mass lesion in the fourth ventricle; however, there was no evidence of recurrence of the primary vermian tumor. Gadolinium-diethylenetriamine penta-acetic acid (Gd-DTPA)-enhanced cranial magnetic resonance (MR) imaging demonstrated multiple leptomeningeal nodular, round masses with no J. Neurosurg. / Volume 77/Novernber, 1992
Disseminated pilocytic astrocytoma
FIG. 1. Initial contrast-enhanced computerized tomography scan showing a multicystic mass in the cerebellar vermis.
evidence of cerebellar tumor recurrence (Fig. 3B). On Gd-DTPA-enhanced spinal MR imaging, subarachnoid metastases were demonstrated at T-3 and T-4 (Fig. 3C). However, the nonenhanced T~- and T~-weighted images (Fig. 3A) did not clearly visualize the metastatic deposits. Cytological examination of the eerebrospinal fluid (CSF) was negative. To clarify the histology of the tumor, a right frontotemporal craniotomy was performed. A soft, reddish-gray tumor was located mainly in the subarachnoid space of the sylvian fissure and was partially adherent to the brain parenchyma. The tumor was totally resected. Pathological Examination. Histologically, the disseminated tumor was essentially the same as the original neoplasm. No nuclear atypism, mitotic figure, necrosis, or vascular endothelial proliferation was observed. Rosenthal fibers were abundantly present. Immunohistological stains revealed the presence of glial fibrillary acidic protein in the tumor cells. A diagnosis of pilocytic astrocytoma was made for this tumor (Fig. 4). Postoperative Course. Radiation therapy with a total dose of 40 Gy was delivered to the cervical and upper-thoracic spinal regions. Three months after completion of radiation therapy, the tumors at T-3 and T4 showed no change in size on MR imaging and the spinal cord was still compressed. Therefore, a decompressive laminectomy from T-2 to T-4 was performed. These tumor masses were primarily extramedullary in location. Histologically, they were similar to the previously resected tumor from the sylvian fissure. To estimate the proliferation potential of the original, we also analyzed the bromodeoxyuridine (BUdR) labeling index (LI) of these tumors. Two hours before spinal tumor resection, the patient received a 150-mg intravenous infusion of BUdR over a period of 30 minutes; the BUdR LI of these tumors was 0.5%. Two years after the diagnosis of dissemination, the radiological findings J. Neurosurg. / Volume 77/November. 1992
FIG. 2. Photomicrograph of the original tumor of the cerebellar vermis. The typical histology of juvenile pilocytic astrocytoma showing interwoven elongated piloid cells with microcystic degeneration is seen. H & E, • 32.
of the residual nodular masses had not changed and the patient remained well. Discussion
This case is unique in that the cerebellar tumor showed no local recurrence and the disseminated tumor demonstrated no anaplastic features. Moreover, the size and number of the disseminated tumor nodules did not change over a 2-year follow-up period. A long interval between the first radiological signs and the beginning of clinical symptoms is one of the characteristic features in this type of CSF dissemination. Generally, seeding of an anaplastic astrocytoma or glioblastoma herald the end stage of disease. ~'~ Therefore, the growth character, biological behavior, and clinical course of the disseminated pilocytic astrocytoma were clearly different from that of the malignant gliomas. It has been reported that the BUdR LI reflects the growth activity of gliomas and is closely correlated to patient prognosis and survival duration. I-Ioshino, et al., ~ reported that low-grade gliomas with a BUdR LI of 1% or more showed a tendency to recur rapidly, whereas patients in whom the glioma BUdR LI is less than 1% survived longer. The BUdR LI and clinical course in this case were consistent with these findings. The possibility exists that the multiplicity of pilocytic astrocytomas might be due to the multiple genesis of the tumors. However, the tumor in this case was located mainly in the CSF space and was loosely attached to the brain parenchyma. Therefore, CSF dissemination of the original tumor is most likely in this case. One mechanism for dissemination is that the viable tumor cells gain access to the subarachnoid or ventricular fluid spaces. In patients with cerebellar pilocytic astrocytomas, extension into the subarachnoid space is common but is not necessarily associated with aggressive behavior or leptomeningeal seedingY '~'--~~ MeLaughlin ~3 reported five cases of extracerebellar pilo789
K. Mishima, et al.
FI6. 3. Follow-up magnetic resonance images obtained 6 years after the initial operation. Multiple nodular masses in the subarachnoid spaces thal cannot be detected on the axial T j-weighted image of the head (A) are seen on the Gd-DTPA-enhanced Tt-weighted image (B, arrowheads). A sagiltal Gd-DTPA-cnhanced T~weighted image (C) of the spine demonstrates several enhancing nodular lesions/arrm~'~') adjacent 1o the spinal cord.
tumor appears to be aggressive surgery, where possible. Recently, the efficacy of MR imaging has been evaluated in patients with meningeal tumor spread. 7'~5 Although noncontrast-enhanced MR imaging is rather insensitive, Gd-DTPA-enhanced MR imaging is useful when searching for leptomeningeal tumor deposits to prevent patient deterioration. In conclusion, although seeding from a cerebellar pilocytic astrocytoma rarely occurs, it is difficult to predict the occurrence of dissemination even by histological examination. Therefore, careful follow-up review with contrast-enhanced MR imaging is important even in cases of histologically benign pilocytic astrocytoma. FiG. 4. Photomicrograph of the disseminated tumors (brain and spinal) showing pilocytic astrocytoma without malignant features. Rosenthal fibers are also seen. H & E, • 32.
cytic astrocytoma demonstrating subarachnoid spread and invasion of surrounding structures. They concluded that a tumor showing nuclear pleomorphism or oligodendrocytomatous areas had a poor prognosis. Shapiro and Shulman ~s reported three of 72 patients with histologically benign cerebellar astrocytomas in whom the tumor seeded the spinal subarachneid space without malignant transformation. They mentioned that the seeding did not indicate the patient's imminent demise and believed that this was part of the natural history of this tumor. The treatment of the disseminated tumor remains controversial. In our patient, radiotherapy to the disseminated lesions was ineffective. Kepes, et al.? ~ and Auer, el al., 2 demonstrated the ineffectiveness of radiotherapy in controlling dissemination. With this background, the most reliable treatment of the disseminated 790
Reference
l. Alpers CE, Davis RL, Wilson CB: Persistence and late malignant transformation of the childhood cerebellar astrocytoma. Case report. J Neurosurg 57:548-551, 1982 2. Auer RN, Rice GPA, Hinton GG, et air Cerebellar astrocytoma with benign histology and malignant clinical course. Case report. J Neurosurg 54:128-132, 1981 3. Awad I, Bay JW, Rogers L: Leptomeningeal metastasis from supratentorial malignant gliomas. Neurosurgery 19: 247-251, 1986 4. Bernell WR, Kepes J J, Seitz EP: Late malignant recurrence of childhood cerebellar astrocytoma. Report of two cases. J Neurosurg 37:470-474, 1972 5. Budka H: Partially resected and irradiated cerebellar astrocytoma of childhood: malignant evolution after 28 years. Acta Neurochir 32:139-146, 1975 6. Burger PC, Scheithauer BW, Vogel FS: Surgical Pathology of the Nervous System and Its Coverings, ed 3. New York: Churchill Livingstone, 1991, pp 251-261 7. Davis PC, Friedman NC, Fry SM, et al: Leptomeningeal metastasis: MR imaging. Radiology 163:449-454, 1987 8. Hoshino T, Rodriguez LA, Cho KG, et al: Prognostic implications of the proliferative potential of low-grade astrocytomas. J Neurosnrg 69:839-842, 1988 J. Neurosurg. / r#)/ume 77/November. 1992
Disseminated pilocytic astrocytoma 9. llgren EB, Stiller CA: Cerebellar astrocytomas. Part I. Macroscopic and microscopic features. Clin Neuropathol 6:185-200, 1987 10. Kandt RS, Shinnar S, D'Souza BJ, et al: Cerebrospinal metastases in malignant childhood astrocytomas. J Neurooncol 2:123-128, t984 1l. Kepes JJ, Lewis RC, Vergara GG: Cerebellar astrocytoma invading the musculature and soft tissues of the neck. Case report. J Neurnsurg 52:414-418, 1980 12. Kleinman GM, Schoene WC, Walshe TM I11, et al: Malignant transformation in benign cerebellar astrocytoma. Case report. J Neurosurg 49:111-118, 1978 13. McLaughlin JE: Juvenile astrocytomas with subarachnoid spread. J Pathol 118:101-107, 1976 14. Ringertz N, Nordenstam H: Cerebellar astrocytoma. J Neuropathol Exp Neuroi 10:343-367, 1951 15. Rippe DJ, Boyko OB, Friedman HS, et ah Gd-DTPAenhanced MR imaging of leptomeningeal spread of primary intracranial CNS tumor in children. AJNR 11: 329-332, 1990 16. Russell DS, Rubinstein LJ: Pathology of Tumours of the Nervous System, ed 5. Baltimore: Williams & Wilkins, 1989, pp 152-159
J. Ne~lrosurg. / Vohtme 77/No'~,ember, 1992
17. Scott RM, Ballantine HT Jr: Cerebellar astrocytoma: malignant recurrence after prolonged postoperative survival. Case report. J Neurosurg 39:777-779, 1973 18. Shapiro K, Shulman K: Spinal cord seeding from cerebellar astrocytomas. Childs Brain 2:177-186, 1976 19. Steinberg GK, Shuer LM, Conley FK, et al: Evolution and outcome in malignant astroglial neoplasms of the cerebellum. J Neurosurg 62:9-17, 1985 20. Szrnfisy J, Slowik F: Prognosis of benign cerebellar astrocytomas in children. Childs Brain 10:39-47, 1983 21. Ushio Y, Arila N, Yoshimine T, et al: Malignant recurrence of childhood cerebellar astrocytoma: case report. Neurosnrgery 21:251-255, 1987
Manuscript received December 13, 1991. Accepted in final form May 13, 1992. Address reprint requests to: Kazuhiko Mishima, M.D., Department of Neurosurgery, Tokyo Metropolitan Komagome General Hospital, 3-18-22, Honkomagome, Bunkyoku, Tokyo 113, Japan.
791
