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Primary rhabdomyosarcoma of the leptomeninx
Primary rhabdomyosarcoma of the leptomeninx Clinical, neuroradioIogi~a1 and pathologica R. Korinthenberg*, R.-P. Miiller****
G. Edel**,
aspects
D. Palm*,
K.-M.
Mi.iller**,
M. Brandt***
and
Introduction Summary
This report concerns a primary intracranial rhabdomyosarcoma originating in the leptomeninx. Due to the diffuse localisation. diagnosis was difficult in spite of severe clinical symptoms. Intracranial rhabdomyosarcomas that are not identified as metastases of an extracranial primary one. are extremely rare. In a survey of 810 brain tumors in children, primary rhabdomyosarcomas were found in only two patienthI:. Case report
F.H., male. born 1977. (J.Nr. 879/X0). The boy was born after an uneventful pregnancy without complicatons. No tumors or neurological diseases are reported in the family. The child’s mental and motor development were normal. On July 1st 1980, the boy had a first epileptic convulsion, starting in the right arm with secondary generalisation. On admission to the hospital he seemed drowsy, with slurred speech. Neurological examination failed to reveal pathologic findings apart from a slight deviation of the tongue towards the right side. EEG showec severe slowing over the left hemisphere, but a brain scan with Tc-glucoheptonat
Report of an eight-year-old boy presenting with untreatable focal epilepsy and sluwly progressing hemiparesis combined with perchanges. Continuous diagnostic sonality efforts eventually resulted in the diagnosis of a intracranial primary rhabd~)myosarc(~ma several months later. The delay in making the correct diagnosis was due to the fact that the malignant process originated as a diffuse involvement of the leptomeninx. and only in later stages a tumor mass developed. Nosology and lllsto~enesis of primary intracranial rhabdomyosarcomas are discussed. Key
words:
domyosarcoma. metastases.
Intracranial tumor, rhabcomputed tomography. spinal
was without pathologic findings. There was no papilledema. CT revealed a distinct dilatation of the ventricles and the subarachnoid space, while in the white matter of the left hemisphere a hypodense area was observed, which showed marked peripheral enhancement after intravenous contrast application. There was also a slight compression of the left lateral ventricle (Fig. 1). An arteri~)gram of the left carotid showed no abnormalities. Because repeated CT’s resulted in identical findings. craniotomy was perform-
t,1g.I. Initial Cl’ scan after contrast application chowvq a hypodense area within the marrow of the left hemisphere. Distinct peripheral enhancement, and a slight compression of the left ventricle.
FL&2. Control Cl‘ scan (2 I .4.8 I ) showing a large tumorous mabs m the tempo-parietal area of the left hemisphere, with irregular contrast enhancement and displacement of midline structures.
ed, suspecting an intracerebral tumor. Over the left frontal and parietal areas the leptomeninx was thickened and whitish. No evidence of a tumor was seen on the brain surface, and after incision of the cortex, there was no tumorous tissue either in the depth of the white matter, and only a slight edema of brain tissue was recognized. Histology revealed no abnormal cells in leptomeningeal and brain tissue. Increase of collagen was found within the leptomeninx, and some regressive changes in the white matter. The ensuing clinical course was marked by frequent partial and generalized epileptic seizures withstanding anticonvulsive medication. Progressive loss of mental and physical abilities was observed over several months, resulting eventually in loss of orientation, mild right-sided hemiparesis, ataxia, and choreiform unvoluntary movements. In addition there was a right-sided peripheral paresis of the hypoglossus nerve, while the other cranial nerves were intact. Monthly CT scans documented the known edema of the left hemisphere to a different ex-
tent. Lumbar puncture was repeated several times, but not until 8 months after the onset of symptoms it revealed CSF pleocytosis (50 macrophages/mm3, no tumor cells), elevation of CSF protein (6512 mg/l), and decrease of CSF glucose (25 mg/dl vs. 125 mg/dl blood glucose). Another CT, performed on April 1st 1981, was the first to show a tumorlike mass within the left frontoparietal hemisphere, with irregular enhancement after intravenous contrast application (Fig. 2). A second neurosurgical exploration revealed a grey-reddish tumor of 5 x 5 cm within the area of the first operation. Its extensive infiltration into the neighboring brain tissue prevented a more than subtotal resection. Postthe patient did not regain operatively consciousness. Flaccid paraparesis, with loss of reaction to pain, appeared on the 4th postoperative day. In view of the infaust prognosis no intensive treatment was begun for the brain tumor and suspected spinal metastases. The patient died of central dysregulation on the 9th postoperative day.
302
Fig. 3. Grey-whitish
tumor
at the left temporal
pole.
a.
Fig. 4. Metastatic
tumor nodules
on the dura of the posterior
fossa.
b.
c. Fig. 5 a) Undifferentiated myoblasts and rhabdomyoblasts at varying grades of maturity in a myxoid h) Well-differentiated myocytes with longitudinal and cross striation. (EvG. x 650) c) Prominent pericytic arrangement of tumor cells. (HE, x 125) d) Bizarre giant tumor cells with pycnotic nuclei in excentric position. (HE, x 130)
Pathologic
findings
On post-mortem examination the brain weighed 1670 g. Besides the marks of the operation there were the typical signs of increased intracranial pressure. Meningeal thickening and
stroma.
(HE, x 300)
grey-whitish opacity was found over large parts of the left hemisphere, over the chiasma opticum. the pons and the cerebellar hemispheres. Near the site of resection some residual tumor tissue was observed with a greywhitish, vitreo-fibrous consistency, apparently 303
originating from the meninges and extending into the brain tissue via the Virchow-Robin spaces. A similar tumorous node of 2.8 cm diameter was located at the left temporal pole (Fig. 3). Numerous liquorogenous metastases were found inside the right lateral ventricle, attached to the meninges of the posterior fossa (Fig. 4). and in the arachnoid involving the whole spinal cord. The tumor tissue showed various histologic structures: Undifferentiated myoblasts and rhabdomyoblasts at varying grades of maturity were seen besides mesenchymal cells of lowgrade differentiation (Fig. 5a). Many .of these cells showed intense and uniform cross-striation (Fig. 5b). The tumor cells often surrounded blood vessels in a rosette-like array (Fig. 5~). There were also some bizarre giant tumor cell. with pycnotic nuclei in excentric position (Fig. 5d). The rate of mitoses was distinctly increased. No tumor tissue was found in extracranial sites even at the most meticulous examination. Discussion
As far as we know only 20 cases of primary intracranial rhabdomyosarcoma have been reported in the literature1-20. Patient’s ages range from 9 months to 52 years, 12 patients were younger than 16 years of age. Most of the tumors presented as space-occupying mass lesions with corresponding clinical symptoms. So far, diffuse meningeal infiltration was reported only oncelg. The tumors were localized within the posterior fossa in lo/20 cases, within the supratentorial space in 9/20 cases, and one case showed spinal localization. In our patient, the early coincidence of right-sided partial epileptic fits with peripheral hypoglossal paresis suggests a multilocular origin of the tumor itself, or a very early onset of metastatic spread via the CSF. No consent is established as yet concerning the histogenesis of primary intracranial rhabdomyosarcomas. Several authors propose a mesenchymal origin, probably from primitive residues of mesenchymal tissue within the neural crest8Jg*20. The ectomesenchyma that normally exists within the neural crest, is capable of differentiating into cartilage, bone, and meningeal tissue6J5. It is also present in the 304
pericapillary areas of the brain, espectally in the pia mater and arachnoid2’. Thus it appears likely that this tissue could differentiate into myoblasts which may give rise to a rhabdomyosarcoma. In this context particular importance is attributed to the findings of striated muscle fibers within the meninges of individuals with brain malformations”-““. The primary rhabdomyosarcomas have to be differentiated from mixed mesenchymal and neuroepithelial tumors. These are composed of gliomas and sarcomas showing varying amounts of fibroblastic. chondroblastic, and rhabdomyoblastic elementsa6-2”. The primary cerebral rhabdomyosarcomas must also be distinguished from the so-called medullomyoblastomas which contain both rhabdoand leiomyoblastic structures and are found almost exclusively in the cerebellum of children, Teratogenic and embryonal mesenchymal origins are discussed for this variety”“J’. Untreated patients with primary intracranial rhabdomyosarcomas usually die within a period of a few weeks to five months. In some cases duration of life could be extended by surgery and irradiation with five months to two years r1.r6. In one case, after treatment consistremoval and polying of a subtotal chemotherapy (vincristin, actinomycin-D, methotrexate i.th.), the cyclophosphamide, child was still disease-free at time of publication, two years later’“. Nearly all other patients died with widespread liquorogenous metastases, often without systemic spread of the tumora. References s, IT0 Y,SHINOZAWA T. A case of primary cerebral rhabdomyosarcoma. No Shinkei Geka (Neurol Surg) 1981; 9: 1067-72. (3~~~110~0 s,GADDONI G. Miosarcomi primitive de1 SNC. Acta Neural (Napoli) 1971; 26:297-302. JELLINGER K, MACHACEK E. Rare intracranial tumours in infancy and childhood. In: Voth D, Gutjahr P, Langmaid C. eds. Tumours of the central nervous system in infancy and childhood. Berlin. Heidelberg, New York: SpringerVerlag. 1982: 44-52. KOIDE o, ISHIZONE s.A case of rhabdomyosarcoma in the brain. No To Shinkei (Brain Nerve) 1958; 10:49-54. LEEDHAM PW. Primary cerebral rhabdomyosarcoma and the problem of medullomyoblastoma. J Neurol Neurosurg Psychiatry 1972; 35% 1-9. LEGIER JF,WELLS HA. Primary cerebellar rhabdomyosarcoma. Case report. J. Neurosurg 1967; 26: 436-8. CHIBA J, FUJINO H, YAGASHITA
i IopEs IX FARIA I. Rhabdomyosarcoma
Arch Pathol
of cerebellum.
1957: 63:234-8.
* MASU~A~AT.SHIMABUKOROH.~AMOS~~TA S,SATOF. The ultra structure of primary cerebral rhabdomyosarcoma. Acta Neuropathol (Berlin) 1982; 56:307-10. !I MATSUKADO y, YAKOTA A, MARUBAYOSHI T. Rhabdomyosarcomaofthe brain. J Neurosurg 1975; 43:215-21. I’) MIN KW, GYORKEY F. HALPERT B Primary rhabdomyosarcoma of the cerebrum. Cancer 1975: 35:1405-i I. ” NAMBA K. ASCHENRRENER C,NIKPOUR M,VAN GILDER JC. Primary rhabdomyosarcoma of the tentorium with peculiar angiographic findings. Surg Nemo1 1979: 1 I :39-43. ‘a O'COWEL JEA.The subarachnoid dissemination of spinal turnouts. J Nemo1 Neurosurg Psychiatry 1946; 9:55-62. I:’ OZ~.KI ‘r. A necropsy case report of primary rhabdomyosarcoma m the cerebrum. Transact Sot Pathol Japon 1960161: 49:750. ” PASQUIER R.CQUDERC P,PASQUlERD,HONG PM,PELLATJ. Primary rhabdomyos~r~oma of the central nervous system. Acta Neuropathol (Berlin) 1975; 33:333-42. ” ROY s,RHATIA R. NANDA NR. Primary rhabdomyosarcoma of the cerebellum. J Pathol 1980; 132:235-41. I” SHIN KH. WHITEHEAD VM. Rhabdomyosarcoma of the brain. Can J Surg 1980: 23:576-8. ‘r SHUANGSHQTI S,PIYARAfN P,VIRIYAPANICH PL. Primary rhabdomyosarcoma of cerebellum. Necropsy report. Cancer 1968: 22:376-81. ‘8 SHUANGSHOTI s. PHONPRASERT c. Primary intracranial rhabd~~myosar~oma producing proptosis. J Neurosurg Psychiatry 1976; 39:531-5. *‘SMITH MI, ARMBRUSTMA~HER VW. VIOLETT TWA. Diffuse meningeal rhabdomyosarcoma. Cancer 1981; 47:2081-6.
s. IICJHY. CHIBA y. I~JINO H. Primary rhabdomyosarcoma of the cerebrum. An u~trastructural study. Acta Neuropathol (Berlin) 1979; 45: I I l-5. %’BL.OOM w, FAWCETT DW. Textbook of histopathology. 8th ed. Philadelphia: W.B. Saunders. 1962; 93-255. p’ AMBLER MW. Striated muscle cells in the teptomeninges in cerebral dysplasia. Acta Neuropathol (Berlin) 1977: 40:268-7 1. ‘t:i FRIEDC RL. Dysplasia ofcerebral cortex. In: Friede RL, ed. Developmental neuropathology. New York: Springer Press. 1975:308. 2-1HOFIMAN SF.RORKE LB. On finding striated muscle in the brain. J Neural Neurosurg Psychiatry 1971: 34:761-4. z JARRELL HR. KRWS HF. SHOCHET ss. ~enjngeal rhabdomyomatosis. Arch Pathol Lab Med 1981; 105:387. x FEIGIN JH. ALLEN LB,LIPKIN L.CROSS SW. The endothelial hyperplasia of cerebral blood vessels with brain tumors and its sarcomatom transformation. Cancer 1958: I1:264-77. z GOLDMAN RL. Gli(~rnyosar~orn~~ of the cerebrum. Report of a unique case. Am J Clin Pathol 3969: 53: 741-4. 2XHOLIMW IL. ROSENRLUM wJ. “Gangltorhabdomyosarcoma”: A tumor of ectomesenchyme. Case report. J Neurosurg 1971; 34:417-22. “a RUBINSTEIN LJ. The development of contiguous sarcomatom and gliomatous tissue in intracranial turnours. J Pathol Bacterial 1956; 71:441-59. Untersuchungen zur :“’ GI~LI.oTIA t. Vergleichende Morphologic und Genese der sogenannten Medulloblastome. Acta Neuropathol (Berlin) 1966; 8:76-83. ‘tt RIISSEL ifs.RC!BINSI~IN w. Pathology of tumours of the nervous system. 4th ed. London. Adward Arnold. 1977:74-7.
Z' YAGASHIIA
305
G. Edel**,
aspects
D. Palm*,
K.-M.
Mi.iller**,
M. Brandt***
and
Introduction Summary
This report concerns a primary intracranial rhabdomyosarcoma originating in the leptomeninx. Due to the diffuse localisation. diagnosis was difficult in spite of severe clinical symptoms. Intracranial rhabdomyosarcomas that are not identified as metastases of an extracranial primary one. are extremely rare. In a survey of 810 brain tumors in children, primary rhabdomyosarcomas were found in only two patienthI:. Case report
F.H., male. born 1977. (J.Nr. 879/X0). The boy was born after an uneventful pregnancy without complicatons. No tumors or neurological diseases are reported in the family. The child’s mental and motor development were normal. On July 1st 1980, the boy had a first epileptic convulsion, starting in the right arm with secondary generalisation. On admission to the hospital he seemed drowsy, with slurred speech. Neurological examination failed to reveal pathologic findings apart from a slight deviation of the tongue towards the right side. EEG showec severe slowing over the left hemisphere, but a brain scan with Tc-glucoheptonat
Report of an eight-year-old boy presenting with untreatable focal epilepsy and sluwly progressing hemiparesis combined with perchanges. Continuous diagnostic sonality efforts eventually resulted in the diagnosis of a intracranial primary rhabd~)myosarc(~ma several months later. The delay in making the correct diagnosis was due to the fact that the malignant process originated as a diffuse involvement of the leptomeninx. and only in later stages a tumor mass developed. Nosology and lllsto~enesis of primary intracranial rhabdomyosarcomas are discussed. Key
words:
domyosarcoma. metastases.
Intracranial tumor, rhabcomputed tomography. spinal
was without pathologic findings. There was no papilledema. CT revealed a distinct dilatation of the ventricles and the subarachnoid space, while in the white matter of the left hemisphere a hypodense area was observed, which showed marked peripheral enhancement after intravenous contrast application. There was also a slight compression of the left lateral ventricle (Fig. 1). An arteri~)gram of the left carotid showed no abnormalities. Because repeated CT’s resulted in identical findings. craniotomy was perform-
t,1g.I. Initial Cl’ scan after contrast application chowvq a hypodense area within the marrow of the left hemisphere. Distinct peripheral enhancement, and a slight compression of the left ventricle.
FL&2. Control Cl‘ scan (2 I .4.8 I ) showing a large tumorous mabs m the tempo-parietal area of the left hemisphere, with irregular contrast enhancement and displacement of midline structures.
ed, suspecting an intracerebral tumor. Over the left frontal and parietal areas the leptomeninx was thickened and whitish. No evidence of a tumor was seen on the brain surface, and after incision of the cortex, there was no tumorous tissue either in the depth of the white matter, and only a slight edema of brain tissue was recognized. Histology revealed no abnormal cells in leptomeningeal and brain tissue. Increase of collagen was found within the leptomeninx, and some regressive changes in the white matter. The ensuing clinical course was marked by frequent partial and generalized epileptic seizures withstanding anticonvulsive medication. Progressive loss of mental and physical abilities was observed over several months, resulting eventually in loss of orientation, mild right-sided hemiparesis, ataxia, and choreiform unvoluntary movements. In addition there was a right-sided peripheral paresis of the hypoglossus nerve, while the other cranial nerves were intact. Monthly CT scans documented the known edema of the left hemisphere to a different ex-
tent. Lumbar puncture was repeated several times, but not until 8 months after the onset of symptoms it revealed CSF pleocytosis (50 macrophages/mm3, no tumor cells), elevation of CSF protein (6512 mg/l), and decrease of CSF glucose (25 mg/dl vs. 125 mg/dl blood glucose). Another CT, performed on April 1st 1981, was the first to show a tumorlike mass within the left frontoparietal hemisphere, with irregular enhancement after intravenous contrast application (Fig. 2). A second neurosurgical exploration revealed a grey-reddish tumor of 5 x 5 cm within the area of the first operation. Its extensive infiltration into the neighboring brain tissue prevented a more than subtotal resection. Postthe patient did not regain operatively consciousness. Flaccid paraparesis, with loss of reaction to pain, appeared on the 4th postoperative day. In view of the infaust prognosis no intensive treatment was begun for the brain tumor and suspected spinal metastases. The patient died of central dysregulation on the 9th postoperative day.
302
Fig. 3. Grey-whitish
tumor
at the left temporal
pole.
a.
Fig. 4. Metastatic
tumor nodules
on the dura of the posterior
fossa.
b.
c. Fig. 5 a) Undifferentiated myoblasts and rhabdomyoblasts at varying grades of maturity in a myxoid h) Well-differentiated myocytes with longitudinal and cross striation. (EvG. x 650) c) Prominent pericytic arrangement of tumor cells. (HE, x 125) d) Bizarre giant tumor cells with pycnotic nuclei in excentric position. (HE, x 130)
Pathologic
findings
On post-mortem examination the brain weighed 1670 g. Besides the marks of the operation there were the typical signs of increased intracranial pressure. Meningeal thickening and
stroma.
(HE, x 300)
grey-whitish opacity was found over large parts of the left hemisphere, over the chiasma opticum. the pons and the cerebellar hemispheres. Near the site of resection some residual tumor tissue was observed with a greywhitish, vitreo-fibrous consistency, apparently 303
originating from the meninges and extending into the brain tissue via the Virchow-Robin spaces. A similar tumorous node of 2.8 cm diameter was located at the left temporal pole (Fig. 3). Numerous liquorogenous metastases were found inside the right lateral ventricle, attached to the meninges of the posterior fossa (Fig. 4). and in the arachnoid involving the whole spinal cord. The tumor tissue showed various histologic structures: Undifferentiated myoblasts and rhabdomyoblasts at varying grades of maturity were seen besides mesenchymal cells of lowgrade differentiation (Fig. 5a). Many .of these cells showed intense and uniform cross-striation (Fig. 5b). The tumor cells often surrounded blood vessels in a rosette-like array (Fig. 5~). There were also some bizarre giant tumor cell. with pycnotic nuclei in excentric position (Fig. 5d). The rate of mitoses was distinctly increased. No tumor tissue was found in extracranial sites even at the most meticulous examination. Discussion
As far as we know only 20 cases of primary intracranial rhabdomyosarcoma have been reported in the literature1-20. Patient’s ages range from 9 months to 52 years, 12 patients were younger than 16 years of age. Most of the tumors presented as space-occupying mass lesions with corresponding clinical symptoms. So far, diffuse meningeal infiltration was reported only oncelg. The tumors were localized within the posterior fossa in lo/20 cases, within the supratentorial space in 9/20 cases, and one case showed spinal localization. In our patient, the early coincidence of right-sided partial epileptic fits with peripheral hypoglossal paresis suggests a multilocular origin of the tumor itself, or a very early onset of metastatic spread via the CSF. No consent is established as yet concerning the histogenesis of primary intracranial rhabdomyosarcomas. Several authors propose a mesenchymal origin, probably from primitive residues of mesenchymal tissue within the neural crest8Jg*20. The ectomesenchyma that normally exists within the neural crest, is capable of differentiating into cartilage, bone, and meningeal tissue6J5. It is also present in the 304
pericapillary areas of the brain, espectally in the pia mater and arachnoid2’. Thus it appears likely that this tissue could differentiate into myoblasts which may give rise to a rhabdomyosarcoma. In this context particular importance is attributed to the findings of striated muscle fibers within the meninges of individuals with brain malformations”-““. The primary rhabdomyosarcomas have to be differentiated from mixed mesenchymal and neuroepithelial tumors. These are composed of gliomas and sarcomas showing varying amounts of fibroblastic. chondroblastic, and rhabdomyoblastic elementsa6-2”. The primary cerebral rhabdomyosarcomas must also be distinguished from the so-called medullomyoblastomas which contain both rhabdoand leiomyoblastic structures and are found almost exclusively in the cerebellum of children, Teratogenic and embryonal mesenchymal origins are discussed for this variety”“J’. Untreated patients with primary intracranial rhabdomyosarcomas usually die within a period of a few weeks to five months. In some cases duration of life could be extended by surgery and irradiation with five months to two years r1.r6. In one case, after treatment consistremoval and polying of a subtotal chemotherapy (vincristin, actinomycin-D, methotrexate i.th.), the cyclophosphamide, child was still disease-free at time of publication, two years later’“. Nearly all other patients died with widespread liquorogenous metastases, often without systemic spread of the tumora. References s, IT0 Y,SHINOZAWA T. A case of primary cerebral rhabdomyosarcoma. No Shinkei Geka (Neurol Surg) 1981; 9: 1067-72. (3~~~110~0 s,GADDONI G. Miosarcomi primitive de1 SNC. Acta Neural (Napoli) 1971; 26:297-302. JELLINGER K, MACHACEK E. Rare intracranial tumours in infancy and childhood. In: Voth D, Gutjahr P, Langmaid C. eds. Tumours of the central nervous system in infancy and childhood. Berlin. Heidelberg, New York: SpringerVerlag. 1982: 44-52. KOIDE o, ISHIZONE s.A case of rhabdomyosarcoma in the brain. No To Shinkei (Brain Nerve) 1958; 10:49-54. LEEDHAM PW. Primary cerebral rhabdomyosarcoma and the problem of medullomyoblastoma. J Neurol Neurosurg Psychiatry 1972; 35% 1-9. LEGIER JF,WELLS HA. Primary cerebellar rhabdomyosarcoma. Case report. J. Neurosurg 1967; 26: 436-8. CHIBA J, FUJINO H, YAGASHITA
i IopEs IX FARIA I. Rhabdomyosarcoma
Arch Pathol
of cerebellum.
1957: 63:234-8.
* MASU~A~AT.SHIMABUKOROH.~AMOS~~TA S,SATOF. The ultra structure of primary cerebral rhabdomyosarcoma. Acta Neuropathol (Berlin) 1982; 56:307-10. !I MATSUKADO y, YAKOTA A, MARUBAYOSHI T. Rhabdomyosarcomaofthe brain. J Neurosurg 1975; 43:215-21. I’) MIN KW, GYORKEY F. HALPERT B Primary rhabdomyosarcoma of the cerebrum. Cancer 1975: 35:1405-i I. ” NAMBA K. ASCHENRRENER C,NIKPOUR M,VAN GILDER JC. Primary rhabdomyosarcoma of the tentorium with peculiar angiographic findings. Surg Nemo1 1979: 1 I :39-43. ‘a O'COWEL JEA.The subarachnoid dissemination of spinal turnouts. J Nemo1 Neurosurg Psychiatry 1946; 9:55-62. I:’ OZ~.KI ‘r. A necropsy case report of primary rhabdomyosarcoma m the cerebrum. Transact Sot Pathol Japon 1960161: 49:750. ” PASQUIER R.CQUDERC P,PASQUlERD,HONG PM,PELLATJ. Primary rhabdomyos~r~oma of the central nervous system. Acta Neuropathol (Berlin) 1975; 33:333-42. ” ROY s,RHATIA R. NANDA NR. Primary rhabdomyosarcoma of the cerebellum. J Pathol 1980; 132:235-41. I” SHIN KH. WHITEHEAD VM. Rhabdomyosarcoma of the brain. Can J Surg 1980: 23:576-8. ‘r SHUANGSHQTI S,PIYARAfN P,VIRIYAPANICH PL. Primary rhabdomyosarcoma of cerebellum. Necropsy report. Cancer 1968: 22:376-81. ‘8 SHUANGSHOTI s. PHONPRASERT c. Primary intracranial rhabd~~myosar~oma producing proptosis. J Neurosurg Psychiatry 1976; 39:531-5. *‘SMITH MI, ARMBRUSTMA~HER VW. VIOLETT TWA. Diffuse meningeal rhabdomyosarcoma. Cancer 1981; 47:2081-6.
s. IICJHY. CHIBA y. I~JINO H. Primary rhabdomyosarcoma of the cerebrum. An u~trastructural study. Acta Neuropathol (Berlin) 1979; 45: I I l-5. %’BL.OOM w, FAWCETT DW. Textbook of histopathology. 8th ed. Philadelphia: W.B. Saunders. 1962; 93-255. p’ AMBLER MW. Striated muscle cells in the teptomeninges in cerebral dysplasia. Acta Neuropathol (Berlin) 1977: 40:268-7 1. ‘t:i FRIEDC RL. Dysplasia ofcerebral cortex. In: Friede RL, ed. Developmental neuropathology. New York: Springer Press. 1975:308. 2-1HOFIMAN SF.RORKE LB. On finding striated muscle in the brain. J Neural Neurosurg Psychiatry 1971: 34:761-4. z JARRELL HR. KRWS HF. SHOCHET ss. ~enjngeal rhabdomyomatosis. Arch Pathol Lab Med 1981; 105:387. x FEIGIN JH. ALLEN LB,LIPKIN L.CROSS SW. The endothelial hyperplasia of cerebral blood vessels with brain tumors and its sarcomatom transformation. Cancer 1958: I1:264-77. z GOLDMAN RL. Gli(~rnyosar~orn~~ of the cerebrum. Report of a unique case. Am J Clin Pathol 3969: 53: 741-4. 2XHOLIMW IL. ROSENRLUM wJ. “Gangltorhabdomyosarcoma”: A tumor of ectomesenchyme. Case report. J Neurosurg 1971; 34:417-22. “a RUBINSTEIN LJ. The development of contiguous sarcomatom and gliomatous tissue in intracranial turnours. J Pathol Bacterial 1956; 71:441-59. Untersuchungen zur :“’ GI~LI.oTIA t. Vergleichende Morphologic und Genese der sogenannten Medulloblastome. Acta Neuropathol (Berlin) 1966; 8:76-83. ‘tt RIISSEL ifs.RC!BINSI~IN w. Pathology of tumours of the nervous system. 4th ed. London. Adward Arnold. 1977:74-7.
Z' YAGASHIIA
305