Meningioma following high-dose radiation therapy Case report and review of the literature
Maurizio Domenicucci, rante*
Marco Artico, Francesco Nucci, Maurizio Salvati and Luigi Fer-
Introduction Summary
The possibility that radiotherapy may be an oncogenic stimulus for the formation of meningiomas has been mentioned in a number of reports over the past decadesl-ls. We present a case of this kind in which a patient, originally operated on for astrocytoma, underwent radiation therapy (40 Gy) and, 11 years later, developed a meningioma in the pathway of the original irradiation. A review of the literature has revealed 14 analogous casesz-4,8*11,‘3-‘7, which, in accordance with other authors4.s, we have classified as “high-dose” post-irradiation meningiomas (PIMs), thereby distinguishing them from “lowdose” PIMs which occur after radiation therapy generally given for tinea cap&isat a dosage of less than 8 Gy. A study of “high-dose” PIMs as compared to those induced by low doses of radiation therapyl.5.Y,l",12 shows the former to have some distinctive features. Case report In December 1982 a 24-year-old male was admitted to our Section with signs of drowsiness, urinary incontinence and, according to his family, personality changes which had set in over the previous six months. He showed a marked
* Department
ofNeuroI~gi~at Sciences, Neurosurgery,
University
A case of meningioma induced by high-dose radiation therapy (40 Gy) is reported. The radiation had been given 11 years previously following operation for cerebral astrocytoma. Pertinent cases of benign meningioma occurring after radiation therapy are reviewed and analyzed. Key words: Meningioma, radiation therapy, astrocytoma. recurrent mixed tumor.
expressive dysphasia. In 1971, when he was 13, this patient had undergone a left fronto-temporal lobectomy to remove a low-grade astrocytoma located in the anterior portion of the left temporal lobe. After surgery he had received radiation therapy (for a total of 40 Gy) in the region of tumor removal. At subsequent checkups in 1972 and 1978 he was found to be in good general health. General physical examination did not reveal signs of neurofibromatosis nor was there a family history of the disease. The skin over the left fronto-temporal region was pale pink and slightly atrophic with alopecia. Blurred mentation, disorientation, expressive-dysphasia and urinary incontinence were found at neurologic examination. CT scan revealed a homogeneous, circum-
af Rome “La Sapienza”, Rome, Italy.
Address&r correspondence and reprint requests: Francesco Nucci, M.D., Universitci di Roma “La Sapienza”, Scienze Neurologiche, Neurochirurgia, Viale deN’Universitri 3OlA, 00185 Roma, Italy.
Dipartimento di
Accepted 3.8.89 Clin Neural Neurosurg 1990. Val. 92-4
349
Figure 1. CT scan after injection ot contrast medium on admission (1982) showing a homogeneously enhancing tumor on the left side of the anterior fossa attached to the falx.
scribed expansive lesion with enhancement after contrast medium intravenous injection in the left frontal region, extending slightly over the midline. There was a rim of decreased density at the posterior end of the mass (Fig. 1). Left carotid angiography showed the typical picture of a meningioma. Left frontal craniotomy disclosed a meningioma attached to the falx and infiltrating the superior longitudinal sinus. Apparently radical excision was accomplished. The histological diagnosis was syncytial meningioma . Postoperatively the patient experienced transient right hemiparesis and was discharged in good health. The patient’s conditions remained good until January 1984 when he died in another Institution from acute subdural hematoma resulting from a road accident. Discussion In the first half of this century, before the introduction of griseofulvin, treatment of tinea cupit& consisted of the Adamson-Kienbock method, namely, irradiation of the scalp with doses not exceeding 8 Gy. The long-term risks of this treatment began to appear in the literature in 1966’. In 1974 Modan et ~l.~, on analyzing 10902 cases of immigrant children in Israel during the period 1948-1951 who had undergone radiation therapy for tinea cupitis, found a statistically significant increase in the number of intracranial meningiomas with respect to an analogous con350
trol group of non-irradiated subjects (4/l). In several cases where a meningioma developed after ventriculography with Thoriumdioxide’ IK-20 ionizing radiation was suggested as having an oncogenic role. From 1974 onwards some publications appeared showing how radiation with doses exceeding 23 Gy, for treatment of intracranial tumors, was later followed by development of a meningioma. A review of the literature disclosed 14 cases of “high-dose” PIMs~~~~~~~~“~‘~-‘~ which, together with our case, have been collected and analyzed (Table 1). In this group no patient referred familial or clinical signs of neurofibromatosis. Iacono et a1.4 and Anderson et al.’ have contributed two cases of multiple PIMs. The average age, at diagnosis of the meningioma, was 31 years the patients ranging from 15 to 51 years of age. The latency period from the time of radiation therapy to diagnosis of PIM varied from a minimum of 11 years to a maximum of 27, the average being 18.4. Radiation therapy was given at an average age of 12.9 years; in 10 cases in pediatric age (under 16) and in the remaining 5 cases between 17 and 29 years of age. The male/female ratio was approximately l/2. It should be noted that in this group of patients diagnosis was made at an average age of 31, significantly lower than the average age at diagnosis in patients with spontaneous meningioma21-24. Soffer et ai.‘O, reporting on 42 cases of “lowdose” PIMs, given an average latency period from radiotherapy to diagnosis of meningioma of 36.8 years and an average age of 45.5 years at diagnosis (ranging from 22 to 63). Similarly Rubinstein et aL9 in a study of 43 “low-dose” PIMs report an average latency period of 38 years and an average age of 45 at diagnosis. From that reported up to now the group of “high-dose” PIMs appears to have an unusually low average age at diagnosis with respect to spontaneous meningiomas and “low-dose” PIMs. Furthermore, the average latency period from irradiation to diagnosis in our group (18.4 years) is significantly shorter than that of the “low-dose” PIMs (37 years) reported by other authorsY,‘“. We therefore suppose that there is a correla-
Table 1. Clinical features in 15 cases of “high-dose PIMs Author
Sex.
Nor-wood et al. 1974
Primary Pathology
Radiant dose (Gy)
Lafency
10 1
36 23
25 15
Temp.pariet.convex. Temp.convex.
60+12
25
Occipital
(yrs)
M F
Optic nerve glioma Medulloblastoma
M F
Medulloblastoma (not verified) Acromegaly
15
61.1
16
Tentorial
Tanaka et al. 1975
F
Fr.oligodendroglioma
17
66.6
23
Frontal falx
Stock et al. 1975
M
Acromegaly
15
30+40
21
Parasellar
Waga & Handa, 1976
F
Craniopharingioma
23
56
12
Tentorial
Robinson 1978
F
Medulloblastoma
13
35
21
Suprasellar
Iacono et al. 1981
F
Medulloblastoma
6
50
27
Multiple mening
Spallone 1982
F F
Chromophobe adenoma Eosinophilic adenoma
25+41 40+22
22 13
Parasellar Olfactory groove
Park et al. 1983
7
Medulloblastoma
2
45
13
Convexity
Anderson & Treip, 1984
F
Medulloblastoma
2
43.4
16
Multiple mening.
Kolodny & Dluhy, 1985
M
Chromophobe adenoma
23
40+27
17
Fronto-temporal
Temporal astrocytoma
13
40
11
Frontal parasagittal
Bogdanowicz & Sachs, 1974
Domenicucci et al. 1988 M
3
29 23
tion between the doses of radiation delivered and tumor growth that justifies the division of PIMs into two groups of “high-dose” and “lowdose” respectively. Our conclusion is that the risk of inducing PIM has greatly diminished since the abolition of low-dose radiation therapy for treatment of tinea cupitis. However, this risk is extremely small even in view of the current use of high doses of radiation therapy for treatment of intracranial tumors.
Z
3
4
5
6 7
References '
Site of Meningioma
Age (yrs) X-ray th.
ALBERT NC, BAER
RE,OMRAN
SCHMIDT RL.
H,
AR,BRAUEREW,DOVE BAUMRING
R, MORRILL
DC,COHEN S, SCHULZ
x R,
Follow-up study of patients treated by X-rays
for tinea capitis. Am .I Public Health 1966; 56:2114-20. JR, TREIP cs. Radiation-induced intracranial neoplasms: a report of three possible cases. Cancer 1984; 53~426-9. BOGDANOWICZ WH, SACHS EJ. The possible role ofradiation in oncogenesis of meningioma. Surg Neurol 1974; 2:379-83. IACONO RP, APUZZ~ MU, DAVIS RL, TSAI N. Multiple meningiomas following radiation therapy for medulloblastoma. Case report. J Neurosurg 1981; 55:282-6. ANDERSON
MODAN
8, BAIDATZ
Radiation-induced 1974; 11277-9. MUNK
J, PEYSER
D, MART
H, STEINITZ
R, LEVIN
head and neck tumours.
E, GRUSZKIEWICZ
J.
Radiation
SG.
Lancet induced
intracranial meningiomas. Clin Radio1 1969; 20:90-4. NORWOODCW,KELLYDL Jr, DAVISCH, Jr, ALEXANDERE. Irradiation-induced mesodermal tumors of the central nervous system: report of two meningiomas following x-ray treatment for gliomas. Surg Neurol 1974; 2:161-4. ROBINSON RG. A second brain tumor and irradiation. J Neurol Neurosurg Psychiatry 1978; 41:1005-12.
351
4
RUBINSTEIN AB, SHALIT MN, COHEN
ML, ZANDBANK
U,
cerebral meningioma: a recognizable entity. J Neurosurg 1984; 61:966-71. REICHENTHAL
‘”
E. Radiation-induced
SOFFER D,PITTALUGA
S,FElNERM,BELLER
AJ. bltrBCra-
nial meningiomas following low-dose irradiation to the head. J Neurosurg 1983; .59:1048-53. ” SPALLONE A. Meningioma as a sequel of radiotherapy for pituitary adenoma. Neurochirurgia 1982; 25:68-72. ‘r SPALL~NE A, GAGLIARDI FM, VAGNOZZI R. Intracranial meningiomas related to external cranial irradiation. Surg Neural 1979; 12:153-9. I3 STOCK JK, GHATAK NR, OPPENHEIMER JH. Unsuspected meningioma in a patient with pituitary gigantism. Case report with autopsy findings. Metabolism 1975; 24:76775. r4 TANAKAJ,GARCIAJH,NETSKYMG,POWELLWILLIAMSJ. Late appearance of meningioma at the site of partially removed oligodendroglioma (case report). J Neurosurg 1975; 43:80-5. I5 WAGA s,HANDA H. Radiation induced meningioma: with review of the literature. Surg Neural 1976; 5:215-9. l6 KOLODNY J, DLUHY RG. Recurrent profactinoma and meningioma
following irradiationand bromocriptine
treatment. Am
352
J Med 1985; 78:153-5.
1:
PARK 'IS,HOFFMAN
HJ, HLNDRLC‘K E:B,HUMPHRLYS
BECKER LE. Medulloblastoma:
RI'.
clinical presentation and management. J Neurosurg 1983; 58:543-Z. ‘s KYLE RH, OLER A. LASSER EC, ROSOMOFI HI_ Meningioma induced by thorium dioxide. N Engl J Med 1963: 268:80-2. IY MEYERMW,POWELLHC,WACiNERM.NIwAYAMA
Maurizio Domenicucci, rante*
Marco Artico, Francesco Nucci, Maurizio Salvati and Luigi Fer-
Introduction Summary
The possibility that radiotherapy may be an oncogenic stimulus for the formation of meningiomas has been mentioned in a number of reports over the past decadesl-ls. We present a case of this kind in which a patient, originally operated on for astrocytoma, underwent radiation therapy (40 Gy) and, 11 years later, developed a meningioma in the pathway of the original irradiation. A review of the literature has revealed 14 analogous casesz-4,8*11,‘3-‘7, which, in accordance with other authors4.s, we have classified as “high-dose” post-irradiation meningiomas (PIMs), thereby distinguishing them from “lowdose” PIMs which occur after radiation therapy generally given for tinea cap&isat a dosage of less than 8 Gy. A study of “high-dose” PIMs as compared to those induced by low doses of radiation therapyl.5.Y,l",12 shows the former to have some distinctive features. Case report In December 1982 a 24-year-old male was admitted to our Section with signs of drowsiness, urinary incontinence and, according to his family, personality changes which had set in over the previous six months. He showed a marked
* Department
ofNeuroI~gi~at Sciences, Neurosurgery,
University
A case of meningioma induced by high-dose radiation therapy (40 Gy) is reported. The radiation had been given 11 years previously following operation for cerebral astrocytoma. Pertinent cases of benign meningioma occurring after radiation therapy are reviewed and analyzed. Key words: Meningioma, radiation therapy, astrocytoma. recurrent mixed tumor.
expressive dysphasia. In 1971, when he was 13, this patient had undergone a left fronto-temporal lobectomy to remove a low-grade astrocytoma located in the anterior portion of the left temporal lobe. After surgery he had received radiation therapy (for a total of 40 Gy) in the region of tumor removal. At subsequent checkups in 1972 and 1978 he was found to be in good general health. General physical examination did not reveal signs of neurofibromatosis nor was there a family history of the disease. The skin over the left fronto-temporal region was pale pink and slightly atrophic with alopecia. Blurred mentation, disorientation, expressive-dysphasia and urinary incontinence were found at neurologic examination. CT scan revealed a homogeneous, circum-
af Rome “La Sapienza”, Rome, Italy.
Address&r correspondence and reprint requests: Francesco Nucci, M.D., Universitci di Roma “La Sapienza”, Scienze Neurologiche, Neurochirurgia, Viale deN’Universitri 3OlA, 00185 Roma, Italy.
Dipartimento di
Accepted 3.8.89 Clin Neural Neurosurg 1990. Val. 92-4
349
Figure 1. CT scan after injection ot contrast medium on admission (1982) showing a homogeneously enhancing tumor on the left side of the anterior fossa attached to the falx.
scribed expansive lesion with enhancement after contrast medium intravenous injection in the left frontal region, extending slightly over the midline. There was a rim of decreased density at the posterior end of the mass (Fig. 1). Left carotid angiography showed the typical picture of a meningioma. Left frontal craniotomy disclosed a meningioma attached to the falx and infiltrating the superior longitudinal sinus. Apparently radical excision was accomplished. The histological diagnosis was syncytial meningioma . Postoperatively the patient experienced transient right hemiparesis and was discharged in good health. The patient’s conditions remained good until January 1984 when he died in another Institution from acute subdural hematoma resulting from a road accident. Discussion In the first half of this century, before the introduction of griseofulvin, treatment of tinea cupit& consisted of the Adamson-Kienbock method, namely, irradiation of the scalp with doses not exceeding 8 Gy. The long-term risks of this treatment began to appear in the literature in 1966’. In 1974 Modan et ~l.~, on analyzing 10902 cases of immigrant children in Israel during the period 1948-1951 who had undergone radiation therapy for tinea cupitis, found a statistically significant increase in the number of intracranial meningiomas with respect to an analogous con350
trol group of non-irradiated subjects (4/l). In several cases where a meningioma developed after ventriculography with Thoriumdioxide’ IK-20 ionizing radiation was suggested as having an oncogenic role. From 1974 onwards some publications appeared showing how radiation with doses exceeding 23 Gy, for treatment of intracranial tumors, was later followed by development of a meningioma. A review of the literature disclosed 14 cases of “high-dose” PIMs~~~~~~~~“~‘~-‘~ which, together with our case, have been collected and analyzed (Table 1). In this group no patient referred familial or clinical signs of neurofibromatosis. Iacono et a1.4 and Anderson et al.’ have contributed two cases of multiple PIMs. The average age, at diagnosis of the meningioma, was 31 years the patients ranging from 15 to 51 years of age. The latency period from the time of radiation therapy to diagnosis of PIM varied from a minimum of 11 years to a maximum of 27, the average being 18.4. Radiation therapy was given at an average age of 12.9 years; in 10 cases in pediatric age (under 16) and in the remaining 5 cases between 17 and 29 years of age. The male/female ratio was approximately l/2. It should be noted that in this group of patients diagnosis was made at an average age of 31, significantly lower than the average age at diagnosis in patients with spontaneous meningioma21-24. Soffer et ai.‘O, reporting on 42 cases of “lowdose” PIMs, given an average latency period from radiotherapy to diagnosis of meningioma of 36.8 years and an average age of 45.5 years at diagnosis (ranging from 22 to 63). Similarly Rubinstein et aL9 in a study of 43 “low-dose” PIMs report an average latency period of 38 years and an average age of 45 at diagnosis. From that reported up to now the group of “high-dose” PIMs appears to have an unusually low average age at diagnosis with respect to spontaneous meningiomas and “low-dose” PIMs. Furthermore, the average latency period from irradiation to diagnosis in our group (18.4 years) is significantly shorter than that of the “low-dose” PIMs (37 years) reported by other authorsY,‘“. We therefore suppose that there is a correla-
Table 1. Clinical features in 15 cases of “high-dose PIMs Author
Sex.
Nor-wood et al. 1974
Primary Pathology
Radiant dose (Gy)
Lafency
10 1
36 23
25 15
Temp.pariet.convex. Temp.convex.
60+12
25
Occipital
(yrs)
M F
Optic nerve glioma Medulloblastoma
M F
Medulloblastoma (not verified) Acromegaly
15
61.1
16
Tentorial
Tanaka et al. 1975
F
Fr.oligodendroglioma
17
66.6
23
Frontal falx
Stock et al. 1975
M
Acromegaly
15
30+40
21
Parasellar
Waga & Handa, 1976
F
Craniopharingioma
23
56
12
Tentorial
Robinson 1978
F
Medulloblastoma
13
35
21
Suprasellar
Iacono et al. 1981
F
Medulloblastoma
6
50
27
Multiple mening
Spallone 1982
F F
Chromophobe adenoma Eosinophilic adenoma
25+41 40+22
22 13
Parasellar Olfactory groove
Park et al. 1983
7
Medulloblastoma
2
45
13
Convexity
Anderson & Treip, 1984
F
Medulloblastoma
2
43.4
16
Multiple mening.
Kolodny & Dluhy, 1985
M
Chromophobe adenoma
23
40+27
17
Fronto-temporal
Temporal astrocytoma
13
40
11
Frontal parasagittal
Bogdanowicz & Sachs, 1974
Domenicucci et al. 1988 M
3
29 23
tion between the doses of radiation delivered and tumor growth that justifies the division of PIMs into two groups of “high-dose” and “lowdose” respectively. Our conclusion is that the risk of inducing PIM has greatly diminished since the abolition of low-dose radiation therapy for treatment of tinea cupitis. However, this risk is extremely small even in view of the current use of high doses of radiation therapy for treatment of intracranial tumors.
Z
3
4
5
6 7
References '
Site of Meningioma
Age (yrs) X-ray th.
ALBERT NC, BAER
RE,OMRAN
SCHMIDT RL.
H,
AR,BRAUEREW,DOVE BAUMRING
R, MORRILL
DC,COHEN S, SCHULZ
x R,
Follow-up study of patients treated by X-rays
for tinea capitis. Am .I Public Health 1966; 56:2114-20. JR, TREIP cs. Radiation-induced intracranial neoplasms: a report of three possible cases. Cancer 1984; 53~426-9. BOGDANOWICZ WH, SACHS EJ. The possible role ofradiation in oncogenesis of meningioma. Surg Neurol 1974; 2:379-83. IACONO RP, APUZZ~ MU, DAVIS RL, TSAI N. Multiple meningiomas following radiation therapy for medulloblastoma. Case report. J Neurosurg 1981; 55:282-6. ANDERSON
MODAN
8, BAIDATZ
Radiation-induced 1974; 11277-9. MUNK
J, PEYSER
D, MART
H, STEINITZ
R, LEVIN
head and neck tumours.
E, GRUSZKIEWICZ
J.
Radiation
SG.
Lancet induced
intracranial meningiomas. Clin Radio1 1969; 20:90-4. NORWOODCW,KELLYDL Jr, DAVISCH, Jr, ALEXANDERE. Irradiation-induced mesodermal tumors of the central nervous system: report of two meningiomas following x-ray treatment for gliomas. Surg Neurol 1974; 2:161-4. ROBINSON RG. A second brain tumor and irradiation. J Neurol Neurosurg Psychiatry 1978; 41:1005-12.
351
4
RUBINSTEIN AB, SHALIT MN, COHEN
ML, ZANDBANK
U,
cerebral meningioma: a recognizable entity. J Neurosurg 1984; 61:966-71. REICHENTHAL
‘”
E. Radiation-induced
SOFFER D,PITTALUGA
S,FElNERM,BELLER
AJ. bltrBCra-
nial meningiomas following low-dose irradiation to the head. J Neurosurg 1983; .59:1048-53. ” SPALLONE A. Meningioma as a sequel of radiotherapy for pituitary adenoma. Neurochirurgia 1982; 25:68-72. ‘r SPALL~NE A, GAGLIARDI FM, VAGNOZZI R. Intracranial meningiomas related to external cranial irradiation. Surg Neural 1979; 12:153-9. I3 STOCK JK, GHATAK NR, OPPENHEIMER JH. Unsuspected meningioma in a patient with pituitary gigantism. Case report with autopsy findings. Metabolism 1975; 24:76775. r4 TANAKAJ,GARCIAJH,NETSKYMG,POWELLWILLIAMSJ. Late appearance of meningioma at the site of partially removed oligodendroglioma (case report). J Neurosurg 1975; 43:80-5. I5 WAGA s,HANDA H. Radiation induced meningioma: with review of the literature. Surg Neural 1976; 5:215-9. l6 KOLODNY J, DLUHY RG. Recurrent profactinoma and meningioma
following irradiationand bromocriptine
treatment. Am
352
J Med 1985; 78:153-5.
1:
PARK 'IS,HOFFMAN
HJ, HLNDRLC‘K E:B,HUMPHRLYS
BECKER LE. Medulloblastoma:
RI'.
clinical presentation and management. J Neurosurg 1983; 58:543-Z. ‘s KYLE RH, OLER A. LASSER EC, ROSOMOFI HI_ Meningioma induced by thorium dioxide. N Engl J Med 1963: 268:80-2. IY MEYERMW,POWELLHC,WACiNERM.NIwAYAMA
