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Multifocal enhancing magnetic resonance imaging lesions following cranial irradiation.

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Muldocal Enhancing Magnetic Resonance
Imaging Lesions Following Cranial Irradiation
Kendra Peterson, MD," H. Brent Clark, MD, PhD,"? Walter A. Hall, MD,S and Charles L. Truwit, MD"B
Radiation necrosis is a delayed complication of cranial irradiation, typically presenting as a single intracerebral mass
that is radiographically indistinguishable from recurrent tumor. We describe 6 patients with a distinct radiographic
syndrome of multifocal enhancing lesions on magnetic resonance images, and their variable clinical courses: some
fluctuating, some spontaneously resolving, and some demonstrating fulminant progression to frank necrosis.
Peterson K, Clark HB, Hall WA, Truwit CL. Multifocal enhancing magnetic resonance
imaging lesions following cranial irradiation. Ann Neurol 1995;38:237-244
Radiation necrosis is a delayed complication of cranial
irradiation. It generally presents clinically as a single
ictracerebral mass resulting in focal neurological deficits or seizures [1-9}. Computed tomography (CT) or
magnetic resonance imaging (MRI) usually demonstrates an irregular, enhancing mass that may have a
necrotic center or hemorrhagic component, and is indistinguishable radiologically from a recurrent neoplasm [lo- 141. W e describe a distinct radiographic
syndrome of multifocal enhancing lesions on MRI developing within the fields of prior cranial irradiation
administered to primary brain tumors, and the clinical
course of 6 patients with these MRI findings.
Materials and Methods
We reviewed the clinical histories, radiographic studies, and
histopathology of 6 patients with multifocal enhancing lesions
on MRI following cranial irradiation. Five were among the
approximately 200 patients with primary brain tumors seen
in the Neuro-Oncology Clinic at the University of Minnesota
Hospital and Clinic from 1992 to 1994; one was seen at the
Veterans Administration Medical Center in Minneapolis.
The results are summarized in the Table, and the case
histories are detailed below. There were 4 men and 2
women, ages 26 to 48 years. All received local-field
external cranial irradiation for the treatment of primary
brain tumors: one astrocytoma, three anaplastic astrocytomas, and two glioblastoma multiforme. Five of the
patients received a total dose of 6,000 to 6,475 cGy
in daily (Monday-Friday [M-F)) fractions of 175
to 200 cGy; the sixth received 7,200 cGy delivered
by twice-daily (M-F) hyperfractionation in 120-cGy
From the Departments of 'Neurology, thborarory Medicine and
Experimental Pathology, $Neurosurgery, and §Radiology, University of Minnesota School of Medicine, Minneapolis, MN.
doses. None of the patients had underlying vasculopathy or other concurrent illness, and none had acute
neurological complications of the radiation therapy
while undergoing treatment. Five patients received
chemotherapy as part of the treatment regimen: 3 received carmustine (BCNU); 1, BCNU and etoposide
(VP-l6)/vincristine/procarbazine;and 1, BCNU, procarbazine/lomustine (CCNU)/vincristine, and intravenous methotrexate.
The MRI abnormalities appeared 8 to 31 months
after completion of radiotherapy. The lesions were
multifocal and dispersed throughout both gray and
white matter within the treatment fields. Some were in
a periventricular location. Some were punctate, while
others were larger with significant surrounding edema
and mass effect. The lesions enhanced after intravenous administration of contrast material, some in a
ringlike pattern. Many of the lesions changed in appearance over time, waxing and waning on serial imaging studies. In 2 patients the lesions resolved completely over the course of 1 year, in 3 the lesions
remained present but stabilized, and in 1 the lesions
developed into frank necrosis and led to the patient's
One of the 6 patients presented with focal neurological symptoms that prompted MRI. Five patients were
asymptomatic at the time the lesions were detected
on routine follow-up scans; 2 remained asymptomatic
while the others subsequently developed symptoms
and signs referable to the location of the MRI lesions.
One patient developed panhypopituitarism as an associated delayed complication of radiotherapy.
The 2 asymptomatic patients were not treated with
corticosteroids or other medications; in 1 the lesions
Received Feb 24, 1995, and in revised form Apr 21. Accepted for
publication Apr 25, 1995.
Address correspondence to Dr Peterson, Box 275, UMHC, 420
Delaware Street SE, Minneapolis, M N 55455.
Copyright 0 1995 by the American Neurological Association
Srrmniap of Results
Dose1Frac tion
C hem0 therapy
6.4 7 51 17 5
31 mo
7,2001 120
8 mo
13 mo
6,1201 180
14 mo
Cognitive decline, hemiparesis
Initial: none
Later: aphasia
11 mo
17 mo
Initial: none
Later: aphasia
Initial: none
Later: hemiparesis, coma
‘Time interval berween completion of radiotherapy and development of MRI abnormalities.
CS = corticosreroid trearment; BCNU = carmustine; VVP = etoposide, vincristine, procarbazine; PCV
Waxlwane; complete
resolution in 12 mo
Stable for 6 mo
Waxlwane; stabilize
with deficits in 24
Progression then resolution in 12 mo;
died of recurrent
Progression then stabilize in 24 mo
Fulminant progression, death
procarbazine,lomustine, vincristine;
= rnethotrexatc.
resolved spontaneously over 1 year, while in the other
they stabilized over 6 months. All 4 patients with
symptomatic lesions received corticosteroids; t h e outc o m e in these patients was variable and it is uncertain
whether or not corticosteroids influenced t h e radiographic o r clinical course.
Two of the patients in this series died, 1 of recurrent
tumor and 1 of fulminant radiation necrosis. Four patients were alive 14 to 50 months after tumor diagnosis, 2 asymptomatic and 2 with residual neurological
deficits resulting from the treatment-related nervous
system injury.
Biopsy of a small lesion at an early stage in an initially asymptomatic patient (Patient 6) revealed perivascular lyrnphocytic infiltrate and gliosis, though n o frank
necrosis was observed in this specimen. Five months
later at autopsy, extensive radiation necrosis was observed (Figs 1, 2). In the 3 o t h e r patients in whom
biopsy of large, symptomatic lesions was performed,
the usual features of radiation necrosis were observed.
Patzetzt 1
A 35-year-old man presented with a seizure and was diagnosed with a left frontal astrocytoma detected by MRI in
January 1390. He underwent surgical resection followed by
local-field external irradiation in 37 daily (M-F) fractions of
175 cGp each through bilateral opposed ports, to a total dose
of 6,475 cGy. He remained neurologically normal.
Thirty-one months after radiotherapy, follow-up MRI revealed multifocal punctate areas of enhancement in both
frontal lobes, within the radiation fields (Figs 3A, 3B). T2weighted images ( n o t shown) revealed diffuse white matter
hyperintensity in the treated fields. Over the next several
months the enhancing lesions waxed and waned, with some
lesions resolving and other new lesions appearing. The pa-
238 Annals of Neurology
Vol 38 No 2 August 1995
tient developed weight loss, generalized fatigue, and decreased motivation, and was found to have panhypopituitarism. His symptoms were alleviated by hormone replacement.
The patient was followed with serial MRIs. H e did not
undergo biopsy or receive other treatment. The MRIdetected lesions gradually resolved completely over 1 year
from the time they were first noted (Figs 3C, 3D). H e remained neurologically normal when last examined in January
Patient 2
In December 1993 a 32-year-old man suffered minor head
trauma with a brief loss of consciousness. He underwent
MRI, which incidentally revealed a left temporal nonenhancing mass. The results of a neurological examination were
normal. He underwent partial resection of the tumor, with
a histological diagnosis of anaplastic astrocytoma.
The patient received local-field external hyperfractionated
irradiation, 120-cGy fractions twice daily (M-F). A dose of
5,760 cGy in 48 fractions was delivered to the tumor and 3
cm surrounding the tissue, and a “boost” of 1,440 cGy in 12
fractions was delivered to the tumor and 2 cm surrounding
the tissue, to a total dose of 7,200 cGy. He complained of
bilateral otitis externa and developed mastoiditis and serous
otitis media requiring tube placement, but otherwise tolerated the radiotherapy without difficulty. Over the next 8
months he also received four courses of intravenous BCNU
(200 mg/m2/dose every 8 weeks, first course concurrent with
He remained well and continued working full-time. A
follow-up MRI in August 1994 showed no evidence of tumor
recurrence at the primary site. However, the scan revealed
multiple enhancing abnormalities in the posterior fossa, appearing to be both meningeal based and intraparenchymal
(Figs 4A, 4B). The lesions were within the treatment fields
(Fig 4C). Analysis of cerebrospinal fluid (CSF) obtained by
both lumbar and cervical puncture revealed entirely normal
findings, with no evidence of malignant cells.
He was followed clinically with serial scans, and no biopsy
or treatment. When last seen in February 1995 the appearance of his scan was unchanged. He was asymptomatic, and
had mildly increased lower-extremity reflexes without ataxia,
gait disorder, or other neurological abnormalities.
Fig 1 . Gross appearance ofthe brain of Patient 6 at the time of
autopsy. There is extensive necrosis in the deep hemispheric
white matter bilaterally with expansion of the corpus cnllosum.
No tumor was present in these areas. There is a defect in the
right lateral temporal lobe from the original resection. Radiation
necrosis was not present in this area.
Fig 2. Photomicrograph of radiation necrosis in [he hemispheric
white matter in Patient 6. There is coagulatrve necrosis of the
uhite matter (lower right) andjibrinohyaline change in an adjacent cerebral zjeuel. ( X I70 before 46% rednction.t
Patient .3
In August 1991 a 45-year-old woman developed weakness
in the distal aspect of the right leg. MRI revealed a nonenhancing left frontal parasagittal mass. She underwent partial
resection, and histopathology revealed anaplastic astrocytoma. She received focal cranial irradiation, 30 daily (M-F)
fractions of 200 cGy each to a total dose of 6,000 cGy
through right and left lateral fields. She also received six
courses of BCNU chemotherapy (the first concurrent with
radiotherapy, other details not known). She had residual right
lower-extremity weakness but was otherwise neurologically
Thirteen months following radiotherapy a follow-up MRI
revealed multifocal areas of abnormal enhancement, all
within the treated fields (Figs 5A, 5B). T2-weighted images
revealed increased signal abnormalities corresponding to the
enhancing lesions (Figs 5C, 5D). She was noted to have mild
global cognitive dysfunction and suffered increasing seizures.
Over the next several months the lesions enlarged and new
lesions appeared. Over the following year the MRI abnormalities waxed and waned, with some lesions improving and
other new ones appearing. The patient had progressive cognitive dysfunction and developed left hemiparesis, mostly affecting her arm. Biopsy of a large right frontal lesion revealed
radiation necrosis. The arm weakness improved with corticosteroids. However, she was unable to care for herself and
was placed in a nursing home.
The appearance of serial MRIs stabilized, with multiple
enhancing lesions remaining. When last seen in February
1995, the corticosteroids had been tapered and discontinued.
She had moderate global cognitive dysfunction, particularly
affecting her memory. She had mild bilateral long tract signs
and was wheelchair dependent due to residual weakness in
her lower extremities.
Patient 4
A 26-year-old woman presented with a seizure and in June
1991 was found by MRI to have a left frontal mass. An
anaplastic astrocytoma was diagnosed by biopsy. She received
partial brain irradiation in 34 daily (M-F) fractions of 180
cGy to a total dose of 6,120 cGy through anteroposterior
fields. She also received four courses of BCNU chemotherapy (200 mglm’ldose every 8 weeks, the first concurrent
with radiotherapy), which because of pulmonary toxicity was
changed to a combination regimen of VP-16 (100 mg/m’/
day x 3 days), vincristine ( 1.4 mg/m’), and procarbazine
(100 mg orally/day x 7 days) (VVP) every 28 days for two
courses. She was neurologically normal and continued to
work full-time.
Fourteen months after completing radiotherapy the patient
developed multiple punctate areas of enhancement throughout the left hemisphere, all within the treated fields. F-18-
Peterson et al: MRI Lesions after Cranial RT
F i g 3 , Patient 1 , (A.
B ) Contra~t-enhancedT1-uieighted images demonstrate miiltifocaal pirnctate enhancing lesions that dewloped J I months after trcatnrent of a left frontal aJtroqtowa.
(C. D , Folfow-up contrast-enharued images at 1 year show rompletr resolution of the nzultifocal images. Note mild atrophy as
240 Annals of Neurology
Vol 38 N O 2
August 1995
fluorodeoxyglucose positron emission tomography (not
shown) revealed hypometabolism throughout the involved
hemisphere. The patient was asymptomatic. Over several
months the lesions evolved radiographically, and a large confluent left frontal enhancing mass developed. The patient
developed language dysfunction characterized by wordfinding difficulty and stuttering. Biopsy revealed radiation
The large left frontal mass and the smaller punctate lesions
remained for about 6 months and then gradually resolved,
so that they were no longer apparent on scans about 1 year
Fig 4. Patient 2. (A, B ) Contrast-enhanced TI -weighted images shoul multifocal enhancing abnormalities that developed 8
months after cotnpletion of radiation. Follow-zip studies at 2. 4,
and 6 months after completion of radiation (not shouwj shwed
no change in the pattern of enhancement and ubere ez~idencethat
the abnormalities did not represent recurrent disseminated tumor. (C) This treatment planning film shows the target areas
for the treatment (small arrow) and “boost”(large arrow), and
demonstrates that the posterior fossa lesions icere ioithin the
treatment field but not at the center of the target tiolume.
later. The patient’s symptoms improved with corticosteroid
therapy. Unfortunately, the patient developed biopsy-proved
recurrent glioblastoma multiforme, posterior to the area of
necrosis, which was unresponsive to additional chemotherapy. She died of progressive tumor in February 1994.
Patient 5
A 45-year-old man was diagnosed in September 1992 with a
left frontal glioblastoma multiforme. He underwent resection
followed by focal irradiation in 30 daily (M-F) fractions of
200 cGy each, to a total dose of 6,000 cGy through right and
left lateral fields. He also received one course of combination
procarbazine/CCNU/vincristine (PCV) (details not known),
one course of BCNU (details not known), three courses of
intravenous methotrexate (6,000mg/dose), and an additional
course of BCNU (200 mg/m2).
Eleven months after treatment the patient was asymptomatic. There was no evidence of recurrent tumor at the primary
site on follow-up MRI. but new multifocal punctate areas
of enhancement developed in both hemispheres within the
treatment fields. Because of the proximity of these lesions
to the ventricular system, he underwent lumbar puncture and
analysis of the CSF revealed 7 white blood cells/mmi, protein
concentration of 165 mg/dl, and no malignant cells.
The patient developed mild aphasia over the next several
months. The left frontal abnormality enlarged, while others
remained stable or improved. Progressive aphasia prompted
surgical debulking of the large left frontal lesion. The histopathological diagnosis was radiation necrosis. After surgical
debulking the patient’s language improved but did not return
to normal. Right hemispheric abnormalities persisted, though
Peterson et al: MRI Lesions after Cranial RT
Fig 5. Patient 3. (A, B ) Contrasi-enhanced TI-weighted images demonstrate multifocal enhancing lesions that developed I 3
months after the completion of radiotherapy. The larger, right
frontal, ring-enhancing lesion waJ confirmed by biopsy to be radionecroszs. (C. D ) T2-weighted images demonstratefocal increased signal abnormalities corresponding to the enhancing lesi0n.c. as well as more diffuse white matter abnormalities
characteristic of the white matter changes frequently obsewed
after radiothevapy.
Annals of Neurology Vol 38 No 2
August 1795
they remained asymptomatic. When last seen in February
1995, the patient was mildly aphasic, which prevented him
from working, but had no long tract signs and was living
Patient 6
In July 1992 a 48-year-old man presented with headaches
and was found to have a large enhancing right temporal mass.
He underwent gross total surgical resection with a histopathological diagnosis of glioblastoma multiforme. He was treated
with local-field radiotherapy. A dose of 4,600 cGy in 23
fractions of 200 cGy was delivered to the tumor and 3 cm
surrounding the tissue, and a “boost” of 1,400 cGy in 7
fractions of 200 cGy each was delivered to the tumor and 2
cm surrounding the tissue, to a total dose of 6,000 cGy
through right and left lateral fields. He also received intravenous BCNU (80 mg/m’/day x 3 days, every 8 weeks x 6,
first course concurrent with radiotherapy). He was neurologically normal except for mild memory deficits.
Seventeen months after completion of radiotherapy the
patient had no new symptoms. The follow-up MRI showed
no evidence of recurrence at the primary site. However,
there were multiple areas of abnormal enhancement seen
throughout the radiation fields, some of which appeared to be
ringlike. Biopsy of a right frontal lesion revealed perivascular
lymphocytic infiltration and gliosis, without evidence of malignancy.
The patient’s course was one of fulminant progression,
both clinically and radiographically. MRIs showed progressive enlargement of the enhancing lesions. He became stuporous, with bilateral long tract signs and refractory seizures.
He died in June 1994. At autopsy the brain contained widespread radiation necrosis with only focal evidence of residual
or recurrent tumor in the original operative site in the temporal lobe.
Radiation necrosis is one of the late delayed complications of cranial irradiation, most commonly developing
1 to 3 years after the completion of treatment. Its incidence is determined by total radiation dose and fraction size, but overall it is described as an uncommon
complication, occurring in about 5% of patients who
receive a total dose of more than 4,500 cGy [2]. Its
typical CT appearance is that of a single, hypodense
mass, primarily in the white matter, which may have
areas of hemorrhage, central necrosis, o r calcification,
and irregular enhancement with contrast agents [lo131. MRI similarly reveals a hypointense, primarily
white matter mass on T1-weighted images that enhances with gadolinium and that appears hyperintense
with surrounding edema o n T2-weighted images [ 11,
141. Following cranial irradiation, another late delayed
radiographic feature is diffuse white matter change o n
C T or MRI, which is frequently seen in conjunction
with focal radiation necrosis and which may coincide
clinically with radiation-induced dementia [I 1- 141.
Radiation necrosis frequently occurs at the site of
the original treated tumor, and cannot be distinguished
radiographically from recurrent tumor. The clinical
presentation of radiation necrosis is also indistinguishable from that of recurrent tumor, presenting with focal neurological deficits o r seizures. Although there are
reports of symptomatic improvement with surgical resection, corticosteroids [b},or anticoagulation [ 153, radiation necrosis is generally an irreversible process.
T h e inability to distinguish radiation necrosis from
tumor clinically and radiographically necessitates biopsy in many instances. T h e histological features of
radiation necrosis have been well described and consist
of a hypocellular lesion often at the gray-white junction, with fibrin exudate and fibrinoid necrosis of small
blood vessels. T h e predominant factor in its pathogenesis is thought to be related to endothelial injury, although direct glial damage o r immunological mechanisms have been suggested to play a contributing role
[ 16-
T h e clinical and radiological syndrome described in
the 6 patients here occurred between 8 and 3 1 months
following the completion of cranial irradiation, in the
same time interval as typical radiation necrosis. T h e
MRI appearance of the lesions described, however, is
distinct from the classic description of radiation necrosis. An analogous C T appearance of this unusual phenomenon was described previously by Safdari and coauthors [ZO]. T h e radiographic features may represent
one stage in a series of events that may be reversible
and resolve entirely, or may ultimately lead to frank
radiation necrosis. In our patients the initial lesions
were multifocal, distributed throughout both gray and
white matter, and often punctate or small ( < I cm in
diameter). T h e lesions were not located at the site of
the primary tumor, and although they were all within
the radiation fields they were not at the site of the
highest calculated radiation dose. T h e appearance was
indistinguishable from recurrent disseminated tumor.
While some lesions evolved into the more typical mass
lesion of necrosis, others resolved entirely. There was
also a spectrum of clinical findings in these patients,
from those who were asymptomatic to others who developed progressive focal neurological symptoms o r
who died.
Biopsy of a single small asymptomatic lesion was
performed and examination of the specimen revealed
gliosis and perivascular lymphocytic infiltrate. Histological examination of large, symptomatic lesions demonstrated the characteristic features of radiation necrosis. T h e pathogenesis of the initial waxing and waning
MRI lesions is unknown, and precise histological definition is hindered by their lack of symptoms and small
size, which often makes biopsy or resection unwarranted or not feasible. W e suspect that they represent
an early, sometimes reversible stage of radiation injury
to the brain. T h e contribution, if any, of chemotherapy
Peterson et
MRI Lesions after Cranial RT
to the development of these MRI abnormalities is unknown but is not essential; 1 of our patients received
no chemotherapy.
When one encounters a patient with these multifocal
MRI abnormalities following cranial irradiation, the
possibility of radiation injury rather than recurrent tumor must be considered. Positron emission tomography or single-photon emission computed tomography
studies may support a diagnosis of either radiation necrosis or recurrent tumor [21-24]. We found that in
the asymptomatic patients a conservative course of observation and serial scans was justified to avoid an unnecessary brain biopsy. In some of these patients the
lesions resolved or stabilized spontaneously. In the patients with symptomatic lesions, biopsy is important to
distinguish radiation injury from recurrent tumor, and
particularly to avoid inappropriate antineoplastic treatment. The role of anticoagulants, corticosteroids, or
other modalities in the trearment of such MFU lesions
is unknown.
The authors are grateful to D r Richard W. Price for his helpful
review of the manuscript.
Presented in part at the American Neurological Association annual
meeting, San Francisco, CA, October 10- 12, 1994.
1. Delattre JY, Fuks 2, Krol G , ‘et al. Cerebral necrosis following
neutron radiation of an extracranial tumor. J Neurooncol 1988;
2. Rottenberg DA. Acute and chronic effects of radiation on the
nervous system. In: Rottenbeg DA, ed. Neurological complications of cancer treatment. Newton, MA: ButtenvorthHeinemann, 199 1:3-1?
3. Marsumura H, Ross ER. Delayed cerebral radionecrosis following treatment of carcinoma of the scalp: clinicopathologic and
ultrastructural study. Surg Neurol 1979;12:193-204
4. Babu R, Huang PP, Epstein F, et al. Late radionecrosis of the
brain: case report. J Neurooncol 1993;1?:37-42
5. Morris JGL, Grarran-Smith P, Panegyres PK, et al. Delayed
cerebral radiation nrcrosis. Q J Med 1994;87:119-129
6. Gutin PH. Treatment of radiation necrosis of the brain. In:
Gutin PH, Leibel SA, Sheline GE, eds. Radiation injury to the
nervous system. New York: Raven, 1901:27 1-282
7. Sheline GE. Irradiation injury of the human brain: a review of
clinical experience. In: Gilbert HA, Kagan AR, eds. Radiation
damage to the nervous system. A delayed therapeutic hazard.
New York: Raven, 1980:39-58
8. Lampert PW, Davis RL. Delayed effects of radiation on the
Annals of Neurology
Vol 38
No 2
August 1995
human central nervous system. “Early” and “late” delayed reactions. Neurology 1964;14:912-917
9. Martins AN, Johnston 1.5, Henry JM. er al. Delayed radiation
necrosis of the brain. J Neurosurg 1977;47:336-345
10. Kmgsley DPE, Kendall BE. CT of the adverse effects of therapeutic radiation of the central nervous system. AJNR 1981;2:
11. Batnitzky S, Halleran WJ, McMillan J H , et al. Radiologic manifestations of delayed radiation necrosis of the brain. Acta Radiol
Suppl (Stockh) 1986;.369:231-234
12. Valk PE, Dillon WP. Diagnostic imaging of central nervous system radiation injury. In: Gutin PH. Leibel SA. Sheline GE,
eds. Radiation injury to the nervous system. New York: Raven,
1991:2 11-238
13. Brismar J. Robertson G H , Davis KR. Radiation necrosis of the
brain. Neuroradiological considerations with computed romography. Neuroradiology 1976;12:109-113
14. Curran WJ. Hecht-Leavit C, Schur L, et al. Magnetic resonance
imaging of cranial radiation lesions. lnr J Radiat Cncol Biol Phys
1987;13: 1003- 1098
I S . Glanrz MJ, Burger PC, Friedman AH, et al. Treatment ofradiarion-induced nervous system injury with heparin and warfarin.
Neurology 1994;44:2020-2026
16. Burger PC, Boyko OB. The pathology of central nervous system radiation injury. In: Gutin PH, Leibel SA, Sheline GE,
eds. Radiation injury to the nervous system. New York: Raven,
1991: 19 1-2 10
17. Llena JF, Cespedes G. Hirano A, er al. Vascular alterations in
delayed radiation necrosis of the brain. An electron microscopical study. Arch Pathol Lab Med 1976;100:531-534
18. Phillips TL. Early and late effects of radiation on normal tissues.
In: Gutin PH, L i b e l SA, Sheline GE, eds. Radiation injury to
the nervous system. New York: Raven, 1991:37-55
10. Yarnaguchi N , Yamashima T, Yamashita J. A histological and
tluw cytometric study of dog brain endothelial cell inpries in
delayed radiation necrosis. J Neurosurg 1991;74.625-632
20. Safdari H , Boluix B, Gros C. Multifocal brain radionecrosis
masquerading as tumor dissemination. Surg Neurol 1984;2 I :
21. DeChiro G , Oldfield E, Wright DC, et al. Cerebral necrosis
after radiotherapy and/or inrraarterial chemotherapy for brain
tumors; PET and neuroparhological studies. Am J Radiol 1988;
22. Patronas NJ, DiChiro G , Brooks RP, et al. Progress: [‘,‘F]fluorodeoxyglucose and positron emission tomography in the evaluation of radiation necrosis of the brain. Radiology 1982;144:
23. Doyle WK, Budinger TF, Valk PE, et al. Differentiation of
cerebral radiation necrosis from tumor recurrence by F- 18-FDG
and Rb-82 positron emission tomography. J Comput Assist
Tomogr 1987;11:563-570
24. Schwartz RB, Carvalho PA, Alexander E, et al. Radiation necrosis vs high-grade recurrent glioma: differenriation by using dual
isotope SPECT with ”’TI and ’““Tc-HMPAO. AJNR 1992;12:
1187-1 192
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multifocal, cranial, lesions, following, magnetic, imagine, enhancing, resonance, irradiation
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