Radiation Necrosis



Radiation necrosis, a focal structural lesion that usually occurs at the original tumor site, is a potential long-term central nervous system (CNS) complication of radiotherapy or radiosurgery. Edema and the presence of tumor render the CNS parenchyma in the tumor bed more susceptible to radiation necrosis. Radiation necrosis can occur when radiotherapy is used to treat primary CNS tumors, metastatic disease, or head and neck malignancies. It can occur secondary to any form of radiotherapy modality or regimen.

In the clinical situation of a recurrent astrocytoma (postradiation therapy), radiation necrosis presents a diagnostic dilemma. Astrocytic tumors can mutate to the more malignant glioblastoma multiforme. Glioblastoma multiforme's hallmark histology of pseudopalisading necrosis makes it difficult to differentiate radiation necrosis from recurrent astrocytoma using MRI. See Medscape Reference articles Neurologic Manifestations of Glioblastoma Multiforme and Low-Grade Astrocytoma.

Therapeutic effects of radiotherapy

Radiation creates ionized oxygen species that react with cellular DNA. Tumor cells have less ability than healthy cells for DNA repair. Thus, between fractionation doses, healthy cells have a greater probability than tumor cells of repairing themselves. With each subsequent mitosis, the cumulative effects of unrepaired DNA result in apoptosis (cell death) of these tumor cells.

Central nervous system syndromes secondary to radiotherapy

Radiation necrosis is part of a series of clinical syndromes related to CNS complications of radiotherapy. These syndromes occur in a distinct chronologic order and have characteristic pathophysiology. While the term radiation necrosis is used to refer to radiation injury, pathology is not limited to necrosis and a spectrum of injury patterns may occur.

Acute encephalopathy occurs during and up to 1 month after radiotherapy. This acute encephalopathy is due to disruption of the blood-brain barrier.

Early delayed complications occur 1-4 months after radiotherapy. Early delayed complications are caused by white matter injury characterized by demyelination and vasogenic edema. Early delayed changes may produce a somnolence syndrome in children, reappearance of the initial tumor's symptomatology, temporary decline in long-term memory, and encephalopathy. In early delayed complications, patients may have increased edema and contrast enhancement on MRI (both symptomatic and asymptomatic) that may resolve spontaneously over a few months. Both the acute and early delayed complications are steroid responsive.

Treatment-induced leukoencephalopathy is the leading toxicity after primary CNS lymphoma and may be seen both early[1] and as a delayed consequence of treatment. It may be seen in greater than 90% of patients older than 60 years who have been successfully treated with combination chemotherapy and whole-brain radiation. A relationship between increased blood-brain barrier permeability and radiation therapy has been posited to contribute to this leukoencephalopathy and to methotrexate-induced vasculopathy. This also may be an etiology for the changes seen with radiation necrosis.

Radiation necrosis and diffuse cerebral atrophy are considered long-term complications of radiotherapy that occur from months to decades after radiation treatment. As opposed to the focal nature of radiation necrosis, diffuse cerebral atrophy is characterized by bihemispheric sulci enlargement, brain atrophy, and ventriculomegaly. Diffuse cerebral atrophy clinically is associated with cognitive decline, personality changes, and gait disturbances.

Recent studies

Liu et al reported that in children with pontine gliomas, a nearly always fatal brain tumor, bevacizumab may provide both therapeutic benefit and diagnostic information. They note that although radiation therapy can provide some palliation in such patients, it can also result in radiation necrosis and neurologic decline. In a study of 4 children, 3 children showed significant clinical improvement with bevacizumab and were able to discontinue steroid use, which, according to the authors, can have numerous side effects that significantly compromise a patient's quality of life. In 1 child who continued to decline on bevacizumab, it was later determined that the patient had disease progression, not radiation necrosis. In all cases, according to the investigators, bevacizumab was well tolerated.[2]

Barajas et al attempted, in a study of 57 patients, to determine whether T2-weighted dynamic susceptibility-weighted contrast material-enhanced (DSC) MRI can differentiate radiation-therapy-induced necrosis from glioblastoma multiforme. They found that mean, maximum, and minimum relative peak height and relative cerebral blood volume were significantly higher in patients with recurrent glioblastoma multiforme than in patients with radiation necrosis. In addition, they determined that mean, maximum, and minimum relative percentage of signal intensity recovery values were significantly lower in patients with recurrent glioblastoma multiforme than in patients with radiation necrosis.[3]

Levin et al designed a class 1 double-blind study to compare the treatment of cerebral radiation necrosis with bevacizumab or placebo in 14 patients. Their protocol use, clinical, imaging, and other measures clearly demonstrated a beneficial effect of bevacizumab. They used 4 cycles at 3-week intervals. The dose was 7.5 mg/kg. Theoretically, bevacizumab blocks the effect of vascular endothelial growth factor (VGEF) and decreases vascular permeability, a critical component of radiation-mediated injury in the brain. The long-term benefit is not known. One of the study patients required an additional dose.[4]

Plimpton et al used MRI to retrospectively study 101 children with solid brain tumors. Median follow-up for all patients was 13 months (range 3-51 mo). They concluded that findings in pediatric patients treated with radiotherapy for solid brain tumor suggests children may have an increased likelihood to develop radiation necrosis compared with adults.[5]


Radiation necrosis is coagulative and predominantly affects white matter. This coagulative necrosis is due to small artery injury and thrombotic occlusion. These small arteries demonstrate endothelial thickening, lymphocytic and macrophagic infiltrates, presence of cytokines, hyalinization, fibrinoid deposition, thrombosis, and finally occlusion.

The primary mechanism of the delayed injury in radiation associated with necrosis is secondary to vascular endothelial injury or direct damage to oligodendroglia. As a result, white matter tissue is often more affected than gray matter tissue. Radiation may have effects on fibrinolytic enzyme systems, with an absence of tissue plasminogen activator and an excess in urokinase plasminogen activator impacting tissue fibrinogen and extracellular proteolysis with subsequent cytotoxic edema and tissue necrosis. Whether immune-mediated mechanisms may also contribute to radiation-induced neurotoxicity is unclear, but an autoimmune vasculitis has been postulated as a secondary host response to tissue damage.

Animals exposed to radiation and given antibodies to cytokines (tumor necrosis factor, interleukin-1, tissue growth factor) have decreased survival compared to animals that do not receive these antibodies. These cytokines may be involved in initially protecting healthy tissue from the effects of radiation. With prolonged radiation exposure, these particular cytokines are overexpressed and result in a cascade of inflammatory events and vascular injury.[6]

In addition to vessel occlusion with resultant tissue necrosis, telangiectatic vessels, which may hemorrhage, occasionally form. Demyelination, oligodendrocyte dropout, axonal swelling, reactive gliosis, and disruption of the blood-brain barrier also can be observed.



United States

Natural history of the tumor in terms of prognosis and survival may affect the occurrence of radiation necrosis in a particular tumor population. In glioblastoma multiforme or metastatic disease with a poor long-term prognosis, the patient may not live long enough to develop radiation necrosis. Radiation necrosis can occur as soon as a few months or as long as decades after treatment. It generally occurs 6 months to 2 years after radiation therapy. Radiation injury may occur in 5-37% of patients treated for intracranial neoplasms.[7]


Radiation necrosis can be fatal. It also can cause problems associated with a mass lesion, such as seizures, focal deficits, increased intracranial pressure, and herniation syndromes.


Radiation necrosis is a focal process that occurs at the initial tumor site.

Breakthrough or new seizures may occur. These seizures may be partial, complex partial, or partial with secondary generalization (grand mal).

Depending on the tumor location and rate of growth, radiation necrosis can present with signs of mass effect, elevated intracranial pressure, obstructive hydrocephalus, or one of the herniation syndromes.

Hemorrhage in late radiation necrosis is a rare but described phenomenon.[8]

Radiation necrosis involving the frontal or temporal lobes may produce cognitive and personality changes.


Evaluate mental status and cortical functioning in patients with radiation necrosis who have a supratentorial lesion or signs of increased intracranial pressure. In cortical testing, examine for aphasia, apraxia, attention, neglect, visuospatial skills, recognition, short-term recall, and calculation.

With the possibility of increased intracranial pressure, examine the fundus for possible papilledema and/or decreased or absent spontaneous venous pulsations.

Since radiation necrosis is a focal lesion, tailor the neurologic exam to look carefully for focality, lateralization, or asymmetry in motor, sensory, or coordination testing.

Since radiation necrosis occurs in the same region as the initial tumor bed, evaluate functions specific to that area of the CNS.


Occurrence generally is related to total radiation doses and fractionation size. The risk increases with increasing doses and larger radiation fraction sizes.

Other predisposing factors include the following:

Laboratory Studies

No specific tests of the serum or cerebrospinal fluid are indicated.

Imaging Studies

A fundamental problem in diagnosis of radiation necrosis is that most imaging studies do not preclude the need for surgical brain biopsy or craniotomy for diagnosis. The typical appearance of brain radiation injury is similar to that of brain tumors, with a contrast-enhancing mass surrounded by edema and mass effect.

With conventional MRI, CT scan, positron emission tomography with [18 F]-labeled fluorodeoxyglucose (PET-FDG), and thallium 201 spectroscopy (single-photon emission CT [SPECT]), differentiating radiation necrosis from recurrent tumor is difficult.[10] Most of the research has been focused on recurrent astrocytoma. See the images below.

View Image

MRI of a patient with symptoms of gait unsteadiness 1 year after being diagnosed with a posterior fossa primitive neuroectodermal tumor (PNET). Treatm....

View Image

Positron emission tomography with [18F]-labeled fluorodeoxyglucose (PET-FDG) performed following the MRI of a patient with symptoms of gait unsteadine....


MRI signal changes in radiation necrosis cannot be differentiated from tumor-related changes.

In a study by Asao et al, diffusion-weighted MRI sequences of radiation necrosis were associated with marked and spotty hypointensity compared with recurrent tumors, with maximal apparent diffusion coefficient values in each lesion being smaller for recurrent tumors versus radiation necrosis.[11]

Dequesada et al noted that lesions containing radiation necrosis never displayed gyriform lesion/edema distribution, marginal enhancement, or solid enhancements.[12]

Dequesada et al reported that the lesion quotient (which is the ratio of the nodule as seen on T2 imaging as compared to the total enhancing area on T1 imaging) was associated with a quotient of 0.6 or greater in all cases of recurrent tumor and a quotient of 0.3 or less was seen in 4 of 5 cases of radiation necrosis.[12]

T1, T1 with gadolinium, T2, T2- fluid-attenuated inversion recovery (FLAIR), and proton density do not adequately enable differentiation of radiation necrosis from tumors.

Reddy el al concluded that enhancement patterns on MRI were just as accurate in predicting pathologic diagnosis as MR spectroscopy.[13]

Previously, radiation necrosis was believed to have greater peripheral than central enhancement with gadolinium. However, this peripheral enhancement pattern is not a consistent finding in radiation necrosis. Tumors also may display a greater peripheral than central enhancement.

MRI patterns that may signal but are not diagnostic for the possibility of radiation necrosis include the following:

CT scan

CT scan is not helpful in making the diagnosis of radiation necrosis.

It is most useful in the acute, clinical decline of a patient with brain tumor to differentiate acute hemorrhage from increased intracranial pressure, obstructive hydrocephalus, or a herniation syndrome.

Dynamic testing

Dynamic testing (eg, PET-FDG, SPECT) detects differences in tissue metabolism.

Tumors have greater metabolism (ie, increased uptake of PET-FDG and SPECT) than healthy brain parenchyma and areas of radiation necrosis.

Radiation necrosis is hypometabolic (ie, decreased uptake of FDG and thallium) compared to healthy brain parenchyma.

PET-FDG uses glucose transport and glycolysis as markers of metabolic activity.

Other PET imaging tracers have been proposed, including fluoride-labeled boronophenylalanine and other amino-acid tracers. These may be more useful in detection of tumors because the background protein metabolism activity is lower than sugar and the background activity of brain glucose metabolism may complicate interpretations of PET-FDG.[14]

13 N-NH3 PET may also be useful because this compound is associated with high uptake in even low-grade astrocytomas, thus possibly allowing clinicians to distinguish between recurrent astrocytoma and radiation necrosis.[15]

Thallium metabolic activity is due to its similarity to potassium.

Thallium SPECT reflects metabolic activity of sodium/potassium ATP-dependent membrane transport, chloride transport, and calcium channels.

In dynamic testing, a region of interest (ROI) is compared to a similar area of healthy brain. A ROI located in one hemisphere is compared to a similar area in the contralateral hemisphere.

For bihemispheric lesions, a ROI is compared to an equivalent region in the anterior-posterior or posterior-anterior areas of brain parenchyma.

Most medical centers use qualitative assessments of ROI rather than quantitative assessments.

Despite diagnostic benefits and limitations of dynamic testing, histology often demonstrates mixed findings of malignant cells and radiation necrosis.

Advantages of PET-FDG [16]

PET-FDG correlates with prognosis and survival for newly diagnosed astrocytoma. Astrocytoma research has demonstrated that increased FDG uptake correlates with decreased survival.

Increased FDG activity on PET is more indicative of higher-grade astrocytoma such as anaplastic astrocytoma or glioblastoma multiforme.

PET-FDG also has assisted in guiding brain biopsy sites. Since brain biopsies are subject to sampling error, PET-FDG can assist the surgeon in obtaining the most metabolically active tissue to allow more accurate tumor staging.

PET-FDG is diagnostically useful in evaluating a tumefactive lesion (ie, structural lesion on MRI that suggests tumor) when clinical history suggests another diagnosis (eg, stroke, demyelination, abscess).

Despite the potential of this tool in a newly diagnosed brain tumor, PET-FDG becomes problematic when differentiating radiation necrosis from tumor recurrence.

Disadvantages of PET-FDG

Its sensitivity and specificity in differentiating radiation necrosis from tumor recurrence are related to various factors. Overall, the sensitivity of FDG-PET has been reported as 80-90%, but the specificity is lower (50-90% depending on the series).[7]

A ROI less than 1.6 cm lowers sensitivity and specificity in the differentiation of radiation necrosis from tumor recurrence.[17]

A ROI located in the temporal lobes and brain stem may have poor resolution due to artifact from nearby bony structures.

Inflammatory cells in areas of radiation necrosis may show increased metabolic activity, which falsely can indicate tumor recurrence.

Tumor cells also may be present in areas of low glucose activity on PET-FDG.

Brain tissue used for comparison to the ROI can become depressed metabolically from radiotherapy and/or chemotherapy.

Carbon C 11–methionine PET scanning may be a complementary study to FDG-PET. In one series, 31 of 35 brain tumors showed increased11 C-methionine despite isometabolism or hypometabolism on FDG-PET scans, and 10 benign lesions (of which 2 were cases of radiation necrosis) showed decreased or normal uptake of11 C-methionine.[18]

Thallium single-photon emission CT scan

Except for being more readily available at more medical centers than PET-FDG, thallium SPECT has the same limitations in dynamic testing.

A thallium index greater than 1.5 generally correlates with an anaplastic astrocytoma, glioblastoma multiforme, primary CNS lymphoma, or metastasis.

Magnetic resonance spectroscopy

Magnetic resonance spectroscopy (MRS) offers a new, quantitative approach to help differentiate radiation necrosis from tumor recurrence.

A few studies with histologic confirmation demonstrate the potential of MRS in differentiating radiation necrosis from tumor recurrence.

Future studies will determine the usefulness of MRS in avoiding biopsy or craniotomy for definitive diagnosis. MRS measures various brain metabolic markers, as follows:

Overall, imaging studies provide additional information, but they cannot provide a definitive diagnosis (ie, to avoid biopsy or craniotomy).


The similarities of radiation necrosis and tumor recurrence in clinical presentation and diagnostic imaging make performing a brain biopsy critical for diagnosis.

Diagnosing radiation necrosis is problematic. The diagnosis depends on obtaining adequate biopsy findings and is prone to sampling error.

A brain biopsy sample must be large enough to exclude tumor recurrence without causing clinically significant neurologic deficits. Areas to avoid include the deep central areas of the thalamus, the motor strip, occipital lobe, and speech centers.

Histologic Findings

Radiation necrosis tissue samples demonstrate necrotic tissue without predominance of malignant cells.

Irradiated tumor may contain necrosis, which does not necessarily signify radiation necrosis.

Some biopsy findings of radiation necrosis show both malignant cells and radiation necrosis.

A hallmark of radiation necrosis is involvement of the white matter with demyelination and oligodendrocyte dropout.

In addition to necrotic tissue, biopsy findings of radiation necrosis may demonstrate thickened vessels with endothelial proliferation and/or hyalinization with fibrosis and moderate infiltration of lymphocytes and macrophages.

Medical Care

Probably the most important factor in providing good care is the clinician's confidence of diagnosis. Exposing a patient with radiation necrosis to unwarranted antineoplastic treatment is not desirable.

A conservative option in treating a patient with radiation necrosis is observation. This may be appropriate for a patient found to have an asymptomatic necrotic mass on follow-up MRI. If the patient is asymptomatic and definitive diagnosis of radiation necrosis or recurrent glioma does not make a difference in clinical management, the patient should be monitored clinically and with serial MRI scans.

For patients with signs and symptoms of mass effect, increased intracranial pressure, or neurologic disability, consider other treatment options. Consider surgical evaluation, steroids, anticoagulation, or hyperbaric oxygen therapy separately or in combination.[20, 21]

A study of 14 patients with radiographic or biopsy proof of central nervous system radiation necrosis and progressive neurologic symptoms or signs responded to bevacizumab with decreases in T(2)-weighted fluid-attenuated inversion recovery and T(1)-weighted gadolinium-enhanced volumes and a decrease in endothelial transfer constant. This trial provided class I evidence of the efficacy of bevacizumab as a treatment for CNS radiation necrosis.[22]

In another study of the efficacy of bevacizumab, researchers reviewed 14 lesions in 11 patients treated with bevacizumab for brain RN secondary to SRS for their brain metastases. The mean percentage decrease in RN volume seen on T1 post-Gadolinium and fluid-attenuated inversion recovery (FLAIR) MRI at first follow-up, at a mean of 26 days (range, 15-43 days), was 64.4% and 64.3%, respectively.[23]

Hyperbaric oxygen promotes perfusion and angiogenesis.

Surgical Care

In addition to providing potential histologic diagnosis, surgery has other therapeutic benefits. Surgical debulking of the lesion can relieve increased intracranial pressure and improve disability. Patients with obstructive hydrocephalus may require a shunting procedure. Surgery, however, is associated with a high risk of complications or neurologic deficit and should be reserved for symptomatic patients in whom medical therapy fails.

Medication Summary

Medical therapy focuses on 2 mechanisms: controlling vasogenic edema and/or controlling vessel thrombosis.

Dexamethasone (Decadron, Dexasone)

Clinical Context:  Glucocorticoids such as dexamethasone have potent anti-inflammatory effects in many disorders. In addition to metabolic effects, they modify immune system response. Lacks salt-retaining property of hydrocortisone.

Patients can be switched from an IV to PO regimen in a 1:1 ratio.

Class Summary

Steroid therapy has only a temporary role in relieving neurologic decompensation and deficits. It relieves any symptomology related to vasogenic edema and disruption of the blood-brain barrier. While administering steroid therapy, the clinician must implement another medical or surgical therapy to treat radiation necrosis and to protect the patient from long-term complications.


Clinical Context:  Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis. Check aPTT after the first 6 h, then periodically q4-6h in early treatment. Dosage is therapeutic when aPTT is adjusted to 1.5 times normal.

Warfarin (Coumadin)

Clinical Context:  Inhibits synthesis of vitamin K-dependent clotting factors (II, VII, IX, X) and anticoagulants (proteins C and S). Vitamin K is a cofactor for postribosomal synthesis of vitamin K-dependent clotting factors, which promote synthesis of gamma-carboxyglutamic acid (necessary for proper coagulation). Reportedly interferes with vitamin K epoxide regeneration. Peak anticoagulant effect is 72-96 h. Like other anticoagulants, warfarin has no effect on a preexisting thrombus.

Individualize dose in response to PT/INR and therapeutic goal. Periodic determination of PT/INR is required.

Class Summary

Because radiation necrosis pathophysiology involves vessel thrombosis and subsequent occlusion, anticoagulant use has been proposed.[24] To date, few case studies have addressed use in this condition; the evidence for anticoagulation is very limited. Patients with radiation necrosis may also be at risk of intracranial hemorrhage, further limiting the presumptive benefits of this therapy. In most of these studies, histologic verification of radiation necrosis was present. Patients received 6 mo of IV heparin, then warfarin with aPTT and PT adjusted to 1.5 times the control. Patients had significant resolution of deficits. When anticoagulation was stopped, symptoms reemerged. Almost immediate resolution of symptoms occurred when anticoagulation was restarted. Before starting anticoagulation therapy, careful diagnostic evaluation and management are needed.

Bevacizumab (Avastin)

Clinical Context:  A recombinant, humanized antibody that inhibits vascular endothelial growth factor (VEGF). VEGF has a significant role in angiogenesis and maintenance of existing blood vessels. By inhibiting VEGF, the antibody would interfere with the blood supply to a tumor, which is thought to be critical to tumor metastasis. By preventing VEGF from reaching leaky capillaries that are associated with brain swelling, bevacizumab may also help in radiation necrosis.

Fifteen patients with malignant brain tumors were treated with bevacizumab or bevacizumab combination n in one study.

Class Summary

Agents in this category are used to decrease blood supply to a tumor by inhibiting angiogenesis.[25, 26]

Further Outpatient Care

Many neuro-oncology patients have significant cognitive and neurologic disabilities. These may require physical therapy, occupational therapy, social work support, and home nursing.

Further Inpatient Care

Consider the special medical needs of immobilized patients with a decreased level of consciousness and paralysis. They are more susceptible to deep venous thrombosis, pulmonary embolism, pneumonia, sepsis, malnutrition, and skin breakdown.

Depending on lesion site and treatment effects, patients with brain tumors may be more predisposed to cognitive difficulties and dementia, which in turn increase the risk of delirium and cognitive difficulties. Prevention and treatment of delirium includes reorientation techniques, frequent interactions with familiar personal contacts (eg, family members), minimal or no exposure to psychotropic medications, control of noxious visual and auditory stimuli, correction of underlying metabolic derangements, and maintenance of a normal sleep-wake schedule.


Prognosis is related to the natural history of underlying tumor and the idiosyncratic nature of radiation necrosis. Some lesions may show no interval growth while others require multiple resections to relieve disability. While long-term survival is uncommon, prolonged survival in the context of radiation necrosis has been described.


Michael J Schneck, MD, MBA, Vice Chair and Professor, Departments of Neurology and Neurosurgery, Loyola University, Chicago Stritch School of Medicine; Associate Director, Stroke Program, Director, Neurology Intensive Care Program, Medical Director, Neurosciences ICU, Loyola University Medical Center

Disclosure: Received honoraria from Boehringer-Ingelheim for speaking and teaching; Received honoraria from Sanofi/BMS for speaking and teaching; Received honoraria from Pfizer for speaking and teaching; Received honoraria from UCB Pharma for speaking and teaching; Received consulting fee from Talecris for other; Received grant/research funds from NMT Medical for independent contractor; Received grant/research funds from NIH for independent contractor; Received grant/research funds from Sanofi for independe.


Anna Janss, MD, PhD, Associate Professor of Pediatric Neuro-oncology, Emory University School of Medicine; Consulting Neuro-oncologist, Children's Healthcare of Atlanta

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Jorge C Kattah, MD, Head, Associate Program Director, Professor, Department of Neurology, University of Illinois College of Medicine at Peoria

Disclosure: Received honoraria from Biogen for consulting; Received honoraria from Bayer Corporation for consulting.

Additional Contributors

Frederick M Vincent, Sr, MD, Clinical Professor, Department of Neurology and Ophthalmology, Michigan State University Colleges of Human and Osteopathic Medicine

Disclosure: Nothing to disclose.


The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Robert Wilson, MD to the development and writing of this article.


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MRI of a patient with symptoms of gait unsteadiness 1 year after being diagnosed with a posterior fossa primitive neuroectodermal tumor (PNET). Treatment during the 1-year interval prior to this MRI consisted of surgical resection, craniospinal radiation of 2340 cGy, boost dose given to the posterior fossa for a total of 5500 cGy, chemotherapy (vincristine, cis-platinum, and cyclohexylchloroethylnitrosurea [CCNU]), and dexamethasone therapy.

Positron emission tomography with [18F]-labeled fluorodeoxyglucose (PET-FDG) performed following the MRI of a patient with symptoms of gait unsteadiness 1 year after being diagnosed with a posterior fossa primitive neuroectodermal tumor (PNET). Treatment during the 1-year interval prior to these studies consisted of surgical resection, craniospinal radiation of 2340 cGy, boost dose given to the posterior fossa for a total of 5500 cGy, chemotherapy (vincristine, cis-platinum, and cyclohexylchloroethylnitrosurea [CCNU]), and dexamethasone therapy. PET-FDG demonstrates hypometabolism consistent with probable radiation necrosis. Four years later, the patient is stable and without evidence of tumor progression.

MRI of a patient with symptoms of gait unsteadiness 1 year after being diagnosed with a posterior fossa primitive neuroectodermal tumor (PNET). Treatment during the 1-year interval prior to this MRI consisted of surgical resection, craniospinal radiation of 2340 cGy, boost dose given to the posterior fossa for a total of 5500 cGy, chemotherapy (vincristine, cis-platinum, and cyclohexylchloroethylnitrosurea [CCNU]), and dexamethasone therapy.

Positron emission tomography with [18F]-labeled fluorodeoxyglucose (PET-FDG) performed following the MRI of a patient with symptoms of gait unsteadiness 1 year after being diagnosed with a posterior fossa primitive neuroectodermal tumor (PNET). Treatment during the 1-year interval prior to these studies consisted of surgical resection, craniospinal radiation of 2340 cGy, boost dose given to the posterior fossa for a total of 5500 cGy, chemotherapy (vincristine, cis-platinum, and cyclohexylchloroethylnitrosurea [CCNU]), and dexamethasone therapy. PET-FDG demonstrates hypometabolism consistent with probable radiation necrosis. Four years later, the patient is stable and without evidence of tumor progression.