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Radiologic—Pathologic Conferences of the University of Texas M. D. Anderson Cancer Center

Delayed Cerebral Radiation Necrosis

¹ Department of Pathology, The University of Texas M. D. Anderson Cancer Center, Box 85, 1515 Holcombe Blvd., Houston, TX 77030.
² Department of Diagnostic Radiology, The University of Texas M. D. Anderson Cancer Center, Box 57, 1515 Holcombe Blvd., Houston, TX 77030.

Received January 4, 2002; accepted after revision May 15, 2002.

 
Address correspondence to G. J. Whitman.

A 75-year-old woman presented with a 1-year history of decreased mental function, apathy, and bradykinesia. The patient had a history of an olfactory neuroblastoma that had initially been diagnosed 26 years previously. The patient had undergone several surgical resections and external beam radiation therapy (total dose, 50 Gy). MR imaging revealed a large right frontal lobe mass (Figs. 1A and 1B). Biopsy of the frontal lobe lesion showed large confluent areas of white matter necrosis with prominent fibrinoid necrosis of the blood vessel walls. Reactive gliosis and thick-walled hyalinized vessels were also identified (Fig. 1C). No evidence of malignancy was found in the biopsy tissue. The clinicopathologic diagnosis was delayed radionecrosis.

View larger version (129K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1A. —75-year-old woman with delayed radiation necrosis. Contrast-enhanced T1-weighted MR image shows area of enhancement in right frontal lobe (large arrow), genu of corpus callosum (small arrow), and septum pellucidum.

View larger version (140K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1B. —75-year-old woman with delayed radiation necrosis. Contrast-enhanced T1-weighted MR image shows enhancing right frontal mass (arrow) with minimal mass effect.

View larger version (151K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1C. —75-year-old woman with delayed radiation necrosis. Photomicrograph shows characteristic fibrinoid necrosis of blood vessel wall (arrow) with surrounding parenchymal necrosis. No evidence of tumor was found. (H and E, x100)

Radiation necrosis is an uncommon side effect of cranial irradiation. Delayed radionecrosis was initially described as a side effect of radiation therapy for extracranial lesions [1]. The first case of radionecrosis was reported in 1930 as a consequence of radiation therapy for treatment of a basal cell epithelioma [2]. Delayed radionecrosis is directly proportional to dose and inversely related to fraction number [1, 3]. The mean interval between irradiation and presentation is approximately 1 year for patients who received a total dose of more than 50 Gy; however, cases of radionecrosis have been reported as early as 3 months and as late as 19 years after radiation therapy [3]. The clinical presentation of radionecrosis is variable and can include headache, seizures, personality changes, and neurologic deficits.

Delayed radionecrosis consists of confluent zones of parenchymal necrosis that most severely affect the white matter and the deep laminae of the overlying cortex with relative sparing of the superficial cortex. During the early phase of radionecrosis, there is highly characteristic fibrinoid necrosis of the blood vessel walls that is followed by necrosis of the surrounding parenchyma. Late vascular changes include wall thickening and hyalinization as well as telangiectasia. Extensive reactive gliosis is commonly observed adjacent to the necrotic foci. Secondary changes in necrotic tissue, including cyst formation and dystrophic calcification, may occur in patients who live with radiation necrosis for an extended period. The principal entity in the differential diagnosis of radionecrosis is usually neoplasm. Careful histologic examination of the biopsy tissue to rule out malignancy is warranted [4].

Cerebral radiation necrosis may appear as an aggressive lesion on imaging studies. Diffuse damage to the blood—brain barrier is present, and intense contrast enhancement is often seen on CT and MR imaging. The degree of enhancement, however, can vary with time. Larger lesions may appear as islands of enhancement surrounded by areas of nonenhancing necrosis. Minimal local mass effect for the size of the lesion is typical. However, reactive vasogenic edema, which often accompanies this condition, can be extensive and can produce substantial regional mass effect on adjacent structures. The possibility of radiation necrosis should be considered in the differential diagnosis for any enhancing lesion in patients with an appropriate clinical history [4].

Several imaging techniques have been evaluated to help distinguish radionecrosis from a recurrent neoplasm. Dynamic contrast-enhanced MR imaging can be used to differentiate radiation necrosis from tumor on the basis of maximal enhancement rates [5]. Using MR spectroscopy, Fulham et al. [6] found decreased levels of choline-containing compounds in areas affected by chronic radiation necrosis compared with tumors. In the future, positron emission tomography with FDG will likely play a larger role in differentiating neoplasm from radiation necrosis on the basis of measurements of glucose metabolism.

Surgical excision is the treatment of choice for patients with radiation necrosis. Corticosteroid therapy often helps ameliorate the clinical manifestations of cerebral radiation necrosis [1].

References

Top References

 

1. Glass JP, Hwang T-L, Leavens ME, Libshitz, HI. Cerebral radiation necrosis following treatment of extracranial malignancies. Cancer 1984;54:1966 -1972[Medline]
2. Fischer AW, Holfelder H. Lokales amyloid im gehirn. Dtsch Z Chir 1930;227:475 -483
3. Marks JE, Wong J. The risk of cerebral radionecrosis in relation to dose, time and fractionation: a follow-up study. Prog Exp Tumor Res 1985;29:210 -218[Medline]
4. 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: 191-208
5. Hazle JD, Jackson EF, Schomer DF, Leeds NE. Dynamic imaging of intracranial lesions using fast spinecho imaging: differentiation of brain tumors and treatment effects. J Magn Reson Imaging 1997;7:1084 -1093[Medline]
6. Fulham MJ, Bizzi A, Dietz MJ, et al. Mapping of brain tumor metabolites with proton MR spectroscopic imaging: clinical relevance. Radiology 1992;185:675 -686[Abstract/Free Full Text]

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