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Imaging Diffusion-weighted Imaging


RN can have variable SIs (hypointense, hyperintense, heterogeneous) and a non-specific appearance on DWI.4,13


Low apparent diffusion


The SI may also be influenced by the presence of haemosiderin (resulting in a low SI because of the T2* effect), calcifications, gliosis or fibrosis caused by radiation when it occurs within the recurrent tumour.3,4,13


Theoretically, ADC ratios in the contrast-enhancing lesion should be lower in recurrent tumour than in RN,3–7,13,22 broad range of overlapping ADC values.4


but there is a relatively In a study by Hein et al.,


mean ADC ratios higher than 1.62 occurred only in RN, while ratios lower than this threshold occurred only in recurrent neoplasm.3


The presence of a peri-lesional hyperintense halo, reflecting restriction of water diffusion secondary to peri-vascular inflammatory changes, should be carefully evaluated as it may indicate progression toward RN. In the experience of the authors, a close follow-up should be recommended.


Radionecrosis and Metastases


In brain metastases, sequential changes identified on MR after RT and/or radiosurgery can be summed up as temporary exacerbation of the lesion, with peri-lesional oedema and central hypointensity on T2-weighted imaging. The lesion presents central loss of contrast enhancement and rim-like enhancement at two to six months. Blurred marginal enhancement can be observed without tumour


1. Valk PE, Dillon WP, Radiation injury of the brain, AJNR Am J Neuroradiol, 1991;12(1):45–62.


2. Mullins ME, Barest GD, Schaefer PW, et al., Radiation necrosis versus glioma recurrence: conventional MR imaging clues to diagnosis, AJNR Am J Neuroradiol, 2005;26(8):1967–72.


3. Hein PA, Eskey CJ, Dunn JF, Hug EB, Diffusion-weighted imaging in the follow-up of treated high-grade gliomas: tumour recurrence versus radiation injury, AJNR Am J Neuroradiol, 2004;25(2):201–9.


4. Pruzincová L, Steno J, Srbeck M, et al., MR imaging of late radiation therapy- and chemotherapy-induced injury: a pictorial essay, Eur Radiol, 2009;19(11):2716–27.


5. Brandes AA, Tosoni A, Spagnolli F, et al., Disease progression or pseudoprogression after concomitant radiochemotherapy treatment: pitfalls in neurooncology, Neuro-Oncology, 2008;10(3):361–7.


6. Brandsma D, Stalpers L, Taal W, et al., Clinical features, mechanisms, and management of pseudoprogression in malignant gliomas, Lancet Oncol, 2008;9(5):453–61.


7. Sundgren PC, MR spectroscopy in radiation injury, AJNR Am J Neuroradiol, 2009;30(8):1469–76.


8. Smith EA, Carlos RC, Junck LR, et al., Developing a clinical decision model: MR spectroscopy to differentiate between recurrent tumour and radiation change in patients with new contrast-enhancing lesions, AJR Am J Roentgenol, 2009;192(2): W45–52.


9. Weybright P, Sundgren PC, Maly P, et al., Differentiation


coefficient (ADC) values have been reported in some studies; this might reflect early necrosis with abundant polymorphonuclear leukocytes and high viscosity, which could restrict water diffusion, as in purulent fluid.4,13


progression. With time, this marginal enhancement becomes more discrete, while tumour volume and peri-lesional signal change (representing glial scarring) usually decrease.22


As mentioned above,


the presence of a hyperintense rim on DWI may indicate a trend towards RN, and follow-up should be recommended.22


The presence


of meningeal and dural sinus adherences should raise suspicion of RN, while the development of a rim of peri-ventricular or ependymal enhancement is more likely related to RN than to metastasis growth.


The previously mentioned parameters of advanced MR sequences are also applicable to metastases. However, it is important to highlight that metastases are more likely to be completely treated with ChRT, such that pure RN or pure tumour recurrence are more frequently observed. Therefore, a lower degree of overlapping spectral patterns and rCBV values can be found, providing more accurate diagnostic information (see Figure 5).


Conclusion


RN and tumoral recurrence often present at MR with overlapping imaging features; therefore, both clinical and imaging follow-up with conventional and advanced MR sequences are essential. If possible, a spectrum of the tumour should be obtained prior to RT and ChT.


Nevertheless, sometimes the diagnosis can be made solely on the basis of histopathological analysis. In the future, validated prediction models combining multiple metabolic ratios, with or without clinical data, will allow rational patient management, resulting in a reduction of the number of patients subjected to unnecessary invasive procedures or treatment. Furthermore, the possibility of this distinction will have important implications for trials on recurrent glioma. n


between brain tumour recurrence and radiation injury using MR spectroscopy, AJR Am J Roentgenol, 2005;185(6): 1471–6.


10. Kumar AJ, Leeds NE, Fuller GN, et al., Malignant gliomas: MR imaging spectrum of radiation therapy- and chemotherapy- induced necrosis of the brain after treatment, Radiology, 2000;217(2):377–84.


11. Schlemmer HP, Bachert P, Henze M, et al., Differentiation of radiation necrosis from tumour progression using proton magnetic resonance spectroscopy, Neuroradiology, 2002;44(3):216–22.


12. Henry RG, Vigneron DB, Fischbein NJ, et al., Comparison of relative cerebral blood volume and proton spectroscopy in patients with treated gliomas, AJNR Am J Neuroradiol, 2000;21(2):357–66.


13. Asao C, Korogi Y, Kitajima M, et al., Diffusion-weighted imaging of radiation-induced brain injury for differentiation from tumour recurrence, AJNR Am J Neuroradiol, 2005;26(6): 1455–60.


14. Gasparetto EL, Pawlak MA, Patel SH, et al., Posttreatment recurrence of malignant brain neoplasm: accuracy of relative cerebral blood volume fraction in discriminating low from high malignant histologic volume fraction, Radiology, 2009;250(3):887–96.


15. Zeng QS, Li CF, Zhang K, et al., Multivoxel 3D proton MR spectroscopy in the distinction of recurrent glioma from radiation injury, J Neurooncol, 2007;84(1):63–9.


16. Barajas RF, Chang JS, Sneed PK, et al., Distinguishing


recurrent intra-axial metastatic tumour from radiation necrosis following gamma knife radiosurgery using dynamic susceptibility-weighted contrast-enhanced perfusion MR imaging, AJNR Am J Neuroradiol, 2009;30(2):367–72.


17. Schlemmer HP, Bachert P, Herfarth KK, et al., Proton MR spectroscopic evaluation of suspicious brain lesions after stereotactic radiotherapy, AJNR Am J Neuroradiol, 2001;22(7): 1316–24


18. Sugahara T, Korogi Y, Tomiguchi S, et al., Posttherapeutic intraaxial brain tumour: the value of perfusion-sensitive contrast-enhanced MR imaging for differentiating tumour recurrence from nonneoplastic contrast-enhancing tissue, AJNR Am J Neuroradiol, 2000;21(5):901–9.


19. Rabin BM, Meyer JR, Berlin JW, et al., Radiation-induced changes in the central nervous system and head and neck, Radiographics, 1996;16(5):1055–72.


20. Van Tassel P, Bruner JM, Maor MH, et al., MR of toxic effects of accelerated fractionation radiation therapy and carboplatin chemotherapy for malignant gliomas, AJNR Am J Neuroradiol, 1995;16(4):715–26.


21. Wen PY, Macdonald DR, Reardon DA, et al., Updated response assessment criteria for high-grade gliomas response assessment in neuro-oncology working group, J Clin Oncol, 2010;28(11):1963–72.


22. Kang TW, Kim ST, Byun HS, et al., Morphological and functional MRI, MRS, perfusion and diffusion changes after radiosurgery of brain metastasis, Eur J Radiol, 2009;72(3):370–80.


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EUROPEAN ONCOLOGY & HAEMATOLOGY


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