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Magnetic Resonance Imaging Findings of Radiation-induced Changes in Malignant Gliomas

Proposed new response criteria suggest that within the first 12 weeks of completion of RT, progression can be determined only if the majority of the new enhancement is outside the radiation field or there is pathological confirmation of progressive disease.21 Pseudoprogression and RN not only occur more frequently after TMZ ChT, but also develop earlier if RT is combined with ChT.5,6,20


reported incidence rates range between 20 and 30% of patients treated with TMZ ChRT.6,21

No other risk factors for pseudoprogression

have been identified. However, the incidence of pseudoprogression is likely to increase with higher doses of RT.6

Late Radiation-induced Injury

Late radiation effects occur months to years post-radiation and are often progressive and irreversible.1,4–6,17,21 several entities:1,4,6,19

This category includes vascular lesions (lacunar infarcts, large-vessel

occlusion [Moyamoya-like syndrome], telangiectasias), parenchymal calcifications (mineralising microangiopathy), radiation-induced tumours (the most common being meningioma), cranial neuropathy (relatively rare, most often related to necrosis of the optic nerve system), leucoencephalopathy syndrome and RN. Only the last two will be discussed further.

Leucoencephalopathy Syndrome and Disseminated Necrotising Leucoencephalopathy Leucoencephalopathy manifests as gait and memory disturbances, urinary incontinence and mental slowing.1,6

ranges between 38 and 100% of patients receiving RT.19 CD

Figure 2: Disseminated Necrotising Leukoencephalopathy in a Right Frontal Glioblastoma Multiforme Treated with Surgery and Temozolomide Chemoradiotherapy


The reported prevalence It is strongly

related to the volume of brain irradiated, the radiation dose, the interval between irradiation and imaging, concomitant medical diseases predisposing to vascular injury, age and concurrent ChT.1,4,6

On fluid-attenuated inversion recovery (FLAIR) and T2-weighted imaging, leucoencephalopathy typically presents as diffuse, symmetric hyperintense foci in the periventricular white matter near the frontal or occipital horns, which may lead to a confluent pattern with scalloped outer margins extending from the ventricles to the corticomedullary junction, with no enhancement or significant mass effect (indistinguishable from the deep white matter changes seen in normal older people and patients with risk factors for cerebral vascular disease).1,4,6,19,20

The corpus callosum and the subcortical

arcuate fibers are initially spared. Additionally, cerebral atrophy with hydrocephalus may be seen.2,4,6,7,10

In severe cases, extensive diffuse white matter injury can lead to disseminated necrotising leucoencephalopathy, which occurs because of the combined effects of ChT and RT.1,4,19

On MR it is similar

to leucoencephalopathy, but presents petechial or ring-shaped haemorrhages and calcification deposits1

along with areas of

contrast enhancement in the white matter at variable distances from the primary tumour1

(with a predilection for peri-ventricular

Leucoencephalopathy and disseminated necrotising leucoencephalopathy may occur together; alternatively, one may follow the other.1,20

and, less commonly, cortical involvement). Enhancement patterns can be nodular, linear or curvilinear in varying sizes and can be single or multiple, therefore mimicking tumour progression (see Figure 2).4,10

These lesions do not warrant biopsy if they remain stable or regress in size. However, progression to RN should be suspected if the lesions increase in size or are accompanied by oedema and mass effect.4,10

follow-up should also be recommended if a peripheral restriction of EUROPEAN ONCOLOGY & HAEMATOLOGY Radionecrosis

RN is the end result of confluent perivascular coagulative necrosis affecting the white matter.10

It generally occurs three to 12 months

after RT, but can occur up to years and even decades afterwards.1,5,6,10,14,18

brain tumours ranges between 5 and 24%.2,4,6–8,10,20

In adults, the reported incidence of RN after RT for Risk factors include

total radiation dose (>6,500–7,000cGy), size of the radiation field and radiation fraction, number and frequency of radiation doses (>200cGy/day), duration of survival, age of the patient at the time of treatment (in older patients, pre-existing vascular pathology and ChRT may have additive effects), treatment duration, re-irradiation and ChRT (increased incidence and earlier appearance).1,3–7,10,14,20,22

In the experience of the authors,


A: Axial T2-weighted image showing diffuse white matter injury (*) secondary to radiotherapy and coarse calcification foci (open arrow); B: Axial contrast-enhanced T1-weighted image showing three lesions with blurred enhancement (solid arrows); C: Apparent diffusion coefficient (ADC) map revealing elevated ADC values – as high as 2.29x10-3mm2/second. On diffusion-weighted imaging, these lesions presented homogeneous low signal intensity (not shown); D: On a relative cerebral blood volume (rCBV) map, rCBV values as low as 0.57 were also observed, suggesting post-treatment changes; E and F: Axial contrast-enhanced T1-weighted image at follow-up studies six and 12 months later, respectively, revealed how these lesions regressed in size.

water diffusion is found on DWI, as it may be indicative of a trend towards RN.

RN is a

dynamic pathophysiological process with a highly variable clinical course (progressive functional and cognitive impairments that may


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