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Especially in the last case this information is extremely

useful preoperatively, allowing the surgeon to aim at gross

total resection without concern for risking postoperative

functional deficit.

Follow-up

Both low and high grade gliomas are followed-up with high

frequency. In principle, all low grade (WHO grade II) gliomas

undergo malignant transformation, mandating a change

in therapy. Traditionally, the MacDonald criteria are used

to monitor gliomas radiologically, in which the enhancing

tumour is measured as the product of the maximum

perpendicular diameters (15). With current and emerging

therapeutic algorithms, which may on the one hand induce

treatment-related enhancement (pseudoprogression)

and on the other hand rapid reduction of enhancement

(pseudoresponse), the MacDonald criteria may no longer be

valid. These, and other limitations have led the Response

Assessment in Neuro-Oncology (RANO) working group to

define new standardised response assessment criteria for

high grade glioma, in which most notably the non-enhancing

tumour components are taken into account (16). In addition

to the RANO criteria, advanced MR imaging techniques

are expected to play an increasingly prominent role in both

low and high grade glioma monitoring. This has led to the

recent development of an imaging protocol by the European

Organisation for Research and Treatment of Cancer (EORTC)

Brain Tumour Group (BTG), which includes diffusion and

perfusion MR imaging (table).

Malignant transformation

It is not known how, why and when low grade gliomas

undergo their transition from silent to aggressive tumours.

The radiological hallmark of malignant transformation is

the appearance of contrast enhancement in a previously

non-enhancing tumour. An important concept in this

context is the so-called angiogenic switch, indicating the

transition of an avascular to a vascular tumour. It is this

angiogenic switch that is assumed to underlie the finding

by Danchaivijitr et al. of a progressive increase of maximum

rCBV ratios in low grade transforming to high grade gliomas

(17). Using longitudinal rCBV ratio measurements, they

were able to predict malignant transformation as early

as 18 months before transformation became apparent as

determined by the current clinical and radiological criteria.

The mean rCBV ratio at the point of transformation (i.e.

appearance of contrast enhancement) was 5.4 ± 3.0, while

mean rCBV ratios in the transformer group were 3.1 and

3.7 at 6 and 12 months respectively before enhancement

became apparent. Not only can MR perfusion imaging be

used to predict malignant transformation in non-enhancing

tumours prior to the appearance of enhancement, it can

also aid in establishing malignant transformation in those

neuroradiologie

tumours that already show enhancement in their low grade

stages.

Radiation necrosis and pseudoprogression

Radiation-induced injury can be divided into acute (1-6

weeks during or after treatment), early delayed (after 3

weeks to several months) and late delayed (after months

to years) injury (18). Histopathologically there is a vascular,

endothelial injury resulting in endothelial proliferation

with occlusive vasculopathy and stroke like episodes.

Furthermore, there is a neurotoxic effect, resulting in white

matter and glial damage. On conventional MR imaging,

changes related to radiation necrosis are generally

indistinguishable from tumour recurrence or progression.

A separate entity, known as pseudoprogression, has

emerged with the introduction of temozolomide combined

with radiotherapy as the standard of care for newly

diagnosed glioblastoma multiforme. Such chemoradiation

therapy for high grade gliomas may result in asymptomatic

pseudoprogressive lesions and increased necrosis in the

peritumoural region, which is also indistinguishable from

tumour progression or recurrence. It usually occurs soon after

end of therapy (within 3 months of treatment) and subsides

over the course of 6 to 9 months after start of treatment. This

is earlier than the delayed radionecrosis. It is probably due

to a subacute radiation encephalitis and treatment-related

necrosis, with a higher degree of tumour cell and endothelial

cell killing resulting in secondary reactions such as oedema

and abnormal vessel permeability mimicking tumour (1).

Such treatment related effects hinder the adequate

adjustment of therapeutic strategy. Attempts are made

with advanced MR imaging techniques to aid differentiating

tumour progression/recurrence from treatment effects, but

so far no unequivocal method or combination of methods

is available. Such attempts are further complicated by the

fact that histopathological correlation is problematic due

to sampling bias as well as the general co-existence of

radiation necrosis and vital tumour.

MR perfusion imaging

DSC perfusion imaging studies show low rCBV ratios in

areas of radiation necrosis with reported thresholds of 0.7

and 0.6 (20) (figure 2). At such thresholds sensitivity is >90%

and specificity approaches 100% (19). As with initial tumour

staging, rCBV ratios are high in progressive tumour, with

reported values of >2.6 (20) (figure 2). An accurate threshold,

however, remains to be established.

With steady-state dynamic contrast enhanced (DCE)

perfusion a measure of vascular permeability (Ktrans) is

obtained. Although there is contrast enhancement, indicating

increased vascular permeability, in both radiation necrosis

and recurrent tumour, enhancement is slow in radiation

necrosis. K trans is therefore low in areas of radiation necrosis

e d u r a d 6 9 - 2 1 - 2 2 e n 2 3 - 2 4 j u n I 2 0 1 1 29

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