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Advanced MR neuroimaging of brain tumours

Mw. Dr. M. Smits

Afdeling radiology, Erasmus MC, Rotterdam

Prof. dr. A. van der Lugt

Afdeling radiology, Erasmus MC, Rotterdam

Learning objectives

1. To know the added value of Magnetic Resonance

(MR) perfusion, diffusion weighted imaging and MR

spectroscopy in the diagnostic work-up, neurosurgical

intervention and follow-up of primary brain tumours.

2. To know the added value of functional MR imaging

and diffusion tensor imaging in guiding neurosurgical

intervention of primary brain tumours.

3. To know the pitfalls of post-therapeutic imaging,

including pseudoprogression and pseudoresponse.

Introduction

Brain neoplasms are divided into primary brain tumours and

metastatic tumours. The most common primary intra-axial

brain tumours are those derived from the neuroepithelial

tissue, the majority of which are gliomas. Indications for

imaging of brain tumour patients can be divided into three

categories: 1) diagnostic work-up; 2) guiding neurosurgical

intervention; and 3) follow-up.

Diagnostic work-up

For the diagnostic work-up of a brain lesion contrastenhanced

MR imaging is the modality of choice,

complemented with computed tomography (CT) for the

assessment of the presence of calcifications.

Differential diagnosis

Localisation, extent, signal intensity characteristics and

contrast enhancement patterns generally make a first

distinction between tumoural and non-tumoural lesions

possible. One of the most commonly encountered diagnostic

dilemmas in this respect is the differentiation between

necrotic tumour and abscess. Both lesions present as a fluidfilled

ring-enhancing lesion and are often indistinguishable

on conventional MR imaging. Diffusion weighted imaging

(DWI) has shown to be an invaluable imaging technique to

make such a distinction possible, demonstrating diffusion

restriction in abscess and elevated diffusion in necrotic

tumours such as metastases and glioblastoma multiforme.

Exceptions, with diffusion restriction in necrotic tumours,

do occur, for instance in the presence of haemorrhagic

components.

Tumour grading

Brain tumours are both classified and graded to predict

biological behaviour. Therapeutic management algorithms

neuroradiologie

are based on tumour grade, indicating the need for accurate

tumour grading. The grading system as proposed by the

World Health Organisation (WHO) is the most widely

used and consists of grades I to IV, with grade I tumours

being the most benign, showing no tendency to malignant

progression, and grade IV tumours being the most malignant.

The histological grading of gliomas is based on the tumour’s

cellularity, mitosis, necrosis, pleomorphism and vascular

proliferation. Radiological tumour grading is commonly

based on the demonstration of enhancement after contrast

administration. Typically, high grade glioma show contrast

enhancement, which is due to the destruction of the bloodbrain

barrier by malignant tumour cells as well as to the

leakage of contrast media from the immature angiogenic

tumour vessels. Conversely, no contrast enhancement is

observed in non-vascular, low grade gliomas.

Despite such typical findings, most anaplastic astrocytomas

(WHO grade III) do not enhance while up to 50% of

oligodendrogliomas (WHO grade II) do show enhancement.

Perfusion imaging

Higher sensitivity and predictive value for tumour grading

and prognosis may be obtained with T2* weighted first-pass

dynamic susceptibility weighted contrast enhanced (DSC)

perfusion imaging (1). The relative cerebral blood volume

(rCBV) is the most widely used parameter obtained with

DSC for brain tumour grading. The rCBV increase shows a

reliable correlation with tumour grade and increased tumour

vascularity (1). The angiogenic activity of high grade tumours

results in the presence of increased microvascular density

and many slow-flowing collateral vessels, resulting in

increase of rCBV in high grade tumours (1).

Maximum rCBV ratios of low grade glioma are reported to

be between 1.1 and 2.1, while those in high grade glioma

are in the range of 3.5 to 7.3 (1). Using an rCBV ratio cut-off

value of 1.75, high grade glioma can be differentiated from

low grade glioma with 95% sensitivity (2). Specificity

is relatively low at 70%, due to the misclassification of

low grade gliomas with elevated rCBV, most notably

oligodendroglioma.

Relative CBV measurement may also be used to obtain

prognostic information. Law et al. showed that patients with

high grade glioma and an rCBV ratio of less than 1.75 had

a stable disease course, while those with an rCBV ratio of

greater than 1.75 showed rapid deterioration (2).

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