Intracranial Tumours

NECT

• Intra-axial tumours: usually of low attenuation on NECT ▸ high attenuation areas within a tumour indicate tumour calcification or recent intratumoural haemorrhage

• Extra-axial tumours: associated with bone erosion or hyperostosis

CECT

Improved visualization of an enhancing mass lesion (e.g. a meningioma or metastases)

CT perfusion

This can assess tumour relative cerebral blood volume (rCBV) and permeability changes ▸ it provides a limited area of coverage (compared with MRI) ▸ unlike MRI it can provide a direct relationship between the CT attenuation value and tissue contrast material concentration

Usual tumour appearance

• T1WI: low SI ▸ T2WI/FLAIR: high SI

• FLAIR: this provides particularly good contrast between normal brain tissue and glial tumours ▸ signal loss is seen within any cystic tumour components

• Highly cellular tumours (e.g. lymphoma): a corresponding decreased water content (relatively low SI on T2WI)

Extra-axial enhancement

• Vascular extra-axial tumours (e.g. meningioma)

Intra-axial enhancement

• Following disruption of the blood–brain barrier (generally high-grade tumours) ▸ it may also be seen with certain low-grade tumours (e.g. pilocytic astrocytomas)

T2*/susceptibility images

• Haemorrhage/calcification becomes more conspicuous

Intratumoural haemorrhage or calcification

• T2WI: low SI ▸ this is more conspicuous on T2*WI (stronger magnetic susceptibility effects)

High SI (T1WI)

• If there is haemorrhage, proteinaceous fluid, melanin (e.g. metastatic melanomas) or fat

Dynamic susceptibility-weighted contrast-enhanced (DSC) MR perfusion imaging

• This can assess tumour blood vessel density (an indirect measure of tumour neovascularity malignancy)

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    rCBV measurements correlate closely with markers of tumour vascularity and angiogenesis

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      indirect measure of tumour neovascularity

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    Higher rCBV values with high-grade tumours

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    rCBV maps can aid stereotactic tumour biopsies

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    In radiation necrosis the residual enhancing lesion has a low rCBV (higher with tumour recurrence due to new vessel formation)

• DSC imaging differs from contrast enhancement, which is an indicator of vascular endothelial (blood–brain barrier) integrity

Dynamic contrast-enhanced (DCE) imaging

T1WI + Gad ▸ DCE imaging can generate time–signal intensity curves, and analysed with mathematical models (e.g. K ^TRANS )

Permeability imaging – the ‘transfer coefficient’ (K ^TRANS )

• This quantifies tumour microvascular permeability and correlates with tumour grade

• Measured using T1W steady-state or first-pass T2*W gradient-echo imaging

Arterial spin labelling

• Labelled endogenous hydrogen measures cerebral blood flow (rCBF)

MR diffusion imaging

• Useful in identifying acute infarcts or abscesses (which can mimic brain tumours)

• ADC measurements correlate inversely with the histological glioma cell count

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    ADC measurements of any enhancing components in radiation necrosis are significantly higher than with recurrent tumour (mirroring the higher cellular density with a recurrent neoplasm)

• Diffusion tensor imaging (DTI) provides additional information about the direction of water diffusion ▸ the normally high anisotropy within white matter tracts can be lost if infiltrated by tumour

MR spectroscopy (MRS)

• MRS is a sensitive but not specific technique

• The common pattern seen with brain tumours:

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    Decreased:

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      N-acetylaspartate (NAA): a neuron-specific marker

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      Creatine (Cr)

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    Increased:

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      Lipids (L)

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      Lactate (Lac): a marker of tumour tissue hypoxia

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      Choline (Cho): a reflection of cell membrane turnover (increased with neoplastic activity)

fMRI

• BOLD imaging detects changes in regional cerebral blood flow during various forms of brain activity

• This is used for preoperative localization of important cortical regions that may have been displaced by tumour

Patient age and tumour site are useful indicators to the likely tumour type

• Children: primary tumours usually occur infratentorially and within the posterior fossa between the ages of 2 and 10 years (e.g. pilocytic astrocytoma, pontine glioma, ependymoma and medulloblastoma) ▸ below 2 and above 10 years of age supratentorial tumours are more common (paediatric supratentorial tumours will preferentially affect the midline structures) ▸ intracranial metastases are rare

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    Astrocytoma: this is the most common primary childhood brain tumour (the majority are pilocytic astrocytomas and characteristically occur within the cerebellum, hypothalamus and optic nerves)

• Adults: 70% of intracranial tumours are primary (30% are metastases) ▸ the vast majority of tumours are supratentorial – the posterior fossa is rarely affected by a primary tumour (a metastasis is more likely at this location)

CT

A well-circumscribed and encapsulated large mass ▸ predominantly cystic (70%) or solid (30%) ▸ an associated strongly enhancing mural nodule when cystic ▸ calcification is rare ▸ no adjacent oedema

• Differential: a medulloblastoma is a hyperdense solid lesion (NECT)

MRI

Cystic component: T1WI: low SI ▸ T2WI: high SI ▸ T1WI + Gad: avid homogeneous enhancement of any solid component

• Optic pathway pilocytic astrocytoma: occurs anywhere along the optic tract (usually at the chiasm) ▸ hypothalamic or chiasmatic tumours may be more aggressive

CT

An enlarged optic nerve (variable enhancement) ▸ often large and lobulated when at the chiasm and can extend into the hypothalamus ▸ haemorrhage and necrosis is uncommon

• No calcification (unlike an optic nerve sheath meningioma or craniopharyngioma)

MRI

An expanded chiasm and hypothalamus ▸ T1WI: low SI ▸ T2WI: high SI

CT

An iso- or hypodense mass ▸ poor enhancement (there is an intact blood–brain barrier) ▸ calcification in 20%

MRI

T1WI: low-to-intermediate SI ▸ T2WI/FLAIR: high SI ▸ T1WI + Gad: enhancement suggests progression to a higher histological grade

CT

More extensive infiltration of peritumoural tissues than with a grade II tumour (+ vasogenic oedema) ▸ may be non-enhancing

MRI

Solid ± central necrosis ± oedema ▸ T1WI/T2WI: heterogeneous SI appearances due to necrosis and haemorrhage ▸ T1WI + Gad: an irregularly thick enhancing peripheral ‘ring’ (active mitosis) ▸ a multicentric tumour with seeding via the CSF space (5%) ▸ a lower ADC than with a low-grade glioma

• ‘Butterfly lesion’: tumour commonly crosses the midline via the corpus callosum (as can a CNS lymphoma)

• Pseudoprogression: due to an inflammatory reaction following chemoradiation (increased enhancement and oedema) ▸ spontaneous improvement

• Pseudoresponse: decreased enhancement and oedema without improved survival

MRI

A diffuse ill-defined ‘mass-like’ lesion with ventricular effacement ▸ T1WI: a homogeneous intermediate-to-low SI infiltrating mass ▸ T2WI/FLAIR: a homogeneous high SI infiltrating mass ▸ T1WI + Gad: no or minimal enhancement

• Differential: lymphomatosis cerebri ▸ viral encephalitis ▸ acute disseminated encephalomyelitis (ADEM) ▸ vasculitis

CT

A hypodense lesion which may involve the cortex (with associated cortical thickening) ▸ cysts or haemorrhage can be seen in 20% but necrosis and oedema is rare

• 50% of tumours will demonstrate variable (and often heterogeneous) contrast enhancement – this is not a reliable indicator of tumour grade (unlike for an astrocytoma)

• Intratumoral haemorrhage

• Calcification is present in up to 90% of cases – this is central, peripheral or gyriform in nature

MRI

T1WI: heterogeneous low-to-intermediate SI ▸ T2WI/FLAIR: heterogeneous high SI ▸ T1WI + Gad: variable and often heterogeneous

CT

An isodense-to-hyperdense, well-demarcated, lobulated mass lesion which takes on the shape of the 4 ^th ventricle (originating from the roof or floor) and frequently extends through the foramina of Magendie and Luschka to seed via the subarachnoid space (a ‘plastic’ ependymoma) ▸ calcification is seen in >50% of cases and cystic elements can also be demonstrated ▸ there can be an associated obstructive hydrocephalus

• Cerebral hemisphere ependymoma: this tends to arise adjacent to the ventricular system (characteristically adjacent to the trigone of the lateral ventricle) and can resemble an astrocytoma ▸ it is more frequently calcified or cystic than an infratentorial tumour

MRI

There are mixed signal intensities ▸ T1WI: normal-to-low SI ▸ T2WI: predominantly high SI ▸ T1WI + Gad: mild-to-moderate enhancement (which is often heterogeneous)

CT/MRI

It usually appears as a cystic mass with an intensely enhancing mural nodule (± haemorrhage) ▸ there is little surrounding oedema ▸ cyst wall enhancement indicates tumour extension (as for a pilocytic astrocytoma)

• It may only consist of strongly enhancing solid components

• Multiple signal voids may be seen with MRI (as the lesion is highly vascular)

Angiography

A vascular nodule within an avascular mass ▸ there may be draining veins present

CT/MRI

It is an expansile and poorly defined pontine lesion (± haemorrhage) ▸ there is poor enhancement ▸ it can encase the basilar artery

CT/MRI

This has similar imaging features to a pilocytic astrocytoma seen elsewhere

NECT

A well-defined and hyperdense (due to its high cellular density) midline vermian mass abutting the roof of the 4 ^th ventricle ▸ there is perilesional oedema (± hydrocephalus) ▸ cystic change, haemorrhage and calcification are frequently seen ▸ brainstem usually displaced anteriorly rather than directly invaded

MRI

T2WI: intermediate-to-low SI ▸ T1WI + Gad: variable patchy enhancement ▸ DWI: restricted diffusion

MRS

There is a reduced N-acetylaspartate (NAA) peak with an increased choline-to-creatine ratio