Radiology - imaging Brain tumours , classification by location, by age ,by types of cell origin,by location , approch to Brain tumours , intra vs extraaxial lesion , midline crossing ,subarchnoid seeding,ependymal seeding , cortical based tumours , t1 hyperintes lesions, t2 hypointense lesions , tumors with calcifications ,low grade tumors vs high grade tumors , tumors with contrast enhancement vs no contrast enhancement , list of tumour mimics ,who classification of tumours ,t2 flair mismatch , primary and secondary cns lymphoma, cystic tumors of brain ,brain stem glioma it type associated ,ependymoma , medulloblastoma ,rossesforming glionuoranal tumors, include all tumors with its association and pathognomic features ,mainigoma,solitary fibrous tumour, pituitary tumors, craniopharyngiomas, rathke cleft cyst, penial gland tumors, benign cyts of Brain intra vs extra axial, swarnoma all lesions to be included, images to be included, mr spectro findings, perfusion findings,adc findings, ct mri appearance , subependymoma, ependymoma,sega ,pxa , pilocystic astrocytoma , dnet, pnet, glionuoranal tumors and cyst, arachnoid cyst epidermoid dermoid cyst, ependymal cyst, radiation necrosis vs pdeudoprogration of tumour

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Brain Tumours - Comprehensive Neuroradiology Reference


PART 1: SYSTEMATIC APPROACH TO BRAIN TUMOURS

When evaluating any intracranial mass, work through these questions in order:
  1. Patient age - determines the differential diagnosis fundamentally
  2. Location - intra vs. extra-axial, anatomical compartment, midline vs. lateral
  3. Number - solitary vs. multifocal
  4. Tissue characteristics - T1/T2 signal, calcification, fat, cysts, necrosis
  5. Enhancement pattern - homogeneous, ring, nodular, absent
  6. Advanced imaging - DWI/ADC, perfusion, MR spectroscopy

PART 2: CLASSIFICATION BY AGE

Paediatric (0-18 years)

LocationCommon Tumours
Posterior fossaPilocytic astrocytoma, Medulloblastoma, Ependymoma, DNET
SupratentorialDNET, Ganglioglioma, PXA, SEGA (tuberous sclerosis)
BrainstemDiffuse intrinsic pontine glioma (DIPG) / DIPG = H3K27M mutant
SellarCraniopharyngioma (adamantinomatous type)
PinealGerminoma, Pineoblastoma

Adults (18-60 years)

  • Glioblastoma (most common intraaxial primary)
  • Oligodendroglioma (IDH-mutant, 1p/19q-codeleted)
  • Astrocytoma (IDH-mutant)
  • Metastases
  • Meningioma (most common intracranial tumour overall)
  • Primary CNS lymphoma
  • Pituitary adenoma
  • Craniopharyngioma (papillary type - adults)

Elderly (>60 years)

  • Glioblastoma (IDH-wildtype, WHO grade 4)
  • Metastases (most common intraaxial in adults)
  • Primary CNS lymphoma (immunocompromised but also de novo elderly)
  • Meningioma

PART 3: CLASSIFICATION BY CELL ORIGIN

Cell TypeTumourWHO Grade
AstrocytesAstrocytoma IDH-mutant2-4
AstrocytesGlioblastoma IDH-wildtype4
AstrocytesPilocytic astrocytoma1
AstrocytesPXA (Pleomorphic xanthoastrocytoma)2-3
OligodendrocytesOligodendroglioma IDH-mutant 1p/19q-codeletion2-3
Ependymal cellsEpendymoma (spinal > fourth ventricle)2-3
Ependymal cellsSubependymoma1
Ependymal cellsMyxopapillary ependymoma2
Ependymal cellsSEGA (subependymal giant cell astrocytoma)1
Neuronal/glialDNET, Ganglioglioma, Gangliocytoma, RGNT1
EmbryonalMedulloblastoma4
EmbryonalPNET/CNS-PNET4
EmbryonalATRT (atypical teratoid/rhabdoid)4
MeningesMeningioma1-3
MeningesSolitary fibrous tumour (SFT/haemangiopericytoma)1-3
Schwann cellsSchwannoma1
Germ cellsGerminoma, Teratoma, NGGCTvaries
PituitaryPituitary adenoma/PitNETvaries
LymphocytesPrimary CNS lymphoma (DLBCL)N/A
Choroid plexusChoroid plexus papilloma/carcinoma1/3
Pineal parenchymaPineocytoma/Pineoblastoma1/4

PART 4: CLASSIFICATION BY LOCATION

Supratentorial

  • Frontal: Glioblastoma, Oligodendroglioma, Lymphoma, DNET (temporal > frontal for DNET)
  • Temporal: DNET, Ganglioglioma, Low-grade glioma, Herpes encephalitis mimic
  • Parietal/Occipital: Metastases, High-grade glioma
  • Intraventricular (lateral): Subependymoma, SEGA (foramen of Monro), Ependymoma, Central neurocytoma, Colloid cyst (3rd ventricle)
  • Sellar/Parasellar: Pituitary adenoma, Craniopharyngioma, Rathke cleft cyst, Meningioma, Germinoma

Infratentorial

  • Cerebellar hemisphere: Pilocytic astrocytoma, Metastases, Hemangioblastoma
  • Cerebellar vermis: Medulloblastoma (children), DNET
  • Fourth ventricle: Ependymoma (children), Subependymoma (adults), Choroid plexus papilloma
  • Brainstem (pons): DIPG, Glioma
  • Cerebellopontine angle (CPA): Schwannoma (VS), Meningioma, Epidermoid

Midline / Deep

  • Corpus callosum: Glioblastoma (butterfly), Lymphoma, Lipoma, Lymphoma
  • Thalamus: Glioma, ASTROBLASTOMA
  • Pineal region: Germinoma, Pineal parenchymal tumour, Dermoid/Epidermoid

PART 5: INTRA-AXIAL vs. EXTRA-AXIAL

This is the first and most important distinction.

Extra-axial Signs

  • CSF cleft between lesion and brain parenchyma
  • Buckling of cortex (white matter pushed inward)
  • Grey matter displaced away from lesion (not surrounding it)
  • Dural attachment / dural tail
  • Hyperostosis of adjacent bone
  • Homogeneous enhancement (no BBB)
  • Expanded subarachnoid space adjacent to lesion

Intra-axial Signs

  • Grey matter surrounding the lesion (engulfed, not displaced)
  • White matter oedema radiating from the lesion
  • No CSF cleft
  • Heterogeneous enhancement (BBB disruption)

Most Common Extra-axial Tumours

  • Meningioma (80% of extra-axial) - broad dural base, homogeneous enhancement, dural tail
  • Schwannoma (vestibular, trigeminal) - CPA cistern, "ice cream cone" through IAM
  • Note: 80% of extra-axial lesions = meningioma or schwannoma

Extra-axial Pitfall

A T2-hypointense mass at the falx appearing like meningioma - if grey matter is seen on both sides, it is intra-axial (e.g., melanoma metastasis). Always check for grey matter engulfment.

PART 6: IMPORTANT SPREADING PATTERNS

Midline Crossing

  • Glioblastoma: "Butterfly glioma" - crosses corpus callosum
  • Lymphoma: periventricular, can cross midline
  • Lymphoma vs GBM: Lymphoma - homogeneous solid enhancement, restricted diffusion (high DWI, low ADC), no necrosis. GBM - heterogeneous ring enhancement with central necrosis.

Subarachnoid / Leptomeningeal Seeding

  • Medulloblastoma (most common paediatric CNS tumour to seed) - "sugar coating" of spinal cord
  • Ependymoma (posterior fossa)
  • GBM (rare)
  • PNET, Pineal tumours, Choroid plexus carcinoma
  • Imaging: Nodular or linear enhancing deposits on surface of brain/cord on post-contrast T1. Whole spine MRI mandatory at staging.

Ependymal Seeding (Subependymal / Periventricular Spread)

  • GBM - subependymal tumour spread
  • Lymphoma - classically periventricular/subependymal
  • Medulloblastoma - ventricular system seeding
  • Pineal tumours / Germinoma
  • Ependymoma
  • Imaging: Enhancing nodular deposits lining ventricles on post-contrast T1

Cortical-Based Tumours

Tumours that involve cortex primarily (important - may mimic stroke, dysplasia):
  • DNET (dysembryoplastic neuroepithelial tumour)
  • Ganglioglioma
  • PXA (pleomorphic xanthoastrocytoma)
  • Low-grade oligodendroglioma
  • LEAT group (long-term epilepsy associated tumours)
  • Imaging feature: Cortical involvement, pseudostratified bubbly appearance, minimal oedema, no/faint enhancement

PART 7: SIGNAL CHARACTERISTICS

T1 Hyperintense Lesions (Bright on T1)

Mnemonic: "Fat, Flow, Fresh Blood, Fluid (proteinaceous), Free Radicals (melanin)"
CauseExample
FatLipoma, Dermoid cyst, Teratoma
Subacute haemorrhage (methaemoglobin)Cavernoma, Haemorrhagic metastasis (melanoma, RCC, choriocarcinoma)
Proteinaceous fluidRathke cleft cyst, Craniopharyngioma (cholesterol-rich)
MelaninMelanoma metastasis
Calcification (some patterns on GRE)Oligodendroglioma
Slow flow in vesselsArtifact on GRE
Contrast enhancementAlways check pre-contrast T1
Manganese/gadolinium accumulationHepatic encephalopathy

T2 Hypointense Lesions (Dark on T2)

Mnemonic: "Fibrosis, Calcification, Haemosiderin, Hypercellular, Hypervascular"
CauseExample Tumours
Dense cellularityLymphoma, Medulloblastoma, PNET
CalcificationOligodendroglioma, Meningioma
Fibrocollagenous matrixMeningioma (psammomatous/fibrotic)
Haemosiderin (old blood)Cavernoma halo, GBM after bleed
High nuclear-to-cytoplasm ratioLymphoma
MelaninMelanoma metastases
Flow voidsHemangioblastoma, AVM

PART 8: TUMOURS WITH CALCIFICATIONS

TumourCalcification Features
OligodendrogliomaAlmost always calcified; gyriform/ribbon-like in cortex; CT hyperdense
Craniopharyngioma"Eggshell" or nodular; 90% of adamantinomatous type; 15% papillary type
MeningiomaPsammomatous (whorled) calcification
DNETFocal cortical calcification possible
GangliogliomaMural nodule or calcification 30-50%
Pilocytic astrocytomaPossible calcification in solid nodule
EpendymomaFocal calcification common
TeratomaMixed calcification, fat, soft tissue
Pineocytoma"Exploded" pineal calcification (displaces normal gland calcium outward)
Choroid plexus papillomaFine calcification
GerminomaEngulfs pineal calcification (calcification within tumour)
CT rule: Oligodendroglioma - gyriform cortical Ca2+; Craniopharyngioma - suprasellar Ca2+; Germinoma vs Pineocytoma - both can show pineal Ca2+

PART 9: LOW GRADE vs. HIGH GRADE TUMOURS

Low Grade Features (WHO 1-2)

  • T2/FLAIR hyperintense, well-circumscribed or infiltrative
  • No contrast enhancement (with exceptions: pilocytic astrocytoma, ganglioglioma DO enhance despite being low grade)
  • No necrosis
  • No haemorrhage
  • Minimal or no oedema
  • High ADC (low cellularity)
  • Low rCBV on perfusion
  • MRS: mild Cho elevation, NAA preserved or mildly reduced

High Grade Features (WHO 3-4)

  • Heterogeneous signal, irregular enhancement (often ring)
  • Central necrosis
  • Haemorrhage
  • Surrounding vasogenic oedema
  • Low ADC (high cellularity)
  • High rCBV on perfusion (>2 x contralateral white matter)
  • MRS: high Cho, low NAA, lipid/lactate peaks

Important Exceptions

  • Pilocytic astrocytoma (WHO 1): vivid cyst-with-mural-nodule enhancement - DO NOT misgrade
  • Ganglioglioma (WHO 1-2): cortical enhancement, calcification
  • DNET (WHO 1): no enhancement (bubbly cortical lesion)
  • PXA (WHO 2-3): may show meningeal contact, cyst + nodule, BRAF V600E

PART 10: CONTRAST ENHANCEMENT PATTERNS

No Enhancement

  • Low-grade astrocytoma (WHO 2, IDH-mutant)
  • DNET
  • Arachnoid cyst
  • Epidermoid cyst
  • Dermoid cyst

Homogeneous Enhancement

  • Metastases (small, solid)
  • Lymphoma (periventricular, homogeneous, ice-ball appearance)
  • Germinoma / Pineal tumours
  • Pituitary macroadenoma
  • Pilocytic astrocytoma (solid component)
  • Ganglioglioma
  • Meningioma (extra-axial, homogeneous)
  • Schwannoma

Ring Enhancement

  • GBM (thick, irregular ring)
  • Metastases (thin, regular ring)
  • Brain abscess (thin, smooth, regular ring - "rim sign"; inner dark rim on T2)
  • Tumefactive MS (incomplete/open ring - "horseshoe" opens toward grey matter)
  • Radiation necrosis (ring-like)
  • Lymphoma in immunocompromised (ring) vs immunocompetent (solid)

Cyst + Mural Nodule Enhancement

  • Pilocytic astrocytoma (classic)
  • Hemangioblastoma (solid enhancing nodule + large cyst, posterior fossa adults, VHL)
  • Ganglioglioma
  • PXA

Dural Tail Enhancement

  • Meningioma (classic)
  • Also seen in: Lymphoma, Sarcoidosis, Chloroma, some metastases - NOT specific

PART 11: MR SPECTROSCOPY FINDINGS

Normal brain metabolites (in order of prominence): NAA > Cr > Cho > mI
MetaboliteNormal roleTumour significance
NAA (N-acetylaspartate, 2.0 ppm)Neuronal markerDecreased in tumour (neuron loss)
Cho (Choline, 3.2 ppm)Membrane turnoverElevated in tumour (proliferation)
Cr (Creatine, 3.0 ppm)Energy metabolismRelatively stable reference
Lipid/Lactate (0.9-1.3 ppm)None normallyElevated in necrosis, high-grade tumour
mI (myo-inositol, 3.5 ppm)Glial markerElevated in low-grade glioma, astrocytoma
Ala (Alanine, 1.47 ppm)Amino acidElevated in meningioma

Tumour-Specific MRS Patterns

TumourMRS Key Features
High-grade glioma (GBM)Very high Cho, very low NAA, prominent lipid/lactate, Cho/NAA >2
Low-grade gliomaMildly elevated Cho, mildly reduced NAA, elevated mI
MeningiomaHigh Cho, absent NAA (no neurons), alanine peak at 1.47 ppm
LymphomaHigh Cho, low NAA, elevated lipid, prominent Cho peak
MetastasisHigh Cho, absent/low NAA at centre, lipid/lactate in necrotic core
Radiation necrosisLarge lipid/lactate, low/absent Cho and NAA
AbscessAmino acids (0.9 ppm) - valine, leucine, isoleucine; absent NAA and Cho
DemyelinationElevated Cho (acutely), elevated Cr, NAA may recover
Key ratio: Cho/NAA > 2.0 = highly suspicious for high-grade tumour

PART 12: PERFUSION MRI FINDINGS

DSC (Dynamic Susceptibility Contrast) - rCBV

TumourrCBV
GBM (WHO 4)Very high (>4-5x contralateral WM)
High-grade glioma (WHO 3)Elevated (2-4x)
Low-grade glioma (WHO 2)Low (<1.5x) - except oligodendroglioma can be higher
LymphomaElevated Cho but PARADOXICALLY LOW rCBV (vessel wall narrowing by tumour cells, not angiogenesis) - KEY DISTINGUISHING FEATURE
MetastasesElevated rCBV in enhancing rim
MeningiomaVery high rCBV
HemangioblastomaVery high rCBV
Radiation necrosisLow rCBV (vs tumour recurrence: high rCBV)
AbscessLow rCBV
Tumefactive MSLow/normal rCBV
Lymphoma vs GBM perfusion: GBM has HIGH rCBV; Lymphoma has LOWER rCBV despite solid enhancement - this is a classic teaching point.

Leakage Correction

Lymphoma shows pronounced contrast leakage curve on DSC (steep K2 leakage) - hallmark.

PART 13: DWI / ADC FINDINGS

TumourDWIADCMechanism
LymphomaBright (restricted)LowDense cellularity, high nuclear-cytoplasm ratio
MedulloblastomaBright (restricted)LowHighly cellular embryonal tumour
PNET/CNS-PNETBrightLowSame as medulloblastoma
Epidermoid cystBrightLow (pseudo-restriction - slow diffusion of solid keratin)Keratin content
AbscessBrightVery lowViscous pus, inflammatory cells
GBMSolid component: intermediate/high; Necrosis: facilitatedMixedNecrosis = high ADC; solid = intermediate
Low-grade gliomaIso/darkHighLow cellularity
Arachnoid cystDarkVery high (CSF equivalent)Free water
Dermoid cystBrightVariableLipid content
Radiation necrosisHigh ADC (vs pseudoprogression: higher ADC in radiation necrosis; recurrence: lower ADC)HighOedema dominates
Key rules:
  • Low ADC = high cellularity = high-grade or lymphoma
  • Epidermoid vs Arachnoid cyst: Epidermoid restricts (bright DWI, dark ADC); Arachnoid does NOT restrict
  • Abscess vs GBM: Abscess has very low ADC in core; GBM necrotic core has HIGH ADC

PART 14: CT vs. MRI APPEARANCE SUMMARY

CT Density Rules

Hyperdense on CTCause
LymphomaDense cellularity
Medulloblastoma (PNET-MB)Dense cellularity
Colloid cystMucoid content
MeningiomaCalcification / fibrous stroma
Epidermoid with proteinAtypical
Haemorrhagic metastasesBlood
Hypodense on CTCause
Low-grade gliomaLow attenuation
Arachnoid cystCSF density
Dermoid/LipomaFat density (-50 to -100 HU)
EpidermoidSlightly above CSF
AbscessCentral low density

PART 15: WHO 2021 CNS TUMOUR CLASSIFICATION (5th Edition)

Key changes from 2016:
  1. Molecular markers are now required for classification (integrated diagnosis)
  2. Glioblastoma is now EXCLUSIVELY IDH-wildtype (previously IDH-mutant GBM reclassified as astrocytoma grade 4)
  3. Diffuse gliomas separated into adult-type and paediatric-type
  4. Grading: now uses Arabic numerals (1, 2, 3, 4) instead of Roman (I, II, III, IV)
  5. New entities: Diffuse midline glioma H3K27-altered, Diffuse hemispheric glioma H3G34-mutant

WHO 2021 Adult Diffuse Glioma Groups

TumourKey MarkersGrade
Astrocytoma, IDH-mutantIDH1/2 mut, ATRX loss, no 1p/19q codeletion2, 3, or 4
Oligodendroglioma, IDH-mutant, 1p/19q-codeletedIDH mut + 1p/19q codeletion2 or 3
Glioblastoma, IDH-wildtypeIDH-wildtype + TERT promoter, EGFR amp, +7/-104
Diffuse midline glioma, H3K27-alteredH3K27M or EZHIP overexpression4
Diffuse hemispheric glioma, H3G34-mutantH3.3G34R/V mutation4

Paediatric-Type Diffuse Gliomas

  • Diffuse low-grade glioma, MAPK-altered
  • Diffuse high-grade glioma, H3-wildtype, IDH-wildtype
  • Infant-type hemispheric glioma (NTRK/ALK/ROS/MET fusions)

PART 16: T2/FLAIR MISMATCH SIGN

Definition: Solid tumour showing VERY high T2 signal that is SUPPRESSED (attenuated) on FLAIR, with a FLAIR-bright peripheral rim.
The sign: T2 = bright. FLAIR = dark centrally with a bright rim.
Specificity: ~100% specific for IDH-mutant astrocytoma (not oligodendroglioma)
Why it occurs: Abundant extracellular fluid / low cell density in IDH-mutant astrocytoma behaves like "near-CSF" signal - T2 bright, FLAIR suppressed.
Clinical utility: If T2/FLAIR mismatch sign is present in a non-enhancing diffuse glioma, the diagnosis is almost certainly IDH-mutant astrocytoma. Can avoid biopsy in appropriate clinical context.
Important: Does NOT apply to oligodendroglioma (they do NOT show this sign despite IDH mutation - they lack this specific architecture).

PART 17: SPECIFIC TUMOURS - IMAGING & ASSOCIATIONS


GLIOBLASTOMA (GBM, WHO Grade 4, IDH-wildtype)

CT: Heterogeneous hypodense mass with central necrosis, vasogenic oedema, mass effect. Thick, irregular hyperdense enhancing rim.
MRI:
  • T1: Hypointense core (necrosis), T1-bright haemorrhage may be present
  • T2/FLAIR: Heterogeneous; central hypointense necrosis; surrounding FLAIR bright oedema
  • DWI: Solid component intermediate-restricted; necrosis = facilitated diffusion
  • ADC: Necrosis >1000; solid component ~745 ± 135 x10⁻⁶ mm²/s
  • Post-contrast: Thick, irregular ring enhancement
  • Perfusion: Very high rCBV
  • MRS: Very high Cho, very low NAA, lipid/lactate
Hallmarks: Butterfly lesion (corpus callosum crossing), subependymal spread, central necrosis, irregular ring enhancement.
Molecular: IDH-wildtype, TERT promoter mutation, EGFR amplification, chromosome 7 gain / chromosome 10 loss, MGMT promoter methylation (prognostic for temozolomide response).

OLIGODENDROGLIOMA (IDH-mutant, 1p/19q-codeleted, WHO 2-3)

Location: Frontal > temporal lobe cortex, subcortical.
CT: Gyriform cortical calcification (70-90%), mixed hypodense/isodense, "ribbon-like" Ca2+ in cortex.
MRI:
  • T2/FLAIR: Hyperintense, may involve cortex
  • No T2/FLAIR mismatch (unlike astrocytoma)
  • ADC: High (facilitates diffusion)
  • Enhancement: 20-30% (grade 2); more in grade 3
  • Perfusion: rCBV elevated (more than astrocytoma of same grade - due to "chicken wire" vasculature)
  • MRS: Elevated Cho/NAA
Key imaging feature: Cortical calcification + frontal lobe location + young adult + seizures = oligodendroglioma until proven otherwise.

DIFFUSE MIDLINE GLIOMA, H3K27-ALTERED (WHO Grade 4)

Includes: DIPG (Diffuse Intrinsic Pontine Glioma) and thalamic/spinal cord equivalents.
Location: Pons (most common in children), thalamus, spinal cord, cerebellum.
MRI:
  • T2/FLAIR: Diffuse hyperintensity engulfing and expanding the pons
  • Basilar artery "engulfed" by tumour (classic pontine sign)
  • Minimal or no contrast enhancement (may enhance at recurrence)
  • Diffuse, poorly defined borders
Associations: Paediatric (median age 6-7 years); H3K27M mutation; median survival <15 months; NO resection possible (biopsy only in selected centres).

PILOCYTIC ASTROCYTOMA (WHO Grade 1)

Location: Cerebellum (most common), hypothalamus/optic chiasm (NF1!), brainstem, spinal cord.
MRI:
  • Classic: Cyst with enhancing mural nodule (60%)
  • Solid with central necrosis (25%)
  • Purely solid (15%)
  • T2: Very hyperintense
  • T1 post-contrast: Vivid nodule enhancement
  • ADC: High (low cellularity)
  • Perfusion: Low rCBV despite enhancement
  • MRS: Mildly elevated Cho
Pathognomonic features:
  • Cyst + brightly enhancing mural nodule in cerebellum of child
  • KIAA1549-BRAF fusion (most common molecular marker)
  • Rosenthal fibres + eosinophilic granular bodies on histology
Associations: NF1 (optic pathway gliomas), sporadic (cerebellar).

PLEOMORPHIC XANTHOASTROCYTOMA (PXA, WHO Grade 2-3)

Location: Superficial temporal lobe cortex (most common), meningeal contact.
MRI:
  • Cyst with enhancing mural nodule (leptomeningeal contact - KEY feature)
  • T2 hyperintense
  • Superficial/cortical location
  • Enhancement: Solid nodule and meningeal enhancement
  • Young adults, chronic epilepsy history
Associations: BRAF V600E mutation (most common - also seen in ganglioglioma, papillary craniopharyngioma). WHO grade 3 (anaplastic PXA) = higher risk recurrence.

DNET (Dysembryoplastic Neuroepithelial Tumour, WHO Grade 1)

Location: Cortex - temporal lobe (most common), frontal lobe. Strictly cortical.
MRI:
  • T2: "Bubbly" multicystic cortical lesion with pseudostratified appearance
  • FLAIR: "Bright rim sign" - peripheral FLAIR hyperintensity, central FLAIR suppression (like T2/FLAIR mismatch in cortex)
  • DWI: No restriction
  • Enhancement: None or very faint (< 30%)
  • No oedema, no mass effect (despite large size)
  • Scalloping of overlying calvarium (chronic pressure)
  • T1: Hypointense
Associations: Long-standing refractory partial seizures in young patients. Often confused with oligodendroglioma. Excellent prognosis - surgery curative.
Pathognomonic feature: Cortical "bubbly" lesion + chronic seizures + no oedema + young patient.

GANGLIOGLIOMA (WHO Grade 1-2)

Location: Temporal lobe (most common - 70%), then frontal, parietal.
MRI:
  • T2: Hyperintense, well-circumscribed, cortical/subcortical
  • Mixed solid-cystic
  • Enhancement: Variable - mural nodule or solid enhancement (30-50%)
  • Calcification: 30-50%
  • DWI: No restriction
  • Low ADC (variable)
  • No significant oedema
Associations: BRAF V600E (common), BRAF fusions; chronic epilepsy; young patients; Lhermitte-Duclos disease (dysplastic gangliocytoma of cerebellum - PTEN hamartoma, "corduroy" MRI pattern).

ROSETTE-FORMING GLIONEURONAL TUMOUR (RGNT, WHO Grade 1)

Location: Fourth ventricle/aqueduct, midline posterior fossa.
MRI:
  • Mixed cystic-solid lesion in fourth ventricle/aqueduct
  • Enhancement: Nodular within the solid component
  • T2: Hyperintense cystic component
  • Young adults (20-30s)
Associations: NF1 occasionally. Biphasic histology: glial component + neuronal rosettes around vessels.

SUBEPENDYMOMA (WHO Grade 1)

Location: Fourth ventricle (most common), lateral ventricle (frontal horn), rarely third ventricle.
MRI:
  • T2: Hyperintense, lobulated intraventricular mass
  • T1: Hypointense
  • Enhancement: None or minimal (KEY - distinguishes from ependymoma)
  • DWI: No restriction
  • Calcification: Possible
  • Incidental finding in middle-aged/older adults
Key feature: Non-enhancing fourth ventricle lesion in adult = subependymoma (vs ependymoma which enhances).

EPENDYMOMA (WHO Grade 2-3)

Location by age/site:
  • Children: Fourth ventricle (intracranial) - "squeezes" through foramina
  • Adults: Spinal cord (most common site in adults), filum terminale (myxopapillary)
  • Supratentorial: RELA fusion type (now WHO molecular classification)
CT: Heterogeneous, calcification common, may have haemorrhage.
MRI:
  • T2: Heterogeneous, intermediate-high signal
  • T1 post-contrast: Moderate heterogeneous enhancement
  • DWI: Variable
  • Calcification, cysts, haemorrhage - "heterogeneous" = classic
  • Fourth ventricle tumour that "squeezes" through foramen of Magendie into cervical canal = PATHOGNOMONIC
  • Haemosiderin capping (on spine): "cap sign" - haemosiderin at superior and inferior poles
Associations: NF2 (spinal ependymoma, grade 2); RELA fusion (supratentorial, more aggressive); H3K27M = infratentorial, worse prognosis.
Seeding: Can seed subarachnoid space - staging spine MRI required.

MEDULLOBLASTOMA (WHO Grade 4)

Location: Cerebellar vermis (children), cerebellar hemisphere (adults, desmoplastic variant).
CT: Hyperdense midline posterior fossa mass.
MRI:
  • T2: Isointense to hypointense (dense cells)
  • DWI: RESTRICTED (bright DWI, dark ADC) - KEY feature
  • T1 post-contrast: Moderate-vivid heterogeneous enhancement
  • Cysts, calcification, haemorrhage possible
  • Hydrocephalus (obstructs 4th ventricle)
  • Perfusion: High rCBV
Molecular subtypes (WHO 2021):
SubtypeMarkerAgeLocationPrognosis
WNT-activatedBeta-catenin nuclear, CTNNB1Children/adultsMidlineBest (>90% OS)
SHH-activated, TP53-mutTP53 mutationChildrenLateral hemispheresWorst
SHH-activated, TP53-wildtypePTCH1/SMOInfants + adultsHemispheresIntermediate
Non-WNT/Non-SHH Group 3MYC amplificationInfants/childrenMidlinePoor
Non-WNT/Non-SHH Group 4PRDM6, CDK6Children/adultsMidlineIntermediate
Seeding: Most common paediatric CNS tumour to seed - "sugar coating" of spine. ALWAYS stage with full spine MRI pre-operatively.

SEGA (Subependymal Giant Cell Astrocytoma, WHO Grade 1)

Location: Foramen of Monro (ALWAYS).
MRI:
  • T2: Heterogeneous, mixed signal
  • T1 post-contrast: Vivid, heterogeneous enhancement
  • Large (>1 cm) enhancing intraventricular nodule at foramen of Monro
  • May cause obstructive hydrocephalus
Associations: TUBEROUS SCLEROSIS COMPLEX (TSC) - PATHOGNOMONIC in context. Also associated TSC2/TSC1 (hamartin/tuberin) mutations. mTOR pathway.
Distinction: Subependymal nodules (tubers) in TSC are small, calcified, non-enhancing and do NOT obstruct. SEGA is large, enhancing, and obstructs.

CENTRAL NEUROCYTOMA (WHO Grade 2)

Location: Lateral ventricle (body), attached to septum pellucidum.
MRI:
  • T2: Heterogeneous, "soap bubble" or sponge-like cystic areas
  • T1 post-contrast: Moderate, heterogeneous enhancement
  • Calcification common
  • DWI: May show mild restriction
  • MRS: Glycine peak at 3.55 ppm (characteristic)
Age: Young adults (20-40 years).

MENINGIOMA (WHO Grade 1-3)

Location: Extra-axial; convexity, parasagittal, falcine, sphenoid wing, CPA, olfactory groove, planum sphenoidale, foramen magnum, tentorial.
CT: Isodense/hyperdense; homogeneous enhancement; hyperostosis of adjacent bone; calcification (psammomatous).
MRI:
  • T1: Isointense to grey matter
  • T2: Variable (isointense to hypointense in fibrotic types)
  • Post-contrast: Vivid homogeneous enhancement
  • Dural tail sign (reactive dural thickening - NOT tumour itself)
  • Restricted diffusion in atypical/malignant meningioma
Subtypes and T2 signal:
  • Fibroblastic/transitional: T2 hypointense (collagen)
  • Meningothelial: T2 isointense
  • Secretory: T2 hypointense
WHO grading:
  • Grade 1 (benign, 80%): Surgical cure, low recurrence
  • Grade 2 (atypical, 18%): Brain invasion, mitoses >4/10 HPF
  • Grade 3 (anaplastic, 2%): Sarcomatous, high recurrence
Associations: NF2 (bilateral meningiomas = NF2), prior radiation, female sex (progesterone receptors), chromosome 22q deletion.
Perfusion: Very high rCBV (extensive vascularity).

SOLITARY FIBROUS TUMOUR (SFT) / Haemangiopericytoma (WHO Grade 2-3)

Location: Dura-based (like meningioma) but more commonly tentorium, falx, CPA.
MRI:
  • T2: "Yin-yang" or "flip-flop" sign - heterogeneous T2 signal (mix of high and low)
  • Post-contrast: Vivid heterogeneous enhancement
  • May have prominent flow voids (vascular)
  • Narrow dural base (vs meningioma which has broad dural base)
  • Can erode bone (vs meningioma which causes hyperostosis)
Key differentiator from meningioma:
  • Heterogeneous T2 (meningioma is more homogeneous)
  • Bone erosion not hyperostosis
  • Narrower base
  • NAB2-STAT6 fusion (molecular diagnosis)
Associations: Extracranial metastases (lung, liver, bone) after long latency - unlike meningioma. Higher recurrence.

PITUITARY TUMOURS (PitNETs - Pituitary Neuroendocrine Tumours)

Classification: Now called PitNETs (WHO 2021 replaces "pituitary adenoma").
  • Microadenoma: < 10mm
  • Macroadenoma: ≥ 10mm
  • Giant adenoma: > 40mm
MRI Protocol: Thin-section coronal T1 (with and without Gd), dynamic contrast (microadenomas).
CT: Enlargement of sella, bony erosion.
Microadenoma MRI:
  • T1: Hypointense relative to normal pituitary (KEY)
  • T2: Variable
  • Dynamic contrast: Enhances LATER than normal pituitary (normal gland enhances first)
  • Stalk deviation away from lesion
Macroadenoma MRI:
  • T1 pre/post: "Snowman" or "figure-of-8" appearance through diaphragma sellae
  • Suprasellar extension - "waist" at diaphragma
  • T2: Heterogeneous (haemorrhage = pituitary apoplexy)
  • Enhancement: Moderate, heterogeneous
  • Optic chiasm compression (superior)
  • Cavernous sinus invasion (lateral) - Knosp grading
Pituitary Apoplexy: Haemorrhage/infarction of macroadenoma - T1 hyperintense, T2 variable, EMERGENCY.
Functional types (clinical-MRI correlation):
  • Prolactinoma (most common): Medical treatment (dopamine agonists)
  • GH-secreting: Acromegaly/gigantism
  • ACTH-secreting: Cushing disease (often very small - needs dynamic study)
  • TSH-secreting: Central hyperthyroidism
  • Non-functioning: Headache, visual field defects

CRANIOPHARYNGIOMA (WHO Grade 1)

Two types:
FeatureAdamantinomatousPapillary
AgeChildren (5-15y) and adultsAdults (40-55y)
LocationSuprasellar/IntrasellarPurely suprasellar/3rd ventricle
Calcification90% (eggshell/nodular)15%
Cyst content"Motor oil" - cholesterol-rich, T1 brightSerous
T1Hyperintense cystic componentHypointense
T2HeterogeneousHyperintense
EnhancementRim/nodular of solid componentSolid component enhances
MutationCTNNB1 (beta-catenin)BRAF V600E
Key imaging: Suprasellar calcified cystic-solid lesion with T1-bright cyst = adamantinomatous craniopharyngioma.

RATHKE CLEFT CYST (RCC)

Location: Intrasellar (most common), can extend suprasellarly.
MRI:
  • T1: Variable (depends on protein content) - 60% T1 bright, 40% T1 dark
  • T2: Variable
  • No enhancement of cyst wall (KEY distinguishing feature)
  • Intracystic nodule (T1 dark, T2 dark): Floating debris = pathognomonic - "pea in a pod" appearance
  • No calcification (vs craniopharyngioma)
Key: Intracystic nodule + no enhancement = Rathke cleft cyst (not craniopharyngioma).

PINEAL GLAND TUMOURS

Differential for pineal region mass:
  1. Germinoma (most common, 50-60% of pineal tumours)
  2. Pineal parenchymal tumour (pineocytoma vs pineoblastoma)
  3. Glioma
  4. Dermoid/Epidermoid/Teratoma
  5. Benign pineal cyst (incidental)

Germinoma

  • Young males (peak 10-25 years)
  • T1: Isointense; T2: Isointense; Vivid homogeneous enhancement
  • "Engulfs" pre-existing pineal calcification (calcium within tumour)
  • Can seed ventricles and subarachnoid space
  • Parinaud syndrome (upgaze palsy - dorsal midbrain compression)
  • HCG and AFP can be elevated (non-germinomatous GCT)

Pineocytoma (WHO Grade 1)

  • Mature pineal cells
  • "Exploded" pineal calcification - calcification displaced to periphery
  • Small, well-circumscribed, homogeneous enhancement

Pineoblastoma (WHO Grade 4)

  • Highly cellular, aggressive embryonal tumour
  • T2: Hypointense (dense cells)
  • DWI: Restricted
  • Heterogeneous enhancement
  • Leptomeningeal seeding common
  • Associated with germline RB1 mutation ("trilateral retinoblastoma")

PART 18: PRIMARY and SECONDARY CNS LYMPHOMA

Primary CNS Lymphoma (PCNSL)

Histology: Diffuse Large B-Cell Lymphoma (DLBCL) in 95% of immunocompetent cases.
Location: Periventricular white matter, corpus callosum, basal ganglia, subependymal region.
CT: Hyperdense (due to dense cellularity).
MRI:
  • T1: Isointense to hypointense
  • T2: Isointense to hypointense (DARK on T2 relative to white matter) - KEY
  • DWI: RESTRICTED (bright DWI, low ADC) - KEY
  • Post-contrast:
    • Immunocompetent: Solid, homogeneous, vivid enhancement ("ice ball")
    • Immunocompromised (HIV/AIDS): Ring enhancement (may look like toxoplasmosis)
  • Perfusion: Elevated Cho, BUT rCBV paradoxically LOW compared to GBM
  • MRS: High Cho, high lipid
Pathognomonic features:
  • Periventricular/subependymal hyperdense mass
  • T2 DARK (not T2 bright like most tumours)
  • Restricted diffusion
  • Solid homogeneous enhancement
  • Dramatic response to steroids ("ghost tumour" - may disappear on steroids - do NOT give steroids before biopsy)
"Ghost Tumour": If steroids are given before biopsy, lymphoma can temporarily completely resolve - diagnostic nightmare. Biopsy first, steroids after.

Secondary CNS Lymphoma

  • From systemic B-cell or T-cell lymphoma
  • Leptomeningeal involvement more common
  • Dural deposits
  • Intraparenchymal rarer

PART 19: CYSTIC TUMOURS OF THE BRAIN

Intra-axial Cystic Tumours

TumourCharacteristics
Pilocytic astrocytomaClassic cyst + mural nodule; enhancing nodule; T2 bright cyst
HemangioblastomaLarge cyst + small enhancing nodule; posterior fossa; VHL
GBMPseudo-cyst (necrosis with irregular ring enhancement)
PXACyst + superficial enhancing nodule
GangliogliomaCyst + nodule; temporal lobe
EpendymomaCystic component within heterogeneous mass
CraniopharyngiomaSuprasellar cyst (T1 bright)
Cystic metastasisRing-enhancing; often at grey-white junction
Brain abscessDWI restriction in core

PART 20: BENIGN CYSTS OF THE BRAIN

Extra-axial Benign Cysts

Arachnoid Cyst

  • Content: CSF - identical signal to CSF on all sequences
  • T1: Hypointense (CSF); T2: Hyperintense (CSF)
  • FLAIR: Suppressed (CSF signal nulled)
  • DWI: NO restriction (unlike epidermoid!)
  • Enhancement: None
  • Scallops adjacent bone (pressure effect)
  • Location: Middle cranial fossa (most common), CPA, suprasellar, posterior fossa
  • Key differentiator from epidermoid: Arachnoid = no DWI restriction; Epidermoid = DWI BRIGHT

Epidermoid Cyst

  • Content: Desquamated keratin from ectoderm
  • T1: Hypointense (slightly higher than CSF)
  • T2: Hyperintense (similar to CSF)
  • FLAIR: Incomplete suppression (slightly higher than CSF)
  • DWI: RESTRICTED (bright DWI, dark ADC) - KEY distinguishing feature from arachnoid cyst
  • Enhancement: None (smooth capsule)
  • Location: CPA cistern (most common), parasellar, fourth ventricle
  • "Cauliflower" or "frond-like" insinuating margins - wraps around neurovascular structures
  • Trigeminal neuralgia if CPA location

Dermoid Cyst

  • Content: All three germ layers - hair, sebaceous glands, fat
  • T1: Very hyperintense (fat!) - BRIGHT on T1
  • T2: Heterogeneous
  • Fat-suppressed sequences: Fat signal suppressed
  • Ruptured dermoid: Fat droplets scattered throughout subarachnoid space - pathognomonic
  • Enhancement: None
  • DWI: Bright (lipid signal, not true restriction)
  • Location: Midline - posterior fossa, suprasellar

Neurenteric / Neuroenteric Cyst

  • Rare; spinal > intracranial
  • Contents = CSF signal or higher protein
  • T1: Variable; T2: Hyperintense

Intra-axial Benign Cysts

Ependymal Cyst (also called "neuroepithelial cyst")

  • Lined by ependymal cells
  • Within brain parenchyma or ventricles
  • CSF-identical signal on ALL sequences including FLAIR
  • No restriction, no enhancement
  • Incidental; near trigone of lateral ventricle

Choroid Plexus Cyst

  • Small cysts within choroid plexus; incidental; may relate to aneuploidy (trisomy 18) in fetal context

Pineal Cyst

  • Very common (up to 40% of population)
  • Simple: < 10mm, no internal septae, thin wall
  • Enhancement: Thin peripheral rim (normal ependyma enhances)
  • T1: Slightly higher than CSF (protein)
  • FLAIR: Incomplete suppression
  • If > 10mm, thick wall, internal nodule, or septa - consider tumour

PART 21: SCHWANNOMA

Origin: Schwann cells (neural crest) of cranial nerve sheaths.
Most Common:
  • Vestibular schwannoma (acoustic neuroma) - CN VIII, CPA cistern, IAC
  • Trigeminal schwannoma - CN V, Meckel cave / middle cranial fossa
  • Facial schwannoma - CN VII
  • Less common: IX, X, XI, XII

Vestibular Schwannoma

MRI:
  • T1: Isointense to hypointense
  • T2: Hyperintense (high fluid-content microcysts)
  • Post-contrast: Vivid, homogeneous enhancement
  • "Ice cream cone" shape - bulb in CPA cistern + cone into IAM
  • Widening of IAC (vs meningioma at CPA which does NOT widen IAC)
  • Cystic change in larger tumours
Extra-axial signs: CSF cleft, no brain engulfment.
Association: NF2 (bilateral vestibular schwannomas = diagnostic of NF2); schwannomatosis (multiple without NF2); sporadic.
Differential at CPA:
  • Meningioma (no IAC widening, broad dural base, hyperdense CT, dural tail)
  • Epidermoid (no enhancement, DWI bright)
  • Facial nerve schwannoma (follows CN VII)

PART 22: BRAINSTEM GLIOMA - TYPES

TypeLocationAgeMRIPrognosis
DIPG (H3K27M)Pons - diffuseChildren (6-7y)Diffuse T2 expansion of pons, minimal enhancementVery poor (<12-15 months)
Focal brainstem gliomaMidbrain/medullaAll agesWell-circumscribed, enhancement variableGood (surgical/radiation)
Dorsal exophytic gliomaDorsal medulla/ponsChildrenExophytic, T2 bright, ±enhancementModerate
Tectal gliomaQuadrigeminal plateChildrenT2 bright enlargement of tectum, NO enhancementExcellent (usually treated with CSF diversion only)
Cervicomedullary gliomaMedulla/cervical cord junctionChildrenT2 bright, usually pilocyticGood
DIPG: Engulfs basilar artery; diffuse, ill-defined; near-universal H3K27M mutation. Now called "diffuse midline glioma" in WHO 2021.

PART 23: MENINGIOMA - COMPLETE

Locations by frequency:
  1. Cerebral convexity
  2. Parasagittal / falcine
  3. Sphenoid wing (inner - cavernous sinus; outer - "en plaque")
  4. Olfactory groove
  5. Planum sphenoidale
  6. Suprasellar / tuberculum sellae
  7. Posterior fossa / CPA
  8. Foramen magnum
  9. Intraventricular
  10. Orbital
En plaque meningioma: Flat sheet of dural tumour (sphenoid wing) - causes exophthalmos.
Imaging tips:
  • T2 signal correlates with subtype: Secretory (very T2 bright) vs Fibroblastic (T2 dark)
  • Perfusion: Very high rCBV
  • MRS: Alanine peak (1.47 ppm) + absent NAA = classic for meningioma
  • ADC: Intermediate; Grade 2/3 = lower ADC (more restricted)

PART 24: TUMOUR MIMICS

These lesions can look like brain tumours and must be excluded:
MimicKey Differentiating Features
Tumefactive MSOpen/incomplete ring enhancement (opens toward grey matter/cortex); young female; other MS lesions; low rCBV; MRS: elevated Cho (acutely) but recovers
Brain abscessDWI bright core (low ADC); ring enhancement; amino acid peaks on MRS; pyogenic fever, source
Cerebral toxoplasmosisHIV+ patient; ring-enhancing; thalamus/basal ganglia; responds to anti-toxo treatment
Tumefactive PMLHIV/immunocompromised; JC virus; no enhancement usually; subcortical, no mass effect
Subacute infarctVascular territory; DWI bright acutely; gyral enhancement; no mass effect beyond first week
ADEMPost-infectious/vaccination; multifocal WM lesions; bilateral; periventricular; cotton-ball appearance
Radiation necrosisPost-treatment; enhancing; low rCBV; large lipid/lactate on MRS; high ADC
Cavernoma"Popcorn" T2 heterogeneous; T2*GRE blooming; no oedema (unless recent bleed); no enhancement in chronic stage
DVA (Developmental venous anomaly)"Caput medusae" on MRA/venous phase; no mass; often has cavernoma nearby
Encephalitis (HSV)Temporal lobe DWI restriction; haemorrhage; CSF PCR
Cortical dysplasia (FCD)Blurring of grey-white junction; transmantle sign; no mass effect; seizure history
Lymphocytic hypophysitisPituitary enlargement; stalk thickening; homogeneous enhancement; post-partum female
SarcoidosisLeptomeningeal nodular enhancement; perivascular spaces; cranial nerve involvement
Langerhans Cell HistiocytosisSkull lesion + pituitary stalk thickening; no posterior pituitary T1 bright spot

PART 25: RADIATION NECROSIS vs. PSEUDOPROGRESSION

Background

  • After treatment of GBM with radiation + temozolomide, new or enlarged enhancement can be seen
  • Must distinguish TRUE progression from treatment-related changes

Pseudoprogression

  • Definition: Treatment-related enhancement increase at 1-3 months post-chemoradiation (early) that RESOLVES spontaneously
  • More common in MGMT-methylated tumours (~50% of MGMT-methylated vs 20% unmethylated)
  • Timing: Within 3 months of completing radiation

Radiation Necrosis

  • Definition: Late treatment effect (months to years post-radiation)
  • Can look identical to tumour recurrence on conventional MRI

Imaging Differentiation

FeatureTumour RecurrenceRadiation Necrosis/Pseudoprogression
Perfusion (rCBV)HIGHLOW
ADCLower (cellular)Higher (oedema/necrosis)
MRSHigh Cho, low NAAHigh lipid/lactate, absent/low Cho
FDG-PETHypermetabolicHypometabolic
MET/FET-PETPositive (amino acid uptake)Negative
DSC leakageModerateHigh (marked leakage curve)
FLAIRMay increaseMay stabilise or decrease
Most reliable non-invasive method: MR perfusion (rCBV) - high rCBV = recurrence; low rCBV = necrosis.
MRS: Large lipid/lactate peak with absent/low Cho = radiation necrosis. High Cho with low NAA = recurrence.
Advanced: Amino acid PET (11C-MET or 18F-FET) is superior to FDG-PET for distinguishing recurrence from necrosis.

PART 26: SUBEPENDYMAL SEEDING / EPENDYMAL SPREAD - Summary

Tumours that spread along ependymal surface:
  • GBM (subependymal spread along ventricles)
  • Lymphoma (classically periventricular)
  • Medulloblastoma (CSF seeding to ventricles)
  • Germinoma (ventricles)
  • Ependymoma
Imaging: Post-contrast T1 - look for enhancing deposits lining ventricles.

PART 27: QUICK REFERENCE - PATHOGNOMONIC FEATURES

FeatureTumour
Restricted diffusion in cystic coreBrain abscess (not GBM)
Cerebellar cyst + mural nodule, childPilocytic astrocytoma
Posterior fossa cyst + mural nodule, adultHemangioblastoma
Periventricular T2-dark, DWI brightLymphoma
Corpus callosum "butterfly"GBM
Cortical bubbly + no oedema + seizuresDNET
FLAIR mismatchIDH-mutant astrocytoma (non-oligo)
Eggshell suprasellar calcificationAdamantinomatous craniopharyngioma
Exploded pineal calcificationPineocytoma
Engulfed pineal calcificationGerminoma
Intraventricular at foramen of Monro + TSSEGA
Fourth ventricle tumour squeezing through foraminaEpendymoma (children)
IAC widening + CPA massSchwannoma
Dural tail + hyperostosis + homogeneous enhancementMeningioma
Alanine peak on MRSMeningioma
Glycine peak (3.55 ppm)Central neurocytoma
T1 bright cyst in suprasellar regionCraniopharyngioma (adamantinomatous)
Intracystic T1/T2 dark nodule in sellaRathke cleft cyst
Fat droplets scattered in subarachnoid spaceRuptured dermoid cyst
DWI bright extra-axial CPA lesion, no enhancementEpidermoid cyst
"Motor oil" signal + calcification + suprasellarCraniopharyngioma
Ghost tumour (disappears with steroids)CNS Lymphoma
Bilateral CPA massesNF2 (bilateral vestibular schwannomas)
Heterogeneous T2 dural mass + bone erosionSFT/haemangiopericytoma
Large cyst + tiny nodule at posterior fossa, adultHemangioblastoma (VHL)
H3K27M + pontine expansion, childDIPG / Diffuse midline glioma
BRAF V600E + cortical + cyst + meningeal contactPXA
Corduroy MRI of cerebellumDysplastic gangliocytoma / Lhermitte-Duclos (PTEN)

SUMMARY APPROACH ALGORITHM

INTRACRANIAL MASS
│
├── EXTRA-AXIAL? (CSF cleft, buckling, no grey matter engulfment)
│   ├── CPA → Schwannoma vs Meningioma vs Epidermoid
│   ├── Dural → Meningioma vs SFT vs Metastasis vs Sarcoidosis
│   └── Sellar → Pituitary vs Craniopharyngioma vs RCC vs Meningioma
│
└── INTRA-AXIAL?
    ├── AGE: Paediatric?
    │   ├── Posterior fossa → Pilocytic vs Medulloblastoma vs Ependymoma
    │   └── Supratentorial → DNET vs Ganglioglioma vs PXA vs SEGA(TS)
    │
    └── AGE: Adult?
        ├── Enhancement + Ring → GBM vs Metastasis vs Abscess vs Lymphoma (HIV)
        ├── Homogeneous + periventricular → Lymphoma
        ├── No enhancement + diffuse → Low-grade glioma (IDH-mutant)
        ├── T2/FLAIR mismatch → IDH-mutant astrocytoma
        ├── DWI bright + low ADC → Lymphoma / Medulloblastoma / Abscess (check MRS)
        └── Perfusion high + necrosis → GBM

Sources: Robbins & Kumar Basic Pathology, Bradley and Daroff's Neurology in Clinical Practice, Grainger & Allison's Diagnostic Radiology, WHO Classification CNS Tumours 2021, Radiology Assistant (radiologyassistant.nl), PMC Brain Tumour Imaging Review, RadioGraphics, Radiopaedia.
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