Brain tumor reading is anatomical + characterizational: where the mass sits (intra-axial vs extra-axial; supra- vs infratentorial; specific lobe; deep gray; CPA; pineal; sellar; intraventricular) narrows the differential dramatically; signal and enhancement characteristics + perfusion / spectroscopy then refine to a working diagnosis. This page focuses on adult tumors with brief pediatric coverage.

🔹 Bottom Line: Brain Tumor Imaging

  • Intra-axial vs extra-axial: changes differential. Extra-axial = CSF cleft, dural tail, vascular displacement; intra-axial = surrounded by brain.
  • Adult intra-axial: glioma (any grade), metastasis (multiple in 50%), lymphoma (often deep, periventricular), demyelinating mimic (tumefactive plaque), abscess.
  • Adult extra-axial: meningioma (commonest), schwannoma (CPA — CN VIII), pituitary, dermoid/epidermoid, dural metastasis.
  • Pediatric posterior fossa: medulloblastoma (vermian, restricting), pilocytic astrocytoma (cystic + enhancing nodule), ependymoma (4th ventricle “plasticity”), brainstem glioma (DIPG).
  • Perfusion (DSC-MR): high rCBV in high-grade glioma; low in lymphoma despite high cellularity.
  • Spectroscopy: high choline / low NAA = tumor; lipid/lactate = necrosis; 2HG peak = IDH-mutant glioma.
  • DWI/ADC: central restriction in abscess (vs ring-enhancing tumor); restriction in lymphoma + medulloblastoma (hypercellular).

Intra-Axial vs Extra-Axial Distinction

Feature Intra-axial Extra-axial
Location Within brain parenchyma Outside brain (epidural, subdural, subarachnoid)
CSF cleft No Yes — between mass and brain
Buckling of gray matter No Yes — gray matter displaced inward
Pial vessels Displaced peripherally Displaced centrally (between mass and brain)
Dural tail No Common (meningioma)
Bone reaction Rare Common (hyperostosis for meningioma)
Examples Glioma, metastasis, lymphoma, abscess, demyelinating Meningioma, schwannoma, pituitary, metastatic dural lesion, epidermoid

Glioma Family (Adult, Intra-Axial)

2021 WHO Classification — Imaging Implications

  • IDH status drives diagnosis: IDH-mutant glioma (oligodendroglioma if 1p/19q codeleted; astrocytoma otherwise) vs IDH-wildtype glioblastoma.
  • MGMT methylation: predicts temozolomide response.
  • Imaging biomarkers: T2-FLAIR mismatch sign (T2 bright + FLAIR dark center, bright rim) is highly specific for IDH-mutant astrocytoma.
  • 2HG peak on spectroscopy: confirms IDH-mutant.

Glioblastoma (IDH-Wildtype Grade 4)

  • Adult, supratentorial, often involves both hemispheres via corpus callosum (“butterfly glioma”).
  • Heterogeneous T2/FLAIR with central necrosis (T2 bright, non-enhancing) + thick irregular ring enhancement.
  • Vasogenic edema surrounds (finger-like, white matter sparing cortex).
  • High rCBV on DSC-MR perfusion (hypervascular).
  • Spectroscopy: high choline / NAA ratio + lipid/lactate.
  • DWI: typically does NOT restrict centrally (vs abscess); rim may restrict.

Lower-Grade Glioma (IDH-Mutant Astrocytoma, Oligodendroglioma)

  • Young adult; supratentorial; often frontal.
  • T2/FLAIR hyperintense, often non-enhancing (enhancement suggests progression).
  • Oligodendroglioma: calcifications (CT, SWI) common; “scrambled egg” appearance.
  • Lower rCBV than high-grade glioma.
  • T2-FLAIR mismatch sign in IDH-mutant astrocytoma.

Diffuse Midline Glioma (H3 K27M-Altered)

  • Children and adults; thalamus, brainstem (pons → DIPG), spinal cord.
  • Diffuse expansion + heterogeneous T2/FLAIR; variable enhancement.
  • Grade 4 by definition.

Brain Metastasis

  • Most common adult intra-axial CNS tumor.
  • Locations: gray-white junction (commonest), watershed, posterior fossa.
  • Multiple in ~50%; solitary in ~30% (consider biopsy if no known primary).
  • Imaging: spherical T1/T2 lesions with ring or nodular enhancement; disproportionate vasogenic edema relative to lesion size.
  • Hemorrhage-prone primaries: melanoma, renal cell, thyroid, choriocarcinoma (“MRTC BC”).
  • Leptomeningeal carcinomatosis: sulcal/leptomeningeal enhancement; CSF cytology / flow cytometry confirms.
  • Skull / dural metastases: bone window CT or T1 marrow signal loss; commonest from breast, prostate.

Primary CNS Lymphoma (PCNSL)

  • Patterns: solitary or multifocal masses in deep white matter, basal ganglia, thalamus, periventricular, corpus callosum.
  • T2: typically iso or slightly hyperintense (less bright than glioma due to hypercellularity).
  • Enhancement: homogeneous solid in immunocompetent; ring in immunocompromised (mimics toxoplasmosis).
  • DWI: restricts centrally (hypercellular).
  • DSC-MR perfusion: low rCBV (distinguishes from glioma despite cellularity).
  • Spectroscopy: high choline + high lipid (necrosis).
  • FDG-PET: highly avid (distinguishes from toxoplasmosis in HIV).
  • Steroids dramatically shrink (sometimes vanish) lymphoma → hold steroids before biopsy if possible.

Abscess vs Tumor (Ring-Enhancing Lesion)

Feature Abscess Tumor (GBM, met, lymphoma)
DWI center Restricts (viscous pus) Does not restrict (lymphoma is exception — restricts solidly)
ADC center Dark Bright (necrotic fluid)
SWI rim Smooth, complete Often irregular
Spectroscopy Amino acids, lactate, succinate, acetate peaks Choline up, NAA down
Perfusion Low rCBV in rim High rCBV in rim (GBM, met)
Surrounding edema Often less than tumor Often massive vasogenic

Meningioma

  • Extra-axial — CSF cleft, buckling of cortex, dural-based.
  • Dural tail: linear dural enhancement adjacent (highly suggestive but not specific).
  • T1 iso to gray matter; T2 iso; intense homogeneous enhancement.
  • Calcification in ~25%.
  • Hyperostosis of overlying skull on CT.
  • Locations: convexity (commonest), parasagittal/falcine, sphenoid wing, olfactory groove, suprasellar, posterior fossa, intraventricular (atrium), cerebellopontine angle.
  • WHO grading: Grade 1 (benign — 80%), Grade 2 (atypical — 18%), Grade 3 (anaplastic — 2%).
  • Hypervascular blush on DSA; embolization sometimes preoperative.

Schwannoma (Vestibular / Other)

  • Vestibular schwannoma (acoustic neuroma): commonest CPA mass.
  • Imaging: extends into internal auditory canal (IAC) — “ice cream on cone” appearance.
  • T1 iso/hypointense; T2 heterogeneous; intense enhancement.
  • Bilateral vestibular schwannomas: pathognomonic for NF2 (see Genetics).
  • Other schwannomas: trigeminal (Meckel’s cave), facial (IAC), jugular foramen.

Sellar / Suprasellar Lesions

  • Pituitary macroadenoma (≥10 mm): enlarges sella; “snowman” if extending superiorly through diaphragma; cavernous sinus invasion possible.
  • Pituitary microadenoma (<10 mm): dynamic post-contrast T1 shows delayed enhancement relative to normal gland (hypoenhancing focus).
  • Craniopharyngioma: suprasellar; cystic + solid + calcified; children and adults bimodal.
  • Rathke cleft cyst: thin-walled, non-enhancing, T1 variable (high protein bright); benign.
  • Meningioma (planum / tuberculum sellae): dural-based, intense enhancement.
  • Hypophysitis: thickened stalk, diffusely enhancing pituitary.
  • Pituitary apoplexy: enlarged heterogeneous pituitary ± hemorrhage on T1/SWI.

Pineal Region Lesions

  • Pineal cyst: benign incidental; thin wall; non-enhancing or thin rim enhancement.
  • Pineocytoma / pineoblastoma: solid enhancing mass; pineoblastoma in children (PNET family).
  • Germ cell tumors (germinoma, teratoma): pineal or suprasellar; germinoma is highly radiosensitive; βhCG / AFP markers.
  • Parinaud syndrome from upward gaze palsy / convergence-retraction nystagmus from dorsal midbrain compression.

Intraventricular Lesions

  • Colloid cyst: third ventricle at foramen of Monro; T1 bright, T2 dark (proteinaceous); can cause obstructive hydrocephalus.
  • Choroid plexus papilloma / carcinoma: cauliflower-like enhancing mass; trigone in adults, 4th vent in children.
  • Subependymoma: 4th ventricle / lateral ventricle; older adult; benign.
  • Central neurocytoma: lateral ventricle near septum pellucidum; young adults; “swiss cheese” appearance.
  • Ependymoma: 4th ventricle in children — “plastic” extends through foramina; supratentorial in adults.

Posterior Fossa Tumors (Pediatric)

  • Pilocytic astrocytoma: cerebellar hemisphere; cystic + enhancing mural nodule; benign, indolent.
  • Medulloblastoma: vermis (midline); DWI restricts (hypercellular); enhances; CSF dissemination (“drop metastases” to spine).
  • Ependymoma: 4th ventricle; “plasticity” through foramina of Luschka and Magendie.
  • Brainstem glioma (DIPG): diffuse pontine expansion; H3 K27M-altered.
  • ATRT (atypical teratoid rhabdoid tumor): infants; aggressive; mimics medulloblastoma but younger.

Hemangioblastoma

  • Cerebellar, brainstem, spinal cord.
  • Cystic + enhancing mural nodule (mimics pilocytic astrocytoma but adult).
  • VHL if multiple — see Genetics.

Recurrence vs Radiation Necrosis

Feature Tumor Recurrence Radiation Necrosis
FDG-PET / amino-acid PET Avid Hypometabolic
DSC perfusion (rCBV) High Low
Spectroscopy High choline / NAA Flat profile + lipid
Location Near original tumor / surgical bed Within radiation port; often perilesional
Time course Progressive Often stable or improves over months

🔹 Clinical Relevance: Imaging-Guided Tumor Workup

  • Ring-enhancing lesion + central DWI restriction → abscess. Order biopsy + drainage; antibiotics.
  • Ring-enhancing lesion + low DWI restriction + high rCBV → likely high-grade glioma or metastasis.
  • Solid, deep, DWI-restricting, low rCBV → lymphoma. Avoid steroids before biopsy.
  • T2-FLAIR mismatch sign → IDH-mutant astrocytoma (specific imaging biomarker).
  • 2HG peak on spectroscopy → IDH-mutant glioma confirmation.
  • Bilateral vestibular schwannomas → NF2 genetic workup.
  • Multiple hemangioblastomas → VHL genetic workup + abdominal imaging.
  • Open-ring enhancement → tumefactive demyelinating plaque (not tumor).
  • Pediatric posterior fossa: midline + DWI-restricting + enhancing = medulloblastoma; lateral cystic + nodular = pilocytic astrocytoma; 4th vent “plastic” = ependymoma; diffuse pontine = DIPG.
  • Carcinomatous meningitis: post-contrast FLAIR + T1 + CSF cytology.

Pitfalls and Pearls

  • Don’t biopsy until you’ve considered abscess — DWI center is the deciding sequence.
  • Steroids shrink lymphoma dramatically — hold steroids before biopsy if at all possible.
  • Lymphoma vs toxoplasmosis (HIV): FDG-PET (lymphoma avid; toxo not), spectroscopy, treatment trial.
  • Solitary brain metastasis without known primary → systemic workup + biopsy.
  • Hemorrhage-prone metastases: melanoma, renal, thyroid, choriocarcinoma.
  • Open-ring enhancement: tumefactive MS, not tumor.
  • Dural tail suggests but does not prove meningioma — solitary fibrous tumor, lymphoma, sarcoidosis, plasmacytoma can also have dural tails.
  • Carcinomatous meningitis on imaging is often subtle — combine post-contrast FLAIR + thin-cuts + CSF flow cytology.
  • T2-FLAIR mismatch sign: highly specific (~100% PPV) for IDH-mutant astrocytoma; sensitivity is lower.
  • Spectroscopy: small voxels near skull base / sinuses are unreliable due to susceptibility artifact.
  • Pineal incidental cyst is common; only worry if >15 mm + enhancement + mass effect.
  • “Drop metastases” to spine: medulloblastoma, ependymoma, germinoma, lymphoma — screen with spine MRI in selected cases.

References

  1. Louis DN, Perry A, Wesseling P, et al. The 2021 WHO Classification of Tumors of the Central Nervous System: a summary. Neuro Oncol. 2021;23(8):1231-1251.
  2. Patel SH, Poisson LM, Brat DJ, et al. T2-FLAIR mismatch, an imaging biomarker for IDH and 1p/19q status in lower-grade gliomas: a TCGA/TCIA project. Clin Cancer Res. 2017;23(20):6078-6085.
  3. Smith AB, Smirniotopoulos JG, Horkanyne-Szakaly I. From the radiologic pathology archives: intraventricular neoplasms — radiologic-pathologic correlation. RadioGraphics. 2013;33(1):21-43.
  4. Pope WB, Mirsadraei L, Lai A, et al. Differential gene expression in glioblastoma defined by ADC histogram analysis: relationship to extracellular matrix molecules and survival. AJNR Am J Neuroradiol. 2012;33(6):1059-1064.
  5. Choi C, Ganji SK, DeBerardinis RJ, et al. 2-hydroxyglutarate detection by magnetic resonance spectroscopy in IDH-mutated patients with gliomas. Nat Med. 2012;18(4):624-629.