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Common Radiological Lesions of the Brain on MRI
Based on Grainger & Allison's Diagnostic Radiology, 7th ed. and supporting neurology textbooks
Understanding MRI Signal Characteristics (Quick Reference)
Before categorising lesions, understanding basic MRI signal behaviour is essential:
| Tissue/State | T1 Signal | T2/FLAIR Signal | DWI |
|---|
| CSF | Dark (hypointense) | Bright; suppressed on FLAIR | Dark (free diffusion) |
| Normal white matter | Intermediate | Dark relative to grey matter | - |
| Oedema / gliosis | Dark | Bright | Variable |
| Acute infarction | Dark | Bright | Bright (restricted) |
| Subacute haemorrhage | Bright (metHb) | Bright | - |
| Chronic haemorrhage | Dark rim (haemosiderin) | Dark rim | - |
| Pus/viscous fluid | Intermediate | Intermediate-bright | Bright (restricted) |
| Fat | Bright | Bright | - |
| Calcification | Dark | Dark | - |
1. Vascular Lesions
1a. Acute Ischaemic Stroke / Infarction
- DWI is the key sequence: shows bright signal within minutes of onset (restricted diffusion)
- Corresponding ADC map shows dark (low) signal - confirming true restriction, not T2 shine-through
- T2/FLAIR: hyperintense, but may lag DWI by 6-12 hours
- T1: hypointense territory
- Cortical gyral enhancement may appear after 1-2 weeks
- Distribution follows a vascular territory (e.g., MCA, ACA)
- Cytotoxic oedema: no ADC elevation on DWI = distinguishes from vasogenic oedema
1b. Intracranial Haemorrhage
MRI signal evolves predictably with time:
| Stage | Timing | T1 | T2 |
|---|
| Hyperacute | <24 h | Iso/hypointense | Hyperintense |
| Acute | 1-3 days | Iso/hypointense | Hypointense (deoxy-Hb) |
| Early subacute | 3-7 days | Hyperintense (met-Hb, intracellular) | Hypointense |
| Late subacute | 1-2 wk | Hyperintense | Hyperintense |
| Chronic | Months | Hypointense rim | Dark rim (haemosiderin) |
- Susceptibility-Weighted Imaging (SWI) is most sensitive for microbleeds, cavernomas and haemorrhagic transformation
- Germinal matrix haemorrhage (neonates): begins under frontal horn ependyma; progresses to intraventricular haemorrhage (IVH) and porencephalic cyst
1c. Subdural Haematoma
- Crescentic collection over the brain surface
- Acute: hyperdense on CT; T1 iso-/hypointense, T2 hypointense
- Subacute: bright on T1 (methaemoglobin)
- Chronic: T1/T2 hyperintense (lysed blood products)
1d. Cerebral Venous Sinus Thrombosis
- Non-arterial territory infarction, often with haemorrhage
- MRV (MR venography) shows filling defect in the affected sinus
- T1 shows hyperintense thrombus in the sinus
2. Infective / Inflammatory Lesions
2a. Brain Abscess
This is one of the most important lesions to recognise on MRI:
- Central cavity: T1 intermediate (between CSF and white matter); T2 iso- to mildly hyperintense
- Abscess rim: T2 hypointense (relatively - caused by free radicals from phagocytosis)
- SWI: rim appears markedly hypointense; a "dual rim" sign (outer hypointense + inner hyperintense) is characteristic
- DWI: central cavity is bright (restricted diffusion) with low ADC - this is the key distinguishing feature from necrotic tumour
- Post-contrast: smooth, thin ring enhancement; the inner margin is smooth; medial wall is thinner than the lateral wall
- Surrounding vasogenic oedema: T1 low, T2/FLAIR high
- Satellite microabscesses are common (10-50% are multiple)
Key distinction: Tumour (GBM, metastasis) tends to have thick, irregular enhancement and does NOT show central restricted diffusion reliably. Dynamic perfusion MRI shows lower rCBV in abscess rim vs. glioma rim.
FLAIR axial image: Listeria meningitis - abnormal high signal in the sulci from pus in the subarachnoid space (Grainger & Allison)
2b. Meningitis
- FLAIR may show failure of CSF suppression (pus in sulci appears hyperintense, as in image above)
- Post-contrast T1: leptomeningeal enhancement (following sulci and gyri)
- May cause complications: cerebral oedema, ventriculitis, empyema, venous thrombosis
2c. Subdural Empyema
- Crescentic collection identical in location to subdural haematoma
- T2/FLAIR: hyperintense; DWI restricted (pus)
- Post-contrast: thick dural enhancement at the deep margin
- Does NOT cross midline (unlike epidural abscess, which can cross)
2d. Epidural Abscess
- Lentiform (biconvex) extradural collection between dura and inner skull table
- T2/FLAIR: hyperintense; DWI: restricted
- Thick, slightly irregular dural enhancement at deep margin
- CAN cross midline (dura not attached at midline anteriorly)
- Common cause: frontal sinusitis, otomastoiditis
2e. Ventriculitis
- Ependymal enhancement around ventricles on post-contrast T1
- T2/FLAIR: periventricular hyperintensity
- DWI: may show restricted diffusion within ventricles (intraventricular pus)
3. Neoplastic Lesions
3a. Classification Framework
Brain tumours are first classified as:
- Intra-axial (within brain parenchyma): gliomas, metastases, lymphoma
- Extra-axial (outside parenchyma, from meninges/nerves/skull): meningioma, schwannoma, epidermoid
Clue: The "claw sign" - cerebral parenchyma surrounding an intra-axial tumour like a claw confirms its parenchymal origin.
3b. Glioblastoma Multiforme (GBM) - WHO Grade IV
- Most common malignant primary brain tumour in adults (mean age 59 years)
- MRI hallmarks:
- Heterogeneous intra-axial mass
- Central necrosis: T1 dark, T2 bright
- Thick, irregular ring enhancement post-gadolinium
- Surrounding T2/FLAIR hyperintensity (vasogenic oedema + infiltrative tumour)
- "Butterfly" appearance when crossing the corpus callosum
- Perfusion MRI: elevated rCBV (hyperperfused)
- MR spectroscopy: elevated choline, reduced NAA, elevated lipids/lactate
3c. Low-Grade Glioma (Astrocytoma/Oligodendroglioma - WHO Grade II)
- Diffuse infiltrating, non-enhancing (typically)
- T2/FLAIR hyperintense white matter expansion with preserved architecture
- Low-grade fibrillary astrocytomas: no enhancement (key feature)
- Pilocytic astrocytoma (WHO Grade I, paediatric): cyst with an enhancing mural nodule, especially in cerebellum
3d. Metastases
- Multiple ring-enhancing lesions at grey-white junction (most common location)
- Often disproportionately large surrounding oedema relative to tumour size
- Central necrosis common in large lesions
- May show restricted diffusion (overlap with abscess)
- Perfusion: elevated rCBV (but lower than GBM)
- Common primaries: lung, breast, melanoma, renal cell, colorectal
3e. Meningioma (Extra-axial)
- Arises from dura; extra-axial location
- T1: isointense to grey matter; T2: variable (may be hypointense)
- Post-contrast: intense, homogeneous enhancement
- Dural tail sign: linear enhancement extending from tumour along dura
- May show calcification (hypointense on all sequences)
- Buckling and displacement of adjacent cortex (not invasion of parenchyma)
3f. Lymphoma (Primary CNS)
- Typically periventricular, corpus callosum, basal ganglia
- T1: isointense; T2: isointense to mildly hyperintense (relatively hypercellular)
- Homogeneous enhancement in immunocompetent patients
- DWI: restricted (highly cellular)
- Perfusion: low rCBV despite enhancement (unlike GBM)
- Dramatically sensitive to corticosteroids ("ghost tumour" - may vanish on MRI after steroids)
3g. Posterior Fossa Tumours (Paediatric)
The most common in children, in order of frequency:
- Medulloblastoma - midline, arises from 4th ventricle roof; DWI restricted; homogeneous enhancement; leptomeningeal spread common
- Pilocytic astrocytoma - cystic with mural nodule; intense enhancement of nodule; favourable prognosis
- Ependymoma - arises from floor of 4th ventricle; "plastic" extension through foramina (Luschka/Magendie); calcification common
- Atypical Teratoid Rhabdoid Tumour (ATRT) - very young children; heterogeneous, aggressive
4. Demyelinating / White Matter Lesions
4a. Multiple Sclerosis (MS)
- Ovoid periventricular lesions oriented perpendicular to ventricles ("Dawson's fingers" on sagittal FLAIR)
- Lesion locations required for diagnosis (2024 McDonald criteria): periventricular, cortical/juxtacortical, infratentorial, spinal cord
- T2/FLAIR: hyperintense
- Active lesions: ring or nodular enhancement on post-gadolinium T1
- Central vein sign: a thin central vein within a lesion (SWI/T2*) - supports MS diagnosis
- Paramagnetic rim lesions (PRL): persistently hypointense rim on SWI/T2* - chronic active inflammation
- Black holes: T1-hypointense lesions = irreversible axonal loss
4b. Posterior Reversible Encephalopathy Syndrome (PRES)
- T2/FLAIR hyperintensity predominantly in parieto-occipital regions
- Vasogenic oedema (ADC elevated - distinguishes from infarction)
- Associated with hypertensive emergency, eclampsia, immunosuppressants
5. Traumatic Lesions
5a. Diffuse Axonal Injury (DAI)
- T2/FLAIR hyperintensities at grey-white junctions, corpus callosum, dorsolateral brainstem
- SWI most sensitive: multiple punctate microhaemorrhages (haemorrhagic DAI)
- May appear normal on CT
5b. Contusional Brain Injury
- Cortical haemorrhagic contusions: SWI/GRE hypointense foci at sites of impact and contrecoup
- Overlying subdural/extradural collections may be present
5c. Intraventricular Haemorrhage (IVH) in Premature Neonates
- Germinal matrix: hyperechogenic on US; MRI signal varies with haemorrhage age
- Late: porencephalic cyst (T2 bright communicating with lateral ventricle)
T2 axial image: dilated lateral ventricles - periventricular white matter thinning, sequela of prematurity (Grainger & Allison)
6. Epilepsy-Associated Structural Lesions
Common structural causes of epilepsy seen on MRI:
- Hippocampal sclerosis: T2 hyperintensity + volume loss in hippocampus; best on coronal FLAIR
- Focal cortical dysplasia (FCD): cortical thickening, blurring of grey-white junction on FLAIR; "transmantle" sign (linear FLAIR hyperintensity from cortex to ventricle)
- DNET (Dysembryoplastic Neuroepithelial Tumour): cortical/subcortical; T2 hyperintense; "bubbly" multilocular; no mass effect; no oedema; characteristic of temporal lobe epilepsy
- Ganglioglioma: T2 hyperintense cortical/subcortical mass; often cystic; may calcify; typically temporal; enhances variably
- Cavernous malformation: "popcorn" appearance on MRI (mixed signal core); dark hemosiderin rim on T2*/SWI; no enhancement; no surrounding oedema
7. Infective Lesions - Special Types
Neurocysticercosis
- Multiple cystic lesions; live cyst = T2 bright with scolex (white dot); dying cyst = ring enhancement + oedema; calcified = T2/SWI dark dot
- Most common cause of seizures due to parasitic CNS infection worldwide
Tuberculoma
- Solid or ring-enhancing nodule(s) with surrounding oedema
- Central T2 signal varies: T2 dark in solid caseating centre (TB-characteristic, unlike pyogenic abscess)
- Preferred locations: cerebral convexities, basal cisterns (basilar meningitis)
Toxoplasma (immunocompromised)
- Multiple ring-enhancing lesions; basal ganglia predilection
- Eccentric target sign on MRI (enhancing nodule within ring) helps distinguish from CNS lymphoma
8. Summary Table - Common MRI Lesion Patterns
| Lesion | T1 | T2/FLAIR | DWI | Enhancement |
|---|
| Acute infarction | Dark | Bright | Bright | Absent early |
| Brain abscess | Intermediate | Intermediate | Bright | Ring (thin, smooth) |
| GBM | Mixed | Bright (oedema) | Variable | Thick, irregular ring |
| Metastasis | Variable | Bright halo | Variable | Ring/nodular |
| Meningioma | Iso | Iso-bright | Variable | Intense, homogeneous + dural tail |
| MS plaque (active) | Dark | Bright | Variable | Ring/nodular |
| PRES | Iso | Bright (parieto-occipital) | Normal/high ADC | Usually absent |
| Lymphoma | Iso | Iso-bright | Bright | Homogeneous |
| Neurocysticercosis (live) | Dark | Bright (with scolex dot) | Variable | None (live) / ring (dying) |
Key MRI Sequences and Their Roles
| Sequence | Primary Use |
|---|
| T1 | Anatomy, haemorrhage stages, contrast enhancement |
| T2 | Oedema, demyelination, white matter disease, tumour extent |
| FLAIR | White matter lesions (suppresses CSF), meningeal disease |
| DWI/ADC | Acute stroke, abscess, lymphoma, prion disease |
| SWI/GRE T2* | Microbleeds, cavernomas, haemorrhage, DAI |
| Post-Gd T1 | Blood-brain barrier breakdown, tumour, infection |
| MR Perfusion | Tumour grading, abscess vs tumour differentiation |
| MR Spectroscopy | Metabolite ratios (Cho/NAA), tumour, demyelination |
| DTI | White matter tract integrity, pre-surgical planning |
Sources: Grainger & Allison's Diagnostic Radiology, 7th ed. | Bradley and Daroff's Neurology in Clinical Practice | Adams and Victor's Principles of Neurology, 12th ed.