Brain MRI Approach
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Direct answer
T1 for anatomy, T2 and FLAIR for pathology, diffusion-weighted imaging for cytotoxic insult, GRE or SWI for blood products, and post-contrast T1 for breakdown of the blood-brain barrier — five questions asked in a fixed order make brain MRI tractable. Cerebrospinal fluid is dark on T1 and bright on T2, suppressed on FLAIR, which is why FLAIR exposes periventricular and cortical lesions that T2 hides within bright fluid. Fat, melanin, methaemoglobin, proteinaceous fluid and gadolinium are bright on T1 — a short memorised list that decodes half of all sequence questions. Location first (intra- or extra-axial, supra- or infratentorial), then signal behaviour across all sequences, then enhancement pattern, and the NEET-PG answer is usually already written.
What you must remember
- Sequence logic: T1 anatomy and contrast studies; T2 water-sensitive pathology; FLAIR suppresses CSF to reveal periventricular plaques and superficial lesions; DWI with ADC for infarct and abscess.
- Bright on T1: fat, melanin, methaemoglobin (subacute blood), high-protein fluid, gadolinium and sometimes calcification — quote the list, not a vague "bright things".
- Extra-axial clues: broad dural base, grey matter buckling, CSF cleft, displaced cortex — meningioma until proven otherwise, with a dural tail on post-contrast T1.
- Multiple sclerosis: ovoid periventricular plaques perpendicular to ventricles (Dawson fingers), callososeptal interface on sagittal FLAIR, juxtacortical and infratentorial lesions.
- GRE or SWI blooming: signals haemosiderin from old microbleeds — hypertensive, cavernoma, diffuse axonal injury, cerebral amyloid angiopathy.
- Ring-enhancement differential: abscess (restricted diffusion in pus), neurocysticercosis (eccentric scolex, "hole with dot"), toxoplasmosis versus lymphoma (the latter restricts on DWI and shows homogenous enhancement when solid).
- Pituitary protocol: dynamic contrast-enhanced thin coronal sections; microadenomas are hypoenhancing early against the vivid normal gland.
- When CT still wins: acute trauma, suspected acute haemorrhage before thrombolysis, and unstable patients — MRI is a problem-solver, not the first responder.
A worked sequence read
A 28-year-old woman with two episodes of transient left-arm weakness. CT was unremarkable. On T2 and FLAIR, three ovoid hyperintense lesions hug the lateral ventricles, one perpendicular to the long axis — Dawson fingers; another sits in the juxtacortical white matter of the right hemisphere. DWI shows no restriction (this is demyelination, not infarct). GRE shows no blooming. Post-contrast T1 shows a single enhancing lesion, meaning one plaque is active while the rest are silent — dissemination in time and space on one study, and clinically isolated syndrome becomes possible multiple sclerosis by the 2017 McDonald criteria, which permit enhancement and spinal lesions to establish dissemination. Now rehearse the contrast pair the examiner will substitute: an extra-axial homogenously enhancing mass with a dural tail is a meningioma; a cyst with an enhancing mural nodule in a young cerebellar patient is a haemangioblastoma; a thick, nodular irregular rim in an immunocompromised patient forces the toxoplasmosis-versus-lymphoma question, where restricted diffusion and periventricular location favour lymphoma.
High-yield viva angles
Reading T2 alone is the cardinal error — a bright lesion on T2 is also bright on DWI by T2 shine-through, and only the ADC map separates true restriction (dark ADC) from spurious brightness; this single distinction is the most repeatedly tested MRI concept. The second slip is ignoring the CSF cleft: a lesion with cortex draped around it is extra-axial, and calling a meningioma "brain tumour" without qualifying extra-axial loses the mark in image-based stems. Third, sequence purpose confusion: FLAIR exists because T2 cannot see through bright CSF, so "FLAIR is a water-sensitive sequence like T2" is only half the answer expected.
Frequently asked questions
Why is FLAIR preferred over T2 for periventricular lesions?
FLAIR suppresses the bright cerebrospinal fluid signal, so plaques abutting the ventricles and cortex stand out against a dark background instead of blending into bright CSF.
What structures appear bright on T1-weighted images?
Fat, melanin, methaemoglobin in subacute haemorrhage, protein-rich fluid and gadolinium — the standard quotable list.
What is the dural tail sign?
Thickening and enhancement of dura tapering away from an extra-axial mass, classically meningioma, reflecting reactive or neoplastic dural involvement.
Which MRI sequences detect old microbleeds?
Gradient echo T2 star-weighted (GRE) and susceptibility-weighted imaging (SWI), where haemosiderin blooms dark — hypertensive microbleeds, cavernomas, amyloid angiopathy and shearing injury.
How does MRI distinguish lymphoma from toxoplasmosis?
Primary CNS lymphoma is typically homogenous, periventricular and shows restricted diffusion, whereas toxoplasmosis enhances in a ring with a non-restricting necrotic centre — the classic IMAGE-pair differential in immunocompromised patients.