MRI Sequences — T1, T2, FLAIR, DWI, SWI, Post-Contrast

This page walks through each routine MRI sequence — what it is sensitive to, classic patterns, and the traps that catch even experienced readers. Pair this with the Physics Primer page for signal-intensity rules; here, the focus is sequence-by-sequence interpretation.

T1-Weighted

Use

• Anatomy + atrophy assessment.
• Identifies fat, methemoglobin, melanin, mineralization, gyriform cortical laminar necrosis.
• Post-contrast T1 detects BBB breakdown / vascular structures.

What to Look For

• Cortical thickness and atrophy patterns — symmetric vs asymmetric, lobar predominance.
• Hippocampal volume — coronal MTL, especially in dementia and epilepsy workup.
• Brainstem volume — midbrain atrophy in PSP; pons + middle cerebellar peduncle atrophy in MSA.
• Bright T1 signal — subacute hemorrhage, melanin (primary melanoma, neurocutaneous melanosis), fat (lipoma, dermoid, marrow), high-protein cysts (colloid, Rathke), manganese (PN, liver failure), gadolinium deposition (dentate, globus pallidus — cumulative dosing).
• Dark T1 cortical band — laminar necrosis (subacute infarct, hypoxia, status epilepticus).

T2-Weighted

Use

• Pathology screen — most lesions are bright on T2.
• Identifies edema, gliosis, cyst, demyelination, tumor, infarct.
• Detects iron, calcium, fibrous/cellular tissue (dark).

What to Look For

• White matter T2 hyperintensity — small vessel ischemia, MS, leukodystrophy, CADASIL (anterior temporal + external capsule), Susac (corpus callosum “snowballs”).
• Deep gray T2 hyperintensity — symmetric: metabolic / toxic / mitochondrial / Wernicke / hypoxic; asymmetric: stroke, encephalitis.
• Cortical T2 hyperintensity — subacute infarct, encephalitis (HSV → medial temporal), autoimmune (limbic), CJD ribbon, status epilepticus.
• Brainstem T2 hyperintensity — pontine perforator infarcts (lacunar pattern), MS, central pontine myelinolysis, NMO, mitochondrial.
• Iron-related T2 darkening — globus pallidus (normal aging, NBIA), substantia nigra (loss of swallow-tail in PD), dentate (CTX), red nucleus.

FLAIR

Use

• T2 with CSF nulled. Sensitive to lesions next to CSF spaces — periventricular and juxtacortical.
• The single most useful sequence for MS, gliosis, low-grade tumor, encephalitis.

Patterns

• Periventricular FLAIR hyperintensity — MS plaques (perpendicular Dawson fingers), small vessel ischemia (more confluent), transependymal CSF flow (smooth halo), CADASIL.
• Juxtacortical FLAIR hyperintensity — MS (especially U-fibers), encephalitis, FCD type IIB (transmantle sign), low-grade glioma.
• Cortical FLAIR hyperintensity — subacute stroke, encephalitis, CJD ribbon, status epilepticus, MELAS stroke-like episode.
• Bilateral mesial temporal FLAIR hyperintensity — herpes encephalitis (asymmetric typically), autoimmune limbic encephalitis (anti-LGI1, anti-CASPR2, anti-Hu), seizure-related, hypoglycemia.
• Sulcal FLAIR hyperintensity — leptomeningeal disease (carcinomatous, infectious meningitis), SAH (hyperacute), hyperoxygenation under anesthesia, propofol, gadolinium leakage in renal failure.
• Splenium of corpus callosum FLAIR hyperintensity — MERS (mild encephalopathy with reversible splenial lesion), CADASIL, AED toxicity, status, MS, ischemia.

FLAIR Pitfalls

• CSF flow artifact in posterior fossa (4th ventricle) — false bright.
• Hyperoxygenation (general anesthesia, high FiO2) → diffuse sulcal FLAIR bright.
• Propofol → sulcal FLAIR brightness.
• Gadolinium leakage into CSF in renal failure or BBB-disrupted states.

DWI / ADC

Use

• Detects water motion restriction.
• True restriction = bright on DWI AND dark on ADC.
• Single most useful sequence for acute ischemic stroke (positive within minutes).

Causes of True Restriction

• Acute ischemic stroke — within minutes; “DWI-positive but FLAIR-negative” identifies treatable window.
• Abscess — central pus restricts; helps distinguish from ring-enhancing tumor.
• Hypercellular tumors — lymphoma, medulloblastoma, glioblastoma (focal areas).
• Prion disease — cortical ribbon + basal ganglia + pulvinar pattern.
• Acute MS / NMO plaque center — transient restriction.
• Herpes encephalitis — medial temporal.
• Wernicke encephalopathy — mammillary bodies, periaqueductal, dorsomedial thalamus.
• Status epilepticus — peri-ictal cortical + ipsilateral thalamus.
• Hypoglycemia — cortical (especially parieto-occipital), hippocampal, splenium.
• Epidermoid cyst — viscous fluid (distinguishes from arachnoid cyst).
• Cytotoxic lesion of corpus callosum — splenium central restriction (MERS, drug-related).
• PRES variant with infarction — late-stage cytotoxic injury.

DWI Traps

• T2 shine-through: high DWI without ADC darkness ≠ restriction. Always confirm ADC.
• T2 black-out: very dark T2 lesions (chronic blood, calcium) can appear “restricted” via inverse artifact. Correlate with SWI/T2*.
• Susceptibility artifact at skull base + posterior fossa (sinus air, dental hardware) obscures DWI — be cautious calling restriction here.

SWI / GRE / T2*

Use

• Susceptibility-weighted; sensitive to anything that distorts the local magnetic field.
• Detects blood, calcium, iron, air, melanin.
• SWI > GRE > T2* in sensitivity.

Key Findings

• Microbleeds — small (<10 mm), round, blooming hypointensities. Patterns:
  • Lobar (cortical / subcortical) → cerebral amyloid angiopathy (CAA).
  • Deep (basal ganglia, thalamus, pons, cerebellum) → hypertensive vasculopathy.
  • Diffuse small + skull base → diffuse axonal injury.
  • Mixed deep + lobar → mixed CAA / hypertensive.
• Cerebral amyloid angiopathy (modified Boston criteria) — multiple lobar microbleeds + cortical superficial siderosis ± lobar ICH in elderly. SWI is critical.
• Cavernous malformation — “popcorn” mixed-signal core + complete dark hemosiderin rim. Often multifocal in familial forms.
• Cerebral venous sinus thrombosis — low signal in occluded sinus + blooming around. Cortical vein thrombosis shows linear dark signal in superficial cortex with adjacent edema.
• Hemorrhagic transformation of infarct — petechial → confluent hyperdensity / blooming.
• Substantia nigra “swallow-tail sign” — normally bright dorsolateral SN compartment; loss = PD or atypical parkinsonism.
• MS — central vein sign — small vein passing through plaque (high specificity for MS vs ischemic white matter disease).
• Calcification — common in normal globus pallidus, choroid plexus, pineal, falx; pathologic in oligodendroglioma, meningioma, Fahr, hypoparathyroidism.

Post-Contrast T1

Use

• Detects BBB breakdown (tumors, abscess, inflammation, demyelination, metastasis).
• Highlights normal vascular structures (vessels, sinuses, choroid, pituitary stalk).

Patterns and Differential

Post-Contrast FLAIR

• Most sensitive sequence for leptomeningeal disease — combines T2 / FLAIR contrast with gadolinium enhancement of pial vessels.
• Sensitive for early infarct cortical enhancement, low-volume hydrocephalus, low-volume SAH.
• Order when carcinomatous or infectious meningitis is suspected.

Specialty Sequences (Briefly)

• DTI / tractography: white matter tract integrity (presurgical planning, TBI, MS, leukodystrophy research).
• MR spectroscopy: metabolic profile of a voxel (NAA, choline, creatine, lipid, lactate). Useful for tumor grade, radiation necrosis vs recurrence, mitochondrial disease, NAA deficits in white matter disease.
• Functional MRI (fMRI): BOLD signal mapping for language, motor, memory; presurgical planning.
• MR perfusion (DSC, ASL): see Perfusion page.
• SVS spectroscopy mnemonic: NAA down (neuronal loss), choline up (cell turnover), lactate up (anaerobic), lipid up (necrosis).
• Time-of-flight MRA / MRV: see Angiography page.

Pitfalls and Pearls

• Always pair DWI with ADC — T2 shine-through is the universal trap.
• Open-ring enhancement = tumefactive demyelination, not abscess or tumor.
• Central vein sign on SWI = high specificity for MS over ischemic white matter lesions.
• Mesial temporal asymmetry on FLAIR + DWI = think HSV (asymmetric, hemorrhagic, often unilateral); autoimmune limbic encephalitis (more bilateral, less aggressive); seizure-related (correlate with EEG).
• Cortical ribbon DWI + pulvinar FLAIR = CJD.
• Pulvinar T2 bright bilaterally = consider variant CJD, Fabry, hypoglycemic injury, mitochondrial.
• Splenium central focal lesion with restriction = MERS, AED-related, ischemic, MS.
• Bilateral basal ganglia symmetric T2 bright = metabolic (hypoxia, CO, methanol), Wernicke, mitochondrial (Leigh), Wilson, NPC, manganese.
• Loss of swallow-tail sign on SWI = Parkinson disease (dopaminergic SN loss).
• Smooth dural enhancement + brain sagging = intracranial hypotension; look for CSF leak.
• Gadolinium leakage into CSF in renal failure can mimic SAH on FLAIR — clinical correlation.
• Don’t read “brain MRI” without checking the cord — sagittal T1/T2 visible through cervicomedullary level.

References

1. Filippi M, Preziosa P, Banwell BL, et al. Assessment of lesions on magnetic resonance imaging in multiple sclerosis: practical guidelines. Brain. 2019;142(7):1858-1875.
2. Osborn AG. Osborn’s Brain. 2nd ed. Elsevier; 2018.
3. Provenzale JM. The role of advanced MR techniques in the diagnosis of brain tumors. Magn Reson Imaging Clin N Am. 2007;15(2):283-298.
4. Vernooij MW, van der Lugt A, Ikram MA, et al. Prevalence and risk factors of cerebral microbleeds: the Rotterdam Scan Study. Neurology. 2008;70(14):1208-1214.