MRI Teaching Case Library
Ten classic “must-not-miss” cases across neuro, spine, MSK and body. Schematic illustrations, not clinical images.
How to use: read the history, form your own impression, then reveal each step in turn — Step 1 findings → Step 2 differential → Step 3 diagnosis & teaching points. Work it like a viva.
1 · Sudden right-arm weakness & aphasia
History68 y, hypertensive, AF. Acute onset left MCA-territory symptoms 90 min ago. Time-critical thrombolysis question.
Step 1 — Key imaging findings
- Wedge-shaped cortical/subcortical region of high signal on DWI conforming to a vascular territory.
- Corresponding low ADC (true restricted diffusion) — confirms cytotoxic oedema, not T2 shine-through.
- DWI–FLAIR mismatch: DWI bright but FLAIR still normal/subtle → lesion likely < ~4.5 h old.
Step 2 — Differential diagnosis
- T2 shine-through (bright DWI but ADC not low) — e.g. vasogenic oedema.
- Seizure-related / status epilepticus cortical restriction (often crosses territories).
- Hypoglycaemia, herpes encephalitis, CJD — pattern & clinical context distinguish.
- Tumour / abscess (abscess core restricts — but ring-enhancing mass, not territorial).
Step 3 — Diagnosis & teaching points
Acute ischaemic stroke (left MCA territory).
- Always confirm ADC is dark — bright DWI alone is not enough.
- DWI–FLAIR mismatch helps date “wake-up”/unknown-onset strokes for thrombolysis.
- Look for a susceptibility “blooming” clot on SWI/GRE and vessel occlusion on MRA.
Related: build the workup in the Differential Diagnosis Guide (restricted-diffusion pathway).
2 · Young woman, optic neuritis + past numbness
History29 y, painful visual loss now; transient limb numbness last year. Query demyelination.
Step 1 — Key imaging findings
- Ovoid periventricular lesions perpendicular to the ventricles — Dawson’s fingers (along medullary veins).
- Lesions of the callososeptal interface / corpus callosum, juxtacortical, infratentorial and cord.
- Some lesions enhance (active); an incomplete “open-ring” enhancement favours demyelination.
Step 2 — Differential diagnosis
- Small-vessel ischaemic disease (spares callosum & U-fibres, older patients).
- ADEM (monophasic, larger confluent lesions, post-infection/vaccine).
- Vasculitis, neurosarcoid, Susac, NMOSD (longitudinally extensive cord, area postrema).
- Migraine white-matter foci (non-specific, subcortical).
Step 3 — Diagnosis & teaching points
Multiple sclerosis (relapsing–remitting).
- Diagnosis needs dissemination in space and time (McDonald 2024 criteria).
- Callosal & juxtacortical involvement helps separate MS from small-vessel disease.
- Always image the cord in suspected MS — adds lesions and prognostic weight.
Related: the Differential Diagnosis Guide white-matter pathway weights callosal & periventricular signs.
3 · Unilateral hearing loss & tinnitus
History54 y, progressive right sensorineural hearing loss, tinnitus, mild imbalance. IAC protocol MRI.
Step 1 — Key imaging findings
- Avidly enhancing mass centred on the internal auditory canal (IAC) extending into the cerebellopontine angle (CPA).
- “Ice-cream cone” shape — CPA component (scoop) with an IAC tail (cone); may widen/flare the porus.
- Acute angles with the petrous bone; heterogeneous with cystic change when large.
Step 2 — Differential diagnosis
- Meningioma: broad dural base, obtuse angles, dural tail, calcifies, off-centre from IAC.
- Epidermoid: restricts on DWI, insinuates, does not enhance.
- Facial nerve schwannoma, aneurysm, metastasis.
Step 3 — Diagnosis & teaching points
Vestibular schwannoma (acoustic neuroma).
- Commonest CPA mass (~80%); arises from CN VIII, usually vestibular division.
- High-resolution T2 (CISS/FIESTA) shows the filling defect within bright CSF/labyrinth.
- Bilateral vestibular schwannomas = neurofibromatosis type 2 until proven otherwise.
Related: CPA-mass discriminators are in the Differential Diagnosis Guide.
4 · Back pain, leg weakness, known cancer
History62 y, prostate cancer, worsening thoracic back pain, bilateral leg weakness & a sensory level. Urgent whole-spine MRI.
Step 1 — Key imaging findings
- Multiple marrow-replacing vertebral lesions: low T1 (replacing bright fatty marrow), variable T2/STIR bright.
- Posterior epidural soft-tissue mass indenting the thecal sac with cord compression and T2 cord signal change.
- Preserved disc height distinguishes tumour from infection.
Step 2 — Differential diagnosis
- Metastatic epidural disease (most common malignant cause).
- Epidural abscess / discitis-osteomyelitis (disc & endplate destruction, restricts).
- Epidural haematoma, lymphoma, myeloma, aggressive haemangioma.
Step 3 — Diagnosis & teaching points
Metastatic epidural spinal cord compression (MSCC).
- Oncological emergency — steroids + urgent onco/surgical/RT referral; outcome depends on pre-treatment neurology.
- Image the whole spine: multilevel disease is common and changes the radiation field.
- Low T1 marrow (darker than adjacent disc/muscle) is the most sensitive screen.
Related: red-flag back pain workup in the Differential Diagnosis Guide.
5 · Back pain, saddle numbness, retention
History41 y, acute severe low-back & bilateral leg pain, saddle anaesthesia, urinary retention, reduced anal tone. Emergency MRI.
Step 1 — Key imaging findings
- Large central/paracentral disc extrusion (commonly L4/5 or L5/S1) filling the canal.
- Severe canal stenosis with obliteration of CSF and crowding/displacement of the cauda equina nerve roots.
- No CSF flow void around the compressed roots on sagittal/axial T2.
Step 2 — Differential diagnosis
- Massive disc herniation (commonest).
- Epidural abscess/haematoma; tumour (ependymoma, mets, lymphoma).
- Severe degenerative canal stenosis; synovial cyst.
Step 3 — Diagnosis & teaching points
Cauda equina syndrome from a large central disc extrusion.
- Surgical emergency — decompression, ideally early, to preserve bladder/bowel & sexual function.
- Correlate imaging with the clinical picture: the syndrome is a clinical diagnosis confirmed by MRI.
- Assess axial images for degree of root crowding — sagittal alone underestimates it.
Related: the Differential Diagnosis Guide flags cauda equina red flags in the history parser.
6 · Locked knee after a twist
History24 y footballer, twisting injury, knee locked in flexion, cannot fully extend. Knee MRI.
Step 1 — Key imaging findings
- Double-PCL sign: a displaced meniscal fragment lies anterior/inferior to the PCL, mimicking a second ligament (sagittal).
- Absent bow-tie sign — fewer than the expected two bow-tie slices of the meniscal body.
- Fragment flipped into the intercondylar notch (double anterior horn / “flipped meniscus”).
Step 2 — Differential diagnosis
- Bucket-handle meniscal tear (the cause of true mechanical locking).
- Displaced flap tear; discoid meniscus with tear.
- Loose body / ACL stump causing pseudo-locking.
Step 3 — Diagnosis & teaching points
Bucket-handle tear of the medial meniscus.
- A vertical longitudinal tear with the inner fragment displaced centrally into the notch.
- Signs cluster: double-PCL, absent bow-tie, flipped-fragment, and a “disproportionate posterior horn”.
- Surgically repairable if peripheral/vascular — report displacement to guide repair vs resection.
Related: meniscal-tear sign checklist in the Differential Diagnosis Guide (MSK pathway).
7 · Pop, effusion, giving-way
History27 y, non-contact pivot injury, heard a “pop”, immediate swelling, knee gives way. Knee MRI.
Step 1 — Key imaging findings
- Primary: discontinuous / non-visualised ACL fibres, abnormal high T2 signal, wavy or absent ligament.
- Secondary signs: “kissing” bone bruises at lateral femoral condyle & posterolateral tibia; anterior tibial translation.
- Deepened lateral femoral notch; uncovered posterior horn of lateral meniscus; PCL buckling.
Step 2 — Differential diagnosis
- Acute complete ACL tear (this pattern).
- Partial ACL tear / mucoid degeneration (intact fibres, “celery-stalk” T2).
- Ganglion cyst of ACL; previous reconstruction/graft.
Step 3 — Diagnosis & teaching points
Acute complete ACL rupture.
- The characteristic bone-bruise pattern reflects the pivot-shift impaction mechanism.
- Look for the O’Donoghue “unhappy triad”: ACL + MCL + medial (or lateral) meniscal tear.
- Also assess for Segond fracture (lateral tibial avulsion) — highly associated with ACL tear.
Related: secondary ACL signs are weighted in the Differential Diagnosis Guide.
8 · Cirrhosis, surveillance mass
History59 y, hepatitis-C cirrhosis, 3 cm liver nodule on surveillance US, rising AFP. Multiphase liver MRI.
Step 1 — Key imaging findings
- Arterial-phase hyperenhancement (APHE) — non-rim — brighter than background liver.
- Washout on portal-venous/delayed phase (hypointense to liver).
- Enhancing capsule; threshold growth on serial imaging. Often mild T2 hyperintensity, may restrict on DWI.
Step 2 — Differential diagnosis
- Hepatocellular carcinoma (this classic pattern).
- Haemangioma (peripheral nodular discontinuous fill-in, T2-bright).
- FNH (central scar, retains hepatobiliary-agent signal); dysplastic nodule; arterioportal shunt.
- Intrahepatic cholangiocarcinoma / metastasis (rim APHE, progressive/target enhancement).
Step 3 — Diagnosis & teaching points
Hepatocellular carcinoma — LI-RADS 5.
- APHE + washout + capsule + threshold growth in a size threshold = LR-5 (definite HCC) in an at-risk liver.
- LI-RADS applies only to at-risk patients (cirrhosis, chronic HBV); don’t apply it to a normal liver.
- Rim APHE / target restriction / progressive enhancement should raise suspicion for non-HCC malignancy (LR-M).
Related: LI-RADS features map to the body pathway in the Differential Diagnosis Guide.
9 · Raised PSA, MRI before biopsy
History66 y, PSA 9.2 rising. Multiparametric prostate MRI (T2 + DWI/ADC + DCE) prior to targeted biopsy.
Step 1 — Key imaging findings
- Peripheral-zone (PZ) focal round/ill-defined low T2 signal.
- Marked restricted diffusion: high on high-b DWI, low on ADC — the dominant sequence in the PZ.
- Focal early enhancement on DCE; measures ≥ 1.5 cm and/or shows extraprostatic extension.
Step 2 — Differential diagnosis
- Clinically significant prostate cancer (this pattern).
- Prostatitis (wedge/band-like, less mass-like, less restriction).
- Post-biopsy haemorrhage (bright on T1 — always check T1); BPH nodule (typically TZ).
Step 3 — Diagnosis & teaching points
Clinically significant prostate cancer — PI-RADS 5.
- PI-RADS v2.1: DWI is the dominant sequence in the peripheral zone; T2 dominates the transition zone.
- Score 4–5 lesions warrant targeted (fusion) biopsy; report extraprostatic extension & seminal-vesicle invasion for staging.
- Always review T1 first — post-biopsy blood mimics/masks tumour.
Related: PI-RADS zone-based scoring logic lives in the Differential Diagnosis Guide.
10 · Headache, bitemporal visual loss
History48 y, chronic headache, bitemporal hemianopia; acute severe headache today with worsening vision. Sella MRI.
Step 1 — Key imaging findings
- Sellar/suprasellar mass > 10 mm expanding the sella, with a “snowman/figure-of-8” waist at the diaphragma sellae.
- Optic chiasm compression from above; possible cavernous-sinus extension encasing the ICA.
- If apoplexy: haemorrhage/infarction — heterogeneous T1-bright blood, fluid–fluid level, restricted diffusion.
Step 2 — Differential diagnosis
- Pituitary macroadenoma (commonest sellar mass in adults).
- Craniopharyngioma (calcified, cystic, children/older adults); Rathke cleft cyst.
- Meningioma (dural base, homogeneous enhancement); aneurysm; metastasis; hypophysitis.
Step 3 — Diagnosis & teaching points
Pituitary macroadenoma with pituitary apoplexy.
- Apoplexy = acute haemorrhage/infarction of an adenoma — thunderclap headache, ophthalmoplegia, visual loss.
- Endocrine emergency: check for hypocortisolism — give stress-dose steroids; urgent endocrine/neurosurgical review.
- Identify the normal gland and chiasm; note cavernous sinus & ICA relationship for surgery.
Related: sellar-mass discriminators are in the Differential Diagnosis Guide.
Educational use only. All illustrations are schematic teaching diagrams — not real patient MRI images — and these cases are simplified for learning. They do not substitute for formal training, local protocols, or clinical judgement, and must not be used to guide the care of any individual patient.