Anatomy, Physiology & Pathophysiology on MRI
A structure-by-structure walk through the body: the normal make-up and job of each part, how it fails, and the signal changes that make that failure visible. Choose a region, then a structure.
On this page
Scroll through real scansBrainHead & NeckSpineMusculoskeletalChest & CardiacAbdomenPelvisVascular & Nerve- An intact blood–brain barrier keeps gadolinium out, so normal brain does not enhance; ischaemia causes cytotoxic oedema with restricted diffusion, while a leaky barrier causes vasogenic oedema and enhancement.
- Normal adult marrow is T1-bright from fat; in an adult, a marrow lesion darker than disc or muscle on T1 should be treated as replacement until proven otherwise.
- Never read an orbital post-contrast series without fat suppression: bright orbital fat drowns pathology, so image the optic nerve with fat-suppressed T2 and T1 post-gadolinium.
- The liver has a dual blood supply (about 75% portal vein, 25% hepatic artery) and HCC typically shows arterial hyperenhancement then washout, so bolus-track the arterial phase: mistime it and the hyperenhancement can be missed.
- CSF pulsation can fake a spinal cord lesion, so make any apparent cord lesion prove itself on two planes before calling it.
Explain it simply
- Healthy brain has a barrier that keeps contrast dye out, so it doesn’t light up. Loss of blood supply makes cells swell and water move less freely; a damaged barrier lets fluid and dye leak in.
- Adult bone marrow is fatty, so it is bright on T1 scans. In adults, a marrow spot darker than the nearby disc or muscle counts as disease moving in until proven otherwise.
- The eye socket is full of fat that shines brightly on scans. Scans of the eye nerve, including those after contrast dye, must dim the fat, or it hides inflamed or abnormal tissue.
- The liver gets about three-quarters of its blood from a vein and a quarter from an artery. Liver cancer usually lights up early, then fades, so time the early scan carefully or it can be missed.
- The movement of spinal fluid can create a fake spot in the spinal cord. Only believe a cord abnormality if it also shows up when viewed from a second direction.
A guide only: follow your departmental protocols and regional requirements.
Scroll through real scans
Brain
CerebrumPosterior fossaSellaVentriclesCranial nerves
Cerebrum
Normal anatomy
Cell-body-rich cortical grey matter sits over lipid-rich myelinated white matter; CSF fills the sulci and ventricles.
Physiology
Signal is driven by water and its microenvironment. An intact blood–brain barrier keeps gadolinium out, so normal brain does not enhance.
When it goes wrong
Ischaemia stalls the Na/K pump → cytotoxic oedema (restricted diffusion). A leaky barrier → vasogenic oedema and enhancement. Demyelination strips myelin lipid.
GM intermediate, WM T1-bright, CSF dark on T1/FLAIR and bright on T2. DWI/ADC for stroke, FLAIR for oedema, T1+Gd for the barrier, SWI for blood.
TechniqueRun DWI early in stroke work, and always read it against ADC to catch T2 shine-through.
PlainThinking cells, insulated wiring and cushioning fluid. Disease shifts how much water is present and how freely it moves, and the scan reads that shift.
Posterior fossa & cerebellum
Normal anatomy
Cerebellar hemispheres and vermis, the brainstem and the fourth ventricle, packed into a tight bony compartment.
Physiology
Coordinates movement and carries cranial-nerve nuclei plus CSF outflow, with almost no room to absorb a mass.
When it goes wrong
Infarct, tumour (medulloblastoma, metastasis, haemangioblastoma) or bleed quickly effaces the fourth ventricle → obstructive hydrocephalus and tonsillar herniation.
Thin-slice T2/FLAIR and DWI; watch fourth-ventricle effacement and tonsil position. Bone/air susceptibility degrades images here.
TechniquePush bandwidth up and slices thin to fight posterior-fossa susceptibility blur.
PlainA small, crowded space at the back of the skull that runs balance. With no spare room, even minor swelling counts.
Sella & pituitary
Normal anatomy
The pituitary sits in the sella with the optic chiasm above and the cavernous sinuses (carotids, CN III–VI) either side.
Physiology
A hormone factory; the posterior lobe stores vasopressin and shows a normal T1-bright “posterior bright spot.”
When it goes wrong
Adenoma (micro or macro), apoplexy or a Rathke cyst. Macroadenomas push up on the chiasm → bitemporal hemianopia.
Dynamic small-FOV coronal T1+Gd: a microadenoma enhances more slowly than normal gland. A missing bright spot hints at diabetes insipidus.
TechniqueTiming is everything. The early dynamic phase is where microadenomas declare themselves.
PlainThe master hormone gland, tucked under the brain right beside the vision nerves, so growths here hit hormones or eyesight.
Ventricles & CSF spaces
Normal anatomy
Paired lateral ventricles, the third and fourth, linked by the foramina and aqueduct; the choroid plexus makes CSF.
Physiology
CSF is made, circulated and reabsorbed in balance, holding intracranial pressure steady.
When it goes wrong
A block (tumour, aqueduct stenosis) gives non-communicating hydrocephalus; poor absorption gives the communicating kind; idiopathic normal-pressure hydrocephalus is a communicating hydrocephalus seen mainly in older adults.
Ventricular size, transependymal oedema on FLAIR, and phase-contrast CSF-flow studies; heavily-T2 sequences pinpoint the level of block.
TechniqueA dilated system with crisp transependymal FLAIR signal points to acute obstruction, not just atrophy.
PlainFluid chambers that cushion the brain. If drainage jams, they swell and press outward on brain tissue.
Cranial nerves · IAC / CPA
Normal anatomy
CN VII and VIII thread the internal auditory canal into the cerebellopontine angle; other cranial nerves leave through skull-base foramina.
Physiology
They carry hearing, balance, facial movement and sensation, and are normally thin, non-enhancing threads in CSF.
When it goes wrong
Vestibular schwannoma, meningioma or epidermoid at the CPA; tumour can also creep along a nerve (perineural spread).
Heavily-T2 CISS/FIESTA outlines nerves against bright CSF; T1+Gd lights up a schwannoma or abnormal nerve.
TechniqueSub-millimetre 3D heavily-T2 is the workhorse; a nerve should be visible as a dark thread in bright fluid.
PlainThe cabling for hearing, balance and the face runs through tiny bony tunnels; scans catch small growths pressing on it.
Head & Neck
OrbitTemporal boneParanasal sinusesSalivary glandsPharynx, larynxThyroid
Orbit & globe
Normal anatomy
The globe, optic nerve and its sheath, the extra-ocular muscles and orbital fat, all inside the bony orbit.
Physiology
Orbital fat gives natural contrast; the optic nerve is a CNS tract wrapped in CSF.
When it goes wrong
Optic neuritis (often MS), thyroid eye disease (muscle-belly enlargement that spares the tendon insertions, often with increased orbital fat), tumours (glioma, meningioma, mets) and cellulitis/abscess.
Fat-suppressed T2 and T1+Gd of the nerve; without fat suppression the bright orbital fat drowns pathology.
TechniqueNever read an orbital post-contrast series without fat suppression; enhancement hides in the fat otherwise.
PlainThe eye and its nerve sit in a fatty socket; dimming the fat lets inflammation or growths show through.
Temporal bone & inner ear
Normal anatomy
The cochlea, semicircular canals and vestibule (the membranous labyrinth), all fluid-filled.
Physiology
A fluid sensory organ for hearing and balance; normally bright on heavily-T2 imaging.
When it goes wrong
Labyrinthitis, endolymphatic hydrops (Ménière), labyrinthitis ossificans, and schwannoma reaching in from the IAC.
3D heavily-T2 shows the fluid spaces; lost fluid signal or abnormal enhancement flags disease. Delayed post-Gd for hydrops.
TechniqueBright, continuous fluid in every turn of the cochlea is the normal you are checking against.
PlainHearing and balance live in tiny fluid loops; the scan reads that fluid to spot inflammation or blockage.
Paranasal sinuses & nasal cavity
Normal anatomy
Air-filled sinuses lined by thin mucosa, draining through ostia into the nasal cavity.
Physiology
Mucociliary clearance keeps them aerated; air reads as low signal, the mucosa a thin line.
When it goes wrong
Sinusitis, mucocele, fungal disease and sinonasal tumours; MRI’s job is to split obstructed secretions from tumour.
T2 bright secretions vs intermediate solid tumour; T1+Gd separates mucosal from solid enhancement. CT still owns the bone.
TechniqueBeware inspissated or fungal secretions; they can go T2-dark and mimic an aerated sinus. Correlate with CT.
PlainAir pockets in the face. MRI tells trapped mucus from a solid growth by how bright the contents look.
Salivary glands
Normal anatomy
Parotid, submandibular and sublingual glands; the facial nerve runs right through the parotid.
Physiology
They secrete serous and mucinous saliva; the fatty parotid gives its own contrast.
When it goes wrong
Pleomorphic adenoma, Warthin tumour, malignancy, sialadenitis and Sjögren syndrome.
T2 and T1+Gd characterise a lesion; ADC helps split benign from malignant. Always check the deep lobe and facial nerve.
TechniqueMap any mass against the facial-nerve plane; deep-lobe involvement changes the operation.
PlainSpit-making glands in the cheeks and jaw; scans grade a lump and check the facial nerve running through it.
Pharynx, larynx & oral cavity
Normal anatomy
Mucosal spaces (naso-, oro- and hypopharynx and larynx) wrapped around the airway with deep fascial planes.
Physiology
Mucosa-lined tubes for air, food and voice; the worry is spread beneath the surface.
When it goes wrong
Squamous cell carcinoma dominates; MRI maps deep and submucosal reach and cartilage invasion for staging.
Fat-suppressed T2 and T1+Gd for extent; DWI for nodes. Cartilage invasion moves the stage.
TechniqueSwallowing and breathing smear neck MRI; fast sequences and a coached, still patient rescue the study.
PlainThe throat and voice box. MRI shows how deep a tumour goes, which CT can under-call.
Thyroid & neck nodes
Normal anatomy
Thyroid lobes straddle the trachea; cervical node chains run down beside the great vessels.
Physiology
An iodine-handling endocrine gland; nodes filter lymph and swell with disease.
When it goes wrong
Goitre, thyroiditis, carcinoma and nodal metastasis or lymphoma; MRI mainly stages substernal reach and nodes.
T2, T1+Gd and DWI; ultrasound and CT lead, MRI steps in for retrosternal extent and vessel involvement.
TechniqueFollow the lower pole into the mediastinum; that substernal component drives surgical planning.
PlainThe neck’s hormone gland and its lymph glands; scans map spread and any dip behind the breastbone.
Spine
VertebraeIntervertebral discSpinal cordNerve rootsSacroiliac joints
Vertebrae & bone marrow
Normal anatomy
Vertebral bodies of trabecular bone holding red (blood-forming) and yellow (fatty) marrow.
Physiology
Marrow converts red-to-fatty with age; normal adult marrow is T1-bright from that fat.
When it goes wrong
Metastasis or myeloma replace the fat; fracture or infection floods it with oedema; degeneration gives Modic endplate change.
T1 marrow darker than disc or muscle suggests infiltration (red-marrow reconversion, oedema from fracture or infection, and Modic type 1 change also lower T1 signal); STIR shows oedema; Dixon fat-fraction quantifies. Tumour and infection enhance.
TechniqueIf a marrow lesion is darker than disc or muscle on T1, treat it as replacement until proven otherwise.
PlainSpine bones hold marrow that is normally fatty and bright; disease that moves in snuffs out that brightness.
Intervertebral disc
Normal anatomy
A gel nucleus pulposus inside the fibrous annulus, sandwiched between vertebral endplates.
Physiology
Proteoglycans bind water, giving the turgor that cushions and spreads axial load; the adult disc is nearly avascular.
When it goes wrong
Proteoglycan loss → dehydration → height loss → annular tears → herniation onto a nerve root.
T2 loss of the bright nucleus (the “black disc”), lower height, Modic change; axial T2 shows the herniation and foraminal narrowing.
TechniqueThe bright nucleus on sagittal T2 is your hydration gauge; when it darkens, that is real water loss.
PlainA water-filled cushion between the bones; with wear it dries, flattens and can bulge onto a nerve.
Spinal cord
Normal anatomy
A central butterfly of grey matter with peripheral white-matter tracts, tapering to the conus.
Physiology
It relays motor and sensory traffic, slung in CSF that gives it T2 contrast all around.
When it goes wrong
Compression (myelopathy), demyelination (MS/NMO), ischaemia, and intramedullary tumour or syrinx.
T2/STIR intramedullary hyperintensity marks oedema or gliosis; T1+Gd for active plaque or tumour; axials localise within the cord.
TechniqueCSF pulsation can fake a cord lesion; make it prove itself on two planes.
PlainThe main nerve cable. A bright signal inside it flags pressure, inflammation or injury.
Nerve roots & cauda equina
Normal anatomy
Roots exit at each level; below the conus they trail as the cauda equina inside the thecal sac.
Physiology
They float free in CSF and are normally thin, evenly spread and non-enhancing.
When it goes wrong
Compression from disc or stenosis, arachnoiditis (clumping), and leptomeningeal tumour (drop metastases).
Axial T2 shows crowding or clumping; T1+Gd reveals an abnormal root or leptomeningeal coating.
TechniqueOn a clean axial the roots sit evenly around the back of the sac; central clumping, or roots stuck to the sac wall (an ‘empty’ sac), is the abnormal you look for.
PlainThe trailing nerve strands of the lower spine; scans show if they are pinched, clumped or coated by disease.
Sacroiliac joints
Normal anatomy
Paired synovial and ligamentous joints between the sacrum and each ilium.
Physiology
They pass load from spine to pelvis with barely any motion.
When it goes wrong
Axial spondyloarthritis brings active change (oedema, capsulitis) and structural change (erosion, ankylosis); infection also occurs.
STIR/T2 FS subchondral marrow oedema that is clearly present, typical in location and highly suggestive of axSpA is the ASAS sign of active sacroiliitis, but oedema meeting this definition is also seen in some healthy people, runners and women after childbirth (extensive oedema is rare in them), so read it with the clinical picture; T1 for erosion, fat metaplasia and ankylosis.
TechniquePlan semicoronal obliques along the sacral axis; off-plane slices hide the joint.
PlainThe joints linking spine to pelvis; a bright “bruise” here can point to inflammatory arthritis, though some is seen in healthy people, runners and after childbirth.
Musculoskeletal
ShoulderElbowWristHipKneeAnkleSkeletal muscleBone marrow (limbs)
Shoulder
Normal anatomy
The glenohumeral joint with its fibrocartilage labrum, the rotator-cuff tendons and the biceps anchor.
Physiology
The labrum deepens a shallow socket; the cuff centres and drives the humeral head.
When it goes wrong
Rotator-cuff tendinopathy and tears, labral tears (Bankart, SLAP), and impingement.
PD/T2 FS shows fluid-bright tendon gaps and labral tears; MR arthrography lifts labral sensitivity.
TechniqueLine obliques up with supraspinatus and the glenoid; off-axis slices fake and hide tears.
PlainA shallow ball-and-socket held by a cartilage rim and tendons; tears read as bright fluid lines.
Elbow
Normal anatomy
A hinge joint with collateral ligaments and the common flexor and extensor tendon origins.
Physiology
Ligaments hold valgus/varus stability; the tendon origins transmit forearm load.
When it goes wrong
Epicondylitis (tendinosis), collateral-ligament tears and osteochondral injury.
PD/T2 FS for tendon and ligament signal and marrow oedema; thin slices for small structures.
TechniqueSmall structures, small FOV. Resolution beats raw signal at the epicondyles.
PlainThe elbow hinge; tennis or golfer’s elbow and ligament sprains show as bright, swollen tendon.
Wrist & hand
Normal anatomy
Carpal bones, the TFCC fibrocartilage, intrinsic ligaments and the flexor/extensor tendons.
Physiology
Complex small-joint mechanics; the TFCC cushions the ulnar side.
When it goes wrong
TFCC and scapholunate ligament tears, avascular necrosis (scaphoid, lunate) and tenosynovitis.
High-resolution small-FOV PD/T2 FS; T1 for marrow (AVN); arthrography for ligament tears.
TechniqueA dedicated coil and a small FOV are non-negotiable for wrist detail.
PlainMany tiny bones and ligaments; high-detail scans find small tears and a bone losing its blood supply.
Hip & pelvis
Normal anatomy
A deep ball-and-socket with an acetabular labrum and strong surrounding muscles and tendons.
Physiology
The labrum seals and steadies the joint; its depth demands good fat suppression.
When it goes wrong
Labral tears and FAI, avascular necrosis of the femoral head, and stress or insufficiency fractures.
T1 for the AVN serpiginous line and marrow; PD/T2 FS and arthrography for the labrum; STIR for an occult fracture.
TechniquePair a large-FOV pelvis with a small-FOV hip, so you catch the other side and still resolve the labrum.
PlainThe hip ball-and-socket with a cartilage seal; scans find tears, hidden fractures and lost blood supply.
Knee
Normal anatomy
The menisci (fibrocartilage), cruciate and collateral ligaments, and hyaline articular cartilage.
Physiology
Menisci spread load, ligaments stabilise, cartilage gives a low-friction glide.
When it goes wrong
Meniscal tears, ACL/PCL rupture, cartilage loss and bone-marrow oedema (bone bruise).
PD/T2 FS: signal clearly reaching an articular surface on two or more images (short-TE) indicates a meniscal tear; discontinuous ACL fibres; a STIR bruise hints at mechanism.
TechniqueA normal meniscus is a uniform black wedge. A tear is signal that clearly reaches an articular surface on at least two images (the two-slice-touch rule, read on short-TE PD images), or an abnormal shape; signal that stays inside the meniscus, or normal vascular signal in a child, is not a tear.
PlainCushions and ligaments in the knee; injury lets bright fluid in, revealing tears and bruising.
Ankle & foot
Normal anatomy
The mortise joint, collateral ligaments, the Achilles and peroneal tendons, and the plantar fascia.
Physiology
Ligaments and tendons balance and propel; hyaline cartilage caps the talar dome.
When it goes wrong
Ligament sprains and tears, Achilles tendinopathy or rupture, osteochondral lesions and plantar fasciitis.
PD/T2 FS for ligament and tendon fluid signal and marrow oedema; sagittal for the Achilles and plantar fascia.
TechniqueMagic-angle signal is common in the ankle tendons in neutral; about 20° of plantar flexion (or prone positioning) reduces it, and long-TE images help before calling tendon signal disease (Mengiardi et al. 2006; Wang et al. 2005).
PlainThe ankle joint with its tendons and ligaments; sprains, ruptures and cartilage chips all show as bright signal.
Skeletal muscle
Normal anatomy
Muscle fibres bundled in fascial compartments with fat planes between them.
Physiology
Contractile tissue: intermediate signal with feathery fat planes when normal.
When it goes wrong
Strain or tear, denervation, myositis, and infiltrating masses.
STIR/T2 FS oedema pinpoints injury (often the myotendinous junction) or inflammation; T1 shows fatty atrophy of chronic denervation.
TechniqueFollow oedema to the myotendinous junction; that is where most strains tear.
PlainMuscle brightens and swells when strained or inflamed, and turns fatty when its nerve fails.
Bone marrow (limbs)
Normal anatomy
Red and yellow marrow within the trabecular bone of the limbs.
Physiology
Fatty conversion with age; reconversion to red marrow under haematopoietic stress.
When it goes wrong
Infiltration (mets, marrow disease), oedema (fracture, infection, transient) and infarct.
T1 loss of bright fat means infiltration; STIR oedema; Dixon fat-fraction and DWI quantify.
TechniqueUse adjacent muscle or disc on T1 as your built-in reference for “too dark.”
PlainThe fatty core of bones is normally bright; disease dims it or lights it up with swelling.
Chest & Cardiac
HeartGreat vesselsBreastMediastinumLungBrachial plexus
Heart (myocardium)
Normal anatomy
Four chambers of muscular myocardium, the valves and the pericardium.
Physiology
A rhythmic pump, so imaging has to be gated to the cardiac cycle and a breath-hold.
When it goes wrong
Infarct and scar, the cardiomyopathies, myocarditis and infiltration (amyloid, sarcoid, iron).
Cine SSFP for function; T2 for oedema; late gadolinium enhancement maps scar; T1/T2 mapping and ECV quantify diffuse disease.
TechniqueThe LGE pattern (subendocardial in a coronary territory versus mid-wall or subepicardial) separates infarct from non-ischaemic disease and narrows the differential (SCMR 2020).
PlainThe heart muscle; timed scans measure the pumping and reveal scar or inflammation.
Great vessels (aorta & pulmonary)
Normal anatomy
The aorta and pulmonary arteries carrying high-flow blood from the heart.
Physiology
Flowing blood gives the signal for angiography; the wall has to hold under pressure.
When it goes wrong
Aneurysm, dissection (an intimal flap), coarctation and vasculitis.
Contrast-enhanced MRA and flow-sensitive sequences show lumen, flap and flow; black-blood T1/T2 for wall inflammation.
TechniqueA dissection flap is a thin line splitting the lumen; confirm true vs false lumen on flow imaging.
PlainThe body’s main pipes; angiography shows bulges, tears or narrowing.
Breast
Normal anatomy
Fibroglandular tissue and ducts in a fatty background, with regional lymph nodes.
Physiology
Glandular tissue shifts with hormones; tumours recruit leaky new vessels (angiogenesis).
When it goes wrong
Invasive and in-situ carcinoma with angiogenesis; benign lesions (fibroadenoma, cyst) behave differently on kinetics.
Dynamic T1+Gd: rapid early enhancement with washout is the kinetic pattern most suggestive of malignancy, but many cancers (including DCIS and invasive lobular carcinoma) plateau or keep enhancing, and morphology comes first (BI-RADS); fat-sat and DWI/ADC add specificity; very high sensitivity for high-risk screening.
TechniqueThe shape of the enhancement curve, not just that it enhances, drives the call, so time the dynamic tightly.
PlainContrast MRI watches how fast a lump takes up dye; many cancers light up quickly then fade, but some keep brightening, so the lump’s shape matters most.
Mediastinum
Normal anatomy
The central chest compartment: thymus, nodes, vessels and the oesophagus.
Physiology
It houses vascular and lymphatic structures; the thymus shrinks with age.
When it goes wrong
Thymoma, lymphoma, germ-cell tumours and cysts; MRI characterises tissue where CT is on the fence.
T2, chemical-shift (thymic hyperplasia loses signal) and T1+Gd tell cystic from solid and fatty from soft tissue.
TechniqueUse in/opposed-phase to unmask thymic hyperplasia; the signal drop settles many equivocal masses.
PlainThe middle of the chest; MRI helps sort cysts, fat and solid growths apart.
Lung & pleura
Normal anatomy
Air-filled alveolar lung and the pleural lining.
Physiology
Low proton density and air–tissue interfaces make lung hard to image, so MRI is a problem-solver, not first-line.
When it goes wrong
Pleural effusion or tumour, and apical (Pancoast) tumour invading chest wall or brachial plexus.
T2/STIR and T1+Gd judge chest-wall, vascular and plexus invasion; CT still owns the parenchyma.
TechniqueSave lung MRI for the specific question (chest-wall or vascular invasion) that CT can’t settle.
PlainAir-filled lungs are tricky for MRI, so it mostly checks whether a tumour has grown into nearby structures.
Brachial plexus
Normal anatomy
Nerve roots C5–T1 forming trunks and cords from the neck to the axilla.
Physiology
They carry arm motor and sensory traffic; thin nerves running among vessels and muscle.
When it goes wrong
Traumatic avulsion, tumour (schwannoma, mets, Pancoast invasion) and radiation plexopathy.
Coronal and sagittal STIR and 3D nerve-selective (neurography) sequences; T1+Gd for tumour; a pseudomeningocele signals avulsion.
TechniqueA pseudomeningocele at the neural foramen strongly suggests root avulsion; look for the absent root itself on thin heavily T2-weighted images (Wade et al. 2019).
PlainThe nerve bundle to the arm; special scans trace it to find stretch injuries or tumours.
Abdomen
LiverBiliary treePancreasSpleenKidneysAdrenal glandsSmall bowel
Liver
Normal anatomy
Segmental parenchyma with a dual blood supply: about 75% portal vein, 25% hepatic artery.
Physiology
Hepatocytes metabolise and excrete (including hepatobiliary contrast); normal liver enhances mostly in the portal-venous phase.
When it goes wrong
HCC (arterial neovascularity), metastases, haemangioma, and diffuse fat, iron or fibrosis.
Dynamic Gd: HCC typically shows nonrim arterial hyperenhancement then washout (LI-RADS, in at-risk patients); hepatobiliary agents show non-uptake; chemical-shift for fat; elastography for fibrosis.
TechniqueBolus-track the arterial phase and aim for the late arterial phase: HCC enhancement is usually strongest then and some HCCs enhance only then, so a mistimed scan can make the hyperenhancement weak or missed (ACR LI-RADS).
PlainThe liver draws blood from two sources; many tumours tap the artery and light up early with dye, then fade.
Biliary tree & gallbladder
Normal anatomy
Intra- and extrahepatic bile ducts draining to the gallbladder and duodenum.
Physiology
Bile is a static fluid, perfect for heavily-T2 imaging (MRCP), no contrast needed.
When it goes wrong
Stones, strictures, cholangiocarcinoma and congenital anomalies.
MRCP (heavily-T2) draws the fluid-bright ductal tree; filling defects are stones or tumour; T1+Gd for wall enhancement.
TechniqueFast the patient to distend the gallbladder and cut bowel-fluid overlap on MRCP.
PlainThe bile pipes; a water-sensitive scan maps them to find stones or narrowings.
Pancreas
Normal anatomy
Exocrine acini and the pancreatic duct, with the islets of Langerhans.
Physiology
It secretes enzymes and hormones; normal gland is T1-bright from its proteinaceous acinar content.
When it goes wrong
Adenocarcinoma (desmoplastic, hypoenhancing), pancreatitis and cystic neoplasms (IPMN).
T1 FS (loss of the normal bright signal in tumour or fibrosis), dynamic Gd (ductal adeno is hypovascular) and MRCP for duct and cysts.
TechniqueLook for adenocarcinoma as a hypoenhancing focus on the pancreatic-phase T1 FS, often with an upstream dilated duct.
PlainThe pancreas is normally bright on MRI; tumours and scarring dim it and block its drainage duct.
Spleen
Normal anatomy
Red and white pulp with a rich sinusoidal vascular network.
Physiology
It filters blood and backs immunity; enhances heterogeneously (“arciform”) early because of variable flow.
When it goes wrong
Infarct, lymphoma or infiltration, cysts, and iron deposition.
T2 and dynamic Gd (don’t mistake early heterogeneity for disease); T2*/susceptibility for iron overload.
TechniqueGive the spleen a few seconds; that early stripey enhancement is normal, not pathology.
PlainA blood-filtering organ; scans check for iron build-up, infarcts and infiltration.
Kidneys & ureters
Normal anatomy
Cortex and medulla with the collecting system and the renal vasculature.
Physiology
They filter blood and concentrate urine; corticomedullary contrast tracks perfusion and function.
When it goes wrong
Renal cell carcinoma, cysts (Bosniak), angiomyolipoma (fat) and obstruction/hydronephrosis.
Fat-suppressed T1 shows the macroscopic fat of classic AML; an opposed-phase signal drop shows intracellular (microscopic) fat, typical of clear-cell RCC and only occasionally of fat-poor AML; dynamic Gd characterises masses; MR urography (heavy-T2) for obstruction.
TechniqueRun in/opposed-phase; an intracellular-fat signal drop reframes the whole differential.
PlainThe kidneys clean blood; MRI grades cysts and tumours and shows any urine blockage.
Adrenal glands
Normal anatomy
A cortex (steroid hormones) and medulla (catecholamines), one perched on each kidney.
Physiology
Endocrine glands; adenomas often carry intracellular lipid.
When it goes wrong
Adenoma (usually lipid-rich), phaeochromocytoma, metastasis and carcinoma.
Chemical-shift in/opposed-phase: a clear signal drop on opposed-phase shows intracellular lipid and strongly favours a lipid-rich adenoma (beware metastases from clear-cell RCC or HCC, and adrenocortical carcinoma, which can contain lipid); no drop is indeterminate, because lipid-poor adenomas don’t drop either.
TechniqueAn opposed-phase signal drop is a fast, no-contrast pointer towards adenoma, not proof; read it with size, history and hormonal work-up.
PlainSmall hormone glands above the kidneys; a specific MRI trick spots the fat inside harmless nodules.
Small bowel & mesentery
Normal anatomy
Loops of small bowel with mucosa and wall layers, and the mesenteric vessels and nodes.
Physiology
A peristaltic absorptive tube; distending it with oral contrast lets you read the wall.
When it goes wrong
Crohn disease (active vs fibrotic strictures), tumours and obstruction.
MR enterography: T2/DWI and dynamic T1+Gd grade active inflammation vs fibrosis with no radiation, ideal for young Crohn patients.
TechniqueAdequate oral distension is essential and an antiperistaltic agent is recommended unless contraindicated (SAR–SPR–AGA and ESGAR–ESPR consensus).
PlainThe gut; a radiation-free scan grades inflammation in conditions like Crohn’s, good for repeat checks in the young.
Pelvis
ProstateUterusOvariesBladderRectum
Prostate
Normal anatomy
A glandular peripheral zone (PZ), a transition zone (TZ) around the proximal urethra, a central zone (CZ) at the base around the ejaculatory ducts, and the anterior fibromuscular stroma; PI-RADS v2.1 names these zones rather than a ‘central gland’.
Physiology
The PZ is packed with fluid-filled acini, so it is normally T2-bright.
When it goes wrong
Cancer swaps open glands for densely packed cells → lower T2 and restricted diffusion.
Multiparametric: focal low T2, DWI/ADC restriction (the dominant read in the PZ) and early DCE (PI-RADS).
TechniquePurge rectal gas and susceptibility so the ADC restriction you see is real, not artefact.
PlainThe gland’s outer zone is normally bright; cancer packs it with cells, darkening it and trapping water.
Uterus & cervix
Normal anatomy
Endometrium, junctional zone and myometrium, with the cervix and its stroma.
Physiology
Hormone-responsive zonal anatomy; the junctional zone is a key T2 landmark.
When it goes wrong
Fibroids and adenomyosis, and endometrial and cervical carcinoma; MRI stages depth of invasion.
High-resolution T2 shows the zones and tumour depth; DWI and dynamic Gd add detection; a junctional zone of 12 mm or more, especially with T2-bright foci, supports adenomyosis; 8–12 mm is indeterminate, and the zone varies with the menstrual cycle and transient contractions (Reinhold et al. 1996).
TechniqueAngle small-FOV T2 to the true uterine and cervical axes; oblique slices over- or under-stage depth.
PlainThe womb shows clear MRI layers; scans reveal fibroids and how deep a cancer has grown.
Ovaries & adnexa
Normal anatomy
The ovaries with their follicles and the neighbouring fallopian tubes.
Physiology
Cyclical follicular activity; simple follicles are thin-walled fluid.
When it goes wrong
Cysts, endometrioma, dermoid (fat) and ovarian carcinoma; MRI characterises the indeterminate adnexal mass.
T1 (blood or fat), fat-suppression (endometrioma “shading”, dermoid fat) and dynamic Gd for solid parts (O-RADS).
TechniqueAlways add fat-sat T1; it is how you prove or exclude fat and haemorrhage in an adnexal lesion.
PlainMRI sorts ovarian cysts by what fills them (clear fluid, blood or fat) to judge the risk.
Bladder
Normal anatomy
A muscular detrusor wall lined by urothelium, filling with urine.
Physiology
A distensible reservoir; urine gives T2-bright contrast against the darker wall.
When it goes wrong
Urothelial carcinoma; MRI grades the depth of muscle invasion for staging.
T2, DWI and dynamic Gd (VI-RADS) judge muscle-layer invasion, the pivotal staging step.
TechniqueWatch the dark muscle line under a tumour; its integrity separates non-muscle-invasive from invasive.
PlainThe urine bag; MRI checks whether a tumour has grown into the muscle wall.
Rectum & anus
Normal anatomy
Rectal wall layers within the mesorectal fascia, and the anal sphincter complex.
Physiology
Continence and storage; the wall layers and fascia are the staging landmarks.
When it goes wrong
Rectal carcinoma (T-stage, mesorectal fascia, EMVI) and perianal fistula.
High-resolution T2 for wall layers and the mesorectal margin; DWI for tumour and nodes; fistula mapping on T2/STIR + Gd.
TechniqueTake thin oblique T2 perpendicular to the tumour axis; that is what defines the mesorectal margin.
PlainMRI maps how far a rectal tumour reaches and traces fistula tracks around the anus.
Vascular & Nerve
Arteries (MRA)
Normal anatomy
The arterial tree from the aorta out to the peripheral run-off vessels.
Physiology
Flowing blood makes the signal; contrast or flow effects build the angiogram.
When it goes wrong
Stenosis or occlusion, aneurysm, dissection and vasculitis.
Contrast-enhanced or non-contrast (TOF, QISS) MRA maps the lumen; black-blood wall imaging for vasculitis; handy when iodinated contrast is out.
TechniqueIn severe renal impairment, non-contrast MRA (TOF/QISS) avoids both iodinated and gadolinium contrast; follow your department’s contrast policy (ACR–NKF consensus statements).
PlainAngiography maps the arteries to find narrowings, bulges or tears, sometimes with no dye at all.
Veins (MRV)
Normal anatomy
The deep and superficial venous systems, including the dural venous sinuses.
Physiology
Lower-flow return circulation; flow patterns enable venography.
When it goes wrong
Thrombosis (DVT, cerebral venous sinus thrombosis) and compression syndromes.
MRV (TOF, phase-contrast or contrast-enhanced) shows filling defects or absent flow; SWI helps with cerebral veins.
TechniqueAbsent flow signal raises suspicion of thrombosis; confirm with contrast-enhanced MRV or CTV and SWI/T2*, remembering sinus hypoplasia and flow gaps (AHA 2024).
PlainVein scans reveal clots by showing where blood flow has gone missing.
Peripheral nerve (neurography)
Normal anatomy
Named peripheral nerves with a fascicular structure, travelling with their vessels.
Physiology
They conduct signals; a healthy nerve is near-isointense to muscle with visible fascicles.
When it goes wrong
Entrapment, traumatic neuroma, nerve-sheath tumour and neuritis.
Fat-suppressed high-resolution T2 / 3D neurography shows thickening, T2 hyperintensity or a mass; denervated muscle shows oedema then fatty atrophy.
TechniqueDenervation oedema (then fatty atrophy) in the target muscle is a reliable secondary sign of a nerve lesion.
PlainHigh-detail scans follow individual nerves to spot pinching, tumours or inflammation.
An educational account of established anatomy, physiology and pathophysiology as it relates to MRI signal, not a substitute for a formal radiology report or clinical judgement. Pairs with the Normal MRI Anatomy Atlas and the MRI Differential Diagnosis guide.