HOYADOCS

Block 6 · CNS · CNS06 · Rev 1.2 · Updated Oct 23, 2026

CNS06 · DRT · Study Guide

Neuroradiology

Learning objectives

LO 1Look at a brain image and say whether it is a CT or an MRI (and, for MRI, which sequence) by reading which tissues are bright and which are dark.
LO 2Apply the core rules of neuroimaging: how CT density and MRI signal work, which study to order first, when contrast helps or hurts, and how edema type, diffusion and enhancement point to a diagnosis.
LO 3Recognize the common intracranial diseases on CT and MRI: the four hemorrhages, ischemic stroke, mass effect and herniation, meningeal disease, and a brain mass.

★ Step 1 HY ⚠ Step 1 trap ✎ Memory tool “ Buzzwords

MAPBig picture

Every study costs money + risk → ask why → will it change management?
CT → density only → fast, everywhere → first study for anything acute (bleed, mass effect, hydrocephalus, edema)
MRI → hydrogen proton signal
- T1 likes fat · T2 loves fluid
- FLAIR · fat-sat · DWI · gadolinium → normal goes dark → disease lights up
Pattern + history → name the pathology (same image → meningitis or carcinomatosis)

LO 1CT or MRI? Which sequence?Read the brightness of bone, CSF, fat, gray and white matter

By the end: you can name any axial brain image as CT, T1, T2, FLAIR, FLAIR + fat-sat or DWI in under 10 seconds, and explain why each tissue looks the way it does.

Q1. What is a CT actually measuring?

CT (computed tomography) sends ionizing radiation (x-rays) through the head and measures how much each voxel attenuates (blocks) the beam.
- More attenuation = denser = whiter. Air blocks nothing → black.
- That is the only thing CT knows → "one-trick pony": it depends only on the density of the object.
The density scale (Hounsfield units, HU) is anchored on water = 0. Less dense than water → negative; denser → positive. Air is the least dense (black).
Vocabulary: hyperdense (brighter), hypodense (darker), isodense (same as brain). Never "hyperintense" on CT.
On a head CT you see 4 densities: bone, gray matter, white matter, CSF (plus scalp soft tissue).

Approximate Hounsfield units. Acute blood (55–75) is denser than any brain tissue, so a fresh bleed is white on non-contrast CT.

CheckWhy is an acute hemorrhage bright on CT but CSF dark?

Clotted blood is packed with protein (hemoglobin) → 55–75 HU, denser than brain (~22–45). CSF is nearly water (0–10 HU), less dense than brain → dark.

Step 1 trap — wrong vocabulary

CT findings are dense (hyper/hypodense); MRI findings are intense (hyper/hypointense, "signal"). An answer choice that calls a CT bleed "hyperintense" is mixing modalities.

Memory tool — D vs I

CT Counts Density. MRI Measures Intensity. If the word is "density", you are on CT.

Q2. Why is gray matter brighter than white matter on CT, and what does it mean when that difference disappears?

Gray matter (cortex, deep nuclei)

Packed with neuronal cell bodies → denser
Hyperdense (brighter) vs WM
High metabolic demand → first to suffer in ischemia

White matter (tracts)

Myelinated axons; myelin is fat (lipid)
Fat is hypodense → WM is darker than GM
Rule: GM should always be slightly brighter than WM

Ischemiablood supply cut off

→

No ATPmitochondria cannot supply it

→

Na⁺/K⁺-ATPase failspump in the plasma membrane stops

→

Gray matter swellswater enters cells

→

GM looks like WMloss of GM/WM differentiation

Loss of gray–white differentiation = the cortex has swollen and become as dark as the white matter. Causes to know: stroke, seizure, infection.
In early MCA stroke this shows up as the insular ribbon sign (the insular cortex fades) and an obscured lentiform nucleus.

CheckWhy is the cortex the first place injured when blood flow stops?

Neuronal cell bodies have the highest energy demand. Their Na⁺/K⁺-ATPase pumps need ATP from mitochondria; without ATP the pumps fail, Na⁺ and water flood in, and the gray matter swells first.

Step 1 HY — early CT signs of ischemic stroke

CT is often normal in the first hours of an ischemic stroke; its first job is to exclude hemorrhage before thrombolysis.
Earliest signs: hyperdense MCA sign (bright clot in the artery), then insular ribbon loss and obscured basal ganglia, then frank hypodensity.

Step 1 trap — where the pump lives

The Na⁺/K⁺-ATPase sits in the plasma membrane; mitochondria only supply its ATP. An option placing the pump "in the mitochondria" is wrong.

Q3. How do I sanity-check a normal axial head CT?

Fold it in half. The two hemispheres should be mirror images. Asymmetry → mass effect or midline shift.
The brain should smile at you (at the level of the 3rd ventricle):
- Eyes = frontal horns of the lateral ventricles
- Nose = 3rd ventricle
- Mouth = quadrigeminal (basal) cistern
- Lost smile → cerebral edema
The 4th ventricle should frown (posterior fossa slice).
- Lost frown → mass effect

Effaced eyes/nose/mouth = cerebral edema. A flattened, pushed or lost frown = posterior fossa mass effect.

CheckThe frontal horns, 3rd ventricle and basal cisterns are all squeezed shut on a trauma CT. What process is this?

Diffuse cerebral edema: the brain has lost its "smile" because swollen tissue effaces CSF spaces. It is a warning sign for herniation.

Memory tool — the face

The supratentorial brain is happy (smile); the posterior fossa is grumpy (frown). A brain that is no longer happy is swollen; a 4th ventricle that stops frowning is being pushed.

Q4. How does MRI make a picture, and how is it different from CT?

"Forget everything you just learned about CT." MRI uses no ionizing radiation, and electron density has no effect on how things look.
The patient sits in a strong magnetic field; radio pulses tip hydrogen protons, and the scanner listens as they relax. Different tissues (fat, water, myelin) have different spin behavior → different signal.
Vocabulary: hyperintense / hypointense / isointense (signal intensity).
Strengths: far better soft-tissue characterization; much more definitive about lesions; special sequences (hemorrhage vs calcification, ultra-thin cuts for cranial nerves, advanced techniques like perfusion and spectroscopy).
Weaknesses (every CT pro is an MRI con): slow, expensive, less available, needs more technologists, and patients must be screened for metal (e.g., pacemakers).

CheckCould a bone fragment and a blood clot look identical on MRI even though their densities differ greatly?

Yes in principle: MRI ignores density and reads proton behavior, so brightness depends on the sequence and the tissue's chemistry (water, fat, blood breakdown products), not on how much it blocks x-rays. Cortical bone has almost no mobile protons → dark on every MRI sequence.

Step 1 HY — MRI safety

Screen for non-MRI-conditional pacemakers/defibrillators, ferromagnetic aneurysm clips, cochlear implants, and metal fragments in the orbit (metalworkers: get orbital x-rays first).
CT radiation matters most in children and pregnancy; MRI is preferred when time allows.

Step 1 trap — "better" is not "first"

MRI is more sensitive for almost everything, but the right first test in an unstable or acutely ill patient is still non-contrast CT (fast, no metal screening, finds blood).

Q5. T1 or T2? The two facts you must memorize

Fact 1 · T1 likes fat

T1 likes fat better than T2 does. Fat (scalp, marrow, orbit, lipoma, myelin) is bright.

Fact 2 · T2 loves fluid

No one loves fluid more than T2. CSF, edema, cysts are bright.

Then look at three things on every MRI: GM vs WM, fluid, and fat. The tissues never change; only the weighting does.

White matter is full of myelin (lipid) → T1 likes it → WM brighter than GM on T1 ("looks like a real brain").
Gray matter holds more water → T2 likes it → GM brighter than WM on T2 (inverted, "negative" look).
Fluid: dark on T1, only bright on T2.
Fat: bright on both (brighter on T1).

Two axial MRI images side by side: left has dark ventricles and bright white matter; right has bright ventricles and darker white matter — **Left = T1**: CSF dark, WM brighter than GM, scalp fat bright. **Right = T2**: CSF bright, GM brighter than WM.

What is white on which scan?

Tissue	CT (non-contrast)	T1	T2	FLAIR	FLAIR + FS
CSF / simple fluid	dark	dark	bright	dark (suppressed)	dark
Edema / abnormal fluid	hypodense	dark	bright	bright (stands out)	bright
Fat (scalp, marrow, lipoma)	very dark (−100)	bright	fairly bright (less than fluid)	bright	dark (suppressed)
White vs gray matter	GM brighter	WM brighter	GM brighter	GM brighter	GM brighter
Cortical bone / air	bone bright, air black	dark on every MRI sequence (few mobile protons)

CheckThe ventricles are white and the cortex is brighter than the white matter. Which sequence?

T2. Bright fluid can only be T2 (T2 loves fluid), and GM > WM fits T2.

CheckOn which sequence is white matter brighter than gray matter, and why?

T1, because white matter is rich in myelin (fat) and T1 likes fat.

Memory tool — WW2 and the fat burger

"World War 2": Water is White on T2.
T1 = 1 fat burger; T2 = H₂O.
T1 "looks like the brain you dissected" (WM pale, ventricles dark); T2 "looks like a photo negative".

Step 1 trap — bright on T1 is not always fat

Things bright on T1: fat, gadolinium enhancement, methemoglobin (subacute blood), melanin, protein-rich fluid. Always compare pre- vs post-contrast T1 and use fat saturation before calling it fat.

Q6. FLAIR and fat saturation: how do we make the normal go dark?

Fluid and fat protons spin so differently from other tissue that we can "saturate" them out (make them dark) on purpose.
FLAIR (fluid-attenuated inversion recovery) = a T2-type image where normal CSF is suppressed (black).
- Abnormal fluid (edema, gliosis, demyelination) stays bright → picked up faster than on plain T2, especially next to the ventricles.
FLAIR + FS (fat saturation) = normal CSF and normal fat both dark (scalp and skull marrow go black).
- Very useful for picking up meningitis quickly: abnormal meningeal/sulcal signal stands out against a dark background.

Three axial MRIs: left with dark ventricles and gray brain, middle with bright ventricles, right with dark ventricles and dark scalp fat — Left → right: **FLAIR** (CSF dark, T2-style brain), T2 (CSF bright), **FLAIR + FS** (CSF and scalp/marrow fat both dark).

CheckVentricles are dark, GM is brighter than WM, and scalp fat is still bright. Name the sequence.

FLAIR (without fat saturation). Dark CSF + T2-type brain = FLAIR; if the scalp fat were dark too it would be FLAIR + FS.

Step 1 HY — FLAIR in multiple sclerosis

MS plaques are T2/FLAIR hyperintense and periventricular, oriented perpendicular to the ventricles ("Dawson fingers"). Active plaques enhance with gadolinium (often an open-ring pattern).

Buzzwords — sequences

"bright ventricles" → T2"dark ventricles, T2-looking brain" → FLAIR"dark scalp fat" → fat-sat (FS)"WM brighter than GM" → T1"restricted diffusion" → DWI bright / ADC dark

ApplyLO 1 application questions

A1An image shows bright white bone, dark ventricles, a grainy brain and cortex slightly brighter than white matter. Modality?

Non-contrast CT. Bright bone (bone is dark on MRI), poor soft-tissue contrast, GM hyperdense to WM.

A2A lesion is bright on T1 and turns dark when fat saturation is applied. What is it made of?

Fat (e.g., a lipoma). T1 likes fat; fat saturation removes fat signal, proving the composition.

A3Predict: on FLAIR, will a periventricular edema rim be easier or harder to see than on T2?

Easier. On T2 both CSF and edema are bright and blur together; FLAIR darkens normal CSF so the bright edema stands out.

A4A 70-year-old's CT shows the left insular cortex blending into the white matter. What does this mean?

Loss of gray–white differentiation (insular ribbon sign) → early left MCA infarct (cytotoxic edema of the cortex). Other causes of lost GM/WM differentiation: seizure, infection.

LO 2Core neuroimaging conceptsPick the study, decide on contrast, read edema, diffusion and enhancement

By the end: you can choose CT vs MRI (with or without contrast) for a given patient, explain vasogenic vs cytotoxic edema and DWI at the cell level, decide whether a lesion is intra- or extra-axial, and use signal + enhancement pattern to build a differential.

Q1. Which study should I order first?

Before ordering, answer three questions: Why am I ordering this? What do I hope it tells me? How will it change management?

Feature	CT	MRI
Physics	Ionizing radiation (x-rays); density	Hydrogen protons in a magnetic field; no ionizing radiation
Words used	Hyper-/hypo-/isodense	Hyper-/hypo-/isointense (signal)
Speed · cost · availability	Fast, cheap, everywhere	Slow, expensive, needs more technologists
Safety screening	None for metal; think radiation (children, pregnancy)	Metal screening (pacemakers, clips, implants)
Soft-tissue detail	Poor	Excellent; definitive about lesions
Best use	First imaging study in the CNS and for any acute process: acute hemorrhage, mass effect, hydrocephalus, cerebral edema, trauma, fractures	Characterize a lesion (tumor, infection, demyelination), DWI for stroke, posterior fossa, cranial nerves
Contrast agent	Iodinated (renal caution)	Gadolinium (avoid in pregnancy)

Non-contrast CT is the first study in the CNS for anything acute. MRI comes next to characterize.

CheckA 30-year-old arrives after a motorcycle crash with GCS 9. First head study?

Non-contrast CT head: fast, no metal screening, detects acute blood, mass effect, hydrocephalus and fractures.

Step 1 HY — classic "next step" imaging

Acute stroke → non-contrast CT to rule out hemorrhage before thrombolysis.
Suspected SAH → non-contrast CT; if negative and suspicion high → LP for xanthochromia.
Suspected meningitis → CT before LP only if signs of ↑ICP or mass (papilledema, focal deficit, altered mental status, seizure, immunocompromise); otherwise LP + antibiotics without delay.

Step 1 trap — DWI is more sensitive, but…

MRI DWI detects ischemia within minutes, yet the first study in a suspected stroke is still non-contrast CT, because the immediate decision (tPA or not) hinges on excluding blood.

Q2. When do we add contrast, and when should we not?

Two axial CT images: left without contrast, right with bright vessels after IV contrast — **Left:** non-contrast CT. **Right:** CT with IV contrast; vessels and dural sinuses are now bright.

Why contrast? To evaluate masses and suspected infection (and vessels). Contrast leaks where the blood–brain barrier is broken or vascularity is high → the lesion "enhances".
Why the first ER CT is non-contrast: acute blood is bright and contrast is bright → contrast can hide a subtle hemorrhage. Subtle hemorrhage suspected? → non-contrast CT.
Iodinated CT contrast affects renal function → check GFR first (GFR > 60 is fine). Low GFR → you cannot use CT contrast.

	CT contrast (iodinated)	MRI contrast (gadolinium)
Use for	Mass, infection, vessels	Enhancing / vascular lesions: tumor, infection, inflammation (the pattern narrows the differential)
Avoid when	Suspected hemorrhage or infarct (first study) · low GFR / high creatinine · contrast allergy	Pregnancy
Low GFR	Cannot use (affects renal function)	Can be given (not nephrotoxic); it just clears more slowly
Looks like	Hyperdense vessels / lesion	Bright on post-contrast T1 ("T1 + C", "T1 post")

CheckA 68-year-old with CKD (GFR 22) has a suspected brain mass. Can you order a contrast CT?

No. Iodinated contrast should not be given with a low GFR. Choose MRI (gadolinium can be given with low GFR in this course's teaching; it clears more slowly) or a non-contrast study.

Step 1 HY — boards phrase gadolinium differently

Boards phrase it as: gadolinium in severe renal failure (GFR < 30, dialysis) carries a risk of nephrogenic systemic fibrosis (skin thickening, joint contractures). Iodinated contrast → contrast-induced nephropathy and allergic-type reactions (premedicate with steroids + antihistamine if prior reaction).

Memory tool — look for blood first

"Blood is bright; contrast is bright, so don't add contrast until you've looked for blood."

Step 1 trap — contrast picks

A pregnant patient with a new seizure: avoid gadolinium, not MRI itself. Non-contrast MRI (or non-contrast CT if acute) is fine.

Q3. Vasogenic vs cytotoxic edema: what is the difference?

Three axial CTs: normal, a hypodense finger-like white matter area, and a swollen hypodense hemisphere involving cortex — Left → right: **normal**; **vasogenic** (dark edema confined to white matter, finger-like, cortex spared); **cytotoxic** (gray + white matter swollen, gray–white junction lost).

Edema and diffusion at the cell level.

Ischemiano ATP

→

Pump failsNa⁺ stays in cell, water follows

→

Cytotoxiccells swell · GM + WM

→

Cells burstBBB disrupted

→

Vasogenicfluid leaks into WM interstitium

Feature	Vasogenic	Cytotoxic
Mechanism	BBB disrupted → fluid leaks into the interstitium	Na⁺/K⁺ pump failure → Na⁺ and water inside cells
Compartment	Extracellular	Intracellular
Where	White matter only (finger-like; cortex spared)	Gray ± white matter (GM/WM junction lost)
Course	Acute; "the brain is irritated"	Acute (mass effect) or chronic (volume loss)
Cell death	No	Yes
Classic causes	Tumor, abscess, trauma; late infarct	Ischemic stroke, hypoxia, ↓O₂-carrying capacity
DWI	Not restricted	Restricted (bright)

Sequence: ischemia → no ATP → Na⁺/K⁺ pump fails → Na⁺ inside cells → water follows → cytotoxic edema (GM + WM).
Cells keep swelling → burst → BBB disrupted → vasogenic edema (WM only).
An infarct always starts as cytotoxic. BBB disrupted = vasogenic.

CheckA metastasis has dark fingers of edema reaching into the white matter but the overlying cortex looks normal. Which edema?

Vasogenic: BBB leak around the tumor, confined to white matter, cortex spared.

Step 1 HY — treating edema

Vasogenic edema (tumor, abscess) responds to dexamethasone (tightens the BBB).
Cytotoxic edema (stroke) does not respond to steroids; manage ICP (elevate head, osmotherapy with mannitol / hypertonic saline, hemicraniectomy for malignant MCA edema).
Third type: interstitial edema from obstructive hydrocephalus (transependymal CSF flow around the ventricles).

Memory tool — V for vessel

Vasogenic = Vessel leak (BBB) → white-matter "V-shaped fingers". Cytotoxic = Cell swells → Cortex involved.

Q4. What does diffusion-weighted imaging (DWI) show?

DWI measures how freely water molecules move in tissue. Normal brain: water wanders between cells → dark.
Anything that shrinks the extracellular space or thickens it restricts diffusion → bright on DWI:
- Acute stroke: cells swell (cytotoxic edema). Bright within minutes; DWI is the most sensitive sequence for acute ischemia.
- Tightly packed, highly cellular tumors (e.g., lymphoma, medulloblastoma).
- Abscess: thick, viscous pus.
ADC map (apparent diffusion coefficient) is the "proof": true restriction = bright on DWI and dark on ADC.
Use DWI to evaluate stroke or cellular lesions: restricted diffusion = acute infarct (cytotoxic edema), hypercellular tumor, abscess.
DWI is built on a T2 image, so a very T2-bright lesion can look bright on DWI too ("T2 shine-through"); it will be bright on ADC as well.

CheckBesides cell swelling in stroke, how else can you "fill the box" so that extracellular water movement decreases?

Pack it with cells (hypercellular tumor) or with viscous fluid (abscess pus). Both are bright on DWI.

Step 1 HY — ring lesion + DWI

A ring-enhancing lesion with a DWI-bright center = abscess (pus restricts). A necrotic tumor center is usually not restricted.

Step 1 trap — shine-through

Bright DWI is not automatically stroke. Check ADC: dark ADC = true restriction; bright ADC = T2 shine-through (e.g., an old infarct or cyst).

Buzzwords — diffusion

"restricted diffusion within minutes" → acute ischemic stroke"DWI bright, ADC dark" → true restriction"bright DWI center of a ring" → abscess

Q5. Is the lesion intra-axial or extra-axial?

Intra-axial

Inside the brain parenchyma, enclosed by the pia mater (which hugs the brain surface)
Most tumors and infections
Most common intra-axial mass: glioma (primary brain tumor)
Bleeds: intraparenchymal hemorrhage, contusion, diffuse axonal injury

Extra-axial

Outside the pia: epidural, subdural, subarachnoid spaces
Most common extra-axial mass: meningioma
Bleeds: epidural, subdural, subarachnoid

Signs a mass is extra-axial

Definitive: something interposed between brain and lesion: a CSF cleft, vessels, cortex, or dura.
Suggestive: broad base along the calvarium, overlying bone change (hyperostosis), enhancement of adjacent meninges (dural tail), brain displaced away from the skull (white matter buckling).

CheckA dural-based mass with a CSF cleft between it and the cortex and an enhancing dural tail. Location and likely diagnosis?

Extra-axial → meningioma. The CSF cleft is a definitive extra-axial sign; the dural tail is suggestive.

Step 1 HY — meningioma and brain tumor epidemiology

Meningioma: arachnoid cap cells, women, dural-based, dural tail, psammoma bodies, whorls; associated with NF2 and prior radiation.
Boards: the most common brain tumors overall in adults are metastases (multiple, at the gray–white junction; lung, breast, melanoma, kidney); the most common malignant primary is glioblastoma.

Step 1 trap — the subarachnoid space is extra-axial

SAH sits in the sulci right against the brain, but it is still outside the pia → extra-axial. Contusion and DAI are intra-axial.

Q6. What is this lesion made of? Match it to a reference tissue on every sequence

The trick: pick a reference you know (CSF, scalp fat) and ask whether the lesion behaves like it on every sequence. If it behaves like CSF, it is CSF.

Axial T1, T2 and FLAIR images of a round left parasagittal lesion that is dark, bright, then dark — **Fluid:** T1 dark (not fat) → T2 bright (fluid) → FLAIR dark (suppressed like CSF) = a CSF cyst (congenital **porencephalic cyst**).

Four axial MRI images of a small round midline posterior lesion: bright on T1 and T1 plus contrast, intermediate on T2, dark on FLAIR with fat saturation — **Fat:** T1 bright → T1 + contrast no real added enhancement → T2 duller than fluid → FLAIR + FS dark = **lipoma**.

Lesion content	T1	T2	FLAIR / FLAIR + FS
Simple CSF (porencephalic cyst)	Dark	Bright	Dark (CSF suppressed)
Fat (lipoma)	Bright	Intermediate (less than fluid)	Dark on FS
Edema / abnormal fluid	Dark	Bright	Stays bright on FLAIR

CheckA lesion is dark T1, bright T2, and bright on FLAIR. Simple CSF cyst?

No. Simple CSF would be suppressed (dark) on FLAIR. Bright FLAIR means abnormal fluid (edema, gliosis, proteinaceous fluid, tumor).

Memory tool — follow the reference

"If it walks like CSF on T1, T2 and FLAIR, it is CSF." "If it vanishes with fat-sat, it was fat."

Q7. How does the enhancement pattern narrow the differential?

On post-contrast images, all white areas are abnormal enhancement (high vascularity or BBB breakdown); the pattern of enhancement helps narrow the differential diagnosis. The shape of the enhancement matters because each pattern has a different differential.

Eight cartoon brains showing leptomeningeal, pachymeningeal, cortical gyral and periventricular, subcortical nodular, dural tail, smooth open ring, smooth closed ring and necrotic ring enhancement — Eight enhancement patterns (labels on each cartoon).

Pattern	What enhances	Think
Leptomeningeal	Pia-arachnoid, follows sulci and cerebellar folia	Meningitis, leptomeningeal carcinomatosis, sarcoid
Pachymeningeal	Dura, smooth along the inner skull	Intracranial hypotension, post-surgery, dural metastases
Cortical gyral & periventricular	Gyri / ependyma	Subacute infarct, encephalitis, ventriculitis
Subcortical nodular	Small dots at the gray–white junction	Metastases, septic emboli
Dural tail	Broad dural-based mass + tapering dura	Meningioma (extra-axial)
Smooth open (incomplete) ring	Ring open toward the cortex	Demyelination (tumefactive MS)
Smooth closed ring	Thin, complete ring	Abscess, metastasis
Necrotic (thick, irregular) ring	Shaggy ring around necrosis	Glioblastoma, necrotic metastasis

Build the differential with a fixed list, then narrow it with signal, enhancement and DWI: Infarct · Mass · Hemorrhage · Infection · Toxic/metabolic · Vascular · Degenerative.

CheckA ring lesion is open on its cortical side. Most likely category?

Demyelination (open-ring sign), rather than abscess or tumor, which form closed rings.

Step 1 HY — ring-enhancing lesions

MAGICAL DR: Metastasis, Abscess, Glioblastoma, Infarct (subacute), Contusion, AIDS (toxoplasmosis, lymphoma), Lymphoma, Demyelination, Radiation necrosis.

AIDS (CD4 < 100): multiple ring lesions in the basal ganglia → toxoplasmosis; single periventricular lesion, EBV-positive CSF → primary CNS lymphoma.

Memory tool — lepto vs pachy

Lepto = "thin" membranes that dip into the sulci (pia-arachnoid). Pachy = "thick" dura that stays smooth against the skull.

ApplyLO 2 application questions

A1A patient with an older, non-MRI-safe pacemaker needs evaluation of a suspected brain mass. GFR is 85. Which study?

CT with IV contrast. MRI is unsafe; contrast CT is indicated for a mass, and renal function is normal.

A2A pregnant woman at 20 weeks has a first seizure and needs a brain MRI. What do you leave out?

Gadolinium. It is contraindicated in pregnancy; do a non-contrast MRI.

A3Predict the DWI and ADC appearance of a brain abscess center versus a simple porencephalic cyst.

Abscess pus: DWI bright, ADC dark (restricted). Cyst: DWI dark, ADC bright (free water). Pus is viscous; CSF is not.

A4One lesion enhances, is surrounded by T2-bright white matter, and is DWI-bright. Another follows CSF on every sequence. Which is more worrying?

The first. Enhancement (BBB breakdown) + vasogenic edema + restricted diffusion (high cellularity) points to tumor or abscess. The second is a benign CSF cyst.

A5A 3-day-old infarct now shows edema spreading through the white matter. Why can a stroke cause vasogenic edema later?

The infarct starts cytotoxic; as swollen cells die and burst, the BBB breaks down and fluid leaks into the white matter interstitium = vasogenic edema.

LO 3Basic intracranial pathologyBleeds, strokes, mass effect, meninges and a mass

By the end: you can name each hemorrhage by its shape and space, date blood on CT and MRI, spot an acute infarct on CT and DWI, call mass effect and herniation, and work through an enhancing mass or meningeal case to a diagnosis and next step.

Q1. Something is bright on a non-contrast CT. Which of the four hemorrhages is it?

Start from the layers. The space the blood is in decides its shape, and the shape gives the diagnosis.

Everything above the pia is extra-axial; blood inside the brain tissue is intra-axial.

Shape = space. Lens vs crescent is one of the most tested image pairs in neuro.

Three non-contrast axial CTs: a bright deep right hemisphere blob, a thin bright crescent along the left convexity, and bright blood in sulci and cisterns — Real cases, left → right: **intraparenchymal** hemorrhage (deep right hemisphere), **acute subdural** hematoma (crescent along the left convexity), **subarachnoid** hemorrhage (blood in sulci and cisterns).

Type	Axial location	CT shape	Vessel / cause	Classic clinical story
Epidural	Extra-axial (skull ↔ dura)	Lens / biconvex; does not cross sutures (dura is stuck there); can cross the falx/tentorium	Middle meningeal artery; temporal bone (pterion) fracture	Young trauma patient, brief LOC → lucid interval → rapid decline
Subdural	Extra-axial (dura ↔ arachnoid)	Crescent along the convexity; crosses sutures, not the midline falx	Torn bridging veins; blunt head trauma	Elderly (atrophy), alcohol use, anticoagulation, shaken baby; gradual confusion
Subarachnoid	Extra-axial (under arachnoid)	Blood in sulci and basal cisterns	Aneurysm rupture or trauma; ADPKD association	"Worst headache of my life", neck stiffness
Intraparenchymal	Intra-axial (within pia)	Bright blob in brain tissue ± surrounding edema	Hypertension (Charcot–Bouchard microaneurysms)	Hypertensive patient with sudden deficit; putamen, thalamus, pons, cerebellum

CheckAn 80-year-old on warfarin falls and becomes progressively confused over a day. CT: hyperdense crescent along the left convexity crossing suture lines. Diagnosis?

Acute subdural hematoma (extra-axial): torn bridging veins; atrophy + anticoagulation are risk factors.

Step 1 HY — epidural vs subdural

Epidural: arterial (middle meningeal a., branch of maxillary a.), lens, does not cross sutures, lucid interval, can cause rapid uncal herniation → emergency evacuation.
Subdural: venous (bridging veins), crescent, crosses sutures, slower. Shaken baby = SDH + retinal hemorrhages.
Hypertensive bleeds: putamen (most common), thalamus, pons, cerebellum. Lobar bleeds in the elderly → cerebral amyloid angiopathy.

Memory tool — lens vs crescent

Epidural = lEns; Arterial; stops at sutures because dura is "glued" there.
Subdural = Sickle (crescent); Slow venous ooze; Senior citizens.

Step 1 trap — sutures vs falx

Epidural blood is limited by sutures but can cross the midline (above the sinus); subdural blood crosses sutures but is stopped by the falx/tentorium. Don't swap them.

Buzzwords — bleeds

"lucid interval" → epidural"biconvex / lens-shaped" → epidural"crescent crossing sutures" → subdural"elderly, alcoholic, fall" → subdural"thunderclap / worst headache" → SAH"hypertensive, putamen" → intraparenchymal

Q2. Subarachnoid hemorrhage: how do I work it up and what goes wrong next?

Thunderclap headache"worst of my life", meningismus, ↓consciousness

→

Non-contrast CTblood in sulci / cisterns (most sensitive in first ~6 h)

→

CT negative?LP: xanthochromia (bilirubin), RBCs that do not clear

→

CT angiographyfind the aneurysm → coil or clip

Causes: overall most common = trauma; most common non-traumatic = ruptured berry (saccular) aneurysm, usually at the anterior communicating artery.
Associations: ADPKD, Ehlers–Danlos, Marfan, coarctation, smoking, hypertension.
Complications: rebleeding (first day), vasospasm with delayed ischemia (~3–10 days; prevent with nimodipine), communicating hydrocephalus (blood blocks arachnoid granulations), hyponatremia (SIADH / cerebral salt wasting).

CheckA 55-year-old with a family history of polycystic kidney disease has a sudden severe headache, BP 180/100. CT: hyperdense blood in the basal cisterns. Diagnosis?

Aneurysmal subarachnoid hemorrhage (ruptured berry aneurysm). ADPKD is a classic association.

Step 1 HY — aneurysm localization

ACom aneurysm: most common; can compress the optic chiasm → bitemporal visual field defect.
PCom aneurysm: CN III palsy with a blown pupil (parasympathetic fibers run on the outside of the nerve).

Step 1 trap — negative CT

A negative CT does not exclude SAH when the headache started many hours ago. Next step is LP, not discharge and not MRI.

Q3. How old is this blood? (CT and MRI)

Blood density on CT falls with time. A severely anemic patient's acute bleed can look isodense.

Stage (time)	Blood product	T1	T2
Hyperacute (< 1 day)	Oxyhemoglobin	Iso	Bright
Acute (1–3 days)	Deoxyhemoglobin	Iso	Dark
Early subacute (3–7 days)	Intracellular methemoglobin	Bright	Dark
Late subacute (1–4 weeks)	Extracellular methemoglobin	Bright	Bright
Chronic (> 1 month)	Hemosiderin (rim)	Dark	Dark

CheckA 2-week-old subdural is barely visible on CT. Why, and what helps?

It is subacute and isodense to brain. Look for indirect signs (effaced sulci, midline shift, buckled gray–white junction), or use MRI (extracellular methemoglobin is bright on T1 and T2).

Memory tool — "It Be, Iddy Biddy, BaBy, Doo Doo"

T1/T2 pairs in order: Iso/Bright → Iso/Dark → Bright/Dark → Bright/Bright → Dark/Dark. Products: oxyHb → deoxyHb → intracellular metHb → extracellular metHb → hemosiderin.

Step 1 HY — hemosiderin "blooms"

Susceptibility sequences (GRE/SWI) make hemosiderin and calcium look black and larger ("blooming"). Many tiny lobar microbleeds in an elderly patient → cerebral amyloid angiopathy; at the gray–white junction after trauma → diffuse axonal injury.

Step 1 trap — isodense subdural

"Normal" CT in a confused elderly patient 2–3 weeks after a fall can hide an isodense subacute SDH. Look for asymmetric sulci and midline shift.

Q4. How does an ischemic stroke look on CT and on DWI?

Cause: lack of blood supply or ↓ oxygen-carrying capacity.
CT of an acute stroke: hypodense territory, hydrocephalus, midline shift → then ask what the presenting symptoms are.
Presentation: contralateral extremity weakness/numbness, aphasia (dominant, usually left hemisphere), dysarthria, facial palsy, altered mental status.
MCA is the most commonly occluded artery (largest territory). MCA pattern: face and arm > leg.
Every infarct starts as cytotoxic edema; later, burst cells and BBB breakdown add vasogenic edema.

Two non-contrast axial CTs: left shows a large dark swollen area on the image-right side with the ventricles pushed across; right is a normal reference — **Left:** acute **left MCA** territory infarct (image right = patient left): large hypodense, swollen territory with loss of gray–white differentiation, **midline shift** toward the patient's right, and **hydrocephalus** of the opposite (trapped) lateral ventricle. **Right:** normal reference.

Time after onset	Non-contrast CT	MRI
Minutes to 6 h	Often normal · hyperdense MCA sign (clot)	DWI bright / ADC dark within minutes
6–24 h	Loss of GM/WM differentiation, insular ribbon sign, obscured lentiform nucleus	FLAIR becomes bright
Days 2–5	Wedge of hypodensity in a vascular territory; swelling peaks → mass effect, herniation risk	DWI still bright
Weeks to months	CSF-dark encephalomalacia, volume loss, ex vacuo ventricular enlargement	Gliosis; DWI fades (ADC normalizes then rises)

Two axial diffusion-weighted images: left with a bright area in the image-right hemisphere; right normal — DWI: bright restricted diffusion in the **left MCA** territory (patient with acute aphasia, right-sided weakness/numbness, altered mental status). Right panel normal.

Several small DWI-bright foci that are bilateral, anterior and posterior, supra- and infratentorial → multiple vascular territories at once → embolic source (heart, e.g., atrial fibrillation; or the proximal aorta).
DWI + symptoms: acute aphasia + right-sided weakness/numbness + altered mental status = acute left MCA infarct.
Differential for multiple DWI-bright foci: acute infarcts (embolic) · hypercellular tumors · abscesses. The vascular-territory pattern and clinical picture favor emboli.

CheckSudden left hemiplegia 1 hour ago. CT parenchyma looks nearly normal, but the right MCA is bright. What is this?

Hyperdense MCA sign: acute thrombus is denser than flowing blood. Suggests a large-vessel occlusion → CTA, consider thrombectomy (and tPA if no blood and in window).

Step 1 HY — acute stroke management

Non-contrast CT first to exclude hemorrhage → IV thrombolysis (alteplase/tenecteplase) within 4.5 h of last known well.
Mechanical thrombectomy for large-vessel occlusion, up to 24 h in selected patients.
Dominant (left) MCA → aphasia; non-dominant (right) MCA → hemineglect. Eyes deviate toward the lesion.
Cerebral cortex neurons: red neurons at 12–24 h; liquefactive necrosis.

Step 1 trap — normal early CT

A normal CT in the first hours does not rule out ischemic stroke. And a bright DWI spot is not always stroke: hypercellular tumors and abscesses restrict too.

Buzzwords — stroke imaging

"hyperdense MCA sign" → acute MCA thrombus"insular ribbon sign" → early MCA infarct"wedge-shaped hypodensity in a vascular territory" → infarct"multiple territories on DWI" → embolic

Q5. What do mass effect, midline shift, hydrocephalus and herniation look like?

Reading a stroke CT: name all three findings (acute stroke, hydrocephalus, midline shift), then ask what symptoms the patient presented with.
Mass effect: anything taking up space (bleed, tumor, swollen infarct) effaces sulci and ventricles, loses the "smile", and flattens the 4th ventricle "frown".
Midline shift: the septum pellucidum and falx are pushed to the opposite side.
Hydrocephalus: enlarged ventricles. A shifted brain can trap the opposite lateral ventricle at the foramen of Monro → it dilates (non-communicating). SAH and meningitis block arachnoid granulations → communicating hydrocephalus.

Coronal view of a left-sided mass. Note the compressed ipsilateral ventricle and the enlarged, trapped contralateral ventricle.

CheckA patient with a large right epidural hematoma develops a fixed, dilated right pupil. Which herniation?

Right uncal (transtentorial) herniation: the uncus compresses the ipsilateral CN III; parasympathetic fibers on its surface are hit first → blown pupil.

Step 1 HY — uncal herniation triad

Ipsilateral dilated pupil / ptosis (CN III).
Contralateral homonymous hemianopia (PCA compression).
Ipsilateral hemiparesis = Kernohan notch (opposite crus pressed against the tentorium), a false localizing sign. Usual hemiparesis is contralateral (ipsilateral crus).

Step 1 trap — hemiparesis on the "wrong" side

Weakness on the same side as the mass does not move the lesion; it signals Kernohan phenomenon.

Memory tool — top to bottom

Herniations go across (subfalcine), over (uncal), down (central), out (tonsillar). The lower it goes, the closer to the breathing center in the medulla.

Q6. Fever, headache and the meninges: what does contrast show, and why does history matter?

Two post-contrast axial MRIs at the level of the cerebellum: left with bright lines along the cerebellar folia, right normal — **Left:** diffuse **leptomeningeal enhancement** throughout the cerebellum (bright lines tracing the folia). **Right:** normal.

56-year-old · 3 days of headache, fever, N/V

Leptomeningeal enhancement → meningitis. Next step: LP.

56-year-old · lung cancer · 3 days of headache, N/V

Same image → leptomeningeal carcinomatosis. Next step: LP (cytology).

Same pattern, different disease. Your history and physical decide the diagnosis; the image narrows the differential.

CheckFebrile patient, neck stiffness, unremarkable CT. Which MRI approach shows meningeal disease best?

FLAIR + FS (normal CSF and fat suppressed) and post-contrast T1, looking for abnormal sulcal signal and leptomeningeal enhancement. Then LP.

Step 1 HY — meningitis and imaging

Imaging is often normal in bacterial meningitis; CSF is the diagnosis. Get CT before LP only when ↑ICP / mass is possible. Leptomeningeal enhancement predominantly at the basal cisterns → think TB (or fungal) meningitis.

Q7. Putting it together: a slowly growing mass

Case. A 56-year-old woman has months of slowly worsening headaches and altered mental status. First study? Non-contrast CT: something is pushing on the ventricles, bilateral but contiguous, with vasogenic edema. CT does not give enough information → contrast-enhanced MRI.

Four axial MRI images of a frontal mass crossing the midline above the lateral ventricles: T2, T1, T1 post-contrast with bright homogeneous enhancement, and DWI — Left → right: T2, T1, **T1 + post-contrast**, **DWI**.

Sequence	Finding	What it means
T2	Lesion hypointense, crossing the corpus callosum; bright surrounding WM	Densely cellular (little free water); vasogenic edema
T1	Hypointense	Not fat, not subacute blood
T1 + contrast	Diffuse homogeneous enhancement	BBB breakdown; solid (not necrotic) tumor
DWI	Mild restricted diffusion	Hypercellular

Run the list: infarct · mass · hemorrhage · infection · toxic/metabolic · vascular · degenerative → Mass: primary CNS lymphoma.

Primary CNS lymphoma homogeneous

Periventricular, crosses corpus callosum, T2 dark, DWI bright, homogeneous enhancement (ring-like in AIDS). B-cell (DLBCL); EBV in AIDS.

Glioblastoma necrotic ring

"Butterfly" across the corpus callosum, thick irregular ring around necrosis, hemorrhage; pseudopalisading necrosis; GFAP+.

Metastases multiple

Multiple, round, at the gray–white junction, lots of vasogenic edema for their size. Lung, breast, melanoma, renal.

Abscess smooth ring

Thin smooth ring, DWI-bright center (pus), edema; fever; spread from sinus/ear, dental, endocarditis.

Toxoplasmosis AIDS

Multiple ring lesions in the basal ganglia / gray–white junction, CD4 < 100. Treat empirically; shrinks in ~2 weeks.

Meningioma extra-axial

Dural-based, dural tail, CSF cleft, hyperostosis, homogeneous enhancement.

CheckWhy is a mass that is dark on T2 and bright on DWI more likely lymphoma than glioblastoma?

Lymphoma is densely packed with cells (high nuclear:cytoplasmic ratio, little free water) → T2 dark + restricted diffusion + homogeneous enhancement. GBM usually has a necrotic center and a thick irregular ring.

Step 1 HY — primary CNS lymphoma

Usually diffuse large B-cell lymphoma; in AIDS it is EBV-driven (EBV DNA in CSF).
Single periventricular lesion in AIDS → lymphoma; multiple basal ganglia lesions → toxoplasmosis.
Steroids can make it shrink or vanish → biopsy before steroids if possible.

Step 1 trap — crossing the corpus callosum

Two tumors classically cross the corpus callosum: GBM (necrotic "butterfly") and lymphoma (homogeneous, DWI bright). Use the enhancement pattern and diffusion to separate them.

ApplyLO 3 application questions

A1A 22-year-old is hit in the temple by a baseball, talks normally for an hour, then becomes unresponsive. Predict the CT.

Biconvex (lens) hyperdense epidural hematoma over the temporal region, not crossing sutures, from a torn middle meningeal artery. Classic lucid interval.

A2DWI shows multiple small bright foci in both hemispheres and the cerebellum. ECG shows atrial fibrillation. Mechanism?

Cardioembolic infarcts: emboli scatter to several vascular territories (bilateral, anterior and posterior circulation).

A3Day 3 after a large right MCA stroke, the patient becomes drowsy and the right pupil dilates. What happened on imaging?

Peak cytotoxic swelling ("malignant MCA edema") → midline shift and right uncal herniation compressing CN III. Consider decompressive hemicraniectomy.

A4MRI of a hemorrhage is bright on both T1 and T2. Roughly how old is it?

Late subacute (about 1–4 weeks): extracellular methemoglobin ("BaBy").

A5A patient with AIDS (CD4 40) has several ring-enhancing lesions in the basal ganglia. Most likely diagnosis and next step?

Toxoplasmosis: start empiric pyrimethamine–sulfadiazine (+ leucovorin) and reimage in ~2 weeks; biopsy if no response (think lymphoma).

IMGImage ID drillName the modality, sequence and finding, then tap to check

How to use: for each image say (1) CT or MRI, (2) which sequence(s), (3) the finding, (4) the next step if relevant. Then open the card.

Two axial CT images, the right one with bright vessels

1 · Two scans, same patient. What changed? (tap for answer)

Non-contrast CT (left) vs contrast CT (right). Vessels and dural sinuses are bright after iodinated contrast. Used for a suspected mass or infection, only with a normal GFR.

Two axial MRIs: dark ventricles on the left, bright ventricles on the right

2 · Which sequence is each? (tap for answer)

Left = T1 (CSF dark, WM brighter than GM). Right = T2 (CSF bright, GM brighter than WM).

Three axial MRIs with varying CSF and fat brightness

3 · Name the three sequences (tap for answer)

FLAIR (CSF dark, T2-type brain) · T2 (CSF bright) · FLAIR + FS (CSF and fat dark; scalp black).

Three axial CTs with different bright collections

4 · Three non-contrast CTs: name each bleed (tap for answer)

Intraparenchymal (hypertension; intra-axial) · acute subdural (crescent; blunt trauma) · subarachnoid (blood in sulci; aneurysm or trauma; ADPKD).

Axial CT with a large dark swollen territory and a normal comparison

5 · Acute aphasia + right weakness. Findings? (tap for answer)

Acute left MCA infarct (hypodense, swollen; cytotoxic edema) with midline shift and hydrocephalus of the trapped opposite ventricle. Right image = normal reference.

Three MRI sequences of a round left parasagittal lesion

6 · What is this lesion made of? (tap for answer)

T1 dark · T2 bright · FLAIR dark = follows CSF on every sequence → porencephalic (CSF) cyst.

Four MRI sequences of a small round midline lesion

7 · T1 · T1 + C · T2 · FLAIR + FS. Diagnosis? (tap for answer)

Bright T1, no real enhancement, duller than fluid on T2, dark with fat saturation → lipoma.

Four diffusion-weighted axial images with several bright spots

8 · DWI at four levels. Findings and mechanism? (tap for answer)

Multiple foci of restricted diffusion, bilateral, anterior and posterior, supra- and infratentorial → acute embolic infarcts (differential: hypercellular tumors, abscesses).

Two post-contrast MRIs at cerebellar level

9 · Post-contrast MRI, fever + headache (right = normal) (tap for answer)

Diffuse leptomeningeal enhancement → meningitis (or carcinomatosis if known cancer). Next step: LP.

Four MRI sequences of a frontal mass crossing the midline

10 · T2 · T1 · T1 + post · DWI. Diagnosis? (tap for answer)

T2-dark mass crossing the corpus callosum, vasogenic edema, homogeneous enhancement, mild restricted diffusion → primary CNS lymphoma.

Image drill · Michigan SecondLook

How to use: name what you see, then tap the card to check. Images credited to the Michigan SecondLook Anki Deck (University of Michigan Medical School).

Unlabeled image for SecondLook drill item 1

1 · T1 or T2? What enhances? (tap for answer)

T1-weighted (pre- and post-gadolinium): CSF is dark; it would be bright on T2.
Abnormality: an enhancing mass in the 4th ventricle extending into the cervical spinal canal, most likely an ependymoma. Annotated answer image for item 1