I now have all the material needed to write a thorough, well-illustrated answer. Here is the complete guide:
Reading Brain CT and MRI: Bleed vs. Infarct with Temporal Staging
Part 1 - How to Approach a Brain CT
The Systematic "ABCDE" Window Approach
Always view brain CT in at least two window settings:
- Brain window (WW ~80, WL ~35): evaluates parenchyma, gray-white differentiation, blood
- Bone window (WW ~2000, WL ~300): evaluates skull fractures, calvarium
For stroke, a "stroke window" (WW ~35, WL ~35) improves sensitivity for early ischemic changes by widening the contrast between normal and ischemic parenchyma.
CT Density (Hounsfield Units - HU)
| Structure | HU |
|---|
| Air | -1000 |
| Fat | -100 |
| Water/CSF | 0 |
| Normal gray matter | ~35-40 |
| Normal white matter | ~25-30 |
| Acute blood | ~50-90 |
| Bone | ~700-1000 |
The golden rule: blood is white (hyperdense), infarct is dark (hypodense) on CT.
Part 2 - CT Appearance: Hemorrhage vs. Infarct
Hemorrhage on CT
Acute hemorrhage is hyperdense (bright white) relative to brain. This is due to clot retraction and increased protein concentration of coagulated blood.
"Fresh intracranial hemorrhage coagulates nearly immediately and therefore shows up on CT scans as hyperdense areas relative to brain. Fresh hemorrhage may appear about as white as bone."
- Neuroanatomy through Clinical Cases, 3rd Ed.
"The area of ischemic injury on brain CT scan appears as a relative hypodensity, in contrast to brain hemorrhage, which appears hyperdense compared with the surrounding brain."
Timeline of hemorrhage on CT:
| Phase | Time | CT Appearance |
|---|
| Hyperacute | 0-6 hrs | Hyperdense (white, ~60-80 HU) |
| Acute | 1-3 days | Hyperdense, may develop hypodense ring (edema) |
| Subacute | 3-14 days | Becomes isodense (similar to brain, ~35 HU) - can be missed! |
| Chronic | >14 days | Hypodense (darker than brain), may calcify; subdurals form crescent-shaped dark collections |
Important: In severely anemic patients, acute blood can appear isodense or even hypodense - always correlate clinically.
Infarct on CT
Ischemic infarction appears hypodense (dark) and is often subtle in the first 6 hours.
Early CT signs of ischemic stroke (first 6 hours):
- Loss of gray-white differentiation - the insular cortex and basal ganglia lose their normal contrast with white matter
- "Insular ribbon sign" - loss of the normally sharp insular cortex outline (sensitive for MCA territory ischemia)
- Sulcal effacement - gyri swell and compress the sulci
- Hyperdense vessel sign - a dense MCA or basilar artery indicates acute thrombosis
- "One-third rule" - if more than 1/3 of the MCA territory is already hypodense, thrombolysis is contraindicated (increased hemorrhage risk)
"Brain swelling on CT without accompanying low density does not always progress to infarction. Such cases may be due to abnormal perfusion, but a compensatory increase in CBV rather than a reduction."
- Grainger & Allison's Diagnostic Radiology
CT Timeline of Infarction:
| Phase | Time | CT Appearance |
|---|
| Hyperacute | 0-6 hrs | Normal OR very subtle hypodensity, sulcal effacement |
| Acute | 6-24 hrs | Definite hypodensity in affected territory, gray-white blurring |
| Subacute | 1-7 days | Progressively more hypodense, mass effect peaks at 3-5 days |
| Fogging effect | ~1-3 wks | Temporarily appears isodense (macrophage infiltration, petechial hemorrhage) - can be falsely normal |
| Chronic | >3 wks | Well-defined hypodense area, ex-vacuo ventricular dilation (encephalomalacia) |
Part 3 - MRI Approach and Sequences
Each sequence has a specific role. From Adams and Victor's Principles of Neurology:
| Sequence | Best For | Bright | Dark |
|---|
| T1 | Anatomy, subacute blood | Subacute blood, fat, methemoglobin | CSF, edema, deoxyhemoglobin |
| T2 | Edema, infarcts, inflammation | CSF, edema, late subacute blood | Acute blood (deoxyhemoglobin), calcium |
| FLAIR | Periventricular lesions, SAH, subacute infarct | Edema, gliosis, SAH | CSF (suppressed) |
| DWI | Acute infarction (gold standard) | Acute ischemia (minutes to ~7 days) | Blood after several days |
| ADC map | Confirm true restriction vs. T2 shine-through | - | True infarct (dark = restricted diffusion) |
| SWI/GRE | Microhemorrhages, venous blood | - | All blood products, calcification (blooms dark) |
The DWI-ADC Rule
This is the most important concept in acute stroke MRI:
- Acute infarct: DWI bright + ADC dark = true restricted diffusion = infarction
- Chronic lesion (gliosis): DWI dark + ADC bright = T2 shine-through without restriction
- T2 shine-through (subacute): DWI bright + ADC bright/normal = not infarction, just T2 effect
"DWI has a preeminent role in acute stroke imaging due to its extremely high sensitivity and specificity, with parenchymal hyperintensity as early as 5 minutes following the onset of infarction."
- Grainger & Allison's Diagnostic Radiology
Acute left MCA infarct (7 hours after onset). CT (A) shows subtle hypodensity, T2/FLAIR (B, C) show parenchymal signal change, DWI (D) shows full hyperintensity, ADC (E) confirms restricted diffusion - Grainger & Allison's Diagnostic Radiology
Acute left MCA infarct: (A) DWI shows bright hyperintensity with mass effect; (B) ADC map confirms corresponding hypointensity (restricted diffusion) - Bradley and Daroff's Neurology in Clinical Practice
Part 4 - MRI Timeline of Intracerebral Hemorrhage
The appearance of blood on MRI depends entirely on the oxidation state of hemoglobin and its location (intracellular vs. extracellular). This is from Neuroanatomy through Clinical Cases, 3rd Ed.:
| Stage | Timeframe | Hemoglobin Form | T1 | T2 | Mechanism |
|---|
| Hyperacute | 0-6 hours | Intracellular oxyhemoglobin | Gray (isointense) | Light gray (slightly bright) | Oxyhemoglobin has no unpaired electrons - no T1 shortening |
| Acute | 1-3 days | Intracellular deoxyhemoglobin | Gray (isointense) | Dark gray (hypointense) | Deoxyhemoglobin has unpaired electrons - T2 shortening; intact RBCs prevent T1 effect |
| Early subacute | 3-7 days | Intracellular methemoglobin | White (bright) | Dark gray (hypointense) | Methemoglobin shortens T1 strongly; still intracellular so T2 remains dark |
| Late subacute | 7->30 days | Extracellular methemoglobin | White (bright) | White (bright) | RBC lysis releases methemoglobin extracellularly - now both T1 and T2 bright |
| Chronic | >14 days | Hemosiderin (outer rim) | Dark gray | Black (markedly hypointense) | Hemosiderin (ferritin/hemosiderin in macrophages) causes susceptibility effect - "blooms" dark |
"The actual sequence of changes can be fairly complicated and variable, depending on brain microenvironment and individual scanners."
Memory aid: "Be A Bright White Rim"
- Be = acute (Black on T2 at 1-3 days, deoxy)
- A = acute-subacute transition (starts to brighten T1)
- Bright White = subacute (methemoglobin, bright on both)
- Rim = chronic (dark hemosiderin rim on T2/SWI)
Part 5 - MRI Timeline of Ischemic Infarction
From Bradley and Daroff's Neurology in Clinical Practice:
| Phase | Timeframe | DWI | ADC | T2/FLAIR | T1 |
|---|
| Hyperacute | 0-6 hrs | Bright (from ~5 min) | Dark | Subtle/normal | Normal |
| Acute | 6 hrs - 5 days | Bright | Dark | Clearly hyperintense + gyral swelling | Hypointense |
| Subacute | 5-14 days | Fading bright (T2 shine-through takes over) | Normalizing (pseudonormalization ~days 7-10) | Bright, mass effect peaks then resolves | Hypointense |
| Chronic | >3 weeks | Dark (gliosis, unrestricted) | Bright | Bright (gliosis) | Hypointense; may see gyral enhancement with contrast |
Pseudonormalization trap: Around days 7-14, ADC may normalize due to vasogenic edema developing, making the ADC map look normal even though infarction has occurred. Always use clinical context + FLAIR/T2.
"Initially, the hyperintense signal on DWI is caused by decreased water diffusivity due to swelling of the ischemic nerve cells (for the first 5-7 days); then it increasingly results from the abnormal T2 properties of the infarcted tissue (T2 shine-through). For this reason, a reliable estimation of the age of the ischemic lesion is not possible by looking at DWI images alone."
- Bradley and Daroff's Neurology in Clinical Practice
Part 6 - Key Differentiating Features at a Glance
CT: Bleed vs. Infarct
| Feature | Hemorrhage | Infarct |
|---|
| Density | Hyperdense (white) acutely | Hypodense (dark) |
| Timing of visibility | Immediately visible | Subtle <6 hrs; clear >6 hrs |
| Shape | Round/oval, well-defined | Follows vascular territory (wedge-shaped or territorial) |
| Location | Any (hypertensive: basal ganglia, thalamus, cerebellum, pons) | Cortex + subcortex in artery territory |
| Mass effect | Yes - surrounding edema | Peaks at 3-5 days with large infarcts |
| Hemorrhagic transformation | N/A | Can occur (petechial or confluent) in large infarcts |
| Contrast enhancement | Peripheral ring (subacute) | Gyral enhancement after ~1-2 weeks |
MRI: Quick Reference Summary
| Phase | Infarct DWI | Infarct ADC | Hemorrhage T1 | Hemorrhage T2/SWI |
|---|
| Hyperacute (0-6h) | Bright | Dark | Gray | Light gray / Bright |
| Acute (1-3d) | Bright | Dark | Gray | Dark (deoxy) |
| Early subacute (3-7d) | Bright | Dark | Bright | Dark (intracel methHb) |
| Late subacute (7d-4wks) | Fading | Pseudonorm | Bright | Bright (extracel methHb) |
| Chronic (>4wks) | Dark | Bright | Dark | Black rim (hemosiderin) |
Part 7 - Practical Workflow in Emergency Setting
- First: Non-contrast CT - rule out hemorrhage, mass lesion, or hemorrhagic transformation before giving thrombolytics
- If CT negative but stroke suspected within 6 hours: MRI with DWI/ADC is the gold standard - bright DWI + dark ADC = confirmed ischemic infarct
- CTA (CT Angiography): Aortic arch to intracranial vessels - look for large vessel occlusion (LVO), hyperdense vessel sign, and collateral flow
- CT perfusion / MR perfusion: Identifies the penumbra (salvageable ischemic tissue = MTT prolonged but CBV preserved) vs. core infarct (CBV reduced)
- SWI/GRE: Detects microhemorrhages (amyloid angiopathy), thrombosed veins, and acute thrombus in vessels with "blooming" effect
"DWI is the most sensitive imaging sequence for the detection of acute ischemic infarction and can show infarcted tissue within minutes of stroke onset, considerably earlier than CT and other MRI sequences."
- Adams and Victor's Principles of Neurology, 12th Ed.
Quick Memory Tables
Hemorrhage on CT (Rule of 2 weeks)
- <7 days: White (hyperdense)
- ~7-14 days: Isodense (can be invisible - look for mass effect)
- >14 days: Dark (hypodense), may calcify or become cystic
FLAIR in Stroke
- Infarct <4.5 hours: DWI bright but FLAIR normal or subtle = safe thrombolysis window ("DWI-FLAIR mismatch" for wake-up strokes)
- Infarct >4.5 hours: Both DWI and FLAIR bright
- SAH: Hyperintense CSF in sulci on FLAIR (FLAIR more sensitive than CT at 24-48 hrs)
Sources: Adams and Victor's Principles of Neurology 12th Ed. | Bradley and Daroff's Neurology in Clinical Practice | Grainger & Allison's Diagnostic Radiology | Neuroanatomy through Clinical Cases 3rd Ed. | Goldman-Cecil Medicine