CT Brain in Stroke & Head Injury
Radiology · Neuroradiology · lean revision notes
CT Brain in Stroke & Head Injury
Non-contrast CT (NCCT) of the brain is the single most exam-relevant imaging investigation in NEET PG neuroradiology. It is the first-line, immediate, gold-standard initial test in acute stroke and in head injury because it is fast, universally available, and exquisitely sensitive to two things that change management within minutes: fresh blood and bone. This chapter builds a systematic NCCT reading approach and then drills the high-yield signs of ischaemia, intracranial haemorrhage, and traumatic brain injury.
Why NCCT first — physics and density logic
CT measures X-ray attenuation expressed in Hounsfield Units (HU), calibrated so that water = 0 HU and air = −1000 HU. Reading any CT brain is fundamentally about recognising whether a structure is hyperdense (whiter) or hypodense (darker) relative to normal grey/white matter.
| Tissue / substance | Approximate HU | CT appearance |
|---|---|---|
| Air | −1000 | Black |
| Fat | −50 to −100 | Dark |
| Water / CSF | 0 | Dark grey |
| White matter | 20–30 | Grey |
| Grey matter | 35–45 | Slightly whiter than white matter |
| Acute clotted blood | 50–100 | Hyperdense (white) |
| Calcification | 100–400 | Very white |
| Cortical bone / metal | >1000 | Brilliant white |
High-yield: Acute blood is hyperdense (~60–80 HU) because of the high protein content of haemoglobin within the clot — NOT because of iron. As the clot retracts and breaks down, density falls roughly 1–2 HU/day, so haematomas become isodense at ~1 week and hypodense at 2–3 weeks.
High-yield: NCCT is the investigation of choice to exclude haemorrhage before thrombolysis. The crucial decision in acute stroke is haemorrhagic vs. ischaemic, and CT detects blood instantly while early infarct is subtle.
Systematic reading approach (the "Blood Can Be Very Bad" mnemonic)
A reproducible search pattern prevents missed lesions.
Blood → Cisterns → Brain → Ventricles → Bone
- Blood — scan for any hyperdensity: extra-axial (EDH/SDH/SAH) or intra-axial (intracerebral haemorrhage).
- Cisterns — basal cisterns (suprasellar, quadrigeminal, ambient): effacement = raised ICP or SAH; asymmetry = herniation.
- Brain — grey–white differentiation, sulcal effacement, mass effect, hypodensities (infarct/oedema), midline shift.
- Ventricles — size (hydrocephalus), intraventricular blood, compression.
- Bone (bone window) — fractures, pneumocephalus, sinuses.
High-yield: Always look at both brain windows (window width ~80, level ~40) for soft tissue and bone windows (width ~2000) for fractures. A subtle linear skull fracture is invisible on brain windows.
Ischaemic Stroke on NCCT
Timeline of CT findings
In hyperacute ischaemia the CT may be completely normal — this is expected and does NOT exclude stroke.
| Time from onset | NCCT finding |
|---|---|
| 0–6 h (hyperacute) | Often normal; earliest signs: hyperdense MCA sign, insular ribbon loss, obscured lentiform nucleus, sulcal effacement |
| 6–24 h (acute) | Wedge-shaped hypodensity (grey + white matter), loss of grey–white differentiation, mass effect develops |
| 1–7 days (subacute) | Maximal oedema/mass effect (peaks day 3–5); well-defined hypodensity |
| 2–3 weeks | Fogging effect — infarct becomes isodense and may look "normal" |
| >1 month (chronic) | Encephalomalacia, CSF-density cavity, volume loss, ex-vacuo ventricular dilatation |
Early ischaemic signs (very high-yield)
- Hyperdense MCA sign — the most classic. A thrombus within the M1 segment makes the artery appear bright (~ 40–60 HU) against the dark Sylvian fissure. Implies a large-vessel occlusion and a poor prognosis. The equivalent at the Sylvian branches is the "MCA dot sign" (hyperdense dot in the insula).
- Insular ribbon sign — loss of the normally visible grey-matter density of the insular cortex.
- Obscuration of the lentiform nucleus — the basal ganglia become indistinct due to cytotoxic oedema (early, as basal ganglia are end-artery territory).
- Loss of grey–white matter differentiation and sulcal effacement from cytotoxic oedema.
High-yield: A hyperdense MCA sign represents the clot itself, whereas the hypodensity that appears later represents the dying brain. Don't confuse a hyperdense MCA with calcified atheroma (which is much denser, >100 HU, and often bilateral).
ASPECTS score
The Alberta Stroke Program Early CT Score (ASPECTS) is a 10-point score for MCA-territory infarcts. Start at 10 and subtract 1 for each affected region (caudate, lentiform, internal capsule, insula, and M1–M6 cortical zones).
- Score ≥6 → favourable; eligible for thrombectomy/thrombolysis.
- Score <6 (or large established hypodensity) → larger core, higher haemorrhagic-transformation risk.
High-yield: Loss of grey–white differentiation in more than one-third of the MCA territory is a relative contraindication to thrombolysis because of high risk of haemorrhagic transformation.
MRI vs. CT in ischaemia
| Feature | NCCT | MRI (DWI) |
|---|---|---|
| Detect haemorrhage | Excellent, immediate | Good (GRE/SWI) |
| Detect hyperacute infarct (<6 h) | Poor | Excellent (DWI positive in minutes) |
| Speed / availability | Fast, ubiquitous | Slower, limited |
| First test in acute stroke | Yes | If CT equivocal / posterior fossa |
High-yield: DWI (diffusion-weighted MRI) is the most sensitive modality for early ischaemic infarct (restricted diffusion = bright on DWI, dark on ADC). But NCCT remains the first test because the immediate clinical question is haemorrhage exclusion.
Intracerebral Haemorrhage (ICH)
Spontaneous (non-traumatic) ICH appears as an acute hyperdense intra-axial mass, often with surrounding hypodense vasogenic oedema and mass effect.
- Hypertensive haemorrhage — classic sites: basal ganglia (putamen, most common), thalamus, pons, cerebellum. Caused by rupture of Charcot–Bouchard microaneurysms of lenticulostriate perforators.
- Cerebral amyloid angiopathy — lobar haemorrhages in the elderly, often recurrent, peripheral/cortical.
- "Spot sign" on CT angiography = contrast extravasation within the haematoma → predicts ongoing bleeding and expansion.
High-yield: Putamen (lentiform nucleus) is the commonest site of hypertensive intracerebral bleed. Pontine bleeds present with pinpoint pupils and coma; cerebellar bleeds >3 cm warrant surgical evacuation.
Subarachnoid Haemorrhage (SAH)
Blood in the subarachnoid space, most often from a ruptured berry (saccular) aneurysm at the circle of Willis (commonest: anterior communicating artery).
- NCCT is the initial test — sensitivity is ~95–98% within the first 6–24 h, falling thereafter.
- Appearance: hyperdensity filling the basal cisterns, Sylvian and interhemispheric fissures, and sulci — a star-shaped pattern in the suprasellar cistern.
- CT angiography localises the aneurysm; DSA (digital subtraction angiography) is the gold standard for aneurysm characterisation.
- If CT is negative but suspicion remains → lumbar puncture looking for xanthochromia (yellow CSF from bilirubin, takes ~12 h to develop; differentiates true SAH from a traumatic tap).
High-yield: Clinical clue = "thunderclap headache / worst headache of life." A negative CT does NOT exclude SAH → do LP for xanthochromia. The modified Fisher grade (based on CT blood thickness + IVH) predicts vasospasm risk; vasospasm peaks day 4–14 and is treated/prevented with oral nimodipine.
Head Injury: Extra-axial Haematomas
The single most tested radiology discrimination in trauma is extradural vs. subdural haematoma morphology.
| Feature | Extradural (Epidural) Haematoma | Subdural Haematoma |
|---|---|---|
| Location | Between skull and dura | Between dura and arachnoid |
| Shape on CT | Biconvex / lentiform (lens) | Crescent (concavo-convex) |
| Crosses suture lines | No (dura adherent at sutures) | Yes |
| Crosses dural reflections (falx/tentorium) | Yes | No |
| Source of bleed | Middle meningeal artery (arterial) | Bridging cortical veins (venous) |
| Typical fracture | Temporo-parietal (pterion) | May/may not |
| Classic course | Lucid interval then deterioration | Insidious, fluctuating |
| Age group | Young | Elderly, alcoholics, infants |
Extradural haematoma (EDH)
- Arterial, fast-accumulating, biconvex because tightly bound dura limits spread; stops at sutures.
- Caused by middle meningeal artery tear, classically with a pterion fracture (thinnest part of skull).
- Classic triad/course: head trauma → brief unconsciousness → lucid interval → rapid deterioration (expanding clot, herniation).
High-yield: Biconvex + does NOT cross sutures + lucid interval + middle meningeal artery + pterion fracture = EDH. A swirl sign (hypodense areas within a hyperdense EDH) indicates active bleeding/unclotted blood → emergency.
Subdural haematoma (SDH)
- Venous (bridging veins), crescent-shaped, crosses sutures but not midline (falx).
- Acute SDH (<3 days):** hyperdense crescent. **Subacute (3 days–3 weeks):** **isodense** (easy to miss — look for effaced sulci and midline shift). **Chronic (>3 weeks): hypodense crescent.
- Risk groups: elderly (brain atrophy stretches bridging veins), alcoholics, anticoagulated, infants (suspect non-accidental injury / shaken baby — bilateral SDH + retinal haemorrhages).
High-yield: An isodense subacute SDH can be invisible against grey matter — clue is unilateral sulcal effacement and midline shift. Bilateral isodense SDH can mask itself by symmetry ("hidden" SDH).
Head Injury: Intra-axial & Other Findings
Cerebral contusion
- "Bruise" of the brain — heterogeneous hyperdense (haemorrhagic foci) within hypodense (oedema) lesion, typically at sites where brain meets bony ridges: inferior frontal lobes and anterior/inferior temporal lobes.
- Coup = injury at site of impact; contrecoup = opposite to impact (often larger).
- Contusions classically "blossom" (enlarge) on repeat CT over 24–48 h.
Diffuse axonal injury (DAI)
- Shearing of axons from rotational/acceleration–deceleration forces (e.g., high-speed RTA).
- Classic locations: grey–white matter junction, corpus callosum (especially splenium), and dorsolateral midbrain.
- NCCT is frequently NORMAL or shows only tiny petechial haemorrhages despite a deeply comatose patient — a key clinical–radiological mismatch.
High-yield: If a patient has a Glasgow Coma Scale far worse than the CT suggests, think DAI. MRI (GRE/SWI sequences) is far more sensitive for the microhaemorrhages of DAI than CT.
Traumatic SAH
- Commonest CT finding after significant head trauma; blood layers in sulci/cisterns, often over the convexity (vs. aneurysmal SAH which centres on basal cisterns).
Skull fracture & secondary signs
- Pneumocephalus (air in cranium) implies a fracture communicating with sinuses/mastoid or open injury.
- Base-of-skull fracture signs (clinical): raccoon eyes (periorbital bruising), Battle's sign (mastoid bruising), CSF rhinorrhoea/otorrhoea, haemotympanum.
Mass effect, midline shift & herniation
- Midline shift is measured at the level of the septum pellucidum / foramen of Monro; report the distance the midline structures are pushed across.
- Herniation patterns: subfalcine (cingulate under falx), uncal/transtentorial (uncus → CN III palsy: fixed dilated pupil + "down and out" eye), tonsillar (cerebellar tonsils through foramen magnum → respiratory arrest).
High-yield: A fixed, dilated pupil with a unilateral expanding mass = uncal herniation compressing CN III → neurosurgical emergency.
Stepwise Acute Stroke Imaging Pathway
Suspected acute stroke → immediate NCCT brain → is there blood?
- Blood present → haemorrhagic stroke → BP control, reverse anticoagulation, neurosurgery referral; no thrombolysis.
- No blood + within window (≤4.5 h) + no contraindication → IV thrombolysis (alteplase/tenecteplase).
- Large-vessel occlusion (hyperdense MCA, good ASPECTS) → add mechanical thrombectomy (window extendable to 24 h with perfusion imaging — DAWN/DEFUSE-3 criteria).
- CT equivocal / posterior fossa stroke suspected → MRI with DWI.
Key Differentials
- Hyperdense MCA sign vs. calcified atheroma: thrombus ~40–60 HU and unilateral; calcification >100 HU and often bilateral.
- Acute SDH vs. EDH: crescent + crosses sutures vs. biconvex + stops at sutures.
- Aneurysmal SAH (basal cisterns) vs. traumatic SAH (convexity sulci).
- Hypertensive ICH (deep: basal ganglia/thalamus) vs. amyloid angiopathy (lobar, elderly).
- Isodense subacute SDH vs. normal brain: look for midline shift and sulcal effacement.
- Ring-enhancing lesion differentials (on contrast CT/MRI): metastasis, abscess, glioblastoma, tuberculoma, toxoplasmosis (MAGIC TR mnemonic).
Recently asked / exam angle
- Image-based MCQs showing a biconvex vs. crescent extra-axial collection asking for the diagnosis and the artery/vein involved (middle meningeal artery for EDH; bridging veins for SDH).
- "Which does NOT cross suture lines?" → Extradural haematoma.
- "Hyperdense MCA sign indicates?" → acute thromboembolic MCA occlusion / ischaemic stroke.
- "Investigation of choice to exclude haemorrhage before thrombolysis" → NCCT brain.
- "Most sensitive test for hyperacute infarct" → MRI DWI.
- "Commonest site of hypertensive bleed" → putamen / basal ganglia.
- "CSF finding when CT is negative but SAH suspected" → xanthochromia on LP.
- "Best sequence for diffuse axonal injury" → MRI GRE/SWI; CT often normal.
- "Drug to prevent vasospasm in SAH" → nimodipine.
- "Lucid interval is characteristic of" → extradural haematoma.
- Density questions: HU of acute blood (~60–80), reason for hyperdensity (protein/clot, not iron).
Rapid revision
- NCCT brain is the first-line test in acute stroke and head injury — detects fresh blood and bone instantly.
- Acute blood = hyperdense (~60–80 HU) due to clot protein; becomes isodense at ~1 week, hypodense at 2–3 weeks.
- Hyperdense MCA sign = thrombus in M1 = large-vessel ischaemic stroke; earliest CT sign.
- DWI MRI is most sensitive for hyperacute infarct; CT may be normal in first 6 h.
- Avoid thrombolysis if hypodensity involves >1/3 of MCA territory or ASPECTS <6.
- EDH: biconvex, middle meningeal artery, does NOT cross sutures, lucid interval, pterion fracture.
- SDH: crescent, bridging veins, crosses sutures, elderly/alcoholic/infant; subacute SDH is isodense.
- Aneurysmal SAH fills basal cisterns (star sign); commonest source = anterior communicating artery; negative CT → LP for xanthochromia.
- Nimodipine prevents SAH-related vasospasm (peaks day 4–14).
- Hypertensive ICH = deep (putamen #1); amyloid angiopathy = lobar in elderly.
- DAI: clinical–radiological mismatch (deep coma, near-normal CT); seen at grey–white junction & corpus callosum; MRI GRE best.
- Contusions favour inferior frontal/temporal lobes, coup–contrecoup, and "blossom" on repeat scan.
- Uncal herniation → ipsilateral fixed dilated pupil (CN III) → neurosurgical emergency.
- Read every trauma CT on bone windows to avoid missing fractures and pneumocephalus.