Non-Contrast CT — Signs and Interpretation

Non-contrast CT remains the workhorse of acute neurologic imaging — it is fast, ubiquitous, and excellent for blood, mass effect, herniation, and bone. The trade-off is poor sensitivity for hyperacute ischemia and for non-hemorrhagic mass lesions. This page covers what NCT shows, what it misses, and the high-yield signs.

What Non-Contrast CT Is Good For

• Acute hemorrhage — sensitive within minutes; persists hyperdense ~7–10 days.
• Skull / facial / cervical fracture.
• Mass effect, midline shift, herniation, hydrocephalus.
• Calcified lesions (oligodendroglioma, meningioma, congenital).
• Foreign body, air, shunt position.
• Triage of acute stroke — rules out hemorrhage before tPA.
• Initial assessment of TBI, altered mental status, severe headache.

What Non-Contrast CT Misses

• Hyperacute ischemia (often normal <6 hours).
• Small posterior fossa / brainstem lesions (beam hardening artifact).
• Subtle non-hemorrhagic masses, low-grade tumors.
• MS plaques, most demyelinating disease.
• Most encephalitis, abscess (early).
• Small subarachnoid hemorrhage (more sensitive within first 6 hours; sensitivity drops to ~50% by 1 week).
• Isodense subdural hematomas (subacute, anemic patient).

Acute Ischemia Signs

Hyperdense Vessel Sign

• Acute thrombus is denser than circulating blood (~70–90 HU vs ~40 HU).
• Hyperdense MCA sign (M1) — most common; high specificity for acute LVO.
• MCA dot sign — distal M2/M3 branch in Sylvian fissure.
• Hyperdense basilar artery sign — easily missed; check brainstem level on every CT.
• Caveats: a calcified atherosclerotic vessel can mimic; high hematocrit makes vessels look denser bilaterally.

Loss of Gray-White Differentiation

• Insular ribbon sign — loss of normal cortex vs white matter density at the insular cortex.
• Obscured lentiform nucleus — basal ganglia (specifically lentiform) becomes isodense to internal capsule.
• Loss of cortical sulci on the affected side — early swelling.
• Hypodensity evolves over hours; well-developed by 24–48 hours.

ASPECTS (Alberta Stroke Program Early CT Score)

10-point scale for MCA territory. Subtract 1 for each region with early ischemic change. ≥6 favors thrombectomy; ≤5 reduces benefit.

• Two ganglionic slices (caudate, lentiform, internal capsule, insular ribbon, M1–M3 cortex) = 7 points.
• Two supraganglionic slices (M4–M6 cortex) = 3 points.
• 10 = normal. 0 = entire MCA territory infarcted.

Intracranial Hemorrhage (ICH)

Acute ICH on CT

• Acute blood ~50–80 HU (hyperdense to brain).
• Density decreases over time: ~1–2 HU/day. By 1–2 weeks isodense; by ~3 weeks hypodense.
• Spot sign (CTA): focus of contrast extravasation within ICH → predicts expansion.

Location Predicts Cause

Hematoma Expansion Risk

• Spot sign on CTA → high risk.
• Larger initial volume (>30 mL).
• Heterogeneous density / fluid-fluid level → suggests active bleeding or coagulopathy.
• Anticoagulant use.
• Time from onset to imaging <6 hours.

Subarachnoid Hemorrhage (SAH)

CT Sensitivity

• ~95–98% within 6 hours of onset (with modern multi-detector CT).
• ~85–90% within 24 hours.
• ~50% by 1 week.
• If CT negative + clinical suspicion, do LP (xanthochromia) or MRI FLAIR + SWI.

Distribution Predicts Aneurysm Location

Hunt-Hess and Fisher Grades (Bedside Reading)

• Fisher (CT-based): I = no SAH; II = thin diffuse SAH; III = thick SAH (>1 mm in cisterns); IV = ICH or IVH ± thin SAH. Higher = higher vasospasm risk.
• Modified Fisher: incorporates IVH; better vasospasm prediction.

Complications to Look For

• Hydrocephalus (obstructive from IVH or communicating from arachnoid blood).
• Vasospasm (typically days 3–14; CTA/CTP for screening).
• Rebleeding (especially before securing aneurysm).
• Cerebral edema, mass effect, herniation.

Subdural Hematoma (SDH)

• Shape: crescentic, conforms to brain surface.
• Crosses sutures (does NOT cross dural reflections like falx or tentorium).
• Mechanism: bridging vein tear (deceleration, fall, atrophy in elderly).
• Density evolution:
  • Acute: hyperdense.
  • Subacute (~7–21 d): isodense — easy to miss; use wide subdural window (e.g., WL 75 / WW 250) + look for sulcal effacement and midline shift.
  • Chronic: hypodense.
  • Mixed-density = acute on chronic, common in elderly.
• Bilateral isodense SDH — easy to miss; can give “empty sulci” appearance.

Epidural Hematoma (EDH)

• Shape: biconvex (lentiform).
• Does NOT cross sutures (limited by dural attachment).
• Mechanism: middle meningeal artery laceration from temporal bone fracture (most common); venous EDH at vertex possible.
• Lucid interval classically described — immediate LOC → wake up → secondary deterioration as EDH expands.
• Swirl sign within hyperdense EDH → active bleeding → surgical urgency.
• Surgical emergency for symptomatic / expanding EDH; small asymptomatic can be observed with serial CT.

Mass Effect, Midline Shift, Herniation

Midline Shift

• Measure at the septum pellucidum or third ventricle.
• Mild (<5 mm), moderate (5–10 mm), severe (>10 mm).
• Decompressive craniectomy considered for severe shift with malignant edema.

Herniation Patterns

• Subfalcine: cingulate gyrus pushed under falx → ACA territory infarct.
• Uncal (transtentorial, descending): medial temporal lobe over tentorium → CN III palsy (ipsilateral pupil dilation), PCA compression, Duret hemorrhages in brainstem.
• Central (downward): bilateral diencephalon and brainstem pushed inferiorly → progressive rostrocaudal deterioration.
• Tonsillar: cerebellar tonsils through foramen magnum → brainstem compression → respiratory arrest.
• Ascending transtentorial: cerebellar/posterior fossa mass pushes upward → midbrain compression, aqueduct obstruction.
• External: brain herniates through skull defect (craniectomy site).

Hydrocephalus

• Obstructive (non-communicating): blockage of ventricular outflow (aqueduct stenosis, colloid cyst, IVH, tumor compressing 4th ventricle). Dilated ventricles ABOVE the obstruction.
• Communicating: impaired absorption (SAH, meningitis, NPH, leptomeningeal disease).
• Signs: ventricular enlargement (Evans index >0.3), transependymal CSF flow (periventricular T2/FLAIR halo), bowing of corpus callosum, effaced cortical sulci, large temporal horns.
• NPH triad: gait apraxia + urinary incontinence + cognitive decline. Ventriculomegaly out of proportion to sulcal atrophy + DESH (disproportionately enlarged subarachnoid space hydrocephalus) pattern.

Bone Window — Don’t Skip

• Skull fractures (linear, depressed, basilar).
• Pneumocephalus (post-fracture, post-surgical).
• Lytic lesions: metastases (breast, lung, prostate, multiple myeloma), hemangioma, eosinophilic granuloma.
• Sclerotic lesions: meningioma (hyperostosis), Paget, sclerotic metastases (prostate, breast).
• Sinus disease: opacification, air-fluid levels, bone destruction (suggests aggressive process).
• Mastoiditis: opacification + erosion of bony septations.
• Otomastoiditis with intracranial extension → epidural / temporal lobe abscess.

Pitfalls and Pearls

• Isodense subdural = bilateral SDH on a chronic patient with anemia — easy miss. Look for sulcal effacement + use wide subdural window.
• Posterior fossa beam hardening obscures brainstem / cerebellum. MRI if concern for posterior fossa pathology.
• Hyperdense MCA can be artifactual in patients with calcified atherosclerosis or high hematocrit — compare both sides.
• Subarachnoid blood at the base = aneurysmal SAH until proven otherwise → CTA next.
• “Pseudo-SAH”: diffuse cerebral edema with effaced cisterns can mimic SAH (brain density falls below vessel/cistern density).
• Calcified choroid plexus, pineal, basal ganglia are normal — don’t confuse with hemorrhage.
• Globus pallidus low attenuation in young patients: CO poisoning, hypoxic injury, methanol, mitochondrial.
• Hyperdense basilar is missed routinely — check at the brainstem level on every NCT in acute presentations.
• Vertex SDH is missed routinely — scroll all the way to the top.
• Mass effect with no obvious mass: think encephalitis, status epilepticus, PRES, MS tumefactive plaque, early infarct.
• Spot sign on CTA = active bleeding within ICH → reverse coagulopathy + close surgical evaluation.

References

1. Barber PA, Demchuk AM, Zhang J, Buchan AM. Validity and reliability of a quantitative computed tomography score in predicting outcome of hyperacute stroke before thrombolytic therapy. Lancet. 2000;355(9216):1670-1674.
2. Demchuk AM, Dowlatshahi D, Rodriguez-Luna D, et al. Prediction of haematoma growth and outcome in patients with intracerebral haemorrhage using the CT-angiography spot sign (PREDICT). Lancet Neurol. 2012;11(4):307-314.
3. Perry JJ, Stiell IG, Sivilotti ML, et al. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage. BMJ. 2011;343:d4277.
4. Heit JJ, Iv M, Wintermark M. Imaging of intracranial hemorrhage. J Stroke. 2017;19(1):11-27.