The hyperdense vessel on a non-contrast CT
A 71-year-old man presents 2 hours after sudden onset of dense left hemiparesis (NIHSS 14). Blood pressure 168/94 mmHg, glucose 6.8 mmol/L, no anticoagulation, no prior stroke. A non-contrast CT head is performed. The reporting radiologist notes a hyperdense right middle cerebral artery (MCA) sign and asks you, as the on-call registrar, whether this represents thrombus within the M1 segment or calcification of the vessel wall. The scan is 5 mm thick, and the hyperdense segment measures approximately 12 mm in length. There is no visible parenchymal hypodensity. You must decide whether to proceed directly to CT angiography (CTA) or to request a repeat thinner-section scan first.
1. How would you distinguish a hyperdense MCA sign due to acute thrombus from incidental MCA calcification on this scan, and what are the anatomical and technical factors that affect your confidence?
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A true hyperdense MCA sign reflects acute intraluminal thrombus in the proximal M1 segment. Key discriminators:
Morphology and distribution
- Thrombus is typically linear, follows the entire course of the visible M1 segment, and extends distally to the bifurcation. Calcification is usually punctate, nodular, or confined to the vessel wall rather than filling the lumen.
- Thrombus is seen in the proximal MCA only; calcification may also involve the carotid siphon, vertebral arteries, and choroid plexus.
Attenuation
- Thrombus density is usually 60–90 HU, whereas calcification exceeds 100–120 HU. On a 5 mm scan, partial volume averaging degrades this discrimination.
Anatomical pitfalls
- The M1 segment runs horizontally in the Sylvian fissure; the adjacent sphenoid ridge and orbital roof can produce beam-hardening artefact.
- The basilar artery and distal internal carotid can also show hyperdensity.
Technical factors
- Thin-section (≤2.5 mm) reconstruction reduces partial volume averaging and improves confidence. Multiplanar reformats along the M1 axis help.
- The length (12 mm) and the absence of calcification elsewhere favour thrombus.
Given the high pre-test probability (NIHSS 14, 2-hour window, no parenchymal change), the correct action is to proceed to CTA rather than delay for a repeat scan. CTA will confirm the occlusion, define the clot burden, and assess collateral status, all of which guide thrombectomy decisions. The hyperdense sign is supportive but not definitive; CTA is the reference standard.
2. If CTA confirms a right M1 occlusion, what anatomical features on the CTA would you assess to determine eligibility for endovascular thrombectomy, and why do they matter?
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Clot location and length
- Confirm occlusion of the M1 segment and measure the clot length. A long clot (>8 mm) may be less responsive to aspiration or stent-retriever alone and influences device choice.
Collateral circulation
- Assess leptomeningeal collaterals from the anterior cerebral artery (ACA) and posterior cerebral artery (PCA) territories. Good collaterals (e.g., >50% of the MCA territory) predict a favourable penumbra and better outcomes after thrombectomy.
- Collateral status is a stronger predictor of outcome than time from onset in some series.
Vessel anatomy
- The M1 segment arises from the internal carotid bifurcation, runs laterally to the limen insulae, and bifurcates into superior and inferior trunks. The site of occlusion determines the territory at risk (superior trunk: frontal and parietal; inferior trunk: temporal and parietal).
- Tortuosity of the cervical and intracranial internal carotid affects catheter navigation.
Circle of Willis variants
- A fetal origin of the PCA or a hypoplastic A1 segment alters collateral pathways and the size of the penumbra.
Contraindications
- Large established infarct core (>1/3 MCA territory) or haemorrhage excludes thrombectomy.
These features determine whether the patient has salvageable tissue and whether the procedure is technically feasible.