How do you systematically interpret a non-contrast (NC) computed tomography (CT) scan?

Systematic Interpretation of Non-Contrast CT Head

Adopt a structured anatomical approach that systematically evaluates blood, brain parenchyma, ventricles, and bone to avoid missing critical pathology, as this method is recommended by the American College of Radiology for acute neurological presentations 1.

Initial Technical Assessment

Before interpreting the scan, verify technical adequacy:

• Confirm adequate coverage from vertex to foramen magnum with contiguous 5-10mm thick sections parallel to the canthal-meatal line 1
• Check for motion artifact or beam hardening that may limit sensitivity, particularly in the posterior fossa where artifact can obscure small brainstem infarcts 1

Step 1: Blood (Hyperdensity Assessment)

Begin by systematically searching for hemorrhage, as this is the primary indication for non-contrast CT in acute neurological presentations 1.

Acute Hemorrhage Detection

• Scan all brain parenchyma for hyperdensity (typically 50-90 Hounsfield Units), checking intraparenchymal, subarachnoid, subdural, epidural, and intraventricular spaces 1, 2
• Examine for specific hemorrhage expansion markers including the blend sign (heterogeneous density within hematoma), black hole sign (hypoattenuating area within hematoma), island sign (separate hematoma fragments), and hypodensities within the hemorrhage, as these predict expansion and poor outcomes 3
• Note that CT can miss small hemorrhages, particularly hemorrhagic transformation of infarcts, with MRI being more sensitive for detecting microbleeds and chronic hemorrhage 4, 5

Vascular Hyperdensity

• Look for hyperdense vessel signs (dense MCA sign, dense basilar sign) indicating acute thrombus, though this requires correlation with clinical presentation 1
• Evaluate dural venous sinuses for hyperdensity suggesting venous thrombosis, though only 30% of venous sinus thrombosis cases show abnormalities on non-contrast CT 1

Step 2: Brain Parenchyma (Gray-White Differentiation)

Systematically assess each vascular territory for early ischemic changes, as these determine treatment eligibility and prognosis 1.

Acute Ischemic Changes

• Apply the ASPECTS (Alberta Stroke Program Early CT Score) to quantify early infarct signs in the MCA territory, examining for loss of gray-white differentiation, sulcal effacement, and hypoattenuation 1
• Recognize that CT significantly underestimates acute ischemia compared to MRI, with beam hardening artifact particularly limiting detection of small brainstem infarcts 1
• Identify hypodensity of the caudate nucleus, lentiform nucleus, insular ribbon, or cortical regions as markers of established ischemic core 1

Chronic Changes

• Document chronic small vessel ischemic changes appearing as white matter hypodensities and lacunar infarcts, though CT significantly underestimates the extent compared to MRI 6
• Note that moderate to severe white matter changes indicate established cerebrovascular disease requiring aggressive vascular risk factor modification 6

Mass Effect and Edema

• Assess for mass effect including midline shift, sulcal effacement, ventricular compression, and cisternal effacement 1, 7
• Evaluate for progressive edema in known pathology, as this may indicate clinical deterioration requiring urgent intervention 1, 7

Step 3: Cerebrospinal Fluid Spaces

Examine ventricular size and configuration, as hydrocephalus requires urgent intervention 1, 7.

Ventricular System

• Compare ventricular size to prior studies when available, looking for acute enlargement suggesting obstructive hydrocephalus or shunt malfunction 7
• Assess for intraventricular hemorrhage, which complicates management and worsens prognosis 1, 7
• Evaluate temporal horns and third ventricle disproportionately, as early enlargement may indicate developing hydrocephalus 7

Cisterns and Sulci

• Check basal cisterns (suprasellar, ambient, quadrigeminal) for effacement indicating increased intracranial pressure or herniation 1
• Assess sulcal spaces for asymmetric effacement suggesting focal pathology or edema 1

Step 4: Bone and Extracranial Structures

Systematically review all visualized bone and soft tissues, as incidental findings may explain symptoms or require follow-up 1.

Skull Base and Calvarium

• Examine for fractures, particularly in trauma settings where CT rapidly identifies skull fractures and foreign bodies 1
• Assess skull base foramina for erosion or expansion suggesting perineural tumor spread or chronic infection 1

Paranasal Sinuses and Mastoids

• Document mucosal thickening or opacification, though this is often incidental and only requires treatment if symptomatic 6
• Note mastoid air cell opacification, which may indicate infection in appropriate clinical context 1

Critical Pitfalls to Avoid

• Never rely solely on CT to exclude acute ischemia in the first 6 hours, as early infarct signs may be subtle or absent 1
• Do not assume CT excludes all hemorrhage—small hemorrhagic transformations and microbleeds are frequently missed 4, 5
• Avoid misinterpreting contrast staining from prior procedures as hemorrhage, though distinguishing these can be challenging (hyperdensity >90 HU suggests hemorrhage) 8
• Do not overlook posterior fossa pathology where beam hardening artifact significantly limits sensitivity 1
• Remember that venous sinus thrombosis is missed on 70% of non-contrast CTs, requiring CTV or MRV for definitive diagnosis 1

When Non-Contrast CT is Insufficient

Recognize that non-contrast CT serves primarily to exclude hemorrhage and detect large established infarcts, but MRI is superior for detecting acute ischemia, small hemorrhages, posterior fossa pathology, and chronic small vessel disease 1, 6, 4, 5.

• Consider immediate MRI with DWI for suspected acute stroke when CT is normal but clinical suspicion remains high 1, 5
• Add CTA immediately after non-contrast CT in suspected large vessel occlusion to guide endovascular therapy decisions 1
• Reserve contrast-enhanced CT only for specific concerns about infection, tumor, or inflammatory conditions, as it adds no value for routine stroke or hemorrhage evaluation 1, 7