01Purpose and principlesWhat the assessment is for and the core concepts behind it.
CT assigns a number to x-ray attenuation and displays it through chosen window settings. Air is dark, CSF is low attenuation, brain is intermediate, acute clot is commonly bright, and calcium or bone is very bright. Those relative appearances change with acquisition, reconstruction, windowing, haemoglobin and time, so comparison with anatomy and prior images is safer than a single density label.
The initial question is often exclusionary: is there blood, mass effect, hydrocephalus or a large established infarct that changes immediate treatment? A scan may answer that question while remaining unable to exclude small infarction, cerebral venous thrombosis, encephalitis, meningitis or subtle posterior-fossa disease. The report and clinical plan should state what remains unresolved.
Pattern recognition must lead to action. Extra-axial blood, basal cisternal blood, asymmetric low attenuation, compressed ventricles or obliterated cisterns demand different vascular and specialist pathways. Image interpretation should be integrated with onset time, trauma, anticoagulants, fever, malignancy, pregnancy and examination rather than used as a stand-alone diagnosis.
Key points
- Non-contrast CT is fast and excellent for acute haemorrhage, hydrocephalus, skull injury and substantial mass effect; it is less sensitive for early ischaemia and some posterior-fossa lesions.
- Review systematically: technical adequacy, extra-axial spaces, cisterns and sulci, ventricles, parenchymal symmetry and grey–white differentiation, posterior fossa, skull and extracranial tissues.
- Fresh blood is usually hyperattenuating, but anaemia, very small volume, lesion age and artefact can alter conspicuity; describe compartment and mass effect before inferring cause.
- Loss of the insular ribbon, obscured lentiform nucleus, sulcal effacement and a dense artery can support early ischaemia, yet a normal scan never ends a time-critical stroke pathway.
- For suspected SAH, a radiologist-reported negative CT within six hours may avoid routine LP; after six hours, consider LP and wait at least 12 hours from onset for spectrophotometry.
- Repeat or escalate imaging when neurology deteriorates, the first study is technically limited, or the modality cannot answer the persisting high-risk clinical question.
02Indications, selection and cautionsWhen it is useful, when urgency changes and important limitations.
Search sulci, basal cisterns, fissures, ventricles, brain parenchyma and extra-axial spaces. State side, compartment, volume impression, ventricular extension and associated oedema or shift.
Compare hemispheres for grey–white loss, focal hypoattenuation, sulcal effacement and a dense artery. Small or very early infarcts may remain invisible, especially in the posterior fossa.
Assess sulci, ventricles, basal cisterns, midline position and herniation corridors. Millimetres of shift alone do not determine clinical severity; lesion location and trajectory matter.
Judge ventricular size against age and prior imaging, then look for transependymal CSF seepage and an obstructing lesion. Acute ventricular enlargement with declining consciousness is an emergency.
Check motion, coverage, reconstruction thickness and window settings. Beam hardening near the skull base can conceal posterior-fossa haemorrhage or infarction and should be named explicitly.
Define the disease, timing and image quality before calling CT reassuring. A negative result is meaningful only for the question and population in which its performance is known.
03Method and interpretationA systematic approach to the test and its findings.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Non-contrast CT headFirst step - Why
- Identify acute blood, major mass effect, hydrocephalus, fracture and established infarction rapidly.
- Interpretation and limitations
- A negative study does not universally exclude early infarction or SAH. Review time from onset, technical adequacy, haemoglobin, artefact and the suspected compartment.
- 02
CT angiography - Why
- Identify arterial occlusion, aneurysm or vascular lesion when the presentation and initial CT require vascular definition.
- Interpretation and limitations
- CTA adds contrast and timing dependence. It follows the relevant stroke, SAH or ICH pathway and should not be ordered as a generic substitute for clinical formulation.
- 03
CT perfusion - Why
- Estimate infarct core and hypoperfused tissue in selected reperfusion pathways.
- Interpretation and limitations
- Maps depend on acquisition and software thresholds and can be distorted by motion, delay or poor cardiac output; interpret with symptoms, non-contrast CT and CTA.
- 04
MRI brain with diffusion sequences - Why
- Detect small, early or posterior-fossa infarction and characterise lesions unresolved by CT.
- Interpretation and limitations
- Diffusion restriction is sensitive but not perfectly specific, and occasional very early strokes are DWI-negative. MRI must not create avoidable reperfusion delay.
- 05
Lumbar puncture after negative CT for suspected SAH - Why
- Detect bilirubin when later CT has not resolved a high-probability SAH presentation.
- Interpretation and limitations
- Consider after a negative scan performed more than six hours from onset; wait at least 12 hours, confirm procedural safety and use spectrophotometry.
- 06
Repeat CT head - Why
- Detect evolution after neurological deterioration or reassess a study limited by motion or timing.
- Interpretation and limitations
- Repeat urgently for a new deficit, GCS decline or other defined change. Routine repetition without a clinical question adds radiation without resolving uncertainty.
04Clinical next stepsHow the result changes management or prompts escalation.
01Worked acute pathwayThunderclap headache with a negative scanFirst stepAn adult presents after sudden maximal-at-onset headache and initial non-contrast CT shows no blood.+
- 1Confirm exact onset, neurological state, scan timing and technical adequacy, while maintaining urgent SAH assessment.
- 2If CT was obtained and radiologist-reported within six hours, use the NG228 pathway rather than adding routine LP automatically.
- 3If imaging occurred after six hours and suspicion persists, consider LP when safe and at least 12 hours after onset, with bilirubin spectrophotometry.
- 4EscalationEscalate to specialist and vascular imaging routes when blood or an aneurysmal pattern is demonstrated.
02Stroke pathwayAcute focal deficit with no haemorrhageNon-contrast CT shows no acute blood in a patient with a disabling focal deficit.+
- 1Keep the stroke call active and assess reperfusion eligibility from last-known-well time, deficit, premorbid state and contraindications.
- 2Obtain CTA promptly when thrombectomy is a possibility and use perfusion or MRI only where the pathway requires it.
- 3Do not wait for a mature low-attenuation infarct before making time-critical treatment decisions.
03Deterioration pathwayEarlier reassuring CT but worsening neurologyConsciousness or focal signs worsen after an initially normal or minor CT finding.+
- 1Repeat ABC assessment, glucose, pupils, GCS and limb findings and call senior neurological support immediately.
- 2Re-review the first images and report for timing, posterior-fossa coverage and other stated limits.
- 3AlternativeArrange urgent repeat or alternative imaging based on the suspected complication while treating life-threatening physiology.
05Risks, monitoring and follow-upComplications, safety checks and further assessment.
- Timestamp GCS components, pupils, limb power, speech and vital signs so a change can be distinguished from sedation, fatigue or documentation variation.
- After a negative or limited study, document the residual differential and the explicit trigger for CTA, MRI, LP or repeat CT.
- Track contrast exposure, renal context and allergies when CTA or perfusion is added, but do not delay life-saving emergency imaging for routine laboratory results.
- Ensure urgent and unexpected findings are communicated directly to the responsible clinical team with acknowledgement and an agreed next action.
- Review final reports and addenda against treatment already given; a provisional interpretation should not become the unexamined endpoint.
06Special situationsVariants, exceptions and circumstances that change the usual approach.
Windows alter visibility
Brain, subdural and bone windows emphasise different attenuation ranges; a systematic review uses each to avoid missing thin extra-axial blood or fracture.
Density evolves
Clot generally becomes less conspicuous over time, and profound anaemia can reduce the brightness of acute blood, so pattern and context remain essential.
Posterior fossa is difficult
Dense skull-base bone creates artefact and small brainstem infarcts may be occult; MRI is often the problem-solving modality when signs persist.
Negative means question-specific
A scan can exclude a large haemorrhage yet fail to exclude a small infarct, venous thrombosis, meningitis or later-presenting subarachnoid haemorrhage.
Comparison adds trajectory
Prior imaging helps separate chronic ventriculomegaly, calcification and old infarction from new oedema, haemorrhage or developing hydrocephalus.
07Common pitfallsFrequent interpretation and management errors.
- 01
Calling an early normal CT a rule-out test for acute ischaemic stroke and allowing the reperfusion pathway to stop.
- 02
Applying the six-hour SAH rule without a secure onset time, adequate scan or radiologist interpretation.
- 03
Ignoring posterior-fossa artefact when the clinical syndrome localises to cerebellum or brainstem.
- 04
Describing blood without its compartment, ventricular extension, mass effect or likely need for vascular imaging.
- 05
Repeating CT by habit while failing to define the clinical change or the unresolved question.