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Textbook/Clinical imaging and interpretation/Raised intracranial pressure and mass effect
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Raised intracranial pressure and mass effect

Recognise CT and MRI signs of raised intracranial pressure, localise mass effect and hydrocephalus, and communicate imaging limits so urgent treatment is driven by the patient and lesion rather than shift alone.

26 min full readUK scopeSources checked 13 Sept 2026Clinical review pending
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Herniation is a clinical and imaging emergency

Declining consciousness, new anisocoria, extensor posturing or abrupt respiratory change can indicate tissue displacement before every radiological sign is fully developed.

Action: Activate emergency neurological support, optimise oxygenation and circulation, elevate and align the head where appropriate, obtain urgent CT when safe, and progress definitive decompression or CSF diversion with neurosurgery.

Open the sections you need. The overview is shown first.
01Purpose and principlesWhat the assessment is for and the core concepts behind it.

Intracranial volume is shared by brain, blood and CSF. Compensation can initially hide pressure rise, but once exhausted small volume changes produce steep physiological deterioration. Imaging reveals the lesion, displaced compartments and CSF obstruction; the clinical examination supplies the rate and functional consequence. They should be interpreted together.

Horizontal displacement is seen as midline shift, subfalcine herniation and ventricular compression. Descending transtentorial movement crowds the suprasellar and ambient cisterns, displaces the medial temporal lobe and can compress the third nerve and brainstem. Tonsillar descent at the foramen magnum threatens the medulla. Upward posterior-fossa herniation is another confined-compartment pattern.

Ventricular enlargement is not synonymous with acute hydrocephalus. Atrophy enlarges ventricles and sulci together, while obstructive hydrocephalus preferentially expands compartments upstream of blockage and may produce transependymal low attenuation. Communicating hydrocephalus enlarges the system more diffusely. Prior imaging and clinical tempo are essential.

Key points

  • Raised intracranial pressure is a physiological state; CT and MRI show causes and consequences but a normal scan does not universally exclude elevated pressure.
  • Assess sulci, ventricles, midline, basal cisterns, medial temporal lobes, brainstem and foramen magnum in a fixed sequence before quantifying any single sign.
  • Mass effect includes sulcal effacement, ventricular compression, cisternal obliteration, shift and herniation; location and rate often matter more than a millimetre value alone.
  • Hydrocephalus is interpreted by ventricular pattern, sulcal context, transependymal CSF flow and comparison; localise obstruction rather than merely calling ventriculomegaly.
  • Urgent non-contrast CT is usually the first test in acute deterioration, while MRI characterises tumour, infection, venous disease and posterior-fossa anatomy once safe and feasible.
  • Never use imaging to delay resuscitation or definitive specialist treatment, and never treat a normal scan as automatic clearance for lumbar puncture.
02Indications, selection and cautionsWhen it is useful, when urgency changes and important limitations.
Sulcal and cisternal effacementRed flag

Compare hemispheres and inspect suprasellar, ambient and quadrigeminal cisterns. Loss of normal CSF spaces signals crowding but may be subtle or symmetrical.

Midline displacement

Measure at a reproducible landmark and state the direction and source lesion. Shift summarises geometry but does not replace examination or location-specific risk.

Uncal and central descentRed flag

Look for medial temporal displacement, asymmetric ambient cisterns, third-nerve compression pattern and progressive brainstem crowding.

Posterior-fossa crowdingRed flag

Review fourth ventricle, prepontine cistern, brainstem contour and foramen magnum. Beam-hardening artefact on CT can limit confidence and favour MRI after stabilisation.

Obstructive hydrocephalusRed flag

Determine which ventricles are enlarged and identify the transition point. Transependymal CSF seepage and clinical decline support an acute pressure consequence.

Normal imaging boundary

Early pressure elevation can occur without dramatic CT signs, particularly in comatose paediatric severe TBI; do not let one scan overrule clinical trajectory.

Red flags requiring action

  • A falling GCS with a newly dilated pupil or progressive motor asymmetry is an immediate herniation warning; do not wait for the complete Cushing triad.
  • Effaced basal cisterns, ventricular compression, increasing midline shift or downward tonsillar displacement requires urgent communication even if the report is provisional.
  • Acute hydrocephalus with drowsiness, vomiting or sixth-nerve dysfunction may deteriorate rapidly and needs neurosurgical assessment for CSF diversion.
  • A posterior-fossa lesion can obstruct the fourth ventricle and compress the brainstem with little supratentorial shift, so the compartment must be reviewed directly.
  • Lumbar puncture is unsafe when a space-occupying lesion, obstructive hydrocephalus or evolving herniation creates a pressure gradient.
03Method and interpretationA systematic approach to the test and its findings.
Investigation order

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.

  1. 01
    Urgent non-contrast CT headFirst step
    Why
    Identify haemorrhage, oedema, hydrocephalus, mass lesion and gross herniation rapidly.
    Interpretation and limitations
    Review cisterns and posterior fossa as well as shift. A normal study cannot universally exclude pressure elevation and should not end assessment of a deteriorating patient.
  2. 02
    Contrast-enhanced MRI brain
    Why
    Characterise tumour, abscess, inflammation, venous disease and posterior-fossa anatomy once the patient is stable enough.
    Interpretation and limitations
    MRI offers superior tissue contrast but longer acquisition and monitoring constraints; it is a problem-solving study, not a reason to postpone emergency decompression.
  3. 03
    CT angiography or venography
    Why
    Assess arterial or venous causes of swelling, haemorrhage or impaired drainage.
    Interpretation and limitations
    Choose the vascular study from the lesion pattern. Poor timing or motion can make a negative examination non-definitive.
  4. 04
    Serial CT
    Why
    Evaluate evolving oedema, haemorrhage, hydrocephalus or response after intervention.
    Interpretation and limitations
    Repeat because examination or management changed. Compare ventricles, cisterns and lesion size directly rather than relying on an isolated shift value.
  5. 05
    Invasive intracranial-pressure monitoring
    Why
    Guide selected neurocritical-care management when examination and imaging cannot provide continuous physiology.
    Interpretation and limitations
    Thresholds are population-specific; adult and paediatric severe-TBI values must not be applied to every tumour, stroke or infection.
  6. 06
    Formal ophthalmic assessment
    Why
    Confirm papilloedema and measure visual function in selected stable pressure disorders.
    Interpretation and limitations
    Fundoscopy, fields and acuity support chronic pathways, but absence of papilloedema does not exclude acute herniation and should not delay emergency imaging.
04Clinical next stepsHow the result changes management or prompts escalation.
01Worked emergency pathwayDeterioration with new anisocoriaFirst stepA patient with a known intracranial lesion develops reduced consciousness and a unilateral dilated pupil.
  1. 1Call anaesthesia and neurosurgery immediately, secure oxygenation and circulation, align and elevate the head when appropriate, and avoid hypotension.
  2. 2Obtain urgent non-contrast CT when transport is safe while initiating specialist-directed temporary pressure rescue.
  3. 3Describe lesion, cisterns, ventricles, shift and herniation route directly to the treating team rather than waiting for routine report delivery.
  4. 4DefinitiveProceed to definitive decompression, lesion treatment or CSF diversion as determined by the cause and specialist assessment.
02Hydrocephalus pathwayVentricular enlargement with clinical declineImaging shows acute ventricular expansion and transependymal flow in a drowsy patient.
  1. 1Localise the obstruction from the pattern and inspect for haemorrhage, tumour or posterior-fossa lesion.
  2. 2Contact neurosurgery immediately and avoid lumbar puncture because an obstructive pressure gradient may be present.
  3. 3Use specialist-led urgent ventricular drainage or cause control, followed by clinical and imaging reassessment.
03Discordant pathwayStrong pressure syndrome with limited CTThe examination worsens but the CT report describes no major mass effect.
  1. 1Reassess GCS, pupils, motor pattern, physiology and confounders, and re-review the actual images for subtle cisternal or posterior-fossa change.
  2. 2Consider repeat CT, MRI or invasive monitoring according to stability, suspected cause and neurocritical-care advice.
  3. 3EscalationMaintain treatment and escalation for the clinical syndrome while the unresolved imaging question is addressed.
05Risks, monitoring and follow-upComplications, safety checks and further assessment.
  • Use timestamped GCS components, pupils, motor response and vital signs; changes should trigger immediate clinical reassessment rather than passive interval imaging.
  • After any pressure intervention, reassess the neurological examination and compare cisterns, ventricles and lesion effect on appropriately timed imaging.
  • Monitor oxygenation, carbon dioxide, blood pressure, temperature, glucose and sodium under the cause-specific critical-care pathway because secondary insults amplify injury.
  • For ventricular drains or invasive monitors, follow the authorised unit protocol and interpret numbers alongside waveform, examination and CT rather than in isolation.
  • Document direct communication of acute hydrocephalus, new herniation or unexpected mass effect, including recipient, time and agreed action.
06Special situationsVariants, exceptions and circumstances that change the usual approach.

Pressure is not a picture

Imaging displays anatomy at one moment; intracranial pressure is dynamic and may require physiological monitoring in selected critically ill patients.

Shift is not universal severity

A slowly growing hemispheric lesion may generate substantial shift with modest symptoms, while a small posterior-fossa lesion can rapidly threaten the brainstem.

Cisterns show crowding

Suprasellar and ambient cisternal asymmetry may reveal transtentorial displacement before a large midline measurement develops.

Ventricular geometry localises

Enlargement upstream from a narrow transition helps identify obstruction at the foramen of Monro, aqueduct or fourth-ventricular outlets.

LP clearance is clinical

A scan cannot certify every lumbar puncture as safe; the indication, examination, coagulation and possibility of a pressure gradient remain decisive.

07Common pitfallsFrequent interpretation and management errors.
  1. 01

    Waiting for hypertension and bradycardia before recognising a patient with clear early signs of herniation.

  2. 02

    Reporting only midline shift while omitting basal cisterns, ventricular obstruction and posterior-fossa crowding.

  3. 03

    Calling every enlarged ventricle hydrocephalus without examining sulci, prior images and the pattern upstream of obstruction.

  4. 04

    Sending an unstable patient for prolonged MRI when CT already shows a lesion requiring emergency specialist treatment.

  5. 05

    Using a normal CT as universal proof that intracranial pressure is normal or that lumbar puncture is safe.

Practice

Two practice questions

Question 1 of 20 correct
Clinical imaging and interpretationOriginal SBA

Deterioration with uncal signs

A patient with a known temporal mass becomes drowsy and develops a newly dilated poorly reactive ipsilateral pupil. What is the best immediate imaging-related action?

Sources and review status4 sources · checked 13 Sept 2026 · clinical review pending
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 13 Sept 2026; clinical approval remains outstanding.

  • ENLS Intracranial Hypertension and Herniation Protocol version 6.0Version 6.0, updated September 2024; communication, diagnosis, Tier Zero and Tier One sections read. Multi-aetiology professional consensus for the first hours of an ICP crisis, not a UK national or disease-specific outcomes guideline. Applied specifically to Raised intracranial pressure and mass effect.
  • NICE NG232 head injury recommendationsPublished 18 May 2023; recommendations on acute assessment, CT criteria, neurosurgical discussion and neurological deterioration read 13 September 2026. This source governs traumatic head injury across ages and was not generalised to spontaneous disease. Applied specifically to Raised intracranial pressure and mass effect.
  • Brain Trauma Foundation paediatric severe TBI guideline, third editionPublished 2019; neuroimaging, ICP and CPP sections read. Applies only to severe paediatric traumatic brain injury; an initially normal CT does not exclude raised ICP in a comatose child, and adult thresholds were not imported. Applied specifically to Raised intracranial pressure and mass effect.
  • ESO/EANS 2025 guideline on spontaneous intracerebral haemorrhagePublished 22 May 2025; diagnostic-cause imaging, prognostic-score, blood-pressure, haemostatic, hydrocephalus and surgery sections read. European adult spontaneous ICH guidance; many recommendations are weak and do not govern traumatic haemorrhage. Applied specifically to Raised intracranial pressure and mass effect.
Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom