01Core principlesThe concepts and mechanisms needed to understand the subject.
The rigid adult skull contains brain tissue, blood and cerebrospinal fluid. Compensation initially displaces venous blood and CSF, so pressure may remain modest despite added volume. Once this reserve is exhausted, small further increases in tumour, haematoma, oedema, venous blood or CSF can produce a steep pressure rise, reduce cerebral perfusion and create pressure gradients that shift brain tissue. Infants with open sutures can partly accommodate chronic expansion through head growth, which changes the signs but does not prevent injury.
Symptoms are sensitive to rate, cause and location. A slowly growing lesion may cause progressive headache, cognitive change, papilloedema or sixth-nerve palsy. Acute haemorrhage, obstructive hydrocephalus or diffuse swelling may present with abrupt vomiting, falling consciousness, pupillary asymmetry, weakness or seizure. Neither a morning headache nor vomiting is specific, and pain pattern alone cannot determine pressure. The clinical task is to recognise a concerning cluster, compare it with baseline, seek the cause and respond to deterioration.
Raised pressure and herniation are related but not identical. An instrumented patient can have sustained raised ICP without a focal herniation syndrome, while a dangerous compartmental gradient can cause herniation signs without a globally high measured value. The examination therefore complements monitoring and imaging. Treat the patient’s trajectory, lesion and physiology rather than waiting for one number or the traditional triad.
Key points
- Raised intracranial pressure is a physiological state with many causes; headache and vomiting may suggest it, but deterioration in consciousness, pupils, motor responses or breathing determines emergency urgency.
- Do not wait for the complete Cushing triad: hypertension, bradycardia and irregular breathing commonly appear together only late in an intracranial pressure crisis.
- Age changes the presentation: infants may show head enlargement, a tense fontanelle and irritability, while older children and adults more often report headache, vomiting, transient visual obscurations or diplopia.
- Serial examination is more informative than a single reassuring value; document separate GCS components, pupils, limb responses, vital signs and the direction and speed of change.
- Acute CT identifies haemorrhage, hydrocephalus, oedema and mass effect; papilloedema without instability usually needs urgent brain imaging with venography before a diagnostic lumbar puncture is considered.
- Absence of papilloedema, normal early imaging or temporary symptom improvement does not universally exclude raised pressure, particularly in acute deterioration, young children or intermittently raised pressure.
02Mechanisms and patternsImportant relationships and how to distinguish them.
Ask about progression, nocturnal waking, early-morning severity, worsening with cough or posture, repeated vomiting and change from the person’s usual headache. These features raise concern but remain non-specific; migraine, infection and systemic illness can resemble them.
Look for slowing, confusion, irritability, agitation, drowsiness and reduced GCS. Record eye, verbal and motor components separately and compare with a reliable baseline. A small sustained motor decline can be more consequential than an unchanged total score suggests.
Measure pupil size and light response, eye position, facial movement and limb power. New unilateral pupillary dilation with reduced consciousness and opposite-sided weakness is a cardinal transtentorial herniation pattern, although atypical or bilateral findings occur.
Transient greying of vision, blurred vision, pulsatile tinnitus, binocular horizontal diplopia or disc swelling may accompany sustained pressure. Sixth-nerve palsy impairs abduction and can be a false localising sign; papilloedema threatens visual fields even with preserved acuity.
Assess feeding, irritability, lethargy, vomiting, developmental change, head circumference trajectory, fontanelle tension, sutures and eye position. Use age-appropriate GCS and experienced paediatric observation because adult symptom descriptions and thresholds cannot simply be transferred.
Systemic hypertension, often with widened pulse pressure, bradycardia and irregular respiration or apnoea represents brainstem compromise. The full Cushing response is uncommon and late, so its absence cannot reassure after earlier neurological deterioration.
03Interpreting evidenceInformation, measurements and their limitations.
Consider the information, its meaning and its limitations before deciding what follows.
- 01
Serial structured neurological observations - Why
- Detect clinically meaningful change in consciousness, pupils, limb movement and cardiorespiratory physiology rather than relying on one examination.
- Interpretation and limitations
- In traumatic head injury, NICE specifies GCS components, pupil size and reactivity, limb movements, respiratory rate, heart rate, blood pressure, temperature and oxygen saturation. Any confirmed deterioration triggers urgent medical reassessment and consideration of immediate CT.
- 02
Non-contrast CT head - Why
- Rapidly detect haemorrhage, hydrocephalus, mass effect, herniation, compressed basal cisterns and major cerebral oedema in an acute or unstable presentation.
- Interpretation and limitations
- A causative lesion redirects immediately to neurosurgical and cause-specific treatment. In comatose paediatric severe TBI, a normal initial CT at zero to six hours must not be used to exclude elevated ICP; unexplained deterioration still requires specialist reassessment and sometimes repeat or different imaging.
- 03
MRI brain with venous imaging - Why
- Evaluate a stable subacute presentation, posterior-fossa or infiltrative disease, and exclude cerebral venous sinus thrombosis when papilloedema suggests intracranial hypertension.
- Interpretation and limitations
- Structural, meningeal or venous abnormalities establish secondary disease. Imaging signs associated with IIH can support but do not independently prove the diagnosis, and urgent CT is preferable when MRI would delay an unstable patient.
- 04
Ophthalmic examination and perimetry - Why
- Confirm true papilloedema, grade disc swelling and measure visual function that may be threatened before central acuity falls.
- Interpretation and limitations
- Document acuity, pupils, colour vision where appropriate, formal fields and dilated fundus findings. Disc swelling is a sign requiring an explanation; optic-disc drusen, optic neuritis, ischaemic disease and malignant hypertension remain competing diagnoses.
- 05
Invasive intracranial pressure monitoring - Why
- Guide neurocritical treatment in selected severe brain injury when clinical examination and imaging cannot quantify pressure burden continuously.
- Interpretation and limitations
- Thresholds are population-specific. Adult severe-TBI guidance recommends treatment above 22 mmHg alongside the examination and CT, whereas paediatric severe-TBI guidance suggests targeting below 20 mmHg; neither value is a universal diagnostic cut-off.
04Applied reasoningWorked examples connecting principles to decisions.
01Worked case: acute deteriorationHeadache, vomiting and declining consciousnessA patient becomes drowsier with a new pupil or focal motor change, with or without a known intracranial lesion.+
- 1Recognise an intracranial pressure crisis from the trajectory, call senior emergency, anaesthetic and neurosurgical teams, and perform simultaneous airway, breathing and circulation assessment with continuous oxygen saturation and blood-pressure monitoring.
- 2Protect the airway when indicated, avoid hypoxaemia and hypotension, elevate the head more than 30 degrees and keep it midline if spinal and circulatory safety permit, while documenting GCS components, pupils and limb responses.
- 3Obtain immediate non-contrast CT as soon as the patient can be positioned safely; do not send an unstable patient away from resuscitation or delay presumptive herniation treatment for a complete classic triad.
- 4Treat the identified cause with the neurocritical and neurosurgical team, reassess after every intervention, and escalate persistent herniation signs to hyperosmolar, CSF-diversion or operative pathways matched to aetiology and age.
- 5Verify response through repeated examination, cardiorespiratory physiology, imaging and ICP data when present; continued decline overrides an initially reassuring result.
02Urgent diagnostic pathwayPapilloedema without immediate instabilityNew optic-disc swelling or visual obscurations are found in an alert patient without acute herniation signs.+
- 1Arrange urgent ophthalmic and neurological assessment, quantify visual acuity and fields, and ask about headache, diplopia, pulsatile tinnitus, medicines, thrombosis risk and systemic disease.
- 2Obtain urgent brain imaging with venography to exclude mass lesion, hydrocephalus and cerebral venous sinus thrombosis before considering lumbar puncture.
- 3If imaging and clinical review establish that lumbar puncture is safe, measure opening pressure correctly and analyse CSF; do not diagnose IIH from one pressure value in isolation.
- 4Escalate rapidly worsening fields or acuity as threatened vision requiring urgent specialist rescue rather than routine headache follow-up.
03Age-adjusted pathwayPossible raised pressure in a childAn infant or child has progressive vomiting, behaviour change, head-growth abnormality, drowsiness or focal neurological signs.+
- 1Use age-appropriate history, GCS and examination, including head circumference and fontanelle in infants, while checking for trauma, infection, hydrocephalus, tumour and toxic or metabolic mimics.
- 2Involve experienced paediatric and neuroscience clinicians early; a tense fontanelle, focal deficit, seizure or abnormal drowsiness changes urgency and imaging decisions.
- 3Apply paediatric imaging and neurocritical thresholds rather than adult severe-TBI numbers, and continue serial observation because early CT and absent papilloedema do not universally exclude rising pressure.
05Checking understandingVerify the reasoning, revisit uncertainties and apply feedback.
- Trend the separate eye, verbal and motor GCS components, pupil size and reactivity, limb movement, respiratory pattern, heart rate, blood pressure, temperature and oxygen saturation.
- Record exact timing and direction of headache, vomiting, visual symptoms, seizure, behavioural change and interventions so that deterioration is apparent across handovers.
- After positioning, airway support or pressure-lowering treatment, repeat the neurological examination and evaluate whether oxygenation, circulation and cerebral perfusion have improved.
- For papilloedema, follow formal visual fields, acuity and disc grade; symptom improvement alone does not prove that optic-nerve risk has resolved.
- In infants and young children, use serial head circumference, fontanelle and developmental observations alongside age-appropriate consciousness assessment.
06Special situationsVariants, exceptions and circumstances that change the usual approach.
Rate shapes the phenotype
Slow expansion permits compensation and may produce weeks of headache or visual symptoms, whereas acute blood or obstructed CSF can exhaust reserve quickly and present with collapse.
Trend beats snapshot
GCS 14 has different meaning in a stable baseline patient and in someone who was fully alert minutes earlier. The change, component and associated pupil or motor findings drive action.
Papilloedema can lag
Disc swelling takes time to develop and can be absent during an acute pressure crisis. Its absence must not delay treatment of rapidly evolving neurological signs.
Pressure may be compartmental
A focal mass can shift tissue and compress the brainstem even when a distant monitor does not show a dramatic global pressure rise. Examination and imaging remain essential.
Children are not small adults
Open sutures, preverbal behaviour and age-dependent physiology alter recognition and targets. Experienced paediatric observation and matching severe-TBI guidance prevent unsafe extrapolation.
07Common pitfallsFrequent interpretation and management errors.
- 01
Waiting for hypertension, bradycardia and abnormal breathing to coexist before treating a deteriorating patient.
- 02
Calling progressive headache or vomiting diagnostic without checking consciousness, pupils, focal signs and relevant competing causes.
- 03
Using absence of papilloedema or one normal CT as a universal rule-out for raised pressure or later deterioration.
- 04
Performing lumbar puncture in a patient with mass effect, evolving focal signs or impaired consciousness before specialist assessment and appropriate imaging.
- 05
Applying adult severe-traumatic-brain-injury ICP, CPP or blood-pressure targets to children, IIH, tumour or spontaneous haemorrhage.
- 06
Allowing transfer to imaging to interrupt airway, circulation, cervical-spine precautions or continuous neurological observation.