Headache and raised intracranial pressure

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Headache in advanced illness is common and often benign, but a new progressive pattern requires neurological formulation. Raised intracranial pressure classically causes morning or recumbent worsening, vomiting, transient visual obscurations and pain with cough or strain, yet these features are neither universal nor specific. Cognitive change, seizure, focal deficit and altered consciousness increase urgency more than headache intensity alone.

Examination should be serial. Record Glasgow Coma Scale or another clear arousal measure, pupils, visual fields, eye movements, facial function, speech, limb power, sensation, reflexes, coordination and gait when safe. Look for papilloedema, but its absence does not exclude pressure rise. Bradycardia, hypertension and irregular breathing are late signs and should not be awaited.

Imaging sequence follows acuity. Non-contrast CT rapidly shows haemorrhage, hydrocephalus and major mass effect. Contrast-enhanced MRI more sensitively defines metastases, primary tumour, posterior fossa disease, leptomeningeal patterns and surrounding oedema. If MRI is unsafe or unavailable, neuroradiology advises alternatives. Do not perform lumbar puncture when mass effect or obstructed flow is possible.

Dexamethasone reduces vasogenic tumour oedema rather than tumour size. A moderate symptomatic presentation may respond to 4 to 8 mg daily; severe focal deficit, vomiting or pressure may require 16 mg daily. Give once daily or divided earlier in the day according to protocol. Improvement often occurs within 24 to 72 hours. Lack of benefit should prompt diagnosis and treatment review rather than indefinite dose escalation.

Steroid safety begins at the first dose. Check glucose and infection, review diabetes treatment, prescribe gastric protection only when gastrointestinal risk warrants and warn about insomnia, agitation and mood change. Monitor proximal strength because steroid myopathy can erase neurological gains. After surgery or radiotherapy begins, taper as rapidly as clinically tolerated; abrupt cessation after sustained therapy risks adrenal insufficiency.

Definitive options depend on number and location of lesions, histology, extracranial disease, performance, prognosis and patient goals. Surgery can relieve mass effect and provide tissue; stereotactic radiotherapy treats selected limited lesions; whole-brain radiotherapy and systemic therapy have context-specific roles. Hydrocephalus may benefit from diversion. Palliative symptom care continues before, during and after these decisions.

In the final phase, a person may decline transfer or intervention. Continue headache analgesia, antiemetic, seizure rescue, steroid when it remains beneficial and family explanation. Review the oral route and renal or hepatic clearance. A DNACPR recommendation does not decide imaging, corticosteroid, anticonvulsant or hospital treatment, so document each ceiling and the process used if capacity is lost.

Key points

Ask about onset speed, progression, morning or positional pattern, cough or strain, vomiting, seizure, cognition, focal symptoms and analgesic or steroid exposure.
First-line examination records consciousness, pupils, cranial nerves, power, sensation, coordination, gait, fundoscopy when feasible and vital signs.
Urgent non-contrast CT is first-line for acute haemorrhage, major mass effect and hydrocephalus; contrast MRI is the gold-standard definition of brain tumour and metastatic burden after stabilisation.
Never perform lumbar puncture before excluding unsafe raised intracranial pressure when papilloedema, focal deficit, seizure or altered consciousness is present.
For symptomatic tumour-related oedema, dexamethasone commonly starts at 4 to 8 mg daily for moderate symptoms and up to 16 mg daily for severe pressure features under specialist guidance.
Give dexamethasone early in the day where possible, monitor glucose and mental state and use the lowest effective dose with a written taper linked to surgery or radiotherapy.
Definitive treatment may be neurosurgical resection, cerebrospinal-fluid diversion, stereotactic treatment, whole-brain radiotherapy or systemic therapy according to tumour, function and goals.
Do not start antiseizure medication solely as prophylaxis in every seizure-naive brain-tumour patient; treat an actual seizure through the neurological pathway.
The gold-standard plan connects imaging, steroid goal and taper, definitive treatment, seizure rescue, analgesia and escalation ceiling while preserving comfort if intervention is declined.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Intracranial tumour and oedema

Primary tumour and metastasis create mass effect, vasogenic oedema, haemorrhage, seizure and obstruction of cerebrospinal-fluid pathways.

Vascular emergency

Intracerebral or subarachnoid haemorrhage, venous sinus thrombosis, infarction and hypertensive crisis can produce acute headache and pressure change.

Hydrocephalus and infection

Obstructed cerebrospinal-fluid flow, meningitis, encephalitis and abscess raise pressure and alter consciousness through distinct urgent mechanisms.

Primary and medication headache

Migraine, tension headache, analgesic overuse, corticosteroid withdrawal and other common causes remain possible in advanced illness.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Monro-Kellie constraint
The fixed skull contains brain, blood and cerebrospinal fluid, so rising volume eventually causes steep pressure increase after compensation is exhausted.
2
Vasogenic oedema
Tumour disrupts the blood-brain barrier, allowing extracellular fluid accumulation that responds to corticosteroid reduction of vascular permeability.
3
Cerebrospinal-fluid obstruction
Mass at ventricular outlets or impaired absorption enlarges ventricles, stretches pain-sensitive structures and compresses surrounding brain.
4
Reduced cerebral perfusion
Rising intracranial pressure lowers cerebral perfusion pressure, causing progressive ischaemia, cytotoxic oedema and further dangerous pressure elevation.
5
Tissue displacement
Pressure gradients shift brain across rigid dural partitions, compressing cranial nerves and brainstem and producing herniation syndromes.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Raised-pressure headache

Progressive morning or recumbent pain, cough or strain aggravation, vomiting and transient visual symptoms supports intracranial pressure rise.

Focal mass effect

New weakness, aphasia, visual-field loss, cranial neuropathy, ataxia or personality change localises dysfunction and increases imaging urgency.

Papilloedema

Optic-disc swelling, enlarged blind spots and transient obscurations support raised pressure, but absence does not provide safe exclusion.

Hydrocephalus

Headache, vomiting, gait decline, drowsiness and cognitive change with ventricular enlargement suggests obstructed cerebrospinal-fluid flow.

Steroid neuropsychiatric effect

Insomnia, agitation, pressured speech, paranoia or hallucinations after dexamethasone can mimic tumour progression or delirium.

Impending herniationRed flag

Rapid coma, unequal pupils, extensor posturing or Cushing physiology requires immediate emergency neurological management.

Red flags requiring action

Thunderclap onset, meningism, fever, collapse or new neurological deficit requires immediate haemorrhage, infection and vascular assessment.
Progressive morning or positional headache with vomiting, papilloedema, focal signs or cognitive change suggests raised intracranial pressure.
Reduced consciousness, unequal pupils, extensor response or Cushing physiology is a late herniation sign and requires emergency action.
Do not perform lumbar puncture when mass lesion, obstructive hydrocephalus, papilloedema or focal deficit raises herniation risk.
New seizure or persistent postictal deficit requires urgent glucose, imaging and seizure management rather than analgesia alone.
Dexamethasone can cause severe hyperglycaemia, infection, psychosis, insomnia, gastrointestinal harm and proximal weakness and needs the lowest effective dose and taper plan.
NSAIDs and contrast require renal and bleeding review, while valproate and many sedatives require hepatic caution.

05InvestigationsWhat to request, why it matters and how to interpret it.

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.

01
First-line serial neurological examinationFirst stepFirst line
Why
Document arousal, pupils, cranial nerves, fields, speech, limbs, coordination, gait and fundoscopy to identify change and localisation.
Interpretation and limitations
Falling consciousness, new pupil or focal deficit accelerates emergency imaging and specialist treatment; one normal examination does not end surveillance.
02
Urgent non-contrast CT head
Why
Detect acute haemorrhage, hydrocephalus, large mass, oedema, midline shift and other immediately actionable structural disease.
Interpretation and limitations
CT is fast for emergency triage but can miss small, posterior fossa or leptomeningeal disease that MRI defines better.
03
Contrast-enhanced brain MRI
Why
Characterise number, location, tissue effect, oedema, primary tumour, metastasis and leptomeningeal or treatment-related change.
Interpretation and limitations
This is the reference-standard tumour assessment after stabilisation and guides neurosurgery, stereotactic or other oncological treatment.
04
Targeted metabolic and infection tests
Why
Assess glucose, sodium, calcium, renal and liver function, infection and coagulopathy that mimic or modify neurological symptoms.
Interpretation and limitations
Correct reversible contributors and use organ results to adjust analgesic, antiseizure, antiemetic and sedative treatment.
05
Steroid baseline and response review
Why
Record glucose, infection, mood, sleep, proximal power, gastrointestinal risk and neurological target before and after dexamethasone.
Interpretation and limitations
Clinical improvement supports oedema response; absent benefit or toxicity drives taper or diagnostic reassessment rather than automatic continuation.
06
Lumbar puncture safety decision
Why
Determine whether cerebrospinal-fluid sampling is necessary and safe after imaging and neurological assessment.
Interpretation and limitations
Mass effect, obstructive hydrocephalus, papilloedema, focal deficit or depressed consciousness makes lumbar puncture hazardous without specialist clearance.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Migraine

Recurrent similar unilateral throbbing headache with sensory sensitivity and fully reversible aura supports migraine but new change still needs review.

Meningitis or abscess

Fever, neck stiffness, immunosuppression, altered consciousness and focal signs indicate infection and imaging or antimicrobial urgency.

Subarachnoid haemorrhage

Instant maximal thunderclap pain, collapse, meningism or exertional onset requires the acute haemorrhage pathway even in known cancer.

Cerebral venous thrombosis

Progressive headache, papilloedema, seizure and focal deficit in malignancy or thrombosis risk may require venographic imaging.

Medication and systemic cause

Opioid toxicity, hypercapnia, hypertension, infection and analgesic overuse cause headache or reduced consciousness without primary mass progression.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Emergency pressureStabilise and image before deteriorationFirst stepHeadache accompanies falling consciousness, new pupil change, focal deficit, repeated vomiting, seizure or late pressure signs.

1Call neurological and critical-care help, use ABCDE care, elevate the head about 30 degrees, maintain neutral neck and correct hypoxia, hypotension and glucose disturbance.
2Obtain urgent non-contrast CT and give dexamethasone promptly for suspected tumour oedema; use hyperosmolar treatment only through the acute specialist protocol.
3Coordinate neurosurgery, cerebrospinal-fluid diversion, radiotherapy or comfort-focused care based on pathology, reversibility, capacity and the documented treatment ceiling.

02Symptomatic tumour oedemaUse the lowest effective corticosteroidImaging or clinical assessment supports brain tumour with headache, vomiting or focal pressure symptoms.

1Define the neurological target and start dexamethasone 4 to 8 mg daily for moderate symptoms or up to 16 mg daily for severe features under specialist guidance.
2DefinitiveDose earlier in the day, check glucose, infection, mood, sleep and gastrointestinal risk and arrange definitive tumour treatment assessment.
3DefinitiveReview within 24 to 72 hours and taper as rapidly as tolerated after response or definitive therapy, increasing only with documented recurrent oedema symptoms.

03Persistent headacheReassess mechanism rather than escalating steroidEscalationHeadache continues despite initial analgesia or dexamethasone, without current herniation signs.

1Review imaging, migraine and tension features, medication overuse, hypercapnia, infection, blood pressure, sleep and steroid adverse effects.
2Optimise appropriate analgesic and antiemetic therapy with renal and hepatic checks and seek neurology, oncology or palliative advice for difficult mechanisms.
3Repeat examination and imaging when pattern changes and avoid prolonged high-dose steroid when no oedema response is evident.

04Comfort-focused phasePreserve relief when intervention is not wantedThe person declines or cannot benefit from neurosurgical or oncological intervention and symptom relief is the agreed goal.

1Confirm capacity or lawful decision process, explain expected neurological change and retain dexamethasone only while it provides more benefit than toxicity.
2Provide route-appropriate analgesia, antiemetic, seizure rescue, mouth and nursing care and convert essential medicines safely if swallowing fails.
3Document hospital and ventilation ceilings separately from CPR, give family a crisis contact and review agitation, pain, seizure and caregiver distress frequently.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

Reduces vasogenic oedema, headache, vomiting and focal deficit while definitive surgery, radiotherapy or systemic treatment is considered.

Dexamethasone for tumour-related cerebral oedema

Use 4 to 8 mg orally or intravenously daily for moderate symptomatic tumour oedema and up to 16 mg daily for severe pressure symptoms under the local neuro-oncology protocol, usually given once or in earlier divided doses with a documented taper.

Monitor glucose, infection, mood, psychosis, insomnia, proximal weakness, gastrointestinal risk and adrenal suppression; use the lowest effective dose and avoid abrupt cessation after sustained therapy.

Provides non-sedating analgesia for mild headache or as part of multimodal relief while intracranial causes are evaluated.

Paracetamol for headache

For an adult at least 50 kg without liver-risk factors, give 500 mg to 1 g orally every 4 to 6 hours as required, maximum 4 g in 24 hours; reduce the maximum for low weight, malnutrition, alcohol excess or hepatic disease.

Reconcile combination products and all routes and do not allow symptomatic relief to delay imaging for red flags or pressure deterioration.

Relieves severe tumour-related headache when non-opioid measures and oedema treatment are insufficient or definitive treatment is pending.

Morphine for severe headache when appropriate

Use a patient-specific immediate-release rescue based on current opioid exposure and the palliative formulary; in an opioid-naive frail adult, a cautious oral starting dose may be 2.5 mg with response and respiratory review.

Sedation can obscure neurological decline; monitor pupils, consciousness, breathing and bowel function and use a renal-appropriate alternative when morphine metabolites may accumulate.

Temporarily reduces intracranial pressure during impending herniation while urgent definitive neurosurgical or other treatment is organised.

Mannitol for acute specialist pressure reduction

When the emergency neurocritical protocol selects it, give 20% mannitol intravenously as a weight-based bolus, commonly 0.25 to 1 g/kg, with serum osmolality, renal, fluid and haemodynamic monitoring.

Not routine palliative headache treatment; renal failure, hypotension, dehydration, electrolyte change and rebound pressure require critical-care supervision and may favour protocol-selected hypertonic saline.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Cerebral herniation

Tissue shift compresses brainstem, pupil pathways and respiratory centres, causing coma, profound cardiorespiratory instability and death.

Seizure and injury

Cortical irritation produces focal or bilateral seizures, aspiration, traumatic injury and prolonged postictal loss of neurological function.

Permanent neurological deficit

Compression and ischaemia cause weakness, visual loss, aphasia, cognitive change and loss of bladder, mobility and decision capacity.

Corticosteroid toxicity

Prolonged high-dose dexamethasone causes disabling myopathy, diabetes, infection, psychosis, insomnia, skin fragility, adrenal suppression and gastrointestinal complications.

Unsafe procedural deterioration

Lumbar puncture or delayed imaging in a mass lesion can worsen pressure gradients and precipitate fatal herniation.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Repeat consciousness, pupils and focal neurological examination after every deterioration, seizure, opioid dose and steroid or definitive treatment change.
Track headache pattern, vomiting, visual symptoms, gait and the patient's chosen functional outcome rather than intensity alone.
During dexamethasone monitor capillary glucose, infection, mood, sleep, proximal strength, gastrointestinal symptoms and skin integrity.
Record steroid dose, timing, indication, response and taper in every care setting and prevent abrupt interruption during transfer.
Review renal and hepatic function and sedation during opioid, antiemetic and antiseizure treatment.
After treatment reassess seizures and do not initiate prophylactic antiseizure medicine automatically in a seizure-naive patient.
Revisit imaging and escalation choices if capacity, function, tumour treatment or the patient's goals change.
Support family understanding of possible drowsiness, weakness, seizure and terminal neurological change and give a clear urgent contact.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Papilloedema can be absent

A normal optic-disc examination does not exclude acute pressure rise, particularly when deterioration is rapid.

Steroid treats oedema

Dexamethasone can improve mass-effect symptoms without shrinking tumour and should not be interpreted as definitive cancer treatment.

More steroid is not always better

Lack of response may reflect haemorrhage, hydrocephalus, migraine or irreversible deficit while toxicity rises with dose and duration.

Opioid can obscure the trend

Analgesia remains important, but new sedation after dosing must be distinguished from neurological pressure deterioration.

Lumbar puncture changes gradients

Removing spinal cerebrospinal fluid below a mass can worsen downward displacement and precipitate herniation.

A taper is active treatment

Reducing dexamethasone prevents cumulative myopathy and metabolic harm while monitoring for recurrent oedema symptoms.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting for Cushing physiology before treating raised intracranial pressure.
02
Using a normal fundoscopy examination to exclude mass effect.
03
Performing lumbar puncture before imaging a focal or pressure presentation.
04
Escalating analgesia while delaying CT for a new neurological deficit.
05
Continuing 16 mg dexamethasone indefinitely without response and toxicity review.
06
Giving dexamethasone late at night and worsening sleep or delirium unnecessarily.
07
Stopping prolonged corticosteroid abruptly and causing adrenal insufficiency.
08
Starting antiseizure prophylaxis automatically in every seizure-naive tumour patient.
09
Using NSAIDs without renal, bleeding and corticosteroid gastrointestinal review.
10
Assuming DNACPR prohibits imaging, dexamethasone or neurosurgical discussion.