raised intracranial pressure and brain tumours — The Herniating Brain and the Space-Occupying Lesion

The answer first

Raised intracranial pressure (ICP) is a pathophysiological state in which the volume of brain, blood, or cerebrospinal fluid (CSF) within the rigid skull exceeds the compensatory reserve, driving cerebral perfusion down and ultimately forcing brain tissue through dural edges — the herniation syndromes. Brain tumours are the most common space-occupying cause encountered by the physician in the emergency department, the ward and the outpatient clinic, and the urgency of every decision rests on whether the intracranial compartment is tolerating the lesion or decompensating. ^[1]

A physician-level answer rests on four pillars: ^[1]

1. Recognise the decompensating brain before it is too late. The early signs of raised ICP — headache worst on waking and on bending or coughing, vomiting without nausea, papilloedema, declining GCS, new focal deficit — are windows of opportunity; the late signs (Cushing's triad of bradycardia with widened pulse pressure and irregular breathing, fixed dilated pupil, decerebrate posturing) are pre-terminal. Escalate empirically with hyperosmolar therapy and airway control while arranging emergency CT, because waiting for imaging in a herniating patient is the single most avoidable cause of death on the ward. ^[1]
2. Map the herniation syndrome to the lesion. Each syndrome (subfalcine, uncal, central, tonsillar, upward, external) predicts the clinical deficit and points to the location of the mass: a third-nerve palsy with ipsilateral fixed dilated pupil is uncal; leg weakness and contralateral frontal signs are subfalcine; respiratory arrest with downbeat nystagmus is tonsillar. Naming the syndrome is a DCE short-case expectation. ^[2]
3. Reduce intracranial volume while planning definitive treatment. Head of bed 30 degrees, normocapnia (PaCO₂ 35 to 40 mmHg), normoxia, normoglycaemia, normothermia, euvolaemia, and — when there is vasogenic tumour oedema — dexamethasone 4 to 16 mg per day; hyperosmolar therapy (mannitol 0.25 to 1 g/kg or 3 percent hypertonic saline to target sodium 145 to 155 mmol/L) for acute decompensation. ^{[3] [4] [5]}
4. Treat the tumour by grade, molecular marker and performance status. Glioblastoma is Stupp chemo-radiotherapy with concomitant and adjuvant temozolomide 75 mg/m² daily during radiotherapy then 150 to 200 mg/m² for 6 to 12 cycles, with tumour-treating fields added; low-grade and atypical meningioma decisions hinge on WHO grade and Simpson resection; brain metastases are managed with surgery or stereotactic radiosurgery, reserving whole-brain radiotherapy for extensive disease. ^{[6] [7] [8] [9]}

DWE high-yield: "Stupp is the standard." Concomitant temozolomide with 60 Gy radiotherapy in 30 fractions followed by six adjuvant 5-day cycles of 150 to 200 mg/m² temozolomide is the bedrock of glioblastoma care, with median survival of 14.6 months versus 12.1 months for radiotherapy alone, and the addition of tumour-treating fields (TTFields) in EF-14 extended median survival to roughly 21 months. ^{[6] [7]}

References12ShowHide

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12. [12]Nail J, Herendeen J Postoperative Considerations Following Decompressive Hemicraniectomy. Neurosurg Clin N Am, 2026.PMID 41967895