GC111 Raised Intracranial Pressure And Hydrocephalus
Raised intracranial pressure is an elevation of pressure within the cranial cavity above normal (> 20 mmHg), often caused by mass lesions, cerebral edema, or hydrocephalus—a pathological accumulation of cerebrospinal fluid within the ventricular system due to impaired production, flow, or absorption.
Raised Intracranial Pressure & Hydrocephalus
Big Idea: The brain lives in a rigid, non-expandable box (the skull). Any increase in the volume of its contents — brain, blood, or CSF — will eventually cause a rise in intracranial pressure (ICP). Raised ICP reduces cerebral perfusion, causes brain herniation, and kills patients rapidly. Understanding the Monro-Kellie doctrine, the ICP–volume relationship, cerebral perfusion pressure, and the principles of ICP management is foundational to neurosurgery, neurology, critical care, and emergency medicine. Hydrocephalus is a specific cause of raised ICP with its own classification, clinical features, and surgical management.
Learning Objectives (from the lecture): [1]
- Common causes, pathophysiology, and clinical presentation of raised ICP
- Principles of management of raised ICP
- Pathophysiology of hydrocephalus
- Principles of management of hydrocephalus
Core Concepts and Mechanisms
The lecture describes pressure measurement referenced to the external auditory meatus (approximately the level of the foramen of Monro). Normal adult ICP = 10–15 mmHg; normal infant ICP = 1–6 mmHg. [1]
Continuous ICP is usually measured with an intraventricular catheter (which can also drain CSF) or an intraparenchymal monitor. Lumbar puncture measures lumbar CSF opening pressure, not continuously monitored cranial ICP, and must not be used when clinical or imaging features make a dangerous craniospinal pressure gradient possible. [12][13]
Reading the waveform shown on slide 3: the cardiac-linked peaks are P1 (percussion), P2 (tidal/compliance) and P3 (dicrotic). With preserved compliance, P1 is usually taller than P2. As compliance worsens, P2 rises to equal or exceed P1: the waveform can therefore warn of lost intracranial reserve even before a single mean-pressure value tells the whole story.
Why these numbers matter: The brain has no pain receptors for pressure itself — symptoms arise because raised ICP compresses structures, reduces perfusion, and causes herniation. Knowing the normal range lets you interpret monitoring data and recognise pathology.
Do Not Mix the Units or Contexts
The slide's > 20 cmH₂O (about 15 mmHg) refers to an abnormal CSF opening pressure range. It is not the same as the treatment threshold used for monitored severe TBI. Current Brain Trauma Foundation guidance recommends treating ICP > 22 mmHg (about 30 cmH₂O), while integrating the trend, examination and CT rather than acting on one number alone. [1][12]
The adult skull is a rigid box containing Brain + Blood + CSF. A mass lesion initially displaces venous blood and CSF. [1]
First principles explanation:
- Brain parenchyma ≈ 80%, Blood ≈ 10%, CSF ≈ 10% of intracranial volume [2]
- The skull cannot expand (unlike infant skulls with open fontanelles/sutures)
- Therefore, if any one compartment increases in volume, the other compartments must decrease to compensate
- Compensation mechanisms (in order):
- Venous blood outflow — fastest; venous blood is squeezed out of the cranium through jugular veins
- CSF displacement — CSF shifts from the ventricles/cisterns into the spinal thecal sac
- Once these buffers are exhausted → decompensation → exponential rise in ICP for even small additional volume increases
This is the classic "ICP vs SOL Volume" curve (the pressure-volume curve):
"Talk... and die." Initial compensation allows the patient to remain conscious, but once decompensation occurs, ICP rises exponentially and rapidly. [1]
Clinical pearl: This is why a patient can go from GCS 14 to GCS 5 in one hour — you go to lunch, they start dying. The slide literally shows: "1:00 p.m. Alert & Talking GCS=14 → 2:00 p.m. Comatose GCS=5. You went to lunch." [1]
CPP = MAP − ICP. Normal CPP = 60–80 mmHg. CBF = CPP / CVR. Normal CBF = 45–65 ml/min/100 g tissue. [1]
Why this matters:
- If ICP rises and MAP stays the same → CPP falls → CBF falls → cerebral ischaemia
- If MAP falls (e.g., from haemorrhagic shock) and ICP is normal → CPP still falls
- The brain's oxygen consumption is high and constant; it cannot tolerate ischaemia
Brain cells don't like ischaemia: obligate aerobic respiration; can only use glucose (& ketones in emergency); injured neurons can't recycle lactate → lactic acidosis; vicious cycles of glutamate release (excitotoxicity), calcium influx, energy failure & DNA damage → rapid cell death. [1]
The vicious cycle: Ischaemia → cell death → brain swelling (oedema) → further ICP rise → further ischaemia → more swelling. This is the slide titled "Vicious Cycle of Ischaemia & Brain Swelling." [1]
Reading the CBF–EEG–cell-response diagram (slide 12): the lecture shows a staged loss of function as CBF falls. These are approximate teaching bands, not bedside treatment cut-offs—duration, temperature, collateral flow and tissue state alter reversibility.
| Approximate CBF (mL/100 g/min) | Visualised progression |
|---|---|
| 35–50 | EEG may remain near normal while protein synthesis falls |
| 25–35 | Faster EEG frequencies are lost; anaerobic metabolism and neurotransmitter release begin |
| 18–25 | Slow-wave activity increases, lactate accumulates and ATP falls—the slide marks an ischaemic threshold in this region |
| 12–18 | Electrical failure with membrane-pump failure and ionic/water shifts |
| Below about 10–12 | EEG suppression, calcium accumulation, anoxic depolarisation and cell death—the slide's infarction range |
| Type | Mechanism | BBB Status | Location | Classic Cause | Steroid Response |
|---|---|---|---|---|---|
| Vasogenic | Fluid leaks from capillaries through damaged BBB into extracellular space (white matter) | Disrupted | Extracellular | Tumour (peri-tumoural oedema), abscess | Yes ✓ |
| Cytotoxic | Defective Na⁺/K⁺ ATPase → intracellular swelling | Intact | Intracellular | Ischaemia/infarction, hypoxia | No ✗ |
| Interstitial | CSF forced into periventricular extracellular space | N/A | Periventricular | Obstructive hydrocephalus | No |
High Yield – Steroids
Dexamethasone can reduce selected symptomatic tumour-related vasogenic oedema. Corticosteroids should not be used to improve outcome or reduce ICP after TBI; high-dose methylprednisolone increased mortality in the CRASH trial. They are not routine treatment for cerebral oedema after ischaemic stroke. [1][12] This is a favourite MCQ discriminator.
Space-occupying mass lesion (haematoma, tumour, abscess); Hydrocephalus (communicating/non-communicating); Brain swelling (focal/diffuse); Hyperaemia; Venous congestion. [1]
| Category | Examples |
|---|---|
| Mass lesion | Intracerebral haemorrhage, brain tumour, brain abscess, epidural/subdural haematoma |
| Hydrocephalus | Communicating (post-SAH, post-meningitis), non-communicating (tumour obstructing aqueduct/ventricle) |
| Brain swelling | Massive infarction, diffuse cerebral oedema (post-TBI, hypoxic-ischaemic encephalopathy) |
| Hyperaemia | Loss of cerebral autoregulation (post-TBI) |
| Venous congestion | Venous sinus thrombosis, jugular vein compression, midline tumour compressing sagittal sinus |
| Others | Idiopathic intracranial hypertension (IIH), seizure |
Pattern Recognition on the Six CT/MR Examples (Slide 5)
| Image label | What the image is teaching you to recognise |
|---|---|
| Hydrocephalus | Ventricular enlargement (rounded frontal/temporal horns) disproportionate to the sulci; look for periventricular transependymal oedema |
| Cerebral oedema | Diffuse sulcal and cisternal effacement with reduced grey–white differentiation; ventricles may be compressed rather than enlarged |
| Intracerebral haemorrhage | Acute hyperdense intraparenchymal blood, often with surrounding low-density oedema and mass effect/midline shift |
| Massive infarction | Territorial hypoattenuation, loss of grey–white differentiation and sulcal effacement; malignant swelling can displace the midline |
| Brain abscess | A smooth ring-enhancing lesion with a low-density centre and marked surrounding vasogenic oedema on contrast imaging |
| Brain tumour | An enhancing solid or heterogeneous mass with surrounding vasogenic oedema; imaging pattern narrows the differential but does not replace definitive diagnosis |
Clinical Features of Raised ICP
Headache (supine > erect; worse early a.m.); Vomiting (might transiently relieve headache); Blurring of vision & diplopia (CN VI); Deterioration in consciousness; Papilloedema (late). [1]
- Headache worse supine and early morning: Lying down increases venous return to the head → increased intracranial blood volume → increased ICP. During sleep, hypoventilation → ↑ PaCO₂ → cerebral vasodilation → ↑ ICP [3]
- Vomiting: Direct pressure on area postrema (vomiting centre) in the medulla. Vomiting transiently relieves headache because the Valsalva effect during emesis initially raises ICP, but subsequent changes in posture and CSF dynamics can temporarily relieve pressure
- CN VI palsy (diplopia): CN VI (abducens) has the longest intracranial course → most vulnerable to stretching by diffusely raised ICP. This is a false localising sign — it doesn't tell you where the lesion is
- Papilloedema: Raised ICP is transmitted along the subarachnoid space surrounding the optic nerve sheath → impedes axoplasmic flow → axonal swelling at the optic disc. It is a late sign [1][4]
- Deterioration in consciousness: Compression of the reticular activating system (brainstem) and global cerebral ischaemia
Brain "herniates" across intracranial compartments. Basal cistern obliterated. Brainstem compressed. [1]
The lecture uses the analogy: basal cistern patent = brainstem "smiling"; basal cistern obliterated = "not smiling" [1].
How to read the slide's CT pair: a patent suprasellar/perimesencephalic cistern leaves low-density CSF visible around the midbrain. Effacement removes that dark CSF outline: the brainstem is crowded, the basal cisterns are "not smiling", and impending transtentorial herniation must be assumed in the right clinical setting. This is a morphology clue, not a substitute for the whole scan (midline shift, ventricular trapping, mass effect and lesion type).
Types of herniation (supplemented from past papers [5]):
| Type | Structures Involved | Key Clinical Features |
|---|---|---|
| Uncal (transtentorial) | Medial temporal lobe through tentorial notch | Ipsilateral fixed dilated pupil (CN III compression), contralateral hemiplegia, ↓consciousness |
| Subfalcine (cingulate) | Cingulate gyrus under falx cerebri | Contralateral leg weakness (ACA compression), can compress ACA → infarction |
| Tonsillar | Cerebellar tonsils through foramen magnum | Brainstem compression → Cushing's triad, respiratory arrest, death |
| Upward (transtentorial) | Cerebellum herniates upward through tentorial notch | Posterior fossa mass pushing upward |
| External | Brain through skull defect | Through traumatic/surgical skull defect |
Combination of sympathetic & parasympathetic activation: Hypertension, Bradycardia, Irregular respiration (rapid & shallow). Also: Cushing ulcer, fixed dilated pupil (CN III). [1]
Why the Cushing reflex occurs:
- Brainstem ischaemia (from ICP approaching MAP)
- The vasomotor centre in the medulla responds by firing maximally → systemic hypertension (sympathetic surge to try to maintain CPP)
- Baroreceptors detect hypertension → reflex bradycardia (vagal)
- Respiratory centres in the medulla are compressed → irregular/agonal breathing
Critical Distinction
The Cushing reflex is a terminal, pre-mortem event. If you see the triad, the patient is about to die. Don't wait for it to diagnose raised ICP.
Glasgow Coma Scale (GCS)
Objective & reproducible way to assess consciousness. Admission GCS is prognostic. Trend reflects deterioration/improvement. Quantitative (3–15) but not a linear scale. Three components: Eye opening (E1-4), Motor response (M1-6), Verbal response (V1-5). [1]
| Component | Score | Response |
|---|---|---|
| Eye Opening (E) | 4 | Spontaneous |
| 3 | To voice* | |
| 2 | To pain | |
| 1 | None | |
| Verbal Response (V) | 5 | Oriented** |
| 4 | Confused | |
| 3 | Inappropriate words | |
| 2 | Incomprehensible sounds (moaning) | |
| 1 | None | |
| Motor Response (M) | 6 | Obeys commands |
| 5 | Localises pain | |
| 4 | Withdrawal (flexion) | |
| 3 | Abnormal flexion (decorticate) | |
| 2 | Extension (decerebrate) | |
| 1 | None |
*Try to wake up by calling the patient by name [1] **Oriented in person, space & time [1]
Motor score is indicative of extent of injury & prognostic. Painful stimuli applied over CNV territory. Best response of limbs. M5 – UL raised above clavicle. M4 – UL withdraw but not above clavicle. M3 (Decorticate Posture) – Injury to corticospinal tract above midbrain. M2 (Decerebrate Posture) – Injury to midbrain or upper pons. [1]
Why M is most prognostic: The motor pathways span the entire neuroaxis — their integrity reflects the global state of the brain better than eye or verbal responses.
Decorticate vs Decerebrate:
- M3 Decorticate (abnormal flexion): Arms flexed, legs extended. Lesion is ABOVE the red nucleus (in the midbrain) — the rubrospinal tract is intact and drives flexion
- M2 Decerebrate (extension): All limbs extended. Lesion is AT the midbrain/upper pons — the vestibulospinal tract dominates, driving extension
E1M5V2 (eyes closed, localises pain, moaning) vs E1M4V2 (eyes closed, flexion withdrawal, moaning) vs E1M3V1 (eyes closed, abnormal flexion, no sound) vs E1M2V1 (eyes closed, extension, no sound). [1]
E – swollen/no eye post-trauma; M – spinal cord injury, limb injury, muscle relaxant; V – language barrier, intubation/tracheostomy (VT); Total score can mean many things; Effect of shock – use post-resuscitation GCS; Effect of sedative drugs (e.g., for mechanical ventilation). [1]
Key exam point: Always use the best response. If the right arm localises but the left arm only flexes, record M5. Document components separately (e.g., E2M5V3 = GCS 10), not just the total.
The observation-chart visual (slide 20) adds a time sequence: falling eye/verbal/motor responses and new focal deficits usually precede the late autonomic pattern of rising blood pressure, bradycardia and disordered breathing. Plot and escalate a trend; do not wait for the Cushing response. In trauma, classify severity using the post-resuscitation GCS: 13–15 mild, 9–12 moderate and ≤8 severe in the lecture's scheme. [1]
ICP Monitoring
Lecture indications: no reliable GCS (e.g., sedation, muscle paralysis), GCS ≤8, or an evolving disease process. Relative concerns include an awake examinable patient and bleeding tendency. [1]
Current severe-TBI framing: monitoring-guided management reduces early mortality. The classic selection criteria are post-resuscitation GCS 3–8 with an abnormal CT (haematoma, contusion, swelling, herniation or compressed basal cisterns); older criteria also considered selected severe-TBI patients with a normal CT plus risk factors. GCS ≤8 prompts urgent airway assessment, but does not by itself prove loss of airway reflexes or create a universal indication for an ICP bolt. [12]
Manometric principle for monitoring intracranial CSF pressure. Therapeutic by draining CSF for decompression. Risk of infection, iatrogenic trauma. LP contraindicated if raised ICP (with exception…). [1]
Reading the EVD diagram: the ventricular catheter connects through a closed system to a pressure transducer/manometer and drainage chamber/bag. The system is levelled to the prescribed cranial reference; changing the chamber height changes the pressure at which CSF drains. It can both monitor and treat, but incorrect levelling, inadvertent clamping/opening, infection and catheter-related haemorrhage can cause harm.
Lumbar Puncture Safety — Corrected
Communicating hydrocephalus does not make LP automatically safe. The slide's communicating/non-communicating distinction explains the physiology: draining lumbar CSF is particularly dangerous when an obstruction or mass creates a pressure gradient. In actual practice, defer LP and obtain appropriate assessment/imaging when there is papilloedema, GCS below 10, focal signs or cranial-nerve deficits, a new adult seizure, severe immunocompromise, cardiorespiratory instability, bleeding risk, or suspected mass effect/midline shift. A normal scan does not cancel an unsafe clinical picture. If meningitis is suspected, cultures and empiric treatment must not be delayed while LP is deferred. [13]
Initial GCS = E1M4V2. Intubated, ventilated & observed. ICP progressively increased from 16 to 28 cmH₂O. Definitely abnormal > 20 cmH₂O. Suggests worsening conditions → Repeat imaging studies → Escalate treatment. [1]
Management of Raised ICP
Protect uninjured brain. Salvage injured brain. Treat underlying cause. ALWAYS resuscitate first. Clinical/ICP monitoring. Control ICP & maintain cerebral perfusion. Neuroprotective therapies. [1]
ABC before ICP!! Airway, Breathing (protect C-spine), Circulation (not CT scan!), Disability, Exposure/Environment. [1]
ABC before ICP
Never skip resuscitation to get a CT scan. A dead patient doesn't need imaging. Stabilise the patient first, then investigate. [1]
| Any Doctor Can Do | Neurosurgeon/ICU |
|---|---|
| Head elevation 30° | ICP monitoring + CSF drainage (EVD) |
| Optimise ventilation | Controlled hyperventilation |
| Maintain MAP | Barbiturate coma |
| Osmotherapy (mannitol, hypertonic saline) | Surgical removal of SOL |
| Sedation | Decompressive craniectomy |
| Optimise electrolyte/glucose level | |
| Prevent/control seizures | |
| Prevent pyrexia |
Avoid neck rotation. Remove neck collar if not indicated. Head elevation ~30°. Maintain vascular volume & BP. [1]
Why 30° head elevation: Promotes venous drainage via the internal jugular veins → reduces intracranial venous blood volume → reduces ICP. Neck rotation or tight collars compress the jugular veins and impede outflow.
What the angle graph adds: ICP generally falls as the head is raised, but excessive elevation can also lower arterial pressure at brain level and therefore CPP. About 30° with a neutral, unobstructed neck is the usual starting compromise; reassess ICP, MAP/CPP and spinal precautions rather than treating the angle as a fixed prescription.
Normally vasoreactivity maintains stable CBF. Brain injury might impair vasoreactivity: Pressure active: ↑MAP → ↓ICP; Pressure passive: ↑MAP → ↑ICP. Aim: CPP ~60–70 mmHg. [1]
Explanation:
- In a pressure-active (intact autoregulation) brain: raising MAP causes reflex vasoconstriction → decreased cerebral blood volume → ICP actually decreases. This is desirable.
- In a pressure-passive (lost autoregulation) brain: raising MAP directly increases cerebral blood volume → ICP increases. This is dangerous.
- You don't always know which state the patient is in, so aim for a CPP sweet spot of 60–70 mmHg.
↓CO₂ → ↑Vasoconstriction → ↓ICP. But: CBF = CPP/CVR. ↑Vasoconstriction → ↑CVR → ↓CBF. Aim: PaCO₂ ~3.0–3.5 kPa. To buy time (e.g., on way to OT). [1]
PREVENT these: [1]
- ❌ Prophylactic hyperventilation
- ❌ Prolonged hyperventilation
- ❌ Without raised ICP
- ❌ Without monitoring
- ❌ Stopping suddenly (rebound vasodilation → ICP spike)
Hypoglycaemia → seizure & brain injury. Hyperglycaemia → lactic acidosis. Seizure → ↑metabolic demand, ↑brain swelling → Phenytoin (loading + infusion). Electrolyte imbalance. Fever → All contribute to acidosis. [1]
Mannitol (e.g., 100 ml 20% i.v.): Osmotic effect (needs intact BBB); ↓Blood viscosity, ↑CBF, ↓CBV; but also ↓Vascular volume, haemoconcentration, renal failure. CI: shock, ↑Na. Foley's catheter required (osmotic diuresis). Loop diuretics (e.g., frusemide). Hypertonic saline (better in multiply injured patients?). [1]
No Mannitol if Shocked
Mannitol causes osmotic diuresis and can aggravate hypovolaemia or hypotension, lowering CPP. First resuscitate shock and choose hyperosmolar therapy with senior/neurocritical-care input, guided by haemodynamics, sodium/osmolality and renal function. Hypertonic saline is often favoured when volume depletion is a concern, but the Brain Trauma Foundation found insufficient comparative evidence to mandate one agent for all severe-TBI patients; the lecture's fixed 100 mL example is not a universal dose. [1][12]
Aim at "burst suppression" on EEG. ↓Neuronal activities → ↓CBF & ↓ICP. Side effects: hypotension, myocardial depression. [1]
Why it works: Decreasing neuronal metabolic activity reduces oxygen demand → reflex cerebral vasoconstriction (metabolic autoregulation) → decreased cerebral blood volume → decreased ICP. But the trade-off is systemic cardiovascular depression.
Recognise the EEG target in the slide: high-amplitude bursts alternate with near-isoelectric suppression. This is a monitored rescue endpoint for selected refractory ICP, not a bedside diagnosis or first-line treatment.
The 2023 slide presents early cooling to 32–34°C as established post-cardiac-arrest therapy and controversial in stroke/TBI. [1]
Current AHA guidance is broader: use a deliberate, protocolised temperature-control strategy for adults who remain unresponsive after return of spontaneous circulation and maintain 32–37.5°C; evidence does not establish routine 32–34°C cooling as superior to controlled normothermia/fever prevention. Prophylactic hypothermia is not a routine raised-ICP treatment in TBI or stroke. Pneumonia, arrhythmia and coagulopathy remain relevant adverse effects of deeper cooling. [14]
| Procedure | Description | Indication |
|---|---|---|
| EVD | Release CSF ± ICP monitoring | Hydrocephalus, raised ICP monitoring |
| Craniostomy (burr hole) | Drainage of superficial fluid collection | Chronic subdural haematoma |
| Craniotomy | Skull flap raised & replaced; removal of haematoma/tumour | Acute epidural/subdural haematoma, tumour |
| Decompressive craniectomy | Skull flap removed (not replaced) | Massive infarction, post-TBI brain swelling with refractory raised ICP |
Decompressive craniectomy: Bone flap not replaced. Effective in lowering ICP & mortality. Massive infarction or post-TBI brain swelling. Primary pathology (deficit) unchanged. Quality of survival variable. Ethical & philosophical issues. [1]
Reading the operative images: a craniotomy raises a bone flap for evacuation/resection and replaces it; a craniectomy leaves the flap off so swollen brain can expand outward. The before/after craniectomy CTs show the intended mechanical effect—more extracranial room and less intracranial compression—but decompression does not reverse the primary infarct or traumatic damage.
Hydrocephalus
Production: Choroid plexus in ventricles, ~450 ml/day in adults. Absorption: Arachnoid granulations at venous sinuses. Hydrocephalus if: ↑Production, Flow obstruction, ↓Absorption. [1]
CSF pathway: Lateral ventricles → Foramen of Monro → 3rd ventricle → Aqueduct of Sylvius → 4th ventricle → Foramina of Luschka (lateral) & Magendie (medial) → subarachnoid space → arachnoid granulations → superior sagittal sinus [6]
Key numbers:
| Feature | Communicating | Non-communicating (Obstructive) |
|---|---|---|
| Site of problem | Arachnoid granulations (impaired absorption) | Within ventricular system (flow obstruction) |
| Ventricle appearance | ALL ventricles dilated (including 4th) | Ventricles proximal to block dilated; 4th ventricle may be normal |
| Lumbar drainage | May be possible in carefully selected patients after safety assessment | Avoid when obstruction/mass effect creates a pressure gradient; use ventricular access when urgent diversion is needed |
This is a critical distinction. [1]
Acquired: ↑CSF production (choroid plexus papilloma); Flow obstruction (tumour, haematoma); ↓Absorption (meningitis, SAH). Congenital: Aqueductal stenosis, Arnold-Chiari malformation, Dandy-Walker syndrome, Neural tube defect, Congenital infection, Congenital mass lesions. [1]
| Classification | Causes |
|---|---|
| Communicating – Acquired | Post-SAH, post-meningitis (arachnoid granulation adhesions), leptomeningeal carcinomatosis, IVH, NPH |
| Non-communicating – Acquired | CPA tumours, posterior fossa tumours (cerebellar tumour obstructing 4th ventricle), colloid cyst in 3rd ventricle, aqueductal stenosis (post-infective), brain abscess |
| Congenital | Aqueductal stenosis, Arnold-Chiari malformation (Type II), Dandy-Walker syndrome, congenital infection |
| Overproduction (rare) | Choroid plexus papilloma |
Depends on age, cause, chronicity, brain compliance. Infants: large head, dilated scalp veins, tense fontanelle, sunset eyes, irritability, developmental delay. Adults: ICP symptoms, motor deficit, cognitive dysfunction, urinary incontinence, drowsiness, coma. Insidious onset, or can be rapidly fatal. [1]
Why infants are different: Sutures are open → skull can expand → ICP may remain relatively compensated for longer, but head circumference increases. In adults, the rigid skull means raised ICP symptoms develop earlier.
A potentially surgically treatable cause of cognitive decline. Complex pathophysiology of abnormal brain compliance. ICP is not persistently high despite large ventricles. Classic clinical triad: gait disturbance, cognitive decline, urinary incontinence. Selected patients may improve after CSF diversion (e.g., VP shunting); distinguish competing causes such as Alzheimer disease. [1]
Why is ICP "normal" in NPH? The pressure reaches a new equilibrium — the ventricles dilate until an equilibrium is reached where production ≈ absorption at a normal pressure, but the expanded ventricles exert local pressure effects on periventricular structures (especially the corona radiata carrying leg fibres → gait disturbance appears first).
Key differential: Alzheimer's disease. Both present with cognitive decline in older patients. NPH may improve after shunting in appropriately selected patients, whereas a primary neurodegenerative dementia will not be corrected by CSF diversion. CT/MRI shows ventriculomegaly out of proportion to sulcal enlargement in NPH (vs proportional ventricular and sulcal enlargement in cerebral atrophy). [7]
Clinical suspicion. Imaging studies — ventricular dilatation, change in morphology & periventricular oedema. MRI CSF studies. Lumbar puncture — measures CSF pressure, trial drainage BUT BE CAREFUL!! EVD — rarely. [1]
Imaging checklist from slides 44–47:
- Trace the ventricular pathway and ask where calibre changes. Dilated lateral and 3rd ventricles with a normal 4th localise obstruction near the aqueduct; a colloid cyst can obstruct the foramina of Monro, while a posterior-fossa mass can obstruct the 4th-ventricle outlets.
- Look for rounded frontal horns and visible temporal horns. Periventricular low attenuation on CT or T2/FLAIR hyperintensity on MRI suggests transependymal CSF flow (interstitial oedema), supporting active pressure rather than simple atrophy.
- Compare ventricles with cortical sulci. Proportionate ventricular and sulcal enlargement suggests ex-vacuo change; ventriculomegaly out of proportion to the sulci supports hydrocephalus/NPH in the right syndrome.
- Search for the cause and danger signs: haemorrhage (especially SAH/IVH), tumour/cyst, midline shift, compressed basal cisterns and a trapped ventricle.
For NPH specifically:
- CT/MRI: ventriculomegaly out of proportion to sulcal widening
- A supervised high-volume tap or drainage trial may assess gait response only after LP contraindications have been excluded. Improvement supports shunt responsiveness, but shunting is a specialist decision and benefit is not guaranteed. [7][13]
ABC first. The lecture lists lumbar drainage for selected communicating cases and EVD if there is doubt or an unstable/evolving condition. Definitive measures: CSF shunting (VP, VA), endoscopic third ventriculostomy (ETV), or treatment of the cause (e.g., haematoma/tumour removal). [1]
Do not turn the slide into an automatic rule: route and urgency of diversion depend on the cause, compartments, examination and imaging. Suspected obstructive hydrocephalus or mass effect needs urgent neurosurgical assessment; an EVD provides proximal diversion and monitoring.
Complications: Infection (10% or 20%); Blockage → hydrocephalus; Dislodgement/Fracture → hydrocephalus; Over-shunting → CSDH; Abdominal pseudocyst; Slit ventricle syndrome; Nephritis (VA); Bowel perforation (VP). Avoid shunting if possible! [1]
| Complication | Mechanism/Explanation |
|---|---|
| Infection | Most common organism: S. epidermidis, S. aureus. Presents with fever, meningism, raised ICP signs |
| Blockage | 80% proximal (choroid plexus/brain debris), 10% valve, 10% distal. Most common mechanical failure |
| Over-shunting | Too much CSF drained → low ICP → bridging veins stretch → chronic subdural haematoma (CSDH) |
| Slit ventricle syndrome | Chronic over-shunting → ventricles collapse → catheter tip obstructed → intermittent raised ICP |
| Abdominal pseudocyst | CSF-filled cyst forms around distal VP catheter in peritoneum |
| Bowel perforation | VP catheter erodes into bowel → peritonitis |
| Nephritis | VA shunt → immune-complex (shunt) nephritis |
Recognising the devices and complication images: a VP shunt runs from a ventricular catheter through a one-way valve/reservoir to the peritoneum; a VA shunt terminates in the venous circulation/right atrium. On CT, over-drainage may produce subdural collections and very small ventricles; slit-ventricle syndrome combines slit-like ventricles with intermittent pressure symptoms. An abdominal pseudocyst appears as a loculated fluid collection around the distal catheter. Bowel perforation may present with peritonitis or extrusion of distal tubing and requires urgent surgical/infectious-disease management.
| Scenario | Think About |
|---|---|
| Recurrent hydrocephalic symptoms | Blocked shunt → test shunt if competent |
| Raised ICP + focal deficit | CSDH? (especially elderly on aspirin — from over-shunting) |
| Postural headache (worse erect) | Intracranial hypotension from over-shunting (without CSDH) |
| Fever + abdominal pain | Shunt infection → peritonitis? OR peritonitis → shunt infection? → Externalise shunt + antibiotics |
Allows post-op transcutaneous adjustment of shunt valve setting. Tailored to individual patients' needs. Affected by external magnetic field. Check before and after MRI. [1]
Fenestrate III ventricle floor. Bypass obstruction & restore CSF flow. Avoid permanent shunting. Enable tumour biopsy. [1]
When to use ETV: For non-communicating (obstructive) hydrocephalus only. The 3rd ventricle floor is fenestrated endoscopically → CSF can flow directly from the 3rd ventricle into the basal cisterns, bypassing the blocked aqueduct. This is NOT effective in communicating hydrocephalus because the problem is at the arachnoid granulations, not flow obstruction.
Raised ICP can have insidious onset or be rapidly fatal. CPP = MAP − ICP; CBF = CPP/CVR; GCS = E+M+V (3–15). ABC before ICP. Avoid prophylactic/prolonged uncontrolled hyperventilation, do not use corticosteroids to treat TBI, and do not give mannitol without addressing shock. [1]
Current safety overlay: in severe TBI, treat sustained ICP > 22 mmHg and target CPP 60–70 mmHg while integrating clinical/CT findings. Communicating anatomy alone never proves LP safety. [12][13]
Integration with Related Material
- Meningitis → meningeal adhesions → communicating hydrocephalus and raised ICP
- Post-meningitic hydrocephalus is often communicating, but LP still requires a clinical safety screen; do not delay antibiotics for imaging or a deferred LP. [13]
- ICP monitoring in raised ICP from stroke
- Surgical decompression of supratentorial infarct: quality of life not improved, best in young patients with non-dominant infarct
- Cerebellar infarct → direct brainstem compression → drainage of hydrocephalus, posterior fossa decompression
- Obstructive hydrocephalus: lateral ventricles dilated out of proportion to sulcal spaces
- SAH → IVH → obstructive hydrocephalus
- Differentiate from "hydrocephalus ex vacuo" (cerebral atrophy — proportional ventricular and sulcal enlargement)
- Papilloedema = optic disc swelling from raised ICP only
- Transient visual obscurations (TVOs): fleeting monocular visual disturbance
- Evaluation: urgent neuroimaging to look for a mass/venous cause; LP follows only if the overall clinical and imaging assessment shows no contraindication. [13]
- The CRASH trial found increased mortality with high-dose methylprednisolone in clinically significant TBI
- Do not use corticosteroids to improve outcome or reduce ICP after TBI [12]
While not the focus of this lecture, it is mentioned as a cause of raised ICP and is frequently tested:
- Typical patient: Obese young woman with headache and visual disturbance [7]
- CT brain: Normal (to rule out SOL)
- LP: Elevated opening pressure (> 25 cmH₂O) with normal CSF composition
- Management: Weight reduction, acetazolamide (1st line), frusemide (2nd line), optic nerve sheath fenestration or LP shunt if refractory [7]
| Trap | Correct Answer |
|---|---|
| "Give steroids for raised ICP in head trauma" | Do not — high-dose methylprednisolone increased mortality and corticosteroids are not recommended to improve outcome or reduce ICP in TBI |
| "Give mannitol to all patients with raised ICP" | NOT if shocked — will worsen hypotension |
| "Communicating hydrocephalus means LP is safe" | False — anatomy is only one part of the safety assessment; papilloedema, low/falling GCS, focal signs, seizure, instability, bleeding risk or mass effect require deferral/imaging |
| "Hyperventilate prophylactically" | NEVER prophylactic or prolonged — only to buy time |
| "20 cmH₂O and 20 mmHg are interchangeable" | False — 20 cmH₂O ≈15 mmHg; the severe-TBI treatment threshold is sustained ICP > 22 mmHg |
| "Papilloedema is an early sign of raised ICP" | It is a LATE sign |
| "GCS 8 means the same thing regardless of components" | E2M4V2 ≠ E1M5V2 — always report components separately |
| "NPH = high ICP" | ICP is normal — the pathology is abnormal compliance with local pressure effects |
| "ETV works for all hydrocephalus" | Only for non-communicating (obstructive) hydrocephalus |
| "CPP = SBP − ICP" | CPP = MAP − ICP (not systolic BP!) |
High Yield Summary
-
Raised ICP
- Normal adult ICP is about 10–15 mmHg. In severe TBI, treat sustained ICP > 22 mmHg while integrating examination and CT. Causes: SOL, hydrocephalus, brain swelling, hyperaemia, venous congestion.
-
Monro-Kellie Doctrine
- Brain + Blood + CSF in rigid skull. Compensation (venous outflow, CSF displacement) then decompensation (exponential ICP rise). "Talk and die."
-
CPP = MAP − ICP
-
Clinical features
- Morning headache, vomiting, CN VI palsy, papilloedema (LATE), deteriorating consciousness. Terminal: Cushing triad (HTN, bradycardia, irregular breathing), fixed dilated pupil.
-
GCS
- E(1-4) + M(1-6) + V(1-5) = 3–15. Motor score most prognostic. M3 = decorticate (above midbrain). M2 = decerebrate (midbrain/pons).
-
Management
- ABC FIRST → Head about 30° with neutral neck → Maintain CPP 60–70 → Protocolised osmotherapy → Controlled hyperventilation only as a monitored bridge for acute herniation/refractory ICP → Seizure/fever/glucose control → Dexamethasone for selected tumour-related vasogenic oedema, not TBI → Surgical: EVD, lesion evacuation, decompressive craniectomy.
-
Hydrocephalus
- Communicating (impaired absorption) vs non-communicating (obstruction). Communicating anatomy does not automatically make LP safe. CSF production ~450 mL/day. Causes include SAH, meningitis, tumour and congenital abnormalities.
-
NPH
- Wet (incontinence), Wacky (cognitive decline), Wobbly (gait). Selected patients may improve with VP shunting; assess competing neurodegenerative and vascular causes.
-
Shunt complications
- Infection, blockage (80% proximal), over-shunting → CSDH, abdominal pseudocyst, slit ventricle, bowel perforation, nephritis (VA).
-
ETV
- For obstructive hydrocephalus only. Fenestrates 3rd ventricle floor → bypasses obstruction.
- LP requires a clinical and imaging safety assessment; do not rely on “communicating” anatomy alone.
Active Recall - Raised ICP and Hydrocephalus
[1] Lecture slides: GC 111. Raised intracranial pressure and hydrocephalus.pdf [2] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (Increased ICP section) [3] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (Brain tumour headache section) [4] Senior notes: Ryan Ho Opthalmology.pdf (Papilloedema section) [5] Past papers: 2018 Fourth Summative SAQ.pdf (Q8); 2022 Fourth Summative SAQ.pdf (Q9) [6] Senior notes: Maksim Surgery Notes.pdf (Hydrocephalus section) [7] Senior notes: Maksim Medicine Notes.pdf (NPH and IIH sections) [8] Lecture slides: GC 051. Fever and confusion_meningitis and encephalitis; suppurative brain infection.pdf [9] Lecture slides: GC 087. Sudden hemiplegia dysphagia.pdf [10] Lecture slides: Neuroradiology Cases studies_Updated by Chu C Y_June 2023.pptx.pdf [12] Brain Trauma Foundation. Guidelines for the Management of Severe Traumatic Brain Injury, 4th Edition: https://braintrauma.org/coma/guidelines/severe-tbi [13] World Health Organization. WHO guidelines on meningitis diagnosis, treatment and care (2025): https://www.who.int/publications/i/item/9789240108042 [14] American Heart Association. 2025 Guidelines, Part 11: Post-Cardiac Arrest Care: https://cpr.heart.org/en/resuscitation-science/cpr-and-ecc-guidelines/post-cardiac-arrest-care
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