Canonical Question

Neuro Measurement – ICP

V5 H2.i Historical V4 K1.ii, K5.i 2 appearances

Master answer

Definition:

ICP: hydrostatic pressure within the cranial vault
Normal value is 5-15 mmHg
focal ischaemia when ICP > 20 mmHg
global ischaemia when ICP > 50mmHg

Munro-Kellie Doctrine

The rigid and closed cranial vault forms a fixed brain volume containing
- Brain parenchyma (80%, 1400 g)
- CSF (10%; 75 mL)
- Cerebral blood and vessels (10%; 75 mL)
Δ’s in volume of any components → Δ’s in others or and increase in ICP

CSF Production / Absorption

CSF Production:

60-70% of the CSF is formed by the choroid plexuses
30-40% by the cerebral vessels lining the ventricular walls
Normal rate is 20mL/hour
Formation independent of ventricular pressure
Mechanism
- From Coroid Plexus by net transport of Na+, K+, Cl-, HCO3- and water, from plasma to ventricles
- Na down Conc grad
- Others down electro chem grads

CSF Absorption:

Absorbed through the arachnoid villi into the cerebral venous sinuses
- Absorption by bulk flow, is proportional to ventricular pressure
- If pressure < 7 cmH2O, CSF absorption ceases
- Above 7cmCSF absorption is linear
- At approximately 11 cmH2O, CSF Absorption = Formation

Control of ICP

ICP is regulated via volume buffering
- i.e. increase in volume of one intracranial component leads to compensatory decrease in volume of other intracranial components
When volume buffering mechanism is exhausted → rapid increase in ICP (decompensation)
- Movement of cerebral venous blood = rapid compensation, lower capacity
- Movement of CSF = gradual compensation, larger capacity

Determinants of ICP:

Brain
- Age / Mass
- Space occupying lesions
- Cerebral Oedema
CSF
- CSF production
- CSF Absorption
Cerebral Blood Volume
- Cerebral autoregulation: Flow-metabolic coupling
- Cerebral metabolic rate
- Increase in systemic blood pressure / flow
- Venous Outflow obstruction
- Vasoactive agents
Monro-Kellie Doctrine
- Loss of above – e.g. Fractures, surgery

Compensation for Elevated ICP (Intracranial Pressure)

Early compensation

Δ CSF distribution and flow
CSF is displaced to spinal subarachnoid space
↑’d resorption rate

Late compensation

↑ ICP → ↓ CBF → ↓ in cerebral blood volume → cerebral ischaemia

Decompensation

↑ICP → ↓ in cerebral tissue volume → brain herniation
Cushing Reflex
- Hypertension, bradycardia and abnormal breathing associated with raised ICP
Mechanism:
- Stage 1:
  - ↑ ICP → ↓ blood supply to vasomotor area → Local hypoxia/hypercarbia → ↑ SNS >> ↑ PSPS vasomotor stimulation
  - ↑ TPR → ↑ MAP
  - ↑ HR → ↑ CO
  - → compensatory ↑CBF
- Stage 2:
  - ↑ CO → Baroreceptor stimulation → ↑ Vagus nerve stimulation → Bradycardia and ↓ contractility.

Gladwin / JC 2020

Methods of Measurement of ICP (Outline)

Invasive

Method	Advantages	Disadvantages
Intraventricular catheter (EVD)	Provides ‘ture’ global ICP Allows for CSF drainage and administration of drugs In-vivo calibration possible via external pressure transducer	Infection Difficult iinsertion
Epidural catheter	Ease of insertion Minimal risk of infection (no penetration of dura)	Low accuracy
Lumbar CSF puncture	Extracranial procedure Can be performed ambulatory	May not reflect ICP Dangerous if ICP high
Catheter-tip micro transducers (subdural or intra-parenchymal)	Rare complications during procedure Low risk of infections Can be made permanent implants	Drift of transducer output over time In-vivo calibration not possible Inaccurate if intraparenchymal gradient exists

Non-Invasive

Non-invasive methods like pupillometry, CT, MRI, TCD provide an adjunct to clinical examination of high ICP, but are not a surrogate for invasive ICP measurement.

Gladwin / JC 2020

Answer by Gladwin, JC

Exam appearances

Exam	Exact wording	Relationship	Success
2016B Q18	Discuss the determinants of intracranial pressure (80% of marks). Outline how it can be measured (20% of marks).	historical_member	55.00%
2022A Q10	Discuss the determinants of intracranial pressure (80% marks) and outline how it can be measured (20% marks).	historical_member	64.00%