#Intracranial pressure

#Discuss the determinants of intracranial pressure

#Definition and normal values

Intracranial pressure (ICP) is the pressure within the cranial vault, reflecting the combined volumes of brain tissue, blood, and cerebrospinal fluid (CSF).

In normal adults:

• ICP is 5–15 mmHg
• Sustained ICP >20 mmHg is associated with cerebral ischaemia

The cranial contents are distributed approximately as:

• Brain tissue: 1500 mL (~80%)
• Blood: 150 mL (~10%)
• CSF: 150 mL (~10%)

These proportions emphasise that ICP is determined by the interaction between compartments, not a single component.

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#Monroe–Kellie doctrine

The Monroe–Kellie doctrine describes the fundamental constraint governing ICP:

The cranium is a rigid, fixed-volume container. Therefore, an increase in one intracranial component must be offset by a decrease in another, otherwise ICP will rise.

This principle underpins all ICP physiology. Early in disease, compensatory mechanisms maintain ICP, but once exhausted, ICP rises rapidly.

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#Intracranial pressure-volume relationship and compensation

The relationship between intracranial volume and pressure is described by the intracranial pressure-volume curve.

When ICP is low, changes in volume do not significantly affect ICP. However when ICP is higher, even small changes in volume can cause a massive rise in ICP.

By Harary et al. Intracranial Pressure Monitoring—Review and Avenues for Development.

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#Compensated phase

In the early phase, increases in volume produce minimal rises in ICP due to buffering:

• Venous blood displacement out of the cranial vault
• CSF displacement into the spinal subarachnoid space
• Increased CSF absorption via arachnoid granulations

CSF absorption is pressure dependent:

• Minimal when ICP <7 mmHg
• Rises linearly with ICP above this threshold

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#Decompensated phase

Once compensatory reserve is exhausted:

• Small increases in volume → large increases in ICP
• Leads to:
  • ↓ CPP (CPP = MAP − ICP)
  • ↓ CBF (CBF = CPP / vascular resistance)
  • → cerebral ischaemia

Critical thresholds:

• ~20 mmHg → onset of ischaemia
• ~40 mmHg → critical ischaemia and risk of herniation

#Cushing's reflex

Cushing's reflex is a late sign of severe intracranial hypertension.

Mechanism:

• ↑ ICP → ↓ CPP → brainstem ischaemia
• → massive sympathetic activation

Clinical features:

• Hypertension due to sympathetic activation
• Bradycardia mediated by the baroreceptor reflex response to hypertension
• Irregular respiration due to brainstem dysfunction or herniation

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#Determinants of intracranial pressure

#Cranium

The cranium is normally fixed in volume.

A reduction in ICP occurs if cranial volume increases, for example due to decompressive craniectomy or open skull fracture.

#Brain parenchyma

Brain parenchymal volume is generally not modifiable under normal physiological conditions. However, changes to brain tissue may occur due to pathological processes.

Increase in volume → ↑ICP:

• Tumour
• Abscess
• Intracranial haemorrhage
• Cerebral oedema

Decrease in volume → ↓ICP:

• Age-related atrophy
• Surgical resection
• Drainage of mass lesions

#Cerebrospinal fluid (CSF)

CSF is produced by the choroid plexus (~500 mL/day) and absorbed via arachnoid granulations.

ICP depends on production and drainage:

• ↓ production → ↓ ICP (e.g. hypovolaemia)

• ↓ drainage → ↑ ICP (e.g. obstructive hydrocephalus)

• ↑ drainage → ↓ ICP (e.g. external ventricular drain (EVD) or ventriculoperitoneal shunt)