A rigid box,
and what happens when the reserve runs out.

Every normal value comes with its conditions

• Posture. ICP is posture-dependent. Head-up tilt lowers it; head-down or flat raises it. A value quoted without a posture is incomplete — which is also why head-up positioning is a therapeutic manoeuvre and not merely nursing convention.
• It is not a steady number. ICP varies through the cardiac cycle (the pulse waveform of §11) and through the respiratory cycle (the baseline drift on the same trace).
• Transients are large. Even in a normal brain, coughing, straining and sneezing take ICP transiently to around 50 mmHg. That is normal in a compliant skull and dangerous in a non-compliant one.
• Units. mmHg is conventional for ICP and necessary for calculating cerebral perfusion pressure, since arterial pressure is in mmHg. cmH₂O appears for CSF pressure at lumbar puncture; 1 mmHg ≈ 1.36 cmH₂O.
• Reference level. An external transducer must be zeroed to atmosphere at a fixed cranial reference — conventionally the external auditory meatus, which approximates the foramen of Monro. Change the head height without re-levelling and the number changes without the physiology changing.

What is actually being measured, and by what

ICP cannot be estimated reliably from clinical signs; it has to be measured invasively.

Which compartments actually displace, and in what order

The doctrine says a compartment must shrink; it does not say which one can. In practice only two can, and both have hard limits.

1. CSF, first and most. CSF is translocated out of the cranium into the spinal subarachnoid space, and because absorption is pressure-dependent, absorption also rises. This is the first and the most important compensatory mechanism, and the one most often left out of an account of compensation.
2. Venous blood, second. The dural venous sinuses are compressed and venous blood is displaced into the internal jugular veins. This reserve is smaller and is used up quickly.
3. After that, only bad options. A fall in arterial blood volume as perfusion pressure drops, and displacement of brain tissue itself between compartments or through the foramen magnum.

Why different lesions behave differently

The clinically important corollary. An identical added volume produces a completely different pressure change in two different patients, because what determines the pressure rise is not the volume added but how much compensatory reserve was left before it was added. That is exactly what the next section’s curve draws.

The ICP wave is generated by the arterial pulse in the large cerebral vessels and transmitted through the CSF, so one cycle lasts one cardiac cycle and the trace lags slightly behind the arterial trace. It is measured through an external ventricular drain placed in the anterior horn of a lateral ventricle, or through an intraparenchymal probe.

Three components

• The pulse wave — the three peaks below, at heart rate.
• A respiratory component — the baseline moves with the respiratory cycle.
• Slow waves — changes in the baseline itself, over minutes.

Slow waves

Slow, or Lundberg, waves are changes in the baseline rather than in the pulse waveform. They are usually pathological.

In practice ICP monitoring is used mostly to read the mean value and calculate cerebral perfusion pressure; the waveform and slow waves are additional signals rather than the primary purpose.

The chain is always the same shape, and stating it explicitly is what separates a mark-earning answer from a list: variable changes → physiological mechanism → intracranial component changes → ICP consequence.

The arterial compartment is set by cerebral blood flow

Three of the rows above — carbon dioxide, oxygen and cerebral metabolic rate — and autoregulation all act by setting cerebral vascular resistance, and therefore cerebral blood flow, and therefore cerebral blood volume, which is the term that appears in the Monro-Kellie balance. Those four relationships, with the curves you should be able to draw for each, are taught in lesson 8 — cerebral blood flow. The short version needed here:

• Autoregulation holds flow near 50 mL/100 g/min across a mean arterial pressure of about 70-150 mmHg in most adults by a myogenic mechanism. Within that range a rising pressure constricts the vessels, so cerebral blood volume falls slightly. Outside it, flow and volume are pressure-passive.
• Carbon dioxide is a fast lever: flow rises by roughly 1-2 mL/100 g/min per mmHg, so volume and therefore ICP rise with it.
• Oxygen has almost no effect until PaO₂ falls below about 60 mmHg (8 kPa), below which there is abrupt vasodilatation and a sharp rise in volume.
• Metabolic rate drives flow through coupling, so anything that raises it — arousal, pain, seizures, fever — raises cerebral blood volume too.

Stage 1 — compensation

1. CSF is displaced from the cranium into the spinal subarachnoid space. This is the first and most important compensatory mechanism.
2. CSF absorption increases, because absorption at the arachnoid villi is pressure-dependent and CSF pressure has risen. The effective intracranial CSF volume falls further.
3. Venous blood is displaced. The dural venous sinuses are compressed and venous blood moves into the internal jugular veins, reducing intracranial blood volume.
4. Throughout this stage, ICP is nearly unchanged — the flat limb of the volume-pressure curve.

Stage 2 — the reserve runs out

1. Compliance falls and elastance rises. The curve passes its knee — the point of decompensation.
2. ICP rises steeply. Each further increment of volume now produces a much larger pressure rise than the same increment did an hour earlier.
3. Cerebral perfusion pressure falls, because CPP = MAP − ICP and MAP has not changed.

Stage 3 — ischaemia and positive feedback

1. Once CPP falls below about 50 mmHg, the cerebral arterioles are already maximally dilated and autoregulation fails. Cerebral blood flow becomes pressure-passive and falls below the normal 50 mL per 100 g per minute.
2. Cerebral ischaemia begins — first focal, in the least well-perfused regions, then global.
3. Ischaemia produces further vasodilatation and cytotoxic oedema, both of which add volume. That volume raises ICP further, which lowers CPP further: positive feedback, and the reason deterioration accelerates.

Stage 4 — late systemic response and herniation

1. The Cushing response. Brainstem ischaemia drives a massive increase in sympathetic outflow from the vasomotor area, producing intense systemic arteriolar vasoconstriction and systemic hypertension — which raises MAP and so restores CPP to the brainstem. The arterial baroreceptors sense the hypertension and produce reflex bradycardia. Brainstem compression produces an abnormal respiratory pattern. Together: Cushing’s triad.
2. Herniation. Brain tissue is displaced between compartments — subfalcine, uncal (transtentorial), cerebellar and transcalvarial routes are described — most dangerously the cerebellar tonsils through the foramen magnum, compressing the brainstem.
3. Brainstem failure — irregular breathing and apnoea, a falling conscious level, and finally hypotension as the vasomotor centre itself is compressed.

When ICP is not the relevant downstream pressure

CPP is a gradient across the cerebral circulation, so the correct downstream term is whichever pressure the vessels actually empty against. Stated in full: CPP is mean arterial pressure minus intracranial pressure, or minus central venous pressure, whichever is higher.

Normally ICP exceeds central venous pressure, so CPP = MAP − ICP holds. Where central venous pressure is high — high positive end-expiratory pressure (PEEP), jugular obstruction, right heart failure, straining — CVP becomes the effective downstream pressure, and using ICP alone overestimates perfusion.

Rearranged, CBF = CPP ÷ CVR. This form is the more useful one when the question is about what changes flow: autoregulation works by adjusting CVR to hold CBF constant as CPP varies, across a range of pressure. In most adults the lower limit is not less than a mean arterial pressure of 70 mmHg, which with a normal CSF pressure is a CPP of 60 to 65 mmHg, and the upper limit is about 150 mmHg. Outside that range flow is pressure-passive. Lassen’s original curve put the lower limit at 50 mmHg, and some texts still draw it there; current evidence places it higher and finds considerable variation between individuals, so the plateau is better thought of as a family of curves than a single one.