Methods of intracranial pressure monitoring

There are several means of getting information about intracranial pressure. These are only two of the methods in common use: the external ventriular drain and the parenchymal pressure transducer. The alternative, also presented here, is a clinical assessment.

This chapter answers the question as to how one might monitor intracranial pressure, rather than asking whether one should (the indications for ICP monitoring being the subject of another chapter).

Questions on this topic have included the following:

In brief summary:

Clinical Intracranial Pressure Monitoring
These are the clinical features of increasing intracranial pressure.They were asked about in Question 5.2 from the second paper of 2010

Cardinal features:

  • Decreased level of consciousness
  • Bradycardia and hypertension
  • Papilloedema
  • Unilateral or bilateral pupil dilatation

Associated features:

  • Headache and vomiting
  • Seizures
  • ST segment changes, T wave inversion
  • QT prolongation
A Comparison of Invasive ICP Monitoring Equipment
Advantages and Disadvantages of Two Common Instruments


Codman Microsensor

Gold standard of ICP monitoring

Similar accuracy to EVD

Pressure is transmitted to a Wheatsone bridge transducer via fluid-filled non-compressible tubing

Piesoelectric strain gauge pressure sensor is intracranial; connected to the monitor via fiberoptic cable

Requires a certain expertise to place correctly.
About 12% are placed into an inappropriate position.

Requires less expertise to place (however, this should still be done by somebody with neurosurgical experience)

More traumatic owing to depth of insertion and diameter of catheter

Less traumatic, because the catheter placement is not as deep, and the catheter tip is finer. The Codmans typically sits about 2cm below the cerebral surface.

CSF can be drained though the EVD

CSF cannot be drained or sampled

The catheter can become blocked by clots or debris

The catheter cannot block

Measures intraventricular pressure,
which is thought to be representative of the pressure within the intracranial CSF

Measures local parenchymal pressure

Can be re-zeroed to atmorpsheric pressure

Cannot be re-zeroed after insertion;
calibration tends to drift after 72 hours

Insertion is impossible if the ventricles are collapsed

Does not rely on venticular placement, and thus is the only option in a patient with small collapsed ventricles

Dangerous in coagulopathy. Even when non-coagulopathic, the risk of haemorrhagic complications is around 5-7% on average

Coagulopathy is only a relative contraindication; hemorrhagic complications are infrequent. One study puts the rate of bleeding at 1.1%.

Places the patient at risk of ventriculitis after 5 days. Bacterial colonisation rates range up to 27%, but studies vary in their definition of what a clinically significant infection actually is.

Less likely to become infected; highly unlikely to cause ventriculitis, as it does not communicate with the entricles.
One study puts the infection rate at 0.6%.



In greater detail:

Clinical assessment of intracranial pressure: the cardinal features

There are several general remarks one could make about the clinical signs of increased intracranial pressure, using Plum and Posner's great textbook as a source.

  • Increases in ICP are tolerated remarkably well, as long as they progress relatively slowly.
  • Clinical assessment of a raised ICP is non-inferior to direct measurement of raised ICP when it comes to mortality in the general trauma population (though severe TBI patients still benefit from routine EVD insertion).
  • Physical signs are generally neither very specific nor very sensitive for subtle changes in intracranial pressure. They become more and more obvious as the pressure rises.
  • Papilloedema and a decrease in the level of consciousness are probably the first signs
  • Dilated pupils and the Cushing reflex tend to occur very late in the process.

Decreased level of consciousness

The decrease in the level of consciousness due to raised intracranial pressure is generally due to the effect of increased ICP on arterial blood flow. It is therefore a fairly sensitive indicator of terrible pathology, but not a very sensitive indicator of early gradual increases in ICP. In short, a decline in the level of consciousness should not be interpreted as an early warning sign. Plum and Posner report that cerebral arterial blood flow in a haemodynamically normal individual would become impaired only at an ICP around 45-50 mmHg, i.e. when the (average-ish) MAP of 80 mmHg is only resulting in a cerebral perfusion pressure of around 30-35 mmHg.

Chronically, intracranial pressure can rise to as high as 60cmH2O (i.e. around 45mm Hg), and yet have little effect on the level of consciousness. Slow and long-lasting ICP increases are better tolerated than acute changes.

Relevance of the level of consciousness as a marker of raised ICP

  • The level of consciousness decreases as a late sign of raised ICP.
  • It tends to occur due to impaired cerebral blood flow.
  • Once it drops, it is likely to keep dropping rapidly.


The direction of axoplasmic flow in the optic nerve, as well as retinal venous blood flow, is into the head - though the retina, down the optic nerve and into the cavernous sinus. Normally, there is no pressure gradient acting on the optic nerve. The intraocular pressure is usually about the same as the normal intracranial pressure (i.e. in the range of single digits or early teens of mmHg), and venous blood flow continues unimpeded.

Components of papilloedema, in order of progression

  • Decreased and ultimately absent retinal venous pulsation
  • Engorgement of retinal veins
  • Loss of the border of the optic disc
  • Enlarging scotoma
  • Concentric loss of vision

Thus, the first finding of a rising ICP is a loss of venous pulsation in the retinal vein. As ICP rises above systemic venous pressure, retinal venous pulsation disappears (i.e. the drainage of venous blood through the optic nerve is no longer possible).

The retinal veins become engorged, and more obvious on fundoscopy. The axoplasmic flow in the axons of the optic nerve is also interupted, and this leads to axonal oedema. The increased water content of the optic nerve results in the "spreading" of the optic disk, a blurring of its margins. The patient- provided they are conscious - may complain of a loss of vision in a scotoma within the visual field. As papilloedema progresses, ganglion cells begin to die in the retina, a progress which progresses inwards (towards the macula) causing concentric peripheral visual loss.

Cushing reflex

This is the observed tendency of patients with raised intracranial pressure to become bradycardiac and hypertensive. This phenomenon is discussed in satisfying detail by the authors of a 2006 article from Neurosurgery. Named after the Pope of Neurosurgery, the discovery of this process should probably be attributed to von Bergmann and Cramer, who did fascinating research on intracranial pressure in the 1870s (eg. observing the brain vessels directly through a glass window cut in the skull of an experimental animal, while injecting various substances (spongy or gelatinous) into the cranial cavity).

The reflex consists of bradycardia and hypertension, and it forms a part of Cushing's Triad, of which the third leg is an abnormal respiratory pattern. It was thought to be a protective reflex, a desperate order issued by a dying brain to maintain its perfusion at any cost. It turns ot that one can generate a very convincing Cushing response by some "electrical stimulation or distension of tissues within a thin strip of brain along the floor of the fourth ventricle in the rostral medulla and caudal pons."

Without electrical stimulation, pressure on the rostral medulla results in the same effects; this underlies the association of the Cushing reflex with increased intracranial pressure. However, it is unreliable, largely because it takes a fair amount of pressure to squeeze the rostral medulla. In a series of patients undergoing endoscopic neurosurgery, very few of the anaesthetised patients developed a Cushing reflex with a cerebral perfusion pressure around 30mmHg. They would be unconscious with that sort of CPP, but the Cushing reflex identified their problem with a sensitivity of only 39%, and a specificity of 73%.

The reflex confidently identified raised intracranial pressure only in patients whose CPP had dropped to 15mmHg. The authors of the paper were able to state that "no observable effects are seen with a cerebral perfusion pressure >40 mm Hg, independent of the intracranial pressure".

The Cushing Reflex as a marker of raised ICP

  • Bradycardia and hypertension are a very late late sign
  • The reflex has good sensitivity and specificity only when the ICP is enormous
  • The absence of the Cushing reflex does not exclude severely decreased cerebral perfusion pressure, which would be enough to cause profound long-term disability.

Dilated Pupils

The "blown pupil" as a sign of raised intracranial pressure is discussed in greater detail in the chapter on pupillary abnormalities. In brief:

The unilateral or bilateral dilated pupil as a marker of raised ICP

  • Pupil dilation occurs when the thrid nerve is stretched over the petroclinoid ligament, or crushed against it in uncal herneation.
    • In that case, the pupils will be very dilated.
    • In uncal herneation, the dilated pupil occurs on the same side as the lesion.
  • When the hernation is central, the pupils are usually small, and mid-dilate when the brainstem is completely destroyed.


Pre-LP assessment for features of a space-occupying lesion

The abovelisted clinical features all suggest that the patient has increased intracranial pressure, and that there is a risk they will herniate if you perform a lumbar puncture. In addition to these obvious signs, there are focal neurological features and aspects of history which might prompt one to scan the head first.

This precise scenario was presented in Question 25.1 from the second paper of 2009. Thankfully, a nice article from 2004 (Clinical Infectious Diseases) presents a set of recommended criteria for adult patients with suspected bacterial meningitis who should undergo CT prior to lumbar puncture.

These recommendations are presented as a table, which - with minimal modification - is reproduced below. In diluted grey, ther author adds his own remarks, which do not belong in the original canonical table, but which seemed relevant.

Who Should Undergo a Head CT prior to LP?

Immunocompromised host

  • HIV or AIDS
  • On immunosuppressant drugs, including steroids
  • Post transplant (any sort of transplant)
  • Post-splenectomy patients, particularly when under-immunised.

History of focal CNS disease

  • Known tumour
  • Known stroke
  • Known focal infection

New onset of seizures

  • Within 1 week of presentation

Ongoing or recent seizures

  • Prolonged seizures
  • Within 30 minutes of the last seizure

(Seizures in general seem to cause an increase in intracranial pressure, in the absence of a space-occupying lesion, and with a deceptively normal head CT.)


  • Normal venous pulsations suggest a normal ICP

Decreased level of consciousness

  • Irrespective of focal neurology (or the desire to do an LP) this finding alone would probably make the head CT mandatory.

Focal neurological signs

  • Dilated unreactive pupil
  • Cranial nerve signs
  • Unilateral weakness
  • Partial seziures

It must be mentioned that a head CT does not completely exclude the possibility that the patient will cone and die as a result of your LP (however, the likelihood diminishes into the realm of case reports).

Nor is the presence of increased intracranial pressure necessarily a recipe for brainstem herniation.

Recently, the Swedes did away with the recommendation to routinely scan heads in adult meningitis patients with altered levels of consciousness, and saw an improvement in door-to-antibiotics time.

The interval between presentation and diagnosis is all-important: mortality increases by 12.6% per hour of delay. By forgetting about the CT head, the LP could be done earlier and the antibiotics could be started sooner (on average 1.6 hours sooner) with a paradoxical improvement in mortality and morbidity.

External Ventricular Drain (EVD)

This is a thin tube inserted into the cerebral ventricle. Generally held to be the "gold standard" of ICP monitoring, it also offers a means of sampling the CSF and draining it off if the need arises. Because the CSF spaces (usually) communicate, pressure of the whole system can be measured from any one of these spaces.

The disadvantage of the EVD is the fact that it is relatively wide-bore, and its insertion results in some degree of parenchymal trauma. Yes, there can be haemorrhage. Yes, it can get infected. Freehand insertion can occasionally lodge the catheter into parenchyma (where its useless) or worse yet, into an "eloquent" region such as the thalamus or brainstem.

Furthermore, if there is significant midline shift or cerebral oedema and the ventricles are very small, the EVD cannot be inserted safely. In such a situation, one must rely on a parenchymal catheter to measure the pressure of the brain tissue rather than CSF.

The Brain Trauma Foundation salutes the EVD as a cheap and accurate means of monitoring intracranial pressure, and insists we use then whenever possible.

Parenchymal catheter (eg. Codman catheter)

These are either strain-gauge or fiberoptic catheters inserted into the brain parenchyma. Thus, you're not measuring the CSF pressure but rather the parenchymal pressure. The two are closely correlated, but there is an element of inaccuracy, especially considering that different parts of the parenchyma may be experiencing different pressure.

Haemorrhage and infection can also affect these catheters, but not as often as the EVD. Another advantage is the simplicity of insertion - you don't need to hit the ventricle for it to be effective. As it is a narrower catheter, there is less collateral damage to the healthy brain.

The disadvantages are that you cant get CSF when you need it, and the catheters malfunction more frequently. There is a well-know phenomenon of "drift", where the catheter gradually deviates away from the zeroed value and because it cant be re zeroed it gives progressively less and less accurate readings (it is suspected that the sensitive tip becomes caked with proteinaceous filth).

A good article evaluates the various advantages and disadvantages of EVDs and Codman catheters, and on this basis a table of comparison can be constructed, which is presented in the "brief summary" above.

Anatomy of the The Extraventricular Drain

anatomy of the evd

The EVD is a thin tube inserted into the lateral ventricle. The point of insertion (which is performed blindly) is about 2.5 centimetres left or right from the midline, 11cm posterior to the junction between the frontal bone and the nasal bones (the "nasion", which is the depression between the bow ridges above the nose). One aims away from the motor cortex.

The drain connects to the transducer via a three-way tap; the waveform is only generated when the drain is closed (turned off to the cylinder)- if you were measuring an open drain all you would get would be the pressure in the column of CSF in the tubing above the transducer.

The transducer is zeroed to atmospheric pressure at the level of the tragus.

The height of the drain is set to a certain specified height (in cm) above the patients tragus. When the drain is open, this allows CSF to drain out of the ventricle, which keeps the pressure in the ventricle under control. Lets say the drain is fixed at 15cm- then, obviously if the pressure in the ventricle increases beyond 15cmH2O the CSF comes out of the drain into the cylinder, and continues coming out while the pressure remains above 15cmH2O.

Once enough CSF has exited the ventricle the pressure decreases and the CSF stops draining.

Weaning off the EVD

While the EVD is connected, there is continuos drainage. Every hour the nurses will clamp the drainage catheter and measure the ICP, recording its value.

At a stage in the disease process, as the patient is weaned off sedation and their ICP measurements become more stable, the EVD can be clamped for a 24-48 hour period. During this time, the ICP is measured continuously. If it remains within a relatively normal range (say, less than 25-20), one can assume that it will continue to remain within this range, and the EVD can be safely removed.

How much should be coming out?

It is said that the rate of CSF production is about 0.4ml per minute, or about 24ml per hr; this causes one to arrive at a figure of 576ml per day. That sounds about right. Given that the total CSF volume is less than 160ml, this makes for a rapid rate of turnover. The reabsorption seems to be driven by a simple pressure gradient: observations suggest that CSF resorption subsides and essentially ceases when the ICP is about 5mmHg.


A series of excellent resource were available from the NSW ICU protocols and publications, but the links broke. Thank you Ganesh for identifying this problem. New links have been added (until they break too).

Medtronic have this brochure to describe the bedside use of their DUET drain system.

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Catherine J. Kirkness, Pamela H. Mitchell, R bert L. Burr, Karen S. March, David W. Newell Intracranial Pressure Waveform Analysis: Clinical and Research Implications Journal of Neuroscience Nursing, Oct, 2000

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Glimåker, Martin, et al. "Adult Bacterial Meningitis: Earlier Treatment and Improved Outcome Following Guideline Revision Promoting Prompt Lumbar Puncture." Clinical Infectious Diseases (2015): civ011.