Intracranial pressure

2 Increased ICP

Intracranial pressure (ICP) is the pressure inside the

skull and thus in the brain tissue and cerebrospinal uid
(CSF). The body has various mechanisms by which it
keeps the ICP stable, with CSF pressures varying by
about 1 mmHg in normal adults through shifts in production and absorption of CSF. CSF pressure has been shown
to be inuenced by abrupt changes in intrathoracic pressure during coughing (intraabdominal pressure), valsalva
(Queckenstedts maneuver), and communication with the
vasculature (venous and arterial systems). ICP is measured in millimeters of mercury (mmHg) and, at rest, is
normally 715 mmHg for a supine adult. [1] Changes in
ICP are attributed to volume changes in one or more of
the constituents contained in the cranium.
Intracranial hypertension, commonly abbreviated IH,
IICP or raised ICP, is elevation of the pressure in the
cranium. ICP is normally 715 mm Hg; at 2025 mm
Hg, the upper limit of normal, treatment to reduce ICP
may be needed.[2]

Severely high ICP can cause the brain to herniate.

The Monro-Kellie hypothesis

One of the most damaging aspects of brain trauma

and other conditions, directly correlated with poor outcome, is an elevated intracranial pressure.[6] ICP is very
likely to cause severe harm if it rises too high.[7] Very
high intracranial pressures are usually fatal if prolonged,
but children can tolerate higher pressures for longer
periods.[8] An increase in pressure, most commonly
due to head injury leading to intracranial hematoma or
cerebral edema, can crush brain tissue, shift brain structures, contribute to hydrocephalus, cause brain herniation, and restrict blood supply to the brain.[9] It is a cause
of reex bradycardia.[10]

The pressure-volume relationship between ICP, volume

of CSF, blood, and brain tissue, and cerebral perfusion
pressure (CPP) is known as the Monro-Kellie doctrine or
the Monro-Kellie hypothesis.[3][4][5]
The Monro-Kellie hypothesis states that the cranial compartment is incompressible, and the volume inside the
cranium is a xed volume. The cranium and its constituents (blood, CSF, and brain tissue) create a state of
volume equilibrium, such that any increase in volume of
one of the cranial constituents must be compensated by a
decrease in volume of another.[5]
The principal buers for increased volumes include CSF
and, to a lesser extent, blood volume. These buers respond to increases in volume of the remaining intracranial constituents. For example, an increase in lesion volume (e.g. epidural hematoma) will be compensated by
the downward displacement of CSF and venous blood.[5]
These compensatory mechanisms are able to maintain a
normal ICP for any change in volume less than approximately 100120 mL.

2.1 Pathophysiology

The cranium and the vertebral canal, along with the relatively inelastic dura, form a rigid container, such that the
increase in any of its contentsbrain, blood, or CSF
will tend to increase the ICP. In addition, any increase
in one of the components must be at the expense of the
other two; this relationship is known as the Monro-Kellie
doctrine. Small increases in brain volume do not lead
It is named after Edinburgh doctors Alexander Monro to immediate increase in ICP because of the ability of
and George Kellie.
the CSF to be displaced into the spinal canal, as well as
1

2
the slight ability to stretch the falx cerebri between the
hemispheres and the tentorium between the hemispheres
and the cerebellum. However, once the ICP has reached
around 25 mmHg, small increases in brain volume can
lead to marked elevations in ICP; this is due to failure of
intracranial compliance.
Traumatic brain injury is a devastating problem with both
high subsequent morbidity and high mortality. Injury to
the brain occurs both at the time of the initial trauma (the
primary injury) and subsequently due to ongoing cerebral
ischemia (secondary injury). Cerebral edema, CSF hypertension, circulatory hypotension, and hypoxic conditions are well recognized causes of this secondary injury.
In the intensive care unit, raised intracranial pressure (intracranial hypertension) is seen frequently after a severe
diuse brain injury (one that occurs over a widespread
area) and leads to cerebral ischemia by compromising
cerebral perfusion.

2 INCREASED ICP

2.2 Stages of intracranial hypertension

Minimal increases in ICP due to compensatory mechanisms are known as stage 1 of intracranial hypertension.
When the lesion volume continues to increase beyond the
point of compensation, the ICP has no other resource but
to increase. Any change in volume greater than 100120
mL would mean a drastic increase in ICP. This is stage
2 of intracranial hypertension. Characteristics of stage 2
of intracranial hypertension include compromise of neuronal oxygenation and systemic arteriolar vasoconstriction to increase MAP and CPP. Stage 3 intracranial hypertension is characterised by a sustained increased ICP,
with dramatic changes in ICP with small changes in volume. In stage 3, as the ICP approaches the MAP, it becomes more and more dicult to squeeze blood into the
intracranial space. The bodys response to a decrease in
CPP is to raise blood pressure and dilate blood vessels in
the brain. This results in increased cerebral blood volume, which increases ICP, lowering CPP and perpetuating this vicious cycle. This results in widespread reduction in cerebral ow and perfusion, eventually leading to ischemia and brain infarction. Neurologic changes
seen in increased ICP are mostly due to hypoxia and hypercapnea and are as follows: decreased level of consciousness (LOC), CheyneStokes respiration, hyperventilation, sluggish dilated pupils and widened pulse pressure.

Cerebral perfusion pressure (CPP), the pressure of blood

owing to the brain, is normally fairly constant due to
autoregulation, but for abnormal mean arterial pressure
(MAP) or abnormal ICP the cerebral perfusion pressure
is calculated by subtracting the intracranial pressure from
the mean arterial pressure: CPP = MAP ICP .[1][11] One
of the main dangers of increased ICP is that it can cause
ischemia by decreasing CPP. Once the ICP approaches
the level of the mean systemic pressure, cerebral perfusion falls. The bodys response to a fall in CPP is to raise
systemic blood pressure and dilate cerebral blood vessels.
This results in increased cerebral blood volume, which 2.3 Causes
increases ICP, lowering CPP further and causing a vicious cycle. This results in widespread reduction in cere- Causes of increased intracranial pressure can be classied
bral ow and perfusion, eventually leading to ischemia by the mechanism in which ICP is increased:
and brain infarction. Increased blood pressure can also
mass eect such as brain tumor, infarction with
make intracranial hemorrhages bleed faster, also increasedema, contusions, subdural or epidural hematoma,
ing ICP.
or abscesses all tend to deform the adjacent brain.
Severely raised ICP, if caused by a unilateral spaceoccupying lesion (e.g. a hematoma) can result in midline
generalized brain swelling can occur in ischemicshift, a dangerous sequela in which the brain moves toanoxia states, acute liver failure,[13] hypertensive enward one side as the result of massive swelling in a
cephalopathy, hypercarbia, and Reye hepatocerecerebral hemisphere. Midline shift can compress the
bral syndrome. These conditions tend to decrease
ventricles and lead to hydrocephalus.[12] Prognosis is
the cerebral perfusion pressure but with minimal tismuch worse in patients with midline shift than in those
sue shifts.
without it. Another dire consequence of increased ICP
increase in venous pressure can be due to venous
combined with a space-occupying process is brain hersinus thrombosis, heart failure, or obstruction of suniation (usually uncal or tonsilar). In uncal herniation,
perior mediastinal or jugular veins.
the uncus hippocampus becomes compressed against the
free edge of the tentorium cerebelli, frequently leading
obstruction to CSF ow and/or absorption can
to brainstem compression. If brainstem compression is
occur in hydrocephalus (blockage in ventricles or
involved, it may lead to respiratory depression and is posubarachnoid space at base of brain, e.g., by
tentially fatal. This herniation is often referred to as conArnold-Chiari malformation), extensive meningeal
ing.
disease (e.g., infection, carcinoma, granuloma, or
Major causes of morbidity due to raised intracranial pressure are due to global brain infarction as well as decreased
respiratory drive due to brain herniation.

hemorrhage), or obstruction in cerebral convexities

and superior sagittal sinus (decreased absorption).
Main article: hydrocephalus

2.5

Treatment

increased CSF production can occur in 2.5 Treatment

meningitis, subarachnoid hemorrhage, or choroid
plexus tumor.
The treatment for IH depends on the etiology. In addition
to management of the underlying causes, major consid Idiopathic or unknown cause (idiopathic intracranial erations in acute treatment of increased ICP relates to the
management of stroke and cerebral trauma.
hypertension)
craniosynostosis

2.4

Signs and symptoms

In general, symptoms and signs that suggest a rise in

ICP including headache, vomiting without nausea, ocular
palsies, altered level of consciousness, back pain and
papilledema. If papilledema is protracted, it may lead to
visual disturbances, optic atrophy, and eventually blindness. The headache is classically a morning headache
which may wake them from sleep. The brain is relatively
poorly supplied by oxygen as a result of mild hypoventilation during the sleeping hours, and also cerebral oedema
may worsen during the night due to the lying position.
The headache is worse on coughing / sneezing / bending,
and progressively worsens over time. There may also be
personality or behavioral changes.
In addition to the above, if mass eect is present with
resulting displacement of brain tissue, additional signs
may include pupillary dilatation, abducens palsies, and
the Cushings triad. Cushings triad involves an increased systolic blood pressure, a widened pulse pressure,
bradycardia, and an abnormal respiratory pattern.[14] In
children, a low heart rate is especially suggestive of high
ICP.
Irregular respirations occur when injury to parts of the
brain interfere with the respiratory drive. Cheyne
Stokes respiration, in which breathing is rapid for a period and then absent for a period, occurs because of
injury to the cerebral hemispheres or diencephalon.[15]
Hyperventilation can occur when the brain stem or
tegmentum is damaged.[15]
As a rule, patients with normal blood pressure retain normal alertness with ICP of 2540 mmHg (unless tissue
shifts at the same time). Only when ICP exceeds 4050
mmHg do CPP and cerebral perfusion decrease to a level
that results in loss of consciousness. Any further elevations will lead to brain infarction and brain death.
In infants and small children, the eects of ICP dier because their cranial sutures have not closed. In infants, the
fontanels, or soft spots on the head where the skull bones
have not yet fused, bulge when ICP gets too high.
Papilledema, or the swelling of the optic disc, can be a
reliable sign that ICP is elevated. Unlike other conditions that may result in the swelling of the optic disc, it
is in the case of papilledema that vision may go largely
unaected.[16]

A very common treatment for long-term, especially

idiopathic, cranial hypertension is medication with a special diuretic, especially one prescribed by a neurologist.
In patients who have high ICP due to an acute injury,
it is particularly important to ensure adequate airway,
breathing, and oxygenation. Inadequate blood oxygen
levels (hypoxia) or excessively high carbon dioxide levels (hypercapnia) cause cerebral blood vessels to dilate,
increasing the ow of blood to the brain and causing the
ICP to rise.[17] Inadequate oxygenation also forces brain
cells to produce energy using anaerobic metabolism,
which produces lactic acid and lowers pH, also dilating blood vessels and exacerbating the problem.[6] Conversely, blood vessels constrict when carbon dioxide levels are below normal, so hyperventilating a patient with
a ventilator or bag valve mask can temporarily reduce
ICP. Hyperventilation was formerly a part of the standard
treatment of traumatic brain injuries, but the induced
constriction of blood vessels limits blood ow to the brain
at a time when the brain may already be ischemichence
it is no longer widely used.[18] Furthermore, the brain adjusts to the new level of carbon dioxide after 48 to 72
hours of hyperventilation, which could cause the vessels
to rapidly dilate if carbon-dioxide levels were returned
to normal too quickly.[18] Hyperventilation is still used
if ICP is resistant to other methods of control, or there
are signs of brain herniation, because the damage herniation can cause is so severe that it may be worthwhile
to constrict blood vessels even if doing so reduces blood
ow. ICP can also be lowered by raising the head of the
bed, improving venous drainage. A side eect of this is
that it could lower pressure of blood to the head, resulting in a reduced and possibly inadequate blood supply to
the brain. Venous drainage may also be impeded by external factors such as hard collars to immobilize the neck
in trauma patients, and this may also increase the ICP.
Sandbags may be used to further limit neck movement.
In the hospital, the blood pressure can be articially increased in order to increase CPP, increase perfusion,
oxygenate tissues, remove wastes, and thereby lessen
swelling.[18] Since hypertension is the bodys way of forcing blood into the brain, medical professionals do not
normally interfere with it when it is found in a patient with a head injury.[15] When it is necessary to decrease cerebral blood ow, MAP can be lowered using
common antihypertensive agents such as calcium channel blockers.[6] If there is an intact bloodbrain barrier,
osmotherapy may be carried out by administering IV
mannitol to create a hypertonic solution within the blood
to draw water out of the neurons. This helps to reduce the
uid within the intracranial space; however, prolonged

administration may lead to increase in ICP.[19]

REFERENCES

Main article: Cerebrospinal uid leak

Struggling, restlessness, and seizures can increase

metabolic demands and oxygen consumption, as well as
increasing blood pressure.[17][20] Analgesia and sedation
(particularly in the pre-hospital, ER, and intensive care
setting) are used to reduce agitation and metabolic needs
of the brain, but these medications may cause low blood
pressure and other side eects.[6] Thus if full sedation
alone is ineective, patients may be paralyzed with drugs
such as atracurium. Paralysis allows the cerebral veins to
drain more easily, but can mask signs of seizures, and the
drugs can have other harmful eects.[17] Paralysing drugs
are only introduced if patients are fully sedated (this is
essentially the same as a general anaesthetic)

Spontaneous intracranial hypotension may occur as a result of an occult leak of CSF into another body cavity.
More commonly, decreased ICP is the result of lumbar
puncture or other medical procedures involving the brain
or spinal cord. Various medical imaging technologies exist to assist in identifying the cause of decreased ICP. Often, the syndrome is self-limiting, especially if it is the
result of a medical procedure. If persistent intracranial
hypotension is the result of a lumbar puncture, a blood
patch may be applied to seal the site of CSF leakage.
Various medical treatments have been proposed; only the
intravenous administration of caeine and theophylline
[22]
Intracranial pressure can be measured continuously with has shown to be particularly useful.
intracranial transducers. A catheter can be surgically inserted into one of the brains lateral ventricles and can
be used to drain CSF (cerebrospinal uid) in order to de- 4 See also
crease ICPs. This type of drain is known as an EVD
(extraventricular drain).[6] In rare situations when only
Brain Trauma Foundation
small amounts of CSF are to be drained to reduce ICPs,
Neurocritical care
drainage of CSF via lumbar puncture can be used as
a treatment. There are many clinical studies of non Cushings triad
invasive intracranial pressure measurement methods currently being proposed, aimed at nding reliable and accu Traumatic brain injury
rate ways to measure ICP non-invasively. Such methods
external ventricular drain
could improve diagnostics of traumatic brain injury and
many other conditions associated with intracranial hyper Non-invasive intracranial pressure measurement
tension.
methods
Craniotomies are holes drilled in the skull to remove
intracranial hematomas or relieve pressure from parts of
the brain.[6] As raised ICPs may be caused by the pres5 References
ence of a mass, removal of this via craniotomy will decrease raised ICPs.
A drastic treatment for increased ICP is decompressive
craniectomy,[21] in which a part of the skull is removed
and the dura mater is expanded to allow the brain to swell
without crushing it or causing herniation.[18] The section
of bone removed, known as a bone ap, can be stored in
the patients abdomen and resited back to complete the
skull once the acute cause of raised ICPs has resolved.
Alternatively a synthetic material may be used to replace
the removed bone section (see cranioplasty)

Low ICP

Main article: Intracranial hypotension

It is also possible for the intracranial pressure to drop below normal levels, though increased intracranial pressure
is a far more common (and far more serious) sign. The
symptoms for both conditions are often the same, leading many medical experts to believe that it is the change in
pressure rather than the pressure itself causing the above
symptoms.

[1] Steiner LA, Andrews PJ (2006). Monitoring the injured

brain: ICP and CBF. British Journal of Anaesthesia 97
(1): 2638. doi:10.1093/bja/ael110. PMID 16698860.
[2] Ghajar J (September 2000). Traumatic brain injury. Lancet 356 (9233): 9239. doi:10.1016/S01406736(00)02689-1. PMID 11036909.

[3] Monro A (1783). Observations on the structure and function of the nervous system. Edinburgh: Creech & Johnson.
[4] Kellie G (1824). Appearances observed in the dissection
of two individuals; death from cold and congestion of the
brain. Trans Med Chir Sci Edinb 1: 84169.
[5] Mokri B (June 2001). The Monro-Kellie hypothesis:
applications in CSF volume depletion. Neurology 56
(12): 17468. doi:10.1212/WNL.56.12.1746. PMID
11425944.
[6] Orlando Regional Healthcare, Education and Development. 2004. Overview of Adult Traumatic Brain Injuries. Accessed January 16, 2008.
[7] Dawodu S. 2005.
Traumatic Brain Injury:
Denition,
Epidemiology,
Pathophysiology
Emedicine.com.Accessed January 4, 2007.

[8] Tolias C and Sgouros S. 2006. Initial Evaluation and

Management of CNS Injury. Emedicine.com. Accessed
January 4, 2007.
[9] Graham DI and Gennareli TA. Chapter 5, Pathology of
Brain Damage After Head Injury In, Cooper P and Golnos G. 2000. Head Injury, 4th Ed. Morgan Hill, New
York.
[10] Deepak A. Rao; Le, Tao; Bhushan, Vikas (2007). First
Aid for the USMLE Step 1 2008 (First Aid for the Usmle
Step 1). McGraw-Hill Medical. ISBN 0-07-149868-0.
Page 254
[11] Duschek S, Schandry R (2007). Reduced brain perfusion and cognitive performance due to constitutional hypotension. Clinical Autonomic Research 17 (2): 6976.
doi:10.1007/s10286-006-0379-7. PMC 1858602. PMID
17106628.
[12] Downie A. 2001. Tutorial: CT in Head Trauma Accessed January 4, 2007.
[13] Polson J, Lee WM (2005). AASLD position paper: the
management of acute liver failure. Hepatology 41 (5):
117997. doi:10.1002/hep.20703. PMID 15841455.
[14] Sanders MJ and McKenna K. 2001. Mosbys Paramedic
Textbook, 2nd revised Ed. Chapter 22, Head and Facial
Trauma. Mosby.
[15] Singh J and Stock A. 2006.
Head Trauma.
Emedicine.com. Accessed January 4, 2007.
[16] http://emedicine.medscape.com/article/
1217204-overview
[17] Su F and Huh J. 2006. Neurointensive Care for Traumatic Brain Injury in Children. Emedicine.com. Accessed January 4, 2007.
[18] Shepherd S. 2004. Head Trauma. Emedicine.com. Accessed January 4, 2007.
[19] Trauma.org 2000.
TRAUMA.ORG: Neurotrauma:
Control of Intracranial Hypertension Trauma.org. Accessed March 18, 2009.
[20] Bechtel K. 2004. Pediatric Controversies: Diagnosis and
Management of Traumatic Brain Injuries. Trauma Report. Supplement to Emergency Medicine Reports, Pediatric Emergency Medicine Reports, ED Management,
and Emergency Medicine Alert. Volume 5, Number 3.
Thomsom American Health Consultants.
[21] Sahuquillo J, Arikan F (2006).
Sahuquillo, Juan,
ed. Decompressive craniectomy for the treatment
of refractory high intracranial pressure in traumatic
Cochrane Database Syst Rev (1):
brain injury.
CD003983.
doi:10.1002/14651858.CD003983.pub2.
PMID 16437469.
[22] Paldino M, Mogilner AY, Tenner MS (December
2003). Intracranial hypotension syndrome: a comprehensive review. Neurosurg Focus 15 (6): ECP2.
doi:10.3171/foc.2003.15.6.8. PMID 15305844.

6 External links
Gruen P. 2002. Monro-Kellie Model Neurosurgery Infonet. USC Neurosurgery. Accessed January 4, 2007.
National Guideline Clearinghouse.
2005.
Guidelines for the management of severe traumatic brain injury. Firstgov. Accessed January 4,
2007.
Intracranial Pressure at the US National Library of
Medicine Medical Subject Headings (MeSH)

7 TEXT AND IMAGE SOURCES, CONTRIBUTORS, AND LICENSES

Text and image sources, contributors, and licenses

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Intracranial pressure Source: http://en.wikipedia.org/wiki/Intracranial%20pressure?oldid=628067368 Contributors: Metasquares,

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Images

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CC BY 2.0 Contributors: Rocque BG, Bakaya MK (2008). Spontaneous acute subdural hematoma as an initial presentation of
choriocarcinoma: A case report. J Med Case Reports 2: 211. doi:10.1186/1752-1947-2-211. PMID 18565226. PMC 2442118
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