Intracranial pressure

Intracranial pressure (ICP) is the pressure inside the skull and thus in the brain tissue and cerebrospinal fluid (CSF). ICP is measured in millimeters of mercury (mmHg) and, at rest, is normally 7–15 mmHg for a supine adult.^[1] 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. Changes in ICP are attributed to volume changes in one or more of the constituents contained in the cranium. CSF pressure has been shown to be influenced by abrupt changes in intrathoracic pressure during coughing (intra-abdominal pressure), valsalva maneuver, and communication with the vasculature (venous and arterial systems).

Intracranial hypertension, commonly abbreviated IH, IICP or raised ICP, is elevation of the pressure in the cranium. ICP is normally 7–15 mm Hg; at 20–25 mm Hg, the upper limit of normal, treatment to reduce ICP may be needed.^[2]

Contents

• 
  1 The Monro–Kellie hypothesis
  


• 
  2 Increased ICP
  
  
  
  • 
    2.1 Signs and symptoms
    
  
  
  • 
    2.2 Causes
    
  
  
  • 
    2.3 Pathophysiology
    
  
  
  • 
    2.4 Diagnosis
    
  
  
  • 
    2.5 Treatment
    
  
  
  
  


• 
  3 Low ICP
  


• 
  4 See also
  


• 
  5 References
  


• 
  6 External links
  

The Monro–Kellie hypothesis

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 that the volume inside the cranium is fixed. 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 buffers for increased volumes include CSF and, to a lesser extent, blood volume. These buffers 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]

The Monro–Kellie hypothesis is named after Edinburgh doctors Alexander Monro and George Kellie.

Increased ICP

Severely high ICP can cause the brain to herniate.

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 reflex bradycardia.^[10]

Signs and symptoms

In general, symptoms and signs that suggest a rise in ICP include 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 edema may worsen during the night due to the lying position. The headache is worse on coughing, sneezing or bending and progressively worsens over time. There may also be personality or behavioral changes.

In addition to the above, if mass effect is present with resulting displacement of brain tissue, additional signs may include pupillary dilatation, abducens palsies, and the Cushing's triad. Cushing's triad involves an increased systolic blood pressure, a widened pulse pressure, bradycardia, and an abnormal respiratory pattern.^[11] 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. Biot's 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.^[12]Hyperventilation can occur when the brain stem or tegmentum is damaged.^[12]

As a rule, patients with normal blood pressure retain normal alertness with ICP of 25–40 mmHg (unless tissue shifts at the same time). Only when ICP exceeds 40–50 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 effects of ICP differ 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. ICP correlates with intraocular pressure (IOP) but seems to lack the accuracy necessary for close management of intracranial pressure in the acute posttraumatic period.^[13]

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 unaffected.^[14]

Causes

Causes of increased intracranial pressure can be classified by the mechanism in which ICP is increased:

• Mass effect such as brain tumor, infarction with edema, contusions, subdural or epidural hematoma, or abscesses all tend to deform the adjacent brain.


• Generalized brain swelling can occur in ischemic-anoxia states, acute liver failure,^[15]hypertensive encephalopathy, hypercarbia (hypercapnia), and Reye hepatocerebral syndrome. These conditions tend to decrease the cerebral perfusion pressure but with minimal tissue shifts.


• Increase in venous pressure can be due to venous sinus thrombosis, heart failure, or obstruction of superior mediastinal or jugular veins.


• Obstruction to CSF flow and/or absorption can occur in hydrocephalus (blockage in ventricles or subarachnoid space at base of brain, e.g., by Arnold-Chiari malformation), extensive meningeal disease (e.g., infection, carcinoma, granuloma, or hemorrhage), or obstruction in cerebral convexities and superior sagittal sinus (decreased absorption).


• Increased CSF production can occur in meningitis, subarachnoid hemorrhage, or choroid plexus tumor.


• Idiopathic or unknown cause (idiopathic intracranial hypertension, a common cause in otherwise well people especially younger obese women)


• Craniosynostosis

Pathophysiology

Cerebral perfusion pressure (CPP), the pressure of blood flowing 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][16] 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 body’s 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 increases ICP, lowering CPP further and causing a vicious cycle. This results in widespread reduction in cerebral flow and perfusion, eventually leading to ischemia and brain infarction. Increased blood pressure can also make intracranial hemorrhages bleed faster, also increasing ICP.

Severely raised ICP, if caused by a unilateral space-occupying lesion (e.g. a hematoma) can result in midline shift, a dangerous sequela in which the brain moves toward one side as the result of massive swelling in a cerebral hemisphere. Midline shift can compress the ventricles and lead to hydrocephalus.^[17]

Diagnosis

The most definitive way of measuring the intracranial pressure is with transducers placed within the brain. A catheter can be surgically inserted into one of the brain's lateral ventricles and can be used to drain CSF (cerebrospinal fluid) in order to decrease ICP's. This type of drain is known as an extraventricular drain (EVD).^[6] This is rarely required outside brain injury and brain surgery settings.

In situations when only small amounts of CSF are to be drained to reduce ICP's (e.g. in IIH), drainage of CSF via lumbar puncture can be used as a treatment. Non-invasive measurement of intracranial pressure is being studied.

Treatment

The treatment for IH depends on the cause. In addition to management of the underlying causes, major considerations in acute treatment of increased ICP relates to the management of stroke and cerebral trauma.

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 flow of blood to the brain and causing the ICP to rise.^[18] 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 flow to the brain at a time when the brain may already be ischemic—hence it is no longer widely used.^[19] 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.^[19] 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 flow. ICP can also be lowered by raising the head of the bed, improving venous drainage. A side effect 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 artificially increased in order to increase CPP, increase perfusion, oxygenate tissues, remove wastes, and thereby lessen swelling.^[19] Since hypertension is the body's 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.^[12] When it is necessary to decrease cerebral blood flow, MAP can be lowered using common antihypertensive agents such as calcium channel blockers.^[6] If there is an intact blood–brain 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 fluid within the intracranial space; however, prolonged administration may lead to increase in ICP.^[20]

Struggling, restlessness, and seizures can increase metabolic demands and oxygen consumption, as well as increasing blood pressure.^[18][21] 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 effects.^[6] Thus if full sedation alone is ineffective, 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 effects.^[18] Paralysing drugs are only introduced if patients are fully sedated (this is essentially the same as a general anaesthetic)

Craniotomies are holes drilled in the skull to remove intracranial hematomas or relieve pressure from parts of the brain.^[6] As raised ICP's may be caused by the presence of a mass, removal of this via craniotomy will decrease raised ICP's.

A drastic treatment for increased ICP is decompressive craniectomy,^[22] 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.^[19] The section of bone removed, known as a bone flap, can be stored in the patient's abdomen and resited back to complete the skull once the acute cause of raised ICP's has resolved. Alternatively a synthetic material may be used to replace the removed bone section (see cranioplasty)

Low ICP

Main article: Cerebrospinal fluid leak

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 caffeine and theophylline has shown to be particularly useful.^[23]

See also

• Brain Trauma Foundation


• Neurocritical care


• Cushing's triad


• Traumatic brain injury


• external ventricular drain


• Non-invasive intracranial pressure measurement methods


• Pressure reactivity index (PRx)

References

1. 
   ^ ^ab Steiner LA, Andrews PJ (2006). "Monitoring the injured brain: ICP and CBF". British Journal of Anaesthesia. 97 (1): 26–38. doi:10.1093/bja/ael110. PMID 16698860..mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"""""""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("//upload.wikimedia.org/wikipedia/commons/thumb/6/65/Lock-green.svg/9px-Lock-green.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("//upload.wikimedia.org/wikipedia/commons/thumb/d/d6/Lock-gray-alt-2.svg/9px-Lock-gray-alt-2.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("//upload.wikimedia.org/wikipedia/commons/thumb/a/aa/Lock-red-alt-2.svg/9px-Lock-red-alt-2.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
   


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   ^ 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: 84–169.
   


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   ^ ^abc Mokri B (June 2001). "The Monro-Kellie hypothesis: applications in CSF volume depletion". Neurology. 56 (12): 1746–8. doi:10.1212/WNL.56.12.1746. PMID 11425944.
   


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   ^ ^abcdef Orlando Regional Healthcare, Education and Development. 2004. "Overview of Adult Traumatic Brain Injuries." Accessed January 16, 2008. Archived February 27, 2008, at the Wayback Machine.
   


7. 
   ^ Traumatic Brain Injury (TBI) - Definition, Epidemiology, Pathophysiology at eMedicine
   


8. 
   ^ Initial Evaluation and Management of CNS Injury at eMedicine
   


9. 
   ^ Graham, D. I.; Gennarelli, T. A. (2000). "Pathology of Brain Damage After Head Injury". In Cooper, Paul Richard; Golfinos, John. Head Injury (4th ed.). McGraw-Hill. pp. 133–54. ISBN 978-0-8385-3687-2.
   


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. p. 254. ISBN 0-07-149868-0.
    


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    ^ Sanders MJ and McKenna K. 2001. Mosby’s Paramedic Textbook, 2nd revised Ed. Chapter 22, "Head and Facial Trauma." Mosby.
    


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13. 
    ^ Spentzas, Thomas; Henricksen, Jared; Patters, Andrea B.; Chaum, Edward (2010-09-01). "Correlation of intraocular pressure with intracranial pressure in children with severe head injuries". Pediatric Critical Care Medicine: A Journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies. 11 (5): 593–598. doi:10.1097/PCC.0b013e3181ce755c. ISSN 1529-7535. PMID 20081553.
    


14. 
    ^ Papilledema at eMedicine
    


15. 
    ^ Polson J, Lee WM (2005). "AASLD position paper: the management of acute liver failure". Hepatology. 41 (5): 1179–97. doi:10.1002/hep.20703. PMID 15841455.
    


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    ^ Duschek S, Schandry R (2007). "Reduced brain perfusion and cognitive performance due to constitutional hypotension". Clinical Autonomic Research. 17 (2): 69–76. doi:10.1007/s10286-006-0379-7. PMC 1858602. PMID 17106628.
    


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    ^ Downie A. 2001. "Tutorial: CT in Head Trauma" Archived 2005-11-06 at the Wayback Machine. Accessed January 4, 2007.
    


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19. 
    ^ ^abcd Head Trauma at eMedicine
    


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    ^ Trauma.org 2000. "TRAUMA.ORG: Neurotrauma: Control of Intracranial Hypertension" Trauma.org. Accessed March 18, 2009.
    


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    ^ 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.
    


22. 
    ^ Sahuquillo J, Arikan F (2006). Sahuquillo, Juan, ed. "Decompressive craniectomy for the treatment of refractory high intracranial pressure in traumatic brain injury". Cochrane Database Syst Rev (1): CD003983. doi:10.1002/14651858.CD003983.pub2. PMID 16437469.
    


23. 
    ^ 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.
    

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)

v t e Physiology of the nervous system
Primarily CNS	Arousal Wakefulness Intracranial pressure Lateralization of brain function Sleep Memory
Primarily PNS	Reflex Sensation
Both	Evoked potential Bereitschaftspotential P300 Auditory evoked potential Somatosensory evoked potentials Visual evoked potential Other short term Neurotransmission Chronaxie Membrane potential Action potential Postsynaptic potential Excitatory Inhibitory Long term Axoplasmic transport Neuroregeneration/Nerve regeneration Neuroplasticity/Synaptic plasticity Long-term potentiation Long-term depression Other Myelinogenesis

v t e Diseases of the nervous system, primarily CNS (G04–G47, 323–349)
Inflammation	Brain Encephalitis Viral encephalitis Herpesviral encephalitis Limbic encephalitis Encephalitis lethargica Cavernous sinus thrombosis Brain abscess Amoebic Spinal cord Myelitis: Poliomyelitis Demyelinating disease Transverse myelitis Tropical spastic paraparesis Epidural abscess Both/either Encephalomyelitis Acute disseminated Myalgic Meningoencephalitis
Brain/ encephalopathy	Degenerative Extrapyramidal and movement disorders Basal ganglia disease Parkinsonism PD Postencephalitic NMS PKAN Tauopathy PSP Striatonigral degeneration Hemiballismus HD OA Dyskinesia Dystonia Status dystonicus Spasmodic torticollis Meige's Blepharospasm Athetosis Chorea Choreoathetosis Myoclonus Myoclonic epilepsy Akathisia Tremor Essential tremor Intention tremor Restless legs Stiff person Dementia Tauopathy Alzheimer's Early-onset Primary progressive aphasia Frontotemporal dementia/Frontotemporal lobar degeneration Pick's Dementia with Lewy bodies Posterior cortical atrophy Vascular dementia Mitochondrial disease Leigh disease Demyelinating autoimmune Multiple sclerosis Neuromyelitis optica Schilder's disease hereditary Adrenoleukodystrophy Alexander Canavan Krabbe ML PMD VWM MFC CAMFAK syndrome Central pontine myelinolysis Marchiafava–Bignami disease Alpers' disease Episodic/ paroxysmal Seizure/epilepsy Focal Generalised Status epilepticus Myoclonic epilepsy Headache Migraine Familial hemiplegic Cluster Tension Cerebrovascular TIA Amaurosis fugax Transient global amnesia Acute aphasia Stroke MCA ACA PCA Foville's Millard–Gubler Lateral medullary Medial medullary Weber's Lacunar stroke Sleep disorders Insomnia Hypersomnia Sleep apnea Obstructive Congenital central hypoventilation syndrome Narcolepsy Cataplexy Kleine–Levin Circadian rhythm sleep disorder Advanced sleep phase disorder Delayed sleep phase disorder Non-24-hour sleep–wake disorder Jet lag CSF Intracranial hypertension Hydrocephalus/NPH Choroid plexus papilloma Idiopathic intracranial hypertension Cerebral edema Intracranial hypotension Other Brain herniation Reye's Hepatic encephalopathy Toxic encephalopathy Hashimoto's encephalopathy
Spinal cord/ myelopathy	Syringomyelia Syringobulbia Morvan's syndrome Vascular myelopathy Foix–Alajouanine syndrome Spinal cord compression
Both/either	Degenerative SA Friedreich's ataxia Ataxia-telangiectasia MND UMN only: Primary lateral sclerosis Pseudobulbar palsy Hereditary spastic paraplegia LMN only: Distal hereditary motor neuronopathies Spinal muscular atrophies SMA SMAX1 SMAX2 DSMA1 Congenital DSMA SMA-PCH SMA-LED SMA-PME Progressive muscular atrophy Progressive bulbar palsy Fazio–Londe Infantile progressive bulbar palsy both: Amyotrophic lateral sclerosis

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