Intracranial pressure: Difference between revisions

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==Overview==
==Overview==


'''Intracranial pressure''', ('''ICP'''), is the pressure in the [[cranium]] and thus in the [[brain]] tissue and [[cerebrospinal fluid]] (CSF); this pressure is exerted on the brain's intracranial [[blood]] circulation vessels. ICP is maintained in a tight normal range dynamically, through the production and absorption of CSF. Because the entire system is contained by bone and strong ligamentous connections, the pressures of the body, such as those caused by straining, exercise, and coughing, do not affect the brain or its environment. ICP is measured in millimeters of mercury ([[mmHg]]) and, at rest, is normally 7–15 mmHg for a [[Supine position|supine]] adult, and becomes negative (averaging &minus;10&nbsp;mmHg) in the vertical position.<ref name="Steiner">{{cite journal | author=Steiner LA, Andrews PJ | title=Monitoring the injured brain: ICP and CBF | journal=British Journal of Anaesthesia | volume=97 | issue=1 | year=2006 | pages=26–38 |url=http://bja.oxfordjournals.org/cgi/content/full/97/1/26 | pmid=16698860  | doi=10.1093/bja/ael110}}</ref> Changes in ICP are attributed to volume changes in one or more of the constituents contained in the cranium.
'''Intracranial pressure''', ('''ICP'''), is the pressure exerted by  three structures inside the [[Cranium (anatomy)|cranium]]; brain parenchyma, CSF and blood. The norma ICP is 10-15 mmHg and is usually maintained by equilibrium of the intracranial contents. '''Intracranial hypertension (''' '''IH)''', is elevation of the pressure in the [[cranium]]. It typically occurs when the ICP is >20 mmHg. Hans Queckenstedt's was the first person to use [[lumbar]] needle for ICP monitoring. Intracranial [[hypertension]] is generally categorized as acute or chronic. The Monro-Kellie hypothesis explains the relationship between the contents of the [[cranium]] and intracranial pressure. It explains the underlying pathophysiology  of elevated intracranial pressure or intracranial hypertension. Several pathophysiologic mechanisms are thought to be involved in the pathogenesis of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH). All mechanisms eventually lead to brain injury from [[brain stem]] compression and decreased cerebral blood supply or ischemia. Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) must be differentiated from other diseases that cause [[headache]], nausea, [[vomiting]] and neurologic deficits such as [[tumor]], [[abscess]] or [[space occupying lesion]], [[Cerebral venous sinus thrombosis|venous sinus thrombosis]],  neck surgery, [[Obstructive hydrocephalus]], [[meningitis]], [[subarachnoid hemorrhage]], [[choroid plexus papilloma]], and [[Malignant hypertension|Malignant systemic hypertension]]. The diagnosis of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) is made when ICP is >20 mmHg. [[CT scan]] or [[MRI]] may be considered initial diagnostic investigations.  Intracranial hypertension is considered to be emergency condition.  Treatment includes resuscitative measures and specific directed therapy.  Resuscitative measures include oxygen, blood pressure and ICP monitoring, [[osmotic diuresis]], head elevation up to 30 degrees, [[therapeutic hypothermia]] and [[seizure]] prophylaxis.    


'''Intracranial hypertension''', commonly abbreviated '''IH''', is elevation of the pressure in the [[cranium]]. ICP is normally 0–10&nbsp;mm Hg; at 20–25&nbsp;mm Hg, the upper limit of normal, treatment to reduce ICP is needed.<ref name="Ghajar00">
==Historical Perspective==
{{
 
cite journal |author=Ghajar J |title=Traumatic brain injury |journal=Lancet |volume=356 |issue=9233 |pages=923–9 |year=2000 |month=September |pmid=11036909 |doi=10.1016/S0140-6736(00)02689-1
*In 1950s, [[therapeutic hypothermia]] (goal core temperature of 32-34C) was first introduced as a treatment for brain injury. <ref name="pmid7373397">{{cite journal |vauthors=Welch K |title=The intracranial pressure in infants |journal=J. Neurosurg. |volume=52 |issue=5 |pages=693–9 |date=May 1980 |pmid=7373397 |doi=10.3171/jns.1980.52.5.0693 |url=}}</ref>
}}
*In early 1800s, the Monro-Kellie hypothesis and the [[CSF]] physiology was first introduced by Alexander Monro and George Kellie.
</ref>  
*Hans Queckenstedt's was the first person to use lumbar needle for ICP monitoring.
 
==Classification==
 
*Elevated intracranial pressure or Intracranial hypertension may be classified into two subtypes/groups:
 
:*[[Acute]]
:*Chronic
 
*Intracranial hypertension may also be classified as various stages:
**Stage 1: Minimal increases in ICP due to compensatory mechanisms
**Stage 2:
***Any change in volume greater than 100–120 mL
***Exhaustion of compensatory mechanisms
***Compromise of [[neuronal]] oxygenation and systemic arteriolar vasoconstriction to increase MAP and CP
**Stage 3:
***Sustained increased ICP
***Dramatic changes in ICP with small changes in volume
***The ICP approaches the MAP
 
'''Intracranial pressure''', ('''ICP'''), is the pressure exerted by three structures inside the cranium; brain parenchyma, CSF and blood. The norma ICP is 10-15 mmHg and is usually maintained by equilibrium of the intracranial contents.
 
'''Intracranial hypertension (''' '''IH)''', is elevation of the pressure in the [[cranium]]. It typically occurs when the ICP is >20 mmHg.
 
==Pathophysiology==
====Intracranial components and their proportions:====
 
*Brain [[parenchyma]] volume: 1400 ml (80%)<ref name="pmid19472865">{{cite journal |vauthors=Whedon JM, Glassey D |title=Cerebrospinal fluid stasis and its clinical significance |journal=Altern Ther Health Med |volume=15 |issue=3 |pages=54–60 |date=2009 |pmid=19472865 |pmc=2842089 |doi= |url=}}</ref>
*[[CSF]] volume: 10 ml (10%)
*Blood volume: 10 ml (10%)
 
====The Monro-Kellie Hypothesis:====
 
*The Monro-Kellie hypothesis explains the relationship between the contents of the [[cranium]] and intracranial pressure. It explains the underlying pathophysiology  of elevated intracranial pressure or intracranial hypertension.
*In normal physiological state, intracranial contents (the brain tissue, the blood, and the [[cerebrospinal fluid]]) maintain an equilibrium state and keep the ICP within normal range by acting as compensatory mechanisms for small volume changes.<ref name="pmid7452330">{{cite journal |vauthors=Bruce DA, Alavi A, Bilaniuk L, Dolinskas C, Obrist W, Uzzell B |title=Diffuse cerebral swelling following head injuries in children: the syndrome of "malignant brain edema" |journal=J. Neurosurg. |volume=54 |issue=2 |pages=170–8 |date=February 1981 |pmid=7452330 |doi=10.3171/jns.1981.54.2.0170 |url=}}</ref>
*Compensatory mechanisms are being exhausted by large volume changes, eventually causing significantly elevated intracranial pressures and potential [[herniation]].<ref name="pmid1738026">{{cite journal |vauthors=Aldrich EF, Eisenberg HM, Saydjari C, Luerssen TG, Foulkes MA, Jane JA, Marshall LF, Marmarou A, Young HF |title=Diffuse brain swelling in severely head-injured children. A report from the NIH Traumatic Coma Data Bank |journal=J. Neurosurg. |volume=76 |issue=3 |pages=450–4 |date=March 1992 |pmid=1738026 |doi=10.3171/jns.1992.76.3.0450 |url=}}</ref>
 
====Intracranial compliance:====
 
*There is an inverse relationship between  intracranial components and the compliance.
*Generally the normal compliance is maintained by compensatory mechanisms such as
**Increased [[CSF]] reabsorption via thecal sac
**Increased venoconstriction to decrease cerebral venous flow
**Decreased cerebral venous flow via increased  extracranial drainage


==The Monro-Kellie Hypothesis==
====Cerebral Blood Flow (Ohm's Law):====


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.<ref>{{cite book | author=Monro A | title=Observations on the structure and function of the nervous system | location=Edinburgh | publisher=Creech & Johnson | year=1783}}</ref><ref>{{cite journal | author=Kelly G | title=Appearances observed in the dissection of two individuals; death from cold and congestion of the brain | journal=Trans Med Chir Sci Edinb | year=1824 | volume=1 | pages=84–169}}</ref><ref name=Mokri>{{cite journal |author=Mokri B |title=The Monro-Kellie hypothesis: applications in CSF volume depletion |journal=Neurology |volume=56 |issue=12 |pages=1746–8 |year=2001 |month=June |pmid=11425944 |doi= |url=http://www.neurology.org/cgi/content/full/56/12/1746}}</ref>
*Cerebral blood flow is generally assessed by subtracting jugular venous pressure from carotid arterial pressure and dividing by cerebrovascular resistance, as follows:<ref name="pmid2757806">{{cite journal |vauthors=Strandgaard S, Paulson OB |title=Cerebral blood flow and its pathophysiology in hypertension |journal=Am. J. Hypertens. |volume=2 |issue=6 Pt 1 |pages=486–92 |date=June 1989 |pmid=2757806 |doi=10.1093/ajh/2.6.486 |url=}}</ref><ref name="pmid6516910">{{cite journal |vauthors=Strandgaard S, Andersen GS, Ahlgreen P, Nielsen PE |title=Visual disturbances and occipital brain infarct following acute, transient hypotension in hypertensive patients |journal=Acta Med Scand |volume=216 |issue=4 |pages=417–22 |date=1984 |pmid=6516910 |doi= |url=}}</ref><ref name="pmid641549">{{cite journal |vauthors=Enevoldsen EM, Jensen FT |title=Autoregulation and CO2 responses of cerebral blood flow in patients with acute severe head injury |journal=J. Neurosurg. |volume=48 |issue=5 |pages=689–703 |date=May 1978 |pmid=641549 |doi=10.3171/jns.1978.48.5.0689 |url=}}</ref>
**CBF = (CAP - JVP) ÷ CVR
**Cerebral perfusion is assessed by cerebral perfusion pressure (CPP). CPP is calculated by subtracting ICP from mean arterial pressure, as follows:
**CPP = MAP - ICP<ref name="pmid4640619">{{cite journal |vauthors=Lassen NA, Agnoli A |title=The upper limit of autoregulation of cerebral blood flow--on the pathogenesis of hypertensive encepholopathy |journal=Scand. J. Clin. Lab. Invest. |volume=30 |issue=2 |pages=113–6 |date=October 1972 |pmid=4640619 |doi=10.3109/00365517209081099 |url=}}</ref>
**In normal physiological states, ICP  and CPP is maintained by [[autoregulation]].<ref name="pmid1738026">{{cite journal |vauthors=Aldrich EF, Eisenberg HM, Saydjari C, Luerssen TG, Foulkes MA, Jane JA, Marshall LF, Marmarou A, Young HF |title=Diffuse brain swelling in severely head-injured children. A report from the NIH Traumatic Coma Data Bank |journal=J. Neurosurg. |volume=76 |issue=3 |pages=450–4 |date=March 1992 |pmid=1738026 |doi=10.3171/jns.1992.76.3.0450 |url=}}</ref>


The Monro-Kellie hypothesis states that the cranial compartment is incompressible, and the volume inside the cranium is a fixed 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.<ref name=Mokri/>
Several pathophysiologic mechanisms are thought to be involved in the pathogenesis of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH). All mechanisms eventually lead to brain injury from brain stem compression and decreased cerebral blood supply or ischemia. These mechanisms are as follows:


The principal buffers for increased volumes include both 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.<ref name=Mokri/>  These compensatory mechanisms are able to maintain a normal ICP for any change in volume less than approximately 100–120 mL.
**'''Mass effect'''
***It can occur secondary to [[brain tumor]], contusions, subdural or epidural [[hematoma]], or [[abscess]]<ref name="pmid1407426">{{cite journal |vauthors=Levin HS, Aldrich EF, Saydjari C, Eisenberg HM, Foulkes MA, Bellefleur M, Luerssen TG, Jane JA, Marmarou A, Marshall LF |title=Severe head injury in children: experience of the Traumatic Coma Data Bank |journal=Neurosurgery |volume=31 |issue=3 |pages=435–43; discussion 443–4 |date=September 1992 |pmid=1407426 |doi=10.1227/00006123-199209000-00008 |url=}}</ref>
**'''Cerebral edema or Generalized brain swelling'''
***It can occur secondary to ischemic-anoxia states, [[hypertensive encephalopathy]], [[pseudotumor cerebri]], and hypercarbia.
***These conditions tend to decrease the cerebral perfusion pressure but with minimal tissue shifts.
**'''Increase in venous pressure'''
***Secondary to [[venous sinus thrombosis]], heart failure, neck surgery or obstruction of superior mediastinal or jugular veins.
**'''Obstruction to CSF flow'''  
***Secondary to [[hydrocephalus]], extensive meningeal disease (e.g., infectious, carcinomatous, granulomatous, or hemorrhagic), or obstruction in cerebral convexities and superior sagittal sinus (decreased absorption).
**'''Increased CSF production'''
***[[Meningitis]], subarachnoid hemorrhage, or choroid plexus tumor.
**Increased cerebral blood flow (CBF)
***Increased CBF is generally seen in conditions associated with hypercapnia and hypoxia
**'''Drugs'''
***[[Albendazole]], [[Ciprofloxacin]]
**Idiopathic
***[[Pseudotumor cerebri]]


==Increased ICP==
<br />
One of the most damaging aspects of [[brain trauma]] and other conditions, directly correlated with poor outcome, is an elevated intracranial pressure.<ref name="orlando">Orlando Regional Healthcare, Education and Development. 2004. [http://www.manimalia.org/docs/TBI.pdf "Overview of Adult Traumatic Brain Injuries."] Accessed September 6, 2007.</ref>  ICP is very likely to cause severe harm if it rises beyond 40 mmHg in an adult.<ref name="Dawodu">Dawodu S. 2005. [http://www.emedicine.com/pmr/topic212.htm "Traumatic Brain Injury: Definition, Epidemiology, Pathophysiology"] Emedicine.com.Accessed January 4, 2007. </ref>  Even intracranial pressures between 25 and 30 mm Hg are usually fatal if prolonged, except in children, who can tolerate higher pressures for longer periods.<ref name="tolias">Tolias C and Sgouros S. 2006. [http://www.emedicine.com/med/topic3216.htm "Initial Evaluation and Management of CNS Injury."] Emedicine.com. Accessed January 4, 2007.</ref>  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 the brain to [[brain herniation|herniate]], and restrict blood supply to the brain, leading to an [[ischemic cascade]].<ref name="graham">Graham DI and Gennareli TA. Chapter 5, "Pathology of Brain Damage After Head Injury" In, Cooper P and Golfinos G. 2000. ''Head Injury'', 4th Ed. Morgan Hill, New York.</ref>


==Causes==
==Causes==
===Common Causes===
===Common Causes===
*[[Aneurysm ]]
*[[Aneurysm ]]
*[[Arnold-chiari malformation]]
*[[Arnold-chiari malformation]]
Line 80: Line 144:
*[[Venous sinus thrombosis]]
*[[Venous sinus thrombosis]]


===Causes by Organ System===
==Differential Diagnosis of Increased Intracranial Pressure (ICP)==
{|style="width:80%; height:100px" border="1"
*Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) must be differentiated from other diseases that cause headache, nausea, vomiting and neurologic deficits such as tumor, abscess or space occupying lesion,  [[Cerebral venous sinus thrombosis|venous sinus thrombosis]],  neck surgery, [[Obstructive hydrocephalus]], [[meningitis]], [[subarachnoid hemorrhage]], [[choroid plexus papilloma]], and [[Malignant hypertension|Malignant systemic hypertension]].
|style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" |'''Cardiovascular'''
=== Differentiating Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) from Other Diseases on the Basis of Seizure, Visual disturbance, and Constitutional Symptoms ===
|style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | [[Aneurysm ]], [[Cerebral venous sinus thrombosis]], [[Dural arteriovenous fistula]], [[Epidural haemorrhage]], [[Epidural hematoma]], [[Heart failure]], [[Hypertension]], [[Hypertensive brain hemorrhage]], [[Hypertensive encephalopathy]], [[Infarction with edema]], [[Intracranial haemorrhage]], [[Intraventricular hemorrhage]], [[Obstruction of superior mediastinal veins]], [[Obstruction of jugular veins]], [[Stroke]], [[Vasculitis]], [[Venous sinus thrombosis]]
On the basis of [[seizure]], [[visual disturbance]], and constitutional symptoms, meningioma must be differentiated from [[oligodendroglioma]], astrocytoma, [[hemangioblastoma]], [[pituitary adenoma]], [[schwannoma]], [[Primary central nervous system lymphoma|primary CNS lymphoma]], [[medulloblastoma]], [[ependymoma]], [[craniopharyngioma]], [[pinealoma]], [[Arteriovenous malformation|AV malformation]], [[brain aneurysm]], [[bacterial]] [[brain]] [[abscess]], [[tuberculosis]], [[toxoplasmosis]], [[hydatid cyst]], [[CNS]] [[cryptococcosis]], [[CNS]] [[aspergillosis]], and [[brain metastasis]].
{|
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
! rowspan="4" |Diseases
| colspan="5" rowspan="1" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Clinical manifestations'''
! colspan="3" rowspan="2" |Para-clinical findings
| colspan="1" rowspan="4" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Gold<br>standard'''
! rowspan="4" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Additional findings
|-
|-
|bgcolor="LightSteelBlue"| '''Chemical/Poisoning'''
| colspan="4" rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Symptoms'''
|bgcolor="Beige"| [[Lead]], [[Vitamin a]]
! rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Physical examination
|-
|-
|-bgcolor="LightSteelBlue"
! rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Lab Findings
| '''Dental'''
! rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |MRI
|bgcolor="Beige"| No underlying causes
! rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Immunohistopathology
|-
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Head-<br>ache
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Seizure
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Visual disturbance
! colspan="1" rowspan="1" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Constitutional
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Focal neurological deficit
|-
|-
|-bgcolor="LightSteelBlue"
! colspan="11" style="background: #7d7d7d; color: #FFFFFF; padding: 5px; text-align: center;" |Adult primary brain tumors
| '''Dermatologic'''
|bgcolor="Beige"| No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Meningioma]]<br><ref name="pmid1642904">{{cite journal |vauthors=Zee CS, Chin T, Segall HD, Destian S, Ahmadi J |title=Magnetic resonance imaging of meningiomas |journal=Semin. Ultrasound CT MR |volume=13 |issue=3 |pages=154–69 |date=June 1992 |pmid=1642904 |doi= |url=}}</ref><ref name="pmid25744347">{{cite journal |vauthors=Shibuya M |title=Pathology and molecular genetics of meningioma: recent advances |journal=Neurol. Med. Chir. (Tokyo) |volume=55 |issue=1 |pages=14–27 |date=2015 |pmid=25744347 |doi=10.2176/nmc.ra.2014-0233 |url=}}</ref><ref name="pmid17509660">{{cite journal |vauthors=Begnami MD, Palau M, Rushing EJ, Santi M, Quezado M |title=Evaluation of NF2 gene deletion in sporadic schwannomas, meningiomas, and ependymomas by chromogenic in situ hybridization |journal=Hum. Pathol. |volume=38 |issue=9 |pages=1345–50 |date=September 2007 |pmid=17509660 |pmc=2094208 |doi=10.1016/j.humpath.2007.01.027 |url=}}</ref>
| '''Drug Side Effect'''
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
|bgcolor="Beige"| [[Accutane]],  [[Albendazole ]],  [[Ciprofloxacin]], [[Claravis]],  [[Isotretinoin]],  [[Minocycline]],  [[Sotret]]
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* Well circumscribed
* Extra-axial [[mass]]
 
* [[Meninges|Dural]] attachment
* [[CSF]] [[vascular]] cleft sign
* Sunburst appearance of the [[Vessel|vessels]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Arachnoid]] origin
 
* [[Psammoma body|Psammoma bodies]]
 
* Whorled spindle cell pattern
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Highest [[incidence]] is between 40 and 50 years of age.
* Most of the time, focal [[neurological]] deficit and [[epileptic seizure]] are the presenting [[signs]].
 
* May be associated with [[Neurofibromatosis type II|NF-2]]
|-
|-
|-bgcolor="LightSteelBlue"
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Glioblastoma multiforme]]<br><ref name="pmid17964028">{{cite journal |vauthors=Sathornsumetee S, Rich JN, Reardon DA |title=Diagnosis and treatment of high-grade astrocytoma |journal=Neurol Clin |volume=25 |issue=4 |pages=1111–39, x |date=November 2007 |pmid=17964028 |doi=10.1016/j.ncl.2007.07.004 |url=}}</ref><ref name="pmid22819718">{{cite journal |vauthors=Pedersen CL, Romner B |title=Current treatment of low grade astrocytoma: a review |journal=Clin Neurol Neurosurg |volume=115 |issue=1 |pages=1–8 |date=January 2013 |pmid=22819718 |doi=10.1016/j.clineuro.2012.07.002 |url=}}</ref><ref name=":0">{{cite book | last = Mattle | first = Heinrich | title = Fundamentals of neurology : an illustrated guide | publisher = Thieme | location = Stuttgart New York | year = 2017 | isbn = 9783131364524 }}</ref>
| '''Ear Nose Throat'''
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
|bgcolor="Beige"| No underlying causes
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" |−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" |−
| style="background: #F5F5F5; padding: 5px;" |
* [[Supratentorial]]
* Irregular ring-nodular enhancing lesions
* Central [[necrosis]]
* Surrounding [[vasogenic edema]]
 
* Cross [[corpus callosum]] ([[butterfly glioma]])
| style="background: #F5F5F5; padding: 5px;" |
* [[Astrocyte]] origin
 
* [[Pleomorphism|Pleomorphic]] cell
 
* Pseudopalisading appearance
 
* [[GFAP]] +
 
* [[Necrosis]] +
 
* [[Hemorrhage]] +
 
* [[Vascular]] prolifration +
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Highest [[incidence]] in fifth and sixth decades of life
* Most of the time, focal [[neurological]] deficit is the presenting [[Sign (medical)|sign]].
|-
|-
|-bgcolor="LightSteelBlue"
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Oligodendroglioma]]<br><ref name="pmid26849038">{{cite journal |vauthors=Smits M |title=Imaging of oligodendroglioma |journal=Br J Radiol |volume=89 |issue=1060 |pages=20150857 |date=2016 |pmid=26849038 |pmc=4846213 |doi=10.1259/bjr.20150857 |url=}}</ref><ref name="pmid25943885">{{cite journal |vauthors=Wesseling P, van den Bent M, Perry A |title=Oligodendroglioma: pathology, molecular mechanisms and markers |journal=Acta Neuropathol. |volume=129 |issue=6 |pages=809–27 |date=June 2015 |pmid=25943885 |pmc=4436696 |doi=10.1007/s00401-015-1424-1 |url=}}</ref><ref name="pmid26478444">{{cite journal |vauthors=Kerkhof M, Benit C, Duran-Pena A, Vecht CJ |title=Seizures in oligodendroglial tumors |journal=CNS Oncol |volume=4 |issue=5 |pages=347–56 |date=2015 |pmid=26478444 |pmc=6082346 |doi=10.2217/cns.15.29 |url=}}</ref>
| '''Endocrine'''
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
|bgcolor="Beige"| [[Hyperthyroidism]],  [[Hypoparathyroidism]],  [[Hypothyroidism]], [[Insulin like growth factor 1]],  [[Pineal tumour]]
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* Almost always in [[Cerebral hemisphere|cerebral hemisphers]] ([[Frontal lobe|frontal lobes]])
 
* Hypointense on T1
* Hyperintense on T2
* [[Calcification]]
 
* Chicken wire capillary pattern
| style="background: #F5F5F5; padding: 5px;" |
* [[Oligodendrocyte]] origin
 
* [[Calcification]] +
 
* Fried egg cell appearance
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Highest [[incidence]] is between 40 and 50 years of age.
* Most of the time, [[epileptic seizure]] is the presenting [[Sign (medicine)|sign]].
|-
|-
|-bgcolor="LightSteelBlue"
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Hemangioblastoma]]<br><ref name="pmid24579662">{{cite journal |vauthors=Lonser RR, Butman JA, Huntoon K, Asthagiri AR, Wu T, Bakhtian KD, Chew EY, Zhuang Z, Linehan WM, Oldfield EH |title=Prospective natural history study of central nervous system hemangioblastomas in von Hippel-Lindau disease |journal=J. Neurosurg. |volume=120 |issue=5 |pages=1055–62 |date=May 2014 |pmid=24579662 |pmc=4762041 |doi=10.3171/2014.1.JNS131431 |url=}}</ref><ref name="pmid17877533">{{cite journal |vauthors=Hussein MR |title=Central nervous system capillary haemangioblastoma: the pathologist's viewpoint |journal=Int J Exp Pathol |volume=88 |issue=5 |pages=311–24 |date=October 2007 |pmid=17877533 |pmc=2517334 |doi=10.1111/j.1365-2613.2007.00535.x |url=}}</ref><ref name="pmid2704812">{{cite journal |vauthors=Lee SR, Sanches J, Mark AS, Dillon WP, Norman D, Newton TH |title=Posterior fossa hemangioblastomas: MR imaging |journal=Radiology |volume=171 |issue=2 |pages=463–8 |date=May 1989 |pmid=2704812 |doi=10.1148/radiology.171.2.2704812 |url=}}</ref><ref name="pmid945331">{{cite journal |vauthors=Perks WH, Cross JN, Sivapragasam S, Johnson P |title=Supratentorial haemangioblastoma with polycythaemia |journal=J. Neurol. Neurosurg. Psychiatry |volume=39 |issue=3 |pages=218–20 |date=March 1976 |pmid=945331 |doi= |url=}}</ref>
| '''Environmental'''
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
|bgcolor="Beige"| No underlying causes
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* [[Infratentorial]]
 
* [[Cyst|Cystic]] lesion with a solid enhancing mural [[nodule]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Blood vessel]] origin
 
* [[Capillary|Capillaries]] with thin walls
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Might secret [[erythropoietin]] and cause [[polycythemia]]
* May be associated with [[Von Hippel-Lindau Disease|von hippel-lindau syndrome]]
|-
|-
|-bgcolor="LightSteelBlue"
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Pituitary adenoma]]<br><ref name="pmid3786729">{{cite journal |vauthors=Kucharczyk W, Davis DO, Kelly WM, Sze G, Norman D, Newton TH |title=Pituitary adenomas: high-resolution MR imaging at 1.5 T |journal=Radiology |volume=161 |issue=3 |pages=761–5 |date=December 1986 |pmid=3786729 |doi=10.1148/radiology.161.3.3786729 |url=}}</ref><ref name="pmid22584705">{{cite journal |vauthors=Syro LV, Scheithauer BW, Kovacs K, Toledo RA, Londoño FJ, Ortiz LD, Rotondo F, Horvath E, Uribe H |title=Pituitary tumors in patients with MEN1 syndrome |journal=Clinics (Sao Paulo) |volume=67 Suppl 1 |issue= |pages=43–8 |date=2012 |pmid=22584705 |pmc=3328811 |doi= |url=}}</ref><ref name=":0" />
| '''Gastroenterologic'''
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
|bgcolor="Beige"| [[Acute liver failure]],  [[Hepatic failure]]
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | + [[Bitemporal hemianopia]]
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* [[Endocrine]] abnormalities as a result of [[Pituitary adenoma|functional adenomas]] or pressure effect of non-functional [[Adenoma|adenomas]]
| style="background: #F5F5F5; padding: 5px;" |
* Isointense to normal [[pituitary gland]] in T1
| style="background: #F5F5F5; padding: 5px;" |
* [[Endocrine]] cell [[hyperplasia]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* It is associated with [[MEN1]] disease.
 
* Initialy presents with upper bitemporal quadrantanopsia followed by [[Bitemporal hemianopia|bitemporal hemianopsia]] (pressure on [[Optic chiasm|optic chiasma]] from below)
 
*
 
*
|-
|-
|-bgcolor="LightSteelBlue"
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Schwannoma]]<br><ref name="DonnellyDaly2007">{{cite journal|last1=Donnelly|first1=Martin J.|last2=Daly|first2=Carmel A.|last3=Briggs|first3=Robert J. S.|title=MR imaging features of an intracochlear acoustic schwannoma|journal=The Journal of Laryngology & Otology|volume=108|issue=12|year=2007|issn=0022-2151|doi=10.1017/S0022215100129056}}</ref><ref name="pmid9639114">{{cite journal |vauthors=Feany MB, Anthony DC, Fletcher CD |title=Nerve sheath tumours with hybrid features of neurofibroma and schwannoma: a conceptual challenge |journal=Histopathology |volume=32 |issue=5 |pages=405–10 |date=May 1998 |pmid=9639114 |doi= |url=}}</ref><ref name="pmid28710469">{{cite journal |vauthors=Chen H, Xue L, Wang H, Wang Z, Wu H |title=Differential NF2 Gene Status in Sporadic Vestibular Schwannomas and its Prognostic Impact on Tumour Growth Patterns |journal=Sci Rep |volume=7 |issue=1 |pages=5470 |date=July 2017 |pmid=28710469 |doi=10.1038/s41598-017-05769-0 |url=}}</ref><ref name="HardellHansson Mild2003">{{cite journal|last1=Hardell|first1=Lennart|last2=Hansson Mild|first2=Kjell|last3=Sandström|first3=Monica|last4=Carlberg|first4=Michael|last5=Hallquist|first5=Arne|last6=Påhlson|first6=Anneli|title=Vestibular Schwannoma, Tinnitus and Cellular Telephones|journal=Neuroepidemiology|volume=22|issue=2|year=2003|pages=124–129|issn=0251-5350|doi=10.1159/000068745}}</ref>
| '''Genetic'''
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
|bgcolor="Beige"| No underlying causes
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* Split-fat sign
* Fascicular sign
* Often have areas of [[hemosiderin]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Schwann cell]] origin
 
* S100+
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* It causes [[hearing loss]] and [[tinnitus]]
 
* May be associated with [[Neurofibromatosis type II|NF-2]] (bilateral [[Schwannoma|schwannomas]])
|-
|-
|-bgcolor="LightSteelBlue"
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Primary central nervous system lymphoma|Primary CNS lymphoma]]<br><ref name="pmid7480733">{{cite journal |vauthors=Chinn RJ, Wilkinson ID, Hall-Craggs MA, Paley MN, Miller RF, Kendall BE, Newman SP, Harrison MJ |title=Toxoplasmosis and primary central nervous system lymphoma in HIV infection: diagnosis with MR spectroscopy |journal=Radiology |volume=197 |issue=3 |pages=649–54 |date=December 1995 |pmid=7480733 |doi=10.1148/radiology.197.3.7480733 |url=}}</ref><ref name="Paulus19992">{{cite journal|last1=Paulus|first1=Werner|journal=Journal of Neuro-Oncology|title=Classification, Pathogenesis and Molecular Pathology of Primary CNS Lymphomas|volume=43|issue=3|year=1999|pages=203–208|issn=0167594X|doi=10.1023/A:1006242116122}}</ref>
| '''Hematologic'''
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
|bgcolor="Beige"| [[Aschemic-anoxia states]],  [[Behçet's disease]],  [[Erdheim-chester disease]],  [[Hypercarbia]],  [[Hypoxemia]],  [[Iron deficiency]],  [[Multiple hamartoma syndrome]],  [[Polycythaemia vera]],  [[Subarachnoid haemorrhage]],  [[Subdural haemorrhage]],  [[Subdural hematoma]]
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* Usually deep in the [[white matter]]
 
* Single [[mass]] with ring enhancement
| style="background: #F5F5F5; padding: 5px;" |
* [[B cell]] origin
 
* Similar to [[Non-Hodgkin lymphoma|non hodgkin lymphoma]] ([[Diffuse large B cell lymphoma|diffuse large B cell]])
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Usually in young [[immunocompromised]] patients ([[HIV]]) or old [[immunocompetent]] person.
 
*
|-
|-
|-bgcolor="LightSteelBlue"
! colspan="11" style="background: #7d7d7d; color: #FFFFFF; padding: 5px; text-align: center;" |Childhood primary brain tumors
| '''Iatrogenic'''
|bgcolor="Beige"| No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Pilocytic astrocytoma]]<br><ref name="pmid179640282">{{cite journal |vauthors=Sathornsumetee S, Rich JN, Reardon DA |title=Diagnosis and treatment of high-grade astrocytoma |journal=Neurol Clin |volume=25 |issue=4 |pages=1111–39, x |date=November 2007 |pmid=17964028 |doi=10.1016/j.ncl.2007.07.004 |url=}}</ref><ref name="pmid228197182">{{cite journal |vauthors=Pedersen CL, Romner B |title=Current treatment of low grade astrocytoma: a review |journal=Clin Neurol Neurosurg |volume=115 |issue=1 |pages=1–8 |date=January 2013 |pmid=22819718 |doi=10.1016/j.clineuro.2012.07.002 |url=}}</ref><ref name=":02">{{cite book | last = Mattle | first = Heinrich | title = Fundamentals of neurology : an illustrated guide | publisher = Thieme | location = Stuttgart New York | year = 2017 | isbn = 9783131364524 }}</ref>
| '''Infectious Disease'''
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
|bgcolor="Beige"| [[Abscess]],  [[Intracranial abscess / granuloma]],  [[Intracranial granuloma]], [[Meningitis]],  [[Neurocysticercosis]]
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* [[Infratentorial]]
 
* Solid and [[Cyst|cystic]] component
* Mostly in [[posterior fossa]]
* Usually in [[Cerebellar hemisphere|cerebellar hemisphers]] and [[Cerebellar vermis|vermis]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Glial cell]] origin
*Solid and [[Cyst|cystic]] component
 
* [[GFAP]] +
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Most of the time, [[Cerebellum|cerebellar]] dysfunction is the presenting [[signs]].
|-
|-
|-bgcolor="LightSteelBlue"
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Medulloblastoma]]<br><ref name="DorwartWara1981">{{cite journal|last1=Dorwart|first1=R H|last2=Wara|first2=W M|last3=Norman|first3=D|last4=Levin|first4=V A|title=Complete myelographic evaluation of spinal metastases from medulloblastoma.|journal=Radiology|volume=139|issue=2|year=1981|pages=403–408|issn=0033-8419|doi=10.1148/radiology.139.2.7220886}}</ref><ref name="Fruehwald-PallamarPuchner2011">{{cite journal|last1=Fruehwald-Pallamar|first1=Julia|last2=Puchner|first2=Stefan B.|last3=Rossi|first3=Andrea|last4=Garre|first4=Maria L.|last5=Cama|first5=Armando|last6=Koelblinger|first6=Claus|last7=Osborn|first7=Anne G.|last8=Thurnher|first8=Majda M.|title=Magnetic resonance imaging spectrum of medulloblastoma|journal=Neuroradiology|volume=53|issue=6|year=2011|pages=387–396|issn=0028-3940|doi=10.1007/s00234-010-0829-8}}</ref><ref name="BurgerGrahmann1987">{{cite journal|last1=Burger|first1=P. C.|last2=Grahmann|first2=F. C.|last3=Bliestle|first3=A.|last4=Kleihues|first4=P.|title=Differentiation in the medulloblastoma|journal=Acta Neuropathologica|volume=73|issue=2|year=1987|pages=115–123|issn=0001-6322|doi=10.1007/BF00693776}}</ref>
| '''Musculoskeletal/Orthopedic'''
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
|bgcolor="Beige"| [[Craniosynostosis]],  [[Crouzon craniofacial dysostosis]],  [[Erdheim-chester disease]]
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* [[Infratentorial]]
 
* Mostly in [[cerebellum]]
 
* Non communicating [[hydrocephalus]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Neuroectoderm]] origin
 
* Homer wright rosettes
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Drop metastasis]] ([[metastasis]] through [[CSF]])
|-
|-
|-bgcolor="LightSteelBlue"
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Ependymoma]]<br><ref name="YuhBarkovich2009">{{cite journal|last1=Yuh|first1=E. L.|last2=Barkovich|first2=A. J.|last3=Gupta|first3=N.|title=Imaging of ependymomas: MRI and CT|journal=Child's Nervous System|volume=25|issue=10|year=2009|pages=1203–1213|issn=0256-7040|doi=10.1007/s00381-009-0878-7}}</ref><ref name=":0" />
| '''Neurologic'''
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
|bgcolor="Beige"| [[Aneurysm ]],  [[Arnold-chiari malformation]],  [[Aschemic-anoxia states]],  [[Brain tumor]],  [[Cerebral oedema]],  [[Cerebral venous sinus thrombosis]],  [[Choroid plexus tumor]],  [[Colloid cyst of third ventricle]],  [[Contusions]],  [[Craniosynostosis]],  [[Crouzon craniofacial dysostosis]],  [[Dandy-walker syndrome]],  [[Dural arteriovenous fistula]],  [[Encephalitis]],  [[Epidural haemorrhage]],  [[Epidural hematoma]],  [[Excess cerebrospinal fluid]],  [[Head trauma]],  [[Hydrocephalus ]],  [[Hypertensive brain hemorrhage]],  [[Hypertensive encephalopathy]],  [[Hypoxemia]],  [[Idiopathic intracranial hypertension]],  [[Infarction with edema]],  [[Intracranial abscess / granuloma]],  [[Intracranial granuloma]],  [[Intracranial haemorrhage]],  [[Intracranial space-occupying lesion]],  [[Intraventricular hemorrhage]],  [[Meningioma]],  [[Meningitis]],  [[Meningoencephalitis]],  [[Multiple hamartoma syndrome]],  [[Neurocysticercosis]],  [[Obstruction of superior mediastinal veins]],  [[Obstruction of jugular veins]],  [[Obstructive sleep apnea]],  [[Pseudotumor cerebri]],  [[Reye hepatocerebral syndrome]],  [[Status epilepticus]],  [[Subarachnoid haemorrhage]],  [[Subdural haemorrhage]],  [[Subdural hematoma]],  [[Sudanophilic cerebral sclerosis]], [[Venous sinus thrombosis]]
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* [[Infratentorial]]
 
* Usually found in [[Fourth ventricle|4th ventricle]]
* Mixed [[Cyst|cystic]]/solid [[lesion]]
 
* Hydrocephalus
| style="background: #F5F5F5; padding: 5px;" |
* [[Ependymal cell]] origin
 
* Peri[[vascular]] pseudorosette
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Causes an unusually persistent, continuous [[headache]] in children.
|-
|-
|-bgcolor="LightSteelBlue"
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Craniopharyngioma]]<br><ref name="pmid12407316">{{cite journal |vauthors=Brunel H, Raybaud C, Peretti-Viton P, Lena G, Girard N, Paz-Paredes A, Levrier O, Farnarier P, Manera L, Choux M |title=[Craniopharyngioma in children: MRI study of 43 cases] |language=French |journal=Neurochirurgie |volume=48 |issue=4 |pages=309–18 |date=September 2002 |pmid=12407316 |doi= |url=}}</ref><ref name="PrabhuBrown2005">{{cite journal|last1=Prabhu|first1=Vikram C.|last2=Brown|first2=Henry G.|title=The pathogenesis of craniopharyngiomas|journal=Child's Nervous System|volume=21|issue=8-9|year=2005|pages=622–627|issn=0256-7040|doi=10.1007/s00381-005-1190-9}}</ref><ref name="pmid766825">{{cite journal |vauthors=Kennedy HB, Smith RJ |title=Eye signs in craniopharyngioma |journal=Br J Ophthalmol |volume=59 |issue=12 |pages=689–95 |date=December 1975 |pmid=766825 |pmc=1017436 |doi= |url=}}</ref><ref name=":0" />
| '''Nutritional/Metabolic'''
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
|bgcolor="Beige"| [[Iron deficiency]]
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | + [[Bitemporal hemianopia]]
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px;" |
* [[Hypopituitarism]] as a result of pressure effect on [[pituitary gland]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Calcification]]
* Lobulated contour
* Motor-oil like fluid within [[tumor]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Ectoderm|Ectodermal]] origin ([[Rathke's pouch|Rathkes pouch]])
 
* [[Calcification]] +
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Initialy presents with lower bitemporal quadrantanopsia followed by [[Bitemporal hemianopia|bitemporal hemianopsia]] (pressure on [[Optic chiasm|optic chiasma]] from above)
|-
|-
|-bgcolor="LightSteelBlue"
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Pinealoma]]<br><ref name="pmid6625640">{{cite journal |vauthors=Ahmed SR, Shalet SM, Price DA, Pearson D |title=Human chorionic gonadotrophin secreting pineal germinoma and precocious puberty |journal=Arch. Dis. Child. |volume=58 |issue=9 |pages=743–5 |date=September 1983 |pmid=6625640 |doi= |url=}}</ref><ref name="Sano1976">{{cite journal|last1=Sano|first1=Keiji|title=Pinealoma in Children|journal=Pediatric Neurosurgery|volume=2|issue=1|year=1976|pages=67–72|issn=1016-2291|doi=10.1159/000119602}}</ref><ref name="Baggenstoss1939">{{cite journal|last1=Baggenstoss|first1=Archie H.|title=PINEALOMAS|journal=Archives of Neurology And Psychiatry|volume=41|issue=6|year=1939|pages=1187|issn=0096-6754|doi=10.1001/archneurpsyc.1939.02270180115011}}</ref>
| '''Obstetric/Gynecologic'''
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
|bgcolor="Beige"| No underlying causes
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | + vertical gaze palsy
| style="background: #F5F5F5; padding: 5px;" |
* B-hCG rise leads to [[precocious puberty]] in [[Male|males]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Hydrocephalus]] (compression of [[cerebral aqueduct]])
| style="background: #F5F5F5; padding: 5px;" |
* Similar to [[testicular seminoma]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* May cause prinaud syndrome ([[Vertical gaze center|vertical gaze]] palsy, pupillary light-near dissociation, lid retraction and convergence-retraction [[nystagmus]]
|-
|-
|-bgcolor="LightSteelBlue"
! colspan="11" style="background: #7d7d7d; color: #FFFFFF; padding: 5px; text-align: center;" |Vascular
| '''Oncologic'''
|bgcolor="Beige"| [[Brain tumor]],  [[Choroid plexus tumor]],  [[Colloid cyst of third ventricle]],  [[Meningioma]],  [[Pineal tumour]]
|-
|-
|-bgcolor="LightSteelBlue"
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Arteriovenous malformation|AV malformation]]<br><ref name="KucharczykLemme-Pleghos1985">{{cite journal|last1=Kucharczyk|first1=W|last2=Lemme-Pleghos|first2=L|last3=Uske|first3=A|last4=Brant-Zawadzki|first4=M|last5=Dooms|first5=G|last6=Norman|first6=D|title=Intracranial vascular malformations: MR and CT imaging.|journal=Radiology|volume=156|issue=2|year=1985|pages=383–389|issn=0033-8419|doi=10.1148/radiology.156.2.4011900}}</ref><ref name="FleetwoodSteinberg2002">{{cite journal|last1=Fleetwood|first1=Ian G|last2=Steinberg|first2=Gary K|title=Arteriovenous malformations|journal=The Lancet|volume=359|issue=9309|year=2002|pages=863–873|issn=01406736|doi=10.1016/S0140-6736(02)07946-1}}</ref><ref name=":0" />
| '''Ophthalmologic'''
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
|bgcolor="Beige"| No underlying causes
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* [[Supratentorial]]: ~85%
* Flow voids on T2 weighted images
| style="background: #F5F5F5; padding: 5px;" |
* We do not perform [[biopsy]] for [[AVM]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Angiography]]
| style="background: #F5F5F5; padding: 5px;" |
* We may see bag of worms appearance in [[CT angiography]]
|-
|-
|-bgcolor="LightSteelBlue"
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Brain aneurysm]]<br><ref name="ChapmanRubinstein1992">{{cite journal|last1=Chapman|first1=Arlene B.|last2=Rubinstein|first2=David|last3=Hughes|first3=Richard|last4=Stears|first4=John C.|last5=Earnest|first5=Michael P.|last6=Johnson|first6=Ann M.|last7=Gabow|first7=Patricia A.|last8=Kaehny|first8=William D.|title=Intracranial Aneurysms in Autosomal Dominant Polycystic Kidney Disease|journal=New England Journal of Medicine|volume=327|issue=13|year=1992|pages=916–920|issn=0028-4793|doi=10.1056/NEJM199209243271303}}</ref><ref name="pmid25632331">{{cite journal |vauthors=Castori M, Voermans NC |title=Neurological manifestations of Ehlers-Danlos syndrome(s): A review |journal=Iran J Neurol |volume=13 |issue=4 |pages=190–208 |date=October 2014 |pmid=25632331 |pmc=4300794 |doi= |url=}}</ref><ref name="SchievinkRaissi2010">{{cite journal|last1=Schievink|first1=W. I.|last2=Raissi|first2=S. S.|last3=Maya|first3=M. M.|last4=Velebir|first4=A.|title=Screening for intracranial aneurysms in patients with bicuspid aortic valve|journal=Neurology|volume=74|issue=18|year=2010|pages=1430–1433|issn=0028-3878|doi=10.1212/WNL.0b013e3181dc1acf}}</ref><ref name="pmid28486967">{{cite journal |vauthors=Germain DP |title=Pseudoxanthoma elasticum |journal=Orphanet J Rare Dis |volume=12 |issue=1 |pages=85 |date=May 2017 |pmid=28486967 |pmc=5424392 |doi=10.1186/s13023-017-0639-8 |url=}}</ref><ref name="pmid27162847">{{cite journal |vauthors=Farahmand M, Farahangiz S, Yadollahi M |title=Diagnostic Accuracy of Magnetic Resonance Angiography for Detection of Intracranial Aneurysms in Patients with Acute Subarachnoid Hemorrhage; A Comparison to Digital Subtraction Angiography |journal=Bull Emerg Trauma |volume=1 |issue=4 |pages=147–51 |date=October 2013 |pmid=27162847 |pmc=4789449 |doi= |url=}}</ref>
| '''Overdose/Toxicity'''
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
|bgcolor="Beige"| No underlying causes
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* In [[magnetic resonance angiography]], we may see [[aneurysm]] mostly in anterior circulation (~85%)
| style="background: #F5F5F5; padding: 5px;" |
* We do not perform [[biopsy]] for [[brain aneurysm]]
| style="background: #F5F5F5; padding: 5px;" |
* MRA and CTA
| style="background: #F5F5F5; padding: 5px;" |
* It is associated with [[autosomal dominant polycystic kidney disease]], [[Ehlers-Danlos syndrome]], [[pseudoxanthoma elasticum]] and [[Bicuspid aortic valve]]
* ([[Angiography]] is reserved for patients who have negative [[Magnetic resonance angiography|MRA]] and [[CT angiography|CTA]])
|-
|-
|-bgcolor="LightSteelBlue"
! colspan="11" style="background: #7d7d7d; color: #FFFFFF; padding: 5px; text-align: center;" |Infectious
| '''Psychiatric'''
|bgcolor="Beige"| No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
| style="background: #DCDCDC; padding: 5px; text-align: center;" |Bacterial [[brain abscess]]<br><ref name="HaimesZimmerman1989">{{cite journal|last1=Haimes|first1=AB|last2=Zimmerman|first2=RD|last3=Morgello|first3=S|last4=Weingarten|first4=K|last5=Becker|first5=RD|last6=Jennis|first6=R|last7=Deck|first7=MD|title=MR imaging of brain abscesses|journal=American Journal of Roentgenology|volume=152|issue=5|year=1989|pages=1073–1085|issn=0361-803X|doi=10.2214/ajr.152.5.1073}}</ref><ref name="BrouwerTunkel2014">{{cite journal|last1=Brouwer|first1=Matthijs C.|last2=Tunkel|first2=Allan R.|last3=McKhann|first3=Guy M.|last4=van de Beek|first4=Diederik|title=Brain Abscess|journal=New England Journal of Medicine|volume=371|issue=5|year=2014|pages=447–456|issn=0028-4793|doi=10.1056/NEJMra1301635}}</ref>
| '''Pulmonary'''
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
|bgcolor="Beige"| [[Obstructive sleep apnea]]
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px;" |
* [[Leukocytosis]]
* Elevated [[ESR]]
* [[Blood culture]] may be positive for underlying [[organism]]
| style="background: #F5F5F5; padding: 5px;" |
* Central hypodense signal and surrounding ring-enhancement in T1
* Central hyperintense area surrounded by a well-defined hypointense capsule with surrounding [[edema]] in T2
| style="background: #F5F5F5; padding: 5px;" |
* We do not perform [[biopsy]] for [[brain abscess]]
| style="background: #F5F5F5; padding: 5px;" |
* History/ imaging
| style="background: #F5F5F5; padding: 5px;" |
* The most common causes of [[brain abscess]] are [[Streptococcus]] and [[Staphylococcus]].
|-
|-
|-bgcolor="LightSteelBlue"
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Tuberculosis]]<br><ref name="MorgadoRuivo2005">{{cite journal|last1=Morgado|first1=Carlos|last2=Ruivo|first2=Nuno|title=Imaging meningo-encephalic tuberculosis|journal=European Journal of Radiology|volume=55|issue=2|year=2005|pages=188–192|issn=0720048X|doi=10.1016/j.ejrad.2005.04.017}}</ref><ref name=":0" /><ref name="pmid19275620">{{cite journal |vauthors=Be NA, Kim KS, Bishai WR, Jain SK |title=Pathogenesis of central nervous system tuberculosis |journal=Curr. Mol. Med. |volume=9 |issue=2 |pages=94–9 |date=March 2009 |pmid=19275620 |pmc=4486069 |doi= |url=}}</ref>
| '''Renal/Electrolyte'''
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
|bgcolor="Beige"| [[Chronic kidney disease]]
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px;" |
* Positive [[acid-fast bacilli]] ([[AFB]]) smear in [[CSF]] specimen
* Positive [[CSF]] [[nucleic acid]] amplification testing
* [[Hyponatremia]] (inappropriate secretion of [[antidiuretic hormone]])
* Mild [[anemia]]
* [[Leukocytosis]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Hydrocephalus]] combined with marked basilar [[Meninges|meningeal]] enhancement
| style="background: #F5F5F5; padding: 5px;" |
* We do not perform [[biopsy]] for [[brain]] [[tuberculosis]]
| style="background: #F5F5F5; padding: 5px;" |
* Lab data/ Imaging
| style="background: #F5F5F5; padding: 5px;" |
* It is associated with [[HIV]] [[infection]]
|-
|-
|-bgcolor="LightSteelBlue"
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Toxoplasmosis]]<br><ref name="pmid74807332">{{cite journal |vauthors=Chinn RJ, Wilkinson ID, Hall-Craggs MA, Paley MN, Miller RF, Kendall BE, Newman SP, Harrison MJ |title=Toxoplasmosis and primary central nervous system lymphoma in HIV infection: diagnosis with MR spectroscopy |journal=Radiology |volume=197 |issue=3 |pages=649–54 |date=December 1995 |pmid=7480733 |doi=10.1148/radiology.197.3.7480733 |url=}}</ref><ref name="pmid27348541">{{cite journal |vauthors=Helton KJ, Maron G, Mamcarz E, Leventaki V, Patay Z, Sadighi Z |title=Unusual magnetic resonance imaging presentation of post-BMT cerebral toxoplasmosis masquerading as meningoencephalitis and ventriculitis |journal=Bone Marrow Transplant. |volume=51 |issue=11 |pages=1533–1536 |date=November 2016 |pmid=27348541 |doi=10.1038/bmt.2016.168 |url=}}</ref>
| '''Rheumatology/Immunology/Allergy'''
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
|bgcolor="Beige"| [[Cushing's syndrome]], [[Systemic lupus erythematosus]]
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px;" |
* Normal [[CSF]]
| style="background: #F5F5F5; padding: 5px;" |
* Multifocal [[Mass|masses]] with ring enhancement
* Mostly in [[basal ganglia]], [[thalami]], and corticomedullary junction.
| style="background: #F5F5F5; padding: 5px;" |
* We do not perform [[biopsy]] for brain [[toxoplasmosis]]
| style="background: #F5F5F5; padding: 5px;" |
* History/ imaging
| style="background: #F5F5F5; padding: 5px;" |
* It is associated with [[HIV]] [[infection]]
|-
|-
|-bgcolor="LightSteelBlue"
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Hydatid cyst]]<br><ref name="pmid27620198">{{cite journal |vauthors=Taslakian B, Darwish H |title=Intracranial hydatid cyst: imaging findings of a rare disease |journal=BMJ Case Rep |volume=2016 |issue= |pages= |date=September 2016 |pmid=27620198 |pmc=5030532 |doi=10.1136/bcr-2016-216570 |url=}}</ref><ref name=":0" />
| '''Sexual'''
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
|bgcolor="Beige"| No underlying causes
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: left;" |
* Positive [[serology]] ([[Antibody]] detection for [[E. granulosus]]'')''
| style="background: #F5F5F5; padding: 5px;" |
* Honeycomb appearance
* [[Necrotic]] area
| style="background: #F5F5F5; padding: 5px;" |
* We do not perform [[biopsy]] for [[Hydatid cyst|hydatid cysts]]
| style="background: #F5F5F5; padding: 5px;" |
* Imaging
| style="background: #F5F5F5; padding: 5px;" |
* [[Brain]], [[eye]], and [[Spleen|splenic]] [[Cyst|cysts]] may not produce detectable amount of [[antibodies]]
|-
|-
|-bgcolor="LightSteelBlue"
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[CNS]] [[cryptococcosis]]<br><ref name="pmid25006721">{{cite journal |vauthors=McCarthy M, Rosengart A, Schuetz AN, Kontoyiannis DP, Walsh TJ |title=Mold infections of the central nervous system |journal=N. Engl. J. Med. |volume=371 |issue=2 |pages=150–60 |date=July 2014 |pmid=25006721 |pmc=4840461 |doi=10.1056/NEJMra1216008 |url=}}</ref>
| '''Trauma'''
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
|bgcolor="Beige"| [[Contusions]], [[Head trauma]]
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px;" |
* Positive [[CSF]] [[antigen]] testing ([[coccidioidomycosis]])
* [[CSF]] [[Lymphocyte|lymphocytic]] [[pleocytosis]]
* Elevated [[CSF]] [[Protein|proteins]] and [[lactate]]
* Low [[CSF]] [[glucose]]
*
| style="background: #F5F5F5; padding: 5px;" |
* Dilated peri[[vascular]] spaces
* [[Basal ganglia]] [[Pseudocyst|pseudocysts]]
 
* Soap bubble brain lesions ([[cryptococcus neoformans]])
*
| style="background: #F5F5F5; padding: 5px;" |
* We may see numerous acutely branching septate [[Hypha|hyphae]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Laboratory|Lab]] data/ Imaging
| style="background: #F5F5F5; padding: 5px;" |
* It is the most common [[brain]] [[fungal infection]]
 
* It is associated with [[HIV]], [[Immunosuppressive therapy|immunosuppressive therapies]], and [[Organ transplant|organ transplants]]
* In may happen in [[immunocompetent]] patients undergoing invasive procedures ( [[neurosurgery]]) or exposed to [[Contamination|contaminated]] devices or [[drugs]]
* Since [[brain]] [[Biopsy|biopsies]] are highly invasive and may may cause [[neurological]] deficits, we [[diagnose]] [[CNS]] [[fungal]] [[Infection|infections]] based on [[laboratory]] and imaging findings
|-
|-
|-bgcolor="LightSteelBlue"
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[CNS]] [[aspergillosis]]<br><ref name="pmid250067212">{{cite journal |vauthors=McCarthy M, Rosengart A, Schuetz AN, Kontoyiannis DP, Walsh TJ |title=Mold infections of the central nervous system |journal=N. Engl. J. Med. |volume=371 |issue=2 |pages=150–60 |date=July 2014 |pmid=25006721 |pmc=4840461 |doi=10.1056/NEJMra1216008 |url=}}</ref>
| '''Urologic'''
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
|bgcolor="Beige"| No underlying causes
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px;" |
* Positive [[galactomannan]] [[antigen]] testing ([[aspergillosis]])
* [[CSF]] [[Lymphocyte|lymphocytic]] [[pleocytosis]]
* Elevated [[CSF]] [[Protein|proteins]] and [[lactate]]
* Low [[CSF]] [[glucose]]
| style="background: #F5F5F5; padding: 5px;" |
* Multiple [[Abscess|abscesses]]
* Ring enhancement
* Peripheral low signal intensity on T2
| style="background: #F5F5F5; padding: 5px;" |
* We may see numerous acutely branching septate [[Hypha|hyphae]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Laboratory|Lab]] data/ Imaging
| style="background: #F5F5F5; padding: 5px;" |
* It is associated with [[HIV]], [[Immunosuppressive therapy|immunosuppressive therapies]], and [[Organ transplant|organ transplants]]
* In may happen in [[immunocompetent]] patients undergoing invasive procedures ( [[neurosurgery]]) or exposed to [[Contamination|contaminated]] devices or [[drugs]]
* Since [[brain]] [[Biopsy|biopsies]] are highly invasive and may may cause [[neurological]] deficits, we [[diagnose]] [[CNS]] [[fungal]] [[Infection|infections]] based on [[laboratory]] and imaging findings
|-
|-
|-bgcolor="LightSteelBlue"
! colspan="11" style="background: #7d7d7d; color: #FFFFFF; padding: 5px; text-align: center;" |Other
| '''Miscellaneous'''
|bgcolor="Beige"| No underlying causes
|-
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Brain metastasis]]<br><ref name="pmid29307364">{{cite journal |vauthors=Pope WB |title=Brain metastases: neuroimaging |journal=Handb Clin Neurol |volume=149 |issue= |pages=89–112 |date=2018 |pmid=29307364 |pmc=6118134 |doi=10.1016/B978-0-12-811161-1.00007-4 |url=}}</ref><ref name=":0" />
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* Multiple [[Lesion|lesions]]
* [[Vasogenic edema]]
*
| style="background: #F5F5F5; padding: 5px;" |
* Based on the primary [[cancer]] type we may have different immunohistopathology findings.
| style="background: #F5F5F5; padding: 5px;" |
* History/ imaging
| style="background: #F5F5F5; padding: 5px;" |
* Most common primary [[Tumor|tumors]] that [[metastasis]] to [[brain]]:
** [[Lung cancer]]
** [[Renal cell carcinoma]]
** [[Breast cancer]]
** [[Melanoma]]
** [[Gastrointestinal tract]]
* If there is any uncertainty about [[etiology]], [[biopsy]] should be performed
|}
|}
'''ABBREVIATIONS'''


===Causes in Alphabetical Order===
[[CNS]]=[[Central nervous system]], AV=Arteriovenous, [[CSF]]=[[Cerebrospinal fluid]], [[NF-2]]=[[Neurofibromatosis type 2]], [[MEN1|MEN-1]]=[[Multiple endocrine neoplasia]], [[GFAP]]=[[Glial fibrillary acidic protein]], [[HIV]]=[[Human Immunodeficiency Virus|Human immunodeficiency virus]], BhCG=[[Human chorionic gonadotropin]], [[ESR]]=[[Erythrocyte sedimentation rate]], [[AFB]]=Acid fast bacilli, [[Magnetic resonance angiography|MRA]]=[[Magnetic resonance angiography]], [[CT angiography|CTA]]=[[CT angiography]]
{{columns-list|
==Epidemiology and Demographics==
 
*[[Abscess]]
*The prevalence of intracranial hypertension is approximately 1.0 per 100,000 individuals worldwide.
*[[Accutane]]
 
*[[Acute liver failure]]
===Gender===
*[[Albendazole ]]
 
*[[Aneurysm ]]
*Idiopathic ICH is more prevalent among women of childbearing age.
*[[Arnold-chiari malformation]]
 
*[[Aschemic-anoxia states]]
==Risk Factors==
*[[Behçet's disease]]
 
*[[Brain tumor]]
*Common risk factors in the development of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) include underlying pathologies such as; mass lesions, abscesses, and hematomas.
*[[Cerebral oedema]]
*Other risk factors include
*[[Cerebral venous sinus thrombosis]]
**[[Obesity]]
*[[Choroid plexus tumor]]
**[[Chronic hypertension]]
*[[Chronic kidney disease]]
**Women of childbearing age
*[[Ciprofloxacin]]
 
*[[Claravis]]
==Natural History, Complications and Prognosis==
*[[Colloid cyst of third ventricle]]
 
*[[Contusions]]
*Early clinical features include nausea, [[vomiting]], and confusion.
*[[Craniosynostosis]]
*If left untreated, patients may progress to have severe neurologic consequences such as brain [[herniation]], brain death, respiratory depression, brain infections, [[coma]] and death.
*[[Crouzon craniofacial dysostosis]]
*Common complications of intracranial hypertension include brain herniation and neurologic deficits.
*[[Cushing's syndrome]]
 
*[[Dandy-walker syndrome]]
==Diagnosis==
*[[Dural arteriovenous fistula]]
===Diagnostic Criteria===
*[[Encephalitis]]
 
*[[Epidural haemorrhage]]
*The diagnosis of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) is made when ICP is >20 mmHg.
*[[Epidural hematoma]]
*[[Erdheim-chester disease]]
*[[Excess cerebrospinal fluid]]
*[[Head trauma]]
*[[Heart failure]]
*[[Hepatic failure]]
*[[Hydrocephalus ]]
*[[Hypercarbia]]
*[[Hypertension]]
*[[Hypertensive brain hemorrhage]]
*[[Hypertensive encephalopathy]]
*[[Hyperthyroidism]]
*[[Hypoparathyroidism]]
*[[Hypothyroidism]]
*[[Hypoxemia]]
*[[Idiopathic intracranial hypertension]]
*[[Infarction with edema]]
*[[Insulin like growth factor 1]]
*[[Intracranial abscess / granuloma]]
*[[Intracranial granuloma]]
*[[Intracranial haemorrhage]]
*[[Intracranial space-occupying lesion]]
*[[Intraventricular hemorrhage]]
*[[Iron deficiency]]
*[[Isotretinoin]]
*[[Lead]]
*[[Meningioma]]
*[[Meningitis]]
*[[Meningoencephalitis]]
*[[Minocycline]]
*[[Multiple hamartoma syndrome]]
*[[Neurocysticercosis]]
*[[Obstruction of superior mediastinal veins]]
*[[Obstruction of jugular veins]]
*[[Obstructive sleep apnea]]
*[[Pineal tumour]]
*[[Polycythaemia vera]]
*[[Pseudotumor cerebri]]
*[[Reye hepatocerebral syndrome]]
*[[Sotret]]
*[[Status epilepticus]]
*[[Stroke]]
*[[Subarachnoid haemorrhage]]
*[[Subdural haemorrhage]]
*[[Subdural hematoma]]
*[[Sudanophilic cerebral sclerosis]]
*[[Systemic lupus erythematosus]]
*[[Vasculitis]]
*[[Venous sinus thrombosis]]
*[[Vitamin a]]
}}


==Complete Differential Diagnosis of Increased Intracranial Pressure (ICP)==  
===History and Symptoms===


In alphabetical order. <ref>Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:77 ISBN 1591032016</ref> <ref>Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:68 ISBN 140510368X</ref>
*Symptoms of elevated intracranial pressure may include the following:


* [[Acromegaly]]
:*[[Headache]]
* [[Addison's Disease]]
:*[[Nausea]]
* [[Antiphospholipid Antibody Syndrome]]
:*[[Vomiting]]
* [[Arteriovenous malformation]]
:*[[Hyperventilation]] (due to injury to [[brain stem]] or [[tegmentum]] is damaged.<ref name="sgo" />
* [[Brain abscess]]
:*Changes in your behavior
* [[Cor pulmonale]]
:*Weakness or problems with moving or talking
* [[Cushing's Disease]]
:*Lack of energy or sleepiness
* [[Decerebrate posture]]
:*Seizure
* [[Decorticate posture]]
* [[Diabetic Ketoacidosis]]
===Physical Examination===
* [[Drugs]]- [[Dexamethasone]], [[Pergolide]], [[toxin]]s
* [[Epidural hemorrhage]]
* [[Encephalitis]]
* [[Hepatic encephalopathy]]
* [[HIV infection]]
* [[Hypercoagulable state]]
* [[Hyperosmolality]]
* [[Hyponatremia]]
* [[Hypoosmolality]]
* [[Hypoparathyroidism]]
* [[Hypothyroidism]]
* Hypoxic-ischemic injury
* [[Idiopathic intracranial hypertension]]
* [[Intraventricular hemorrhage]]
* [[Iron deficiency anemia]]
* Jugular vein cut
* [[Mastoiditis]]
* [[Meningitis]]
* [[Meningoencephalitis]]
* [[Obesity]]
* Orthostatic [[edema]]
* [[Otitis media]]
* [[Polycystic ovary syndrome]]
* [[Pregnancy]]
* [[Reye's Syndrome]]
* Severe head [[trauma]]
* [[Sleep Apnea]]
* [[Subdural hematoma]]
* [[Ddx:Superior Vena Cava Syndrome|Superior Vena Cava Syndrome]]
* [[Systemic Lupus Erythematosus]]
* [[Turner's Syndrome]]
* [[Water intoxication]]


==Pathophysiology==
*Physical examination may be remarkable for


The cranium and the [[vertebral body]], along with the relatively inelastic dura, form a rigid container, such that the increase in any of its contents—brain, blood, or CSF—will 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 to immediate increase in ICP because of the ability of the CSF to be displaced into the spinal canal, as well as 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&nbsp;mmHg, small increases in brain volume can lead to marked elevations in ICP.
:*Ocular palsies (abducens palsy)
:*Periorbital bruising<ref name="pmid15258230">{{cite journal |vauthors=Hadjikoutis S, Carroll C, Plant GT |title=Raised intracranial pressure presenting with spontaneous periorbital bruising: two case reports |journal=J. Neurol. Neurosurg. Psychiatry |volume=75 |issue=8 |pages=1192–3 |date=August 2004 |pmid=15258230 |pmc=1739150 |doi=10.1136/jnnp.2003.016006 |url=}}</ref>
:*Altered level of consciousness
:*[[Papilledema]]<ref name="pmid15046669">{{cite journal |vauthors=Binder DK, Lyon R, Manley GT |title=Transcranial motor evoked potential recording in a case of Kernohan's notch syndrome: case report |journal=Neurosurgery |volume=54 |issue=4 |pages=999–1002; discussion 1002–3 |date=April 2004 |pmid=15046669 |doi=10.1227/01.neu.0000115674.15497.09 |url=}}</ref>
:*[[Pupillary dilatation]]
:*[[Cushing's triad]] ( Elevated [[systolic blood pressure]], a widened [[pulse pressure]], [[bradycardia]], and an abnormal respiratory pattern.
:*[[Cheyne-Stokes respiration]]
:*Bulging of [[fontanel]]s in infants


Traumatic brain injury is a devastating problem with both high mortality and high subsequent morbidity. Injury to the brain occurs both at the time of the initial trauma (the primary injury) and subsequently due to ongoing cerebral ischemia (the secondary injury). Cerebral edema, hypotension, and axonal 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 diffuse brain injury (one that occurs over a widespread area) and leads to cerebral ischemia by compromising cerebral perfusion.
===Laboratory Findings===


[[Cerebral perfusion pressure]] (CPP), the pressure causing blood flow 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:&nbsp;CPP&nbsp;=&nbsp;MAP&nbsp;&minus;&nbsp;ICP&nbsp;<ref name="Steiner" />.<ref>{{cite journal | author=Duschek S, Schandry R | title=Reduced brain perfusion and cognitive performance due to constitutional hypotension | journal=Clinical Autonomic Research  | volume=17 | issue=2 | year=2007 | pages=69–76 |pmc=1858602 | pmid=17106628  | doi=10.1007/s10286-006-0379-7}}</ref> 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, it becomes more and more difficult to squeeze blood into the intracranial space.  The body’s response to a decrease in CPP is to raise [[blood pressure]] and dilate [[blood vessel]]s in the brain. 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 hemorrhage]]s bleed faster, also increasing ICP.  
*There are no specific laboratory findings associated with Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH).


Highly increased ICP, if caused by a one-sided space-occupying process (e.g., hematoma) can result in midline shift, a dangerous condition in which the brain moves toward one side as the result of massive swelling in a [[cerebral hemisphere]].  Midline shift can compress the [[ventricular system|ventricles]] and lead to buildup of CSF.<ref name="Downie">Downie A. 2001. [http://www.radiology.co.uk/srs-x/tutors/cttrauma/tutor.htm "Tutorial: CT in Head Trauma"] Accessed January 4, 2007.</ref>  Prognosis is much worse in patients with midline shift than in those without it.  Another dire consequence of increased ICP combined with a space-occupying process is [[brain herniation]] (usually uncal or cerebellar), in which the brain is squeezed past structures within the skull, severely compressing it. If brainstem compression is involved, it may lead to decreased respiratory drive and is potentially fatal. This herniation is often referred to as "coning".
===Electrocardiogram===


Major causes of [[morbidity]] due to increased intracranial pressure are due to global brain [[infarction]] as well as decreased respiratory drive due to brain [[herniation]].
*There are no ECG findings associated with Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH).


===Intracranial Hypertension===
===X-ray===
Minimal increases in ICP due to compensatory mechanisms is 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 100–120 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 increace 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 difficult to squeeze blood into the intracranial space. The body’s 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 further and causing a vicious cycle. This results in widespread reduction in cerebral flow 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 LOC, [[Cheyne-Stokes respirations]], hyperventilation, sluggish dilated pupils and widened pulse pressure.


==Causes of increased ICP==
*There are no x-ray findings associated with Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH).
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 abscess all tend to deform the adjacent brain.
===CT scan===
*'''generalized brain swelling''' can occur in ischemic-anoxia states, acute liver failure, hypertensive encephalopathy, pseudotumor cerebri, hypercarbia, 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., infectious, carcinomatous, granulomatous, or hemorrhagic), or obstruction in cerebral convexities and superior sagittal sinus (decreased absorption).
{{main|hydrocephalus}}
*'''increased CSF production''' can occur in meningitis, subarachnoid hemorrhage, or choroid plexus tumor.
*'''Drugs''' [[Albendazole]], [[Ciprofloxacin]]


==Signs and symptoms of increased ICP==
*[[CT scan]] may be helpful in the diagnosis of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH).
In general, symptoms and signs that suggest a rise in ICP including [[headache]], [[nausea]], [[vomiting]], ocular palsies, altered level of consciousness, and [[papilledema]]. If papilledema is protracted, it may lead to visual disturbances, optic atrophy, and eventually blindness.  
*Findings on CT scan suggestive of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) include presence of mass lesions, midline shift or hemorrhage.
*CT scan is particularly helpful for people with acute rise in ICP.


In addition to the above, if mass effect is present with resulting displacement of brain tissue, additional signs may include [[pupillary dilatation]], abducens (CrN VI) 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.<ref name="Sanders">Sanders MJ and McKenna K. 2001. ''Mosby’s Paramedic Textbook, 2nd revised Ed''.  Chapter 22, "Head and Facial Trauma." Mosby.</ref> In children, a slow heart rate is especially suggestive of high ICP.
===MRI===


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 hemisphere]]s or [[diencephalon]].<ref name="sgo">Singh J and Stock A. 2006. [http://www.emedicine.com/ped/topic929.htm "Head Trauma."] Emedicine.com.  Accessed January 4, 2007.</ref> [[Hyperventilation]] can occur when the [[brain stem]] or [[tegmentum]] is damaged.<ref name="sgo"/>
*MR venography (MRV) is preferred over MRI for the diagnosis of cerebral venous thrombosis
*[[MRI]] has a greater sensitivity to detect subtle intracranial masses (eg, gliomatosis cerebri) and meningeal-based pathologies and should be done if no contraindications (eg, pacemakers, metallic clips in head, metallic foreign bodies) present


As a rule, patients with normal blood pressure retain normal alertness with ICP of 25 to 40 mmHg (unless there's concurrent tissue shift). Only when ICP exceeds 40 to 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.  
===Other Diagnostic Studies===
Other diagnostic studies for Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) include invasive and non-invasive ICP monitoring, particularly preferred in patients with no CT or MRI findings, at risk of developing increased ICP, and comatosed.


In infants and small children, the effects of ICP differ due to the fact that their cranial sutures have not closed. In infants, the [[fontanel]]s, or soft spots on the head where the skull bones have not yet fused, bulge when ICP gets too high.
*Invasive ICP monitoring usually involves 4 anatomic sites:<ref name="pmid7490638">{{cite journal |vauthors=Rosner MJ, Rosner SD, Johnson AH |title=Cerebral perfusion pressure: management protocol and clinical results |journal=J. Neurosurg. |volume=83 |issue=6 |pages=949–62 |date=December 1995 |pmid=7490638 |doi=10.3171/jns.1995.83.6.0949 |url=}}</ref><ref name="pmid11129833">{{cite journal |vauthors=Lane PL, Skoretz TG, Doig G, Girotti MJ |title=Intracranial pressure monitoring and outcomes after traumatic brain injury |journal=Can J Surg |volume=43 |issue=6 |pages=442–8 |date=December 2000 |pmid=11129833 |pmc=3695200 |doi= |url=}}</ref><ref name="pmid12163808">{{cite journal |vauthors=Bulger EM, Nathens AB, Rivara FP, Moore M, MacKenzie EJ, Jurkovich GJ |title=Management of severe head injury: institutional variations in care and effect on outcome |journal=Crit. Care Med. |volume=30 |issue=8 |pages=1870–6 |date=August 2002 |pmid=12163808 |doi=10.1097/00003246-200208000-00033 |url=}}</ref><ref name="pmid18365169">{{cite journal |vauthors=Mauritz W, Steltzer H, Bauer P, Dolanski-Aghamanoukjan L, Metnitz P |title=Monitoring of intracranial pressure in patients with severe traumatic brain injury: an Austrian prospective multicenter study |journal=Intensive Care Med |volume=34 |issue=7 |pages=1208–15 |date=July 2008 |pmid=18365169 |doi=10.1007/s00134-008-1079-7 |url=}}</ref><ref name="pmid17511545">{{cite journal |vauthors=Bratton SL, Chestnut RM, Ghajar J, McConnell Hammond FF, Harris OA, Hartl R, Manley GT, Nemecek A, Newell DW, Rosenthal G, Schouten J, Shutter L, Timmons SD, Ullman JS, Videtta W, Wilberger JE, Wright DW |title=Guidelines for the management of severe traumatic brain injury. VII. Intracranial pressure monitoring technology |journal=J. Neurotrauma |volume=24 Suppl 1 |issue= |pages=S45–54 |date=2007 |pmid=17511545 |doi=10.1089/neu.2007.9989 |url=}}</ref>
**[[Intraventricular]]<ref name="pmid6694707">{{cite journal |vauthors=Mayhall CG, Archer NH, Lamb VA, Spadora AC, Baggett JW, Ward JD, Narayan RK |title=Ventriculostomy-related infections. A prospective epidemiologic study |journal=N. Engl. J. Med. |volume=310 |issue=9 |pages=553–9 |date=March 1984 |pmid=6694707 |doi=10.1056/NEJM198403013100903 |url=}}</ref><ref name="pmid8751626">{{cite journal |vauthors=Holloway KL, Barnes T, Choi S, Bullock R, Marshall LF, Eisenberg HM, Jane JA, Ward JD, Young HF, Marmarou A |title=Ventriculostomy infections: the effect of monitoring duration and catheter exchange in 584 patients |journal=J. Neurosurg. |volume=85 |issue=3 |pages=419–24 |date=September 1996 |pmid=8751626 |doi=10.3171/jns.1996.85.3.0419 |url=}}</ref>
**[[Intraparenchymal hemorrhage|Intraparenchymal]]<ref name="pmid3598682">{{cite journal |vauthors=Ostrup RC, Luerssen TG, Marshall LF, Zornow MH |title=Continuous monitoring of intracranial pressure with a miniaturized fiberoptic device |journal=J. Neurosurg. |volume=67 |issue=2 |pages=206–9 |date=August 1987 |pmid=3598682 |doi=10.3171/jns.1987.67.2.0206 |url=}}</ref><ref name="pmid1436417">{{cite journal |vauthors=Gambardella G, d'Avella D, Tomasello F |title=Monitoring of brain tissue pressure with a fiberoptic device |journal=Neurosurgery |volume=31 |issue=5 |pages=918–21; discussion 921–2 |date=November 1992 |pmid=1436417 |doi=10.1227/00006123-199211000-00014 |url=}}</ref><ref name="pmid8923072">{{cite journal |vauthors=Bochicchio M, Latronico N, Zappa S, Beindorf A, Candiani A |title=Bedside burr hole for intracranial pressure monitoring performed by intensive care physicians. A 5-year experience |journal=Intensive Care Med |volume=22 |issue=10 |pages=1070–4 |date=October 1996 |pmid=8923072 |doi=10.1007/BF01699230 |url=}}</ref>
**[[Subarachnoid]]<ref name="pmid17511545">{{cite journal |vauthors=Bratton SL, Chestnut RM, Ghajar J, McConnell Hammond FF, Harris OA, Hartl R, Manley GT, Nemecek A, Newell DW, Rosenthal G, Schouten J, Shutter L, Timmons SD, Ullman JS, Videtta W, Wilberger JE, Wright DW |title=Guidelines for the management of severe traumatic brain injury. VII. Intracranial pressure monitoring technology |journal=J. Neurotrauma |volume=24 Suppl 1 |issue= |pages=S45–54 |date=2007 |pmid=17511545 |doi=10.1089/neu.2007.9989 |url=}}</ref>
**[[Epidural]]<ref name="pmid17511545">{{cite journal |vauthors=Bratton SL, Chestnut RM, Ghajar J, McConnell Hammond FF, Harris OA, Hartl R, Manley GT, Nemecek A, Newell DW, Rosenthal G, Schouten J, Shutter L, Timmons SD, Ullman JS, Videtta W, Wilberger JE, Wright DW |title=Guidelines for the management of severe traumatic brain injury. VII. Intracranial pressure monitoring technology |journal=J. Neurotrauma |volume=24 Suppl 1 |issue= |pages=S45–54 |date=2007 |pmid=17511545 |doi=10.1089/neu.2007.9989 |url=}}</ref><ref name="pmid3748354">{{cite journal |vauthors=Miller JD, Bobo H, Kapp JP |title=Inaccurate pressure readings for subarachnoid bolts |journal=Neurosurgery |volume=19 |issue=2 |pages=253–5 |date=August 1986 |pmid=3748354 |doi=10.1227/00006123-198608000-00012 |url=}}</ref>
*Noninvasive devices still need further large randomized trials to prove their clinical efficacy. They are not used in clinical practice but are still under investigation and include:<ref name="pmid9012577">{{cite journal |vauthors=Manno EM |title=Transcranial Doppler ultrasonography in the neurocritical care unit |journal=Crit Care Clin |volume=13 |issue=1 |pages=79–104 |date=January 1997 |pmid=9012577 |doi=10.1016/s0749-0704(05)70297-9 |url=}}</ref><ref name="pmid15591334">{{cite journal |vauthors=Edouard AR, Vanhille E, Le Moigno S, Benhamou D, Mazoit JX |title=Non-invasive assessment of cerebral perfusion pressure in brain injured patients with moderate intracranial hypertension |journal=Br J Anaesth |volume=94 |issue=2 |pages=216–21 |date=February 2005 |pmid=15591334 |doi=10.1093/bja/aei034 |url=}}</ref>
**Transcranial Doppler (TCD)<ref name="pmid7143059">{{cite journal |vauthors=Aaslid R, Markwalder TM, Nornes H |title=Noninvasive transcranial Doppler ultrasound recording of flow velocity in basal cerebral arteries |journal=J. Neurosurg. |volume=57 |issue=6 |pages=769–74 |date=December 1982 |pmid=7143059 |doi=10.3171/jns.1982.57.6.0769 |url=}}</ref>
**Tissue resonance analysis (TRA)<ref name="pmid12066918">{{cite journal |vauthors=Michaeli D, Rappaport ZH |title=Tissue resonance analysis; a novel method for noninvasive monitoring of intracranial pressure. Technical note |journal=J. Neurosurg. |volume=96 |issue=6 |pages=1132–7 |date=June 2002 |pmid=12066918 |doi=10.3171/jns.2002.96.6.1132 |url=}}</ref>
**Ocular sonography<ref name="pmid19636971">{{cite journal |vauthors=Moretti R, Pizzi B, Cassini F, Vivaldi N |title=Reliability of optic nerve ultrasound for the evaluation of patients with spontaneous intracranial hemorrhage |journal=Neurocrit Care |volume=11 |issue=3 |pages=406–10 |date=December 2009 |pmid=19636971 |doi=10.1007/s12028-009-9250-8 |url=}}</ref><ref name="pmid19098619">{{cite journal |vauthors=Moretti R, Pizzi B |title=Optic nerve ultrasound for detection of intracranial hypertension in intracranial hemorrhage patients: confirmation of previous findings in a different patient population |journal=J Neurosurg Anesthesiol |volume=21 |issue=1 |pages=16–20 |date=January 2009 |pmid=19098619 |doi=10.1097/ANA.0b013e318185996a |url=}}</ref>
**[[Intraocular pressure (IOP)|Intraocular pressure]]<ref name="pmid10752710">{{cite journal |vauthors=Sheeran P, Bland JM, Hall GM |title=Intraocular pressure changes and alterations in intracranial pressure |journal=Lancet |volume=355 |issue=9207 |pages=899 |date=March 2000 |pmid=10752710 |doi=10.1016/s0140-6736(99)02768-3 |url=}}</ref><ref name="pmid18570302">{{cite journal |vauthors=Han Y, McCulley TJ, Horton JC |title=No correlation between intraocular pressure and intracranial pressure |journal=Ann. Neurol. |volume=64 |issue=2 |pages=221–4 |date=August 2008 |pmid=18570302 |doi=10.1002/ana.21416 |url=}}</ref>
**Tympanic membrane displacement


==Treatment==
==Treatment==
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.
===Medical Therapy===


One of the most important treatments for high ICP is to ensure adequate [[airway]], breathing, and [[oxygen]]ation, since inadequate oxygen levels or excess [[carbon dioxide]] cause cerebral blood vessels to dilate and ICP to rise.<ref name="Su and Huh">Su F and Huh J. 2006. [http://www.emedicine.com/ped/topic3082.htm "Neurointensive Care for Traumatic Brain Injury in Children."] Emedicine.com.  Accessed January 4, 2007.</ref>  Inadequate oxygen also forces brain cells to produce energy using [[Fermentation (biochemistry)|anaerobic metabolism]], which produces [[lactic acid]] and lowers [[pH]], which dilates blood vessels.<ref name="orlando"/>  On the other hand, 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 but limits blood flow to the brain in a time when the brain may already be ischemic. Artificially ventilating a patient at a fast rate used to be a standard part of head trauma treatment because of its ability to rapidly lower ICP, but the chance of developing [[ischemia]] was later recognized to be too much of a risk.<ref name="Shepherd">Shepherd S. 2004. [http://www.emedicine.com/med/topic2820.htm "Head Trauma."] Emedicine.com.  Accessed January 4, 2007.</ref>  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.<ref name="Shepherd"/>  Now hyperventilation is used when signs of [[brain herniation]] are apparent 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.  Another way to lower ICP is to raise the head of the bed, allowing for venous drainage. A side effect of this is that it could lower pressure of blood to the head, resulting in inadequate blood supply to the brain. Another simple method used to lower ICP (particularly in trauma cases) is to loosen neck collars and clothing. This method is more useful is the patient is sedated and thus movement is minimal.  Sandbags may be used to further limit neck movement.  
*The management of intracranial hypertension is generally directed towards treating the cause/etiology of the raised intracranial pressure.
*Intracranial hypertension is considered a medical emergency and the management includes emergent resuscitative as well as specific treatment.


In the hospital, blood pressure can be artificially raised in order to increase CPP, increase perfusion, oxygenate tissues, remove wastes and thereby lessen swelling.<ref name="Shepherd"/> 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 head injured patient.<ref name="sgo"/> When it is necessary to decrease cerebral blood flow, MAP can be lowered using common [[antihypertensive agent]]s such as [[calcium channel blocker]]s.<ref name="orlando"/>  
====Resuscitation:====
General principles for resuscitation include:<ref name="pmid10961490">{{cite journal |vauthors=Procaccio F, Stocchetti N, Citerio G, Berardino M, Beretta L, Della Corte F, D'Avella D, Brambilla GL, Delfini R, Servadei F, Tomei G |title=Guidelines for the treatment of adults with severe head trauma (part I). Initial assessment; evaluation and pre-hospital treatment; current criteria for hospital admission; systemic and cerebral monitoring |journal=J Neurosurg Sci |volume=44 |issue=1 |pages=1–10 |date=March 2000 |pmid=10961490 |doi= |url=}}</ref><ref name="pmid10961491">{{cite journal |vauthors=Procaccio F, Stocchetti N, Citerio G, Berardino M, Beretta L, Della Corte F, D'Avella D, Brambilla GL, Delfini R, Servadei F, Tomei G |title=Guidelines for the treatment of adults with severe head trauma (part II). Criteria for medical treatment |journal=J Neurosurg Sci |volume=44 |issue=1 |pages=11–8 |date=March 2000 |pmid=10961491 |doi= |url=}}</ref><ref name="pmid10961492">{{cite journal |vauthors=Davella D, Brambilla GL, Delfini R, Servadei F, Tomei G, Procaccio F, Stocchetti N, Citerio G, Berardino M, Beretta L, Della Corte F |title=Guidelines for the treatment of adults with severe head trauma (part III). Criteria for surgical treatment |journal=J Neurosurg Sci |volume=44 |issue=1 |pages=19–24 |date=March 2000 |pmid=10961492 |doi= |url=}}</ref><ref name="pmid11696494">{{cite journal |vauthors=Robinson N, Clancy M |title=In patients with head injury undergoing rapid sequence intubation, does pretreatment with intravenous lignocaine/lidocaine lead to an improved neurological outcome? A review of the literature |journal=Emerg Med J |volume=18 |issue=6 |pages=453–7 |date=November 2001 |pmid=11696494 |pmc=1725712 |doi=10.1136/emj.18.6.453 |url=}}</ref><ref name="pmid15259869">{{cite journal |vauthors=Smith ER, Madsen JR |title=Neurosurgical aspects of critical care neurology |journal=Semin Pediatr Neurol |volume=11 |issue=2 |pages=169–78 |date=June 2004 |pmid=15259869 |doi=10.1016/j.spen.2004.04.002 |url=}}</ref><ref name="pmid15259863">{{cite journal |vauthors=Smith ER, Madsen JR |title=Cerebral pathophysiology and critical care neurology: basic hemodynamic principles, cerebral perfusion, and intracranial pressure |journal=Semin Pediatr Neurol |volume=11 |issue=2 |pages=89–104 |date=June 2004 |pmid=15259863 |doi=10.1016/j.spen.2004.04.001 |url=}}</ref><ref name="pmid1404521">{{cite journal |vauthors=Schmoker JD, Shackford SR, Wald SL, Pietropaoli JA |title=An analysis of the relationship between fluid and sodium administration and intracranial pressure after head injury |journal=J Trauma |volume=33 |issue=3 |pages=476–81 |date=September 1992 |pmid=1404521 |doi=10.1097/00005373-199209000-00024 |url=}}</ref>


Struggling can increase [[metabolism|metabolic]] demands and oxygen consumption, as well as increasing blood pressure.<ref name="bech">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.</ref><ref name="Su and Huh"/> Thus children may be [[paralysis|paralyzed]] with drugs if other methods for reducing ICP fail. Paralysis allows the cerebral veins to drain more easily, but can mask signs of [[seizure]]s, and the drugs can have other harmful effects.<ref name="Su and Huh"/>
*Maintain oxygen
*Head elevation
*[[Hyperventilation]] to achieve a PaCO2 of 26-30 mmHg
*Osmotic diuresis with intravenous [[mannitol]] and [[Lasix]]
*Appropriate sedation, if patient requires intubation.  [[Propofol]] is considered to be the preferred agent.
*[[Therapeutic hypothermia]] to achieve a low metabolic state
*Appropriate choice of fluids to achieve euvolemic state.  Avoid hypotonic agents
*Allow permissive [[hypertension]].  Treat hypertension only when CPP >120 mmHg and ICP >20 mmHg
*[[Seizure]] prophylaxis with anticonvulsant therapy.<ref name="pmid6202480">{{cite journal |vauthors=Gabor AJ, Brooks AG, Scobey RP, Parsons GH |title=Intracranial pressure during epileptic seizures |journal=Electroencephalogr Clin Neurophysiol |volume=57 |issue=6 |pages=497–506 |date=June 1984 |pmid=6202480 |doi=10.1016/0013-4694(84)90085-3 |url=}}</ref>


Pain is also treated to reduce agitation and metabolic needs of the brain, but some pain medications may cause low blood pressure and other side effects.<ref name="orlando"/>  
<br />


Intracranial pressure can be measured continuously with intracranial transducers (only used in neurosurgical intensive care).  A catheter can be surgically inserted into one of the brain's [[ventricular system|lateral ventricle]]s and can be used to drain CSF (cerebrospinal fluid) in order to decrease ICP's. This type of drain is known as an EVD (extraventricular drain).<ref name="orlando"/>  In rare situations when only small amounts of CSF are to be drained to reduce ICP's, drainage of CSF via lumbar puncture can be used as a treatment.
====Other therapies for intracranial hypertension:====


[[craniotomy|Craniotomies]] are holes drilled in the skull to remove [[intracranial hematoma]]s or relieve pressure from parts of the brain.<ref name="orlando"/> As raised ICP's may be caused by the presence of a mass, removal of this via craniotomy will decrease raised ICP's.
*[[Osmotic diuresis]] can be achieved by hypertonic saline bolus or [[mannitol]].  Hypertonic saline is usually considered to be more effective compared to mannitol for acute ICP reduction. Mannitol can be given as a bolus of 1 g/kg when prepared as 20% solution.  The dose is usually repeated every 6-8 hours.  It should be used cautiously in patients with renal insufficiency. Intravenous Lasix (0.5 to 1 mg/kg) is usually given with mannitol.<ref name="pmid2879175">{{cite journal |vauthors=Bell BA, Smith MA, Kean DM, McGhee CN, MacDonald HL, Miller JD, Barnett GH, Tocher JL, Douglas RH, Best JJ |title=Brain water measured by magnetic resonance imaging. Correlation with direct estimation and changes after mannitol and dexamethasone |journal=Lancet |volume=1 |issue=8524 |pages=66–9 |date=January 1987 |pmid=2879175 |doi=10.1016/s0140-6736(87)91908-8 |url=}}</ref><ref name="pmid3086519">{{cite journal |vauthors=Nath F, Galbraith S |title=The effect of mannitol on cerebral white matter water content |journal=J. Neurosurg. |volume=65 |issue=1 |pages=41–3 |date=July 1986 |pmid=3086519 |doi=10.3171/jns.1986.65.1.0041 |url=}}</ref>


A drastic treatment for increased ICP is [[decompressive craniectomy]], 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]].<ref name="Shepherd"/> 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.
*[[Glucocorticoids]] are usually preferred when the underlying etiologies brain tumor are underlying CNS infection.  Their use is contraindicated in head injury, cerebral infarction and intracranial hemorrhage.<ref name="pmid15474134">{{cite journal |vauthors=Roberts I, Yates D, Sandercock P, Farrell B, Wasserberg J, Lomas G, Cottingham R, Svoboda P, Brayley N, Mazairac G, Laloë V, Muñoz-Sánchez A, Arango M, Hartzenberg B, Khamis H, Yutthakasemsunt S, Komolafe E, Olldashi F, Yadav Y, Murillo-Cabezas F, Shakur H, Edwards P |title=Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomised placebo-controlled trial |journal=Lancet |volume=364 |issue=9442 |pages=1321–8 |date=2004 |pmid=15474134 |doi=10.1016/S0140-6736(04)17188-2 |url=}}</ref>
*[[Phenobarbital]] is considered to have a neuroprotective effect by decreasing brain metabolism.  It is given as a loading dose of 5 to 20 mg/kg, followed by 1 to 4 mg/kg per hour.  EEG monitoring is used to guide therapy.  A burst suppression seen on EEG indicates maximal dosing.<ref name="pmid639524">{{cite journal |vauthors=Marshall LF, Shapiro HM, Rauscher A, Kaufman NM |title=Pentobarbital therapy for intracranial hypertension in metabolic coma. Reye's syndrome |journal=Crit. Care Med. |volume=6 |issue=1 |pages=1–5 |date=1978 |pmid=639524 |doi=10.1097/00003246-197801000-00001 |url=}}</ref>


====Contraindicated medications====
===Surgery===
{{MedCondContrAbs|MedCond = Increased intracranial pressure|Nitroglycerin}}
Surgical options for persistent intracranial hypertension include


==Low ICP==
*Surgical evacuation
*[[CSF]] drainage via [[ventriculostomy]]
**CSF is usually drained at a rate of 1 to 2 mL/minute for 2 to 3 minutes. The procedure is repeated after every 2 to 3 minutes, until ICP is less than 20mmHg
*[[Decompressive craniectomy]]<ref name="pmid3075392">{{cite journal |vauthors=Burkert W, Paver HD |title=[Decompressive trepanation in therapy refractory brain edema] |language=German |journal=Zentralbl. Neurochir. |volume=49 |issue=4 |pages=318–23 |date=1988 |pmid=3075392 |doi= |url=}}</ref><ref name="pmid2624017">{{cite journal |vauthors=Burkert W, Plaumann H |title=[The value of large pressure-relieving trepanation in treatment of refractory brain edema. Animal experiment studies, initial clinical results] |language=German |journal=Zentralbl. Neurochir. |volume=50 |issue=2 |pages=106–8 |date=1989 |pmid=2624017 |doi= |url=}}</ref><ref name="pmid3655895">{{cite journal |vauthors=Hatashita S, Hoff JT |title=The effect of craniectomy on the biomechanics of normal brain |journal=J. Neurosurg. |volume=67 |issue=4 |pages=573–8 |date=October 1987 |pmid=3655895 |doi=10.3171/jns.1987.67.4.0573 |url=}}</ref><ref name="pmid3336907">{{cite journal |vauthors=Hatashita S, Hoff JT |title=Biomechanics of brain edema in acute cerebral ischemia in cats |journal=Stroke |volume=19 |issue=1 |pages=91–7 |date=January 1988 |pmid=3336907 |doi=10.1161/01.str.19.1.91 |url=}}</ref><ref name="pmid2089950">{{cite journal |vauthors=Rinaldi A, Mangiola A, Anile C, Maira G, Amante P, Ferraresi A |title=Hemodynamic effects of decompressive craniectomy in cold induced brain oedema |journal=Acta Neurochir Suppl (Wien) |volume=51 |issue= |pages=394–6 |date=1990 |pmid=2089950 |doi=10.1007/978-3-7091-9115-6_132 |url=}}</ref><ref name="pmid477464">{{cite journal |vauthors=Gaab M, Knoblich OE, Fuhrmeister U, Pflughaupt KW, Dietrich K |title=Comparison of the effects of surgical decompression and resection of local edema in the therapy of experimental brain trauma. Investigation of ICP, EEG and cerebral metabolism in cats |journal=Childs Brain |volume=5 |issue=5 |pages=484–98 |date=1979 |pmid=477464 |doi=10.1159/000119844 |url=}}</ref><ref name="pmid8737804">{{cite journal |vauthors=Dam Hieu P, Sizun J, Person H, Besson G |title=The place of decompressive surgery in the treatment of uncontrollable post-traumatic intracranial hypertension in children |journal=Childs Nerv Syst |volume=12 |issue=5 |pages=270–5 |date=May 1996 |pmid=8737804 |doi=10.1007/BF00261809 |url=}}</ref><ref name="pmid3200370">{{cite journal |vauthors=Gower DJ, Lee KS, McWhorter JM |title=Role of subtemporal decompression in severe closed head injury |journal=Neurosurgery |volume=23 |issue=4 |pages=417–22 |date=October 1988 |pmid=3200370 |doi=10.1227/00006123-198810000-00002 |url=}}</ref><ref name="pmid9950487">{{cite journal |vauthors=Guerra WK, Gaab MR, Dietz H, Mueller JU, Piek J, Fritsch MJ |title=Surgical decompression for traumatic brain swelling: indications and results |journal=J. Neurosurg. |volume=90 |issue=2 |pages=187–96 |date=February 1999 |pmid=9950487 |doi=10.3171/jns.1999.90.2.0187 |url=}}</ref>


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.
===Prevention===


''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.<ref name=Paldino>{{cite journal |author=Paldino M, Mogilner AY, Tenner MS |title=Intracranial hypotension syndrome: a comprehensive review |journal=Neurosurg Focus |volume=15 |issue=6 |pages=ECP2 |year=2003 |month=December |pmid=15305844 |doi= 10.3171/foc.2003.15.6.8|url=}}</ref>
*Effective measures for the primary prevention of intracranial hypertension include early detection of underlying intracranial etiology such as tumor or congenital deformities.
*Once diagnosed and successfully treated, patients with intracranial hypertension are followed up every 6 months to 1 year with a head CT scan to prevent secondary complications.


==References==
==References==
Line 388: Line 790:
==Additional Resources==
==Additional Resources==


*Monroe A. Observations on the structure and function of the nervous system, Edinburgh: Creech & Johnson; 1783.  
*Monroe A. Observations on the structure and function of the nervous system, Edinburgh: Creech & Johnson; 1783.
*Kelly G. An account of the appearances observed in the dikssection of two of three individuals presumed to have perished in the storm of the 3rd, and whose bodies were deiscovered in the vicinity of the Leith on the morning of the 4th of November 1821, with some reflections on the pathology of the brain, Trans Med Chir Sci Edinb 1824;1:84–169.
*Kelly G. An account of the appearances observed in the dikssection of two of three individuals presumed to have perished in the storm of the 3rd, and whose bodies were deiscovered in the vicinity of the Leith on the morning of the 4th of November 1821, with some reflections on the pathology of the brain, Trans Med Chir Sci Edinb 1824;1:84–169.


==External links==
==External links==
*Gruen P. 2002. [http://uscneurosurgery.com/infonet/glossary/m/monro%20kellie%20model.htm "Monro-Kellie Model" Neurosurgery Infonet. USC Neurosurgery]. Accessed January 4, 2007.
*Gruen P. 2002. [http://uscneurosurgery.com/infonet/glossary/m/monro%20kellie%20model.htm "Monro-Kellie Model" Neurosurgery Infonet. USC Neurosurgery]. Accessed January 4, 2007.
*National Guideline Clearinghouse. 2005. [http://www.guideline.gov/summary/summary.aspx?doc_id=3794&nbr=003020&string=intracranial+AND+pressure Guidelines for the management of severe traumatic brain injury.] Firstgov. Accessed January 4, 2007.
*National Guideline Clearinghouse. 2005. [http://www.guideline.gov/summary/summary.aspx?doc_id=3794&nbr=003020&string=intracranial+AND+pressure Guidelines for the management of severe traumatic brain injury.] Firstgov. Accessed January 4, 2007.




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Intracranial pressure
Severely high ICP can cause herniation.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S., Sabeeh Islam, MBBS[2]

Overview

Intracranial pressure, (ICP), is the pressure exerted by three structures inside the cranium; brain parenchyma, CSF and blood. The norma ICP is 10-15 mmHg and is usually maintained by equilibrium of the intracranial contents. Intracranial hypertension ( IH), is elevation of the pressure in the cranium. It typically occurs when the ICP is >20 mmHg. Hans Queckenstedt's was the first person to use lumbar needle for ICP monitoring. Intracranial hypertension is generally categorized as acute or chronic. The Monro-Kellie hypothesis explains the relationship between the contents of the cranium and intracranial pressure. It explains the underlying pathophysiology of elevated intracranial pressure or intracranial hypertension. Several pathophysiologic mechanisms are thought to be involved in the pathogenesis of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH). All mechanisms eventually lead to brain injury from brain stem compression and decreased cerebral blood supply or ischemia. Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) must be differentiated from other diseases that cause headache, nausea, vomiting and neurologic deficits such as tumor, abscess or space occupying lesion, venous sinus thrombosis, neck surgery, Obstructive hydrocephalus, meningitis, subarachnoid hemorrhage, choroid plexus papilloma, and Malignant systemic hypertension. The diagnosis of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) is made when ICP is >20 mmHg. CT scan or MRI may be considered initial diagnostic investigations.  Intracranial hypertension is considered to be emergency condition.  Treatment includes resuscitative measures and specific directed therapy.  Resuscitative measures include oxygen, blood pressure and ICP monitoring, osmotic diuresis, head elevation up to 30 degrees, therapeutic hypothermia and seizure prophylaxis.

Historical Perspective

  • In 1950s, therapeutic hypothermia (goal core temperature of 32-34C) was first introduced as a treatment for brain injury. [1]
  • In early 1800s, the Monro-Kellie hypothesis and the CSF physiology was first introduced by Alexander Monro and George Kellie.
  • Hans Queckenstedt's was the first person to use lumbar needle for ICP monitoring.

Classification

  • Elevated intracranial pressure or Intracranial hypertension may be classified into two subtypes/groups:
  • Intracranial hypertension may also be classified as various stages:
    • Stage 1: Minimal increases in ICP due to compensatory mechanisms
    • Stage 2:
      • Any change in volume greater than 100–120 mL
      • Exhaustion of compensatory mechanisms
      • Compromise of neuronal oxygenation and systemic arteriolar vasoconstriction to increase MAP and CP
    • Stage 3:
      • Sustained increased ICP
      • Dramatic changes in ICP with small changes in volume
      • The ICP approaches the MAP

Intracranial pressure, (ICP), is the pressure exerted by three structures inside the cranium; brain parenchyma, CSF and blood. The norma ICP is 10-15 mmHg and is usually maintained by equilibrium of the intracranial contents.

Intracranial hypertension ( IH), is elevation of the pressure in the cranium. It typically occurs when the ICP is >20 mmHg.

Pathophysiology

Intracranial components and their proportions:

  • Brain parenchyma volume: 1400 ml (80%)[2]
  • CSF volume: 10 ml (10%)
  • Blood volume: 10 ml (10%)

The Monro-Kellie Hypothesis:

  • The Monro-Kellie hypothesis explains the relationship between the contents of the cranium and intracranial pressure. It explains the underlying pathophysiology of elevated intracranial pressure or intracranial hypertension.
  • In normal physiological state, intracranial contents (the brain tissue, the blood, and the cerebrospinal fluid) maintain an equilibrium state and keep the ICP within normal range by acting as compensatory mechanisms for small volume changes.[3]
  • Compensatory mechanisms are being exhausted by large volume changes, eventually causing significantly elevated intracranial pressures and potential herniation.[4]

Intracranial compliance:

  • There is an inverse relationship between intracranial components and the compliance.
  • Generally the normal compliance is maintained by compensatory mechanisms such as
    • Increased CSF reabsorption via thecal sac
    • Increased venoconstriction to decrease cerebral venous flow
    • Decreased cerebral venous flow via increased extracranial drainage

Cerebral Blood Flow (Ohm's Law):

  • Cerebral blood flow is generally assessed by subtracting jugular venous pressure from carotid arterial pressure and dividing by cerebrovascular resistance, as follows:[5][6][7]
    • CBF = (CAP - JVP) ÷ CVR
    • Cerebral perfusion is assessed by cerebral perfusion pressure (CPP). CPP is calculated by subtracting ICP from mean arterial pressure, as follows:
    • CPP = MAP - ICP[8]
    • In normal physiological states, ICP and CPP is maintained by autoregulation.[4]

Several pathophysiologic mechanisms are thought to be involved in the pathogenesis of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH). All mechanisms eventually lead to brain injury from brain stem compression and decreased cerebral blood supply or ischemia. These mechanisms are as follows:

    • Mass effect
    • Cerebral edema or Generalized brain swelling
    • Increase in venous pressure
      • Secondary to venous sinus thrombosis, heart failure, neck surgery or obstruction of superior mediastinal or jugular veins.
    • Obstruction to CSF flow
      • Secondary to hydrocephalus, extensive meningeal disease (e.g., infectious, carcinomatous, granulomatous, or hemorrhagic), or obstruction in cerebral convexities and superior sagittal sinus (decreased absorption).
    • Increased CSF production
      • Meningitis, subarachnoid hemorrhage, or choroid plexus tumor.
    • Increased cerebral blood flow (CBF)
      • Increased CBF is generally seen in conditions associated with hypercapnia and hypoxia
    • Drugs
    • Idiopathic


Causes

Common Causes

Differential Diagnosis of Increased Intracranial Pressure (ICP)

Differentiating Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) from Other Diseases on the Basis of Seizure, Visual disturbance, and Constitutional Symptoms

On the basis of seizure, visual disturbance, and constitutional symptoms, meningioma must be differentiated from oligodendroglioma, astrocytoma, hemangioblastoma, pituitary adenoma, schwannoma, primary CNS lymphoma, medulloblastoma, ependymoma, craniopharyngioma, pinealoma, AV malformation, brain aneurysm, bacterial brain abscess, tuberculosis, toxoplasmosis, hydatid cyst, CNS cryptococcosis, CNS aspergillosis, and brain metastasis.

Diseases Clinical manifestations Para-clinical findings Gold
standard 		Additional findings
Symptoms Physical examination
Lab Findings MRI Immunohistopathology
Head-
ache 		Seizure Visual disturbance Constitutional Focal neurological deficit
Adult primary brain tumors
Meningioma
[10][11][12] 		+ +/− +/− − + −
  • Well circumscribed
  • Extra-axial mass
  • Whorled spindle cell pattern
  • May be associated with NF-2
Glioblastoma multiforme
[13][14][15] 		+ +/− +/− − + −
  • Pseudopalisading appearance
Oligodendroglioma
[16][17][18] 		+ + +/− − + −
  • Chicken wire capillary pattern
  • Fried egg cell appearance
Hemangioblastoma
[19][20][21][22] 		+ +/− +/− − + −
Pituitary adenoma
[23][24][15] 		− − + Bitemporal hemianopia − −
  • It is associated with MEN1 disease.
Schwannoma
[25][26][27][28] 		− − − − + −
  • Split-fat sign
  • Fascicular sign
  • Often have areas of hemosiderin
  • S100+
Primary CNS lymphoma
[29][30] 		+ +/− +/− − + −
  • Single mass with ring enhancement
Childhood primary brain tumors
Pilocytic astrocytoma
[31][32][33] 		+ +/− +/− − + −
Medulloblastoma
[34][35][36] 		+ +/− +/− − + −
  • Homer wright rosettes
Ependymoma
[37][15] 		+ +/− +/− − + −
  • Hydrocephalus
  • Causes an unusually persistent, continuous headache in children.
Craniopharyngioma
[38][39][40][15] 		+ +/− + Bitemporal hemianopia − +
Pinealoma
[41][42][43] 		+ +/− +/− − + vertical gaze palsy
  • May cause prinaud syndrome (vertical gaze palsy, pupillary light-near dissociation, lid retraction and convergence-retraction nystagmus
Vascular
AV malformation
[44][45][15] 		+ + +/− − +/− −
Brain aneurysm
[46][47][48][49][50] 		+ +/− +/− − +/− −
  • MRA and CTA
Infectious
Bacterial brain abscess
[51][52] 		+ +/− +/− + +
  • Central hypodense signal and surrounding ring-enhancement in T1
  • Central hyperintense area surrounded by a well-defined hypointense capsule with surrounding edema in T2
  • History/ imaging
Tuberculosis
[53][15][54] 		+ +/− +/− + +
  • Lab data/ Imaging
Toxoplasmosis
[55][56] 		+ +/− +/− − +
  • History/ imaging
Hydatid cyst
[57][15] 		+ +/− +/− +/− +
  • Imaging
CNS cryptococcosis
[58] 		+ +/− +/− + +
  • We may see numerous acutely branching septate hyphae
  • Lab data/ Imaging
CNS aspergillosis
[59] 		+ +/− +/− + +
  • Multiple abscesses
  • Ring enhancement
  • Peripheral low signal intensity on T2
  • We may see numerous acutely branching septate hyphae
  • Lab data/ Imaging
Other
Brain metastasis
[60][15] 		+ +/− +/− + + −
  • Based on the primary cancer type we may have different immunohistopathology findings.
  • History/ imaging

ABBREVIATIONS

CNS=Central nervous system, AV=Arteriovenous, CSF=Cerebrospinal fluid, NF-2=Neurofibromatosis type 2, MEN-1=Multiple endocrine neoplasia, GFAP=Glial fibrillary acidic protein, HIV=Human immunodeficiency virus, BhCG=Human chorionic gonadotropin, ESR=Erythrocyte sedimentation rate, AFB=Acid fast bacilli, MRA=Magnetic resonance angiography, CTA=CT angiography

Epidemiology and Demographics

  • The prevalence of intracranial hypertension is approximately 1.0 per 100,000 individuals worldwide.

Gender

  • Idiopathic ICH is more prevalent among women of childbearing age.

Risk Factors

  • Common risk factors in the development of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) include underlying pathologies such as; mass lesions, abscesses, and hematomas.
  • Other risk factors include

Natural History, Complications and Prognosis

  • Early clinical features include nausea, vomiting, and confusion.
  • If left untreated, patients may progress to have severe neurologic consequences such as brain herniation, brain death, respiratory depression, brain infections, coma and death.
  • Common complications of intracranial hypertension include brain herniation and neurologic deficits.

Diagnosis

Diagnostic Criteria

  • The diagnosis of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) is made when ICP is >20 mmHg.

History and Symptoms

  • Symptoms of elevated intracranial pressure may include the following:

Physical Examination

  • Physical examination may be remarkable for

Laboratory Findings

  • There are no specific laboratory findings associated with Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH).

Electrocardiogram

  • There are no ECG findings associated with Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH).

X-ray

  • There are no x-ray findings associated with Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH).

CT scan

  • CT scan may be helpful in the diagnosis of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH).
  • Findings on CT scan suggestive of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) include presence of mass lesions, midline shift or hemorrhage.
  • CT scan is particularly helpful for people with acute rise in ICP.

MRI

  • MR venography (MRV) is preferred over MRI for the diagnosis of cerebral venous thrombosis
  • MRI has a greater sensitivity to detect subtle intracranial masses (eg, gliomatosis cerebri) and meningeal-based pathologies and should be done if no contraindications (eg, pacemakers, metallic clips in head, metallic foreign bodies) present

Other Diagnostic Studies

Other diagnostic studies for Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) include invasive and non-invasive ICP monitoring, particularly preferred in patients with no CT or MRI findings, at risk of developing increased ICP, and comatosed.

Treatment

Medical Therapy

  • The management of intracranial hypertension is generally directed towards treating the cause/etiology of the raised intracranial pressure.
  • Intracranial hypertension is considered a medical emergency and the management includes emergent resuscitative as well as specific treatment.

Resuscitation:

General principles for resuscitation include:[83][84][85][86][87][88][89]

  • Maintain oxygen
  • Head elevation
  • Hyperventilation to achieve a PaCO2 of 26-30 mmHg
  • Osmotic diuresis with intravenous mannitol and Lasix
  • Appropriate sedation, if patient requires intubation. Propofol is considered to be the preferred agent.
  • Therapeutic hypothermia to achieve a low metabolic state
  • Appropriate choice of fluids to achieve euvolemic state. Avoid hypotonic agents
  • Allow permissive hypertension. Treat hypertension only when CPP >120 mmHg and ICP >20 mmHg
  • Seizure prophylaxis with anticonvulsant therapy.[90]


Other therapies for intracranial hypertension:

  • Osmotic diuresis can be achieved by hypertonic saline bolus or mannitol. Hypertonic saline is usually considered to be more effective compared to mannitol for acute ICP reduction. Mannitol can be given as a bolus of 1 g/kg when prepared as 20% solution. The dose is usually repeated every 6-8 hours. It should be used cautiously in patients with renal insufficiency. Intravenous Lasix (0.5 to 1 mg/kg) is usually given with mannitol.[91][92]
  • Glucocorticoids are usually preferred when the underlying etiologies brain tumor are underlying CNS infection. Their use is contraindicated in head injury, cerebral infarction and intracranial hemorrhage.[93]
  • Phenobarbital is considered to have a neuroprotective effect by decreasing brain metabolism. It is given as a loading dose of 5 to 20 mg/kg, followed by 1 to 4 mg/kg per hour. EEG monitoring is used to guide therapy. A burst suppression seen on EEG indicates maximal dosing.[94]

Surgery

Surgical options for persistent intracranial hypertension include

Prevention

  • Effective measures for the primary prevention of intracranial hypertension include early detection of underlying intracranial etiology such as tumor or congenital deformities.
  • Once diagnosed and successfully treated, patients with intracranial hypertension are followed up every 6 months to 1 year with a head CT scan to prevent secondary complications.

References

  1. ↑ Welch K (May 1980). "The intracranial pressure in infants". J. Neurosurg. 52 (5): 693–9. doi:10.3171/jns.1980.52.5.0693. PMID 7373397.
  2. ↑ Whedon JM, Glassey D (2009). "Cerebrospinal fluid stasis and its clinical significance". Altern Ther Health Med. 15 (3): 54–60. PMC 2842089. PMID 19472865.
  3. ↑ Bruce DA, Alavi A, Bilaniuk L, Dolinskas C, Obrist W, Uzzell B (February 1981). "Diffuse cerebral swelling following head injuries in children: the syndrome of "malignant brain edema"". J. Neurosurg. 54 (2): 170–8. doi:10.3171/jns.1981.54.2.0170. PMID 7452330.
  4. ↑ 4.0 4.1 Aldrich EF, Eisenberg HM, Saydjari C, Luerssen TG, Foulkes MA, Jane JA, Marshall LF, Marmarou A, Young HF (March 1992). "Diffuse brain swelling in severely head-injured children. A report from the NIH Traumatic Coma Data Bank". J. Neurosurg. 76 (3): 450–4. doi:10.3171/jns.1992.76.3.0450. PMID 1738026.
  5. ↑ Strandgaard S, Paulson OB (June 1989). "Cerebral blood flow and its pathophysiology in hypertension". Am. J. Hypertens. 2 (6 Pt 1): 486–92. doi:10.1093/ajh/2.6.486. PMID 2757806.
  6. ↑ Strandgaard S, Andersen GS, Ahlgreen P, Nielsen PE (1984). "Visual disturbances and occipital brain infarct following acute, transient hypotension in hypertensive patients". Acta Med Scand. 216 (4): 417–22. PMID 6516910.
  7. ↑ Enevoldsen EM, Jensen FT (May 1978). "Autoregulation and CO2 responses of cerebral blood flow in patients with acute severe head injury". J. Neurosurg. 48 (5): 689–703. doi:10.3171/jns.1978.48.5.0689. PMID 641549.
  8. ↑ Lassen NA, Agnoli A (October 1972). "The upper limit of autoregulation of cerebral blood flow--on the pathogenesis of hypertensive encepholopathy". Scand. J. Clin. Lab. Invest. 30 (2): 113–6. doi:10.3109/00365517209081099. PMID 4640619.
  9. ↑ Levin HS, Aldrich EF, Saydjari C, Eisenberg HM, Foulkes MA, Bellefleur M, Luerssen TG, Jane JA, Marmarou A, Marshall LF (September 1992). "Severe head injury in children: experience of the Traumatic Coma Data Bank". Neurosurgery. 31 (3): 435–43, discussion 443–4. doi:10.1227/00006123-199209000-00008. PMID 1407426.
  10. ↑ Zee CS, Chin T, Segall HD, Destian S, Ahmadi J (June 1992). "Magnetic resonance imaging of meningiomas". Semin. Ultrasound CT MR. 13 (3): 154–69. PMID 1642904.
  11. ↑ Shibuya M (2015). "Pathology and molecular genetics of meningioma: recent advances". Neurol. Med. Chir. (Tokyo). 55 (1): 14–27. doi:10.2176/nmc.ra.2014-0233. PMID 25744347.
  12. ↑ Begnami MD, Palau M, Rushing EJ, Santi M, Quezado M (September 2007). "Evaluation of NF2 gene deletion in sporadic schwannomas, meningiomas, and ependymomas by chromogenic in situ hybridization". Hum. Pathol. 38 (9): 1345–50. doi:10.1016/j.humpath.2007.01.027. PMC 2094208. PMID 17509660.
  13. ↑ Sathornsumetee S, Rich JN, Reardon DA (November 2007). "Diagnosis and treatment of high-grade astrocytoma". Neurol Clin. 25 (4): 1111–39, x. doi:10.1016/j.ncl.2007.07.004. PMID 17964028.
  14. ↑ Pedersen CL, Romner B (January 2013). "Current treatment of low grade astrocytoma: a review". Clin Neurol Neurosurg. 115 (1): 1–8. doi:10.1016/j.clineuro.2012.07.002. PMID 22819718.
  15. ↑ 15.0 15.1 15.2 15.3 15.4 15.5 15.6 15.7 Mattle, Heinrich (2017). Fundamentals of neurology : an illustrated guide. Stuttgart New York: Thieme. ISBN 9783131364524.
  16. ↑ Smits M (2016). "Imaging of oligodendroglioma". Br J Radiol. 89 (1060): 20150857. doi:10.1259/bjr.20150857. PMC 4846213. PMID 26849038.
  17. ↑ Wesseling P, van den Bent M, Perry A (June 2015). "Oligodendroglioma: pathology, molecular mechanisms and markers". Acta Neuropathol. 129 (6): 809–27. doi:10.1007/s00401-015-1424-1. PMC 4436696. PMID 25943885.
  18. ↑ Kerkhof M, Benit C, Duran-Pena A, Vecht CJ (2015). "Seizures in oligodendroglial tumors". CNS Oncol. 4 (5): 347–56. doi:10.2217/cns.15.29. PMC 6082346. PMID 26478444.
  19. ↑ Lonser RR, Butman JA, Huntoon K, Asthagiri AR, Wu T, Bakhtian KD, Chew EY, Zhuang Z, Linehan WM, Oldfield EH (May 2014). "Prospective natural history study of central nervous system hemangioblastomas in von Hippel-Lindau disease". J. Neurosurg. 120 (5): 1055–62. doi:10.3171/2014.1.JNS131431. PMC 4762041. PMID 24579662.
  20. ↑ Hussein MR (October 2007). "Central nervous system capillary haemangioblastoma: the pathologist's viewpoint". Int J Exp Pathol. 88 (5): 311–24. doi:10.1111/j.1365-2613.2007.00535.x. PMC 2517334. PMID 17877533.
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  22. ↑ Perks WH, Cross JN, Sivapragasam S, Johnson P (March 1976). "Supratentorial haemangioblastoma with polycythaemia". J. Neurol. Neurosurg. Psychiatry. 39 (3): 218–20. PMID 945331.
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Additional Resources

  • Monroe A. Observations on the structure and function of the nervous system, Edinburgh: Creech & Johnson; 1783.
  • Kelly G. An account of the appearances observed in the dikssection of two of three individuals presumed to have perished in the storm of the 3rd, and whose bodies were deiscovered in the vicinity of the Leith on the morning of the 4th of November 1821, with some reflections on the pathology of the brain, Trans Med Chir Sci Edinb 1824;1:84–169.

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