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	Intracranial pressure;
	Severely high ICP can cause herniation.

VisualWikitext

Latest revision as of 04:14, 29 August 2020

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:

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%)^[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
  - It can occur secondary to brain tumor, contusions, subdural or epidural hematoma, or abscess^[9]
- 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

Causes

Common Causes

Differential Diagnosis of Increased Intracranial Pressure (ICP)

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.

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.

	Symptoms				Physical examination	Lab Findings	MRI	Immunohistopathology
Diseases	Clinical manifestations					Para-clinical findings			Gold standard	Additional findings
	Symptoms				Physical examination	Para-clinical findings
	Head- ache	Seizure	Visual disturbance	Constitutional	Focal neurological deficit	Lab Findings	MRI	Immunohistopathology
Adult primary brain tumors
Meningioma ^[10]^[11]^[12]	+	+/−	+/−	−	+	−	Well circumscribed Extra-axial mass Dural attachment CSF vascular cleft sign Sunburst appearance of the vessels	Arachnoid origin Psammoma bodies Whorled spindle cell pattern	Biopsy	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 NF-2
Glioblastoma multiforme ^[13]^[14]^[15]	+	+/−	+/−	−	+	−	Supratentorial Irregular ring-nodular enhancing lesions Central necrosis Surrounding vasogenic edema Cross corpus callosum (butterfly glioma)	Astrocyte origin Pleomorphic cell Pseudopalisading appearance GFAP + Necrosis + Hemorrhage + Vascular prolifration +	Biopsy	Highest incidence in fifth and sixth decades of life Most of the time, focal neurological deficit is the presenting sign.
Oligodendroglioma ^[16]^[17]^[18]	+	+	+/−	−	+	−	Almost always in cerebral hemisphers (frontal lobes) Hypointense on T1 Hyperintense on T2 Calcification Chicken wire capillary pattern	Oligodendrocyte origin Calcification + Fried egg cell appearance	Biopsy	Highest incidence is between 40 and 50 years of age. Most of the time, epileptic seizure is the presenting sign.
Hemangioblastoma ^[19]^[20]^[21]^[22]	+	+/−	+/−	−	+	−	Infratentorial Cystic lesion with a solid enhancing mural nodule	Blood vessel origin Capillaries with thin walls	Biopsy	Might secret erythropoietin and cause polycythemia May be associated with von hippel-lindau syndrome
Pituitary adenoma ^[23]^[24]^[15]	−	−	+ Bitemporal hemianopia	−	−	Endocrine abnormalities as a result of functional adenomas or pressure effect of non-functional adenomas	Isointense to normal pituitary gland in T1	Endocrine cell hyperplasia	Biopsy	It is associated with MEN1 disease. Initialy presents with upper bitemporal quadrantanopsia followed by bitemporal hemianopsia (pressure on optic chiasma from below)
Schwannoma ^[25]^[26]^[27]^[28]	−	−	−	−	+	−	Split-fat sign Fascicular sign Often have areas of hemosiderin	Schwann cell origin S100+	Biopsy	It causes hearing loss and tinnitus May be associated with NF-2 (bilateral schwannomas)
Primary CNS lymphoma ^[29]^[30]	+	+/−	+/−	−	+	−	Usually deep in the white matter Single mass with ring enhancement	B cell origin Similar to non hodgkin lymphoma (diffuse large B cell)	Biopsy	Usually in young immunocompromised patients (HIV) or old immunocompetent person.
Childhood primary brain tumors
Pilocytic astrocytoma ^[31]^[32]^[33]	+	+/−	+/−	−	+	−	Infratentorial Solid and cystic component Mostly in posterior fossa Usually in cerebellar hemisphers and vermis	Glial cell origin Solid and cystic component GFAP +	Biopsy	Most of the time, cerebellar dysfunction is the presenting signs.
Medulloblastoma ^[34]^[35]^[36]	+	+/−	+/−	−	+	−	Infratentorial Mostly in cerebellum Non communicating hydrocephalus	Neuroectoderm origin Homer wright rosettes	Biopsy	Drop metastasis (metastasis through CSF)
Ependymoma ^[37]^[15]	+	+/−	+/−	−	+	−	Infratentorial Usually found in 4th ventricle Mixed cystic/solid lesion Hydrocephalus	Ependymal cell origin Perivascular pseudorosette	Biopsy	Causes an unusually persistent, continuous headache in children.
Craniopharyngioma ^[38]^[39]^[40]^[15]	+	+/−	+ Bitemporal hemianopia	−	+	Hypopituitarism as a result of pressure effect on pituitary gland	Calcification Lobulated contour Motor-oil like fluid within tumor	Ectodermal origin (Rathkes pouch) Calcification +	Biopsy	Initialy presents with lower bitemporal quadrantanopsia followed by bitemporal hemianopsia (pressure on optic chiasma from above)
Pinealoma ^[41]^[42]^[43]	+	+/−	+/−	−	+ vertical gaze palsy	B-hCG rise leads to precocious puberty in males	Hydrocephalus (compression of cerebral aqueduct)	Similar to testicular seminoma	Biopsy	May cause prinaud syndrome (vertical gaze palsy, pupillary light-near dissociation, lid retraction and convergence-retraction nystagmus
Vascular
AV malformation ^[44]^[45]^[15]	+	+	+/−	−	+/−	−	Supratentorial: ~85% Flow voids on T2 weighted images	We do not perform biopsy for AVM	Angiography	We may see bag of worms appearance in CT angiography
Brain aneurysm ^[46]^[47]^[48]^[49]^[50]	+	+/−	+/−	−	+/−	−	In magnetic resonance angiography, we may see aneurysm mostly in anterior circulation (~85%)	We do not perform biopsy for brain aneurysm	MRA and CTA	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 MRA and CTA)
Infectious
Bacterial brain abscess ^[51]^[52]	+	+/−	+/−	+	+	Leukocytosis Elevated ESR Blood culture may be positive for underlying organism	Central hypodense signal and surrounding ring-enhancement in T1 Central hyperintense area surrounded by a well-defined hypointense capsule with surrounding edema in T2	We do not perform biopsy for brain abscess	History/ imaging	The most common causes of brain abscess are Streptococcus and Staphylococcus.
Tuberculosis ^[53]^[15]^[54]	+	+/−	+/−	+	+	Positive acid-fast bacilli (AFB) smear in CSF specimen Positive CSF nucleic acid amplification testing Hyponatremia (inappropriate secretion of antidiuretic hormone) Mild anemia Leukocytosis	Hydrocephalus combined with marked basilar meningeal enhancement	We do not perform biopsy for brain tuberculosis	Lab data/ Imaging	It is associated with HIV infection
Toxoplasmosis ^[55]^[56]	+	+/−	+/−	−	+	Normal CSF	Multifocal masses with ring enhancement Mostly in basal ganglia, thalami, and corticomedullary junction.	We do not perform biopsy for brain toxoplasmosis	History/ imaging	It is associated with HIV infection
Hydatid cyst ^[57]^[15]	+	+/−	+/−	+/−	+	Positive serology (Antibody detection for E. granulosus)	Honeycomb appearance Necrotic area	We do not perform biopsy for hydatid cysts	Imaging	Brain, eye, and splenic cysts may not produce detectable amount of antibodies
CNS cryptococcosis ^[58]	+	+/−	+/−	+	+	Positive CSF antigen testing (coccidioidomycosis) CSF lymphocytic pleocytosis Elevated CSF proteins and lactate Low CSF glucose	Dilated perivascular spaces Basal ganglia pseudocysts Soap bubble brain lesions (cryptococcus neoformans)	We may see numerous acutely branching septate hyphae	Lab data/ Imaging	It is the most common brain fungal infection It is associated with HIV, immunosuppressive therapies, and organ transplants In may happen in immunocompetent patients undergoing invasive procedures ( neurosurgery) or exposed to contaminated devices or drugs Since brain biopsies are highly invasive and may may cause neurological deficits, we diagnose CNS fungal infections based on laboratory and imaging findings
CNS aspergillosis ^[59]	+	+/−	+/−	+	+	Positive galactomannan antigen testing (aspergillosis) CSF lymphocytic pleocytosis Elevated CSF proteins and lactate Low CSF glucose	Multiple abscesses Ring enhancement Peripheral low signal intensity on T2	We may see numerous acutely branching septate hyphae	Lab data/ Imaging	It is associated with HIV, immunosuppressive therapies, and organ transplants In may happen in immunocompetent patients undergoing invasive procedures ( neurosurgery) or exposed to contaminated devices or drugs Since brain biopsies are highly invasive and may may cause neurological deficits, we diagnose CNS fungal infections based on laboratory and imaging findings
Other
Brain metastasis ^[60]^[15]	+	+/−	+/−	+	+	−	Multiple lesions Vasogenic edema	Based on the primary cancer type we may have different immunohistopathology findings.	History/ imaging	Most common primary 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

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
- Obesity
- Chronic hypertension
- Women of childbearing age

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:

Headache
Nausea
Vomiting
Hyperventilation (due to injury to brain stem or tegmentum is damaged.^[61]
Changes in your behavior
Weakness or problems with moving or talking
Lack of energy or sleepiness
Seizure

Physical Examination

Physical examination may be remarkable for

Ocular palsies (abducens palsy)
Periorbital bruising^[62]
Altered level of consciousness
Papilledema^[63]
Pupillary dilatation
Cushing's triad ( Elevated systolic blood pressure, a widened pulse pressure, bradycardia, and an abnormal respiratory pattern.
Cheyne-Stokes respiration
Bulging of fontanels in infants

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.

Invasive ICP monitoring usually involves 4 anatomic sites:^[64]^[65]^[66]^[67]^[68]
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:^[75]^[76]
- Transcranial Doppler (TCD)^[77]
- Tissue resonance analysis (TRA)^[78]
- Ocular sonography^[79]^[80]
- Intraocular pressure^[81]^[82]
- Tympanic membrane displacement

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

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^[95]^[96]^[97]^[98]^[99]^[100]^[101]^[102]^[103]

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

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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.

External links

Gruen P. 2002. "Monro-Kellie Model" Neurosurgery Infonet. USC Neurosurgery. Accessed January 4, 2007.
National Guideline Clearinghouse. 2005. Guidelines for the management of severe traumatic brain injury. Firstgov. Accessed January 4, 2007.

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 }}
 {{SI}}
-{{CMG}} {{AE}} {{LRO}}
+{{CMG}} {{AE}} {{LRO}}, {{SAI}}
 ==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.
+'''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.
-== Historical Perspective[edit | edit source] ==
+==Historical Perspective==
-* [Disease name] was first discovered by [scientist name], a [nationality + occupation], in [year] during/following [event].
+*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 [year], [gene] mutations were first identified in the pathogenesis of [disease name].
+*In early 1800s, the Monro-Kellie hypothesis and the [[CSF]] physiology was first introduced by Alexander Monro and George Kellie.
-* In [year], the first [discovery] was developed by [scientist] to treat/diagnose [disease name].
+*Hans Queckenstedt's was the first person to use lumbar needle for ICP monitoring.
-== Classification[edit | edit source] ==
+==Classification==
-* Elevated intracranial pressure or Intracranial hypertension may be classified into two subtypes/groups:
+*Elevated intracranial pressure or Intracranial hypertension may be classified into two subtypes/groups:
-:* Acute
+:*[[Acute]]
-:* Chronic
+:*Chronic
-* Intracranial hypertension may also be classified as various stages:
+*Intracranial hypertension may also be classified as various stages:
-** Stage 1: Minimal increases in ICP due to compensatory mechanisms
+**Stage 1: Minimal increases in ICP due to compensatory mechanisms
-** Stage 2:
+**Stage 2:
-*** Any change in volume greater than 100–120 mL
+***Any change in volume greater than 100–120 mL
-*** Exhaustion of compensatory mechanisms
+***Exhaustion of compensatory mechanisms
-*** Compromise of neuronal oxygenation and systemic arteriolar vasoconstriction to increase MAP and CP
+***Compromise of [[neuronal]] oxygenation and systemic arteriolar vasoconstriction to increase MAP and CP
-** Stage 3:
+**Stage 3:
 ***Sustained increased ICP
 ***Dramatic changes in ICP with small changes in volume
-***The ICP approaches the MAP,
+***The ICP approaches the MAP
-===Increased ICP:===
 '''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: ===
 '''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: ====
+====Intracranial components and their proportions:====
-* Brain parenchyma volume: 1400 ml (80%)
+*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%)
+*[[CSF]] volume: 10 ml (10%)
-* Blood volume: 10 ml (10%)
+*Blood volume: 10 ml (10%)
-==== The Monro-Kellie Hypothesis: ====
+====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
+*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
+*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
+*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: ====
+====Intracranial compliance:====
-* There is an inverse relationship between  intracranial components and the compliance.
+*There is an inverse relationship between  intracranial components and the compliance.
-* Generally the normal compliance is maintained by compensatory mechanisms such as
+*Generally the normal compliance is maintained by compensatory mechanisms such as
-** Increased CSF reabsorption via thecal sac
+**Increased [[CSF]] reabsorption via thecal sac
-** Increased venoconstriction to decrease cerebral venous flow
+**Increased venoconstriction to decrease cerebral venous flow
-** Decreased cerebral venous flow via increased  extracranial drainage
+**Decreased cerebral venous flow via increased  extracranial drainage
-==== Cerebral Blood Flow (Ohm's Law): ====
+====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:
+*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
+**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:
+**Cerebral perfusion is assessed by cerebral perfusion pressure (CPP). CPP is calculated by subtracting ICP from mean arterial pressure, as follows:
-** CPP = MAP - ICP
+**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.
+**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>
 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'''
-***It can occur secondary to brain tumor, contusions, subdural or epidural hematoma, or abscess
+***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, hypercarbia, and hepatocerebral syndrome.
+***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.
+***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).
+***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.
+***[[Meningitis]], subarachnoid hemorrhage, or choroid plexus tumor.
-** Increased cerebral blood flow (CBF)
+**Increased cerebral blood flow (CBF)
-*** Increased CBF is generally seen in conditions associated with hypercapnia and hypoxia
+***Increased CBF is generally seen in conditions associated with hypercapnia and hypoxia
 **'''Drugs'''
 ***[[Albendazole]], [[Ciprofloxacin]]
-** Idiopathic
+**Idiopathic
-*** Pseudotumor cerebri
+***[[Pseudotumor cerebri]]
 <br />
 ==Causes==
 ===Common Causes===
 *[[Aneurysm ]]
 *[[Arnold-chiari malformation]]
@@ Line 144: / Line 145: @@
 ==Differential Diagnosis of Increased Intracranial Pressure (ICP)==
+*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]].
+=== 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 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
+|-
+| colspan="4" rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Symptoms'''
+! rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Physical examination
+|-
+! rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Lab Findings
+! rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |MRI
+! 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
+|-
+! colspan="11" style="background: #7d7d7d; color: #FFFFFF; padding: 5px; text-align: center;" |Adult primary brain tumors
+|-
+| 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>
+| 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;" |
+* 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]]
+|-
+| 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>
+| 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;" |
+* [[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]].
+|-
+| 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>
+| 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;" |
+* 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]].
+|-
+| 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>
+| 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;" |
+* [[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]]
+|-
+| 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" />
+| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
+| 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)
+*
+*
+|-
+| 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>
+| 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;" |
+* 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]])
+|-
+| 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>
+| 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;" |
+* Usually deep in the [[white matter]]
+* Single [[mass]] with ring enhancement
+| style="background: #F5F5F5; padding: 5px;" |
+* [[B cell]] origin
-* [Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as:
+* 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.
-:* [Differential dx1]
+*
-:* [Differential dx2]
+|-
-:* [Differential dx3]  <br />
+! colspan="11" style="background: #7d7d7d; color: #FFFFFF; padding: 5px; text-align: center;" |Childhood primary brain tumors
-:
+|-
+| 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>
+| 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;" |
+* [[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]].
+|-
+| 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>
+| 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;" |
+* [[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]])
+|-
+| 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" />
+| 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;" |
+* [[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.
+|-
+| 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" />
+| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
+| 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)
+|-
+| 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>
+| 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;" | + 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]]
+|-
+! colspan="11" style="background: #7d7d7d; color: #FFFFFF; padding: 5px; text-align: center;" |Vascular
+|-
+| 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" />
+| 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;" |
+* [[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]]
+|-
+| 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>
+| 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;" |
+* 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]])
+|-
+! colspan="11" style="background: #7d7d7d; color: #FFFFFF; padding: 5px; text-align: center;" |Infectious
+|-
+| 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>
+| 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;" |
+* [[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]].
+|-
+| 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>
+| 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;" |
+* 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]]
+|-
+| 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>
+| 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;" |
+* 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]]
+|-
+| 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" />
+| 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: 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]]
+|-
+| 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>
+| 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;" |
+* 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
+|-
+| 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>
+| 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;" |
+* 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
+|-
+! colspan="11" style="background: #7d7d7d; color: #FFFFFF; padding: 5px; text-align: center;" |Other
+|-
+| 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'''
+[[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]]
 ==Epidemiology and Demographics==
-* The prevalence of [disease name] is approximately [number or range] per 100,000 individuals worldwide.
-* In [year], the incidence of [disease name] was estimated to be [number or range] cases per 100,000 individuals in [location].
+*The prevalence of intracranial hypertension is approximately 1.0 per 100,000 individuals worldwide.
-===Age===
-*Patients of all age groups may develop [disease name].
-*[Disease name] is more commonly observed among patients aged [age range] years old.
-*[Disease name] is more commonly observed among [elderly patients/young patients/children].
 ===Gender===
-*[Disease name] affects men and women equally.
+*Idiopathic ICH is more prevalent among women of childbearing age.
-*[Gender 1] are more commonly affected with [disease name] than [gender 2].
-* The [gender 1] to [Gender 2] ratio is approximately [number > 1] to 1.
-===Race===
-*There is no racial predilection for [disease name].
-*[Disease name] usually affects individuals of the [race 1] race.
-*[Race 2] individuals are less likely to develop [disease name].
 ==Risk Factors==
-*Common risk factors in the development of raised intracranial pressure include underlying pathologies such as; mass lesions, abscesses, and hematomas.
-== Natural History, Complications and Prognosis==
+*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.
-*The majority of patients with [disease name] remain asymptomatic for [duration/years].
+*Other risk factors include
-*Early clinical features include [manifestation 1], [manifestation 2], and [manifestation 3].
+**[[Obesity]]
-*If left untreated, [#%] of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
+**[[Chronic hypertension]]
-*Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
+**Women of childbearing age
-*Prognosis is generally [excellent/good/poor], and the [1/5/10year mortality/survival rate] of patients with [disease name] is approximately [#%].
-== Diagnosis ==
+==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 [disease name] is made when at least [number] of the following [number] diagnostic criteria are met:
-:*[criterion 1]
+*The diagnosis of Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH) is made when ICP is >20 mmHg.
-:*[criterion 2]
-:*[criterion 3]
+===History and Symptoms===
-:*[criterion 4]
-=== History and Symptoms ===
 *Symptoms of elevated intracranial pressure may include the following:
@@ Line 205: / Line 693: @@
 :*Seizure
-=== Physical Examination ===
+===Physical Examination===
 *Physical examination may be remarkable for
-:*Ocular palsies (abducens (CrN VI) palsies)
+:*Ocular palsies (abducens palsy)
-:* Altered level of consciousness
+:*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>
-:*[[Papilledema]]
+:*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.
@@ Line 217: / Line 706: @@
 :*Bulging of [[fontanel]]s in infants
-=== Laboratory Findings ===
+===Laboratory Findings===
-*There are no specific laboratory findings associated with [disease name].
+*There are no specific laboratory findings associated with Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH).
-*A  [positive/negative] [test name] is diagnostic of [disease name].
-*An [elevated/reduced] concentration of [serum/blood/urinary/CSF/other] [lab test] is diagnostic of [disease name].
-*Other laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].
 ===Electrocardiogram===
-There are no ECG findings associated with [disease name].
-OR
+*There are no ECG findings associated with Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH).
-An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
 ===X-ray===
-There are no x-ray findings associated with [disease name].
-OR
+*There are no x-ray findings associated with Increased Intracaranial pressure (ICP) or Intracranial hypertension (ICH).
-An x-ray may be helpful in the diagnosis of [disease name]. Findings on an x-ray suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
-OR
-There are no x-ray findings associated with [disease name]. However, an x-ray may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
-===Echocardiography or Ultrasound===
-There are no echocardiography/ultrasound  findings associated with [disease name].
-OR
-Echocardiography/ultrasound  may be helpful in the diagnosis of [disease name]. Findings on an echocardiography/ultrasound suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
-OR
-There are no echocardiography/ultrasound  findings associated with [disease name]. However, an echocardiography/ultrasound  may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
 ===CT scan===
-There are no CT scan findings associated with [disease name].
-OR
+*[[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.
-[Location] CT scan may be helpful in the diagnosis of [disease name]. Findings on CT scan suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
+===MRI===
-OR
+*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
-There are no CT scan findings associated with [disease name]. However, a CT scan may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
+===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.
-===MRI===
+*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>
-There are no MRI findings associated with [disease name].
+**[[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
-OR
+==Treatment==
+===Medical Therapy===
-[Location] MRI may be helpful in the diagnosis of [disease name]. Findings on MRI suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
+*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.
-OR
+====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>
-There are no MRI findings associated with [disease name]. However, a MRI may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
+*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>
-===Other Imaging Findings===
+<br />
-There are no other imaging findings associated with [disease name].
-OR
-[Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
+====Other therapies for intracranial hypertension:====
-===Other Diagnostic Studies===
+*[[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>
-There are no other diagnostic studies associated with [disease name].
-OR
+*[[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>
-[Diagnostic study] may be helpful in the diagnosis of [disease name]. Findings suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
+===Surgery===
+Surgical options for persistent intracranial hypertension include
-OR
+*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>
-Other diagnostic studies for [disease name] include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].
+===Prevention===
-== Treatment ==
+*Effective measures for the primary prevention of intracranial hypertension include early detection of underlying intracranial etiology such as tumor or congenital deformities.
-=== Medical Therapy ===
+*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.
-*There is no treatment for [disease name]; the mainstay of therapy is supportive care.
-*The mainstay of therapy for [disease name] is [medical therapy 1] and [medical therapy 2].
-*[Medical therapy 1] acts by [mechanism of action 1].
-*Response to [medical therapy 1] can be monitored with [test/physical finding/imaging] every [frequency/duration].
-=== Surgery ===
-*Surgery is the mainstay of therapy for [disease name].
-*[Surgical procedure] in conjunction with [chemotherapy/radiation] is the most common approach to the treatment of [disease name].
-*[Surgical procedure] can only be performed for patients with [disease stage] [disease name].
-=== Prevention ===
-*There are no primary preventive measures available for [disease name].
-*Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
-*Once diagnosed and successfully treated, patients with [disease name] are followed-up every [duration]. Follow-up testing includes [test 1], [test 2], and [test 3].
-==Treatment==
 ==References==
 {{Reflist|2}}
@@ Line 318: / Line 790: @@
 ==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.
 ==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.
 *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.


Intracranial pressure
Severely high ICP can cause herniation.