Intracranial pressure

Severely high ICP can cause herniation.

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

## Overview

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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

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* 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

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* 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

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#### Intracranial components and their proportions:

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

#### The Monro-Kellie Hypothesis:

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* 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:

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* 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):

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* 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

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### Common Causes

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* Aneurysm
* Arnold-chiari malformation
* Behçet's disease
* Brain tumor
* Cerebral edema
* Cerebral venous sinus thrombosis
* Choroid plexus tumor
* Chronic kidney disease
* Colloid cyst of third ventricle
* Contusions
* Crouzon craniofacial dysostosis
* Cushing's syndrome
* Dural arteriovenous fistula
* Encephalitis
* Epidural haemorrhage
* Epidural hematoma
* Erdheim-chester disease
* Excess cerebrospinal fluid
* Head trauma
* Hydrocephalus
* Hypertensive brain hemorrhage
* Hypertensive encephalopathy
* Idiopathic intracranial hypertension
* Insulin like growth factor 1
* Intracranial granuloma
* Intracranial haemorrhage
* Intraventricular hemorrhage
* Meningioma
* Meningitis
* Meningoencephalitis
* Multiple hamartoma syndrome
* Obstruction of superior mediastinal veins
* Obstruction of jugular veins
* Status epilepticus
* Stroke
* Subarachnoid haemorrhage
* Subdural haemorrhage
* Subdural hematoma
* Vasculitis
* Venous sinus thrombosis

## Differential Diagnosis of Increased Intracranial Pressure (ICP)

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* 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

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

Diseases  | Clinical manifestations | Para-clinical findings  | Gold
standard | Additional findings

|
|
|
|

Symptoms | Physical examination
Lab Findings  | MRI  | Immunohistopathology
Head-
ache  | Seizure  | Visual disturbance  | Constitutional  | Focal neurological deficit
Adult primary brain tumors
Meningioma
[10][11][12] | \+  | +/−  | +/−  | −  | \+  | −  |

* Well circumscribed
* Extra-axial mass

* 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

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

### Gender

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

## Risk Factors

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* 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

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* 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

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### Diagnostic Criteria

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

### History and Symptoms

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* 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

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* 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

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

### Electrocardiogram

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

### X-ray

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

### CT scan

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* 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

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* 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

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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]
* Intraventricular[69][70]
* Intraparenchymal[71][72][73]
* Subarachnoid[68]
* Epidural[68][74]
* 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

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### Medical Therapy

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* 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:

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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:

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* 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

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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

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* 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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1. ↑ Welch K (May 1980). "The intracranial pressure in infants". J. Neurosurg. 52 (5): 693–9. doi:10.3171/jns.1980.52.5.0693. PMID 7373397.
2. ↑ Whedon JM, Glassey D (2009). "Cerebrospinal fluid stasis and its clinical significance". Altern Ther Health Med. 15 (3): 54–60. PMC 2842089. PMID 19472865.
3. ↑ Bruce DA, Alavi A, Bilaniuk L, Dolinskas C, Obrist W, Uzzell B (February 1981). "Diffuse cerebral swelling following head injuries in children: the syndrome of "malignant brain edema"". J. Neurosurg. 54 (2): 170–8. doi:10.3171/jns.1981.54.2.0170. PMID 7452330.
4. ↑ 4.0 4.1 Aldrich EF, Eisenberg HM, Saydjari C, Luerssen TG, Foulkes MA, Jane JA, Marshall LF, Marmarou A, Young HF (March 1992). "Diffuse brain swelling in severely head-injured children. A report from the NIH Traumatic Coma Data Bank". J. Neurosurg. 76 (3): 450–4. doi:10.3171/jns.1992.76.3.0450. PMID 1738026.
5. ↑ Strandgaard S, Paulson OB (June 1989). "Cerebral blood flow and its pathophysiology in hypertension". Am. J. Hypertens. 2 (6 Pt 1): 486–92. doi:10.1093/ajh/2.6.486. PMID 2757806.
6. ↑ Strandgaard S, Andersen GS, Ahlgreen P, Nielsen PE (1984). "Visual disturbances and occipital brain infarct following acute, transient hypotension in hypertensive patients". Acta Med Scand. 216 (4): 417–22. PMID 6516910.
7. ↑ Enevoldsen EM, Jensen FT (May 1978). "Autoregulation and CO2 responses of cerebral blood flow in patients with acute severe head injury". J. Neurosurg. 48 (5): 689–703. doi:10.3171/jns.1978.48.5.0689. PMID 641549.
8. ↑ Lassen NA, Agnoli A (October 1972). "The upper limit of autoregulation of cerebral blood flow--on the pathogenesis of hypertensive encepholopathy". Scand. J. Clin. Lab. Invest. 30 (2): 113–6. doi:10.3109/00365517209081099. PMID 4640619.
9. ↑ Levin HS, Aldrich EF, Saydjari C, Eisenberg HM, Foulkes MA, Bellefleur M, Luerssen TG, Jane JA, Marmarou A, Marshall LF (September 1992). "Severe head injury in children: experience of the Traumatic Coma Data Bank". Neurosurgery. 31 (3): 435–43, discussion 443–4. doi:10.1227/00006123-199209000-00008. PMID 1407426.
10. ↑ Zee CS, Chin T, Segall HD, Destian S, Ahmadi J (June 1992). "Magnetic resonance imaging of meningiomas". Semin. Ultrasound CT MR. 13 (3): 154–69. PMID 1642904.
11. ↑ Shibuya M (2015). "Pathology and molecular genetics of meningioma: recent advances". Neurol. Med. Chir. (Tokyo). 55 (1): 14–27. doi:10.2176/nmc.ra.2014-0233. PMID 25744347.
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## Additional Resources

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* 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

[edit | edit source]

* 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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