Intracranial Hypertension

Continuing Education Activity

Intracranial hypertension is a spectrum of neurological disorders where cerebrospinal fluid (CSF) pressure within the skull is elevated. Normal CSF pressure varies by age. In general, CSF pressure above 250 mm H20 in adults and above 200 mm H2O in children signifies increased intracranial pressure (ICP). It may be idiopathic or arise as a result of neurologic insult or injury. This activity reviews the evaluation and treatment of intracranial hypertension and the role of the medical team in evaluating and treating this condition.


  • Review the most common causes of intracranial hypertension.
  • Outline the frequency of intracranial hypertension in the highest risk patients.
  • Summarize the most common signs and symptoms of intracranial hypertension.
  • Review the importance of improving care coordination among medical team members to improve outcomes for individuals with intracranial hypertension.


Intracranial hypertension is a spectrum of neurological disorders where cerebrospinal fluid (CSF) pressure within the skull is elevated. Normal CSF pressure varies by age. In general, CSF pressure above 250 mm H20 in adults and above 200 mm H2O in children signifies increased intracranial pressure (ICP). It may be idiopathic or arise as a result of neurologic insult or injury.[1][2][3][4]


The human skull is a relatively fixed volume structure of approximately 1400 to 1700 mL. Physiologically its components consist of 80% brain parenchyma, 10% cerebrospinal fluid, and 10% blood. Since the skull is considered an unchangeable volume, any increase in the volume of components within the skull or an addition of a pathologic element will result in increased pressure within the skull. Pathologic structures that can cause increased ICP may include mass lesions, abscesses, and hematomas. 

The physiologic volume of the brain parenchyma is a relatively constant value in adults: however, it may be adjusted by mass lesions or in the setting of cerebral edema. Cerebral edema can occur with acute hypoxic encephalopathy, large cerebral infarction, and severe traumatic brain injury. CSF and blood volume in the intracranial space will vary on a regular basis as these are the primary regulators of intracranial pressure. CSF volume is primarily regulated via choroid plexus production at a rate of approximately 20 mL per hour physiologically and through its reabsorption at a similar rate by arachnoid granulations that drain into the venous system of the skull.  The control mechanisms for maintaining appropriate CSF pressures may become damaged in neurological injuries such as stroke or trauma. Increased CSF production above the rate at which it can be reabsorbed such as in the presence of a choroid plexus papilloma leads to increased pressure. 

A failure to reabsorb at a sufficient rate to match normal secretion rate is another possibility and is seen with arachnoid granulation adhesions after bacterial meningitis. Ventricular obstruction may also induce decreased reabsorption of CSF causing hydrocephalus. The primary regulator of blood volume is via cerebral blood flow. Diseases which obstruct venous outflows such as a venous sinus thrombosis, jugular vein compression, or structural changes due to neck surgery may cause blood congestion within the skull, thus increasing pressure. Idiopathic intracranial hypertension, also known as pseudotumor cerebri, is a term for increased intracranial pressure due to unknown causes with no known structural change.[2][5][6]

Etiology of intracranial hypertension can be divided into 2 categories:

Primary or Intracranial Causes

  • Trauma ( epidural hematoma, subdural hematoma, intracerebral hemorrhage or contusions)
  • Brain tumors
  • Stroke
  • Nontraumatic intracerebral Hemorrhage ( aneurysm rupture)
  • Idiopathic or benign intracranial hypertension
  • Hydrocephalus
  • Meningitis

Secondary or Extracranial Causes

  • Hypoventilation (hypoxia or hypercarbia)
  • Hypertension
  • Airway obstruction
  • Metabolic (drug-induced)
  • Seizures
  • Hyperpyrexia
  • High altitude cerebral edema


The exact epidemiology of intracranial hypertension depends on its etiology. However, of special note is idiopathic intracranial hypertension where up to 90% of affected individuals are women of childbearing age. Individuals with chronic hypertension or obesity are also at an increased risk for developing intracranial hypertension. A frequency of occurrence has been established to be 1.0 per 100,000 in the general population, 1.6 to 3.5 per 100,000 in women, and 7.9 to 20 per 100,000 in women who are overweight.


Anytime there is an elevation in ICP, there is the risk of subsequent injury from direct brainstem compression or from a reduction in cerebral blood flow. Clinically, cerebral blood flow is evaluated via measurement of cerebral perfusion pressure where:

Cerebral perfusion pressure = Mean arterial pressure - Intracranial pressure

Cerebral perfusion pressure in simpler terms is the pressure of blood flowing to the brain and is the driving force for the delivery of oxygen necessary for neuronal functioning. Normally, this is a constant value of 50 to 100 mm Hg due to autoregulation. The impact that cerebral perfusion pressure holds is in the concept that blood flow will occur from an area of higher concentration to an area of lower concentration.  When ICP becomes elevated, cerebral perfusion pressures decrease, and the net driving force of blood flow to the brain becomes decreased.  The physiologic autoregulatory response to a decrease in cerebral perfusion pressure is to increase mean arterial pressures systemically and to vasodilate cerebral blood vessels. This results in increased cerebral blood volume that further increases ICP.  Paradoxically, this further reduces cerebral perfusion pressure producing a feedback cycle that results in the total reduction of cerebral flow and perfusion. The result of this feedback loop is cerebral ischemia and brain infarction with neuronal death. In cases where intracranial hypertension is the result of hemorrhage, increased blood pressure will worsen intracranial bleeding, thus worsening intracranial hypertension.

History and Physical

Symptoms of elevated intracranial hypertension are primarily derived from neurological irritation, compression, or displacement and papilledema. Non-specific headaches are recorded in almost all cases and are likely mediated via the pain fibers of the trigeminal nerve in the dura and blood vessels of the brain. Pain is generally diffuse and worse in the mornings with exacerbation by the Valsalva maneuver. Nausea and vomiting are common presentations of elevated ICP. Patients can present with double vision most frequently with horizontal diplopia associated with CN VI palsy from compression. Transient visual abnormalities occur frequently, often described as a gradual dimming of vision in one or both of the eyes. Visual abnormalities worsen with changes in posture. Peripheral visual loss may be reported and most commonly begins in the nasal inferior quadrant with subsequent loss of the central visual field.  Alterations in visual acuity with blurring or distortion may occur.  Variable degrees of loss of color distinction may occur. In more severe or chronic cases, a sudden visual loss can occur due to intraocular hemorrhage. Tinnitus with a pulsing rhythm exacerbated by supine or bending positions and Valsalva maneuvers can occur. Radicular pain, numbness, or paresthesias are possible and most commonly associated with localized compression or possible herniation of the brain. Neurological findings are indications of severe disease. The anatomical locations where herniation is most likely to occur include the subfalcine, central transtentorial, uncal transtentorial, cerebellar tonsillar/foramen magnum, and transcalvarial routes. These types of changes may lead to decreased consciousness or responsiveness. Focal neurological constellations depend on which region of the brain has herniated. Often this results in a stupor state or more severely with coma due to the local effect of mass lesions or pressure on the reticular formations of the midbrain. It may further lead to respiratory compromise.

Physical exam findings can vary widely depending on etiology. A change in mental status or comatose patient should prompt urgent evaluation. A complete neurological assessment is essential whenever intracranial hypertension is suspected. Cranial nerve assessment is particularly important for identifying lesions. Cranial nerve VI palsy is most common. Blunting of the pupillary reflex with fixed dilation of one pupil is also highly associated with herniation syndromes. Spontaneous periorbital bruising may be present as well. A classic triad of bradycardia, respiratory depression, and hypertension is known as Cushing's triad and is highly indicative of intracranial hypertension. Fundoscopic examination looking for retinal hemorrhages or papilledema is essential. Alterations in respiratory drive and effort may occur leading to failure of respiration and oxygenation.

Infants can have a widening of cranial sutures and bulging fontanelle.


Complete blood count (CBC) and complete metabolic panel (CMP) are usually checked in all patients with suspected intracranial hypertension to evaluate for infection, anemia, and electrolyte abnormalities. The initial evaluation should include a head CT scan. CT scan findings of cerebral edema such as compressed basal cisterns and midline shift are predictive of elevated ICP. However, the absence of these findings does not rule out intracranial hypertension. A head MRI is more accurate than head CT in evaluating elevated ICP and to looking for potential etiology. Bedside ultrasonography also can be used to measure the diameter of the optic nerve sheath to determine intracranial hypertension. However, this study is limited by operator skill and not frequently used. A lumbar puncture may sometimes be needed for diagnosis. However, it should be delayed until neuroimaging, especially in those with suspicion of impending herniation. When LP is performed, in addition to measuring opening pressures, CSF should also be tested for infection and other potential etiology. Invasive measurement of ICP is definitive for diagnosis and improves the physician’s ability to maintain adequate cerebral perfusion pressure (CPP). There are 4 main anatomical sites used for clinical measurement of intracranial pressure: intraventricular, intraparenchymal, subarachnoid, and epidural. Ventriculostomy catheter is preferred device for ICP monitoring and can be used even for therapeutic CSF drainage to lower ICP. When ventricles cannot be cannulated, intraparenchymal devices using microsensor and fibreoptic transducer may be used. Subdural and epidural monitors are not as accurate as ventriculostomy and parenchymal monitors.[7][8][9][10]

Treatment / Management

Treatment of chronic intracranial hypertension is mainly focused on treating and reversing the etiology.

A sudden increase in ICP is a neurosurgical emergency, requiring close monitoring in an intensive care unit (ICU) setting. For acute intracranial hypertension, a patient should first be stabilized with healthcare professionals aiming for hemodynamic stability, and preventing and treating factors that may aggravate or precipitate intracranial hypertension. These patients should have close monitoring of heart rate, blood pressure, body temperature, ventilation and oxygenation, blood glucose, input and output, and ECG. Patients with suspected intracranial hypertension, especially with severe traumatic brain injury, should also have ICP monitoring.[11][12][13]

It is vital to prevent and treat factors that may aggravate or precipitate intracranial hypertension. These interventions are used to buy time until the underlying etiology is identified and corrected.

  • Keep the head elevated to 30 degrees and neutrally positioned to minimize venous outflow resistance and improve cerebral spinal fluid displacement from the intracranial to the spinal compartment.
  • Hypoxia and hypercapnia can increase ICP. Controlling ICP through optimal respiratory management is crucial. It is essential to control ventilation to maintain a normal PaCO2 and maintain adequate oxygenation without increasing the PEEP.
  • Agitation and pain can increase blood pressure and ICP. Adequate sedation and analgesia is an important adjunctive treatment. Since most sedating medications can have effects on blood pressure, medications with a minimal hypotensive effect should be preferred. Hypovolemia can precipitate the hypotensive side effects and should be treated before administering sedative agents. Shorter-acting agents have the advantage of allowing brief interruption of sedation to evaluate neurological status.
  • Fever can increase brain metabolic rate and is a potent vasodilator, which in turn increases the cerebral blood flow and leads to an increased ICP. Fever should be controlled with antipyretics and cooling blankets and infectious causes must be ruled out.
  • Elevated blood pressure is commonly seen in patients with intracranial hypertension especially when due to traumatic brain injury. In patients with untreated intracranial mass lesions, cerebral perfusion is maintained by the higher blood pressure, and systemic hypertension should not be treated. The absence of an intracranial mass lesion presents a more individualized, controversial decision when treating systemic hypertension. When antihypertensive are used, the preferred treatment includes beta-blockers like labetalol and esmolol or calcium channel blockers because they reduced blood pressure without affecting ICP. Agents with short half-lives should be preferred. Avoid vasodilators like sodium nitroprusside, nitroglycerin, and nifedipine.
  • Seizures can contribute and complicate elevated ICP and should be prevented by prophylactic medications, especially in severe traumatic brain injuries.

For patients with sustained intracranial hypertension, additional measures are needed to control the ICP.  

  • Emergent surgical management should be considered when there is sudden intracranial hypertension, or it is refractory to medical management.
  • Nondepolarizing muscle relaxants along with sedatives may be used to treat intracranial hypertension caused by posturing, coughing or agitation. When a neuromuscular blockade is used, EEG should be monitored to rule out convulsive states.
  • Hyperosmolar therapy is used for severe, acute intracranial hypertension.

Mannitol is commonly used as a hyperosmolar agent and is usually given as a bolus of 0.25 to 1 g/kg body weight. Serum osmolality should be kept less than 320 mOsm to avoid side effects of therapy like renal failure, hypokalemia, and hypo-osmolarity.

Hypertonic saline can also create an osmotic shift from the interstitial space of brain parenchyma into the intravascular compartment in the presence of an intact blood-brain barrier. Hypertonic saline has an advantage over mannitol for hypovolemic and hypotensive patients. The adverse effects of hypertonic saline administration include hematological and electrolyte abnormalities. Hyponatremia should be excluded before administering hypertonic saline to reduce the risk of central pontine myelinolysis.

  • Hyperventilation can be used for a rapid reduction in ICP if there are clinical signs of herniation or with severe intracranial hypertension. Hyperventilation decreases PaCO2 which causes vasoconstriction of cerebral arteries, resulting in reduced cerebral blood flow and reduced intracranial pressure.
  • Barbiturate coma should be considered for patients with refractory intracranial hypertension.
  • Routine induction of hypothermia is not indicated; however, moderate hypothermia may be an effective adjunctive treatment for increased ICP refractory to other medical management.
  • Steroids are commonly used for primary and metastatic brain tumors to decrease vasogenic cerebral edema. For other neurosurgical disorders like traumatic brain injury or spontaneous intracerebral hemorrhage, steroids have not been shown to have a benefit, and sometimes may even be detrimental.

Surgical Interventions

  • Resection of intracranial mass lesions producing elevated ICP should be done as soon as possible.
  • CSF drainage lowers ICP immediately by reducing intracranial volume. This modality can be an important adjunct treatment for lowering ICP. However, it has limited utility when the brain is diffusely swollen and the ventricles are collapsed.
  • Decompressive craniectomy is used to treat severe uncontrolled intracranial hypertension. It involves surgical removal of part of the calvaria to create a window in the skull, allowing for herniation of swollen brain through the bone window to relieve pressure.

Differential Diagnosis

  • Acute nerve injury
  • Benign intracranial hypertension (Pseudotumor cerebri)
  • Cerebrovascular ischemia/hemorrhage
  • Hydrocephalus
  • Intracranial epidural abscess
  • Intracranial hemorrhage
  • Leptomeningeal carcinoma
  • Low-grade astrocytoma
  • Lyme disease
  • Meningioma
  • Meningitis
  • Migraine headache
  • Papilledema
  • Subarachnoid hemorrhage
  • Venous sinus thrombosis


Prognosis is highly variable depending on etiology and varies from benign to lethal. Children usually can tolerate higher intracranial pressure (ICP) for a longer period.

Enhancing Healthcare Team Outcomes

The management of intracranial hypertension is with an interprofessional team consisting of a neurologist, neurosurgeon, intensivist, ICU nurses, internist, and a pulmonologist. Treatment of chronic intracranial hypertension is mainly focused on treating and reversing the etiology. These patients need ICU admission and continuous monitoring. In addition, the patients  should have close monitoring of heart rate, blood pressure, body temperature, ventilation and oxygenation, blood glucose, input and output, and ECG. Patients with suspected intracranial hypertension, especially with severe traumatic brain injury, should also have ICP monitoring. In patients in whom the intracranial pressure is short-lived and treated promptly, the prognosis is good but in those patients with delay in treatment or a malignant cause, the prognosis is abysmal. even those who survive develop permanent neurological deficits.[14][15](Level V)

Article Details

Article Author

Sandeep Sharma

Article Author

Muhammad Hashmi

Article Editor:

Anil Kumar


5/7/2021 1:26:07 PM



O'Reilly MW,Westgate CS,Hornby C,Botfield H,Taylor AE,Markey K,Mitchell JL,Scotton WJ,Mollan SP,Yiangou A,Jenkinson C,Gilligan LC,Sherlock M,Gibney J,Tomlinson JW,Lavery GG,Hodson DJ,Arlt W,Sinclair AJ, A unique androgen excess signature in idiopathic intracranial hypertension is linked to cerebrospinal fluid dynamics. JCI insight. 2019 Feb 12;     [PubMed PMID: 30753168]


Zanon E,Pasca S, Intracranial haemorrhage in children and adults with haemophilia A and B: a literature review of the last 20 years. Blood transfusion = Trasfusione del sangue. 2019 Feb 4;     [PubMed PMID: 30747705]


Mondragon J,Klovenski V, Pseudotumor Cerebri 2018 Jan;     [PubMed PMID: 30725609]


Stevens SM,McClelland CM,Chen JJ,Lee MS, Idiopathic Intracranial Hypertension in a Mother and Pre-pubertal Twins. Neuro-ophthalmology (Aeolus Press). 2019 Feb;     [PubMed PMID: 30723525]


Baracchini C,Farina F,Pieroni A,Palmieri A,Kulyk C,Viaro F,Gabrieli JD,Cester G,Causin F,Manara R, Ultrasound identification of patients at increased risk of intracranial hemorrhage after successful endovascular recanalization for acute ischemic stroke. World neurosurgery. 2019 Feb 8;     [PubMed PMID: 30743030]


Ma YH,Leng XY,Dong Y,Xu W,Cao XP,Ji X,Wang HF,Tan L,Yu JT, Risk factors for intracranial atherosclerosis: A systematic review and meta-analysis. Atherosclerosis. 2018 Dec 23;     [PubMed PMID: 30658194]


Sun S,Li Y,Zhang H,Wang X,She L,Yan Z,Lu G, The effect of mannitol in the early stage of supratentorial hypertensive intracerebral hemorrhage: a systematic review and meta-analysis. World neurosurgery. 2018 Dec 18;     [PubMed PMID: 30576817]


McHugh DC,Fiore SM,Strong N,Egnor MR, Bifrontal Biparietal Cruciate Decompressive Craniectomy in Pediatric Traumatic Brain Injury. Pediatric neurosurgery. 2019 Jan 3;     [PubMed PMID: 30605902]


Sheikh MF,Unni N,Agarwal B, Neurological Monitoring in Acute Liver Failure. Journal of clinical and experimental hepatology. 2018 Dec;     [PubMed PMID: 30568346]


Godoy DA,Núñez-Patiño RA,Zorrilla-Vaca A,Ziai WC,Hemphill JC 3rd, Intracranial Hypertension After Spontaneous Intracerebral Hemorrhage: A Systematic Review and Meta-analysis of Prevalence and Mortality Rate. Neurocritical care. 2018 Dec 18;     [PubMed PMID: 30565090]


Jha RM,Kochanek PM, A Precision Medicine Approach to Cerebral Edema and Intracranial Hypertension after Severe Traumatic Brain Injury: Quo Vadis? Current neurology and neuroscience reports. 2018 Nov 7;     [PubMed PMID: 30406315]


Hoffmann J,Mollan SP,Paemeleire K,Lampl C,Jensen RH,Sinclair AJ, European headache federation guideline on idiopathic intracranial hypertension. The journal of headache and pain. 2018 Oct 8;     [PubMed PMID: 30298346]


Alali AS,Temkin N,Barber J,Pridgeon J,Chaddock K,Dikmen S,Hendrickson P,Videtta W,Lujan S,Petroni G,Guadagnoli N,Urbina Z,Chesnut RM, A clinical decision rule to predict intracranial hypertension in severe traumatic brain injury. Journal of neurosurgery. 2018 Sep 1;     [PubMed PMID: 30265194]


Sacco TL,Davis JG, Management of Intracranial Pressure Part II: Nonpharmacologic Interventions. Dimensions of critical care nursing : DCCN. 2019 Mar/Apr;     [PubMed PMID: 30702474]


Pal A,Sengupta P,Biswas D,Sen C,Mukherjee A,Pal S, Pattern of Idiopathic Intracranial Hypertension in Indian Population. Annals of Indian Academy of Neurology. 2019 Jan-Mar;     [PubMed PMID: 30692759]