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Brain Herniation

By

Kenneth Maiese

, MD, National Heart, Lung, and Blood Institute

Last full review/revision Sep 2020| Content last modified Sep 2020
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Topic Resources

Brain herniation occurs when increased intracranial pressure causes the abnormal protrusion of brain tissue through openings in rigid intracranial barriers (eg, tentorial notch).

Because the skull is rigid after infancy, intracranial masses or swelling may increase intracranial pressure, sometimes causing protrusion (herniation) of brain tissue through one of the rigid intracranial barriers (tentorial notch, falx cerebri, foramen magnum). When intracranial pressure is increased sufficiently, regardless of the cause, Cushing reflex and other autonomic abnormalities can occur. Cushing reflex includes systolic hypertension with increased pulse pressure, irregular respirations, and bradycardia.

Brain herniation is life threatening.

Brain herniation is classified based on the structure through which tissue is herniated. Types include the following (see figure Brain herniation):

  • Transtentorial (uncal)

  • Subfalcine

  • Central

  • Upward transtentorial

  • Tonsillar

Brain herniation

Increased intracranial pressure sometimes causes protrusion (herniation) of brain tissue through one of the rigid intracranial barriers (tentorial notch, falx cerebri, foramen magnum).

Brain herniation is classified based on the structure through which tissue is herniated:

  • Transtentorial (uncal) herniation: The medial temporal lobe is squeezed by a unilateral mass across and under the tentlike tentorium that supports the temporal lobe.

  • Subfalcine herniation: The cingulate gyrus is pushed under the falx cerebri by an expanding mass high in a cerebral hemisphere.

  • Central herniation: Both temporal lobes herniate through the tentorial notch because of bilateral mass effects or diffuse brain edema.

  • Upward transtentorial herniation: This type can occur when an infratentorial mass (eg, tumor in the posterior fossa, cerebellar hemorrhage) compresses the brain stem, kinking it and causing patchy brain stem ischemia.

  • Tonsillar herniation: Usually, the cause is an expanding infratentorial mass (eg, cerebellar hemorrhage), forcing the cerebellar tonsils, through the foramen magnum.

Brain herniation

Transtentorial herniation

The medial temporal lobe is squeezed by a unilateral mass across and under the tentlike tentorium that supports the temporal lobe. The herniating lobe compresses the following structures:

  • Ipsilateral 3rd cranial nerve (often first) and posterior cerebral artery

  • As herniation progresses, the ipsilateral cerebral peduncle

  • In about 5% of patients, the contralateral 3rd cranial nerve and cerebral peduncle

  • Eventually, the upper brain stem and the area in or around the thalamus

Subfalcine herniation

The cingulate gyrus is pushed under the falx cerebri by an expanding mass high in a cerebral hemisphere. In this process, one or both anterior cerebral arteries become trapped, causing infarction of the paramedian cortex. As the infarcted area expands, patients are at risk of transtentorial herniation, central herniation, or both.

Central herniation

Both temporal lobes herniate through the tentorial notch because of bilateral mass effects or diffuse brain edema. Ultimately, brain death occurs.

Upward transtentorial herniation

Upward transtentorial herniation can occur when an infratentorial mass (eg, tumor in the posterior fossa, cerebellar hemorrhage) compresses the brain stem, kinking it and causing patchy brain stem ischemia. The posterior 3rd ventricle becomes compressed. Upward herniation also distorts the mesencephalon vasculature, compresses the veins of Galen and Rosenthal, and causes superior cerebellar infarction due to occlusion of the superior cerebellar arteries.

Tonsillar herniation

Usually, tonsillar herniation is caused by an expanding infratentorial mass (eg, cerebellar hemorrhage). The cerebellar tonsils, forced through the foramen magnum, compress the brain stem and obstruct cerebrospinal fluid (CSF) flow.

Etiology

Brain herniation is a complication of a disorder that causes increased intracranial pressure (ICP). Increased intracranial pressure may be caused by

  • Space-occupying lesions (eg, brain tumor, edema, or abscess; contusions; hematomas)

  • Generalized swelling or edema of the brain (eg, due to acute liver failure or hypertensive encephalopathy)

  • Increased venous pressure (eg, due to heart failure, obstruction of superior mediastinal or jugular veins, or venous sinus thrombosis)

  • Obstruction of the CSF flow (eg, due to hydrocephalus or extensive meningeal disease)

Symptoms and Signs

Symptoms and signs of brain herniation are listed in the table below. Usually, patients also have signs of the disorder causing herniation; these signs can be nonspecific (eg, impaired consciousness, lethargy).

Table
icon

Effects of Brain Herniation

Type of Herniation

Mechanism*

Findings

Transtentorial

Compression of ipsilateral 3rd cranial nerve

Unilateral dilated, fixed pupil

Oculomotor paresis

Compression of the posterior cerebral artery

Contralateral homonymous hemianopia

Absence of blinking in response to visual threat from the hemianopic side in obtunded patients

Compression of the contralateral 3rd cranial nerve and cerebral peduncle (indented by the tentorium to form Kernohan notch)

Contralateral dilated pupil and oculomotor paresis

Ipsilateral hemiparesis

Compression of the ipsilateral cerebral peduncle

Contralateral hemiparesis

Eventually, compression of the upper brain stem and the area in and around the thalamus

Impaired consciousness

Abnormal breathing patterns

Fixed, unequal pupils

Further compromise of the brain stem

Loss of oculocephalic reflex

Loss of oculovestibular reflex

Loss of corneal reflexes

Decerebrate posturing

Subfalcine (cingulate)

Trapping of one or both anterior cerebral arteries, causing infarction of the paramedian cortex

Contralateral leg paralysis

Expansion of infarcted area

Edema

Increased intracranial pressure

Increased risk of transtentorial herniation, central herniation, or both

Central

Bilateral, more or less symmetric damage to the midbrain

Pupils fixed in midposition

Decerebrate posturing

Many of the same symptoms as transtentorial herniation

Further compromise of the brain stem

Loss of all brain stem reflexes

Disappearance of decerebrate posturing

Cessation of respirations

Brain death

Upward transtentorial

Compression of the posterior 3rd ventricle

Hydrocephalus, which increases intracranial pressure

Distortion of the mesencephalon vasculature

Compression of the veins of Galen and Rosenthal

Superior cerebellar infarction due to occlusion of the superior cerebellar arteries

Early: Nausea, vomiting, occipital headache, ataxia

Later: Somnolence, breathing abnormalities, patchy and progressive loss of brain stem reflexes

Posterior fossa mass (eg, cerebellar hemorrhage)

Ataxia, dysarthria

Progressive brain stem compression

Increasing somnolence

Respiratory irregularities

Patchy but progressive loss of brain stem reflexes

Tonsillar

Compression of the brain stem

Obstruction of cerebrospinal fluid (CSF) flow

Acute hydrocephalus (with impaired consciousness, headache, vomiting, and meningismus)

Dysconjugate eye movements, nystagmus

Later, abrupt respiratory and cardiac arrest

* Not all mechanisms occur in every patient.

CNS = central nervous system.

Diagnosis

  • CT or MRI

After the patient is stabilized, brain imaging with CT or MRI is required to check for mass lesions and help identify displacement of brain tissue and the type of herniation.

Treatment

  • Immediate stabilization (airway, breathing, circulation, or ABCs)

  • Admission to an intensive care unit (ICU)

  • Supportive measures, including control of ICP

  • Treatment of underlying disorder

Treatment of brain herniation is similar to treatment of coma. The cause of brain herniation is treated when possible.

Hypotension must be corrected. Patients are admitted to the ICU so that respiratory and neurologic status can be monitored.

Patients must be stabilized. Airway, breathing, and circulation must be ensured immediately.

If increased ICP is suspected, intubation should be done via rapid-sequence oral intubation (using a paralytic drug) rather than via nasotracheal intubation; nasotracheal intubation in a patient who is breathing spontaneously causes more coughing and gagging, thus increasing ICP, which is already increased because of intracranial abnormalities.

If ICP is increased, intracranial and cerebral perfusion pressure should be monitored (see Intracranial Pressure Monitoring), and pressures should be controlled. The goal is to maintain ICP at ≤ 20 mm Hg and cerebral perfusion pressure at 50 to 70 mm Hg. Cerebral venous drainage can be enhanced (thus lowering ICP) by elevating the head of the bed to 30° and by keeping the patient’s head in a midline position.

  • Sedation: Sedatives may be necessary to control agitation, excessive muscular activity (eg, due to delirium), or pain, which can increase ICP.

  • Hyperventilation: Hyperventilation causes hypocapnia, which causes vasoconstriction, thus decreasing cerebral blood flow globally.

  • Hydration: Isotonic fluids are used. Providing free water through IV fluids (eg, 5% dextrose, 0.45% saline) can aggravate cerebral edema and should be avoided. Fluids may be restricted to some degree, but patients should be kept euvolemic. If patients have no signs of dehydration or fluid overload, IV fluids with normal saline can be started at 50 to 75 mL/h. The rate can be increased or decreased based on serum sodium, osmolality, urine output, and signs of fluid retention (eg, edema).

  • Diuretics: Serum osmolality should be kept at 295 to 320 mOsm/kg. Osmotic diuretics (eg, mannitol) may be given IV to lower ICP and maintain serum osmolality. These drugs do not cross the blood-brain barrier. They pull water from brain tissue across an osmotic gradient into plasma, eventually leading to equilibrium. Fluid and electrolyte balance should be monitored closely while osmotic diuretics are used. A 3% saline solution is another potential osmotic agent to control ICP.

  • Blood pressure (BP) control: Systemic antihypertensives are needed only when hypertension is severe (> 180/95 mm Hg). How much BP is reduced depends on the clinical context. Systemic BP needs to be high enough to maintain cerebral perfusion pressure even when ICP increases.

  • Corticosteroids: Corticosteroids are effective only for tumors and sometimes abscesses of the brain when vasogenic edema (due to disruption of the blood-brain barrier) is present. Corticosteroids are ineffective for cytotoxic edema (due to cell death and breakdown) and can increase plasma glucose, exacerbating cerebral ischemia.

  • Removal of cerebrospinal fluid (CSF): When ICP is increased, CSF can be removed at periodic intervals; it is removed slowly, at a reduced rate of 1 to 2 mL/minutes to help lower ICP.

  • Position: Positioning the patient to maximize venous outflow from the head can help minimize increases in ICP. The head of the bed can be elevated to 30° (with the head above the heart) as long as cerebral perfusion pressure remains at the desired range. The patient’s head should be kept in a midline position, and neck rotation and flexion should be minimized. Tracheal suctioning, which can increase ICP, should be limited.

If ICP continues to increase despite other measures to control it, the following may be used:

  • Titrated hypothermia: When ICP is increased after head trauma or cardiac arrest, hypothermia in the range of 32 to 35° C has been used to reduce ICP to < 20 mm Hg. However, use of hypothermia to lower ICP is controversial; some evidence (1) suggests that this treatment may not effectively lower ICP in adults or children and may have adverse effects.

  • Pentobarbital coma: Pentobarbital can reduce cerebral blood flow and metabolic demands. However, its use is controversial because the effect on clinical outcome is not consistently beneficial, and treatment with pentobarbital can lead to complications (eg, hypotension). In some patients with refractory intracranial hypertension that does not respond to standard hypercapnia and hyperosmolar therapy, pentobarbital can improve functional outcome.

  • Decompressive craniotomy: Craniotomy with duraplasty can be done to provide room for brain swelling. This procedure can prevent deaths, but overall functional outcome may not improve much, and it may lead to complications such as hydrocephalus in some patients (2). It may be most useful for large cerebral infarcts with impending herniation, particularly in patients < 50 yr.

Brain herniation due to tumors is treated with mannitol 25 to 100 g infused IV, a corticosteroid (eg, dexamethasone 16 mg IV, followed by 4 mg orally or IV every 6 hours), and endotracheal intubation. Hyperventilation to a carbon dioxide partial pressure (PCO2) of 26 to 30 mm Hg can help decrease ICP temporarily in emergencies. Mass lesions should be surgically decompressed as soon as possible.

Treatment references

  • 1. Moler FW, Silverstein FS, Holubkov R, et al: Therapeutic hypothermia after in-hospital cardiac arrest in children. N Engl J Med 376 (4):318-329, 2017. doi: 10.1056/NEJMoa1610493.

  • 2. Su TM, Lan CM, Lee TH, et al: Risk factors for the development of posttraumatic hydrocephalus after unilateral decompressive craniectomy in patients with traumatic brain injury. J Clin Neurosci 63:62-67, 2019. doi: 10.1016/j.jocn.2019.02.006. Epub 2019 Mar 1.

Key Points

  • Brain herniation results from increased intracranial pressure (ICP), which may be caused by space-occupying lesions, generalized swelling or edema of the brain, increased venous pressure, or obstruction of cerebrospinal flow (CSF) flow.

  • Specific symptoms vary based on which structures are compressed; patients also have impaired consciousness and other neurologic deficits caused by the disorder causing herniation.

  • After stabilizing the patient, do brain imaging.

  • Monitor and control ICP using sedatives, endotracheal intubation, hyperventilation, hydration, diuretics, measures to control blood pressure, and sometimes corticosteroids.

  • Treat the cause.

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