Brain herniation: causes, symptoms, diagnosis, treatment.


Overview of the Brain  and it’s CT Images

Brain herniation is also called Cerebral herniation, Brain herniation refers to displacement of a portion of the brain from its normal position through openings in the inelastic dura secondary to focal or diffuse intracranial pressure. Recognition of the CT signs of brain herniation on the emergent head CT is critical to proper patient management. The types of brain herniations are schematically illustrated.”:a) ” Subfalcial (cingulate) herniation ; b) uncal herniation ; c) downward (central, transtentorial) herniation ; d) external herniation ; e) tonsillar herniation.Types a, b, & e are usually caused by focal, ipsilateral space occupying lesions, ie., tumor or axial or extra-axial hemorrhage.”

The condition is usually caused by swelling from a head injury, stroke, bleeding, or brain tumor. A brain herniation is a medical emergency and requires immediate medical attention. It’s often fatal if not treated right away. Brain herniation is life threatening.


Types of brain herniation

Brain herniation is classified based on the structure through which tissue is herniated. Types include the following:
  • Transtentorial (uncal) herniation
  • Subfalcine herniation
  • Central herniation
  • Upward transtentorial herniation
  • Tonsillar herniation

Transtentorial (uncal) 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.

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.

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.

Symptoms and Signs

Symptoms and signs of brain herniation are:
  • dilated pupils
  • headache
  • drowsiness
  • difficulty concentrating
  • high blood pressure
  • loss of reflexes
  • seizures
  • abnormal posturing.
  • cardiac arrest
  • loss of consciousness
  • coma

Causes of brain herniation

A brain herniation is typically the result of swelling in the brain. The swelling puts pressure on brain tissues (referred to as increased intracranial pressure), causing the tissue to be forced away from its normal positon.
The most common causes of a brain herniation include:

  • head injury leading to a subdural hematoma (when blood collects on the brain’s surface beneath the skull) or swelling (cerebral edema)
  • stroke
  • brain hemorrhage (bleeding in the brain)
  • brain tumor
Other reasons for an increase in pressure in the skull include:
  • abscess (collection of pus) from a bacterial or fungal infection
  • buildup of fluid in the brain (hydrocephalus)
  • brain surgery
  • a defect in brain structure called Chiari malformation

Diagnosis brain herniation


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 brain herniation

  • 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.
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, incubation 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.

Measures to control Intracranial Pressure Monitoring (ICP) include

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


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